A Short Textbook of Psychiatry, 7Th Edition

A Short Textbook of PSYCHIATRY Every effort has been made to ensure that drug dosage schedules in this book are accurate and conform to the standards accepted at the time of publication. However, as recommendations for treatment vary in the light of continuing research and clinical experience, the reader is advised to verify drug dosage schedules contained in the product information sheets included in the package of each drug as well as Summary of Product Characteristics (SPC), before any drug is administered. It is the responsibility of the treating physician, relying on experience and knowledge about the patient, to determine the dose(s) and the best treatment for the patient. Neither the publisher nor the author assumes responsibility for any possible untoward consequences. A Short Textbook of PSYCHIATRY

Seventh Edition

Niraj Ahuja MBBS MD MRCPsych Consultant Psychiatrist Newcastle Upon Tyne, UK Formerly Associate Professor (Psychiatry) GB Pant Hospital and Associated Maulana Azad Medical College (MAMC) and Lok Nayak Hospital, New Delhi, India Formerly also at Department of Psychiatry Jawaharlal Institute of Postgraduate Medical Education and Research (JIPMER), Pondicherry Lady Hardinge Medical College (LHMC) and Smt. SK Hospital, New Delhi All India Institute of Medical Sciences (AIIMS), New Delhi, India

Contributing Editor Savita Ahuja MBBS DGO DFSRH DRCOG

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First Edition: 1990 Second Edition: 1992 Third Edition: 1995 Fourth Edition: 1999 Fifth Edition: 2002 Sixth Edition: 2006 Reprint: 2009 Seventh Edition: 2011 ISBN: 978-93-80704-66-1 Typeset at JPBMP typesetting unit Printed at For Manisha and Neha

Preface to the Seventh Edition

It is rather humbling to consider that it has been two decades that the Short Textbook of Psychiatry has enjoyed a wide distribution among the undergraduate medical students, interns, junior residents, postgraduate psychiatry students, nursing students, psychology and psychiatric social work students, occupational therapy and physi- otherapy students, general medical practitioners, other physicians and health professionals in India and some other countries. I am really indebted to the many astute readers who have provided a very constructive and useful feedback, along with encouraging comments regarding the existing format and the contents of the book. The seventh edition of the Short Textbook of Psychiatry has been once again extensively revised and updated. Signifi cant changes have been made in almost all the chapters, especially in chapters on diagnosis and classifi cation, psychoactive substance use disorders, psychopharmacology, schizophrenia, mood disorders and other biological methods of treatment. Coloured-shaded boxes have been added at various places in the text to highlight the important points in tables and fi gures. The chapter on psychiatric history and examination contains a summary of laboratory tests in psychiatry, in additions to other signifi cant changes. The appendices have been revised and contain a glossary of common psychiatric terms. The Short Textbook of Psychiatry sincerely hopes to retain its original aim of providing a brief yet comprehensive account of the psychiatric disorders and their allied aspects in a ‘user-friendly’ and ‘easy-to-follow’ manner. I am grateful to Shri Jitendar P Vij, Chairman and Managing Director, Jaypee Brothers Medical Publishers (P) Ltd for his exquisite control over the production and distribution of the Short Textbook of Psychiatry over the last 20 years. I hope you enjoy reading the book and I warmly welcome critical comments and constructive suggestions. Please send your comments by email to [email protected].

July 2010 Niraj Ahuja

Preface to the First Edition

Psychiatry, as a branch of Medicine, has been cold-shouldered by physicians for a long time. There are various reasons for such an attitude. But, the most important exposition is an unfamiliarity with the psychiatric disorders and their treatment. This is easy to understand in the light of the fact that an easily comprehensible, non-intimidating and concise text on psychiatry was not earlier available. Recently too, the various postgraduate entrance examinations have laid an increasing emphasis on psychiatry and its related branches. Keeping this in mind, the Medical Examination Review—Psychiatry (Multiple Choice Questions with Explanatory Answers) was written, the new edition of which appears this year. Its tremendous success during the last four years and encouraging suggestions from the readers have been a source of stimulation for drafting this text. The Short Textbook of Psychiatry aims to provide a brief yet comprehensive account of psychiatric disorders and their allied aspects. While striving to make the book simple and easy-to-follow, an attempt has been made to keep the book aligned to the most recent developments in classifi cation, terminology and treatment methods. The Short Textbook of Psychiatry is addressed to medical students, interested physicians and other health professionals. A postgraduate student in psychiatry will fi nd the text elementary and basic, although a fi rst year postgraduate will fi nd it useful for a broad introduction to the subject. I will like to put on record my deep appreciation for Shri Jitendar P Vij, Managing Director; Mr. Pawaninder Vij, Production Manager and their effi cient staff at the Jaypee Brothers Medical Publishers (P) Ltd, New Delhi for bringing out this volume in a short time. I welcome critical comments and constructive suggestions from the readers.

January 1990 Niraj Ahuja

Contents

1. Diagnosis and Classiﬁ cation in Psychiatry ...... 1 2. Psychiatric History and Examination ...... 5 3. Organic (Including Symptomatic) Mental Disorders ...... 19 4. Psychoactive Substance Use Disorders ...... 33 5. Schizophrenia ...... 54 6. Mood Disorders ...... 69 7. Other Psychotic Disorders ...... 83 8. Neurotic, Stress-related and Somatoform Disorders ...... 89 9. Disorders of Adult Personality and Behaviour ...... 113 10. Sexual Disorders ...... 121 11. Sleep Disorders ...... 133 12. Behavioural Syndromes Associated with Psychological Disturbances and Physiological Factors ...... 142 13. Mental Retardation ...... 153 14. Child Psychiatry ...... 162 15. Psychopharmacology ...... 172 16. Other Biological Methods of Treatment ...... 199 17. Psychoanalysis ...... 205 18. Psychological Treatments ...... 213 19. Emergency Psychiatry ...... 221 20. Legal and Ethical Issues in Psychiatry ...... 229 21. Community Psychiatry ...... 235 Appendices ...... 241 Appendix I: Nobel Prizes in Psychiatry and Allied Disciplines ...... 241 Appendix II: Some Important Contributors in Psychiatry ...... 242 Appendix III: Glossary of Some Important Terms in Psychiatry...... 246 Suggested Further Reading ...... 249 Index ...... 253 Diagnosis and Classification 1 in Psychiatry

Classifi cation is a process by which phenomena are DEFINITION OF A PSYCHIATRIC organized into categories so as to bring together those DISORDER phenomena that most resemble each other and to separate those that differ. Any classifi cation of psychiatric The simplest way to conceptualize a psychiatric disorders, like that of medical illnesses, should ideally disorder is a disturbance of Cognition (i.e. Thought), be based on aetiology. For a large majority of psychiat- Conation (i.e. Action), or Affect (i.e. Feeling), or any ric disorders, no distinct aetiology is known at present, disequilibrium between the three domains. However, although there are many attractive probabilities for this simple defi nition is not very useful in routine several of them. Therefore, one of the most rational clinical practice. ways to classify psychiatric disorders at present is Another way to defi ne a psychiatric disorder or probably syndromal. A syndrome is defi ned as a group mental disorder is as a clinically signifi cant psycho- of symptoms and signs that often occur together, and logical or behavioural syndrome that causes signifi cant delineate a recognisable clinical condition. (subjective) distress, (objective) disabi lity, or loss of The syndromal approach of classifying psychiat- freedom; and which is not merely a socially deviant ric disorders, on the basis of their clinical signs and behaviour or an expected response to a stressful life symptoms, is very similar to the historical approach event (e.g. loss of a loved one). Confl icts between of classifi cation of medical illnesses, when aetiology the society and the individual are not considered of a majority of medical illnesses was still obscure. psychiatric disorders. A psychiatric disorder should There are three major purposes of classifi cation be a manifestation of behavioural, psychological, and/ of psychiatric disorders: or biological dysfunction in that person (Defi ni tion 1. To enable communication regarding the diagnosis modifi ed after DSM-IV-TR, APA). of disorders, Although slightly lengthy, this defi nition defi nes 2. To facilitate comprehension of the underlying a psychiatric disorder more accurately. causes of these disorders, and 3. To aid prediction of the prognosis of psychiatric NORMAL MENTAL HEALTH disorders. This syndromal approach of classifi cation, in the According to the World Health Organization (WHO), absence of clearly known aetiologies, fulfi ls these Health is a state of comp lete physical, mental and purposes reasonably well. social well-being, and not merely absence of disease Before proceeding to look at current classifi cations or infi rmity. of psychiatric disorders, it is important to defi ne what Normal mental health, much like normal health, is is meant by the term, psychiatric disorder. a rather diffi cult concept to defi ne. There are several 2 A Short Textbook of Psychiatry models available for understanding what may consti- Table 1.1: Some Models of Normality in Mental Health tute ‘ normality’ (see Table 1.1). 1. Medical Model (Normality as Health): Normal men- Although, normality is not an easy concept to tal health is conceptualized as the absence of any defi ne, some of the following traits are more com- psychiatric disorder (‘disease’) or psycho pathology. monly found in ‘normal’ individuals. 2. Statistical Model (Normality as an Average): Statisti- 1. Reality orientation. cally normal mental health falls within two standard 2. Self-awareness and self-knowledge. deviations (SDs) of the normal distribution curve for 3. Self-esteem and self-acceptance. the population. 4. Ability to exercise voluntary control over their 3. Utopian Model (Normality as Utopia): In this model, behaviour. the focus in defi ning normality is on ‘optimal func- 5. Ability to form affectionate relationships. tioning’. 6. Pursuance of productive and goal-directive activi- 4. Subjective Model: According to this model, normality ties. is viewed as an absence of dis tress, disability, or any help-seeking behaviour resulting thereof. This defi ni- CLASSIFICATION IN PSYCHIATRY tion is similar in many ways to the medical model. 5. Social Model: A normal person, according to this defi nition, is expected to behave in a socially Like any growing branch of Medicine, Psychiatry has ‘acceptable’ behaviour. seen rapid changes in classifi cation to keep up with a 6. Process Model (Normality as a Process): This model conglomeration of growing research data dealing with views normality as a dynamic and changing process, epidemiology, symptoma tology, prognostic factors, rather than as a static concept. This model can be treatment methods and new theories for the causation combined with any other model mentioned here. of psychiatric disorders. 7. Continuum Model (Normality as a Conti nuum): Although fi rst attempts to classify psychiatric Normality and mental disorder are considered by disorders can be traced back to Ayurveda, Plato (4th this model as falling at the two ends of a continuum, century BC) and Asclepiades (1st century BC), clas- rather than being disparate entities. According to sifi cation in Psychiatry has certainly evolved ever this model, it is the severity (scores above the ‘cut- since. off’) that determines whether a particular person’s At present, there are two major classifi ca tions in experience constitutes a symptom of a disorder or Psychiatry, namely ICD-10 (1992) and DSM-IV-TR falls on the healthy side of the continuum. (2000). ICD-10 (International Classifi cation of Diseases, classifi cation of mental disorders. DSM-IV-TR is a 10th Revision, 1992) is World Health Organisation’s text revision of the DSM-IV which was originally classifi cation for all diseases and related health prob- published in 1994. lems (and not only psychiatric disorders). The next editions of ICD (ICD-11) and DSM Chapter ‘F’ classifi es psychiatric disorders as Men- (DSM-V) are likely to be available in the years tal and Behavioural Disorders (MBDs) and codes them 2012-14. on an alphanumeric system from F00 to F99. ICD-10 For the purpose of this book, it is intended to is now available in several versions, the most impor- follow the ICD-10 classifi cation. ICD-10 is easy to tant of which are listed in Table 1.2. There are several follow, has been tested extensively all over the world versions of ICD-10; some are listed in Table 1.3. (51 countries; 195 clinical centres), and has been found DSM-IV-TR (Diagnostic and Statistical Manual to be generally applicable across the globe. At some of Mental Disorders, IV Edition, Text Revision, 2000) places in the book, DSM-IV-TR diagnostic criteria are is the American Psychiatric Association (APA)’s also discussed, wherever appropriate. Diagnosis and Classification in Psychiatry 3

Table 1.2: Mental and Behavioural Disorders in ICD-10

1. F00-F09 Organic, Including Symptomatic, Mental such as eating disorders, non-organic sleep disor- Disorders, such as deli rium, dementia, organic am- ders, sexual dysfunctions (not caused by organic nestic syndrome, and other organic mental disorders. disorder or disease), mental and behavioural dis- 2. F10-F19 Mental and Behavioural Disorders due to orders associated with puerperium, and abuse of Psychoactive Substance Use, such as acute intoxica- non-dependence-producing substances. tion, harmful use, dependence synd rome, withdrawal 7. F60-F69 Disorders of Adult Personality and Behav- state, amnestic syndrome, and psycho tic disorders iour, such as specifi c personality disorders, enduring due to psychoactive substance use. personality changes, habit and impulse disorders, 3. F20-F29 Schizophrenia, Schizotypal and Delusional gender-identity disorders, disorders of sexual pre- Disorders, such as schizo phrenia, schizotypal dis- ference, and psychological and behavioural dis orders order, persistent delu sional disorders, acute and asso ciated with sexual development and orientation. transient psycho tic disorders, induced delusional 8. F70-F79 Mental Retardation, including mild, moder- disorder, and schizo-affective disorders. ate, severe, and profound mental retar dation. 4. F31-F39 Mood (Affective) Disorders, such as manic 9. F80-F89 Disorders of Psychological Development, episode, depressive episode, bipolar affective disor- such as specifi c developmental disorders of speech der, recurrent depressive disorder, and persistent and language, specifi c developmental disorders of mood disorder. scholastic skills, specifi c developmental dis orders 5. F40-F48 Neurotic, Stress-related and Somatoform of motor function, mixed specifi c develop mental Disorders (There is no category with code number disorders, and pervasive developmental disorders. F49), such as anxiety disorders, phobic anxiety 10. F90-F98 Behavioural and Emotional Disorders with disorders, obsessive-compulsive disorder, dissocia- Onset Usually Occurring in Childhood and Ado- tive (con ver sion) disorders, somatoform disorders, lescence, such as hyper kinetic disorders, conduct reaction to stress, and adjustment disorders, and disorders, mixed disorders of conduct and emotions, other neurotic disorders. tic disorders, and other disorders. 6. F50-F59 Behavioural Syndromes Associated with 11. F99 Unspecifi ed Mental Disorder Physiological Disturbances and Physical Factors,

The presence of a diagnostic hierarchy implied Table 1.3: Some Versions of ICD-10 that the conditions higher up in the hierarchy needed A. Clinical Descriptions and Diagnostic Guidelines to be considered fi rst, before making a diagnosis of (CDDG) those lower down in the hierarchy. For example, it was B. Diagnostic Criteria for Research (DCR) felt that a current diagnosis of organic mental disorder C. Multi-axial Classifi cation Version such as delirium would exclude a diagnosis of anxi- D. Primary Care Version ety disorder in presence of agitation; and alcohol and drug induced disorders would take precedence over a Earlier classifi cations in psychiatry were based on diagnosis of primary mood disorder. hierarchies of diagnoses with presence of a diagnosis The current classifi cations however encourage higher in the hierarchy usually ruling out a diagnosis recording of multiple diagnoses in a given patient (as lower in the hierarchy. This was felt to be in keeping co-morbidity) regardless of any hierarchy. Although with the teaching of Medicine at large at the time, a diagnostic hierarchy makes much clinical sense, where there was emphasis on making a single diag- consideration and recording of co-morbidity can be nosis of one disease rather than explaining different helpful in identifying more of patient’s needs; for symptoms by different disease entities. example, a diagnosis of co-morbid anxiety disorder 4 A Short Textbook of Psychiatry in a patient with bipolar disorder helps identify and Table 1.4: The Five Axes of DSM-IV-TR treat the anxiety component adequately. AXIS I: Clinical Psychiatric Diagnosis AXIS II: Personality Disorders and Mental Retardation MULTI-AXIAL CLASSIFICATION AXIS III: General Medical Conditions AXIS IV: Psychosocial and Environmental Problems The process of making a correct diagnosis is a very AXIS V: Global Assessment of Functioning: Current useful clinical exercise as evidence-based manage- and in past one year ment can be dependent on making a correct diagnosis. (Rated on a scale) However, sometimes making a clinical diagnosis can lead to labelling of patient and can be stigmatizing. This can also degrade the patient to “just another case” In this system, an individual patient is diagnosed on and does not direct attention to the whole individual. fi ve separate axes, ensuring a more through evaluation In the last few decades, there has been an upsurge of needs (see Table 1.4). of interest in multi-axial systems for achieving a This method helps in making a more holistic, more comprehensive description of an individual’s biopsychosocial assessment of an individual patient. clinical problems and needs. The pattern adopted by Recently, ICD-10 has also brought out its own multi- DSM-IV-TR is a very good example of this attempt. axial classifi cation version (see Table 1.3). Psychiatric History 2 and Examination

Familiarity with the technique of psychiatric assess- Table 2.1: Psychiatric vs Medical Interview ment is important not only for a psy chiatrist but A psychiatric interview can be different from a medical also for a medical practitioner or any mental health interview in several ways, some of which can include: professional, since more than one-third of medical 1. Presence of disturbances in thinking, behaviour and patients can present with psychiatric symptoms. emotions can interfere with meaningful communication INTERVIEW TECHNIQUE 2. Collateral information from signifi cant others can be really important In no other branch of Medicine is the history taking 3. Important to obtain detailed information of personal interview as important as in Psychiatry. All physicians history and pre-morbid personality need to communicate with their patients and a skilful 4. Need for more astute observation of patient’s behav- interview can clearly help in obtaining better informa- iour tion, making a more accurate diagnosis, establi shing 5. Diffi culty in establishing rapport may be encountered a better rapport with patients, and working towards more often better adherence with management plan. 6. Patients may lack insight into their illness and may A psychiatric interview is usually different from have poor judgement the rou tine medical interview in several ways (Table 7. Usually more important to elicit information regard- 2.1). A few important points regarding the interview ing stressors and social situation technique are mentioned below. These serve as pointers towards a technique which clearly has to During the interview session(s), the patient should be mastered over a period of time with repeated be put at ease and an empathic relationship should be examinations. established. A consistent scheme should be used each time for In psychiatric assessment, history taking interview recording the interview, although the interview need and mental status examination need not always be not (and should not) follow a fi xed and rigid method. conducted separately (though they must be recorded The interview technique should have flexibility, individually). During assessment, the interviewer varying according to appropriate clinical circum- should observe any abnormalities in verbal and non- stances. verbal communi cation and make note of them. Whenever possible, the patient should be seen fi rst. It is helpful to record patient’s respon ses verba- When the account of historical information given by tim rather than only naming the signs (for example, the patient and the informant(s) is different, it is useful rather than just writing delusion of persecution, it is to record them separately. better to record in addition: “my neighbour is trying to 6 A Short Textbook of Psychiatry poison me”). It is best done in the patient’s own spoken The informants’ identification data should be language, whenever possible. recorded along with their relationship to the patient, It is useful to ask open-ended and non-directive whether they stay with the patient or not, and the questions (for example, “how are you feeling today”?) duration of stay together. rather than asking direct, leading questions (for exam- Finally, a comment should be made regarding the ple, “are you feeling sad at present”?). reliability of the information provided. The reliability Arguably the most important interviewing skills of the information provided by the informants should are listening, and demonstrating that you are interested be assessed on the following parameters: in listening and attending to the patient. It is important 1. Relationship with patient, to remember that listening is an active, and not a 2. Intellectual and observational ability, passive, process. 3. Familiarity with the patient and length of stay with Confi dentiality must always be observed. How- the patient, and ever, in cases of suicidal/homicidal risk and child 4. Degree of concern regarding the patient. abuse, an exception may have to be made (see Chapter The source of referral (such as a letter from 20 for details). Patients suffering from psychiatric patient’s general practitioner or a letter of referral from disorders are usually no more violent than the general the referring physician/surgeon in case of a liaison population. However, it is important to ensure safety psychiatry referral) often provides valuable informa- if any risks are apparent. tion regarding the patient’s condition. A comprehensive psychiatric interview often requires more than one session. The psychiatric assess- PRESENTING (CHIEF) COMPLAINTS ment can be discussed under the following headings. The presenting complaints and/or reasons for con- IDENTIFICATION DATA sultation should be recorded. Both the patient’s and the informant’s version should be recorded, if relevant. If It is best to start the interview by obtaining some the patient has no complaints (due to absent insight) identifi cation data which may include Name (includ- this fact should also be noted. ing aliases and pet names), Age, Sex, Marital status, It is important to use patient’s own words and to Education, Occupation, Income, Residential and note the duration of each presenting complaint. Some Offi ce Address(es), Religion, and Socioeconomic of the additional points which should be noted include: background, as appropriate according to the setting. It 1. Onset of present illness/symptom. is useful to record the source of referral of the patient. 2. Duration of present illness/symptom. In medicolegal cases, in addition, two identifi cation 3. Course of symptoms/illness. marks should also be recorded. 4. Predisposing factors. 5. Precipitating factors (include life stressors). INFORMANTS 6. Perpetuating and/or reliev ing factors.

Since sometimes the history provided by the patient HISTORY OF PRESENT ILLNESS may be incomplete, due to factors such as absent insight or uncooperativeness, it is important to take the When the patient was last well or asymp to matic should history from patient’s relatives or friends who act as be clearly noted. This provides useful information informants and sources of collateral information. It is about the onset as well as duration of illness. Establish- important to take the patient’s consent before taking ing the time of onset is really important as it provides this collateral history unless the patient does not have clarity about the duration of illness and symptoms. capacity to consent. The symptoms of the illness, from the earliest time Psychiatric History and Examination 7 at which a change was noticed (the onset) until the mellitus, hypertension, coronary artery disease, acute present time, should be narrated chronologically, in intermittent porphyria, syphilis and HIV positivity (or a coherent manner. AIDS) should be explored. The presenting (chief) complaints should be expanded. In particular, any disturbances in physio- TREATMENT HISTORY logical functions such as sleep, appetite and sexual functioning should be enquired. One should always Any treatment received in present and/or previous enquire about the presence of suicidal ideation, ideas episode(s) should be asked along with history of of self-harm and ideas of harm to others (see Chapter treatment adherence, response to treatment received, 19 for details), with details about any possible intent any adverse effects experienced or any drug allergies and/or plans. which should be prominently noted in medical records. It is also essential to consider and record any important negative history (such as history of alcohol/ FAMILY HISTORY drug use in new onset psychosis). A life chart (Fig. 2.1) provides a valuable display The family history usually includes the ‘family of of the course of illness, episodic sequence, polarity origin’ (i.e. the patient’s parents, siblings, grandpar- (if any), severity, frequency, relationship to stressors, ents, uncles, etc.). The ‘family of procreation’ (i.e. and response to treatment, if any. the patient’s spouse, children and grandchildren) is conventionally recorded under the heading of personal PAST PSYCHIATRIC AND MEDICAL history. HISTORY Family history is usually recorded under the following headings: Any history of any past psychiatric illness should be 1. Family structure: Drawing of a ‘family tree’ (pedi- obtai ned. Any past history of having received any gree chart) can help in recording all the relevant psychotropic medication, alcohol and drug abuse or information in very little space which is easily dependence, and psychiatric hospitalisation should readable. An example of a typical family tree is be enquired. given in Figure 2.2. It should be noted whether A past history of any serious medical or neuro- the family is a nuclear, extended nuclear or joint logical illness, surgical procedure, accident or hospi- family. Any consanguineous relationships should talisation should be obtained. The nature of treatment be noted. The age and cause of death (if any) of received, and allergies, if any, should be ascertained. family members should be asked. A past history of relevant aetiological causes such 2. Family history of similar or other psychiatric ill- as head injury, convul sions, unconsciousness, diabetes nesses, major medical illnesses, alcohol or drug dependence and suicide (and suicidal attempts) should be recorded. 3. Current social situation: Home circumstances, per capita income, socioeconomic status, leader of the family (nominal as well as functional) and current attitudes of family members towards the patient’s illness should be noted. The communication patterns in the family, range of affectivity, cultural and religious values, and social Fig. 2.1: An Example of Life Chart support system, should be enquired about, where relevant. 8 A Short Textbook of Psychiatry

Fig. 2.2: A Typical Family Tree and Common Pedigree Symbols Psychiatric History and Examination 9

PERSONAL AND SOCIAL HISTORY Any school phobia, non-attendance, truancy, any learning diffi culties and reasons for termi nation of In a younger patient, it is often possible to give studies (if occurs prema turely) should be noted. more attention to details regarding earlier personal history. In older patients, it is sometimes harder to get a Play History detailed account of the early childhood history. Parents The questions to be asked include, what games were and older siblings, if alive, can often provide much played at what stage, with whom and where. Rela- additional information regarding the past personal tionships with peers, particularly the oppo site sex, history. Not all questions need to be asked from all should be recorded. The evaluation of play history patients and personal history (much like rest of the his- is obviously more important in the younger patients. tory taking) should be individualised for each patient. Personal history can be recorded under the follow- Puberty ing headings: The age at menarche, and reaction to menarche (in females), the age at appearance of secondary sexual Perinatal History characteristics (in both females and males), nocturnal Diffi culties in pregnancy (particularly in the fi rst emissions (in males), masturbation and any anxiety three months of gestation) such as any febrile illness, related to changes in puberty should be asked. medications, drugs and/or alcohol use; abdominal trauma, any physical or psychiatric illness should be Menstrual and Obstetric History asked. Other relevant questions may include whether The regularity and duration of menses, the length the patient was a wanted or unwanted child, date of of each cycle, any abnormalities, the last menstrual birth, whether delivery was normal, any instrumenta- period, the number of children born, and termination tion needed, where born (hospital or home), any peri- of pregnancy (if any) should be asked for. natal complications (cyanosis, convulsions, jaundice), APGAR score (if available), birth cry (immediate or Occupational History delayed), any birth defects, and any prematurity. The age at starting work; jobs held in chronological order; reasons for changes; job satisfac tions; ambitions; Childhood History relationships with authorities, peers and subordinates; Whether the patient was brought up by mother or present income; and whether the job is appropriate someone else, breastfeeding, weaning and any history to the educational and family background, should suggestive of maternal deprivation should be asked. be asked. The age of passing each important develop mental milestone should be noted. The age and ease of toilet Sexual and Marital History training should be asked. Sexual information, how acquired and of what kind; The occurrence of neurotic traits should be noted. masturbation (fantasy and activity); sex play, if any; These include stuttering, stammering, tics, enuresis, adolescent sexual activity; pre marital and extramarital encopresis, night terrors, thumb sucking, nail biting, sexual relationships, if any; sexual practices (normal head banging, body rock ing, morbid fears or phobias, and abnormal); and any gender identity disorder, are somnambulism, temper tantrums, and food fads. the areas to be enquired about. The duration of marriage(s) and/or relationship(s); Educational History time known the partner before marriage; marriage The age of beginning and fi nishing formal edu cation, arranged by parents with or without consent, or academic achievements and rela tionships with peers by self-choice with or without parental consent; and teachers, should be asked. number of marriages, divorces or separations; role in 10 A Short Textbook of Psychiatry marriage; interpersonal and sexual relations; contra- One of the most reliable methods of assessment ceptive measures used; sexual satisfaction; mode and of premorbid personality is interviewing an informant frequency of sexual intercourse; and psychosexual familiar with the patient prior to the onset of illness. dysfunction (if any) should be asked. Conventionally, the details of the ‘family of pro- ALCOHOL AND SUBSTANCE HISTORY creation’ are recorded here. Although alcohol and drug history is often elicited as a Premorbid Personality (PMP) part of personal history, it is often customary to record It is important to elicit details regarding the personality it separately. Alcohol and drugs can often contribute of the individual (temperament, if the age is less than to causation of several psychiatric symptoms and are 16 years). Instead of using labels such as schizoid or often present co-morbidly alongside many psychiatric histrionic, it is more useful to describe the personality diagnoses. in some detail. The following subheadings are often used for the PHYSICAL EXAMINATION description of premorbid personality. 1. Interpersonal relationship: Interpersonal rela- A detailed general physical examination (GPE) and tionships with family mem bers, friends, and systemic examination is a must in every patient. work colleagues; introverted/extroverted; ease Physical disease, which is aetiologically important (for of making and maintaining social relationships. causing psychiatric symptomatology), or accidentally 2. Use of leisure time: Hobbies; interests; intel- co-existent, or secon darily caused by the psychiatric lectual activities; critical faculty; energetic/ condition or treatment, is often present and can be sedentary. detected by a good physical examination. 3. Predominant mood: Optimistic/pessimistic; stable/prone to anxiety; cheerful/despondent; MENTAL STATUS EXAMINATION (MSE)* reaction to stressful life events. 4. Attitude to self and others: Self-confi dence Mental status examination is a standardised format in level; self-criticism; self-consciousness; self- which the clinician records the psychiatric signs and centred/thoughtful of others; self-appraisal of symptoms present at the time of the interview. abilities, achievements and failures. MSE should describe all areas of mental function- 5. Attitude to work and responsibility: Decision ing (Table 2.2). Some areas, however, may deserve making; acceptance of responsibility; fl exibility; more emphasis according to the clinical impressions perseverance; foresight. that may arise from the history; for example, mood 6. Religious beliefs and moral attitudes: Religious and affect in depression, and cognitive functions in beliefs; tolerance of others’ standards and delirium and dementia. beliefs; conscience; altruism. 7. Fantasy life: Sexual and nonsexual fantasies; General Appearance and Behaviour daydreaming-frequency and content; recurrent A rich deal of information can be elicited from ex- or favourite daydreams; dreams. amination of the general appearance and behaviour. 8. Habits: Food fads; alcohol; tobacco; drugs; While examining, it is important to remember patient’s sleep. sociocultural background and personality.

* The deﬁ nitions of some MSE terms are described in Appendix III. Psychiatric History and Examination 11

Table 2.2: Mental Status Examination Attitude towards examiner 1. General Appearance and Behaviour Cooperation/guardedness/evasiveness/hostility/com- i. General Appearance bativeness/haughtiness, ii. Attitude towards Examiner Attentiveness, iii. Comprehension Appears interested/disinterested/apathe tic, iv. Gait and Posture Any ingratiating behaviour, v. Motor Activity Perplexity vi. Social Manner vii. Rapport Comprehension 2. Speech Intact/impaired (partially/fully) i. Rate and Quantity ii. Volume and Tone Gait and posture iii. Flow and Rhythm Normal or abnormal (way of sitting, standing, walk- 3. Mood and Affect ing, lying) 4. Thought i. Stream and Form Motor activity ii. Content 5. Perception Increased/decreased, 6. Cognition (Higher Mental Functions) Excitement/stupor, i. Consciousness Abnormal involuntary movements (AIMs) such as ii. Orientation tics, tremors, akathisia, iii. Attention Restlessness/ill at ease, iv. Concentration Catatonic signs (mannerisms, stereotypies, posturing, v. Memory waxy ﬂ exibility, negativism, ambi ten dency, automatic vi. Intelligence obedience, stupor, echopraxia, psychological pillow, vii. Abstract thinking forced grasping) (see Chapter 5 for details), 7. Insight Conversion and dissociative signs (pseudo seizures, 8. Judgement possession states), Social withdrawal, Autism, Understandably, general appearance and behav- Compulsive acts, rituals or habits (for example, nail iour needs to be given more emphasis in the examina- biting), tion of an uncooperative patient. Reaction time General appearance Social manner and non-verbal The important points to be noted are: behaviour Physique and body habitus (build) and physical ap- Increased, decreased, or inappropriate behaviour pearance (approximate height, weight, and appear- Eye contact (gaze aversion, staring vacantly, staring ance), at the examiner, hesitant eye contact, or normal eye Looks comfortable/uncomfortable, contact). Physical health, Grooming, Hygiene, Self-care, Rapport Dressing (adequate, appropriate, any peculiarities), Whether a working and empathic relationship Facies (non-verbal expression of mood), can be established with the patient, should be men- Effeminate/masculine tioned. 12 A Short Textbook of Psychiatry

Hallucinatory Behaviour over time), depth or intensity of affect (normal, increased or blunted) and appropriateness of affect (in Smiling or crying without reason, Muttering or talking relation to thought and surrounding environment). to self (non-social speech). Mood is described as general warmth, euphoria, Odd gesturing in response to auditory or visual elation, exaltation and/or ecstasy (seen in severe hallucinations. mania) in mania; anxious and restless in anxiety and depression; sad, irritable, angry and/or despai- Speech red in depression; and shallow, blunted, indifferent, Speech can be examined under the following headings: restricted, inappro priate and/or labile in schizophrenia. Anhedonia may occur in both schizophrenia and Rate and quantity of speech depression. Whether speech is present or absent (mutism), If present, whether it is spontaneous, whether produc- Thought tivity is increased or decreased, Normal thinking is a goal directed ﬂ ow of ideas, Rate is rapid or slow (its appropriateness), Pressure symbols and associations initiated by a problem or a of speech or poverty of speech. task, characterised by rational connections between successive ideas or thoughts, and leading towards Volume and tone of speech a reality orien ted conclusion. Therefore, thought Increased/decreased (its appropriateness), process that is not goal-directed, or not logical, or does Low/high/normal pitch not lead to a realistic solution to the problem at hand, is not considered normal. Flow and rhythm of speech Traditionally, in the clinical examination, thought Smooth/hesitant, Blocking (sudden), is assessed (by the content of speech) under the four Dysprosody, Stuttering/Stammering/Cluttering, Any headings of stream, form, content and possession of accent, thought. However, since there is widespread disagree- Circumstantiality, Tangentiality, ment regarding this subdivision, ‘thought’ is discussed Verbigeration, Stereotypies (verbal), here under the following two headings of ‘stream and Flight of ideas, Clang associations. form’, and ‘content’. Mood and Affect Stream and form of thought Mood is the pervasive feeling tone which is sustained For obvious reasons, the ‘stream of thought’ overlaps (lasts for some length of time) and colours the total with examination of ‘speech’. Spontaneity, produc- experience of the person. Affect, on the other hand, is tivity, ﬂ ight of ideas, prolixity, poverty of content of the outward objective expression of the immediate, speech, and thought block should be mentioned here. cross-sectional experience of emotion at a given time. The ‘continuity’ of thought is assessed; Whether The assessment of mood includes testing the qual- the thought processes are relevant to the questions ity of mood, which is assessed sub jectively (‘how asked; Any loosening of associations, tangentiality, do you feel’) and objectively (by examination). The circumstantiality, illogical thinking, perseveration, or other components are stability of mood (over a period verbigeration is noted. of time), reactivity of mood (variation in mood with stimuli), and persistence of mood (length of time the Content of thought mood lasts). Any preoccupations; The affect is similarly described under quality of Obsessions (recurrent, irrational, intrusive, ego- affect, range of affect (of emotional changes displayed dystonic, ego-alien ideas); Psychiatric History and Examination 13

Contents of phobias (irrational fears); (i.e. whether the voices were addressing the patient Delusions (false, unshakable beliefs) or Over-valued or were discussing him in third person); also enquire ideas; about command (imperative) hallucinations (which Explore for delusions/ideas of persecution, reference, give commands to the person). grandeur, love, jealousy (infi de lity), guilt, nihilism, Enquire whether the hallucinations occurred dur- poverty, somatic (hypochon driacal) symptoms, hope- ing wakefulness, or were they hypnagogic (occurring lessness, helplessness, worthlessness, and suicidal while going to sleep) and/or hypno pompic (occurring ideation. while getting up from sleep) hallucinations. Delusions of control, thought insertion, thought withdrawal, and thought broadcasting are Schneiderian Illusions and misinterpretations fi rst rank symptoms (SFRS). The presence of neolo- Whether visual, auditory, or in other sensory fi elds; gisms should be recorded here. whether occur in clear consciousness or not; whether any steps taken to check the reality of distorted per- Perception ceptions. Perception is the process of being aware of a sensory experience and being able to recognize it by compar- Depersonalisation/derealisation ing it with previous experiences. Depersonalisation and derealisation are abnormalities Perception is assessed under the following headings: in the perception of a person’s reality and are often described as ‘as-if’ phenomena. Hallucinations The presence of hallucinations should be noted. Somatic passivity phenomenon A hallucination is a perception experienced in the Somatic passivity is the presence of strange sensa- absence of an external stimulus. The hallucinations tions described by the patient as being imposed on can be in the auditory, visual, olfactory, gustatory or the body by ‘some external agency’, with the patient tactile domains. being a passive recipient. It is one of the Schneider’s Auditory hallucinations are commonest types of fi rst rank symptoms. hallucinations in non-organic psychiatric disorders. It is really important to clarify whether they are Others elementary (only sounds are heard) or complex (voices Autoscopy, abnormal vestibular sensations, sense of heard). presence should be noted here. The hallucination is experienced much like a true perception and it seems to come from an external Cognition (Neuropsychiatric) Assessment objective space (for example, from outside the ears in Assessment of the cognitive or higher mental func- the case of an auditory hallucination). If the hallucinations is an important part of the MSE. A signifi cant tion does not either appear to be a true perception or disturbance of cognitive functions commonly points comes from a subjective internal space (for example, to the presence of an organic psychiatric disorder. It inside the person’s own head in the case of auditory is usual to use Folstein’s mini mental state examina- hallucination), then it is called as a pseudohallucination (MMSE) for a systematic clinical examination of tion. higher mental functions. It should be further enquired what was heard, how many voices were heard, in which part of the day, Consciousness male or female voices, how interpreted and whether The intensity of stimulation needed to arouse the these are second person or third person hallucinations patient should be indicated to demonstrate the level of 14 A Short Textbook of Psychiatry alertness, for example, by calling patient’s name in a (also used for testing attention; are described under normal voice, calling in a loud voice, light touch on the attention). arm, vigorous shaking of the arm, or painful stimulus. b. Recent Memory Grade the level of consciousness: conscious/ con- Ask how did the patient come to the room/hospital; fusion/somnolence/clouding/delirium/stupor/coma. what he ate for dinner the day before or for breakfast Any disturbance in the level of consciousness should the same morning. Give an address to be memorised ideally be rated on Glasgow Coma Scale, where a and ask it to be recalled 15 minutes later or at the end numeric value is given to the best response in each of the interview. of the three categories (eye opening, verbal, motor). c. Remote Memory Ask for the date and place of marriage, name and birth- Orientation days of children, any other relevant questions from Whether the patient is well oriented to time (test by the person’s past. Note any amnesia (anterograde/ asking the time, date, day, month, year, season, and retro grade), or confabulation, if present. the time spent in hospital), place (test by asking the present location, building, city, and country) and Intelligence person (test by asking his own name, and whether Intelligence is the ability to think logically, act ration- he can identify people around him and their role in ally, and deal effectively with environment. that setting). Disorientation in time usually precedes Ask questions about general information, keeping disorientation in place and person. in mind the patient’s educational and social background, his experiences and interests, for example, Attention ask about the current and the past prime ministers and Is the attention easily aroused and sustained; Ask the presidents of India, the capital of India, and the name patient to repeat digits forwards and backwards (digit of the various states. span test; digit forward and backward test), one at a Test for reading and writing; Use simple tests of time (for example, patient may be able to repeat 5 calculation. digits forward and 3 digits backwards). Start with two digit numbers increasing gradually up to eight digit Abstract thinking numbers or till failure occurs on three consecutive Abstract thinking is characterised by the ability to: occasions. a. assume a mental set voluntarily, b. shift voluntarily from one aspect of a situation to Concentration another, Can the patient concentrate; Is he easily distractible; c. keep in mind simultaneously the various aspects Ask to subtract serial sevens from hundred (100-7 of a situation, test), or serial threes from fi fty (50-3 test), or to count d. grasp the essentials of a ‘whole’ (for example, backwards from 20, or enumerate the names of the situation or concept), and months (or days of the week) in the reverse order. e. to break a ‘whole’ into its parts. Note down the answers and the time taken to Abstract thinking testing assesses patient’s concept perform the tests. formation. The methods used are: a. Proverb Testing: The meaning of simple proverbs Memory (usually three) should be asked. a. Immediate Retention and Recall (IR and R) b. Similarities (and also the differences) between Use the digit span test to assess the immediate familiar objects should be asked, such as: table/ memory; digit forwards and digit backwards subtests chair; banana/orange; dog/lion; eye/ear. Psychiatric History and Examination 15

Table 2.3: Clinical Rating of Insight The answers may be overly concrete or abstract. The appropriateness of answers is judged. Concretisa- Insight is rated on a 6-point scale from one to six. tion of responses or inappro priate answers may occur 1. Complete denial of illness. in schizophrenia. 2. Slight awareness of being sick and needing help, but denying it at the same time. Insight 3. Awareness of being sick, but it is attributed to exter- Insight is the degree of awareness and understanding nal or physical factors. that the patient has regarding his illness. 4. Awareness of being sick, due to something unknown Ask the patient’s attitude towards his present state; in self. whether there is an illness or not; if yes, which kind of 5. Intellectual Insight: Awareness of being ill and that the symptoms/failures in social adjustment are due illness (physical, psychiatric or both); is any treatment to own particular irrational feelings/thoughts; yet needed; is there hope for recovery; what is the cause of does not apply this knowledge to the current/future illness. Depending on the patient’s responses, insight experiences. can be graded on a six-point scale (Table 2.3). 6. True Emotional Insight: It is different from intellec- Judgement tual insight in that the awareness leads to signifi cant basic changes in the future behaviour. Judgement is the ability to assess a situation correctly and act appropriately within that situation. Both social and test judgement are assessed. Table 2.4: Some Investigations in Psychiatry i. Social judgement is observed during the hospital stay and during the interview session. It includes I. Biological Investigations an evaluation of ‘personal judgement’. Medical Screen ii. Test judgement is assessed by asking the patient Some of the following tests may be useful in screen- what he would do in certain test situations, such ing for the medical disorders causing the psychiatric as ‘a house on fi re’, or ‘a man lying on the road’, symptoms. Some examples of indications are stated in or ‘a sealed, stamped, addressed envelope lying front of the tests (these examples are not intended to be on a street’. comprehensive). Haemoglobin: Routine screen. Judgement is rated as Good/Intact/Normal or Poor/ Total and differential leucocyte counts: Routine screen, Impaired/Abnormal. Treatment with antipsychotics (e.g. clozapine), lithium, carbamazepine. INVESTIGATIONS Mean Corpuscular Volume (MCV): Alcohol dependence (increased). After a detailed history and examination, investi- Urinalysis: Routine screen; Drug screening. gations (laboratory tests, diagnostic standardised Peripheral smear: Anaemia. interviews, family interviews, and/or psychological Renal function tests: Treatment with lithium. tests) are carried out based on the diagnostic and Liver function tests: Treatment with carbamazepine, aetiological possibilities. Some of these investigations valproate, benzodiazepines. Alcohol dependence. are described briefl y in Table 2.4. Serum electrolytes: Dehydration, SIADH, Treatment with carbamazepine, antipsychotics, lithium. FORMULATION Blood glucose: Routine screen (age>35 years), treatment with antipsychotics After a comprehensive psychiatric assessment, a diagnostic formulation summarises the detailed posi- Contd... 16 A Short Textbook of Psychiatry

Contd...

Thyroid function tests: Refractory depression, rapid Brain Imaging Tests (Cranial) cycling mood disorder. Treatment with lithium, car- Computed Tomography (CT) Scan: Dementia, delirium, bamazepine. seizures, ﬁ rst episode psychosis. Electrocardiogram (ECG): Age>35 years, Treatment with Magnetic Resonance Imaging (MRI) Scan: Dementia. lithium, antidepressants, ECT, antipsychotics. Higher resolution than CT scan. HIV testing: Intravenous drug users, suggestive sexual Positron Emission Tomography (PET) Scan: Research tool history, AIDS dementia. for study of brain function and physiology. VDRL: Suggestive sexual history. Single Photon Emission Computed Tomography (SPECT) Chest X-ray: Age>35 years, Treatment with ECT. Scan: Research tool. Skull X-ray: History of head Injury. Magnetic Resonance (MR) Angiography: Research tool Serum CK: Neuroleptic malignant syndrome (markedly Magnetic Resonance Spectroscopy (MRS): Research tool increased levels). Neuroendocrine Tests Toxicology Screen Dexamethasone Suppression Test (DST): Research tool Useful when substance use is suspected; for example, in depression (response to antidepressants or ECT). If alcohol, cocaine, opiates, cannabis, phencyclidine, plasma cortisol is >5 mg/100 ml following administra- benzodia zepines, barbiturates; remember that certain tion of dexamethasone (1 mg, given at 11 PM the night medications can cause false positive results (for example, before and plasma cortisol taken at 4 PM and 11 PM quetiapine for methadone). the next day), it indicates non-suppression. Drug Levels TRH Stimulation Test: Lithium-induced hypothy roidism, Drug levels are indicated to test for therapeutic blood refractory depression. If the serum TSH is >35 mIU/ml levels, for toxic blood levels, and for testing drug (following 500 mg of TRH given IV), the test is positive. compliance. Examples are lithium (0.6-1.0 meq/L), Serum Prolactin Levels: Seizures vs. pseudo seizures, carbamazepine (4-12 mg/ml), valproate (50-100 mg/ galactorrhoea with antipsychotics. ml), haloperidol (8-18 ng/ml), tricyclic antidepres sants Serum 17-hydroxycorticosteroid: Organic mood (depres- (nortriptyline 50-150 ng/ml; imipramine 200-250 ng/ sion) disorder. ml), benzodiazepines, barbiturates and clozapine (350- Serum Melatonin Levels: Seasonal mood disorders. 500 μg/L). Biochemical Tests Electrophysiological Tests 5-HIAA: Research tool (depression, suicidal and/or EEG (Electroencephalogram): Seizures, dementia, pseu- aggressive behaviour). doseizures vs. seizures, episodic abnormal behaviour. MHPG: Research tool (depression). BEAM (Brain electrical activity mapping): Provides Platelet MAO: Research tool (depression). topographic imaging of EEG data. Catecholamine levels: Organic anxiety disorder (e.g. Video-Telemetry EEG: Pseudoseizures vs. seizures. pheochromocytoma). Evoked potentials (e.g. p300): Research tool. Genetic Tests Polysomnography/Sleep studies: Sleep disorders, sei- Cytogenetic work-up is useful in some cases of mental zures (occurring in sleep). The various compo nents in retardation. sleep studies include EEG, ECG, EOG, EMG, airﬂ ow Sexual Disorder Investigations measurement, penile tumescence, oxygen saturation, Papaverine test: Male erectile disorder (intracaver nosal body temperature, GSR (Galvanic skin response), and injection of papaverine is sometimes used to differen tiate body movement. organic from non-organic male erectile disorder). Holter ECG: Panic disorder. Nocturnal penile tumescence: Male erectile disorder.

Contd... Psychiatric History and Examination 17

Contd... Serum testosterone: Sexual desire disorders, Male erectile used projective tests of personality are Rorschach inkblot disorder. test, TAT (Thematic apperception test), DAPT (Draw-a- Penile Doppler: Male erectile disorder. person test), and sentence completion test (SCT). Miscellaneous Tests Neuropsychological Tests Lactate provocation test: Panic disorders (In about 70% Some of the commonly used neuropsychological tests are of patients with panic disorders, sodium lactate infusion Wisconsin card sorting test, Wechsler memory scale, PGI can provoke a panic attack). memory scale, BG test (Bender Gestalt test), BVRT (Benton Drug assisted interview (Amytal interview): Useful in visual retention test), Luria-Nabraska neuro psychological catatonia, unexplained mutism, and dissociative stupor. test battery, Halstead-Reitan neuropsy cholo gical test bat- Discussed in Chapter 18. tery, and PGI battery of brain dysfunction. CSF examination: Meningitis. Rating Scales II. Psychological Investigations Several rating scales are used in psychiatry to quantify the Objective Tests psychopathology observed. Some of the com monly used These are pen-and-paper objective tests, which are scales are BPRS (Brief psychiatric rating scale), SANS employed to test the various aspects of personality and (Scale for assessment of negative symp toms), SAPS (Scale intelligence in a person. for assessment of positive symp toms), HARS (Hamilton’s Objective personality tests: Some examples of objective anxiety rating scale), HDRS (Hamil ton’s depression rating personality tests are MMPI (Minnesota multiple personal- scale), and Y-BOCS (Yale-Brown obsessive-compulsive ity inventory) and 16-PF (16 personality factors). scale). Intelligence tests: Some commonly used tests of intel- Diagnostic Standardized Interviews ligence are WAIS (Wechsler adult intelligence scale), The use of these instruments makes the diagnostic Stanford-Binet test and Bhatia’s battery of intelligence assessment more standardized. These include PSE tests. (Present state examination), SCAN (Schedules for clinical Projective Tests assess ment in neuropsychiatry), SCID (Structured clinical In projective tests, ambiguous stimuli are used which are interview for DSM-IV), and IPDE (International personal- not clear to the person immediately. Some com monly ity disorder examination).

Table 2.5: Diagnostic Formulation tive (and important negative) information regarding the patient under the focus of care, before listing Biological Psychological Social differential diagnosis, prognostic factors, and a man- Predisposing agement plan. Precipitating The diagnostic formulation focuses on aetiological factors based on the biopsychosocial model (Table 2.5; Perpetuating Fig. 2.3). Similarly, it is useful to devise the manage- Protective ment plan based on the biopsychosocial model (Table 2.6). It is possible to use speciﬁ c formulations based on Table 2.6: Management Plan treatment options; for example, a cognitive formulation for CBT and a psychodynamic formulation for Biological Psychological Social psychodynamic psychotherapy. Short-term Thus, psychiatric assessment is an initial step Medium-term towards diagnosis and management of psychiatric disorders. Long-term 18 A Short Textbook of Psychiatry

SPECIAL INTERVIEWS

There are different formats available for detailed evaluation of special populations such as uncooperative patients, hostile and aggressive patients (Chapter 19), suicidal patients (Chapter 19), and children. These Fig. 2.3: Aetiological Factors Drawn on a Timeline formats should be used whenever appropriate. Organic (Including Symptomatic) 3 Mental Disorders

It is assumed that all psychological and behavioural evaluating a patient with any psychological or behav- processes, whether normal or abnormal, are a result of ioural clinical syndrome. The presence of following normal or deranged brain function. A rational corol- features requires a high index of suspicion for an lary would be that all psychiatric disorders are due to organic mental disorder (or what is loosely called as abnormal brain functioning and are therefore organic. organicity): However, this would be a gross oversimplifi cation. 1. First episode. According to our present knowledge, there are 2. Sudden onset. broadly three types of psychiatric disorders: 3. Older age of onset. 1. Those due to a known organic cause. 4. History of drug and/or alcohol use disorder. 2. Those in whose causation an organic factor has 5. Concurrent medical or neurological illness. not yet been found or proven. 6. Neurological symptoms or signs, such as seizures, 3. Those primarily due to psycho social factors. impairment of consciousness, head injury, sensory Only disorders with a known organic cause are or motor distur bance. called organic mental disorders. Thus, organic mental 7. Presence of confusion, disorientation, memory disorders are behavioural or psychological disorders impairment or soft neurological signs. associated with transient or permanent brain dysfunc- 8. Prominent visual or other non-auditory (e.g. olfac- tion and include only those mental and behavioural tory, gustatory or tactile) halluci nations. disorders that are due to demonstrable cerebral disease These disorders can be broadly subcategorised or disorder, either primary (primary brain pathology) into the following categories: or secondary (brain dysfunction due to systemic dis- 1. Delirium, eases). The use of term organic here does not imply 2. Dementia, that other psychiatric disorders are ‘non-organic’ in the 3. Organic amnestic syndrome, and sense of having no biological basis. It simply means 4. Other organic mental disorders. that the organic mental disorders have a demonstrable and independently diagnosable cerebral disease or DELIRIUM disorder, unlike other psychiatric disorders that do not at present. Delirium is the commonest organic mental disorder Since organic brain illness can mimic any psychi- seen in clinical practice. Five to fi fteen percent of atric disorder, especially in the initial stages, organic all patients in medical and surgical inpatient units mental disorder should be the fi rst consideration in are estimated to develop delirium at some time in 20 A Short Textbook of Psychiatry their lives. This percentage is higher in postoperative Lability of affect is usually present. Motor and patients. verbal perse veration, dysno mia, agraphia and Delirium is the most appropriate substitute for a impaired comprehen sion can also be seen. variety of names used in the past such as acute con- fusional states, acute brain syndrome, acute organic Diagnosis reaction, toxic psychosis, and metabolic (and other The diagnosis of delirium is frequently missed, as acute) encephalopathies. the possibility can be overlooked in medical/surgical settings. It is important to recognize delirium at the Clinical Features earliest possible as delirium often has an underlying Delirium is characterised by the following features: aetiology which may be correctable. Any delay in 1. A relatively acute onset, diagnosis, and thus starting treatment, may lead to 2. Clouding of consciousness, characterised by permanent defi cits which can be irrever sible. a decreased aware ness of surroundings and a The diagnosis of delirium is mainly clinical. No decreased ability to respond to environmental ancillary laboratory test is diagnostic, although tests stimuli, and may help in fi nding the aetiology. 3. Disorientation (most commonly in time, then in According to ICD-10, for a defi nite diagnosis place and usually later in person), associated with of delirium, symptoms (mild or severe) should be a decreased attention span and distrac tibility. present in each one of the fi ve areas described. These Marked perceptual disturbances such as illu- include impairment of consciousness and attention (on sions, misinterpretations, and hallucina tions also a continuum from clouding to coma; reduced ability occur. These are most commonly visual though to direct, focus, sustain, and shift attention), global other perceptual domains can also be involved. disturbance of cognition, psychomotor disturbances, There is often a disturbance of sleep-wake cycle; disturbance of sleep-wake cycle, and emotional dis- most commonly, insomnia at night with daytime turbances. drowsiness. Diurnal variation is marked, usually with The onset is usually rapid, the course diurnally worsening of symptoms in the evening and night fl uctuating, and the total duration of the condi tion (called sun downing). There is also an impairment much less than 6 months. The above clinical picture of registration and retention of new memories. is so characteristic that a fairly confi dent diagnosis of Psychomotor disturbance, usually in form of delirium can be made even if the under lying cause is agitation and occasionally retardation, is present. not clearly established. Generalised autonomic dysfunction, speech and A history of underlying physical or brain disease, thought disturbances (such as slurring of speech, and/or evidence of cerebral dysfunction (e.g. an abnor- incoherence, dysarthria, and fl eeting delusions) are mal EEG, usually but not always, showing slowing often present. of the background activity) may help in reaching the The motor symptoms in delirium can include: diagnosis. 1. Asterixis (fl apping tremor), 2. Multifocal myoclonus, Predisposing Factors 3. Carphologia or fl occil lation (picking move ments Presence of certain predisposing factors lowers the at cover-sheets and clothes), threshold for the development of delirium (Table 3.1). 4. Occupational delirium (elaborate pantomimes as if continuing their usual occupation in the hospital Aetiology bed), and The list of possible causes of delirium is virtually 5. Tone and refl ex abnormalities. endless. Any factor which disturbs the meta bolism of Organic (Including Symptomatic) Mental Disorders 21 brain suffi ciently can cause delirium. The aetiology of One of the important causes of delirium, namely delirium demonstrates a threshold phenomenon, with post-cardiac surgery delirium, is discussed in Chapter a combination of factors adding up to cross a threshold 12. The most common causes are listed in Table 3.2. for causing delirium, which appears to be different for each individual. Management 1. In cases where a cause is not obvious (or other contributory causes are suspected), a battery of Table 3.1: Predisposing Factors in Delirium investigations should be done which can include 1. Pre-existing brain damage or dementia complete blood count, urinalysis, blood glucose, 2. Extremes of age (very old or very young) blood urea, serum electrolytes, liver and renal 3. Previous history of delirium function tests, thyroid function tests, serum B12 and 4. Alcohol or drug dependence folate levels, X-ray chest, ECG, CSF examination, 5. Generalised or focal cerebral lesion urine for porphyrins, drug screens, VDRL, HIV 6. Chronic medical illness testing, arterial pO and pCO , EEG, and brain 7. Surgical procedure and postoperative period 2 2 imaging (such as cranial CT scan or MRI scan). 8. Severe psychological symptoms (such as fear) 2. Identification of the cause and its immediate 9. Treatment with psychotropic medicines correction, e.g. 50 mg of 50% dextrose IV for 10. Present or past history of head injury hypoglycaemia, O for hypoxia, 100 mg of B IV 11. Individual susceptibility to delirium 2 1

Table 3.2: Delirium: Some Important Causes Metabolic Causes iv. Anticonvulsants, L-dopa, Opiates i. Hypoxia, Carbon dioxide narcosis v. Salicylates, Steroids, Penicillin, Insulin ii. Hypoglycaemia vi. Methyl alcohol, heavy metals, biocides. iii. Hepatic encephalopathy, Uremic encephalopa- Nutritional Deﬁ ciencies

thy i. Thiamine, Niacin, Pyridoxine, Folic acid, B12 iv. Cardiac failure, Cardiac arrhythmias, Cardiac ii. Proteins arrest Systemic Infections v. Water and electrolyte imbalance (Water, Na+, i. Acute and Chronic, e.g. Septicaemia, Pneumo- K+, Mg++, Ca++) nia, Endocarditis vi. Metabolic acidosis or alkalosis Intracranial Causes vii. Fever, Anaemia, Hypovolemic shock i. Epilepsy (including post-ictal states) viii. Carcinoid syndrome, Porphyria ii. Head injury, Subarachnoid haemorrhage, Sub- Endocrine Causes dural haematoma i. Hypo- and Hyperpituitarism iii. Intracranial infections, e.g. Meningitis, En- ii. Hypo- and Hyperthyroidism cephalitis, Cerebral malaria iii. Hypo- and Hyperparathyroidism iv. Migraine iv. Hypo- and Hyperadrenalism v. Stroke (acute phase), Hypertensive encepha lo- Drugs (Both ingestion and withdrawal can cause pathy delirium) and Poisons vi. Focal lesions, e.g. right parietal lesions (such i. Digitalis, Quinidine, Antihypertensives as abscess, neoplasm) ii. Alcohol, Sedatives, Hypnotics (espe cially bar- Miscellaneous biturates) i. Postoperative states (including ICU delirium) iii. Tricyclic antidepressants, Antipsychotics, An- ii. Sleep deprivation ticholinergics, Disulﬁ ram iii. Heat, Electricity, Radiation 22 A Short Textbook of Psychiatry

for thiamine defi ciency, and IV fl uids for fl uid and Impairment of all these functions occurs globally, electrolyte imbalance. causing inter ference with day-to-day activities and 3. Symptomatic measures: As many patients are interper sonal relationships. There is impairment of agitated, emergency psychiatric treatment may judgement and impulse control, and also impairment be needed. Small doses of benzodiazepines(lora- of abstract thinking. There is however usually no im- zepam or diazepam) or antipsychotics (haloperi- pairment of consciousness (unlike in delirium; Table dol or risperidone) may be given either orally or 3.3). The course of dementia is usually progressive parenterally. Maintenance treatment can continue though some forms of dementia can be reversible. till recovery occurs, usually within a week’s time. Additional features may also be present. These There is an increased risk of stroke in elderly include: patients with dementia with prescription of 1. Emotional lability (marked variation in emotional atypical antipsychotics such as olanzapine and expression). risperidone. 2. Catastrophic reaction (when confronted with an 4. Supportive medical and nursing care. assignment which is beyond the residual intellectual capacity, patient may go into a sudden rage). DEMENTIA 3. Thought abnormalities, e.g. perseveration, delu- Dementia is a chronic organic mental disorder, char- sions. acterised by the following main clinical features: 4. Urinary and faecal incontinence may develop in 1. Impair ment of intellectual functions, later stages. 2. Impairment of memory (predominantly of recent 5. Disorientation in time; disorientation in place and memory, especially in early stages), person may also develop in later stages. 3. Deterioration of personality with lack of personal 6. Neurological signs may or may not be present, care. depending on the underlying cause. Table 3.3: A Comparison of Delirium and Dementia Features Delirium Dementia 1. Onset Usually acute Usually insidious 2. Course Usually recover in 1 week; Usually protracted, although may be reversible may take up to 1 month in some cases 3. Clinical features a. Consciousness Clouded Usually normal b. Orientation Grossly disturbed Usually normal; disturbed only in late stages c. Memory Immediate retention and Immediate retention and recall normal recall disturbed Recent memory disturbed Recent memory disturbed Remote memory disturbed only in late stages d. Comprehension Impaired Impaired only in late stages e. Sleep-wake cycle Grossly disturbed Usually normal f. Attention and concentration Grossly disturbed Usually normal g. Diurnal variation Marked; sundowning may Usually absent be present h. Perception Visual illusions and Hallucinations may occur hallucinations very common i. Other features Asterixis; multifocal myoclonus Catastrophic reaction; perseveration Organic (Including Symptomatic) Mental Disorders 23

Diagnosis 3. Depressive pseudodementia: Depression in the elderly patients may mimic dementia clinically. It Like delirium, the diagnosis of dementia is clinical is called as depressive pseudodementia (Table 3.4). though ancillary laboratory inves ti gations may help Identifi cation of depres sion is very important as it in elucidating the underlying aetiology. is far more easily treatable than dementia. According to ICD-10, the following features are The depressed patients often complain of memory required for diagnosis: evidence of decline in both impairment, diffi culty in sustaining atten tion and memory and thinking, suffi cient enough to impair concentration, and reduced intellec tual capacity. In personal activities of daily living, memory impairment contrast, patients with dementia do not often complain (typically affecting registration, storage, and retrieval of these disturbances. In fact, when confronted with of new information though previously learned material evi dence of memory impairment, they often con- may also be lost particularly in later stages, impaired fabulate. As depression may often be superimposed thinking, presence of clear consciousness (conscious- on dementia, it is at times necessary to undertake a ness can be impaired if delirium is also present), and therapeutic trial with antidepressants, if the clinical a duration of at least 6 months. picture is unclear. The following conditions must be kept in mind in It is useful to differentiate dementia into cortical the differential diagnosis of dementia. and subcortical subtypes (Table 3.5). 1. Normal aging process: Although impairment of memory and intellect are commoner in elderly, Aetiology their mere presence does not justify a diagnosis A large number of conditions can cause dementia of dementia. Dementia is diagnosed only when (Table 3.6). However, a majority of cases are due to there is demonstrable evidence of memory and a few common causes such as Alzhei mer’s disease other intellec tual impair ment which is of suffi cient and multi-infarct dementia. Some clinically important severity to interfere with social and/or occupational types of dementia are briefl y discussed here. func tioning. The normal memory impair ment in old age is called as benign senescent forgetful ness. Alzheimer’s Dementia 2. Delirium: The syndromes of delirium and demen- This is the commonest cause of dementia, seen in tia may overlap. See Table 3.3 for a comparison about 70% of all cases of dementia in USA. It is more of clinical features. commonly seen in women. Earlier, it was differentiated

Table 3.4: Dementia vs Pseudodementia Dementia Pseudodementia (Depressive) 1. Patient rarely complains of cognitive impairment Patient usually always complains about memory impairment 2. Patient often emphasises achievements Patient often emphasises disability 3. Patient often appears unconcerned Patient very often communicates distress 4. Usually labile affect Severe depression on examination 5. Patient makes errors on cognitive examination ‘Do not know’ answers are more frequent 6. Recent memory impairment found on examination Recent memory impairment rarely found on examination 7. Confabulation may be present Confabulation very rare 8. Consistently poor performance on similar tests Marked variability in performance on similar tests 9. History of depression less common Past history of manic and/or depressive episodes may be present 24 A Short Textbook of Psychiatry

Table 3.5: Cortical and Subcortical Dementia Features Cortical Dementia Subcortical Dementia 1. Site of lesion Cortex (frontal and temporoparieto-occipital Subcortical grey matter (thalamus, basal association areas, and hippocampus) ganglia, and rostral brain stem) 2. Examples Alzheimer’s disease, Pick’s disease Huntington’ chorea, Parkinson’s disease, Progressive supranuclear palsy, Wilson’s disease 3. Severity Severe Mild to moderate 4. Motor system Usually normal Dysarthria, ﬂ exed/extended posture, tremors, dystonia, chorea, ataxia, rigidity 5. Other features Simple delusions; depression uncommon; Complex delusions; depression common; severe aphasia, amnesia, agnosia, apraxia, rarely mania acalculia, slowed cognitive speed (bradyphrenia) 6. Memory deﬁ cit Recall helped very little by cues Recall partially helped by cues and (Short-term) recognition tasks

Table 3.6: Some Common Causes of Dementia

A. Parenchymatous brain disease F. Defi ciency dementias Alzheimer’s disease, Pick’s disease, Parkinson’s Pernicious anaemia, pellagra, folic acid defi ciency, disease, Huntington’s chorea, Lewy body dementia, thiamine defi ciency Steel Richardson syndrome ( Progres sive Supra- G. Dementias due to infections nuclear Palsy) Creutzfeldt-Jacob disease, neurosyphi lis, chronic B. Vascular dementia meningitis, viral encep halitis, AIDS dementia, other Multi-infarct dementia, subcortical vascular dementia HIV-related disor ders, sub acute sclerosing panen- ( Binswanger’s disease) cepha litis (SSPE) C. Toxic dementias H. Neoplastic dementias Bromide intoxication, drugs, heavy metals, alcohol, Neoplasms and other intracranial space-occupying carbon monoxide, anal gesics, anti convulsants, ben- lesions zodiazepines, psychotropic drugs I. Traumatic dementias D. Metabolic dementias Chronic subdural haematoma, head injury Chronic hepatic or uraemic encephalopathy, dialysis J. Hydrocephalic dementia dementia, Wilson’s disease Normal pressure hydrocephalus E. Endocrine causes Thyroid, parathyroid, pituitary, adrenal dys function into two forms: a presenile form and a senile form. investi gations. Autopsy shows macroscopic changes Now it is known that these two forms represent the such as enlarged cerebral ventricles, widened cerebral same disease clinically and pathologically. There is sulci and shrinkage of cerebral cortex, as well as some evidence to suggest that Alzheimer’s disease microscopic changes such as senile plaques, neurofi - may have a genetic basis. brillary tangles, cortical nerve cell loss, and granulo- The diagnosis of Alzheimer’s dementia is by vacuolar degeneration. However, these changes are exclusion of all other causes of dementia, as there are only quantitatively, and not qualitatively, different no distinct diagnostic clinical features or laboratory from a normal aged brain. Neurochemically, there is Organic (Including Symptomatic) Mental Disorders 25 a marked decrease in brain choline acetyltransferase (showing focal area of slowing) and brain imaging (CT (CAT) with a similar decrease in brain acetylcho- scan or MRI scan of brain showing multiple infarcts) linesterase (AchE). help in diagnosis. The treatment of the underlying At present, Alzheimer’s dementia is not consi- cause can prevent further deterioration by preventing dered a treatable disorder. However, Cholinesterase further infarctions. Inhibitors such as Rivastig mine (1.5 mg twice a day to 6 mg twice a day), Donepezil (5-10 mg/day), and Hypothyroid Dementia Galantamine (4 mg twice a day to 12 mg twice a day) This has been considered one of the most important have been used in the recent past for treatment of treatable and reversible causes of dementia, second moderate dementia with Alzheimer’s disease. These only to toxic dementias. Although it accounts for elevate acetylcholine (Ach) concentrations in cerebral less than 1% of dementias, hypothyroidism should be cortex by slowing the degradation of acetylcholine suspected in every patient of dementia. released by still intact cholinergic neurons in Alzhe- Since clinical diagnosis of hypothyroid dementia imer’s disease. may be diffi cult, laboratory tests should be used for Memantine (5-20 mg/day), an N-methyl-D- correct diagnosis. Prompt treatment can reverse the aspartate (NMDA) antagonist, is also available for the dementing process and can lead to complete recovery treatment of moderately severe to severe Alzheimer’s if the treatment is started within two years of the onset disease. There are several other drugs (such as ginkgo of dementia. biloba, piracetam, and vitamin C and E) used for treatment, though their value remains uncertain. AIDS Dementia Complex About 50-70% of patients suffering from AIDS exhibit Multi-infarct Dementia a triad of cognitive, behavioural and motoric defi cits Multi-infarct dementia is the second commonest cause of subcortical dementia type and this is known as the of dementia, seen in 10-15% of all cases, though some AIDS-dementia complex (ADC). Dementia can in studies indicate that multi-infarct dementia is prob- fact be an initial presentation in about 25% cases of ably far more common in India. It is also one of the AIDS. important treatable causes of dementia. As the AIDS virus (a lenti-virus, a type of retro- Occurrence of multiple cerebral infarctions can virus) is highly neurotropic and the virus crosses the lead to a progressive disruption of brain function, lead- blood-brain barrier early in the course of the disease ing to dementia. The most typical form of multi-infarct cognitive impairment is nearly ubiquitous in AIDS. dementia is characterised by the following features: The diagnosis is established by ELISA (enzyme- 1. An abrupt onset, linked immuno-sorbent assay) showing anti-HIV anti- 2. Acute exacerbations (due to repeated infarctions), bodies, and the Western Blot test (blotting of antibody 3. Stepwise clinical deterioration (step-ladder pat- specifi cities to HIV-specifi c proteins). A Cranial CT tern), scan can show cortical atrophy 1-4 months before the 4. Fluctuating course, onset of clinical dementia while MRI scan is helpful 5. Presence of hypertension (most commonly) or any in detecting the white matter lesions. other signifi cant cardiovascular disease, and 6. History of previous stroke or transient ischemic Lewy Body Dementia attacks (TIAs). Lewy body dementia is now believed to be the second Focal neurological signs are frequently present. most common cause of the degenerative dementias, Insight into the illness is usually present in the early accounting for about 4% of all dementias. Typically, part of the course. Emotional lability is common. EEG the clinical features of Lewy body dementia include: 26 A Short Textbook of Psychiatry i. Fluctuating cognitive impairment over weeks or hypertension in multi-infarct dementia, thyroxin months, with involvement of memory and higher replacement in hypothyroid dementia, shunting in cortical functions (such as language, visuo-spatial hydro cephalic dementia, levodopa in parkin sonism, ability, praxis and reasoning). Lucid intervals can and removal of the toxic agent in toxic dementias. be present in between fl uctuations. Early treatment can prevent further deterioration of ii. Recurrent and detailed visual hallucinations. dementia. iii. Spontaneous extrapyramidal or parkinsonian symptoms such as rigidity and tremors. Symptomatic Management iv. Neuroleptic sensitivity syndrome, characterised by 1. Environmental manipulation and focus on coping a marked sensitivity to the effects of typical doses skills to reduce stress in day-to-day activities. of antipsychotic drugs (resulting in severe extrapy- 2. Treatment of medical complications, if any. ramidal side-effects with use of antipsychotics). 3. Care of food and hygiene Other clinical features may include repeated falls, 4. Supportive care for the patient and family/carers. autonomic dysfunction (e.g. orthostatic hypoten- 5. Anxiety symptoms can be treated with low dose of sion), urinary incontinence, delusions and depressive a short-acting benzodiazepine (such as Lorazepam features. Although Lewy bodies (intra-cytoplasmic and Oxaze pam), though care should be taken to inclusion bodies) are also present in Parkinson’s prevent benzodiazepine dependence/misuse. disease, the occurrence of Lewy bodies in Lewy body 6. Depression can be treated with low doses of dementia is more widespread. A PET (Positron Emis- SSRIs such as Citalopram or Sertraline as these sion Tomography) or SPECT (Single Photon Emission antidepressants have low anticholinergic activity Computerised Tomography) scan of brain may show and have a safer cardiac profi le. Agents with high low dopamine transporter uptake in basal ganglia. anti cholinergic acti vity can cause confusion or Antipsychotic medication should be avoided (or even frank delirium. used with extreme caution and in low doses) in patients 7. Psychotic symptoms and disruptive behaviours with Lewy body dementia. can be treated with low doses of antipsychotics. Haloperidol and Rispe ri done have usually been Management preferred as they are less sedating and have low Basic Investigations cardiac toxicity, though Risperidone can cause postural hypotension. Recently, the use of anti- The diagnostic tests are of great importance in fi nd- psychotics in treatment of behavioural symptoms ing the cause, or to exclude all other causes before in dementia has decreased markedly due to diagnosing Alzheimer’s dementia. possible association of antipsychotic use with The list of investigations could include complete increased mortality. Antipsychotics should blood count, urinalysis, blood glucose, serum elec tro- also be avoided if Lewy body dementia is lytes, renal function tests, thyroid function tests, serum suspected.

B12 and folate levels, serological tests for syphilis, 8. Short-term hospitalisation may be needed for arterial pO2 and pCO2, X-ray chest, ECG, X-ray skull, emergent symptoms whilst a longer term hospi- EEG, lumbar punc ture, CT scan/MRI scan of brain, talisation or respite placement may be necessary neuropsychological tests, and drug screens. in later stages. 9. Speciﬁ c drug treatment such as cholinesterase Treatment of the Underlying Cause, inhibitors (e.g. donepezil, rivastigmine, galan- if Treatable tamine) in moderate Alzheimer’s disease, or Some underlying causes of dementia are treatable memantine (NMDA antagonist) in moderate to (reversible dementias), for example, treatment of severe Alzheimer’s disease, can be helpful. Organic (Including Symptomatic) Mental Disorders 27

ORGANIC AMNESTIC SYNDROME Transient Global Amnesia A rare disorder with an abrupt onset, it resembles Organic amnestic syndrome is characterised by the amnestic syndrome closely. Differentiation is made following clinical features: on the basis of an abrupt onset and patient’s severe 1. Impairment of memory due to an underlying distress (because of memory loss) in transient global organic cause, amnesia. This syndrome is probably caused by tempo- 2. No severe disturbance of consciousness and atten- rary cerebral ischaemia in the distribution of posterior tion (unlike delirium), and cerebral circu lation. 3. No global disturbance of intellectual function, abstract thinking and personality (unlike dementia). Aetiology The impairment of memory is characterised by a 1. Thiamine defi ciency: The most common cause severe impairment of recent memory or short-term of organic amnestic syndrome is chronic alcohol memory (inability to learn new material). This is as- dependence (alcoholism). It is also called as sociated with impaired remote memory or long-term the Wernicke-Korsakoff syndrome. Wernicke’s memory (inability to recall previously learned mate- encephalopathy is the acute phase of delirium rial). There is however no impairment of immediate preceding the organic amnestic syndrome, while memory (i.e. immediate retention and recall). Korsakoff’s syndrome is the chronic phase of Although recent memory is severely dis turbed, very amnestic syndrome. remote events are better remembered, especially in the 2. Any other lesion involving bilaterally the inner initial stages. Recent memory impairment also leads to core of limbic system (i.e. mammillary bodies, disorientation in time and place. To fi ll in the memory fornix, hippocampus and para-hippocampal gaps, the patient uses imaginary events in the early structures of medial temporal lobe, pos terior phase of illness (confabulation ). With the progression hypothalamus and dorsomedial thalamic nuclei), of the disease, confabulation often disappears. such as: i. Head trauma, Diagnosis ii. Surgical procedure (e.g. bilateral temporal According to ICD-10, the fol lowing features are re- lobectomy), quired for the diagnosis: recent memory impairment iii. Hypoxia, (anterograde and retrograde amnesia), no impair- iv. Posterior cerebral artery stroke (bila teral), ment of immediate retention and recall, attention, v. Herpes simplex encephalitis, and consciousness, and global intellectual functioning, vi. Space occupying lesions in the region of III and historical or objective evidence of brain disease ventricle (e.g. neoplasms). or injury (occurs particularly with bilateral involvement of diencephalic and medial temporal structures). Management 1. Treatment of the underlying cause, e.g. thiamine Differential Diagnosis (high doses) in Wernicke-Korsakoff syndrome. Amnestic syndrome should be differentiated from However usually the treatment is of not much help, delirium, dementia, non-organic mental disorders and except in prevention of further deterioration and transient global amnesia. Differen tiation from the fi rst the prognosis is often poor. three is relatively easy on the basis of the pattern of 2. Supportive care for general condition and treat- memory loss. ment of the associated medical illness. 28 A Short Textbook of Psychiatry

OTHER ORGANIC MENTAL ORGANIC HALLUCINOSIS DISORDERS (DUE TO BRAIN DAMAGE AND DYSFUNCTION, AND TO According to ICD-10, presence of persistent or recur- PHYSICAL DISEASES) rent hallucinations due to an underlying organic cause This group includes miscellaneous mental disorders is required for the diagnosis of organic hallucinosis, which are causally related to brain dysfunction due to in addition to the general guide lines for the diagnosis primary cerebral disease, systemic disease (second- of other organic mental disorders, described earlier. ary), or toxic sub stances. It is important to rule out any major disturbance of According to ICD-10, an evidence of cerebral consciousness, intelligence, memory, mood or disease, damage or dysfunction, or of systemic thought. physical disease, known to be associated with one These hallucinations can occur in any sensory of the listed syndromes is required, with a temporal modality but are usually visual (most common) or relationship between development of the underlying audi tory in nature. In many cases, they depend on disease and the onset of the mental syndrome, with the underlying cause. These halluci nations can range recovery from the mental disorder following removal from very simple and unformed, to very complex and or improvement of the underlying presumed cause, well-organised. Usually the patients realise that the and an absence of evidence to suggest an alternative hallucinations are not real but sometimes there may cause of the mental syndrome (such as a strong family be a delusional elaboration of hallu cinations. history or precipitating stress). If conditions 1 and 2 are present, a provisional Aetiology diagnosis can be made; if all four are present, the 1. Drugs: Hallucinogens (LSD, psilocybin, mesca- certainty of diagnosis is signiﬁ cantly increased. line), cocaine, cannabis, phencyclidine (PCP), The following clinical conditions are known to levodopa, bromocriptine, amanta dine, ephedrine, be associated with an increased risk for these other propranolol, pentazocine, methyl pheni date, imi- organic mental disorders: pramine, anticholiner gics, bromide. 2. Alcohol: In alcoholic hallucinosis, auditory hal- Primary Cerebral Diseases lucinations are usually more common. Epilepsy, limbic encephalitis, Huntington’s disease, 3. Sensory deprivation. head trauma, brain neoplasms, vascular cerebral dis- 4. ‘Release’ hallucinations due to sensory pathway ease, cerebral malformations. disease, e.g. bilateral cataracts, otoscle rosis, optic neuritis. Systemic Diseases 5. Migraine. Extracranial neoplasms (e.g. carcinoma pancreas), 6. Epilepsy: Complex partial seizures. collagen diseases (e.g. SLE), endocrine disease (e.g. 7. Intracranial space occupying lesions. hypothyroidism, hyperthyroidism, Cushing’s disease), 8. Temporal arteritis. metabolic disorders (e.g. hypoglycaemia, porphyria, 9. Brain stem lesions (peduncular hallucinosis). hypoxia); infectious diseases (e.g. trypanosomiasis). Management Drugs 1. Treatment of the underlying cause, if treatable. Steroids, propranolol, levodopa, methyldopa, antihy- 2. Symptomatic treatment with a low dose of an pertensives, antimalarials, alcohol and other psychoac- antipsychotic medication (such as Haloperidol, tive substances. Risperidone and Olanzapine) may be needed. Organic (Including Symptomatic) Mental Disorders 29

ORGANIC CATATONIC DISORDER earlier. It is important to rule out any major disturbance of consciousness, orientation, memory, or mood. According to the ICD-10, the fol lowing features The delusions are variable and the type depends on are required for the diagnosis of organic catatonic the underlying aetiology. The most common delusions disorder, in addition to the general guidelines for the are persecutory in nature. Hallucinations (visual more diagnosis of other organic mental disorders, described often than auditory) may accompany the delusions. earlier: Schneiderian fi rst rank symptoms (SFRS) are usually 1. Stupor (diminution or complete absence of sponta- not seen the organic delusional disorder (in contrast neous movement with partial or complete mutism, to schizophrenia). negativism, and rigid posturing); 2. Excitement (gross hypermotility with or without Diagnosis a tendency to assaultiveness); Organic delusional disorder secondary to ampheta- 3. Mixed (shifting rapidly and unpredictably from mine use may be diffi cult to differen tiate from para- hypo- to hyperactivity). noid schizophrenia. The differen tiating points are an The presence of other catatonic symptoms and acute onset, history of amphetamine use prior to the signs increases the confi dence in the diagnosis. The onset, predominant visual hallucinations which may catatonic symptoms and signs are described in detail be fl eeting, absence of formal thought disorder and a in Chapter 5. more ‘appropriate’ affect. Aetiology Aetiology The aetiology and management of organic catatonic 1. Drugs: Amphetamines, hallucinogens, cannabis, disorder is described in detail in Chapter 19. disulfi ram 2. Complex partial seizures (e.g. temporal lobe Management epilepsy) 1. Treatment of the underlying cause, if amenable to 3. Huntington’s chorea (initial stages), Parkinson’s treatment. disease, Wilson’s disease, and idiopathic basal 2. Symptomatic treatment with low dose of a short- ganglia calcifi cation acting benzodiazepine (e.g. Lorazepam), or elec- 4. Right parietal lobe lesions, especially vas cular troconvulsive therapy (if needed). Antipsychotics lesions should usually be avoided as they can make 5. Lesions involving limbic system (e.g. tumours) catatonic features worse; however small doses 6. Spinocerebellar degeneration of atypical antipsychotics such as Risperidone, 7. Cerebral malaria Olanzapine, Aripiprazole or Quetiapine can be 8. Herpes simplex encephalitis

used with care. 9. Nutritional deﬁ ciencies (Vitamin B12, iron) 10. Demyelinating disorders (such as multiple scle- ORGANIC DELUSIONAL rosis, metachromatic leukodystrophy) (SCHIZOPHRENIA-LIKE) DISORDER Management According to ICD-10, presence of predominant 1. Treatment of the underlying cause such as removal delusions caused by an underlying organic cause is of toxic agent in amphetamine psychosis. required for the diagnosis of organic delusional dis- 2. Symptomatic management with a low dose of an order, in addition to the general guidelines for the antipsychotic medication (such as Risperidone, Halo- diagnosis of other organic mental disorders, described peridol, Olanzapine, or Quetiapine) may be needed. 30 A Short Textbook of Psychiatry

ORGANIC MOOD (AFFECTIVE) 4. Post-viral illnesses: Infl uenza, infectious mono- DISORDER nucleosis, viral pneumonia, infectious hepatitis. 5. Defi ciencies: Pellagra, defi ciency of thiamine,

According to ICD-10, presence of prominent and folate, niacin, folate, B12. persistent mood disturbance caused by an underlying 6. Others: Carcinoma pancreas (depression), SLE, organic cause is required for the diagnosis of organic perni cious anaemia, temporal arteritis (depres- mood disorder, in addition to the general guidelines sion), carcinoid syndrome (mania). for the diagnosis of other organic mental disorders, described earlier. It is important to rule out any major Management disturbance of consciousness, orientation, or memory. 1. Management of the underlying organic cause, if The mood disturbance can be a major depres sive treatable. episode, a manic episode, or a mixed affective episode. 2. Symptomatic management, if the episodes are The severity may vary from mild to severe. severe. For example, for a manic episode, low dose antipsychotic medication (such as risperidone, Aetiology haloperidol, olanzapine) and/or a mood stabiliser Some of the causes of organic mood disorder are (such as valproate); and for a depres sive episode, listed below: low dose antidepressants (such as sertraline or mir- 1. Drugs: tazapine). Antipsychotics are not recommended Mania: INH, Levodopa, Bromide, LSD, Corti- in patients who have suffered from stroke and/or costeroids (hypomania), Hallucinogens, Tricyclic dementia as the risk of mortality is higher. antidepressants, Cocaine, Baclofen, Ampheta- Pathological laughter and crying (associated mines, Bromocriptine, Cimetidine, Procyclidine with multiple sclerosis or stroke) can similarly Depression: Reserpine, Ethanol, Clonidine, respond to small dose SSRIs or small dose am- Methyldopa, Propranolol, Corticosteroids, An- itriptyline. tipsychotics (particularly typical antipsychotics), Cimetidine, Anticancer chemo therapy, Oral con- ORGANIC ANXIETY DISORDER traceptives. Any drug a depressed person is taking should be According to ICD-10, presence of prominent and considered a potential factor in the causation of persistent generalised anxiety or panic caused by an depressive episode. underlying cause is required for diagnosis of organic 2. Endocrine disorders: anxiety disorder, in addition to the general guidelines Mania: Hyperthyroidism for the diagnosis of other organic mental disorders, Depression: Hypothyroidism, Cushing’s syn- described earlier. It is important to rule out any major drome, Addison’s disease, hyper- and hypo- disturbance of consciousness, orientation, memory, parathyroidism. personality, thought, perception, or mood. 3. CNS disorders: Parkinsonism, Huntington’s chorea, PSP (progressive supranuclear palsy; Aetiology depression more likely), CVAs (cerebrovascular 1. Drugs and toxins: Cocaine, caffeine, amphe- accidents; left-sided anterior lesions and right- tamines and other sympathomimetics, alcohol and sided posterior lesions cause depression in stroke), drug withdrawal, heavy metals, penicillin. cerebral tumours, epilepsy (com plex partial 2. Endocrine disorders: Thyroid, pituitary, parathy- seizures), neurosyphilis (GPI), head injury (mania roid, or adrenal dysfunction; pheochro mocytoma; more likely), multiple sclerosis. fasting hypoglycaemia, carci noid syndrome. Organic (Including Symptomatic) Mental Disorders 31

3. Systemic diseases: Cardiac arrhythmias, mitral apathy, accentuation of earlier personality traits, or valve prolapse syndrome, chronic obstructive hostility. pulmonary disease, coronary artery disease, According to ICD-10, the following features are pulmonary embolism, anaemia, fever, defi ciency required for diagnosis of organic personality disorder, diseases. in addition to the general guidelines for the diagnosis 4. CNS diseases: Cerebral tumours, epilepsy (espe- of other organic mental disorders, described earlier. cially complex partial seizures of temporal lobe In addition to an established history or other evidence origin), cerebrovascular disease, postconcussional of brain disease, damage, or dysfunction, a defi nitive syndrome. diagnosis requires the presence of two or more of six features described. These include consistently reduced Management ability to persevere with goal-directed activities, 1. Treatment of the underlying organic cause, if altered emotional behaviour (emotional lability, treatable. euphoria, inappro priate jocularity, irritability or 2. Symptomatic treatment with benzodiazepines, short-lived anger outbursts), expression of needs and beta-blockers (such as propranolol), cognitive impulses without consideration of the consequences, behaviour therapy, and relaxation techniques may cognitive disturbances (such as suspiciousness, para- be needed. noid ideation, and/or excessive preoccupation with a single theme), marked alteration of language produc- ORGANIC PERSONALITY DISORDER tion (such as circumstantiality, over-inclusiveness, (PERSONALITY AND BEHAVIOURAL visco sity, and hypergraphia), and altered sexual DISORDERS DUE TO BRAIN DISEASE, behaviour. DAMAGE AND DYSFUNCTION) Aetiology The organic personality disorder is characterised by 1. Temporal lobe epilepsy (complex partial seizures) a signifi cant alteration of the pre morbid personality which can be associated with temporal lobe (perso- caused by an underlying organic cause without major nality) syndrome (see Table 3.7). disturbance of consciousness, orientation, memory 2. Concussion ( postconcussional syndrome). or per cep tion. The personality change may be char- 3. Encephalitis (postencephalitis syndrome). acterised by poor impulse control, emotional lability, 4. Multiple sclerosis (early).

Table 3.7: Organic Personality Disorders Organic Personality Disorder Clinical Features 1. Frontal lobe syndrome (Types) a. Orbito-frontal syndrome Disinhibition, jocularity, impulsivity, impaired insight and judgement (Pseudo-psychopathic) b. Frontal convexity type Apathy, lack of initiative, retardation, perseveration (Pseudo-depressive) c. Medial frontal syndrome Akinesis, incontinence, poor verbal output (Akinetic) 2. Temporal lobe syndrome Egocentricity, explosive affect, perseveration, excessive religiosity, obsessional traits 3. Bilateral temporal lobe or Emotional placcidity, hyper-orality, altered sexual behaviour, limbic system lesions excessive exploration of environment (hyper-metamorphosis) 32 A Short Textbook of Psychiatry

5. Cerebral neoplasms, especially in frontal lobe (fron- dyscontrol, and/or antipsychotics (occasio nally) tal lobe syndromes) and parietal lobe (see Table 3.7). for violent behaviour may be needed. 6. Cerebrovascular disease. MISCELLANEOUS ORGANIC 7. Psychoactive drugs (rarely). MENTAL DISORDERS

Management Other organic mental disorders described in ICD-10 1. Treatment of the underlying cause, if treatable. include organic dissociative disorder, organic emo- 2. Symptomatic treatment, with lithium or car- tionally labile (asthenic) disorder, and mild cognitive bamazepine for aggressive behaviour and impulse disorder. Psychoactive Substance 4 Use Disorders

A drug is defi ned (by WHO) as any substance that, renal failure or idiosyncratic sensitivity) even a low when taken into the living organism, may modify one dose may lead to intoxication. The intensity of intoxi- or more of its functions. This defi ni tion conceptual- cation lessens with time, and effects eventually disap- ises ‘drug’ in a very broad way, including not only pear in the absence of further use of the substance. The the medi ca tions but also the other pharmacologically recovery is therefore complete, except where tissue active substances. damage or another complication has arisen. The words ‘drug addiction’ and ‘drug addict’ were The following codes may be used to indicate dropped from scientifi c use due to their derogatory whether the acute intoxication was associated with connotation. Instead ‘ drug abuse’, ‘ drug dependence’, any complications: ‘ harmful use’, ‘misuse’, and ‘psychoactive substance i. uncomplicated (symptoms of varying seve rity, use disorders’ are the terms used in the current nomen- usually dose-dependent, particularly at high clature. A psychoactive drug is one that is capable of dose levels); altering the mental functioning. ii. with trauma or other bodily injury; There are four important patterns of substance use iii. with other medical complications (such as hae- disorders, which may overlap with each other. matemesis, inhalation of vomitus); 1. Acute intoxication, iv. with delirium; 2. Withdrawal state, v. with perceptual distortions; 3. Dependence syndrome, and vi. with coma; 4. Harmful use. vii. with convulsions; and viii. pathological intoxication (only for alcohol). Acute Intoxication According to the ICD-10, acute intoxication is a Withdrawal State transient condition following the administration of A withdrawal state is characterised by a cluster of alcohol or other psychoactive substance, resulting symp toms, often specifi c to the drug used, which in disturbances in level of consciousness, cognition, develop on total or partial withdrawal of a drug, usu- perception, affect or behaviour, or other psychophysio- ally after repeated and/or high-dose use. This, too, is lo gical func tions and responses. This is usually associ- a short-lasting syndrome with usual duration of few ated with high blood levels of the drug. hours to few days. However, in certain cases where the threshold is Typically, the patient reports that the withdrawal low (due to a serious medical illness such as chronic symptoms are relieved by further substance use. 34 A Short Textbook of Psychiatry

The withdrawal state is further classifi ed as: 5. Progressive neglect of alternative pleasures or i. uncomplicated; interests because of psychoactive substance use, ii. with convulsions; and increased amount of time necessary to obtain or iii. with delirium. take the substance or to recover from its effects. 6. Persisting with substance use despite clear evi- Dependence Syndrome dence of overtly harmful consequences, such as According to the ICD-10, the depen dence syndrome is harm to the liver through excessive drinking, a cluster of physio logical, behavioural, and cognitive depressive mood states conse quent to periods of phenomena in which the use of a substance or a class heavy substance use, or drug-related impairment of substances takes on a much higher priority for a of cognitive functioning; efforts should be made given individual than other behaviours that once had to determine that the user was actually, or could greater value. be expected to be, aware of the nature and extent A central descriptive characteristic of the de- of the harm. pendence syndrome is the desire (often strong and A narrowing of personal repertoire of patterns of sometimes overpowering) to take psychoactive psychoactive substance use has also been described as substances (which may or may not have been medi- a characteristic feature of the dependence syndrome cally prescribed), alcohol, or tobacco. There may be (e.g. a tendency to drink in the same way on weekdays evidence that return to substance use after a period and weekends, regardless of the social constraints that of abstinence leads to a more rapid reappearance of determine appropriate drinking behaviour). other features of the syndrome than occurs with non- The dependence syndrome can be further coded dependent individuals. as (ICD-10): A defi nite diagnosis of dependence should usually i. currently abstinent; be made only if at least three of the following have ii. currently abstinent, but in a protected environ ment been experienced or exhibited at sometime during the (e.g. in hospital, in a therapeutic community, in p revious year: prison, etc.); 1. A strong desire or sense of compulsion to take the iii. currently on a clinically supervised maintenance substance. or replacement regime (controlled dependence, 2. Diffi culties in controlling the substance-taking e.g. with methadone; nicotine gum or nicotine behaviour in terms of its onset, termination, or patch); levels of use. iv. currently abstinent, but receiving treatment with 3. A physiological withdrawal state when the sub- aversive or blocking drugs (e.g. naltrexone or stance use has ceased or reduced, as evidenced disulfi ram); by the characteristic withdrawal syndrome for v. currently using the substance (active depen dence); the substance; or use of the same (or a closely vi. continuous use; and related) substance with the intention of relieving vii. episodic use ( dipsomania). or avoiding withdrawal symptoms. The dependence can be either psychic, or physical, 4. Evidence of tolerance , such that increased doses of or both. the psychoactive substance are requi red in order to achieve effects originally produced by lower doses Harmful Use (clear examples of this are found in the alcohol- Harmful use is characterised by: and opiate-dependent individuals who may take 1. Continued drug use, despite the awareness of daily doses that are suffi cient to incapacitate or harmful medical and/or social effect of the drug kill non-tolerant users). being used, and/or Psychoactive Substance Use Disorders 35

2. A pattern of physically hazardous use of drug (e.g. 6. Hallucinogens, e.g. LSD, phencyclidine (PCP) driving during intoxication). 7. Sedatives and hypnotics, e.g. barbiturates The diagnosis requires that the actual damage 8. Inhalants, e.g. volatile solvents should have been caused to the mental or physical 9. Nicotine, and health of the user. Harmful use is not diagnosed, if a 10. Other stimulants (e.g. caffeine). dependence syndrome is present. DSM-IV-TR uses the The various psychoactive substances are sum- term substance abuse instead, with minor variations marised in Table 4.1. in description. The other syndromes associated with the psycho- Aetiology active substance use in ICD-10 include psychotic dis- The various aetiological factors in substance use disorder, amnesic syndrome, and residual and late-onset orders are brieﬂ y summarised in Table 4.2. (delayed onset) psychotic disorder. ALCOHOL USE DISORDERS Psychoactive Substances The major dependence producing drugs are: Alcohol dependence was previously called as alcohol- 1. Alcohol ism. This term much like ‘addiction’ has been dropped 2. Opioids, e.g. opium, heroin due to its derogatory meaning. 3. Cannabinoids, e.g. cannabis According to Jellinek, there are ﬁ ve ‘species’ of 4. Cocaine alcohol dependence (alcoholism) on the basis of the 5. Amphetamine and other sympatho mimetics patterns of use (and not on the basis of severity).

Table 4.1: Psychoactive Substance Use Disorders Drug Usual Route of Physical Psychic Tolerance Administration Dependence Dependence 1 Alcohol Oral ++ ++ + 2 Amphetamines Oral, Parenteral ++ ++ +++ 3 Barbiturates Oral, Parenteral ++ ++ +++ 4 Benzodiazepines Oral, Parenteral + + + 5 Caffeine Oral + ++ + 6 Cannabis Smoking, Oral ± ++ + ( Marihuana) 7 Cocaine Inhalation, Oral, ± ++ – Smoking, Parenteral 8 Lysergic acid Oral – + + diethylamide ( LSD) 9 Nicotine Oral, Smoking + ++ + 10 Opioids Oral, Parenteral, Smoking +++ +++ +++ 11 Phencyclidine (PCP) Smoking, Inhalation, Parenteral, Oral ± + + 12 Volatile solvents Inhalation ± ++ + – = None; ± = Probable/Little; + = Some/Mild; ++ = Moderate; +++ = Severe. The dependence can be either psychic, or physical, or both. 36 A Short Textbook of Psychiatry

Table 4.2: Aetiological Factors in Substance Use A. Alpha (α) Disorders i. Excessive and inappropriate drinking to relieve physical and/or emotional pain. 1. Biological Factors ii. No loss of control. i. Genetic vulnerability (family history of substance use disorder; for example in type II alcoholism) iii. Ability to abstain present. ii. Co-morbid psychiatric disorder or personality B. Beta (β) disorder i. Excessive and inappropriate drinking. iii. Co-morbid medical disorders ii. Physical complications (e.g. cirrhosis, gastritis and iv. Reinforcing effects of drugs (explains continu- neuritis) due to cultural drinking patterns and poor ation of drug use) nutrition. v. Withdrawal effects and craving (explains con- iii. No dependence. tinuation of drug use) C. Gamma (γ); also called as malignant alcoholism vi. Biochemical factors (for example, role of i. Progressive course. dopamine and norepinephrine in cocaine, ii. Physical dependence with tolerance and with- ethanol and opioid dependence) drawal symptoms. 2. Psychological Factors iii. Psychological dependence, with inability to con- i. Curiosity; need for novelty seeking trol drinking. ii. General rebelliousness and social non-conform- D. Delta (δ) ity i. Inability to abstain. iii. Early initiation of alcohol and tobacco ii. Tolerance. iv. Poor impulse control iii. Withdrawal symptoms. v. Sensation-seeking (high) iv. The amount of alcohol consumed can be control- vi. Low self-esteem (anomie) led. vii. Concerns regarding personal autonomy v. Social disruption is minimal. viii. Poor stress management skills E. Epsilon (ε) ix. Childhood trauma or loss i. Dipsomania (compulsive-drinking). x. Relief from fatigue and/or boredom ii. Spree-drinking. xi. Escape from reality Earlier, it was believed that γ-alcoholism was more xii. Lack of interest in conventional goals xiii. Psychological distress common in America, while δ-alcoholism was com- 3. Social Factors moner in the wine-drinking countries such as France. i. Peer pressure (often more important than At present the existence of this pattern of distribution parental factors) is doubted and its inclusion in this book is mainly for ii. Modelling (imitating behaviour of important historical reasons. others) Cloninger has classiﬁ ed alcoholism into two types, iii. Ease of availability of alcohol and drugs on the basis of the relative importance of genetic and iv. Strictness of drug law enforcement environ mental factors (Table 4.3). v. Intrafamilial conﬂ icts Alcohol dependence is more common in males, vi. Religious reasons and has an onset in late second or early third decade. vii. Poor social/familial support The course is usually insidious. There is often an viii. ‘Perceived distance’ within the family associated abuse or dependence of other drugs. If the ix. Permissive social attitudes onset occurs late in life, especially after 40 years of x. Rapid urbanisation. age, an underlying mood disorder should be looked for. Psychoactive Substance Use Disorders 37

Table 4.3: Classifi cation of Alcoholism Factors Type I Type II Synonym Milieu-limited Male-limited Gender Both sexes Mostly in males Age of onset > 25 years < 25 years Aetiological factors Genetic factors important; strong Heritable; environmental environmental infl uences are infl uences are limited contributory Family history May be positive Parental alcoholism and antisocial behaviour usually present Loss of control Present No loss of control Other features Psychological dependence; Drinking followed by aggressive and guilt present behaviour; spontaneous alcohol seeking Pre-morbid Harm avoidance; Novelty-seeking personality traits high reward dependence

Certain l aboratory markers of alcohol depen dence Acute Intoxication have been suggested. These include: i. GGT (γ-glutyl-transferase) is raised to about After a brief period of excitation, there is a generalised 40 IU/L in about 80% of the alcohol dependent central nervous system depression with alcohol use. individuals. GGT returns to normal rapidly (i.e. With increasing intoxication, there is increased reac- within 48 hours) on abstinence from alcohol. An tion time, slowed thinking, distractibility and poor increase of GGT of more than 50% in an abstinent motor control. Later, dysarthria, ataxia and incoordina- individual signifi es a resumption of heavy drinking tion can occur. There is progressive loss of self-control or an abnormality of liver function. with frank disinhibited behaviour. ii. MCV (mean corpuscular volume) is more than The duration of intoxication depends on the 92 fl (normal = 80-90 fl ) in about 60% of the amount and the rapidity of ingestion of alcohol. Usu- alcohol dependent individuals. MCV takes ally the signs of intoxication are obvious with blood several weeks to return to normal values after levels of 150-200 mg%. With blood alcohol levels abstinence. of 300-450 mg%, increasing drowsiness followed iii. Other lab markers include alkaline phosphatase, by coma and respiratory depression develop. Death AST, ALT, uric acid, blood triglyce rides and CK. occurs with blood alcohol levels between 400 to 800 GGT and MCV together can usually identify three mg% (Table 4.6). out of four problem drinkers. In addition, BAC (blood Occasionally a small dose of alcohol may produce alcohol concentration) and breath analyser can be used acute intoxication in some persons. This is known as for the purpose of identifi cation. pathological intoxication. Another feature, sometimes For detection of the problem drinkers in the com- seen in acute intoxication, is the development of munity, several screening instruments are available. amnesia or blackouts . MAST (Michigan Alcoholism Screening Test) is frequently used for this purpose whilst CAGE ques- Withdrawal Syndrome tionnaire (Table 4.5) is the easiest to be administered The most common withdrawal syndrome is a hangover (it takes only about 1-2 minutes). on the next morning. Mild tremors, nausea, vomiting, 38 A Short Textbook of Psychiatry weakness, irritability, inso mnia and anxiety are the Multiple seizures (2-6 at one time) are more com- other common withdra wal symptoms. Sometimes mon than single seizures. Sometimes, status epilep- the withdrawal synd rome may be more severe, char- ticus may be precipitated. In about 30% of the cases, acterised by one of the following three disturbances: delirium tremens follows. delirium tremens, alcoholic seizures and alcoholic 3. Alcoholic hallucinosis hallucinosis. It is important to remember that alcohol Alcoholic hallucinosis is characterised by the presence withdrawal syndrome can be associated with marked of hallucinations (usually auditory) during partial or morbidity as well as signifi cant mortality, and it is complete abstinence, following regular alcohol intake. important to treat it correctly. It occurs in about 2% of patients. 1. Delirium tremens These hallucinations persist after the withdrawal Delirium tremens (DT) is the most severe alcohol syndrome is over, and classically occur in clear con- withdrawal syndrome. It occurs usually within 2-4 sciousness. Usually recovery occurs within one month days of complete or signifi cant abstinence from heavy and the duration is very rarely more than six months. alcohol drinking in about 5% of patients, as compared to acute tremulousness which occurs in about 34% Complications of Chronic Alcohol Use of patients. Alcohol dependence is often associated with several The course is short, with recovery occurring within complications; both medical and social (Table 4.4). 3-7 days. This is an acute organic brain syndrome Some withdrawal and intoxication related complica- (delirium) with characteristic features of: tions have described above whilst the neuropsychiatric i. Clouding of consciousness with disorien tation in complications are discussed below. time and place. Wernicke’s encephalopathy ii. Poor attention span and distractibility. This is an acute reaction to a severe defi ciency of iii. Visual (and also auditory) hallucinations and illu- thiamine, the commonest cause being chronic alcohol sions, which are often vivid and very frightening. use. Characteristically, the onset occurs after a period Tactile hallucina tions of insects crawling over the of persistent vomiting. The important clinical signs body may occur. are: iv. Marked autonomic disturbance with tachy cardia, i. Ocular signs: Coarse nystagmus and ophthal - fever, hypertension, sweating and pupillary dilata- moplegia, with bilateral external rectus paralysis tion. occurring early. In addition, pupillary irregulari- v. Psychomotor agitation and ataxia. ties, reti nal haemorrhages and papil loedema can vi. Insomnia, with a reversal of sleep-wake pattern. occur, causing an impairment of vision. vii. Dehydration with electrolyte imbalance. ii. Higher mental function disturbance: Disorien- Death can occur in 5-10% of patients with delirium tation, confusion, recent memory distur bances, tremens and is often due to cardiovascular collapse, poor attention span and distractibility are quite infection, hyperthermia or self-infl icted injury. At common. Other early symptoms are apathy and times, intercurrent medical illnesses such as pneumo- ataxia. nia, fractures, liver disease or pulmonary tuberculosis Peripheral neuropathy and serious malnut ri tion may complicate the clinical picture. are often co-existent. Neuropatho logically, neuronal 2. Alcoholic seizures (‘ rum fi ts’) degeneration and haemorrhage are seen in thalamus, Generalised tonic clonic seizures occur in about 10% hypotha lamus, mammil lary bodies and midbrain. of alcohol dependence patients, usually 12-48 hours Korsakoff’s psychosis after a heavy bout of drinking. Often these patients As Korsakoff’s psychosis often follows Wernicke’s have been drinking alcohol in large amounts on a encephalopathy; these are together referred to as regular basis for many years. Wernicke-Korsakoff syndrome. Psychoactive Substance Use Disorders 39

Table 4.4: Some Complications of Alcohol Dependence I. Medical Complications ii. Foetal alcohol syndrome (craniofacial ano malies, A. Gastrointestinal System growth retardation, major organ system malfor- i. Fatty liver, cirrhosis of liver, hepatitis, liver cell mations) carcinoma, liver failure iii. Alcoholic hypoglycaemia and ketoacidosis ii. Gastritis, refl ux oesophagitis, oesophageal vari ces, iv. Cardiomyopathy, cardiac beri-beri Mallory-Weiss syndrome, achlorhydria, peptic v. Alcoholic myopathy ulcer, carcinoma stomach and oeso phagus vi. Anaemia, thrombocytopenia, Vitamin K factor iii. Malabsorption syndrome, protein-losing enter- defi ciency, haemolytic anaemia opathy vii. Accidental hypothermia iv. Pancreatitis: acute, chronic, and relapsing viii. Pseudo-Cushing’s syndrome, hypogonadism, B. Central Nervous System gynaecomastia (in men), amenorrhoea, infer tility, i. Peripheral neuropathy decreased testosterone and increa sed LH levels ii. Delirium tremens ix. Risk for coronary artery disease iii. Rum fi ts (Alcohol withdrawal seizures) x. Malnutrition, pellagra iv. Alcoholic hallucinosis xi. Decreased immune function and proneness to v. Alcoholic jealousy infections such as tuberculosis vi. Wernicke-Korsakoff psychosis xii. Sexual dysfunction vii. Marchiafava-Bignami disease II. Social Complications viii. Alcoholic dementia i. Accidents ix. Suicide ii. Marital disharmony x. Cerebellar degeneration iii. Divorce xi. Central pontine myelinosis iv. Occupational problems, with loss of pro ductive xii. Head injury and fractures. man-hours C. Miscellaneous v. Increased incidence of drug dependence i. Acne rosacea, palmar erythema, rhinophyma, vi. Criminality spider naevi, ascitis, parotid enlargement vii. Financial diffi culties.

Table 4.5: CAGE Questionnaire Table 4.6: Body Fluid Alcohol Levels The CAGE questionnaire basically consists of four BAC* (mg%) Behavioural Correlates questions: 25-100 Excitement i. Have you ever had to Cut down on alcohol (amount)? 80 Legal limit for driving (in UK)** ii. Have you ever been Annoyed by people’s criticism 100-200 Serious intoxication, slurred speech, of alcoholism? incoordination, nystagmus iii. Have you ever felt Guilty about drinking? 200-300 Dangerous 300-350 Hypothermia, dysarthria, cold sweats iv. Have you ever needed an Eye opener drink (early 350-400 Coma, respiratory depression morning drink)? >400 Death may occur A score of 2 or more identifi es problem drinkers. Urinary Diagnostic Equivalent BAC Clinically, Korsakoff’s psychosis presents as an Alcohol (mg%) Use (mg%) organic amnestic syndrome, characterised by gross >120 Suggestive 80 memory disturbances, with confabulation. Insight >200 Diagnostic 150 is often impaired. The neuropathological lesion is *BAC - Blood Alcohol Concentration usually wide-spread, but the most consistent changes **30 mg/100 ml in India (Section 185 of the Motor are seen in bilateral dorsomedial nuclei of thalamus Vehicle Act, 1988) 40 A Short Textbook of Psychiatry and mammillary bodies. The changes are also seen unless the risks of acute discontinuation are felt to be in periventricular and periaqueductal grey matter, high by the treating team. This decision is often based cerebellum and parts of brain stem. on several factors including chronicity of alcohol The underlying cause is believed to be usually dependence, daily amount consumed, past history of severe untreated thiamine defi ciency secondary to alcohol withdrawal complications, level of general chronic alcohol use. health and the patient’s wishes. Marchiafava-Bignami disease The usual duration of uncomplicated withdrawal This is a rare disorder characterised by disorien tation, syndrome is 7-14 days. The aim of detoxifi cation is epilepsy, ataxia, dysarthria, hallucina tions, spastic sympto matic management of emergent withdrawal limb paralysis, and deterioration of personality and symptoms. intellectual functioning. There is a widespread demy- The drugs of choice for detoxifi cation are usually elination of corpus callosum, optic tracts and cerebel- benzodiazepines. Chlordiazepoxide (80-200 mg/day in lar peduncles. The cause is probably an alcohol-related divided doses) and diazepam (40-80 mg/day in divided nutri tional defi ciency. doses) are the most frequently used benzo diazepines. The higher limit of the normal dose range is used in Other Complications delirium tremens. These include: A typical dose of Chlordiazepoxide in moderate i. Alcoholic dementia. alcohol dependence is 20 mg QID (four times a day) ii. Cerebellar degeneration. on day 1, 15 mg QID on day 2, 10 mg QID on day 3, iii. Peripheral neuropathy. 5 mg QID on day 4, 5 mg BD on day 5 and none on iv. Central pontine myelinosis. day 6. However, in more severe dependence, higher doses are needed for longer periods (up to 10 days). Treatment These drugs are used in a standardised protocol, with Before starting any treatment, it is important to follow the dosage steadily decreasing everyday before being these steps: stopped, usually on the tenth day. Clormethiazole (1-2 i. Ruling out (or diagnosing) any physical disorder. g/day) and carbamaze pine (600-1600 mg/day) are ii. Ruling out (or diagnosing) any psychiatric disorder experimental drugs and should not be used routinely and/or co-morbid substance use disorder. for detoxifi cation. iii. Assessment of motivation for treatment. In addition, vitamins should also be adminis tered. iv. Assessment of social support system. In patients suffering from (or likely to suffer from) v. Assessment of personality characteristics of the delirium tremens, peripheral neuropathy, Wernicke- patient. Korsakoff syndrome, and/or with other signs of vita- vi. Assessment of current and past social, interper- min B defi ciency (especially thiamine and nicotinic sonal and occupational functioning. acid), a preparation of vitamin B containing 100 mg

The treatment can be broadly divided into two of thiamine (vitamin B1) should be administered categories which are often interlinked. These are parente rally, twice everyday for 3-5 days. This should detoxifi cation and treatment of alcohol depen dence. be followed by oral adminis tration of vitamin B1 for at least 6 months. Detoxifi cation Care of hydration is another important step; it is Detoxifi cation is the treatment of alcohol withdrawal extremely important not to administer 5% dextrose symptoms, i.e. symptoms produced by the removal of (or any carbohydrate) in delirium tremens (or even in the ‘toxin’ (alcohol). The best way to stop alcohol (or uncomplicated alcohol withdrawal syndrome) without any other drug of dependence) is to stop it suddenly thiamine. Psychoactive Substance Use Disorders 41

Although detoxifi cation can be achieved on an religious in nature, many patients derive benefi ts outpatient (OPD) basis, some patients do require from the group meetings which are non-professional hospitalisation. These patients may present with: in nature. i. Signs of impending delirium tremens (tremor, iv. Deterrent agents autonomic hyperactivity, disorientation, or per- The deterrent agents are also known as alcohol sen- ceptual abnormali ties), or sitising drugs. ii. Psychiatric symptoms (psychotic disorder, mood Disulfi ram (tetraethyl thiuram disulfi de) was dis- disorder, suicidal ideation or attempts, alcohol- covered in 1930s, when it was observed that workers induced neuro psychiatric disorders), or in the rubber industry developed unpleasant reactions iii. Physical illness (caused by chronic alcohol use or to alcohol intake, due to accidental absorption of incidentally present), or antioxidant disulfi ram. The mechanism of action of iv. Inability to stop alcohol in the home setting. disulfi ram is summarised in Figure 4.1. Detoxifi cation is the fi rst step in the treatment of When alcohol is ingested by a person who is on alcohol dependence. disulfi ram, alcohol-derived acetal de hyde cannot be oxidised to acetate and this leads to an accumulation Treatment of Alcohol Dependence of acetaldehyde in blood. This causes the important After the step of detoxifi cation is over, there are sev- disulfiram-ethanol reaction (DER) characterised eral methods to choose from, for further management. by fl ush ing, tachycardia, hypotension, tachypnoea, Some of these important methods include: palpitations, headache, sweating, nausea, vomiting, i. Behaviour therapy giddiness and a sense of impending doom associated The most commonly used behaviour therapy in the with severe anxiety. past has been aversion therapy, using either a sub- The onset of the reaction occurs within 30 minutes, threshold electric shock or an emetic such as apomor- becomes full blown within 1 hour, and subsides usu- phine. Many other methods (covert sensitisation, ally within 2 hours of ingestion of alcohol. In sensitive relaxation techniques, assertiveness training, self- patients or in those who have ingested a large amount control skills, and positive reinforcement) have been of alcohol, DER can be very severe and life threatening used alone or in combination with aversion therapy. due to one or more of the following: shock, myocardial Currently, in most settings, it is considered unethical infarction, convulsions, hypoxia, confusion and coma. to use aversion therapy for the treatment of alcohol Therefore, treatment with disulfi ram is usually dependence. begun in an inpatient hospital setting, usually after ii. Psychotherapy a challenge test with alcohol to demonstrate that Both group and individual psychotherapy have been unpleasant and dangerous side-effects occur, if either used. The patient should be educated about the risks alcohol or alcohol-containing eatable/drink is con- of continuing alcohol use, asked to resume personal sumed whilst treatment is continued with disulfi ram. respon sibility for change and be given a choice of The usual dose of disulfi ram is 250-500 mg/day options for change. Motivational enhancement therapy (taken before bedtime to avoid drowsiness in daytime) with or without cognitive behaviour therapy and life- in the fi rst week and 250 mg/day subsequently for style modifi cation is often useful, if available. the maintenance treatment. The effect begins within iii. Group therapy 12 hours of fi rst dose and remains for 7-10 days after Of particular importance is the voluntary self-help the last dose. The patient should carry a warning card group known as AA (Alcoholics Anonymous), with detailing the forbidden alcohol-containing articles, the branches all over the world and a membership in hun- possible effects and their emergency treatment, along dreds of thousands. Although the approach is partly with patient identifi cation details. 42 A Short Textbook of Psychiatry

Fig. 4.1: Disulfiram: Mode of Action

The contraindications of disulfi ram use are fi rst Acamprosate (the Ca++ salt of N-acetyl-homo taurinate) trimester of pregnancy, coronary artery disease, liver interacts with NMDA receptor-mediated glutamater- failure, chronic renal failure, peripheral neuropathy, gic neurotransmission in the various brain regions muscle disease and psychotic symptoms presently or and reduces Ca++ fl uxes through voltage-operated in the past. channels. In selected patients (such as an older age group, Naltrexone (oral opioid receptor antagonist) prob- good motivation, good social support, absent under- ably interferes with alcohol-induced reinfor cement lying psychopathology and good treatment concord- by blocking opioid receptors. Fluoxetine (and other ance), the response can be dramatic. In addition to SSRIs) have been occasionally used as anti-craving oral prepara tions, subcu taneous disulfi ram implants agents in their usual antidepressant doses. are also now available. However, they provide unpre- vi. Other medications dictable blood levels of disulfi ram. A variety of other medicines such as benzodia- Other deterrent agents zepines, antidepressants, antipsychotics, lithium, 1. Citrated calcium carbimide (CCC): The mecha- carbamazepine, and even narcotics have been tried. nism of action is similar to disulfi ram but onset of These should be used only if there is a special indi- action occurs within 1 hour and is reversible. The cation for their use (for example, antidepressants for usual dosage is 100 mg/d in two divided doses. underlying depression). 2. Metronidazole. vii. Psychosocial rehabilitation 3. Animal charcoal, a fungus (Coprinus atra men - Rehabilitation is an integral part of the multi-modal tarius), sulfonylureas and certain cephalos porins treatment of alcohol dependence. also cause a disulfi ram like action. v. Anti-craving agents OPIOID USE DISORDERS Acamprosate, naltrexone and SSRIs (such as fl uoxetine) are among the medications tried as anti-craving Dried exudate obtained from unripe seed capsules of agents in alcohol dependence. Papaver somniferum has been used and abused for Psychoactive Substance Use Disorders 43

Table 4.7: Opioid Derivatives centuries. The natural alkaloids of opium and their synthetic preparations are highly dependence produc- A. Natural Alkaloids of Opium ing. These are listed in Table 4.7. 1. Morphine In the last few decades, use of opioids has in- 2. Codeine creased markedly all over the world. India, surrounded 3. Thebaine on both sides by the infamous routes of illicit trans port, 4. Noscapine namely the Golden Triangle (Burma-Thailand-Laos) and the Golden Crescent (Iran-Afghanistan-Pakistan) 5. Papaverine has been parti cularly severely affected. B. Synthetic Compounds The most important dependence producing de- 1. Heroin rivatives are morphine and heroin. They both like 2. Nalorphine majority of dependence producing opioids bind to 3. Hydromorphone μ (mu) opioid receptors. The other opioid receptors 4. Methadone are k (kappa, e.g. for pentazocine), δ (delta, e.g. for a 5. Dextropropoxyphene type of enkephalin), σ (sigma, e.g. for phencyclidine), 6. Meperidine (Pethidine) ε (epsilon) and λ (lambda). Heroin or di-acetyl-morphine is about two times 7. Cyclazocine more potent than morphine in injectable form. Apart 8. Levallorphan from the parenteral mode of admini stration, heroin can 9. Diphenoxylate also be smoked or ‘chased’ (chasing the dragon), often in an impure form (called ‘ smack’ or ‘ brown sugar’ yawning, tachycardia, mild hyperten sion, insomnia, in India). Heroin is more addicting than morphine raised body temperature, muscle cramps, generalised and can cause dependence even after a short period bodyache, severe anxiety, piloerection, nausea, vomit- of exposure. Tolerance to heroin occurs rapidly and ing and anorexia. can be increased to up to more than 100 times the ﬁ rst There are marked individual differen ces in pres- dose needed to produce an effect. entation of withdrawal symptoms. Heroin withdrawal syndrome is far more severe than the withdrawal Acute Intoxication syndrome seen with morphine. Intoxication is characterised by apathy, bradycardia, hypotension, respiratory depression, subnormal core Complications body temperature, and pin-point pupils. Later, delayed The important complications of chronic opioid use reﬂ exes, thready pulse and coma may occur in case may include one or more of the following: of a large overdose. In severe intoxication, mydriasis 1. Complications due to illicit drug (conta minants): may occur due to hypoxia. Parkinsonism, degeneration of globus pallidus, peripheral neuro pathy, amblyopia, transverse Withdrawal Syndrome myelitis. The onset of withdrawal symptoms occurs typically 2. Complications due to intravenous use: AIDS, within 12-24 hours, peaks within 24-72 hours, and skin infection(s), thrombophlebitis, pulmo nary symptoms usually subside within 7-10 days of the embolism, septicaemia, viral hepatitis, tetanus, last dose of opioid. endocarditis. The characteristic symptoms include lacrimation, 3. Drug peddling and involvement in criminal activi- rhinorrhoea, pupillary dilation, sweating, diarrhoea, ties (social complication). 44 A Short Textbook of Psychiatry

Treatment argue that one type of dependence is often replaced Before treatment, a correct diagnosis must be made by another (methadone). on the basis of history, examination (pin-point pupils 2. Clonidine is an α2 agonist that acts by inhibiting during intoxication or withdrawal symptoms) and/or norepinephrine release at presynaptic α2 recep- laboratory tests. These tests are: tors. The usual dose is 0.3-1.2 mg/day, and drug 1. Naloxone challenge test (to precipitate withdrawal is tapered off in 10-14 days. It can be started after symptoms). stoppage of either the opioid itself or the substitu- 2. Urinary opioids testing: With radioimmunoassay tion drug (methadone). The important side effects (RIA), free radical assay technique (FRAT), of clonidine are excessive sedation and postural thin layer chromatography (TLC), gas-liquid hypotension. Clonidine treatment is usually started chromatography (GLC), high pressure liquid in an inpatient psychiatric or specialist alcohol and chromatography (HPLC) or enzyme-multiplied drug treatment centre setting. immunoassay technique (EMIT). 3. Naltrexone with Clonidine: Naltrexone is an orally The treatment can be divided into three main types: available narcotic antagonist which, when given to 1. Treatment of overdose. an opioid dependent individual, causes withdrawal 2. Detoxifi cation. symptoms. These symptoms are managed with the 3. Maintenance therapy. addition of clonidine for 10-14 days after which clonidine is withdrawn and the patient is continued Treatment of Opioid Overdose on naltrexone alone. Now if the person takes an An overdose of opioid can be treated with narcotic opioid, there are no pleasu rable experiences, as antagonists (such as naloxone, naltrexone). Usually an the opioid receptors are blocked by naltrexone. intravenous injection of 2 mg naloxone, followed by a Therefore, this method is a combination of detoxi- repeat injection in 5-10 minutes, can cause reversal of fi cation and maintenance treatment. The usual overdose. But as naloxone has a short half-life repeated dose of naltrexone is 100 mg orally, administered doses may be needed every 1-2 hours. This should be on alternate days. Once again treatment is usually combined with general care and supportive treatment. started in an inpatient psychiatric or specialist alcohol and drug treatment centre setting. Detoxifi cation 4. Other Drugs: The other detoxifi cation agents This is a mode of treatment in which the dependent include LAAM (levo-alpha-acetyl-metha dol), person is ‘taken off’ opioids. This is usually done propoxyphene, diphenoxy late, bup re norphine abruptly, followed by management of emergent (long acting synthetic partial μ-agonist which can withdrawal symptoms. It is highly recommended that be administered sublingually), and lofexidine (α2 detoxifi cation is conducted in a safe manner under agonist, similar to clonidine). expert guidance of a specialist. In particular, Buprenorphine has recently been The withdrawal symptoms can be managed by one used widely for detoxifi cation as well as for main- of the following methods: tenance treatment in many parts of the World. Care 1. Use of substitution drugs such as methadone (not must be exercised as there is potential for misuse available in India at present) to ameliorate the with buprenorphine. withdrawal symptoms. Maintenance Therapy The aim is to gradually taper off the patient from methadone (which is less addicting, has a longer After the detoxifi cation phase is over, the patient is half-life, decreases possible criminal behaviour, maintained on one of the following regi mens: and has a much milder withdrawal syndrome). 1. Methadone maintenance However, relapses are common and its opponents (Agonist substitution therapy) Psychoactive Substance Use Disorders 45

This a very popular method used widely in the 4. Psychosocial rehabilitation Western World. 20-50 mg/day of methadone is given This is a very important step in the post-detoxifi cation to the patients to ‘shift’ them from ‘hard’ drugs, thus phase, in the absence of which relapse rates can be decreasing IV use and criminal behaviour. Its use very high. Rehabilitation should be at both occupa- in India has not been recommended by an expert tional and social levels. committee for de-addiction services. Other drugs such as LAAM and buprenorphine CANNABIS USE DISORDER can be used for main tenance treatment. 2. Opioid antagonists Cannabis is derived from the hemp plant, Cannabis Opioid antagonists have been in use for a long time sativa, which has several varieties named after the but they were either partial antagonists (such as nalor- region in which it is found (e.g. sativa indica in India phine) or had to be administered parenterally (such as and Pakistan, and americana in America). naloxone). Now with the availability of orally effective Cannabis (street names: grass, hash or hashish, and very potent antagonists, such as naltrexone, the marihuana) produces more than 400 identifiable use of opioid antagonists in routine practice has been chemicals of which about 50 are cannabinoids, the simplifi ed. The usual maintenance dose is 100 mg on most active being Δ-9- tetrahydrocannabinol (Δ9- Mondays and Wednesdays, and 150 mg on Fridays. THC). The pistillate form of the female plant is more Naltrexone combined with clonidine, as described important in cannabis production (Table 4.8). above, is a very effective method for detoxifi cation Recently, a Gi-protein (inhibitory G-protein) linked as well as for maintenance treatment. cannabinoid receptor has been found (in basal ganglia, 3. Othe r methods hippocampus and cerebellum) which inhibits the ade- These include individual psychotherapy, behaviour nylate cyclase activity in a dose-dependent manner. therapy, interpersonal therapy, cogni tive behaviour Cannabis produces a very mild physical depend- therapy (CBT), motivational enhancement therapy, ence, with a relatively mild with drawal syndrome, self-control strategies, psychotropic drugs for asso- which is characterised by fine tremors, irritabil- ciated psycho pathology, family therapy, and group ity, restlessness, nervousness, insomnia, decreased therapy (e.g. in therapeutic communities such as Syna- appetite and craving. This syn drome begins within non, self-help groups such as Narcotic Anonymous or few hours of stopping cannabis use and lasts for 4 to NA). These methods have to be tailored for use in an 5 days. However, some health professionals feel that individual patient. there is no true physical dependence with cannabis.

Table 4.8: Cannabis Preparations Cannabis Portion of Plant THC Content (%) Potency Preparation (as compared to ‘Bhang’) 1 Hashish/Charas Resinous exudate from the fl owering 8-14 10 tops of cultivated plantsh 2 Ganja Small leaves and brackets of infl orescence 1-2 2 of highly cultivated plants 3 Bhang Dried leaves, fl owering shoots and 1 1 cut tops of uncultivated plants 4 Hash oil Lipid soluble plant extract 15-40 25 46 A Short Textbook of Psychiatry

On the other hand, psychological dependence 2. Amotivational syndrome: Chronic cannabis use is ranges from mild (occasional ‘trips’) to marked (com- postulated to cause lethargy, apathy, loss of inter- pulsive use). All the active ingredients are called as est, anergia, reduced drive and lack of ambition. marijuana or marihuana. Cannabis can be detected The aetiological role of cannabis in this disorder in urine for up to 3 weeks after chronic heavy use. is however far from proven. 3. ‘Hemp insanity’ or cannabis psychosis: Indian Acute Intoxication hemp insanity was fi rst described by Dhunjibhoy Mild cannabis intoxication is characterised by mild in 1930. Thereafter, several reports appeared impairment of consciousness and orientation, light- in literature from India, Egypt, Morocco and headedness, tachycardia, a sense of fl oating in the Nigeria. It was described as being similar to an air, a euphoric dream-like state, alternation (either acute schizoph reni form disorder with disorien- an increase or decrease) in psychomotor activity and tation and confusion, and with a good prognosis. tre mors, in addition to photophobia, lacrimation, The validity of this specifi c disorder is currently tachycardia, reddening of conjunctiva, dry mouth and doubted. increased appetite. There is often a curious splitting of 4. Other complications: Chronic cannabis use some- consciousness, in which the user seems to observe his times leads to memory impairment, worsening own intoxication as a non-participant observer, along or relapse in schizophrenia or mood disorder, with a feeling that time is slowed down. chronic obstructive airway disease, pulmonary Perceptual disturbances are common and can malignancies, alteration in both the humoral and include depersonalisation, derealisation, synaesthe- cell-media ted immunity, decreased testosterone sias (sensation in one sensory modality caused by a levels, anovulatory cycles, reversible inhibi tion sensation in another sensory modality, e.g. ‘seeing’ of spermato genesis, blockade of gonado tropin the music) and increased sensitivity to sound. How- releasing hormone, and increased risk for the ever, hallucinations are seen only in marked to severe develo ping foetus (if taken during pregnancy). intoxication. These are often visual, ranging from elementary fl ashes of lights and geometrical fi gures Treatment to complex human faces and pictures. As the withdrawal syndrome is usually very mild, the Mild cannabis intoxication releases inhibitions, management consists of supportive and symp tomatic which is expressed in words and emotions rather than treatment, if the patient comes to medical attention. in actions. ‘ Flashback phenomenon’ has been descri- The psychiatric symptoms may require appropriate bed, and is characterised by a recurrence of cannabis psychotropic medication and sometimes hospitali- use experience in the absence of current cannabis use. sation. Psychotherapy and psychoeducation are very important in the management of psychic Complications dependence. The complications of cannabis use can include: 1. Transient or short-lasting psychiatric disorders: COCAINE USE DISORDER Acute anxiety, paranoid psychosis, hys terical fugue-like states, suicidal ideation, hypo mania, Cocaine is an alkaloid derived from the coca bush, schizophrenia-like state (which is charac terised by Erythroxylum coca, found in Bolivia and Peru. It was persecutory delusions, hallucina tions and at times isolated by Albert Neimann in 1860 and was used by catatonic symptoms), acute organic psychosis and, Karl Koller (a friend of Freud) in 1884 as the fi rst very rarely, depression. effective local anesthetic agent. Psychoactive Substance Use Disorders 47

Cocaine (common street name: Crack) can be output may be present. Later, judgement is impaired administered orally, intranasally, by smo king ( free and there is impairment of social or occupational basing) or parenterally, depending on the preparation functioning. available (Fig. 4.2). Cocaine HCl is the commonest form used, followed by the free base alkaloid. Both Withdrawal Syndrome intravenous use and free base inhalation produce a Cocaine use produces a very mild physical, but a ‘rush’ of pleasurable sensations. very strong psychological, dependence. A triphasic Cocaine is a central stimulant which inhibits the withdrawal syndrome usually follows an abrupt dis- reuptake of dopamine, along with the reuptake of continuation of chronic cocaine use (Table 4.9). norepinephrine and serotonin. In animals, cocaine is the most powerful reinforcer of the drug-taking Complications behaviour. A typical pattern of cocaine use is cocaine The complications of chronic cocaine use include ‘runs’ (binges), followed by the cocaine ‘crashes’ acute anxiety reaction, uncontrolled compulsive (interruption of use). Cocaine is sometimes used in behaviour, psychotic episodes (with persecutory delu- combination with opiates like heroin (‘speed ball’) sions, and tactile and other hallucinations), delirium or at times amphetamines. Previously uncommon, and delusional disorder. High doses of cocaine can cocaine misuse appears to be recently a growing often lead to seizures, respiratory depression, cardiac problem in the metros of India. arrhythmias, coronary artery occlusion, myocardial infarction, lung damage, gastroin testinal necrosis, Acute Intoxication foetal anoxia and perforation of nasal septum. Acute cocaine intoxication is characterised by pupillary dilatation, tachycardia, hyperten sion, sweating, Treatment and nausea or vomiting. A hypomanic picture with Before starting treatment, it is essential to diagnose increased psycho motor activity, grandiosity, ela- (or rule out) co-existent psychiatric and/or physical tion of mood, hypervigilance and increased speech disorder, and assess the motivation for treatment.

Fig. 4.2: Cocaine Preparations 48 A Short Textbook of Psychiatry

Table 4.9: Phases in Cocaine Withdrawal Syndrome Phase Sub-stage Duration Clinical Features I (Crash phase) i 9 hours Agitation, depression, anorexia, to craving +++ ii 4 days Fatigue, depression, sleepiness, craving + iii after discontinuation Exhaustion, hypersomnia with intermittent awakening, hyperphagia, craving ± II i 4 to 7 days Normal sleep, improved mood, craving ± after discontinuation ii Anxiety, anergia, anhedonia, craving ++ III (Extinction phase) After 7-10 days of No withdrawal symptoms, increased discontinuation vulnerability to relapse

Cocaine use disorder is commonly associated with therapy, are useful in the post-with drawal treatment mood disorder, particularly major depression and and in the prevention of relapse. cyclothymia. AMPHETAMINE USE DISORDER Treatment of Cocaine Overdose The treatment of overdose consists of oxyge nation, Though synthesised by Edleano in 1887, it was intro- muscle relaxants, and IV thiopentone and/or IV duced in Medicine in 1932 as benzedrine inhaler, for diazepam (for seizures and severe anxiety). the treatment of coryza, rhinitis and asthma. Later, it IV propranolol, a speciﬁ c antagonist of cocaine- was recom mended for a variety of conditions such as induced sympathomimetic effects, can be helpful, narcolepsy, postencephalitic parkinsonism, obesity, administered by a specialist. Haloperidol (or pimoz- depression, and even to heighten energy and capac- ide) can be used for the treatment of psychosis, as ity to work. well as for blocking the cardio-stimulatory effects of Amphetamine refers to a unique chemical which cocaine. These must be administered very carefully is basically phenyl-iso-propylamine or methyl- by an expert specialist. phenethylamine. It is a powerful CNS stimulant, with peripheral sympathomimetic effects too. The Treatment of Chronic Cocaine Use dextro-amphetamine isomer is nearly 3-4 times more The management of underlying (or co-existent) psy- potent than the levo-isomer. It acts primarily on nore- chopathology is probably the most important step in pinephrine release in brain, along with an action on the management of chronic cocaine use. the release of dopamine and serotonin. The pharmacological treatment includes the Although still clinically indicated for narcolepsy use of bromocriptine (a dopaminergic agonist) and and attention deﬁ cit hyperactivity disorder (and very amantadine (an antiparkinsonian) in reducing cocaine rarely for obesity and mild depression), one of the craving. commonest patterns of ‘use’ is seen amongst the Other useful drugs are desipramine, imipra mine students and sports-persons to overcome the need for and trazodone (both for reducing craving and for sleep and fatigue. Tolerance usually develops to the antidepressant effect). The goal of the treatment is central as well as cardiovascular effects of ampheta- total abstinence from cocaine use. mines. The psychosocial management techniques, such as Recently, there has been a resurgence of amphe- supportive psychotherapy and contingent behaviour tamine use in USA and Europe, with the availability of Psychoactive Substance Use Disorders 49

‘designer’ amphetamines, such as MDMA (3,4-methy- Treatment lenedioxy-amphetamine; street name: ecstasy or Treatment of Intoxication XTC). Acute intoxication is treated by symptomatic meas- Intoxication and Complications ures, e.g. hyperpyrexia (cold sponging, parenteral The signs and symptoms of acute ampheta mine antipyretics), seizures (parenteral diazepam), psy- intoxication are primarily cardiovascular (tachycar- chotic symptoms (antipsychotics), and hypertension dia, hypertension, haemorrhage, cardiac failure and (antihypertensives). Acidifi cation of urine (with oral cardiovascular shock) and central (seizures, hyperpy- NH4Cl; 500 mg every 4 hours) facilitates the elimina- rexia, tremors, ataxia, euphoria, pupillary dilatation, tion of ampheta mines. tetany and coma). The neuropsychiatric manifes ta tions include anxiety, panic, insomnia, restless ness, irrita- Treatment of Withdrawal Symptoms bility, hostility and bruxism. The presence of severe suicidal depression may necessitate Acute intoxication may present as a para noid hal- hospitalisation. The treat ment includes symptomatic lucinatory syndrome which closely mimics paranoid management, use of antidepressants and supportive schizophrenia. The distin guishing features include psychotherapy. The management of withdrawal syndrome rapidity of onset, prominence of visual hallucinations, is usually the fi rst step towards successful management absence of thought disorder, appropriateness of affect, of amphetamine dependence. fearful emotional reaction, and presence of confusion. However, a confi dent diagnosis requires an estimation LSD USE DISORDER of the recent urinary amphetamine levels. Ampheta- mine-induced psychosis usually resolves within seven Lysergic acid diethylamide, fi rst synthesised by Albert days of urinary clearance of amphetamines. Hoffman in 1938 and popularly known as ‘acid’, is a Chronic amphetamine intoxication leads to severe powerful hallucinogen. It is related to the psychedelic and compulsive craving for the drug. A high degree compounds found in the ‘morning glory’ seeds, the of tolerance is characteristic, with the dependent lysergic acid amides. As little as 100 μg of LSD is individual needing up to 15-20 times the initial dose, suffi cient to produce behavioural effects in man. LSD in order to obtain the pleasurable effects. A common presumably produces its effects by an action on the pattern of chronic use is a cycle of runs (heavy use 5-HT levels in brain. for several days) followed by crashes (stopping the Although tolerance as well as psychological drug use). dependence can occur with LSD use, no physical Tactile hallucinations, in clear conscious ness, dependence or withdrawal syndrome is reported. A may sometimes occur in chronic amphetamine common pattern of LSD use is a trip (occasional use intoxication. followed by a long period of abstinence). Withdrawal Syndrome Intoxication The withdrawal syndrome is typically seen on an The characteristic features of acute LSD intoxication abrupt discontinuation of amphetamines after a period are perceptual changes occurring in a clear conscious- of chronic use. The syndrome is charac terised by ness. These perceptual changes include deperson- depression (may present with suicidal ideation), alisation, derealisation, intensifi cation of perceptions, marked asthenia, apathy, fatigue, hyper somnia alterna- synaesthesias (for example, colours are heard, and ting with insomnia, agitation and hyperphagia. sounds are felt), illusions, and hallucina tions. 50 A Short Textbook of Psychiatry

In addition, features suggestive of autonomic hy- it has been described separately as it has some distinc- peractivity, such as pupillary dilatation, tachycardia, tive features. sweating, tremors, incoordi nation, palpitations, raised Since their introduction in 1903, barbiturates have temperature, piloerection and giddiness, can also be been used as sedatives, hypnotics, anticonvulsants, present. anaesthetics and tranquilisers. The commonly abused These changes are usually associated with marked barbiturates are secobar bital, pentobarbital and amo- anxiety and/or depression, though euphoria is more barbital. Their use has recently decreased markedly common in small doses. Persecutory and referential as benzodiazepines have replaced barbiturates in the ideation may also occur. majority of their clinical uses. Sometimes, acute LSD intoxication presents with Barbiturates produce marked physical and psy- an acute panic reaction, known as a bad trip, in which chological dependence. Tolerance (both central and the individual experiences a loss of control over his metabolic) develops rapidly and is usually marked. self. The recovery usually occurs within 8-12 hours of There is also a cross tolerance with alcohol. the last dose. Rarely, the intoxication is severe enough to produce an acute psychotic episode resembling a Intoxication and Complications schizo phreniform psychosis. Acute intoxication, typically occurring as an episodic phenomenon, is characterised by irritability, Withdrawal Syndrome increased productivity of speech, lability of mood, No withdrawal syndrome has been described with disinhibited behaviour, slur ring of speech, incoor- LSD use. dination, attentional and memory impairment, and However, sometimes, there is a spontaneous recur- ataxia. Mild barbi turate intoxication resembles alcohol rence of the LSD use experience in a drug free state. intoxication; severe forms may present with diplopia, Described as a fl ashback, it usually occurs weeks to nystagmus, hypotonia, positive Romberg’s sign and months after the last experience. Such episodes are suicidal ideation. Drug automatism may sometimes often induced by stress, fatigue, alcohol intake, severe lead to lethal accidents. physical illness or marihuana intoxication. Intravenous use can lead to skin abscesses, cel- lulitis, infections, embolism and hypersen si tivity Complications reactions. Long-term LSD use is not a common pheno menon. The complications of chronic LSD use include psy- Withdrawal Syndrome chiatric symptoms (anxiety, depression, psychosis or The barbiturate withdrawal syndrome can be very visual hallucinosis) and occasionally foetal abnor- severe. It usually occurs in individuals who are taking malities. more than 600-800 mg/day of secobarbital equivalent for more than one month. Treatment It is usually characterised by marked restlessness, The treatment of acute LSD intoxication consists tremors, hypertension, seizures, and in severe cases, of symptomatic management with antianxiety, anti- a psychosis resembling delirium tremens. The with- depressant or antipsychotic medication, along with drawal syndrome is at its worst about 72 hours after supportive psycho therapy. the last dose. Coma, followed by death, can occur in some cases. BARBITURATE USE DISORDER Treatment Barbiturate use disorder is now subsumed under seda- The barbiturate intoxication should be treated sympto- tive, hypnotic and anxiolytic use disorders. However, matically. If patient is conscious induction of vomiting Psychoactive Substance Use Disorders 51 and use of activated charcoal can reduce drug absorp- to heavy doses (more than 60-80 mg per day of diation. If coma ensues, intensive care measures should zepam), is characterised by marked anxiety, irritability, be employed on an emergency basis. tremors, insomnia, vomi ting, weakness, autonomic The treatment of withdrawal syndrome is usually hyperactivity with postural hypotension, and seizures. conservative. However, pentobarbital substitution Depres sion, transient psychotic episodes, suicidal therapy has been suggested for treatment of withdrawal ideation, perceptual disturbances and rarely delirium from short-acting barbiturates. After detoxifi cation have also been reported in withdrawal period. phase is over, follow-up supportive treatment and treatment of associated psychiatric disorder, usually Treatment depression, are important steps to prevent relapses. The treatment of benzodiazepine intoxication is usually symptomatic. However, in cases of coma BENZODIAZEPINES AND OTHER caused by benzodiazepine overdose, fl u ma zenil (a SEDATIVE-HYPNOTIC USE DISORDER benzodiazepine receptor anta gonist) can be used in a dose of 0.3-1.0 mg IV, administered over 1-2 minutes. Since the discovery of chlordiazepoxide in 1957 The treatment of low dose dependence syn drome by Sternbach, benzodiazepines have replaced other (~15 mg/day of diazepam) is abrupt withdrawal and sedative-hypnotics in treatment of insomnia and symptomatic management of withdrawal symptoms. anxiety. These are currently one of the most often pre- However, moderate to high dose dependence is best scribed drugs. Benzodiazepines produce their effects managed by gradual withdrawal in a step-wise manner by acting on the benzodiazepine receptors (GABA- (a reduction of ~10% of the dose every day). Sometimes benzodiazepine receptor complex), thereby indirectly a slower withdrawal is clinically indicated (see Ashton increasing the action of GABA, the chief inhibitory Manual in Suggested Further Reading List). neurotransmitter in the human brain. The best treatment is probably prevention by limit- Benzodiazepine (or sedative-hypnotic) use disor- ing benzodiazepine use to no more than 2-4 weeks of der can be either iatrogenic or originating with illicit prescription at most. drug use. Dependence, both physical and psychologi- After the detoxifi cation phase, an adequate follow-up cal, can occur and tolerance is usually moderate. and supportive treatment is essential to prevent relapses.

Intoxication and Complications INHALANTS OR VOLATILE SOLVENT Acute intoxication resembles alcohol intoxication USE DISORDER whilst chronic intoxication causes tole rance, especially to the sedative and anticonvulsant actions of The commonly used volatile solvents include gaso- benzodiazepines. Excessive doses can lead to respira- line (petrol), glues, aerosols (spray paints), thinners, tory depression, coma and death while chronic use has varnish remover and industrial solvents. The active been reported to cause amnestic syndrome. ingredients usually include toluene, benzene, acetone Some of the other complications of benzodi- and halogenated hydrocarbons. azepines, particularly with high dose and chronic Volatile solvent misuse is more common in early use, include behavioural disinhibition, impulsivity, adolescence as a group activity, particularly in low blackouts, memory loss, worsening of depression and socioeconomic status groups (e.g. rag-pickers in interactions with other prescribed medications. Mumbai and Delhi). Withdrawal Syndrome Intoxication and Complications A typical withdrawal syndrome, after cessa tion of Inhalation of a volatile solvent leads to euphoria, ex- prolonged use (more than 4-6 weeks) of moderate citement, belligerence, dizziness, slurring of speech, 52 A Short Textbook of Psychiatry apathy, impaired judgement, and neurological signs depression and impairment in cognitive functions (such as decreased refl exes, ataxia, nystagmus, incoor- have been reported. dination and coma). Death can occur due to respiratory depression, cardiac arrhythmias, or asphyxia. Treatment The complications include irreversible damage to The treatment of PCP intoxication is sympto matic and liver and kidneys, peripheral neuropathy, perceptual usually involves gastric lavage, isolation, and use of disturbances and brain damage. anticonvulsants (for seizures) and antipsychotics (for There appears to be no specifi c treatment of the PCP induced psychosis). inhalant use disorder. There is often an asso ciated psy- There is no specifi c treatment for phencyclidine chiatric disorder (usually schizo phrenia or personality withdrawal syndrome. disorder, particularly in solitary sniffers), or there is a history of criminal background. The prognosis is OTHER USE DISORDERS usually guarded. Caffeine and nicotine are among the most widely used PHENCYCLIDINE USE DISORDER substances, as they are both legally available. Both of these can cause intoxi cation, dependence, tolerance, Phencyclidine (PCP) was introduced as a dissociative and with drawal syndrome. anaesthetic agent (similar to ketamine) in 1950s. Nicotine use (often in the form of smoking) is more However, its use was soon restricted to veterinary common in schizophrenia and depression. Smoking anaesthesia as some human subjects developed predisposes to increased risk of cardiovascular dis- delirium while emerging from anaesthesia. Classifi ed ease, respiratory disease and cancer, and can affect as an atypical hallucinogen (street names: Peace pill; metabolism of several psychotropic drugs. Smoking angel dust), PCP selectively antagonises the neuronal also decreases serum levels of clozapine (and other action of NMDA (N-methyl-D-aspartate). drugs such as olanzapine, duloxetine, fl uphenazine) PCP is usually taken either occasionally or in by up to 50%. Clozapine levels can therefore rise binges (called as runs ); however, some individuals do signifi cantly after smoking cessation even whilst the take PCP in a regular manner. It can be administered patient is on nicotine replacement therapy. This is due orally, intravenously or by snorting. to induction of liver enzymes CYP1A2 (cytochrome P450 1A2) by hydrocarbons in tobacco smoke rather Intoxication and Complications than nicotine. Acute PCP intoxication produces euphoria in small Nicotine withdrawal can occur 12-14 hours after doses; higher doses produce dysphoria. Other features last smoke and can present with anxiety, restless- may include impulsiveness, agitation, impaired social ness, poor concentration, decreased sleep, increased judgement, assaultative ness, feeling of numbness appetite and exacerbation of psychiatric symptoms in and inability to move. PCP intoxication can some- those with pre-existing psychiatric disorder(s). times present with psychiatric syndromes ( catatonic Nicotine replacement therapy is widely used syndrome, delirium, stupor, paranoid hallucinatory despite equivocal evidence, delivered in a variety psychosis, mania or depression) and/or neurological of preparations such as a sublingual tablet (2 mg), symptoms (nystagmus, ataxia, dysarthria, rigidity, lozenge (1, 2 or 4 mg), chewing gum (2 or 4 mg), seizures or coma). nasal spray (0.5 mg), inhalator (10 mg), and patches (7, 14 or 21 mg). Withdrawal Syndrome In addition, bupropion (also called as amfeb- Although no clear-cut withdrawal syndrome has utamone; a norepinephrine and dopamine reuptake been described, craving, social withdrawal, anxiety, inhibitor – NDRI antidepressant) and varenicline Psychoactive Substance Use Disorders 53

(a partial α4β2 nicotinic acetylcholine receptor partial arrhythmia, periods of inexhaustibility and psychomo- agonist) are pharmacological agents recently used in tor agitation. promoting smoking cessation as adjuncts to behav- These symptoms should be accompanied by ioural or cognitive behavioural treatment(s). These clinically signifi cant distress or impairment in social, should only be initiated after a discussion of possible occupational or other areas of functioning, and the adverse effects with the patient. symptoms should not be better accounted by a general Similarly, caffeine is widely used in general medical condition or another mental disorder. population as well as in patients with psychiatric The typical content of caffeine in the commonly disorders. DSM-IV-TR defi nes caffeinism (caffeine used drinks is usually as follows: tea (45 mg/cup), intoxication) as a recent consumption of caffeine, instant coffee (60 mg/cup), brewed coffee (100 mg/ usually in excess of 250 mg per day, along with fi ve cup), and cola drinks (25-50 mg/can). Caffeine is also or more of the following: restlessness, nervousness, present in chocolate. Caffeine can affect metabolism excitement, insomnia, fl ushed face, diuresis, GI (gas- of several psychotropic drugs, most importantly trointestinal) disturbance, muscle twitching, rambling clozapine. It can elevate the levels of clozapine (and fl ow of thought and speech, tachycardia or cardiac other drugs) by inhibiting CYP1A2. 5 Schizophrenia

Schizophrenia has puzzled physicians, philosophers, outcome (dementia: deterioration; praecox: early and general public for centuries. The systematic onset). study of schizophrenia, however, is but a century old. He recognised the characteristic features of de- A clinical syndrome with a profound infl uence on mentia praecox, such as delusions, hallucinations, public health, schizophrenia has been called “arguably disturbances of affect and motor disturbances. the worst disease affecting mankind, even AIDS not excepted” (Nature 1988). Eugen Bleuler To understand what schizophrenia is, it is impor- Eugen Bleuler (1911), while renaming demen tia tant to have a brief look at the history of evolution of praecox as schizophrenia (meaning mental splitting), the concept of schizophrenia. recognised that this disorder did not always have a poor prognosis as described by Kraepelin. He also HISTORICAL BACKGROUND recognised that schizophrenia consisted of a group of disorders rather than being a distinct entity. Therefore, Although earlier descriptions of schizoph renia-like he used the term, a group of schizophrenias. illness are recorded in literature (such as in Ayurveda; Bleuler described the characteristic symptoms Morel’s description of demence precoce; Kahlbaum’s (fundamental symp toms) which were then thought description of catatonia; Hecker’s descrip tion of to be diagnostic of schizophrenia (Table 5.1). He hebephrenia), the scientifi c study of the disorder also described accessory symptoms of schizo phrenia began with the description of dementia praecox by (thought to be secondary to funda mental symptoms). Emil Kraepelin. These accessory symptoms included delusions, hallucinations and negativism. Emil Kraepelin In 1896, Emil Kraepelin differentiated the major Kurt Schneider psychiatric illnesses into two clinical types: Dementia Kurt Schneider (1959) described symptoms which, praecox, and Manic depressive illness. though not specifi c of schizophrenia, were of great Under dementia praecox, he brought together the help in making a clinical diagnosis of schizophrenia. various psychiatric illnesses (such as paranoia, cata- These are popularly called as Schneider’s fi rst rank tonia and hebephrenia), which were earlier thought symptoms of schizo phrenia (FRS or SFRS) (Table 5.2). to be distinct illnesses. The emphasis in diagnosis of He also described the second rank symptoms of dementia praecox was on an early onset and a poor schizophrenia (which were conside red by him as less Schizophrenia 55

Table 5.1: Eugen Bleuler’s Fundamental Symptoms of infl uen ced the diagnostic criteria and classifi cation Schizophrenia (Also called as 4 A’s of Bleuler) of schizophrenia and other related psychotic disor- 1. Ambivalence: Marked inability to decide for or ders. As mentioned earlier, SFRS are not specifi c for against schizophrenia and may be seen in other psychiatric 2. Autism: Withdrawal into self disorders such as mood disorders and organic psy- 3. Affect disturbances: Disturbances of affect such as chiatric disorders. inappropriate affect 4. Association disturbances: Loosening of associations; EPIDEMIOLOGY thought disorder According to the World (Mental) Health Report 2001, about 24 million people worldwide suffer from Table 5.2: First Rank Symptoms (SFRS) of Schizophrenia schizophrenia. The point prevalence of schizophrenia 1. Audible thoughts: Voices speaking out thoughts aloud is about 0.5-1%. Schizophrenia is prevalent across or ‘ thought echo’. racial, sociocultural and national boundaries, with a 2. Voices heard arguing: Two or more hallu cinatory few exceptions in the prevalence rates in some isolated voices discussing the subject in third person. communities. 3. Voices commenting on one’s action. The incidence of schizophrenia is believed to be 4. Thought withdrawal: Thoughts cease and subject about 0.5 per 1000. The onset of schizophrenia occurs experiences them as removed by an external force. usually later in women and often runs a relatively more 5. Thought insertion: Experience of thoughts imposed benign course, as compared to men. by some external force on person’s passive mind. 6. Thought diffusion or broadcasting: Experience of thoughts escaping the confi nes of self and as being CLINICAL FEATURES experienced by others around. 7. ‘ Made’ feelings or affect. Schizophrenia is characterised by disturbances in 8. ‘Made’ impulses. thought and verbal behaviour, percep tion, affect, 9. ‘Made’ volition or acts: In ‘made’ affect, impulses motor behaviour and relationship to the external and volitions, the person experiences feelings, impul- world. The diagnosis is entirely clinical and is based ses or acts which are imposed by some external on the following clinical features, none of which are force. In ‘made’ volition, for example, one’s own pathognomonic if present alone. acts are experienced as being under the control of some external force. Thought and Speech Disorders 10. Somatic passivity: Bodily sensations, espe cially Autistic thinking is one of the most classical features sensory symptoms, are expe rienced as imposed on of schizophrenia. Here thinking is governed by pri- body by some external force. vate and illogical rules. The patient may consider two 11. Delusional perception: Normal perception has a things identical because they have identical predicates private and illogical meaning. or properties (von Domarus Law); for example, Lord Hanuman was celibate, I am celibate too; So, I am important for diagnosis of schizophrenia), such as Lord Hanuman. other forms of hallucina tions, perplexity, and affect Loosening of associations is a pattern of spontane- disturbances. ous speech in which things said in juxtaposition lack These symptoms (SFRS) have been described in a meaningful relationship or there is idiosyncratic some detail here as they have very often been used shifting from one frame of reference to another. The for diagnosis of schizo phrenia and have signifi cantly speech is often des cribed as being ‘disjointed’. If 56 A Short Textbook of Psychiatry the loosen ing becomes very severe, speech becomes The commonly seen delusions in schizophrenia virtually incom prehensible. This is then known as include: incoherence. 1. Delusions of persecution (being persecuted Thought blocking is a characteristic feature of against, e.g. ‘people are against me’). schizophrenia, although it can also be seen in com- 2. Delusions of reference (being referred to by others; plex partial seizures (temporal lobe epi lepsy). There e.g. ‘people are talking about me’). is a sudden interruption of stream of speech before 3. Delusions of grandeur (exaggerated self-impor- the thought is completed. After a pause, the subject tance; e.g. ‘I am God almighty’). cannot recall what he had meant to say. This may at 4. Delusions of control (being controlled by an exter- times be associated with thought withdrawal. nal force, known or unknown; e.g. ‘My neighbour Neologisms are newly formed words or phrases is controlling me”). whose derivation cannot be understood. These are 5. Somatic (or hypochondriacal) delusions (e.g. created to express a concept for which the subject ‘there are insects crawling in my scalp’). has no dictionary word. Sometimes, normal words The other clinical features of schizophrenic are used in an unconventional or distorted way but the thought disorder include: overinclusion (tending to derivation can be under stood, even if bizarre. These include irrelevant items in speech), impaired abstrac- are called word approximations or parapha sias; for tion (loss of ability to genera lise), concreteness (due example, describing stomach as a ‘food vessel’. to impaired abstrac tion), perplexity and ambivalence. A patient with schizophrenia may show complete Schneider’s fi rst rank symptoms (such as thought mutism (with no speech production), poverty of speech insertion, thought withdrawal, thought broadcasting, (decreased speech production), poverty of ideation ‘made’ feeling, ‘made’ impulses and ‘made’ volitions), (speech amount is adequate but content conveys little which have already been discussed earlier (Table 5.2), information), echolalia (repetition or echoing by the may also be present. patient of the words or phrases of examiner), perseveration (persistent repetition of words beyond their Disorders of Perception relevance), or verbigeration (senseless repetition of Hallucinations (perceptions without stimuli) are com- same words or phrases over and over again). These mon in schizophrenia. Auditory hallucinations are by are disorders of verbal behaviour or speech. far the most frequent. These can be: Delusions are false unshakable beliefs which are i. Elementary auditory hallucinations (i.e. hearing not in keeping with patient’s socio-cultural and edu- simple sounds rather than voices) cational background. These are of two types: primary ii. ‘ Thought echo’ (‘ audible thoughts’) and secondary. iii. ‘Third person hallucinations’ (‘voices heard argu- 1. Primary delusions arise de novo and cannot be ing’, discussing the patient in third person) explained on the basis of other experiences or iv. ‘Voices commenting on one’s action’. perceptions. Also known as autochthonous de- Only the ‘third person hallucinations’ are believed lusions, these are though to be characteristic of to be characteristic of schizophrenia. Visual halluci- schizo phrenia and are usually seen in early stages. nations can also occur, usually along with auditory 2. Secondary delusions are the commonest type of hallucinations. The tactile, gustatory and olfactory delusions seen in clinical practice and are not types are less common. diagnostic of schizophrenia as these can also be seen in other psychoses. Secondary delusions Disorders of Affect can be explained as arising from other abnormal The disorders of affect include apathy, emotional experiences. blunting, emotional shallowness, anhedonia (inability Schizophrenia 57 to experience pleasure) and inappropriate emotional 6. There is usually variability in sympto matology response (emotional response inappropriate to over time which in some cases can be marked. thought). 7. There is no obvious underlying organic cause that The diffi culty of a patient with schizophrenia in can explain the causation of the symptoms. establishing emotional contact with other individuals 8. There is no prominent mood disorder of depres sive can lead to lack of rapport with the physician. or manic type. Disorders of Motor Behaviour Suicide in Schizophrenia There can be either a decrease (decreased spontaneity, Suicide can occur in schizophrenia due to several inertia, stupor) or an increase in psychomotor activity reasons. Some of the common reasons can include (excitement, aggressi veness, restlessness, agitation). the presence of co-morbid depressive symptoms, Mannerisms, grimacing, stereotypies (repeti tive command halluci nations comman ding the patient strange behaviour), decreased self-care, and poor to commit suicide, impulsive behaviour, presence grooming are common features. Catatonic features are of anhedo nia, and/or return of insight in the illness commonly seen in the catatonic subtype of schizophre- (with the painful awareness that one has suffered from nia (and are discussed in detail under that heading). schizophrenia or psychosis). It is important to be aware of possibility of suicide Negative Symptoms whilst treating a patient with schizophrenia so that the The prominent negative symptoms of schizo phrenia various risk factors can be addressed in management. include affective fl attening or blunting, attentional impairment, avolition-apathy (lack of initiative as- DIAGNOSIS sociated with psychomotor slowing), anhedonia , asociality (social withdrawal), and alogia (lack of According to ICD-10, for the diagnosis of schizophre- speech output). There is poor verbal as well as non- nia, a minimum of 1 very clear symptom (and usually verbal communication with poor facial expression, 2 or more if less clear cut) belonging to any one of the decreased eye contact, with usually poor self-care and groups referred to as (a) to (d) or symptoms from at social interaction. least 2 of the groups referred to as (e) to (h), should have been clearly present for most of the time during Other Features a period of 1 month or more ( DSM-IV-TR on the 1. Decreased functioning in work, social relations other hand requires a minimum period of 6 months). and self-care, as compared to the earlier levels If the duration of illness is less than 1 month, then achieved by the individual. a diagnosis of acute schizophrenia-like psychotic 2. Loss of ego boundaries (feeling of blurring of disorder should be made. These symptoms include boundaries of self with the environment; uncer- (ICD-10): tainty and perplexity regarding own identity and Thought echo/insertion/withdrawal/broadcasting; meaning of existence). delusions of control/infl uence/passivity; delusional 3. Multiple somatic symptoms, especially in the early perception; hallucinatory voices commenting or stages of illness. discussing the patient, or other voices coming from 4. Insight (into the illness) is absent and social judge- some part of body; and/or persistent culturally inap- ment is usually poor. propriate delusions are included in groups (a) to (d) 5. There is usually no clinically signifi cant distur- mentioned above. bance of conscious ness, orientation, attention, Persistent hallucinations in any modality, or by memory and intelligence. persistent overvalued ideas; incoherence or irrelevant 58 A Short Textbook of Psychiatry speech; neologisms; catatonic behaviour; negative 3. No prominent disturbances of affect, volition, symptoms not due to depression or antipsychotics are speech, and/or motor behaviour. included in groups (a) to (d) mentioned above. Personality deterioration in the paranoid subtype is This is associated with a signifi cant and consist- much less than that seen in other types of schizophre- ent change in personal behaviour, manifest as loss of nias. The patient may be quite apprehensive (due to interest, aimlessness, or social withdrawal. delusions and hallucinations) and anxious, and appear If the patient also meets the criteria for manic epi- evasive and guarded on mental status examination. sode or depressive episode, the guidelines mentioned The onset of paranoid schizophrenia is usually above must have been met before the disturbance of insidious, occurs later in life (i.e. late 3rd and early mood developed. The disorder is not diagnosed in the 4th decade) as compared to the other subtypes of presence of overt brain disease, or alcohol- or drug- schizophrenia. The course is usually progressive and rela ted intoxication, dependence, or withdrawal. complete recovery usually does not occur. There may be frequent remissions and relapses. At other times, the CLINICAL TYPES functional capability may be only slightly impaired. The differential diagnosis is usually from delusional Schizophrenia can be classifi ed into several subtypes (or paranoid) disorders and paranoid personality dis- (Table 5.3). The catatonic and hebephrenic subtypes orders. of schizophrenia together have been called as nuclear schizophrenia , as they present with typical symptoma- Disorganised (or Hebephrenic) tology of schizophrenia and can most frequently result Schizophrenia in personality deterioration over time (especially if Disorganised schizophrenia is characterised by the chronic). following features, in addition to the general guidelines of schizophrenia described earlier: Paranoid Schizophrenia 1. Marked thought disorder, incoherence and severe Paranoid schizophrenia is characterised by the fol- loosening of associations. Delusions and halluci- lowing clinical features, in addition to the general nations are fragmentary and changeable. guidelines of schizophrenia described earlier: 2. Emotional disturbances (inappropriate affect, 1. Delusions of persecution, reference, gran deur (or blunted affect, or senseless giggling), manne- ‘grandiosity’), control, or infi delity (or ‘jealousy’). risms, ‘ mirror-gazing’ (for long periods of time), The delusions are usually well-systematised (i.e. disinhibited behaviour, poor self-care and hy- thematically well connected with each other). giene, markedly impaired social and occupational 2. The hallucinations u sually have a persecu tory or functioning, extreme social withdrawal and other grandiose content. oddities of behaviour. ICD-10 recommends a period of 2 or 3 months of continuous observation for a confi dent diagnosis Table 5.3: Clinical Types of Schizophrenia of disorganised (or hebephrenic) schizophrenia to be 1. Paranoid schizophrenia made. 2. Hebephrenic schizophrenia The onset is insidious, usually in the early 2nd 3. Catatonic schizophrenia decade. The course is progressive and downhill. The 4. Residual schizophrenia recovery from the episode is classically poor. Severe 5. Undifferentiated schizophrenia deterioration, without any signifi cant remissions, 6. Simple schizophrenia usually occurs over time. Hebephrenic schizophrenia 7. Post-schizophrenic depression has one of the worst prognoses among the various 8. Others subtypes of schizophrenia. Schizophrenia 59

Catatonic Schizophrenia Table 5.4: Some Important Clinical Features of Retarded Catatonia Catatonic schizophrenia (Cata: disturbed, tonic: tone) is characterised by a marked disturbance of motor 1. Mutism: Complete absence of speech behaviour, in addi tion to the general guidelines of 2. Rigidity: Maintenance of a rigid posture against ef- schizo phrenia described earlier. forts to be moved It can present in three clinical forms: excited cata- 3. Negativism: An apparently motiveless resistance to tonia, stuporous catatonia, and catatonia alternating all commands and attem pts to be moved, or doing between excitement and stupor. just the oppo site 4. Posturing: Voluntary assumption of an inappropriate Excited Catatonia and often bizarre posture for long periods of time 5. Stupor: Akinesis (no movement) with mutism but This is characterised by the following featu res: with evidence of relative preservation of conscious 1. Increase in psychomotor activity, ranging from awareness restlessness, agitation, excitement, aggres sive ness 6. Echolalia: Repetition, echo or mimic king of phrases to, at times, violent behaviour (furore). or words heard 2. Increase in speech production, with increased 7. Echopraxia: Repetition, echo or mimic king of actions spontaneity, pressure of speech, loose ning of as- observed sociations and frank incoherence. 8. Waxy fl exibility: Parts of body can be placed in The excitement has no apparent relationship with positions that will be main tained for long periods of the external environment; instead inner stimuli (e.g. time, even if very uncomfortable; fl exible like wax thought and impulses) infl uence the excited behaviour. 9. Ambitendency: Due to ambivalence, confl icting im- So, the excitement is not goal-directed. pulses and tentative actions are made, but no goal Sometimes the excitement can become very se- directed action occurs, e.g. on asking to take out vere, and is accompanied by rigidity, hyperthermia tongue, tongue is slightly protruded but taken back and dehy dration, fi nally culmi na ting in death. It is again then known as acute lethal catatonia or pernicious 10. Other signs such as mannerisms, stereotypies (verbal catatonia. Fortunately, with the availability of new and behavioural), automatic obedience (commands treatment choices, and early diagnosis and treatment, are followed automatically, irrespective of their lethal catatonia has become increasingly rare in most nature) and verbigeration (incom prehensible speech). parts of the world. The onset of catatonic schizo phrenia is usually Stuporous (or Retarded) Catatonia acute, usually in the late 2nd and early 3rd decade. The This is characterised by extreme retardation of course is often episodic and recovery from the episode psychomotor function. The characteristic cata tonic is usually complete. However, residual features are signs (Table 5.4) are usually observed. Delusions and present after two or more episodes. Differential di- hallucinations may be present but are usually not agnosis is from other causes of stupor and catatonia. prominent. Not all the features are present at the (This is discussed in further detail in Chapter 19). same time. Residual and Latent Schizophrenia Catatonia Alternating between Residual schizophrenia is similar to latent schizo- Excitement and Stupor phrenia and symptoms are similar to prodromal This clinical picture is very common with fea tures symptoms of schizophrenia. The only difference is of both excited catatonia and stuporous catatonia that residual schizophrenia is diagnosed after at least alternatingly present. one episode has occurred. 60 A Short Textbook of Psychiatry

There are prominent negative symptoms described Other Subtypes above, with absence or marked reduction of fl orid Historically, there have been many other subtypes psychotic symptoms such as delusions and hallucina- of schizophrenia described, but a majority of them tions. It is important to rule out antipsychotic-induced would easily fi t in one of the above-mentioned seven negative symptoms as well as negative symptoms subtypes. A few are briefl y mentioned due to their secondary to associated depression, organic brain historical interest and their popular names; though disease or institutionalisation. others are important in their own right. Undifferentiated Schizophrenia Pseudoneurotic Schizophrenia This is a very common type of schizophrenia and is Pseudoneurotic schizophrenia was fi rst described by diagnosed either: Hoch and Polatin. In initial phases, there are predomi- 1. When features of no subtype are fully present, or nant neurotic symptoms that last for years and show 2. When features of more than one subtype are ex- a poor response to treatment. hibited, and the general criteria for diagnosis of The three classical features described are pananxi- schizophrenia are met. ety (diffuse, free-fl oating anxiety which hardly ever subsides), pan-neurosis (almost all neurotic symptoms Simple Schizophrenia may be present) and pansexuality (constant preoccupa- Although called simple, it is one of the subtypes which tion with sexual problems). is the most diffi cult to diagnose. It is characterised Nowadays, this subtype is subsumed under bor- by an early onset (early 2nd decade), very insidious derline personality disorder. and progressive course, presence of characteristic ‘negative symptoms’ of residual schizophrenia (such Schizophreniform Disorder as marked social withdrawal, shallow emotional This is a diagnostic category in DSM-IV-TR with response, with loss of initiative and drive), vague features of schizophrenia as diagnostic criteria. hypochondriacal features, a drift down the social The only difference is that the duration is less than ladder, and living shabbily and wandering aimlessly. 6 months and prognosis is usually better than that of Delusions and hallucinations are usually absent, and schizophrenia. This term was originally introduced by if present they are short lasting and poorly syste- Langfeldt (1961) to designate good prognosis cases, matised. distinct from “true” schizophrenia. A similar condition The prognosis is usually very poor. in ICD-10 is called acute schizophrenia-like psychotic disorder (see Chapter 7 for details). Post-Schizophrenic Depression Some schizophrenic patients develop depressive Oneiroid Schizophrenia features within 12 months of an acute episode of Described fi rst by Mayer-Gross, this is a subtype of schizophrenia. The depressive features develop in the schizophrenia with an acute onset, clouding of con- presence of residual or active features of schizophrenia sciousness, disorientation, dream-like states (oneiroid and are associated with an increased risk of suicide. means ‘dream’), and perceptual disturbances with The depressive features can occur due to side-effect rapid shifting. of antipsychotics, regaining insight after recovery, or Classically, the episode is usually brief. just be an integral part of schizophrenia. It is important to distinguish the depressive features Van Gogh Syndrome from negative symptoms of schizophrenia and extrapy- Dramatic self-mutilation occurring in schizo phrenia ramidal side-effects of antipsychotic medication. has been also called as Van Gogh syndrome, after the Schizophrenia 61 name of the famous painter Vincent Van Gogh who Although a useful concept theoretically, it has not had cut his ear during the active phase of illness. been found to be valid in the recent research studies. Very few patients have a pure Type I or Type II syn- Late Paraphrenia drome, and admixtures are far more common. Described by Sir Martin Roth, this is a disorder which Table 5.5 summarises symptom clusters in schizo- occurs late in life, usually in the sixth decade. It is phrenia with enumeration of positive, negative and more common in women, especially unmarried or disorganised symptoms. widowed women. Delusions of persecution are seen, with bizarre and fantastic content (for example, being DIFFERENTIAL DIAGNOSIS raped or gassed or strangers entering their rooms and interfering with them). The fi rst step in the differentia l diagnosis is to ex- Hallucinations of all kinds (visual, auditory, tactile, clude psychoses with known organic causes, such gustatory and olfactory) can be present. Intelligence as complex partial seizures, drug-induced psy cho ses and social judgement outside the arena of persecutory (such as amphetamine-induced psychoses), metabolic delusions are usually normal. Approximately 25-40% disturbances, or cerebral space occupying lesions. of the patients have some defect of sight or hearing. There would often be clinical features suggestive of At present, this syndrome is placed under paranoid underlying disorders in these conditions. schizophrenia, late onset type. The second step is to rule out a possibility of mood disorder (such as mania, depression, or mixed affective Pfropf Schizophrenia disorder) or schizo-affective disorder. This is a syndrome of schizophrenia occurring in the The third step is to exclude the possibility of other presence of mental retardation. It differs from schizo- nonorganic psychoses such as delusional disorders, or phrenia in only that there is often a poverty of ideation acute and transient psychotic disorders (ATPD). and delusions are not usually very well-systematised. In addition to the main diagnosis, it is also impor- Therefore, behavioural disturbances are much more tant to look for co-morbid medical (such as diabetes, prominent than delusions and hallucinations. How- hypertension) and/or psychiatric disorders (such as ever, both ICD-10 and DSM-IV-TR do not suggest depression, anxiety, alcohol or drug misuse, or per- a separate category and it is best to diagnose both sonality disorder) on a multi-axial diagnostic system schizophrenia and mental retardation, when present (see Table 1.4). together. PROGNOSIS Type I and Type II Schizophrenia TJ Crow had divided schizophrenia into two sub- The important prognostic factors in schizo phrenia are types, namely Type I and II schizophrenias. The Type I summarised in Table 5.6. syndrome is characterised by positive symptoms while the Type II syndrome is predominantly characterised COURSE AND OUTCOME by presence of negative symptoms. Type I syndrome is supposed to have an acute Since the time of Kraepelin, when the disorder was con- presentation, good response to medication and a good ceptualised as dementia paecox, schizophrenia has been outcome, while Type II is theorised to be chronic in associated with a progressive downhill course, with a course, have a poor response to medication and a poor large number of patients hospitalised in mental asylums. outcome. Crow also described dilated ventricles on However, the longitudinal studies of schizophrenia CT Scan of Brain in Type II syndrome. suggest that this pattern occurs in only a minority of 62 A Short Textbook of Psychiatry

Table 5.5: Symptom Clusters in Schizophrenia Positive Symptoms Negative Symptoms Disorganised Symptoms Delusions Affective ﬂ attening Inappropriate affect Hallucinations Alogia (poverty of speech) Disorganised behaviour Anhedonia—asociality Thought disorder Avolition—apathy Loosening of associations Attentional impairment

Table 5.6: Prognostic Factors in Schizophrenia

Good Prognostic Factors Poor Prognostic Factors 1. Acute or abrupt onset Insidious onset 2. Onset >35 years of age (late onset) Onset <20 years of age (early onset) 3. Presence of precipitating stressor Absence of stressor 4. Good premorbid adjustment Poor premorbid adjustment 5. Catatonic subtype (paranoid subtype has an Disorganised, simple, undifferentiated, or chronic intermediate prognosis) catatonic subtypes 6. Short duration (< 6 months) Chronic course (> 2 years) 7. Presence of depression Absence of depression 8. Predominance of positive symptoms Predominance of negative symptoms 9. Family history of mood disorder Family history of schizophrenia 10. First episode Past history of schizophrenia 11. Pyknic (fat) physique Asthenic (thin) physique 12. Female sex Male sex 13. Good social support Poor social support or unmarried 14. Presence of confusion, perplexity, or disorientation Flat or blunted affect in the acute phase 15. Proper treatment, good treatment concordance, Absence of proper treatment or poor response to and good response to treatment treatment 16. Outpatient treatment Institutionalisation (long-term hospitalisation) 17. Normal cranial CT scan Evidence of ventricular enlargement on cranial CT scan patients. According to a major study (Luc Ciompi A Study of Factors Associated with Course and 1980), where 5661 cases were followed up for an Outcome of Schizophrenia ( SOFACOS) was conduct- average of 36.9 years, the outcome was as follows: ed by ICMR (Indian Council of Medical Research) • Complete remission (27%) at three centres (Vellore, Madras and Lucknow) in • Remission with minor residual deﬁ cit (22%) India. A total of 386 patients were followed up for a • Intermediate outcome (24%) period of 5 years (1981 to 1986), at the end of which • Severe disability (18%) the outcome was as follows: • Unstable or uncertain outcome (9%). • Very favourable outcome (27%) So, almost 50% patients reached complete or near • Favourable outcome (40%) complete recovery, and only 18% were left with severe • Intermediate outcome (31%) disability, with only 9% needing institutio na lisation. • Unfavourable outcome (2%). Schizophrenia 63

So, about two-thirds (67%) of the patients had help-seeking behaviour, decreased activity levels, a favourable outcome as compared to 50% in Luc higher incidence of suicide, and metabolic syndrome. Ciompi’s study. The International Pilot Study on Schizophrenia AETIOLOGY (IPSS), conducted on 811 schizophrenic patients selected in 1968-1969 (patients selected from 9 coun- The aetiology of schizophrenia is currently unknown. tries, namely USA, Columbia, UK, Czechoslovakia, However, several theories have been propounded; USSR, India, Nigeria, Denmark and China), found these include the follow ing: interesting outcome results. It was apparent that the course and prognosis of schizophrenia was better in Biological Theories the developing countries such as Nigeria and India, as compared to the developed countries (Fig. 5.1). Genetic Hypothesis In ICD-10, the course of schizophrenia is speci fi ed About 8-10% of fi rst degree relatives (and 3% of under the categories of: second degree relatives and 2% of third degree i. Continuous; relatives) of patients with schizophrenia can present ii. Episodic with pro gres sive defi cit; with schizophrenia, as compared with the 0.5-1% iii. Episodic with stable defi cit; prevalence rate in general population. iv. Episodic remittent; The concordance rate for monozygotic twins is v. Incomplete remission; and 46% and for dizygotic twins is 14%. If one parent has vi. Complete remission. schizophrenia, the chances of the child develo ping If the period of observation is less than one year, schizophrenia are 10-12%. However, if both parents the course is not specifi ed. have schizophrenia, chances of the child developing Some studies have suggested that longer the DUP schizophrenia increase to about 40%. (duration of untreated psychosis), worse is the out- Therefore, genetic factors are very impor tant in come, underlining the importance of early diagnosis making an individual vulnerable to schizo phrenia. and treatment of schizophrenia. There is an increased However, environmental factors and stress are prob- mortality in patients with schizophrenia by almost one ably also important in precipitating an episode in and half times. The most important cause of death several individuals. is suicide, the life-time risk of which is about 5-10 times higher in schizophrenia as compared to normal Biochemical Theories population. Schizophrenia is presently thought to be probably due There is also a higher prevalence of metabolic to a functional increase of dopa mine at the postsyn- syndrome (characterised by abdominal obesity, athero- genic dyslipidaemia, hypertension, raised fasting blood glucose, and insulin resistance) in schizophrenia which can be worsened by administration of antipsychotic medication. Patients with schizophrenia can die 10-15 years prematurely as compared to general population. There are several factors responsible for this increased morbidity and mortality, including high prevalence of smoking, caffeine, alcohol and drug misuse, obesity, poor treatment concordance, poor Fig. 5.1: IPSS Outcome 64 A Short Textbook of Psychiatry aptic receptor, though other neurotransmitters such as serotonin (especially 5-HT2 receptors), GABA and acetyl choline are also presumably involved. Brain Imaging Cranial CT Scan, MRI Scan, and postmortem studies show enlarged ventricles (not amounting to hydrocephalus) and mild cortical atrophy (with an overall reduction in brain volume and cortical grey matter by 5-10%) in some patients of schizophrenia. PET (positron emission tomography) scan shows Fig. 5.2: Stress Vulnerability Hypothesis in hypofrontality and decreased glucose utilisation in the Schizophrenia. dominant temporal lobe. Attempts are being made to Ref: Zubin and Spring (1977) localise symp toms of schizophrenia (such as auditory hallucinations, negative symptoms) to the various Psychological Theories brain regions by PET studies. At present brain imaging does not have a role in Stress confi rming a diagnosis of schizophrenia though it Increased number of stressful life events before can be used to rule out an organic basis of psychotic the onset or relapse probably has a triggering ef- symptoms where clinically appropriate. fect on the onset of schizophre nia, in a gene tically vulne rable person (Stress-Vulnerability Hypothesis) Other Theories (Fig. 5.2). According to this hypothesis, higher the The following fi ndings also point towards a biological genetic vulnerability in a person, lesser the environ- basis of schizophrenia. Antipsychotics, which act by mental stress needed to precipitate a relapse. blocking the dopamine ( D2) receptor, cause signifi cant Increased expressed emotions (EE; such as hosti- improvement in schizophrenia and relapse usually lity, critical comments, emotional over-involvement) occurs on stopping antipsychotic medication. The of ‘signifi cant others’ in the family can lead to an early newer, atypical antipsychotics (such as risperidone, relapse. Figure 5.3 depicts the 9-month relapse rates in olanzapine, quetiapine) are D2-5-HT2 antagonists. patients with schizophrenia in the study conducted by Drugs such as amphetamines and mesca line can Vaughn and Leff in 1976. In this study, patients who cause schizophrenia-like symptoms in normal subjects. were without any antipsychotic medication and were Organic mental disorders with schizophrenia-like exposed to more than 35 hours contact per week with symptoms may be seen in Huntington’s chorea (early a ‘signifi cant other’ with expressed emotions, were stages), homocystinuria, acute intermittent porphyria, particularly likely to relapse (92%). The compa rable Wilson’s disease and haemachromatosis. rate in patients who received anti psychotic medication Soft neurological signs (SNS), minor physi- and faced less expressed emotions was 12%. In the cal anomalies, and impaired eye tracking (smooth research conducted in the last 30 years, these fi ndings pursuit eye movements) are more often seen in have been replicated all over the globe, though the patients with schizophrenia than in persons without period of 35 hours/weeks has not been found to be the disease. signifi cant. Viral and autoimmune factors have also been implicated by some, while others (e.g. Wein berger) Family Theories have suggested a neurodeve lopmental hypothesis for Several theories have been propounded in the past schizophrenia. but are currently of doubtful value. These include Schizophrenia 65

loss of ego-boundaries (descri bed by Federn), with a loss of touch with reality. Sociocultural Theories Although the prevalence of schizophrenia is quite uniform across cultures, it was found to be more common in lower socioeconomic status in some studies. This has now been explained due to a ‘ downward social drift’, which is a result of having developed schizophrenia rather than causing it. Higher rates of schizophrenia have been found among some migrants, not only among the first generation migrants but also among the second generation. 9 months relapse rate in 128 patients with schizophrenia (Vaughn and Leff 1976) MANAGEMENT Fig. 5.3: Expressed Emotions (EE) in Schizophrenia The treatment of schizophrenia can be discussed under the following major headings: ‘schizophrenogenic mothers’, lack of ‘real’ parents, 1. Somatic treatment dependency on mother, anxious mother, parental a. Pharmacological treatment marital schism or skew, double-bind theory, commu- b. Electro-convulsive therapy (ECT) nication deviance, and pseudomutuality. c. Miscellaneous treatments. Some of these theories were unfortunately re- 2. Psychosocial treatment and rehabilitation. sponsible for arousing a sense of unnecessary guilt in parents for causation of schizophrenia in their Pharmacological Treatment children. The fi rst drug to be used with benefi cial effect in schizophrenia was probably reserpine ( Rauwolfi a Information Processing Hypothesis serpentina extract), in India by Sen and Bose (1931). Disturbances in attention, inability to maintain a set, Reserpine is no longer used for the treatment of and inability to assimilate and integrate percepts are schizophrenia for a variety of reasons, including its common fi ndings in schizophrenia. Patients with propensity to cause severe and suicidal depression. schizophrenia may at first be overly attentive to Antipsychotics were formally discovered by Delay stimuli but later may reduce or exclude attention to and Deniker in 1952. Since their introduction, they stimuli. There is possibly a breakdown in the internal have changed the outcome of schizophrenia signifi - representation of mental events. cantly. These are discussed in some detail in Chapter 15. Only some relevant clinical points are briefl y Psychoanalytical Theories mentioned here. A list of commonly used antipsy- According to Freud, there is regression to the preoral chotics with their routinely used doses is available (and oral) stage of psychosexual deve lop ment, with in Table 5.7. the use of defense mecha nisms of denial, projection, Atypical (or the second generation) antipsychotic and reaction formation (see Table 17.1). There is a drugs, such as risperi done, olanzapine, quetiapine, 66 A Short Textbook of Psychiatry

Table 5.7: Antipsychotic Dose in Schizophrenia Drug Oral Dose Range Parenteral Dose Equivalent Oral Dose* (mg/day) (mg/day) (Equal to 100 mg CPZ) A. Typical/Traditional/First Generation Antipsychotics 1. Chlorpromazine (CPZ) 300-1000 50-100 IM 100 2. Flupentixol 3-18 — 2 3. Haloperidol 5-30 5-10 IM 2-3 4. Loxapine 25-250 — 10 5. Pimozide 4-12 — 2 6. Prochlorperazine 45-150 40-80 IM 15 7. Sulpiride 400-2400 — 200 8. Thioridazine 300-600 — 100 9. Trifl uoperazine 15-50 1-5 IM 5 10. Trifl upromazine 100-400 30-60 IM 25 11. Zuclopenthixol 25-150 50-100 IM 25 B. Atypical/Second Generation Antipsychotics 12. Amisulpride 400-1200 — — 13. Aripiprazole 5-30 5.25-15 IM — 14. Clozapine 50-900 — 50 15. Olanzapine 5-20 2.5-10 IM 2-3 16. Paliperidone 3-12 — — 17. Quetiapine 150-800 — 50-100 18. Risperidone 2-16 — 0.5-1.0 19. Ziprasidone 40-160 — 20 20. Zotepine 75-300 — — *Equivalent doses are at best approximations only. The dose in a particular patient should be chosen on an individualised basis by the treating professional. aripiprazole, and ziprasidone, are more commonly Drug treatment is usually administered in the used than the older typical (or fi rst generation) anti- outpatient setting as: psychotics such as trifl uoperazine and haloperidol, in 1. There are very few number of psychiatric beds in acute stages. Atypical anti psychotics are also more India, useful when negative symptoms are prominent, e.g. 2. Majorities of families are willing to care for the in chronic schizo phrenia. patients at home, and Clozapine, another atypical antipsychotic, is 3. Majority of patients do not require hospitalisa- available in the Indian market. The clinical trials have tion. shown that clozapine is effective in about 30% of However, hospitalisation is indicated if there is: patients who had no benefi cial res ponse to traditional 1. Neglect of food and water intake, (typical and atypical) antipsy chotics. It is an effective 2. Danger to self or others, drug; however, as it can cause agranu locytosis and 3. Poor treatment adherence, seizures as side-effects, it should be used with caution, 4. Signifi cant neglect of self-care, or with regular WBC and neutrophil counts as advised 5. Lack of social support with evidence of above- by the Summary of Product Characteristics (SPC). mentioned risks. Schizophrenia 67

In the presence of acute excitement, haloperidol Antipsychotics probably act by blocking the post-

5 mg IV or IM, with/without 10 mg diazepam or synaptic dopamine ( D2) receptors in the mesolimbic 50 mg of promethazine can be administered. Given system. Other receptors such as 5-HT, muscarinic IM, chlorpromazine can cause painful injection receptors and GABA are also probably important. abscess at the injection site. It should never be given Atypical antipsychotics are also called as Serotonin- IV, as severe hypoten sion can occur. It is really Dopamine Antagonists (SDAs) due of their action on important to exercise care in administering parenteral both dopamine and 5-HT. antipsychotics to any patient, but particularly one who is treatment (antipsychotic) naïve. Oral antipsychotics Electroconvulsive Therapy (ECT) are preferable to parenteral antipsychotic in routine Schizophrenia is not a primary indication for ECT. clinical practice. The indications for ECT in schizophrenia include: A majority of patients require maintenance treat- 1. Catatonic stupor. ment with antipsychotics to prevent relapse. Generally, 2. Uncontrolled catatonic excitement. the treatment is continued for 6 months to 1 year for 3. Acute exacerbation not controlled with drugs. the fi rst episode, for 1-2 years for the subsequent epi- 4. Severe side-effect with drugs, in presence of un- sodes, and for indefi nite period for repeated episodes treated schizophrenia. or persistent symptoms. However, the decision regard- Usually 8-12 ECTs are needed (although up to 18 ing the duration of treatment in a particular case has to have been given in poor responders), administered two be assessed individually by the treating psychiatrist in or three times a week. consultation with the patient and family (if appropriate), in view of past history and possible risks. Miscellaneous Treatments To ensure drug concordance, depot anti psychotic Psychosurgery is not routinely indicated in the treat- prepara tions with long duration of action can be used. ment of schizophrenia. It is a treatment which is (See Table 15.5 for some common preparations of extremely rarely used in clinical practice. When used, depot antipsychotics). the treatment of choice is limbic leucotomy (a small Many patients require adjuvant antiparkin sonian subcaudate lesion with a cingulate lesion) in some medication to prevent extrapyramidal side-effects; cases with severe and very prominent depression, for example, trihexiphenidyl 6 mg/day, orphenadrine anxiety or obsessional symptoms. 150 mg/day, procycli dine 7.5-15 mg/day. This is Severely deteriorated patients are unlikely to particularly true if the patient is receiving an older, benefi t. The maximum benefi t would be in acute typical antipsychotic (such as haloperidol). However, episo des, but antipsychotics are far better obviously at times atypical antipsy chotics such as risperi done both in effi cacy and safety. can also cause extrapyramidal symptoms, particularly Many other methods such as megavitamin therapy, in higher doses. dialysis, malaria therapy, high dose propranolol and Ideally speaking, during hospitalisation, no patient insulin coma therapy have been used in past but are should receive anticholinergic antiparkin sonian no longer used in clinical practice due to either poor medication till extrapyramidal side-effects appear. evidence for effi cacy and/or risks to the patient. Anticholinergics can worsen cognitive function, have an abuse poten tial, can cause delirium (especially Psychosocial Treatment in elderly), can worsen or contribute to negative Psychosocial treatment is an extremely important symptoms in schizophrenia, and may increase the risk component of comprehensive management of schizo- of tardive dyskinesia. But, in routine clinical practice, phrenia. It can be divided in following steps: often a majority of patients do receive anticholinergics 1. Psychoeducation of the patient and espe cially the in addition to traditional anti psychotics. family/carers (with patient’s consent) regarding 68 A Short Textbook of Psychiatry

the nature of illness, and its course and treatment. the current consensus does not recommend the Psycho education helps in establishing a good use of psychoanalytic psycho therapy in routine therapeutic relationship with the patient (and the treatment of schizo phrenia. family). Psychoeducation also involves explaining Several centres (and guidelines) recom mend the the stress-vulnerability model of schizophrenia to use of cognitive behaviour therapy (CBT) in the the patient and carer(s). treatment of schizophrenia [e.g. NICE (National 2. Group psychotherapy is particularly aimed Institute of Clinical Excellence, UK) Guidelines at teaching problem solving and communica- for Schizophrenia 2009]. Delivery of CBT in tion skills. This can be conducted in a form schizophrenia needs specialised training and is which is known as the ‘ social skills training pack- often conducted as an adjunct to psychopharma- age’. cological therapy. 3. Family therapy: Apart from psychoeducation, 6. Psychosocial rehabilitation is used, usually along family members are also provided social skills with milieu therapy. This includes activity therapy, training to enhance comm unication and help to develop the work habit, training in a new voca- decrease intrafamilial ‘tensions’. Attempts are tion or retraining in a previous skill, vocational also made to decrease the ‘ expres sed emotions’ guidance, independent job placement, sheltered (EE) of ‘signiﬁ cant others’ in the family. The employ ment or self-employment, and occupa- family members’ awareness is raised regarding tional therapy. decreasing expectations and avoiding critical However, antipsychotic drug treatment in the acute remarks, emotional over-involve ment, and hostility. stages, as well as for maintenance treatment, is the 4. Milieu therapy (or therapeutic community) in- mainstay of management of schizo phrenia. cludes treatment in a living, learning or working Psychosocial treatment is an important adjunct environment ranging from inpatient psychiatric to drug treatment which enhances its efﬁ cacy and unit to day-care hospitals and half-way homes. leads to a more complete recovery and rehabilitation. 5. Individual psychotherapy is usually sup portive However, it is unlikely that psychosocial treatment, in nature. Rarely, psychoanalytically oriented in the absence of drug treatment, will be able to treat psychodynamic psychotherapy is used. However, schizophrenia effectively. 6 Mood Disorders

Broadly speaking, the emotions can be described as with all medical disorders, and not only psychiatric two main types: disorders. The World Health Report 2001 estimates 1. Affect, which is a short-lived emotional response that there are 121 million people worldwide suffering to an idea or an event, and from depression. 2. Mood, which is a sustained and pervasive emotional response which colours the whole psychic CLASSIFICATION life. So according to these definitions, depres sion The classifi cation of mood disorders is an area which is and mania are mood disorders and not ‘affective fraught with multiple controversies. According to the disorders’ as they have been called so frequently in ICD-10, the mood disorders are classifi ed as follows: the past. Throughout this chapter (and this book), the 1. Manic episode more correct word mood disorder will be used (as 2. Depressive episode indeed in DSM-IV-TR and ICD-10). 3. Bipolar mood (affective) disorder Mood disorders have been known to man since 4. Recurrent depressive disorder antiquity. The Old Testament describes King Saul 5. Persistent mood disorder (including cyclo thymia as suffering from severe depressive episodes and and dysthymia) responding slightly to David’s soothing music. While 6. Other mood disorders (including mixed affective Hippocrates coined the words mania and melancholia, episode and recurrent brief depres sive disorder). it was Aretaeus who fi rst described mania and depression occurring in the same individual. Emil Kraepelin, CLINICAL FEATURES AND DIAGNOSIS borrowing from the work of Kahlbaum, Falret and Baillarger, described the manic-depressive illness as Manic Episode separate from dementia praecox on the basis of course, clinical symptoms and outcome. The life-time risk of manic episode is about 0.8- Recently, the World Health Report 2001 has identi- 1%. This disorder tends to occur in episodes lasting fi ed unipolar depression as the 4th cause of Disability- usually 3-4 months, followed by complete clinical Adjusted Life Years (DALYs) in all ages, and the recovery. The future episodes can be manic, depres- 2nd cause in the age group of 15-44 years. Unipolar sive or mixed. depression is also the 1st cause of YLD (Years of Life A manic episode is typically characterised by the Lived with Disability) in all ages. The comparison was following features (which should last for at least one 70 A Short Textbook of Psychiatry week and cause disruption in occupa tional and social Later, there is ‘ fl ight of ideas’ (rapidly produced activities). speech with abrupt shifts from topic to topic, using external environmental cues. Typically the connec- Elevated, Expansive or Irritable Mood tions between the shifts are apparent). When the The elevated mood can pass through following four ‘fl ight’ becomes severe, incoherence may occur. A less stages, depending on the severity of manic episode: severe and a more ordered ‘fl ight’, in the absence of a. Euphoria (mild elevation of mood): An increased pressure of speech, is called ‘prolixity’. sense of psychological well-being and happiness, There can be delusions (or ideas) of grandeur not in keeping with ongoing events. This is usually (grandiosity), with markedly infl ated self-esteem. seen in hypomania (Stage I). Delusions of persecution may sometimes deve lop b. Elation (moderate elevation of mood): A feeling of secondary to the delusions of grandeur (e.g. I am so confi dence and enjoyment, along with an increased great that people are against me). Hallucinations (both psychomotor activity. Elation is classically seen auditory and visual), often with religious content, in mania (Stage II). can occur (e.g. God appeared before me and spoke to c. Exaltation (severe elevation of mood): Intense me). Since these psychotic symptoms are in keeping elation with delusions of grandeur; seen in severe with the elevated mood state, these are called mood- mania (Stage III). congruent psychotic features. d. Ecstasy (very severe elevation of mood): Intense Distractibility is a common feature and results in sense of rapture or blissfulness; typically seen in rapid changes in speech and activity, in response to delirious or stuporous mania (Stage IV). even irrelevant external stimuli. Along with these variations in elevation of mood, expansive mood may also be present, which is an Goal-directed Activity unceasing and unselective enthusiasm for interac ting The person is unusually alert, trying to do many things with people and surrounding environment. At times, at one time. elevated mood may not be apparent and instead an In hypomania, the ability to function becomes irritable mood may be predomi nant, especially when much better and there is a marked increase in pro- the person is stopped from doing what he wants. There ductivity and creativity. Many artists and writers may be rapid, short lasting shifts from euphoria to have contributed signifi cantly in such periods. As depression or irritability. past history of hypomania and mild forms of mania is often diffi cult to elicit, it is really important to take Psychomotor Activity additional historical information from reliable infor- There is an increased psychomotor activity, ranging mants (e.g. family members). from overactiveness and restlessness, to manic excite- In mania, there is marked increase in activity ment where the person is ‘on-the-toe-on-the-go’, (i.e. with excessive planning and, at times, execution of involved in ceaseless activity). The activity is usually multiple activities. Due to being involved in so many goal-oriented and is based on external environmental activities and distrac tibility, there is often a decrease cues. Rarely, a manic patient can go in to a stuporous in the functioning ability in later stages. There is state (manic stupor). marked increase in socia bility even with previously unknown people. Gradually this soci a bility leads to Speech and Thought an interfering behaviour though the person does not The person is more talkative than usual; des cribes recognise it as abnormal at that time. The person thoughts racing in his mind; develops pressure of becomes impulsive and disinhi bited, with sexual speech; uses playful language with punning, rhyming, indiscretions, and can later become hypersexual and joking and teasing; and speaks loudly. promiscuous. Mood Disorders 71

Due to grandiose ideation, increased sociability, The loss of interest in daily activities results in overactivity and poor judgement, the manic person social with drawal, decreased ability to func tion in is often involved in the high-risk activities such as occupa tional and interpersonal areas and decreased buying sprees, reckless driving, foolish business involvement in previously pleasurable activities. In investments, and distributing money and/or personal severe depression, there may be complete anhedonia articles to unknown persons. He is usually dressed up (inability to experience pleasure). in gaudy and fl amboyant clothes, although in severe mania there may be poor self-care. Depressive Ideation/Cognition Sadness of mood is usually associated with pessimism, Other Features which can result in three common types of depressive Sleep is usually reduced with a decreased need for ideas. These are: sleep. Appetite may be increased but later there is a. Hopelessness (there is no hope in the future). usually decreased food intake, due to marked over- b. Helplessness (no help is possible now). activity. Insight into the illness is absent, especially c. Worthlessness (feeling of inadequacy and inferior- in severe mania. ity). Psychotic features such as delusions, hallucina- The ideas of worthlessness can lead to self- tions which are not understandable in the context of reproach and guilt-feelings. The other features are mood disorder (called mood incongruent psy chotic diffi culty in thinking, diffi culty in concen tra tion, features), e.g. delusions of control, may be present in indecisiveness, slowed thinking, subjec tive poor some cases. memory, lack of initiative and energy. Often there are ruminations (repetitive, intrusive thoughts) with pes- Absence of Underlying Organic Cause simistic ideas. Thoughts of death and preoccupation If manic episode is secondary to an organic cause, a with death are not uncom mon. diagnosis of organic mood disorder should be made. Suicidal ideas may be present. In severe cases, delusions of nihilism (e.g. ‘world is coming to an Depressive Episode end’, ‘my brain is completely dead’, ‘my intestines The life-time risk of depression in males is 8-12% and have rotted away’) may occur. in females is 20-26%. However, the life-time risk of major depression (or depres sive episode) is about 8%. Psychomotor Activity The typical depressive episode is characterised by In younger patients (< 40 year old), retarda tion is more the following features (which should last for at least common and is characterised by slowed thinking and two weeks for a diagnosis to be made): activity, decreased energy and monotonous voice. In a severe form, the patient can become stuporous Depressed Mood ( depressive stupor). The most important feature is the sadness of mood In the older patients (e.g. post-menopausal or loss of interest and/or pleasure in almost all ac- women), agitation is commoner. It often presents with tivities (pervasive sadness), present throughout the marked anxiety, restlessness (inability to sit still, hand- day (persistent sadness). This sadness of mood is wriggling, picking at body parts or other objects) and quantitatively as well as qualitatively different from a subjective feeling of unease. the sadness encoun tered in ‘normal’ sadness or grief. Anxiety is a frequent accompaniment of depres- The depressed mood varies little from day to day sion. Irritability may present as easy annoyance and and is often not responsive to the environmental frustration in day-to-day activities, e.g. unusual anger stimuli. at the noise made by children in the house. 72 A Short Textbook of Psychiatry

Physical Symptoms nature of the disturbance. It often also implies a good Multiple physical symptoms (such as heaviness of response to somatic methods of treatment (e.g. phar- head, vague body aches) are particularly com mon in macotherapy, ECT). the elderly depressives and depressed patients from the develo ping countries (such as India). Psychotic Features However, the recent literature has shown that About 15-20% of depressed patients have psychotic multiple physical symptoms (called general aches symptoms such as delusions, hallucina tions, grossly and pains) are present in most patients even in the inappropriate behaviour or stupor. The psychotic Western world and they can be elicited only if physi- features can be either mood-con gruent (e.g. nihilistic cians routinely ask the patients for their presence. delusions, delusions of guilt, delusions of poverty, Hypo chondria cal features may be present in up stupor) which are understandable in the light of to a quarter of depres sives presenting for treat ment. depressed mood, or can be mood-incongruent (e.g. These physical symptoms are almost always present delusions of control) which are not directly related to in severe depressive episode. depres sive mood. Another common symptom is the complaints of reduced energy and easy fatigability. The patients, Suicide therefore, not surprisingly attribute their symptoms Suicidal ideas in depression should always be taken to physical cause(s) and consult a physician instead very seriously. Although there is a risk of suicide in of a psychiatrist. every depressed patient with suicidal ideation, presence of certain fac tors increases the risk of suicide Biological Functions (Table 6.2). Disturbance of biological functions is common, with insomnia (or sometimes increased sleep), loss of Absence of Underlying Organic Cause appetite and weight (or sometimes hyperphagia and If depressive episode is secondary to an organic cause, weight gain), and loss of sexual drive. a diagnosis of organic mood disorder should be made. When the disturbance is severe, it is called as In ICD-10, the severity of depressive episode is melancholia (somatic syndrome in ICD-10-DCR; defi ned as mild, moderate or severe, depending prima- Diagnostic Criteria for Research). The somatic syn- rily on the number of the symptoms, but also on the drome of depression is described in Table 6.1. severity of symp toms and the degree of impairment. The presence of somatic syndrome in depres sive disorder signifi es higher severity and more biological Table 6.2: Suicidal Risk: Some Important Factors Suicidal risk is much more in the presence of following Table 6.1: Somatic Syndrome in Depression (ICD-10) factors: The somatic syndrome is characterised by: a. Presence of marked hopelessness a. Signifi cant decrease in appetite or weight b. Males; age>40; unmarried, divorced/widowed b. Early morning awakening, at least 2 (or more) c. Written/verbal communication of suicidal intent hours before the usual time of awakening and/or plan c. Diurnal variation, with depression being worst in d. Early stages of depression the morning e. Recovering from depression (At the peak of d. Pervasive loss of interest and loss of reactivity to depression, the patient is usually either too de- pleasurable stimuli pressed or too retarded to commit suicide) e. Psychomotor agitation or retardation. f. Period of 3 months from recovery. Mood Disorders 73

Bipolar Mood (or Aff ective) Disorder Persistent Mood Disorder This disorder, earlier known as manic depres sive psy- These disorders are characterised by per sistent mood chosis (MDP), is characterised by recur rent episodes symptoms which last for more than 2 years (1 year in of mania and depression in the same patient at different children and adoles cents) but are not severe enough times (Fig. 6.1). to be labelled as even hypomanic or mild depressive These episodes can occur in any sequence. The episode. patients with recurrent episodes of mania (unipolar If the symptoms consist of persistent mild depres- mania) are also classifi ed here as they are rare and sion, the disorder is called as dysthymia ; and if symp- often resemble the bipolar patients in their clinical toms consist of persistent instability of mood between features. mild depression and mild elation, the disorder is called The current episode in bipolar mood disorder is as cyclothymia. specifi ed as one of the following (ICD-10): i. hypomanic, Other Mood Disorders ii. manic with out psy chotic symptoms, This category includes the diagnosis of mixed affec- iii. manic with psychotic symp toms, tive episode. This is a frequently missed diagnosis iv. mild or moderate depression, clinically. In this type, the full clinical picture of v. severe depression, without psychotic symptoms, depression and mania is present either at the same time vi. severe depression, with psychotic symptoms, intermixed (Fig. 6.1), or alternates rapidly with each vii. mixed, or other (rapid cycling), without a normal intervening viii. in remission. period of euthymia. Bipolar mood disorder is further classifi ed in to bipolar I and bipolar II disorders (Table 6.3). COURSE AND PROGNOSIS

Recurrent Depressive Disorder Bipolar mood disorder has an earlier age of onset This disorder is characterised by recurrent (at least (third decade) than recurrent depres sive (uni polar) two) depressive episodes ( unipolar depression). disorder. Unipolar depression, on the other hand, is The current episode in recurrent depressive disor- common in two age groups: late third decade and ﬁ fth der is speciﬁ ed as one of the following: to sixth decades. i. mild, An average manic episode lasts for 3-4 months ii. moderate, while a depressive episode lasts from 4-6 months. iii. severe, without psychotic symp toms, Unipolar depression usually lasts longer than bipolar iv. severe, with psychotic symptoms, depression. With rapid institution of treatment, the v. in remission. major symptoms of mania are controlled within 2 weeks and of depression within 6-8 weeks.

Table 6.3: Subtypes of Bipolar Disorder 1. Bipolar I Characterised by episodes of severe mania and severe depression 2. Bipolar II Characterised by episodes of hypomania (not requir- Fig. 6.1: Bipolar Disorder: Clinical Picture ing hospitalisation) and severe dep ression 74 A Short Textbook of Psychiatry

Nearly 40% of depressives with episodic course There is an increased mortality in patients with improve in 3 months, 60% in 6 months and 80% mood disorders by almost two times the general popu- improve within a period of one year. 15-20% of lation. The most important cause of death is suicide, patients develop a chronic course of illness, which the life-time risk of which is 10-15 times higher in may last for two or more years. depression. Patients with depression also have higher Chronic depression is usually characterised by mortality rates from cardiovascular diseases and co- less intense depression, hypochon driacal symptoms, morbid alcohol and drug use disorders. Patients with presence of co-morbid disorders (such as dysthymic depres sion also exhibit a variety of disturbances in disorder, alcohol dependence, perso nality disorders immune function. and medi cal disorders), presence of ongoing stressors and unfavourable early environment. As the age PROGNOSIS advances, the intervals between two episodes shorten and, the dura tion of the episodes and their frequency Classically, the prognosis in mood disorders is gener- tends to increase. Although not all patients have relap- ally described as better than in schizophrenia. Some ses, it has been estimated that up to 75% of patients of the good (and poor) prognostic factors in mood have a second episode within 5 years. disorders are described in Table 6.4. Some patients with bipolar mood disorder have more than 4 episodes per year; they are known as rapid Table 6.4: Some Prognostic Factors in Mood Disorders cyclers (Figure 6.2). About 70-80% of all rapid cyclers Good Prognostic Factors are women. When phases of mania and depression 1. Acute or abrupt onset alternate very rapidly (e.g. in matter of hours or days), 2. Typical clinical features the condition is known as ultra-rapid cycling. Some 3. Severe depression of the factors associated with rapid cycling include the 4. Well-adjusted premorbid personality use of antidepressants (especially tricyclic antidepres- 5. Good response to treatment. sants), low thyroxin levels, female gender, bipolar II Poor Prognostic Factors pattern of illness, and the presence of neurological 1. Co-morbid medical disorder, personality dis order or disease. alcohol dependence 2. Double depression (acute depressive epi sode superimposed on chronic depression or dysthymia) 3. Catastrophic stress or chronic ongoing stress 4. Unfavourable early environment 5. Marked hypochondriacal features, or mood-incongruent psychotic features 6. Poor drug compliance.

AETIOLOGY Over the years, a vast amount of literature has emerged probing the aetiology of mood dis orders. However, the aetiology of mood disorders is not known currently, Fig. 6.2: Bipolar Disorder: Rapid Cycling Clinical despite several theories having been propounded. Picture Some of these include: Mood Disorders 75

Biological Theories decrease in the serotonergic function, evidenced by The following fi ndings (and theories) point towards decreased urinary and plasma 5-HIAA levels and the a biological basis of mood disorders. postmortem studies. Genetic Hypothesis Neuroendocrine Theories The life-time risk for the fi rst degree relatives of Mood symptoms are prominently present in many bipolar mood disorder patients is 25%, and of recurrent endocrine disorders, such as hypothyroidism, depressive disorder patients is 20%. Cushing’s disease, and Addison’s disease. The life-time risk for the children of one parent Endocrine function is often disturbed in depres- with bipolar mood disorder is 27% and of both parents sion, with cortisol hypersecretion, non-suppression with bipolar mood disorder is 74%. with dexamethasone challenge (Dexamethasone sup- The concor dance rate in bipolar disorders for pression test or DST), blunted TSH response to TRH, mono zygotic twins is 65% and for dizygotic twins is and blunted growth hor mone (GH) production during 20%; the concordance rate in unipolar depression for sleep. monozygotic twins is 46% and for dizygotic twins is The neuroendocrine and biochemical mechanisms 20%. are closely inter-related. Therefore, genetic factors are very impor tant in making an individual vulnerable to mood disorders, Sleep Studies particularly so in bipolar mood dis orders. However, Sleep abnormalities are common in mood dis orders environmental factors are also probably important. (e.g. decreased need for sleep in mania; insomnia and frequent awakenings in depres sion). Biochemical Theories In depression, the commonly obser ved abnor- There are several biochemical hypotheses for the malities include decreased REM latency (i.e. the time causation of mood disorders. The monoamine between falling asleep and the fi rst REM period is hypothesis suggests an abnorma lity in the monoamine decreased), increased duration of the fi rst REM period, [catecholamine (norepi nep hrine and dopamine) and and delayed sleep onset. serotonin] system in the central nervous system at one or more sites. Acetylcholine and GABA are also Brain Imaging presum ably involved. In mood disorders, brain imaging studies (CT scan/ The earlier models of a functional increase (in ma- MRI scan of brain, PET scan, and SPECT) have nia) or decrease (in depression) of amines at the syn- yielded inconsistent, yet suggestive fi ndings. aptic cleft now appear simp listic, though urinary and These fi ndings include ventricular dilatation, white CSF levels of amine metabolites indicate decreased matter hyper-intensities, and changes in the blood fl ow norepinep hrine and/or 5-HT function in depression, and metabolism in several parts of brain (such as pre- and increased nor epinephrine in mania. frontal cortex, anterior cingulate cortex, and caudate). The postsynaptic events involving the second messenger system, and alterations in the receptor Psychosocial Theories number and function, are also important in addition Psychoanalytic Theories to the synaptic and presynaptic events. The effects of antidepressants and mood stabilisers In depression, loss of a libidinal object, introjection in mood disorders also provide additional evidence to of the lost object, fi xation in the oral sadistic phase the biochemical hypothesis of mood disorders. of development, and intense craving for narcissism Patients suffering from severe depression with or self-love are some of the postulates of different suicidal intent/attempt appear to have a marked psychodynamic theories. 76 A Short Textbook of Psychiatry

Mania represents a reaction formation (Table 17.1) Table 6.5: Some Commonly used Antidepressants to depression according to the psychodynamic theory. Generic Name Usual Therapeutic Stress Range (mg/day) Increased number of stressful life events before the 1. Agomelatin 25-50 onset or relapse has a formative rather than a pre- 2. Amitriptyline 75-300 cipitating effect in depression though they can serve 3. Amoxapine 150-300 4. Bupropion 150-450 a precipitant role in mania. Increased stressors in 5. Citalopram 10-40 the early period of development are probably more 6. Clomipramine 75-250 important in depression. 7. Doxepine 75-300 Cognitive and Behavioural Theories 8. Dosulepin/Dotheipin 75-150 9. Duloxetine 30-120 The mechanisms of causation of depression, according 10. Escitalopram 10-20 to these theories, include depressive negative 11. Fluoxetine 20-60 cognition (cognitive theory), learned helplessness 12. Fluvoxamine 50-200 (animal model), and anger directed inwards. These 13. Imipramine 75-300 concepts are useful in the psycho logical treatment of 14. Lofepramine 140-210 mild (to moderate) depression. 15. Mianserin 30-120 Several other theories have also been pro pounded 16. Mirtazapine 15-45 but are currently considered to be of doubtful value 17. Moclobemide 300-600 as theories of causation of depression. 18. Nortriptyline 150-300 19. Paroxetine 10-40 DIFFERENTIAL DIAGNOSIS 20. Reboxetine 10-12 21. Sertraline 50-200 The ﬁ rst step in the differential diagnosis of any mood 22. Tianeptin 37.5 disorder is to exclude a disorder with known organic 23. Trazodone 300-600 cause, e.g. organic (especially drug-induced) mood 24. Venlafaxine 75-375 dis orders and dementia (differential diagnosis from depressive pseudo dementia). anxiety, panic, alcohol or drug misuse, or person- The second step is to rule out a possibility of acute ality disorder) on a multi-axial diagnostic system and transient psychotic disorders, schizo-affective (Table 1.4). disorder, and schizophrenia. The third step is to exclude the possibility of other MANAGEMENT non-organic psychoses such as delusional disorders. The fourth step is to exclude the possibility of Somatic Treatment adjustment disorder with depressed mood, gene ra lised anxiety disorder, normal grief reaction, and obses- Antidepressants sive compulsive disorder (with or without secondary Antidepressants are the treatment of choice for a vast depression). majority of depressive episodes. Some of the com- In addition to the main diagnosis, it is also impor- monly used antidepressants with their usual range of tant to look for co-morbid medical (such as diabetes, therapeutic dosage are listed in Table 6.5. (Antide- hypertension) and/or psychiatric disorders (such as pressants are discus sed in more detail in Chapter 15). Mood Disorders 77

The usual starting dose is about 75-150 mg of There are three main phases of treatment: imipramine equivalent. The clinical improve ment i. Acute treatment (till remission occurs), is assessed after about two weeks. In case of non- ii. Continuation treatment (from remission till end improvement, the dose can usually be increased up of treat ment), and to 300 mg of imipramine equivalent. iii. Maintenance treatment (to prevent further recur- It should be remembered that it may take up to rences). 3 weeks before any appreciable response may be Maintenance treatment may be indicated in the noticed. Before stopping or changing a drug, the following patients: particular drug should be given in a therapeutically i. Partial response to acute treatment. adequate dose for at least 6 weeks. ii. Poor symptom control during the continuation A variety of antidepressants are now available treatment. in the market. Since almost all antidepressants are iii. More than 3 episodes (90% chances of recur- equal in antidepressant effi cacy and there is no single rence). antidepressant effective for all depressed patients, the iv. More than 2 episodes with early age of onset, choice of anti depressant is often dictated by other fac- or recurrence within 2 years of stopping tors. These factors include cost and ease of availability antidepressants, or severe and/or life-threatening of the drug, the side-effect profi le of the drug, past depression, or family history of mood disorder. history of response and (any) co-morbid medical or v. Chronic depression (> 2 years) or double depres- psychiatric disorders. An individua lised choice has to sion. be made in each patient, keeping these various fac- About 20-35% of depressed patients are refractory tors in mind. to antidepressant medication. The management of a Imipramine, amitriptyline and other rela ted drugs treatment refractory depres sed patient is best done are called tricyclic antidepres sants (TCAs). The by a psychiatrist, often at a tertiary care centre. These newer antidepressants such as selective serotonin patients may require one of the following alternatives: reuptake inhibitors ( SSRIs) (e.g. fl uoxetine, sertraline, i. A change of antidepressant (Switch), citalopram), mirtazapine, and serotonin norepine- ii. Combination of two types of antidep ressants, phrine reuptake inhibitors (SNRIs) (e.g. venlafaxine, iii. Augmentation with lithium, duloxetine) have very little anticholinergic side iv. Augmentation with T3 or T4, effects and, hence, are generally safer drugs to use in v. Augmentation with antipsychotics, elderly patients with benign hypertrophy of prostate. vi. Electroconvulsive therapy, or However, both venlafaxine and duloxetine have been vii. Use of newer and experimental techni ques. associated with hypertension and should be used with One type of depression, namely delusional depres- care in those with a history of cardiac illness. sion (depression with psychotic features), is usually The antidepressant dosage is monitored on the refractory to antidepressants alone. The treatments of basis of clinical improvement. Routine monitoring choice in this condition include: of blood levels is not usually indicated. i. An antidepressant with ECT, or For the fi rst, uncomplicated, depressive epi sode, ii. An antidepressant with antipsychotics, or the patient should receive full therapeutic dose of the iii. An antidepressant with lithium. chosen antidepressant for a period of 6-9 months, after achieving full remission. It is wise to taper the Electroconvulsive Therapy (ECT) anti depressant medication, when the treatment is to The indications for ECT in depression include: be stopped after the continuation phase. i. Severe depression with suicidal risk. 78 A Short Textbook of Psychiatry

ii. Severe depression with stupor, severe psycho- A blood lithium level of >2.0 mEq/L is often motor retardation, or somatic syndrome. associated with toxicity, while a level of more than iii. Severe treatment refractory depression. 2.5-3.0 mEq/L may be lethal. iv. Delusional depression (psychotic fea tures). Although lithium is indicated for therapeutic use v. Presence of significant antidepressant side- in all manic episodes, the preventive use is best in effects or intolerance to drugs. usually those patients with bipolar disorder, in whom Severe depression with suicidal risk is the fi rst and the frequency of episodes is 1-3 per year or 2-5 per foremost indication for use of ECT. The prompt use two years. of ECT can be life-saving in such a situation. The common acute toxic symptoms of lithium are The response is usually rapid, resulting in a marked neurological while the common chronic side-effects improvement. In most clinical situations, usually 6-8 are nephrological and endocrinal (usually hypothy- ECTs are needed, given three times a week. When six roidism). ECTs are administered, the usual pattern is three ECTs The important investigations before star ting in the fi rst week, two in the second week and one in lithium therapy include a complete general physical the third week. examination, full blood counts, ECG, urine routine However, improvement is not sustained after exami nation (with/without 24 hour urine volume), stopping the ECTs. Therefore, antidepressants are renal function tests and thyroid function tests. often needed along with ECTs, in order to maintain the improvement achieved. The safety of the ECT Antipsychotics procedure has now been well-established. Antipsychotics are an important adjunct in the ECT can also be used for acute manic excite ment, treatment of mood disorder. The commonly used if it is not adequately responding to antipsychotics and drugs include risperidone, olan zapine, quetia pine, mood stabilisers. haloperidol, and aripiprazole. It is customary to use the atypical antipsychotics fi rst, before considering Lithium (Li) the older typical antipsy chotics. Lithium has traditionally been the drug of choice for Some of the indications include: the treatment of manic episode (acute phase) as well 1. Acute manic episode as for prevention of further episodes in bipolar mood • Along with mood stabilisers for the first few disorder. It has also been used in treatment of depres- weeks, before the effect of mood stabilisers sion with less success. (Lithium is discussed in detail becomes apparent. in Chapter 15). • Where mood stabilisers are not effective, not indi- There is usually a 1-2 week lag period before any cated, or have signifi cant side-effects. appreciable response is observed. So, for treatment • Given parenterally (IM or IV) for emer gency of acute manic episode, antipsycho tics are usually treatment of mania. administered along with lithium, in order to provide • Recently, there has been some early evidence that cover for the fi rst few weeks. atypical antipsychotics (e.g. olanzapine) might The usual therapeutic dose range is 900-1500 mg have some mood stabilising properties. of lithium carbonate per day. Lithium treatment needs 2. Delusional depression to be closely monitored by repeated blood levels, as As stated above, antipsychotics are important adjuncts the difference between the therapeutic and lethal blood in the treatment of delusional depression. Once again, levels is not very wide (narrow therapeutic index). it is customary to use atypical antipsychotics such as Therapeutic blood lithium = 0.8-1.2 mEq/L olanzapine, quetiapine, risperidone, and ziprasidone Prophylactic blood lithium = 0.6-1.2 mEq/L fi rst, although any antipsychotic can be used. Mood Disorders 79 iii. Bipolar depression 4. Lamotrigine is particularly effective for bipolar There is recent evidence that quetiapine has antide- depression and is recommended by several guidelines. pressant effi cacy in bipolar depression. 5. T3 and T 4 as adjuncts for the treatment of rapid cy- iv. Maintenance or prophylactic treatment in bipolar c ling mood disorder and resistant depression. disorder Recent evidence shows that several atypical antipsy- Other Treatments chotics such as olanzapine, quetiapine and aripiprazole Psychosurgery is an extremely rarely used method can be successfully used in the maintenance treatment of treatment and is resorted to only in excep tional of bipolar disorder. circumstances. In depressive episode, which is either chronic or Other Mood Stabilisers persistently recurrent with a limited or absent response The other mood stabilisers which are used in the treat- to other modes of treatment, one of the following ment of bipolar mood disorders include: procedures may very rarely be performed: 1. Sodium valproate i. Stereotactic subcaudate tractotomy, or • For acute treatment of mania and prevention of ii. Stereotactic limbic leucotomy. bipolar mood disorder. In carefully selected patients, the results are • Particularly useful in those patients who are refrac- reported to be satisfactory. However, in the current tory to lithium. day and age, psychosurgery is hardly ever considered • The dose range is usually 1000-3000 mg/day (the in routine clinical practice. therapeutic blood levels are 50-125 mg/ml). • It has a faster onset of action than lithium, there- Psychosocial Treatment fore, it can be used in acute treatment of mania Although somatic treatment appears to be the primary effectively. mode of management in major mood disorders, psy- 2. Carbamazepine and Oxcarbazepine chosocial treatment is often helpful. These indications • For acute treatment of mania and prevention of include: bipolar mood disorder. i. As an adjunct to somatic treatment. • Particularly useful in those patients who are refrac- ii. In mild to moderate cases of depression. tory to lithium and valproate. iii. Certain selected cases. • Particularly effective when EEG is abnormal These methods include (see Chapter 18 for details): (although this is not necessary for the use of carbamazepine). Cognitive Behaviour Therapy • The dose range of carbamazepine is 600-1600 mg/ Cognitive behaviour therapy (CBT) aims at correct- day (the therapeutic blood levels are 4-12 mg/ml). ing dep ressive negative cognitions (ideations) such • The use of carbamazepine in treatment of bipolar as hopelessness, worthlessness, helplessness and pes- disorder has recently declined, partly due to its simistic ideas, and replacing them by new cognitive potential for drug interactions. and behavioural responses. • Oxcarbazepine has a narrow evidence base and its CBT is useful in mild to moderate, non-bipolar use in bipolar disorder is quite recent. depression and can be used with or without somatic 3. Benzodiazepines treatment. Lorazepam (IV and orally) and clonazepam are used for the treatment of manic episode alone rarely; how- Interpersonal Therapy ever, they have been used more often as adjuvants to Interpersonal therapy (IPT) attempts to recognise antipsychotics. and explore interpersonal stressors, role disputes and 80 A Short Textbook of Psychiatry transitions, social isolation, or social skills defi cits, OTHER SYNDROMES OF DEPRESSION which act as precipi tants for depression. AND MANIA It is useful in the treatment of mild to moderate Involutional Melancholia unipolar depression, with or without antidepressants. Described by Kraepelin, this is a form of severe de- Psychoanalytic Psychotherapy pression which occurs in the involutional period of The short-term psychoanalytic psychotherapies aim life (i.e. 40-65 years of age). at changing the personality itself rather than just It is typically characterised by marked agitation, ameliorating the symptoms. presence of psychotic features (such as delusions of Their usefulness is uncertain, particularly in fl orid persecution, tactile and auditory hallucinations) and depressive or manic episode. These techniques are multiple somatic symptoms (or hypochondriacal however helpful in the treatment of selected patients delu sions). Presently, it is no longer thought of as an (such as dysthymic disorder, depression co-morbid independent entity but the term is used to describe the with personality disorders, or depression with history severity of a depressive episode. of childhood loss/child abuse). Mixed Anxiety Depressive Disorder Behaviour Therapy This disorder is characterised by the presence of This includes the various short-term modalities such depressive and anxiety symptoms which result in as social skills training; problem solving techniques, signifi cant distress or disability in the person. The assertiveness training, self-control the rapy, activity symptoms should not meet the criteria of either an scheduling and decision-making techniques. anxiety disorder or a mood disorder. It can be useful in mild cases of depression or as This disorder is apparently seen more fre quently an adjunct to antidepressants in moderate depression. in the medical outpatient departments and primary care centres. Several cases pro bably exist untreated Group Therapy in the general population, but rarely come to medical Group psychotherapy can be useful in mild cases of attention. depression. It is a very useful method of psychoeduca- In clinical practice, it is important to consider tion in both recurrent depressive disorder and bipolar a diagnosis of either a mood disorder or an anxi- disorder. ety disorder, before attempting a diagnosis of mixed anxiety-depressive disorder. Family and Marital Therapy Apart from educating the family about the nature of Masked Depression illness and the usefulness of somatic treatment, family In masked depression, the depressive mood is not eas- therapy has not been found very useful in treatment ily apparent and is usually hidden behind the somatic of mood disorders per se. symptoms. This is especially common in the elderly, These therapies can however help decrease the where the somatic symp toms range from chronic pain, intrafamilial and interpersonal diffi culties, and to re- insomnia, atypical facial pain, and paraesthesias. The duce or modify stressors, which may help in a faster depressive symptoms can also be masked by drug and/ and more complete recovery. Their most common use or alcohol misuse. However, a more detailed exami- in clinical practice is to ensure continuity of treatment nation will bring out the tell-tale symptomatology of (such as lithium prevention in patients with bipolar depression. disorder) and adequate drug concordance. The treatment is similar to a depressive episode. Mood Disorders 81

Depressive Equivalents Atypical depression usually has an onset in These are certain conditions which, though not a part the teens and runs a chronic course. Hyper somnia, of the depressive syndrome, are still thought be com- hyperphagia, reactive nature of symp toms, rejection parable to depression (affective spectrum disorders). sensitivity and lethargy (leaden paralysis) are some Some of these show clinical response to anti depressant of the charac teristic features. treatment whilst others appear related to depression The importance of diagnosing atypical depression due to multiple complex reasons. lies in the fact that many of these patients respond These disorders include agoraphobia, chronic pain, better to MAOIs (mono amine oxidase inhibitors), paraesthesias, panic attacks, alcoholism, drug abuse, although SSRIs (Selective Serotonin Reuptake Inhibi- hysteria, obses sive compulsive disorder and eating tors) and TCAs (Tricyclic Antidepressants) should be dis orders ( anorexia nervosa and bulimia nervosa). tried fi rst. This term presently has an uncertain nosological status. Double Depression This is a major depressive episode (usually acute), Atypical Depression(s) superimposed on an underlying dysthy mia or neurotic These are depressive syndromes which do not present depression (usually chronic). The response to treat- with classical or typical features of depression. These ment is usually poor. include: 1. Depression with predominant anxiety: The anxi- Agitated Depression ety here is far more subjective, in contrast to the This is a type of severe depression with marked motor objective restlessness seen in agitated depression. restlessness or agitation. It is either seen alone or along The treat ment is usually by anti depressants. with involutional melancholia. It is more common 2. Phobic-anxiety-depersonalisation syndrome ( PAD after the age of 40 years. syndrome): Described by Roth, this syndrome The treatment of agitated depression usually is commoner in women aged 20-40 years. It requires addition of antipsychotics or benzodiazepines is characterised by diffuse anxiety and panic to the antidepressant therapy. attacks, multiple phobias (such as agorapho bia and claustro phobia), deper sonal isation, derealisation Seasonal Mood Disorder and depres sive features. The treatment is usually This is either a bipolar mood disorder or recurrent by antidepressants. It is recognised that ECTs may depressive episode which tends to occur in the same make the condition worse. season on each occasion. It is usually more commonly 3. Non-endogenous depression: Atypical depression seen in women. of the non-endogenous type is characterised by For example, in a bipolar seasonal mood dis order, absence of neurotic traits and signifi cant stressful depression would tend to occur in the same months life events. This differentiates it from neurotic or every time (usually winter months), while mania reactive depression. would occur in the months of some other season every 4. Hysteroid-dysphoric depression: In this type, there episode (usually summer months). are marked fl uctuations of mood, ranging from This is thought to be due to changes in the length near normal to severe depression. Any stress leads of the day (and light) and its effect on hypothalamus. to an abrupt onset of depression, with marked anxi- The characteristic symptoms of winter depression are ety, pallor and changes in physical appearance. dysphoria, decreased activity and atypical depressive The person usually has histrionic personality traits symp toms (increased fatigue, increased sleep, increa- or disorder. sed appetite and weight, and carbohydrate cra ving). 82 A Short Textbook of Psychiatry

The prevalence of winter seasonal mood disorder 4. Suicidal threats and gestures are more common increases with increasing latitude. than completed suicide. However, as suicide may The treatment, in addition to the usual modes be completed accidentally, all such threats should of management, also includes photo therapy, which be taken seriously. consists of increasing the number of hours of day-light An episode of major depression may become (using artifi cial, full-spectrum, white light of 2,500- superimposed on an underlying neurotic dep ression. 10,000 lux intensity, in the early morning, with eyes This is then known as double depression. open) for the treatment of depression. The recent NICE Neurotic depression has been renamed as dys- guidelines for treatment of depression cast some doubt thymia or dysthymic disorder in DSM-IV-TR and on effi cacy of light therapy. ICD-10. This category does not require the presence Secondary Depression and Secondary of stress as a precipitating factor, and does not put Mania emphasis on the presence of other neurotic symptoms or traits. Dysthymia is defi ned as any mild depression Both depressive and manic episodes can occur sec- which is not severe enough to be called a depressive ondary to certain physical diseases and drugs. These episode, and lasts for two years or more. This is more have been discussed under organic mood disorders (Chapter 3). common in females, with an average age of onset in late third decade. Neurotic Depression A large number of psychotherapies have been Neurotic depression is usually characterised by the advocated for neurotic depression. The choice of following clinical features: therapy mainly rests on the therapist’s expertise in 1. Presence of mild to moderate depression. a particular mode of therapy. Two important issues 2. Depressive symptoms usually occur in response which often need to be addressed in the therapeutic to a stressful situation but are often quite dispro- relation ship are: portionate to the seve rity of stress. i. Dependency needs of the patient, and 3. Other ‘neurotic’ symptoms such as anxiety, obses- ii. Manipulative behaviour. sive symptoms, phobic symptoms, and multi ple Supportive psychotherapy is an important adjunct somatic symptoms, are often present. to the treatment. 4. Preoccupation with the stressful condition is com- When depression is significant and/or is not mon. responding to psychotherapy, antidepressants should The typical course of neurotic depression is be used. As mixed depres sion and anxiety are very chronic, with fl uctuations. Delusions, hallu cinations common, addition of small doses of benzo diazepines and other psychotic features are characteristically to antidepressants may be needed for the fi rst one absent. The other common features include: or two weeks. However, one must be careful as 1. The reactivity of mood is preserved, i.e. the patient benzodiazepines tend to get abused if prescribed for is able to emotionally react to the events occurring more than four weeks at one time. in his surroundings. For non-responders to TCAs and SSRIs, and/or 2. There may be insomnia or hypersomnia. There is when other neurotic symptoms (such as hypochondria- usually diffi culty in initiating sleep and some times cal symptoms or depersonalisation) are prominent, diffi culty in awakening in the morning. MAOIs are the drugs of choice. Occasionally, am- 3. The mood may be worse in the evening, at the end of the day. The mood may also become better in phetamines (such as methyl phenidate) may be useful social gatherings and whilst engaged in recrea- in mild depression; however, there is a signifi cant risk tional activities. of dependence. 7 Other Psychotic Disorders

Table 7.1: Defi nition of Psychosis The major nonorganic psychotic disorders are schizophrenia and mood disorders. In addi tion to these two, The term psychosis is defi ned as: there are other nonorganic psychoses some of which 1. Gross impairment in reality-testing (‘not in contact’ have been sometimes labelled as the third psychoses with reality). or other psychotic disorders (psychosis is defi ned 2. Marked disturbance in personality, with impairment in Table 7.1). These conditions are discussed in this in social, interpersonal and occupational functioning. chapter. 3. Marked impairment in judgement and absent understanding of the current symptoms and behaviour PERSISTENT DELUSIONAL DISORDERS (loss of insight). 4. Presence of the characteristic symptoms, like delu- This category in ICD-10 includes all disorders in sions and hallucinations. which persistent delusions are the prominent and most important clinical features. though stressors are not always evident in seve ral other cases. The aetiology of delusional disorders, similar Delusional Disorder to several other psychiatric disorders, appears to be This disorder, also previously called as paranoid multifactorial. disorder, is characterised by the following clinical It is a disorder with usually a relatively stable and features in ICD-10. Persistent delusions must be chronic course. It is characterised by presence of well- present for at least 3 months and these can include systematised delusions of nonbizarre type (cf. bizarre delusions of persecution (being persecuted against), delusions can occur in schizophrenia). The emotional delusions of grandeur (infl ated self-esteem and self response and behaviour is often understandable in the image), delusions of jealousy (infi delity), somatic light of their delusional beliefs, with behaviour out side (hypochondriacal) delusions, erotomanic delusions the ‘limits’ of delusions usually almost normal. Very (delusions of love), and/or other non-bizarre delusions. often, these individuals are able to carry on a near It is important to note absence of prominent halluci- normal social and occupational life without arousing nations, organic mental disorders, schizophrenia and suspicion regarding their delusional disorder. It is only mood disorders. when the area of delusions is probed or confronted that The common aetiology appears to be an abrupt the dysfunction becomes evident. change in the environment, for example, in prison When the content of delusions is predomi nantly inmates, and in immigrants (to a different cul ture), persecutory (as is often the case), it is important to 84 A Short Textbook of Psychiatry

Table 7.2: Differential Diagnosis of Delusional Disorders Features Paranoid Schizophrenia Delusional Disorder Paranoid Personality ( Paranoid disorder) Disorder 1. General behaviour Eccentricities, mannerisms, Eccentricities, decreased Restrained social inter- stereotypies, decreased social interaction action self-care, social withdrawal, guarded and evasive 2. Personality Disorganised (although Disturbed in delusional No deterioration deterioration is much less area, near normal in other than in other types of areas schizophrenia 3. Thought disorder Delusions, Schneiderian FRS, Nonbizarre delusions No thought disorder loosening of associations, which are well-systema- formal thought disorder; delu- tised, no other thought sions may be bizarre disorder 4. Hallucinations Auditory hallucinations com- Uncommon. If present, are Absent mon not persistent 5. Contact with reality Markedly disturbed Disturbed in area of delu- Intact sional belief 6. Insight Absent Absent Present 7. Affect/mood in Often inappropriate Usually appropriate Usually appropriate relation to thought differentiate delusional disorder from paranoid schizo- erotomania. Occurring most often in women, there phrenia and paranoid personality disorder (Table 7.2). is an erotic conviction that a person with (usually a) When the content of delusions is predomi nantly higher status is in love with the patient. jealousy (inﬁ delity) involving the spouse, it is called When the content of delusions is predominan- as Othello syndrome or conjugal paranoia. tly grandiose, then the patient usually has delusions A syndrome of late paraphrenia has also been with religious or political content and may believe described in the elderly. Although it was earlier consid- self to be a leader with ‘higher’ aims of spreading ered a subtype of delusional disorders, it is presently peace, making war or spreading a message in the diagnosed under paranoid schizo phrenia. world. When the content of delusions is predomi nantly characterised by presence of hypochondriacal delu- Other Persistent Delusional Disorders sions, it is called as monosymptomatic hypochon- This is a residual category in ICD-10 for other persist- driacal psychosis (MHP), delusional parasitosis, or ent delusional disorders, which do not fulﬁ l the criteria hypochondriacal paranoia. The common delusions for delusional disorders. The examples of disorders include infestations by worms or foreign bodies, included here are: emitting a foul odour (delusional halitosis), body 1. Delusions associated with persistent hallu ci na tory (or its parts) being ugly or misshapen ( delusional voices (but a diagnosis of schizophrenia cannot be dysmorphophobia). made). When content of delusions is erotic (erotomanic) 2. Delusional disorders with duration of less than 3 the condition is known as Clerambault’s syndrome or months. Other Psychotic Disorders 85

Differential Diagnosis clinical picture, and usually had a better prognosis The conditions from which delusional disorders than schizophrenia. should be differentiated include para noid schizo- In a study conducted by the Indian Council of phrenia, mania, depression, paranoid personality dis- Medical Research (ICMR) on acute psychoses (1989), order and organic delusional disorder (see Table 7.2). the following fi ndings were apparent: 1. 85% of these patients exhibited full recovery. Treatment 2. Recovery occurred in several cases even in the 1. Antipsychotics are used to control agitation and absence of treatment. treat the psychotic features. For MHP ( monosymp- 3. 50% of patients had a psychological stressor and tomatic hypochondriacal psychosis) or delusional 20% of patients had a somatic stressor before the disorder with somatic (hypochondriacal) delu- onset of illness. sions, pimozide has classically been the drug of 4. The onset occurred in less than 48 hours in 50% choice, though other antipsychotics with or with- of cases. out antidepres sants have been used as effectively. ICD-10 has included a new category of ‘ acute and Recently, the use of pimozide has declined sharply transient psychotic disorders’ (ATPD) in the section on due to concerns regarding its cardiac adverse ‘schizophrenia, schizotypal and delusional disorders’. effects. According to ICD-10, these disor ders have an 2. Supportive psychotherapy. abrupt (less than 48 hours) or acute (less than 2 weeks) 3. Antidepressants (such as fl uoxetine) and/or ECT onset. The onset is often associated with an easily iden- may be needed for secondary depression. tifi able acute stress (though not necessarily always so) that would be regarded as stressful to most people in INDUCED DELUSIONAL DISORDER similar circumstances, within the culture of the person concerned. The typical events would include bereave- This is an uncommon delusional disorder character- ment, unexpected loss of partner or job, marriage, or ised by a sharing of delusions between usually two the psycho logical trauma of combat, terrorism, and (folie å deux) or occasionally more persons (folie torture. Longstanding diffi culties or pro blems are not å trios, folie å quatre, folie å famille), who usually included here as stressful. have a closely knit emotional bond. Only one person Acute onset is probably associated with a good usually has authentic delusions due to an underlying outcome, and it seems that more abrupt the onset, the psychiatric disorder, most often schizophrenia or better is the outcome. A complete recovery usually delusional disorder. occurs within 2-3 months, often even much earlier. On separation of the two, the dependent individual These disorders should not satisfy the crite ria for may give up his/her delusions and the patient with the organic mental disorders, psychoactive substance use primary delusions should then be treated appropriately. disorders, schizophrenia, or mood disorders. The subtypes of acute and transient psychotic ACUTE AND TRANSIENT PSYCHOTIC disorders include the following: DISORDERS 1. Acute polymorphic psychotic disorder without symptoms of schizophrenia. A large number of psychiatrists, especially from the 2. Acute polymorphic psychotic disorder with symp- developing countries such as India and Africa, report- toms of schizophrenia. ed that many patients developed an acute psychotic 3. Acute schizophrenia-like psychotic dis order. disorder that neither fol lowed the classical course 4. Other acute predominantly delusional psychotic of schizophrenia nor resembled mood disorders in disorders. 86 A Short Textbook of Psychiatry

The various subtypes of acute and transient psy- polymorphic) and fulfi l the criteria for schizophrenia chotic disorders are further classifi ed as: but have lasted for less than 1 month. i. without associated acute stress, and Some degree of emotional variability or instability ii. with associated acute stress. may be present, but not to the extent described in the acute polymorphic psychotic disorder. The criteria for Acute Polymorphic Psychotic Disorder acute polymorphic psychotic disorder should not be without Symptoms of Schizophrenia fulfi lled. According to ICD-10, this disorder is characterised If the schizophrenic symptoms persist for more by an acute onset (from a nonpsychotic state to a than 1 month, the diagnosis should be changed to clearly psychotic state within 2 weeks) and polymor- schizophrenia. phic picture (unstable and markedly variable clinical picture that changes from day to day or even from Other Acute Predominantly Delusional hour to hour). Psychotic Disorders There are several types of hallucinations and/or According to ICD-10, this disorder is characterised delusions, changing in both type and intensity from by an acute onset of a psychotic disorder in which day to day or within the same day. Marked emotional comparatively stable delusions or hallucinations are turmoil, which ranges from intense feelings of hap- the main clinical features, but do not fulfi l the criteria piness and ecstasy to anxiety and irritability, is also for schizophrenia. frequently present. Delusions of persecution or reference are com- This disorder is particularly likely to have an mon, and hallucinations are usually auditory (voices abrupt onset (within 48 hours) and a rapid resolution talking directly to the patient). The criteria for acute of symptoms; in a large proportion of cases there polymorphic psychotic disorder or schizophrenia is no obvious precipitating stress. If the symptoms should not be fulfi lled. persist for more than 3 months, the diagnosis should If delusions persist for more than 3 months, the be changed. In spite of the variety of symptoms, none diagnosis should be changed to persistent delusional should be present with suffi cient consistency to fulfi l disorder. If only hallucinations persist for more than the criteria for schizophrenia or mood disorder. 3 months, the diagnosis should then be changed to other nonorganic psychotic disorder. Acute Polymorphic Psychotic Disorder with Symptoms of Schizophrenia Differential Diagnosis According to ICD-10, this disorder meets the descrip- The conditions from which acute and transient tive criteria for acute polymorphic psychotic disorder psychotic disorders should be differentiated include but in which typically schizo phrenic symptoms are organic mental disorders, psychoactive substance also consis tently present. use disorders, schizophrenia, mood disor ders, and If the schizophrenic symptoms persist for more delusional disorders. than 1 month, the diagnosis should be changed to schizophrenia. Prognosis The good prognostic factors in acute and transient Acute Schizophrenia-like Psychotic psychotic disorders are as follows: Disorder 1. Well adjusted premorbid personality. According to ICD-10, this disorder is characterised 2. Absence of family history of schizophrenia. by an acute onset of a psychotic disorder in which the 3. Presence of severe precipitating stressor before psychotic symptoms are comparatively stable (and not the onset. Other Psychotic Disorders 87

4. Sudden onset of symptoms. There are three types described: 5. Presence of affective symptoms, confusion, per- 1. Schizoaffective disorder, manic (or bipolar) type. plexity and/or disorientation in clinical picture. 2. Schizoaffective disorder, depressed type. 6. Short duration of symptoms. 3. Schizoaffective disorder, mixed type. 7. First episode. The course is usually episodic (particularly in manic subtype), although a chronic course in some Treatment patients has been described (parti cularly in the 1. Antipsychotics are the mainstay of treatment, depressed subtype). The prognosis is better than and are used to control agitation and psychotic that in schizophrenia but is worse than that in mood features. Usually lower doses of antipsy cho tics disorders. are needed. The treatment is with mood stabilisers (such as However, in the initial stages the patient may not lithium or valproate), antipsychotics, anti depressants take oral medi cation. In such cases, parenteral and/or ECT, depending on the predominant sympto- administration of antipsychotics (with or without matology. benzodiazepines such as lorazepam or diazepam) may be needed. CAPGRAS’ SYNDROME The fi rst use of parenteral antipsychotics in an (THE DELUSION OF DOUBLES) antipsychotic-naive patient should be carefully considered, as there is a higher risk of neuroleptic Capgras’ syndrome is a syndrome that is closely malignant syndrome (NMS) in these patients. related to delusional disorders and is characterised Long-term use of antipsychotics should be prefer- by a delusional conviction that other persons in the ably avoided in these patients (see Chapter 15 for environment are not their real selves but are their further details). own doubles. 2. ECT may be needed in cases with marked agitation It is one of the several delusional misidentifi cation and emotional turmoil, as well as in cases where syndromes, of which there are four types described: there is a danger to self and/or others. 1. Typical Capgras’ syndrome (Illusion des sosies): 3. Antidepressants may be rarely needed as adju vants Here the patient sees a familiar person as a in some cases with associated depression. complete stranger who is imposing on him as a 4. Psychotherapy and other psychological inter- familiar person. ventions may be needed in cases with associated 2. Illusion de Fregoli: The patient falsely identifi es stress, as well as for psychoeducation for the stranger(s) as familiar person(s). patient and family. Engagement with psychologi- 3. Syndrome of subjective doubles: The patient’s own cal treatment is usually after the acute episode is self is perceived as being replaced by a double. under control and the patient can communi cate 4. Intermetamorphosis: Here the patient’s misiden- his/her fears and anxieties. tifi cation is complete and the patient misidenti- fies not only the ‘external appearance’ (as in SCHIZOAFFECTIVE DISORDER the previous three types) but also the complete personality. This is a disorder which lies on the borderland between The syndrome is commonly seen in psycho tic schizophrenia and mood disorders. In this disorder, conditions with delusional symptomatology, such as the symptoms of schizophrenia and mood disorders paranoid schizophrenia (most frequently), delusional are prominently present within the same episode. The disorders and organic delusional disorder. symptoms of both disorders may be present simultane- The treatment consists of adequately treating the ously or may follow within few days of each other. underlying disorder. 88 A Short Textbook of Psychiatry

REACTIVE PSYCHOSIS 3. A clear temporal relation between stress and the onset of psychotic symptoms. Reactive psychosis is characterised by following 4. No organic cause underlying the psychosis. features: The usual duration of illness is less than one month 1. A sudden onset of symptoms. and recovery is usually complete. Currently a majority of cases of reactive psychosis 2. Presence of a major stress before the onset (the would be classiﬁ ed under acute and transient psychotic quantum of stress should be severe enough to be disorder with associated stress (in ICD-10) or brief stressful to a majority of people). reactive psychosis (in DSM-IV-TR). Neurotic, Stress-related and 8 Somatoform Disorders

The terms neurosis (Table 8.1) and psychosis are cur- Table 8.1: Defi nition of Neurosis rently not widely used. The defi nitions and descrip- The term neurosis has been variously defi ned as meeting tions of these terms are far from perfect and there are one or more of the following criteria: clearly exceptions to the rules. These terms also have 1. The presence of a symptom or group of symp toms psychodynamic connotations. As current classifi ca- which cause subjective dist ress to the patient. tory systems are largely theoretical, any aetiological 2. The symptom is recognised as undesirable (i.e. meaning is not very helpful. insight is present). DSM-IV-TR does not use these terms at all and 3. The personality and behaviour are rela tively pre- although ICD-10 still mentions the term neurotic in served and not usually grossly disturbed. the classifi cation, it discourages the use of the terms 4. The contact with reality is preserved. neurosis and psychosis. 5. There is an absence of organic causative factors. In ICD-10, ‘ neurotic, stress-related and somato- 6. Reaction to severe stress, and adjustment form disorders have been classifi ed into the following disorders, types: 7. Dissociative ( conversion) disorders, 1. Phobic anxiety disorder, 8. Somatoform disorders, and 2. Other anxiety disorders (called simply anxiety 9. Other neurotic disorders. disorder in this book), 3. Obsessive compulsive disorder. Normal anxiety becomes pathological when it causes signifi cant subjective distress and/or impair- ANXIETY DISORDER ment in functioning of an individual. Some authors separate anxiety into two types: Anxiety is the commonest psychiatric symp tom in 1. Trait anxiety: This is a habitual tendency to be clinical practice and anxiety disorders are one of the anxious in general (a trait) and is exemplifi ed by commonest psychiatric disorders in general popula- ‘I often feel anxious’. tion. 2. State anxiety: This is the anxiety felt at the present, Anxiety is a ‘normal’ phenomenon, which is cross-sectional moment (state) and is exemplifi ed characterised by a state of apprehension or unease by ‘I feel anxious now’. arising out of anticipation of danger. Anxiety is often Persons with trait anxiety often have episodes of differentiated from fear, as fear is an apprehension in state anxiety. The symptoms of anxiety can be broadly response to an external danger while in anxiety the classifi ed in two groups: physical and psycho logical danger is largely unknown (or internal). (psychic) (Table 8.2). 90 A Short Textbook of Psychiatry

Table 8.2: Symptoms of Anxiety with often a chronic course. The panic attacks occur 1. Physical Symptoms recurrently every few days. There may or may not be A. Motoric Symptoms: Tremors; Restlessness; an underlying generalised anxiety disorder. Muscle twitches; Fearful facial expression The episode is usually sudden in onset, lasts for a B. Autonomic and Visceral Symptoms: Palpitations; few minutes and is characterised by very severe anxi- Tachycardia; Sweating; Flushes; Dyspnoea; ety. Classically the symptoms begin unexpectedly or Hyperventilation; Constriction in the chest; Dry ‘out-of-the-blue’. Usually there is no apparent precipi- mouth; Frequency and hesitancy of mic tu rition; tating factor, though some patients report exposure to Dizziness; Diarrhoea; Mydria sis phobic stimuli as a precipitant. 2. Psychological Symptoms The differential diagnosis is from organic anxiety A. Cognitive Symptoms: Poor concentration; Dis- disorder (Chapter 3) (e.g. secondary to hypoglycae- tractibility; Hyperarousal; Vigilance or scan- mia, hyperthyroidism, phaeochromocytoma) and ning; Negative automatic thoughts cardiac disorders (e.g. MVPS or mitral valve prolapse B. Perceptual Symptoms: Derealisation; Deperson- syndrome). alisation The life time prevalence of panic disorder is C. Affective Symptoms: Diffuse, unpleasant, and 1.5-2%, with 3-4% reporting subsyndromal panic vague sense of apprehen sion; Fearfulness; In- symptoms (i.e. panic symptoms not severe enough to ability to relax; Irritability; Feeling of impending qualify for panic disorder). Panic disorder is usually doom (when severe) seen about 2-3 times more often in females. Panic D. Other Symptoms: Insomnia (initial); Increased disorder can present either alone or with agoraphobia. sensitivity to noise; Exaggerated startle response. Aetiology The cause of anxiety disorders is not clearly known. Generalised Anxiety Disorder There are however several theories, of which more This is characterised by an insidious onset in the third than one may be applicable in a particular patient. decade and a stable, usually chronic course which may 1. Psychodynamic Theory or may not be punctuated by repea ted panic attacks According to this theory, anxiety is a signal that (episodes of acute anxiety). The symptoms of anxi- something is disturbing the internal psychological ety should last for at least a period of 6 months for a equilibrium. This is called as signal anxiety . This diag nosis of genera lised anxiety disorder to be made. signal anxiety arouses the ego to take defensive action The one year prevalence of generalised anxiety which is usually in the form of repres sion, a primary disorder in the general population is about 2.5-8%. It defense mechanism. Ordinarily when repression fails, is the com monest psychiatric disorder in the popula- other secondary defense mechanisms (such as conver- tion. As anxiety is a cardinal feature of almost all sion, isolation) are called into action. psychiatric disorders, it is very important to exclude In anxiety, repression fails to function ade- other diagnoses. The most important differential diag- quately but the secondary defense mechanisms are nosis is from depressive disorders and organic anxiety not activated. Hence, anxiety comes to the fore-front disorder. unopposed. Developmentally, primitive anxiety is mani fested as somatic symptomatology while deve- Panic Disorder lopmentally advanced anxiety is signal anxiety. Panic This is characterised by discrete episodes of acute anxiety, according to this theory, is closely related to anxiety. The onset is usually in early third decade the separation anxiety of childhood. Neurotic, Stress-related and Somatoform Disorders 91

2. Behavioural Theory tory effect on the CNS) relieve anxiety and that According to this theory, anxiety is viewed as an benzodiazepine-antagonists (e.g. fl umazenil) and unconditioned inherent response of the organism to inverse agonists (e.g. β-carbolines) cause anxiety, painful or dangerous stimuli. In anxiety and phobias, lends heavy support to this hypothesis. this becomes attached to relatively neutral stimuli by iv. Other neurotransmitters: Norepinephrine, 5-HT, conditioning. dopamine, opioid recep tors and neuroendocrine 3. Cognitive Behavioural Theory (CBT) dysfunction have also been implicated in the According to cognitive behaviour theory, in anxiety causation of anxiety disorders. disorders there is evidence of selective information v. Neuroanatomical basis: Locus coeruleus, limbic processing (with more attention paid to threat-related system, and prefrontal cortex are some of the areas information), cognitive distortions, negative automatic implicated in the aetiology of anxiety disorders. thoughts and perception of decreased control over both Regional cere bral blood fl ow (rCBF) is increased internal and external stimuli. in anxiety, though vasoconstriction occurs in se- 4. Biological Theory vere anxiety. i. Genetic evidence: About 15-20% of fi rst degree vi. Organic anxiety disorder: This disorder is char- relatives of the patients with anxiety disorder ex- acterised by the presence of anxiety which is hibit anxiety disorders themselves. The concord- secondary to the various medi cal disorders (e.g. ance rate in the monozygotic twins of patients with hyperthyroidism, phaeochromocytoma, coronary panic disorders is as high as 80% (4 times more artery disease). If anxiety symptoms can occur than in dizygotic twins). secondary to medical disorders, it seems possible ii. Chemically induced anxiety states: Infusion of than that anxiety has a biological basis. chemicals (such as sodium lactate, isoproterenol and caffeine), ingestion of yohim bine and inha- Treatment

lation of 5% CO2 can produce panic episodes in The treatment of anxiety disorders is usually multi- predisposed individuals. Administration (oral) of modal. MAOIs before the lactate infusion protects the 1. Psychotherapy individual(s) from panic attack, thus providing a Psychoanalytic psychotherapy is not usually indi- probable clue to the biological model of anxiety. cated, u nless characterological (perso nality) problems iii. GABA- benzodiazepine receptors: This is one of co-exist. Usually supportive psychotherapy is used the most recent advances in the search for the ae- either alone, when anxiety is mild, or in combina- tiology of anxiety disorders. The benzodiazepine tion with drug therapy. The establishment of a good receptors are distributed widely in the central therapist-patient relationship is often the ﬁ rst step in nervous system. Presently, two types of benzodi- psycho therapy. azepine receptors have been identiﬁ ed. The type Recently, there has been an increasing use of CBT

I (ω1) is GABA and chloride independent, while in the management of anxiety disorders, particularly

type II (ω2) is GABA and chloride dependent. panic disorders (with or without agoraphobia). CBT GABA (Gamma amino butyric acid) is the can be used either alone or in conjunction with SSRIs. most prevalent inhibitory neurotransmitter in the 2. Relaxation Techniques central nervous system. It has been suggested In patients with mild to moderate anxiety, relaxation that an alteration in GABA levels may lead to techniques are very useful. These techniques are used production of clinical anxiety. The fact that the by the patient himself as a routine exercise everyday benzodiazepines (which facilitate GABA trans- and also whenever anxiety-provoking situation is at mission, thereby causing a generalised inhibi- hand. 92 A Short Textbook of Psychiatry

These techniques include Jacobson’s progressive able to benzo diazepines for the long-term management relaxation technique, yoga, pranayama , self-hypno- of anxiety disorder. It, however, has not much role in sis, and meditation (including TM or trans cendental the management of panic disorder. meditation). 3. Other Behaviour Therapies PHOBIC DISORDER The behaviour therapies include biofeedback and hyperventilation control. These methods are important Phobia is defi ned as an irrational fear of a specifi c adjuncts to treat ment. object, situation or activity, often leading to persis tent 4. Drug Treatment avoidance of the feared object, situation or activity. The differential response of generalised anxiety and The characteristic features of phobia are described panic to drug treatment has lead to what is called as in Table 8.3. The common types of phobias are: the pharmacological dissection of anxiety disorders 1. Agoraphobia, though this differentiation has become much more 2. Social phobia, and diluted recently with antidepressants used in treatment 3. Specifi c ( Simple) phobia. of both conditions. The drugs of choice for generalised anxiety disor- Agoraphobia der have traditionally been benzodiazepines, and for Agoraphobia is an example of irrational fear of situa- panic disorder, antidepressants. Both benzodiazepines tions. It is the commonest type of phobia encountered and antidepres sants are discussed in detail in Chapter in clinical practice. Women far out-number men in 15. It is useful to begin the treatment of panic disorders suffering from agoraphobia in the Western countries. with small doses of anti depressants, usually SSRIs It is characterised by an irrational fear of being (e.g. fl uoxetine). in places away from the familiar setting of home. Benzodiazepines (such as alprazolam and clon- Although it was earlier thought to be a fear of open azepam) are useful in short-term treatment of both spaces only, now it includes fear of open spaces, pub- generalised anxiety and panic disorders. However, lic places, crowded places, and any other place from tolerance and dependence potential limit the use of where there is no easy escape to a safe place. these drugs. Several antidepressants (such as sertraline) are now licensed for treatment of anxiety and Table 8.3: Phobia: Some Characteristic Features panic disorders. β-blockers such as propranolol and atenolol are 1. Presence of the fear of an object, situation or activity. particularly useful in the management of antici patory 2. The fear is out of proportion to the dangerous ness anxiety (e.g. anxiety occurring before going on stage perceived. or before examinations). However, due care must be 3. Patient recognises the fear as irrational and unjusti- exercised in the use of propranolol in the patients with fi ed ( Insight is present). history of asthma, bradycardia or heart block. Atenolol 4. Patient is unable to control the fear and is very does not cross the blood brain barrier and takes care distressed by it. of only the peripheral symptoms of anxiety. It also has 5. This leads to persistent avoidance of the particular object, situation or activity. less likelihood of causing bronchial constriction than 6. Gradually, the phobia and the phobic object become propranolol. a preoccupation with the patient, resulting in marked Buspirone is an anti-anxiety drug (discussed in distress and restriction of the freedom of mobility Chapter 15) which does not have any dependence (afraid to encounter the phobic object; phobic avoid- potential, unlike benzodia zepines. It takes about 2-3 ance). weeks before its action is apparent. It may be prefer- Neurotic, Stress-related and Somatoform Disorders 93

In fact, the patient is afraid of all the places or Specifi c phobia is characterised by an irrational situations from where escape may be perceived to be fear of a specifi ed object or situation. Anticipatory diffi cult or help may not be available, if he suddenly anxiety leads to persistent avoidant behaviour, while develops embarrassing or incapacitating symp toms. confrontation with the avoided object or situation leads These embarrassing or incapacitating symp toms are to panic attacks. Gradually, the phobia usually spreads the classical symptoms of panic. to other objects and situations. A full-blown panic attack may occur (agora phobia The disorder is diagnosed only if there is marked with panic disorder) or only a few symptoms (such distress and/or disturbance in daily functioning, in as dizziness or tachycardia) may occur (agoraphobia addition to fear and avoidance of the specifi ed object without panic disorder). or situation. Some of the examples of simple phobia As the agoraphobia increases in severity, there is include acrophobia (fear of high places), zoophobia a gradual restriction in the normal day-to-day activi- (fear of animals), xenophobia (fear of strangers), ties. The activities may become so severely restricted algophobia (fear of pain), and claustro phobia (fear that the person becomes self-imprisoned at his home. of closed places). One or two persons (usually close relations or friends) The list of specifi c phobias is virtually endless. may be relied upon, with whom the patient can leave Course home. Hence, the patient becomes severely dependent on these phobic companion(s). Phobias are generally more common in women with an onset in late second decade or early third decade. Social Phobia Typically, the onset is sudden without any apparent This is an example of irrational fear of activities or cause. The course is usually chronic with gradually social interaction, characterised by an irrational fear of increasing restriction of daily activities. Sometimes, performing activities in the presence of other people phobias are spontaneously remitting. or interacting with others. The patient is afraid of his own actions being viewed by others critically, result- Aetiology ing in embarrassment or humiliation. Psychodynamic Theory There is marked distress and disturbance in rou- As discussed in the aetiology of anxiety disorders, tine daily functioning. Some of the examples include anxiety is usually dealt with the defense mecha nism fear of blushing (erythrophobia ), eating in company of repression . When repression fails to function of others, public speaking, public performance (e.g. adequately, other secondary defense mechanisms of on stage), participating in groups, writing in public ego come into action. (e.g. signing a check), speaking to strangers (e.g. for In phobia, this secondary defense mecha nism asking for directions), dating, speaking to authority is displacement . By using displacement, anxiety is fi gures, and urinating in a public lavatory (shy blad- transferred from a really dangerous or frightening der). Sometimes, alcohol (and sometimes, other drugs) object to a neutral object. These two objects are often is used to overcome the anxiety occurring in social connected by symbolic associations. situations. The neutral object chosen unconsciously is the Specifi c (Simple) Phobia one which can be easily avoided in day-to-day life, in contrast to the frightening object (frightening to the In contrast to agoraphobia and social phobia where the patient only, due to oedipal genital drives). stimuli are generalised, in specifi c phobia the stimulus In agoraphobia, loss of parents in childhood and is usually well circum scribed. This is an example of separation anxiety have been theorised to contribute irrational fear of objects or situations. to causation. 94 A Short Textbook of Psychiatry

From a psychobiological perspective, the trau- fi nd ways to limit their lives within the limitations matic experiences of childhood may affect the child’s imposed by phobias, they experience little, if any, developing brain in such a manner that the child anxiety. When they are forced to face the phobic situ- becomes susceptible to anxiety and fear in childhood ation, anxiety mounts and they then seek treatment. and later life. The patients with more than one phobia and presence of panic symptoms often seek treatment earlier. Behavioural Theories The treatment approach is usually multi-modal. The behavioural theories explain phobia as a conditioned refl ex. Initially, the anxiety provoked by Psychotherapy a naturally frightening or dangerous object occurs Psychodynamically oriented psychotherapy is not in conti guity with a second neutral object. If this usually helpful in treatment of phobias. This approach happens often enough, the neutral object becomes a is however indicated when there are characterological conditioned stimulus for causing anxiety. or personality diffi culties as well. Supportive psycho- In 1920, John Watson experimentally produced therapy is a helpful adjunct to behaviour therapy and phobia in an 11 month old boy who came to be know drug treatment. as ‘Little Albert’. Using classical conditioning, he As stated earlier, cognitive behaviour therapy paired white objects to a loud noise. ‘Little Albert’ (CBT) can be used to break the anxiety patterns in gradually developed a fear of all white objects. Of phobic disorder. It is usual to combine CBT with course, it would be completely unethical to replicate behavioural techniques. this experiment in the present day. Although the behavioural theory does not explain Behaviour Therapy all the features of phobic disorders adequately, it is If properly planned, this mode of treatment is usually very helpful in planning systematic treatment. successful. The behavioural thera pies are discussed in Chapter 18 and only the names of important tech- Biological Theories niques are mentioned here. All phobias, especially agoraphobia, are closely linked 1. Flooding. to panic disorders. It has been suggested that probably 2. Systematic desensitisation. the biological models of panic apply to phobias too. 3. Exposure and response prevention. However, the evidence for this view is not strong 4. Relaxation techniques. at present, except for the importance of genetic factors in specifi c phobias of blood-injury type. There is also Drug Treatment some evidence for the presence of familial factors in The drugs used in the treatment of phobia are: social phobias. 1. Benzodiazepines (Chapter 15) are useful in reducing the anticipatory anxiety. Alprazolam is stated Differential Diagnosis to have anti-phobic, anti-panic and anti-anxiety The differential diagnoses include anxiety disorder, properties. So, it is the drug of choice, when panic disorder, major depression, avoidant personality benzodia zepines are used. However, long-term, disorder, obsessive compulsive disorder, delusional double-blind randomised controlled trials are disorder, hypochondriasis, and schizophrenia. needed. The other drugs used include clonazepam and diazepam. Treatment However, long-term use of benzodiazepines is Most patients with phobic disorder rely on avoidance fraught with the dangers of tolerance and depend- to manage their fears and anxieties. As long as they ence. Neurotic, Stress-related and Somatoform Disorders 95

2. Among the antidepressants (discussed in Chapter 5. The behaviour is performed with a sense of subjec- 15), SSRIs are currently drugs of choice, with tive compulsion (urge or impulse to act). paroxetine being the most widely used drug. Other Compulsions may diminish the anxiety associated SSRIs, such as fl uoxe tine and sertraline are also with obsessions. equally effective. Fluoxetine has the advantage of a longer half-life. Other antidepressants such as Epidemiology, Course and Outcome imipramine (TCA) and phenelzine (MAOI), are In India, obsessive compulsive disorder (OCD) is also helpful in treating the panic attacks asso ciated more common in unmarried males, while in other with phobias, thereby decreasing the distress. countries, no gender differences are reported. This dis- As mentioned earlier, multiple approaches are order is commoner in persons from upper social strata usually combined together in treatment of a particular and with high intelligence. The average age of onset patient. is late third decade (i.e. late 20s) in India, while in the Western countries the onset is usually earlier in life. OBSESSIVE-COMPULSIVE DISORDER Recent studies show the life-time prevalence of OCD to be as high as 2-3%, though the Indian data An obsession is defi ned as: shows a lower prevalence rate. Although classically 1. An idea, impulse or image which intrudes into the thought to have a steady chronic course, the longitu- conscious awareness repeatedly. dinal profi le of this disorder can also be episodic. 2. It is recognised as one’s own idea, impulse or A summary of long-term follow-up studies shows image but is perceived as ego-alien (foreign to that about 25% remained unimproved over time, 50% one’s personality). had moderate to marked impro vement while 25% had 3. It is recognised as irrational and absurd (insight is recovered completely. present). 4. Patient tries to resist against it but is unable to. Clinical Syndromes 5. Failure to resist, leads to marked distress. ICD-10 classifi es OCD into three clinical sub types: Differentiation has to be made clinically from 1. Predominantly obsessive thoughts or rumina tions, delusion and thought insertion. A delusion is rec- 2. Predominantly compulsive acts (compul sive ritu- ognised as one’s own idea but is not reco gnised as als), and ego-alien. In fact, it is strongly believed; hence it 3. Mixed obsessional thoughts and acts. is not thought to be irrational and is never resisted. Depression is very commonly associated with Thought insertion is not thought of as one’s own idea, obsessive compulsive disorder. It is estimated that at but instead somebody else’s thought being forcibly least half the patients of OCD have major depressive inserted into one’s mind. episodes while many other have mild depression. An obsession is usually associated with Premorbidly obsessional or anankastic personality compulsion(s). A compulsion is defi ned as: disorder or ‘traits’ may be commoner than in rest of 1. A form of behaviour which usually follows obses- the popu lation. sions. Four clinical syndromes have been des cribed in 2. It is aimed at either preventing or neutralising the literature, although admixtures are commoner than distress or fear arising out of obsession. pure syndromes. 3. The behaviour is not realistic and is either irrational or excessive. Washers 4. Insight is present, so the patient realises the This is the commonest type. Here the obsession is of irrationality of compulsion. contamination with dirt, germs, body excretions and 96 A Short Textbook of Psychiatry the like. The compulsion is washing of hands or the 1. Aggressive obsessions whole body, repeatedly many times a day. It usually 2. Contamination obsessions spreads on to washing of clothes, washing of bath- 3. Sexual obsessions room, bedroom, door knobs and personal articles, 4. Hoarding/Saving obsessions gradually. 5. Religious/Scrupulous obsessions The person tries to avoid contamination but is 6. Obsession with need for symmetry or exactness unable to, so washing becomes a ritual. 7. Somatic obsessions 8. Miscellaneous obsessions Checkers 9. Cleaning/washing compulsions In this type, the person has multiple doubts, e.g. the 10. Checking compulsions door has not been locked, kitchen gas has been left 11. Repeating rituals open, counting of money was not exact, etc. The com- 12. Counting compulsions pulsion, of course, is checking repeatedly to ‘remove’ 13. Ordering/arranging compulsions the doubt. 14. Hoarding/collecting compulsions Any attempt to stop the checking leads to mount- 15. Miscellaneous compulsions. ing anxiety. Before one doubt has been cleared, other doubts may creep in. Aetiology Several causative factors have been explored in the Pure Obsessions past but no clear aetiology of obsessive compulsive This syndrome is characterised by repetitive intrusive disorder is known yet. Some of the important theories thoughts, impulses or images which are not associated include: with compulsive acts. The content is usually sexual or aggressive in nature. The distress associated with these Psychodynamic Theory obsessions is dealt usually by counter-thoughts (such Sigmund Freud found obsessions and phobias to be as counting) and not by behavioural rituals. psychogenetically related. This theory can be ex- A variant is obsessive rumination, which is a pre- plained in a fl ow diagram (Fig. 8.1). occupation with thoughts. Here, the person repetitively Isolation of Affect: By this defense mechanism, ruminates in his mind about the pros and cons of the ego removes the affect (isolates the affect) from the thought concerned. anxiety-causing idea. The idea is thus weakened, but remains still in the consciousness. The affect how- Primary Obsessive Slowness ever becomes free and attaches itself to other neutral A relatively rare syndrome, it is characterised by idea(s) by symbolic associations. Thus, these neutral severe obsessive ideas and/or extensive compulsive ideas become anxiety-provoking and turn into obses- rituals, in the relative absence of manifested anxiety. sions. This leads to marked slowness in daily activities. This happens only when isolation of affect is This subtype is quite diffi cult to diagnose in the not fully successful (incomplete isolation of affect). routine clinical practice, unless the possibility of this When it is fully successful, both the idea and affect subtype is kept in mind. are repressed and there are no obsessions. In clinical practice, one of the most useful scales Undoing: This defense mechanism leads to is the Y-BOCS (Yale-Brown Obsessive Compulsive compul sions, which prevent or undo the feared con- Scale). It can be used to elicit the symptomatology sequences of obsessions. and rate the severity of OCD. The Y-BOCS classifi es Reaction formation results in the formation of the symptoms and signs of OCD as follows: obsessive compulsive personality traits rather than Neurotic, Stress-related and Somatoform Disorders 97

Fig. 8.1: Psychodynamic Theory of Obsessive Compulsive Disorder: A Brief Summary contributing to obsessive compulsive symptoms, Behavioural or learning theory is not able to while displacement leads to forma tion of phobic explain the causation of OCD adequately but is very symptoms. These defense mechanisms are discussed useful in its treatment. in Table 17.1. This mechanism has been explained in slight Biological Theories detail as this theory attempts to describe the probable 1. Obsessive compulsive symptoms can occur causation of OCD in a remarkably syste matic man- secondary to many illnesses such as von Econ- ner. However, it must be remembered that this is only omo’s encephalitis, basal ganglia lesions, Gilles a theory and whether it is true or not, is a matter of de la Tourette syndrome, and hypothalamic and conjecture. third ventricle lesions. Thus, the psychodynamic theory explains OCD 2. Obsessive compulsive disorder is found in 5-7% by a defensive regression to anal-sadistic phase of of ﬁ rst degree relatives of the patients with development with the use of isolation, undoing and OCD. displacement to produce obsessive-compulsive symp- 3. Psychosurgery has been successfully used for toms. treat ment of OCD. 4. Biochemically, the central 5-HT system seems Behavioural Theory to be involved in OCD, as SSRIs are useful in The behavioural theory explains obsessions as condi- the treatment of OCD. tioned stimuli to anxiety (similar to phobias). Compul- Some authors pointed at cingulum (gyrus) as the sions have been described as learned behaviour which probable site of lesion, while others have found EEG decrease the anxiety associated with obsessions. abnormalities most marked over the temporal lobes. This decrease in anxiety positively reinforces the However, at the present moment, there is no con- compulsive acts and they become ‘stable’, learned clusive evi dence for OCD having a clearly proven behaviours. organic aetiology. 98 A Short Textbook of Psychiatry

Treatment (20-40 mg/day) and sertraline (50-200 mg/day) Psychotherapy are also effective in some patients. 3. Antipsychotics: These are occasionally used in 1. Psychoanalytic psychotherapy is used in certain low doses (e.g. haloperidol, risperi done, olan- selected patients, who are psychologically ori- zapine, aripiprazole, pimozide) in the treat ment ented. of severe, disabling anxiety. 2. Supportive psychotherapy is an important ad- 4. Buspirone has also been used benefi cially as junct to other modes of treatment. Supportive an adjunct for aug mentation of SSRIs, in some psychotherapy is also needed by the family patients. members. Electroconvulsive Therapy Behaviour Therapy and Cognitive In presence of severe depression with OCD, ECT may Behaviour Therapy be needed. ECT is particularly indicated when there is Behaviour modification is an effective mode of a risk of suicide and/or when there is a poor response therapy, with a success rate as high as 80%, especially to the other modes of treatment. However, ECT is not for the compulsive acts. It is customary these days to the treatment of fi rst choice in OCD. combine CBT with BT at most centres. The techniques used are listed below (They are Psychosurgery described in Chapter 18): Psychosurgery can be used in treatment of OCD that i. Thought-stopping (and its modifi cations). has become intractable, and is not responding to other ii. Response prevention. methods of treat ment. It is worth mentioning that iii. Systematic desensitisation. psychosurgery is only available as a treatment choice iv. Modelling. at a very few centres throughout the world. The best responders are usually those who have Drug Treatment significant associated depression, although pure 1. Benzodiazepines (e.g. alprazolam, clonazepam) obsessives also do respond. The main benefi t is the have a limited role in controlling anxiety as marked reduction in associated distress and severe adjuncts and should be used very sparingly. anxiety. 2. Antidepressants: Some patients may improve The procedures which can be employed are: dramatically with speci fi c sero tonin reup take i. Stereotactic limbic leucotomy. inhibitors (SSRIs). ii. Stereotactic subcaudate tractotomy. Clomipramine (75-300 mg/day), a nonspecifi c Psychosurgery is usually followed by intensive serotonin reuptake inhibitor (SRI), was the fi rst behaviour therapy aimed at rehabilitation. However, drug used effectively in the treatment of OCD. with the easy availability of SSRIs, and a good re- The response is better in the presence of depres- sponse of OCD symptoms to SSRIs and other phar- sive symptoms, but many patients with pure macological measures, psychosurgery is very rarely OCD also improve substantially. used in the treatment of OCD. Fluoxetine (20-80 mg/day) is a good alterna- Very often, a comprehensive treatment of OCD tive to clomipramine and often preferred these requires that multiple treatment modalities (e.g. drug days for its better side-effect profi le. Fluvoxam- treatment and BT/CBT) be combined in a specifi c ine (50-200 mg/day) is marketed as a specifi c manner, suitable to the particular patient being treated anti-obsessional SSRI drug, whilst paroxetine at the time. Neurotic, Stress-related and Somatoform Disorders 99

DISSOCIATIVE AND CONVERSION Conversion Disorder DISORDERS Conversion disorder is characterised by the following clinical features: The word hysteria has been used in so many contexts 1. Presence of symptoms or defi cits affecting motor by psychiatrists, physicians and non-professionals or sensory function, suggesting a medical or that it no longer has any one meaning. These various neurological disorder. contexts include: 2. Sudden onset. 1. Impulsive, uncontrolled behaviour (impulse dy- 3. Development of symptoms usually in the pre sence scontrol). of a signifi cant psychosocial stressor(s). 2. Manipulative, exhibitionistic, emotional, dra- 4. A clear temporal relationship between stressor and matic, and/or seductive behaviour (histrionic development or exacerbation of symp toms. personality traits). 5. Patient does not intentionally produce the symp- 3. Absence of objective signs of organic illness. toms. 4. Presence of multiple vague somatic symp toms, 6. There is usually a ‘ secondary gain’ (though not especially in a female patient (masked depression, required by ICD-10 for diagnosis). somatisation disorder or Briquet’s hysteria). 7. Detailed physical examination and inves tigations 5. Hypochondriasis. do not reveal any abnormality that can explain the 6. Any mental illness. symptoms adequately. 7. Presence of certain symptoms which are not ex- 8. The symptom may have a ‘symbolic’ relationship plainable in the context of present organic illness with the stressor/confl ict. ( functional overlay, con version symp toms). There can be two different types of distur ban ces 8. Diffi cult patient; poor doctor-patient communica- in conversion disorder; motor and sensory. Autonomic tion. nervous system is typically not involved, except when 9. ‘ Sick’ role or ‘ abnormal illness behaviour’. the voluntary musculature is involved, e.g. vomiting, 10. Psychosomatic disorders. globus hystericus. 11. Malingering. In ICD-10, conversion disorder is subsumed under 12. Psychosexual dysfunctions. ‘dissociative disorders of movement and sensation’, a This list is not exhaustive. Therefore, it is not sur- subtype under ‘dissociative (conversion) disorders’. It prising that the word hysteria has been removed from is further classifi ed in to dissociative motor disorders, DSM-IV-TR as well as the ICD-10. The term hysteria disso ciative anaesthesia and sensory loss, and disso- has now been replaced in the ICD-10 by ‘conversion ciative convulsions. and dissociative disorders’ and in DSM-IV-TR, by conversion and disso ciative disorders. Dissociative Motor Disorders The motor disturbance usually involves either paraly- Epidemiology sis or abnormal movements. The ‘paralysis’ may be a Hysteria (comprising of conversion, dissociation and monoplegia, paraplegia or quadri plegia. somatisation disorder) constitutes about 6-15% of Classically, the symptom distribution is according all outpatient diagnoses and 14-20% of all neurotic to the patient’s knowledge of nervous system. The ex- disorders. Females usually out num ber males, but in amination shows normal or voluntarily increased tone children the percentage tends to be similar in boys and normal refl exes. However, a prolonged ‘paralysis’ and girls. may lead to the development of contractures. 100 A Short Textbook of Psychiatry

The abnormal movements can range from tremors, of convulsive movements and partial loss of con- choreiform movements and gait disturbances, to consciousness. This is a very common disorder in India vulsive movements. These movements either occur or and other developing countries, though some patients increase when attention is directed towards them, and may present with only a partial, brief unresponsive- may disappear when patient is watched unobserved. ness, in the absence of convulsive movements (called These movements do not fi t the ‘typical’ clini- as brief dissociative stupor or simple dissociative cal picture of the abnormal involuntary movement disorder). disorders. The gait disturbance (astasia abasia) is Clearly, differential diagnosis with true seizures usually charac terised by a wide-based, jerky, stag- is important. The main differentiating points between gering, dra ma tic and irregular gait with exaggerated epileptic seizures and dissociative convulsions are body movements. listed in Table 8.4. Dissociative Anaesthesia and Sensory Loss Dissociative Disorder (Sensory Disorders) These disorders are characterised by the follo wing The sensory disturbance is exemplifi ed by a ‘glove clinical features: and stocking’ anaesthesia (absence of all sensations 1. Disturbance in the normally integrated functions with an abrupt boundary, not conforming to the of consciousness, identity and/or memory. distribution of dermatomes, and usually limiting at 2. Onset is usually sudden and the distur bance is wrists and ankles), hemi-anaesthesias, blindness or usually temporary. Recovery is often abrupt. contracted visual fi elds (tubular vision), and deafness. 3. Often, there is a precipitating stress before the The detailed examination usually shows absence of onset. There is a clear temporal relation ship objective signs of the particular illness and the dis- between the stressor and the onset of the illness. turbance is usually based on patient’s knowledge of A frequent stressful situation is an ongoing war. that illness. 4. A ‘secondary gain’ resulting from the development Sensory disturbances are inconsistent with the ana- of symptoms may be found. tomic patterns expected. Often all sensory modalities 5. Detailed physical examination and investi ga tions (such as touch, pain, temperature and position sense) do not reveal any abnormality that can explain the are affected at the same level. In conversion disorder, symptoms adequately. the loss of vibration sense maintains a strict midline The common clinical types are described below: separation, in spite of the fact that vibrations can be perceived on the other side of body through bone Dissociative Amnesia conduction. However, this is not a fool-proof test. This is the commonest clinical type of dis socia tive A patient with bilateral conversion blindness is disorder. Occurring mostly in adolescent and young able to go about his way reasonably well and doesn’t adults (females more than males, except in war), it is injure himself by walking into obstacles. In unilat- characterised by a sudden inability to recall important eral conversion blindness, the pupillary refl ex of the personal information (amnesia), particularly concern- affected eye is normal. ing stress ful or trau matic life events. The amnesia can Mixed presentations, with both sensory and motor not be explained by everyday forgetfulness and there symptoms, are quite common. is no evidence of an underlying medical illness. Most often, dissociative amnesia follows a trau- Dissociative Convulsions (Hysterical Fits) matic or stressful life situation. Sometimes, imagined Earlier known as ‘ hysterical fi ts’ or pseudo seizures, stressors or expression of ‘forbidden’ impulses may dissociative convulsions are characterised by presence also precipitate the onset of amnesia. Neurotic, Stress-related and Somatoform Disorders 101

Table 8.4: Dissociative Convulsions and Epileptic Seizures Clinical Features Epileptic Seizures Dissociative Convulsions (Hysterical Fits) 1. Attack pattern Stereotyped, known clinical patterns Absence of any established clinical pattern. Purposive body movements occur 2. Place of occurrence Anywhere Usually indoors or at safe places 3. Warning Both prodrome and aura are stereotyped Variable 4. Time of day Anytime. Can occur during sleep Never occur during sleep 5. Tongue bite Usually present Usually absent. Cheek and lip bite may be present 6. Incontinence of urine Can occur Very rare and faeces 7. Injury Can occur Very rare. If occurs, it is minor or may be accidental 8. Speech No verbalisation during the seizure Verbalisation may occur during the ﬁ t 9. Duration Usually about 30-70 sec. (Short) 20-800 sec. (Prolonged) 10. Head turning Unilateral Side to side turning 11. Eye gaze Staring, if eyes are open Avoidant gaze 12. Amnesia Complete Partial 13. Neurological signs Present, e.g. up-going plantars Absent 14. Post-ictal confusion Present Absent 15. Stress Present in 25% Present much more often 16. EEG - Inter-ictal Usually abnormal; Usually normal - Ictal Abnormal Normal 17. Serum prolactin Increased in post-ictal period (15-20 minutes Usually normal after seizure; returns back to normal in 1 hour)

This amnesia is of four types (Table 8.5). During the Table 8.5: Types of Dissociative Amnesia amnesic period, there may be slight clouding of con- 1. Circumscribed amnesia (commonest type): There is sciousness. In the post-amnesic period, the awareness an inability to recall all the personal events during a of disturbance of memory is present. circumscribed period of time, usually corresponding with the presence of the stressor. Dissociative Fugue 2. Selective amnesia (less common): This is similar to Dissociative fugue is characterised by episodes of circumscribed amnesia but there is an inability to wandering away (usually away from home). During recall only some selective personal events during the episode, the person usually adopts a new identity that period while some other events during the same with complete amnesia for the earlier life. The onset period may be recalled. is usually sudden, often in the presence of severe 3. Continuous amnesia (rare): In this type, there is an stress. The termination too is abrupt and is followed inability to recall all personal events following the by amnesia for the episode, but with recovery of stressful event, till the present time. memories of earlier life. The characteristic feature 4. Generalised amnesia (very rare): In this type, there is is the assumption of a purposeful new identity, with an inability to recall the personal events of the whole absence of awareness of amnesia. life, in the face of a stressful life event. 102 A Short Textbook of Psychiatry

An important differential diagnosis is from fugue Psychodynamic Theory states seen in complex partial seizures or temporal The explanation given by this theory can be summa- lobe epilepsy. In complex partial seizures, there is no rised in a fl ow diagram (Fig. 8.2). For further details assumption of a new identity, confusion or disorienta- regarding the defense mechanisms and Freudian tion is present during the episode and the episodes are theory, see Tables 17.1 and 17.2. not only linked to any precipitating stress. Behavioural Theory Multiple Personality According to this theory, dissociative (and conver sion) ( Dissociative Identity) Disorder symptoms are learned responses in the face of stress. In this dissociative disorder, the person is dominated For the fi rst time, the symptom may be learned from by two or more personalities, of which only one is the surrounding environ ment (e.g. seeing a paralysed being manifest at a time. These personalities are patient). usually different, at times even opposing. Each per- The development of the symptom brings about sonality has a full range of higher mental functions, psychological relief by avoidance of stress and is thus and performs complex behaviour patterns. secondarily reinforced. Usually one personality is not aware of the existence of the other(s), i.e. there are amnesic barriers Biological Theory between the personalities. Both the onset and termina- The biological basis of dissociative (conversion) disor- tion of control of the each personality is sudden. ders is far from proven. Some long-term studies (e.g. Classical examples in the published literature Slater) have found that up to 80% of patients, diag- include ‘Three faces of Eve’ and ‘Sybil’. nosed as ‘hysteria’, were later found to have physical illnesses. However, replications of such studies have Trance and Possession Disorders not found such high fi gures. Trance and possession disorders (possession hysteria) Conversion symptoms are frequently seen in the are characterised by the control of person’s personality patients with epilepsy and it may at times be diffi cult by a ‘spirit’, during the episodes. Usually the person is to differentiate between true seizures and pseudo- aware of the existence of the other (i.e. ‘possessor’), seizures. unlike in multiple personality. This disorder is very Similarly, ‘conversion-release’ symptoms are seen commonly seen in India and certain African countries. in some cerebral cortex lesions. However, these are only conversion symptoms and are not dissociative Other Dissociative Disorders (and conversion) disorders [i.e. other features for Ganser’s syndrome ( hysterical pseudodementia ) is diag nosis of dissociative (conversion) disorders are commonly found in prison inmates. The characteristic not present]. Hence, these are of doubtful help in feature is vorbeireden, which is also called as ‘ approxi- elucidating the aetiology of dissociative (and conver- mate answers’. The answers are wrong but show that sion) disorders. the person understands the nature of question asked. For example; when asked the colour of a red pen, the Diagnosis patient calls it blue. Diagnosis is based not merely on the absence of objective signs of physical illness, although it is very impor- Aetiology tant to exclude an underlying or associated physical The aetiological theories of dissociative (and con- illness. The presence of positive points in history and ver sion) disorders are predominantly of three types: examination should be present, before a diagnosis of Neurotic, Stress-related and Somatoform Disorders 103

Fig. 8.2: Psychodynamic Theory of Dissociative (Conversion) Disorder dissociative (and conversion) disorders can be made. Treatment These positive points are the characteristic clinical features listed previously. Behaviour Therapy As dissocia tive (and conversion) disorders and Since the patients with dissociative disorders can be physical illness can be co-existent, a detailed exami- attention seeking and their symptoms increase with nation is a must. Dissociative (conversion) symptoms focus of attention, the symptoms should not be un- appearing for the first time in an elderly male, duly focussed on. These patients should be treated as especially in a male more than 50 years old, a strong normal, and not encouraged to stay in a sick-role. Any sus picion of underlying physical or major psychia tric improvement in sympto matology should be actively illness should be kept in mind. encouraged. Other clinical features of dissociative (conversion) Since these patients can also very suggestible, they disorders include la-belle-indifférence , which is a lack respond quickly to the above-stated methods, with a of concern towards the symptoms, despite the apparent consistently ﬁ rm but empathic attitude. severity of the disability pro duced. Although earlier When there is a sudden, acute symptom, its prompt thought to be a hallmark of dissociative (conversion) removal may prevent habituation and future disabil- disorders, it is now known to be present even in ity. This may be achieved by one of the following physical illnesses. In addition, it is not always present methods: in dissociative (con version) disorders. i. Strong suggestion for a return to normalcy. Premorbid histrionic personality traits are often ii. Aversion therapy (liquor ammonia; aversive present, although a personality disorder is less com- electric stimulus; pressure just above eye balls monly present. or tragus of ear; closing the nose and mouth) are occasionally employed carefully in resistant cases. 104 A Short Textbook of Psychiatry

However, the use of aversion therapy has been Drug Therapy decried as it: Drug treatment has a very limited role in dissociative a. tends to get over-used; (and conversion) disorders (apart from the use of IV b. may harm the patient; thiopentone, amytal or diazepam in abreaction). A few c. violates the basic human rights of the patient; patients have disabling anxiety (although anxiety as a and rule is rather uncommon in ‘hysteria’) and may need d. can lend a wrong mental picture of the patient short-term benzodiazepines. in the physician’s mind, i.e. of a ‘manipulator’ needing punishment! SOMATOFORM DISORDER The current status is that aversion therapy is not a preferred treatment choice. The somatoform disorders are characterised by iii. Amplifi cation of suggestion with hypno sis, free- repeated presentation with physical symp toms which association, intravenous amytal or thiopentone, or do not have any adequate physical basis (and are not intra venous diazepam. explained by the presence of other psychiatric disorders), and a persistent request for investigations and treatment Psychotherapy with Abreaction despite repeated assurances by the treating doctors. Abreaction is bringing to the conscious awareness, In ICD-10, somatoform disorders are divided into thoughts, affects and memories for the fi rst time. This the following categories. may be achieved by: i. Hypnosis. Somatisation Disorder ii. Free association. Somatisation disorder is characterised by the follow- iii. Intravenous thiopentone or diazepam: The aim ing clinical features: of abreaction with IV thiopentone is, both, to 1. Multiple somatic symptoms in the absence of any make the confl icts conscious and to make the physical disorder. patient more suggestible to therapist’s advice. 2. The symptoms are recurrent and chronic (of many Once the confl icts have become conscious and years duration, usually); at least 2 year duration is their affects (emotions) have been released, needed for diagnosis. the conversion or dissociative symptom disap- 3. The symptoms are vague, presented in a dramatic pears. manner, and involve multiple organ systems. The common symptoms include gastrointes tinal Supportive Psychotherapy (abdominal pain, beltching, nausea, vomiting, Supportive psychotherapy is needed especially when regurgitation), abnormal skin sensations (numb- the confl icts (and the current problems) have become ness, soreness, itching, tingling, burning), and conscious and have to be faced in routine life. It is an sexual and menstrual complaints (menorrhagia, important adjunct to treatment. dysmenorrhoea, dyspareunia). 4. There is frequent change of treating physicians. Psychoanalysis 5. Persistent refusal to accept the advice or reassur- This mode of treatment is chosen not on the basis of ance of several doctors that there is no physical conversion/dissociative symptoms but on the total explanation for the symptoms. personality structure of the patient. Several patients 6. Some degree of impairment of social and family respond remarkably well. The total length of therapy functioning attributable to the nature of the symp- in classical psycho analysis is usually fi ve years or toms and resulting behaviour. more. 7. Presence of conversion symptoms is common. Neurotic, Stress-related and Somatoform Disorders 105

This disorder usually begins in second or third somatic symptoms are interpreted as the pre sence decade of life and is much more common in females. of a serious body disease. In the fi rst degree relatives of patients with somatisa- 4. Conversion disorder: Although conversion tion disorder, disorders such as somatisation disorder symptoms are common in somatisation disorder, (in females), and alcoholism and psychopathy (in they are classified separately. The number of males) are common. Histrionic personality traits or symptoms in conversion disorder is far less (one disorder may also be present. or two) than in somatisation disorder (usually more than ten). Differential Diagnosis 5. Delusional disorders: Somatic delusions may It is important to rule out physical disorders be- be present in delusional disorders (e.g. mono- fore making a diagnosis of somatisation disorder. symptomatic hypochondriacal psychosis). In de- Particularly those physical disorders, which often lusional disorders, there is a delusional conviction present with apparently vague and multiple somatic of somatic symptoms, with far fewer symptoms. symptoms, must be kept in mind. This is especially so if the onset of symptoms is in the later part of Treatment life (> 35 years of age; more so if > 45 years of age) The treatment is often diffi cult. It mainly consists of: and in male patients. These physical disorders 1. Supportive psychotherapy: The treatment of include: choice is usually supportive psychotherapy. The 1. Multiple sclerosis. fi rst step is to enlist the patient in the therapeutic 2. Hypothyroidism. alliance by establishing a rapport. It is useful 3. Acute intermittent porphyria. to demonstrate the link between psychosocial 4. Systemic lupus erythematosus (SLE). confl ict(s) and somatic symptoms, if it is apparent. 5. Hyperparathyroidism. In chronic cases, ‘symptom reduction’ rather than 6. Carcinoma pancreas. ‘complete cure’ might be a reasonable goal. Somatisation sometimes presents as an ‘idiom of 2. Behaviour modifi cation: After rapport is estab- distress’ in the absence of a diagnosable psychiatric lished, attempts at modifying behaviour are made, disorder. However, certain psychiatric disorders must for example, not focusing on the symptoms per se, be ruled out. and positively reinforcing normal functioning. 1. Schizophrenia: In the initial (prodromal) stages, 3. Relaxation therapy, with graded physical exercises. multiple somatic symptoms may be present but 4. Drug therapy: Antidepressants and/or ben- later typical features of schizophrenia are mani- zodiazepines can be given on a short-term basis fested. for associated depression and/or anxiety. Benzo- 2. Major depression: Particularly in developing diazepines should be used with great caution, as countries such as India, multiple somatic symp- the risk of dependence and misuse is high in these toms are common in major depre ssion. The patients. presence of depressed mood, depres sive ideation and disturbances of biological functions in major Hypochondriasis depression helps in differen tiation. Occasionally, (Hypochondriacal Disorder) differential diagnosis with masked depression may Hypochondriasis is defi ned as a persistent preoccupa- be diffi cult. tion with a fear (or belief) of having one (or more) 3. Hypochondriasis: In somatisation disorder, there serious disease(s), based on person’s own interpre- are multiple, vague somatic symptoms, while in tation of normal body function or a minor physical hypochondriasis, normal body functions or minor abnormality. 106 A Short Textbook of Psychiatry

The other important features of hypochondriasis 1. Supportive psychotherapy. are: 2. Treatment of associated or underlying depression 1. Complete physical examination and investi gations and/or anxiety, if present. do not show presence of any signifi cant abnormality. Somatoform Autonomic Dysfunction 2. The fear or belief persists despite assurance to the According to ICD-10, in this disor der, symptoms contrary by showing normal reports to the patient. are presented by the patient as if they were due to 3. The fear or belief is not a delusion but is instead a physical disorder of an organ system that is pre- an example of an overvalued idea. The patient may dominantly under autonomic control, e.g. heart and agree regarding the possibility of his exaggerating cardio vas cular system (such as palpitations), upper the graveness of situation, at that time. gastro intestinal tract (such as aerophagy, hiccough), 4. A preoccupation with medical terms and syn- lower gastrointestinal tract (such as fl atulence, irritable dromes is quite common. The patient tends to bowel), respiratory system (such as hyperventi la tion), change the physician frequently, in order to get genitourinary system (such as dysuria), or other organ investigated again. systems. The usual age of onset is in the late third decade. There is preoccupation with, and distress regard- The course is usually chronic with remissions and ing, the possibility of a serious (but often unspecifi ed) relapses. Obsessive perso na lity traits and narcissistic disorder of the particular organ system. Physical personality features are frequently seen, in addition examination and investigations do not however show to associated anxiety and depression. presence of any signifi cant abnormality. The preoccupation persists despite repeated assurances and Aetiology explanations. The cause of hypochondriasis is not known. The important theories are mentioned below: Treatment 1. Psychodynamic Theory The treatment consists of: Hypochondriasis is believed to be based on a narcis- 1. Supportive psychotherapy. sistic personality, caused by a narcissistic libido. Here 2. Drug treatment: The symptoms of anxiety and/or other parts of body become erotogenic zones, which depression usually respond to short-term use of act as substitutes for genitals. Hypochondriacally benzodiazepines and antidepressants. focused organs symbolise the genitals. It must be Some other common disorders are described in remembered that this is only a theoretical psychody- some detail below: namic construct. 2. As a Symptom of Depression Hyperventilation Syndrome (HVS) Hypochondriacal symptoms are commonly present This is a very common clinical syndrome which is in major depression. In fact, according to some, often missed, particularly when it does not present in hypochondriasis is almost always a part of another its full blown form. The syndrome is characterised by a psychiatric syndrome, most commonly a mood dis- ‘habit’ of hyperventilation which becomes particularly order. Thus, hypo chondriasis has been visualised as marked in the presence of psychosocial stress, or any a masked depression or depressive equivalent, though emotional upheaval. not everyone agrees with this view. In its mild form, it is characterised by excessive fatigue, chest pain, headache, palpitations, sweating Treatment and a feeling of ‘lightheadedness’. In severe hyper- The treatment of hypochondriasis is often diffi cult. It ventilation syndrome, carpopaedal spasm (tetany), basically consists of: paraesthesias and loss of consciousness may occur. Neurotic, Stress-related and Somatoform Disorders 107

These symptoms are produced by hypo capnia (or ii. Slow respiration with passive expiration, with- a decrease in arterial pCO2). The sequence of events in out muscular effort. hyperventilation syndrome is explained in Figure 8.3. iii. A short rest cycle to be voluntarily introduced The diagnosis is usually easy, if the possi bility after each respiratory cycle. of hyperventilation is remembered. Apart from the 3. Treatment of underlying anxiety or depres sion, clinical history and presence of frequent ‘sighing’ if present, with antidepressants and/or short-term during the interview, a simple test would demonstrate benzodiazepines. the symptomatology. The patient is asked to breathe 4. Breathing-in-bag technique: The aim of this rapidly and deeply for 2-3 minutes. This pro duces technique is to have the patient re-breathe the the classical physical symptoms. If carried on longer, expired air. This prevents the decrease in pCO2 tetany and unconsciousness would result; therefore, which causes physical symptoms, or causes an due care should be undertaken in performing this test. increase in pCO2 where physical symptoms have already developed. Re-breathing in a paper bag, Treatment which is carried by the patient, quickly reverts the 1. Relaxation techniques: Jacobson’s progres sive symptoms. It is really important to emphasise a muscular relaxation, autohypnosis or hypno sis, safe use of the bag, to prevent the possibility of yoga, transcendental meditation (TM), and/or suffo cation. There is some recent evidence doubt- biofeedback. ing the efﬁ cacy of this approach. 2. Teaching relaxed breathing techniques, which include: Irritable Bowel Syndrome (IBS) i. Breathing more from the abdomen, thus avoid- This is a common syndrome, often known by a large ing the use of accessory muscles of expiration. variety of names, such as spastic colitis, irritable

Fig. 8.3: Physiology of Hyperventilation Syndrome 108 A Short Textbook of Psychiatry colon syndrome, nervous diarrhoea, mucus colitis, sometimes be useful. A trial of fi bre (wheat bran, and colon neurosis. psyllium, methylcellulose) is reasonable in some The principal abnormality in IBS is a disturbance patients with irritable bowel syndrome. of bowel mobility, which is modifi ed by psychosocial factors. The patients usually pre sent with one or more Premenstrual Syndrome of the following symptoms: Premenstrual syndrome or premenstrual tension 1. Abdominal pain, discomfort or cramps. (PMT—as it has been commonly called) is charac- 2. Alteration of bowel habits (diarrhoea or constipa- terised by a variety of physical, psychological and tion). behavioural symptoms occurring in the second half of 3. A sensation of incomplete evacuation. menstrual cycle. Typically, the symptoms start after Quite often, all three features (abdominal pain a few days of ovulation, reach a peak about 4-5 days and diarrhoea alternating with constipation) are before menstrua tion and disappear usually around present together; also associated is fl atulence. The menstruation. The period between menstruation and patients often describe their stools in a dramatic next ovulation is normal. manner. The syndrome is characterised by feelings of It is a fairly common disorder occurring in nearly irritability, depression, crying spells, restlessness and 40% of all patients attending a gastroenterology (GE) anxiety. These are associated with changes in appetite, clinic. Although females more frequently have IBS in signs and symptoms of water retention (such as pedal America, in India males are more often affected. It is oedema, weight gain, swelling of breasts, a sense of more or less a stable disorder with frequent exacerba- bloating of abdomen), gastroenterological changes, tions. headache and fatigue. The typical mode of onset or exacerbation is with The aetiology is probably multifactorial. The occurrence of a psychosocial stressor or emotional biological factors include faulty luteinisation, excess upheaval. Physiologically, there are two changes pos- of oestrogens, and progesterone defi ciency. The psy- sible in the bowel motility. chosocial factors encompass educa tion, expectations 1. Hypomotility, which is often associated with pain- and attitudes towards menstruation and femininity less diarrhoea. (‘tension’ about menstruation). 2. Hypermotility, which presents clinically as painful constipation or rarely painful diarrhoea. Treatment 1. The treatment of water retention can be by diu- Treatment retics, and restricting the fl uid intake. Thiazide 1. A stable and trustful doctor-patient relation ship. diuretics are often prescribed but spironolactone 2. Supportive psychotherapy is best carried out in (an aldosterone anta gonist) is probably superior. medical or GE clinic by the treating physi cian. 2. Psychotherapy may be helpful in some cases where These patients often resent psychiatric referrals. confl icts regarding menstruation and/or femininity 3. Identifi cation of current life stressors, environ- are present. mental manipulation, and learning of coping skills 3. Hormonal treatment with oral or parenteral pro- aimed at dealing with stressors are very helpful. gesterone has been recommended by some, with 4. Anti-anxiety and antidepressant medication may good results. be helpful at times. At other times, they just act 4. In resistant cases, other drugs such as lithium, like placebos. bromocrip tine, pyridoxine, antidepressants and 5. Symptomatic management is often unsuc cess ful. anti-anxiety agents have been used with varying However, prokinetic agents (e.g. cisapride) may success. Neurotic, Stress-related and Somatoform Disorders 109

Persistent Somatoform Pain Disorder Persisting/distressing complaints of increased It was previously called as psychogenic pain disorder. fatigue after mental effort, or of weakness/exhaustion In this disorder, persistent, severe and distressing after minimal effort; with two or more of the follow- pain is the main feature which is, either grossly in ing: feelings of muscular aches/pains, dizziness, ten- excess of what is expected from the physical fi nd ings, sion headaches, sleep disturbances, inability to relax, or inconsistent with the anatomical distri bution of irritability and dyspepsia. It is important to rule out nervous system. Preoccupation with pain is common. other mental disorders which may fully explain the There is often a precipitating stressful event and symptoms. secondary gain may be present. Repeated change of This is clearly a poorly defi ned syndrome and its physicians (doctor-shopping) is common. The affected independence as a diagnosis is doubtful. A differen tial person often assumes a ‘sick-role’ or an ‘invalid-role’. diagnosis with CFS (chronic fatigue syndrome), and Abuse and dependence of analgesics and minor tran- other medical and psychiatric disorders pre senting quilisers is common, particularly when the course is with fatigue, is important before diag nosing neuras- chronic. thenia. This disorder is more common in females, with CFS is characterised by profound fatigue (present an onset in the third or fourth decade of life. at rest, and made worse by physical and mental effort), muscle pains, headache, sore throat, functional impair- Treatment ment and nonspecifi c ‘soft’ physical signs, e.g. mild 1. The patients usually refuse psychiatric interven- fever, mild lymphadenopathy. CFS is diagnosed in the tion; therefore treatment is often managed by the absence of medical or other psychiatric disorder(s), treating physician. though neuropsychiatric symptoms may be present. 2. Drug therapy should be avoided if possible as the risk of iatrogenic drug abuse is quite high. Depersonalisation Disorder 3. In the absence of other modes of successful (or Depersonalisation-Derealisation treatment, a supportive relationship with a physi- Syndrome) cian will prevent doctor-shopping and provide Depersonalisation is characterised by an altera tion in relief. the perception or experience of self, so that the feeling of one’s own reality is temporarily changed or lost. Other Somatoform Disorders It is an ‘as if’ phenomenon. The person affected In ICD-10, this category includes other soma toform is not delusionally convinced about the change, and disorders not classifi ed in the previous four catego- instead describes it to have occurred, as-if. This is ries, e.g. ‘ globus hystericus’, psychogenic torticollis, often accompanied by derealisation , which is an psychogenic pruritus, psychogenic dysmenorrhoea, alteration in the perception or experience of the teeth-grinding. external world, so that the feeling of reality of external world is temporarily changed or lost. This too is an OTHER NEUROTIC DISORDERS ‘as if’ phenomenon. Derealisation is a larger concept which also encompasses depersonalisation. As they In ICD-10, the other neurotic disorders are divided both often occur together the syndrome is also called into the following categories: as depersonalisation-derealisation syndrome. As both depersonalisation and derealisation occur Neurasthenia in many other disorders (Table 8.6), the term deper- According to ICD-10, this disorder is characterised sonalisation dis order should be used only when other by: disorders have been ruled out. 110 A Short Textbook of Psychiatry

The other associated clinical features may include: Table 8.6: Depersonalisation: Causes 1. The episodes of depersonalisation and/or dere- 1. Psychiatric Disorders alisation causing signifi cant social, interpersonal i. Depersonalisation disorder or occupational impairment. The episodes recur ii. Phobic-anxiety-depersonalisation (PAD) frequently. syndrome 2. The onset and termination of episodes is usually iii. Anxiety disorder sudden. iv. Panic disorder 3. Marked distress and anxiety results, as the experi- v. Agoraphobia ence is highly unpleasant. vi. Schizophrenia 4. Insight into the illness is usually present. vii. Depression 5. A feeling of loss of control on one’s action and 2. Neurological Disorders speech may occur. i. Complex partial seizures 6. The episodes occur in the presence of a clear ii. Migraine sensorium. iii. Cerebral tumours (especially affecting non- The age of onset is usually late second or early dominant parietal lobe) third decade. The course is usually chronic. iv. Encephalitis 3. Other Causes Treatment i. Hyperventilation The treatment is usually not very successful though ii. Alcohol and drug dependence co-morbid symptoms of anxiety and depression can iii. Hypoglycaemia often be treated. The various methods which can be iv. Fatigue tried include: v. Grief 1. Supportive psychotherapy. vi. Sensory deprivation 2. Drug therapy with antidepressants; rarely antipsychotics may also be tried. 4. Anxiety or depression may be present. 5. Sexual dysfunction may occur. Other Specifi ed Neurotic Disorders Dhat is a whitish discharge passed in urine and (Culture Bound Syndromes) believed to be semen by the patient. According to an In ICD-10, this category includes miscellaneous disor- ancient sociocultural belief prevalent in the Indian ders which are of uncertain aetiology and nosological society, semen is an ‘extremely precious’ body element status, and which occur in certain cultures, e.g. dhat which is produced from several drops of blood. Hence, syndrome, koro, latah, wihtigo, piblokto and amok. it follows from this view that loss of semen will be These are called as culture-bound syndromes, as they perceived to lead to weakness and sexual dysfunction. are localised to certain geographical areas only, and are Often, masturbatory anxiety and overconcern with not usually seen in the Western, developed countries. nocturnal emissions are also associated with other clinical symptoms. Dhat Syndrome Treatment Dhat syndrome is a culture-bound syndrome, which 1. Counselling and Psychotherapy: This is the most is prevalent in the Indian subcontinent. This is char- important method of treatment directed towards acterised by: removing misconcep tions regarding apprehension 1. Complaint of passage of dhat in urine. of semen loss. This counselling is combined with 2. Multiple somatic symptoms. general sex educa tion. Specifi cally, fears regar ding 3. Asthenia (physical or mental exhaustion). masturbation and nocturnal emissions are allayed. Neurotic, Stress-related and Somatoform Disorders 111

Cognitive behavioural techniques can easily be extremely cold conditions. She may imitate the cry of incorporated in the psychotherapy model applied. a bird or an animal. 2. Symptomatic treatment: The treatment of under- The episode usually lasts for 1-2 hours, followed lying anxiety, depression, hypochon driasis and/or by amnesia for the events. It is most probably a type sexual dysfunction by the usual means may also be of dissociative disorder. necessary. Several patients present with underlying (or co-morbid) depression and anxiety, and Latah (Startle Reaction) may need psychopharmacological management This syndrome is reported from south-east Asia of these symptoms. and Japan. Occurring more often in women, latah is typically characterised by the presence of auto- Amok matic obedience, echolalia, and echopraxia. It is often Amok is characterised by a sudden, unpro voked precipitated by a sudden stimulus, such as loud sound. episode of rage, in which the affected person runs about (runs ‘amok’) and indis criminately injures Some Indian Culture-bound Syndromes or kills any person who is encountered on the way. In addition to dhat syndrome, amok and koro This condition is usually seen in south-east Asia (e.g. (described above), the other culture-bound syndromes Malaysia). seen in India include Suchi-bai (purity mania), ascetic syndrome, nupital psy chosis, and Jhinjhinia. Koro Koro is a culture-bound syndrome seen in Asia (in- REACTION TO STRESS AND cluding India). The affected male person has the belief ADJUSTMENT DISORDERS that his penis is shrinking and may disappear in to his abdominal wall and he may then die. This category in ICD-10 consists of disorders which Females are also affected infrequently, with a cor- are temporally related to an exceptionally stressful responding belief that their breasts (and/or vulva) are life event (acute stress reaction and post-traumatic shrinking. stress disorder) or a signifi cant life change (adjustment Koro often spreads rapidly to the other members disorders) immediately before the onset of illness. of community in an epidemic form. It is usually based on the culturally elabo rated fears regarding nocturnal Acute Stress Reaction emission and masturbation (particularly in men). According to ICD-10, in this disorder there is an immediate and clear temporal relationship between an Wihtigo (Windigo) exceptional stressor (such as death of a loved one, This syndrome is seen in native American-Indians. natural catastrophe, accident, rape) and the onset of The affected person has the belief that he has been symptoms. The symptoms show a mixed and chang- transformed in to a wihtigo, a cannibal monster. The ing picture. This disorder is more likely to develop in episodes are known to have occurred especially during presence of physical exhaustion and in extremes of times of starvation. age. It is also more commonly seen in female gender and people with poor coping skills. Piblokto (Arctic Hysteria) The symptoms range from a ‘dazed’ condition, This culture-bound syndrome occurs in Eskimos. anxiety, depression, anger, despair, overactivity or The affected person is often a female, who screams withdrawal, and constriction of the fi eld of conscious- and tears-off her clothes, and throws herself on ice in ness. The symptoms resolve rapidly (within few hours 112 A Short Textbook of Psychiatry usually), if removal from the stressful environment is 4. Cognitive behaviour therapy (CBT). possible. If the stress continues or cannot be reversed, 5. Drug treatment: Antidepressants and benzo- the resolution of symptoms begins after 1-2 days and diazepines (in low doses for short periods) is usually minimal after about three days. are useful in treatment, if anxiety and/or depression are important compo nents of the clinical Treatment picture. The treatment consists of removal of the patient from the stressful environment and helping the patient to Adjustment Disorders ‘pass through’ the stressful experience. IV or oral Adjustment disorders are one of the commoner benzodiazepines (such as diazepam) may be needed psychiatric disorders seen in the clinical practice. They in cases with marked agitation. are most frequently seen in ado les cents and women. Although adjustment disorder is often precipitated by Post-traumatic Stress Disorder (PTSD) one or more stressors, it usually represents a maladap- According to ICD-10, this disorder arises as a delayed tive response to the stressful life event(s). and/protracted response to an exceptionally stressful In ICD-10, this disorder is characterised by those or catastrophic life event or situation, which is likely disorders which occur within 1 month of a signifi cant to cause pervasive distress in ‘almost any person’ (e.g. life change (stressor). This disorder usually occurs disasters, war, rape or torture, serious acci dent). The in those individuals who are vulnerable due to poor symptoms of PTSD may develop, after a period of coping skills or perso nality factors. It is assumed that latency, within six months after the stress or may be the disorder would not have arisen in the absence of delayed beyond this period. the stressor(s). The duration of the disorder is usually PTSD is characterised by recurrent and intrusive less than 6 months, except in the case of pro longed recollections of the stressful event, either in fl ash- depressive reaction. backs (images, thoughts, or perceptions) and/or in The various subtypes include brief or prolonged dreams. There is an associated sense of re-experienc- depres sive reaction, mixed anxiety and depressive ing of the stressful event. There is marked avoidance reaction, and adjustment disorder with predominant of the events or situations that arouse recol lections of disturbance of other emotions and/or predomi nant the stressful event, along with marked symptoms of disturbance of conduct. anxiety and increased arousal. Most patients recover within a period of three The other important clinical features of PTSD months. include partial amnesia for some aspects of the stressful event, feeling of numbness, and anhedonia Treatment (inabi lity to experience pleasure). 1. Supportive psychotherapy remains the treatment of choice. Treatment 2. Crisis intervention is useful in some patients, The treatment consists of the following mea sures: by helping to quickly resolve the stressful life 1. Prevention: Anticipation of disasters in the high situation which has led to the onset of adjustment risk areas, with the training of per sonnel in disaster disorder. management. 3. Stress management training and Coping skills 2. Disaster management: Here the speed of provi ding training. practical help is of paramount importance. This is 4. Drug treatment may be needed in some patients also a preventive measure. for the management of anxiety (benzodiazepines) 3. Supportive psychotherapy. and/or depressive symp toms ( antidepressants). Disorders of Adult 9 Personality and Behaviour

SPECIFIC PERSONALITY DISORDERS co-morbidity) is com mo ner than single (pure) personality disorders. Personality is defi ned as a deeply ingrained pattern of In DSM-IV-TR, the personality disorders (and behaviour that includes modes of perception, relating traits) are coded on Axis II (on the multi-axial system) to and thinking about oneself and the surrounding (see Chapter 1) and have been divided into three environment. Personality traits are normal, prominent clusters. aspects of personality. Personality disorders result Cluster A contains disorders which are thought when these personality traits become abnormal, i.e. to be “odd and eccentric” and on a “schizophrenic- become infl exible and maladaptive, and cause signifi - continuum”. These include Paranoid, Schizoid and cant social or occupational impairment, or signifi cant Schizotypal personality disorders. subjective distress. Cluster B consists of disorders considered “dra- Although personal distress may occur in some matic, emotional and erratic” and on a “psychopathic personality disorders, classically the abnormal per- continuum”. These include Antisocial (or Dissocial), sonality traits are ‘ego-syntonic’. This is in sharp Histrionic, Narcissistic and Borderline (or Emotion- contrast to the symptoms in neurotic disorders, which ally Unstable) personality disorders. are ego-dystonic and hence cause signifi cant distress Cluster C has disorders considered “anxious and to the patient. So, unlike the patients with neurotic fearful” and characterised by “introversion”. These disorders, several personality disorder patients do not include Anxious (Avoidant), Dependent and Obsessive usually seek psychiatric help unless other psychiatric Compulsive (or Anankastic) personality disorders. symptoms co-exist. In addition to these three clusters, some other Although personality disorders are usually rec- personality disorders such as passive-aggressive ognisable by early adolescence, they are not typi- personality disorder and depressive personality dis- cally diagnosed before early adult life. The symptoms order have been included in the section on ‘Criteria continue unchanged through the adult life and usually provided for further study’ in DSM-IV-TR. In ICD-10, become less obvious in the later years of life (after 40 the personality disorders are listed under the section years of age). on ‘Disorders of adult personality and behaviour’. The life-time prevalence of personality disorders in the general population is about 5-10%. Often Diagnosis symptoms of more than one personality disorder are According to ICD-10, the diag nostic guidelines for present in one person. In fact, it is now believed that specifi c personality disorder include conditions not the occurrence of mixed personality disorders (i.e. directly attributable to gross brain damage or disease, 114 A Short Textbook of Psychiatry or to another psychiatric disorder, meeting the fol- Psychodynamically, the underlying defense mecha- lowing criteria. nism is projection. 1. Markedly disharmonious attitudes and behaviour, Paranoid personality disorder is common in the involving usually several areas of func tioning, premorbid personality of some patients of paranoid e.g. affectivity, arousal, impulse control, ways of schizo phrenia. However whether its presence predis- perceiving and thinking, and style of relating to poses to the deve lopment of paranoid schizophrenia others; is not known. The diffe rential diagnosis is from 2. The abnormal behaviour pattern is endu ring, of delusional (paranoid) disorders and paranoid schizo- long standing, and not limited to episodes of phrenia. mental illness; Treatment 3. The abnormal behaviour pattern is pervasive and 1. Individual psychotherapy. clearly maladaptive to a broad range of personal 2. Supportive psychotherapy. and social situations; The response to treatment is usually poor. The 4. The above manifestations always appear during patients often do not seek treatment on their own childhood or adolescence and continue into adult- and may resent treatment. Drug treatment has a very hood; limited role. 5. The disorder leads to considerable personal distress but this may only become apparent late in its Schizoid Personality Disorder course; According to ICD-10, the diagnostic guidelines for 6. The disorder is usually, but not invariably, associ- schizoid personality disorder include the following ated with signifi cant problems in occupational and features (in addition to the general features of per- social performance. sonality disorders). Clear evidence is usually required of the presence of at least three out of nine traits or Clinical Subtypes behaviours given in the clinical description. These traits include emotional coldness, lack of pleasure Paranoid Personality Disorder from activities, limited capacity to express feelings According to ICD-10, the diagnostic guidelines for towards others, apparent indifference to praise or paranoid personality disorder include the following criticism, little interest in sexual experiences, prefer- features (in addition to features of personality disor- ence for solitary activities, excessive preoccupation ders in general, described above). with fantasy and introspection, lack of close friends, Clear evidence is usually required of the pres- and marked insensitivity to prevailing social norms ence of at least three out of seven traits or behaviours and conventions. given in the clinical description in ICD-10. These The features of this disorder may overlap with traits include excessive sensitiveness, tendency to paranoid and schizotypal personality disorders, which persistently bear grudges, signifi cant suspiciousness, too belong to the Cluster-A. Psychotic features are a combative and tenacious sense of personal ‘right’, typically absent. The disorder is usually more common recurrent suspicions about fi delity of partner without in men. justifi cation, tendency to experience excessive self- Psychodynamically, the disorder is supposed to importance, and preoccupation with unsubstantiated result from ‘cold and aloof’ parenting in a child with ‘conspi ratorial’ explanations of events. introverted temperament. However, this hypothesis is The patients may become involved in litigation on far from proven in the research con ducted so far. small issues. The disorder is com moner in men, and it Like all personality disorders, schizoid personality is more common in minority groups and immigrants. disorder has an onset in early childhood with stable Disorders of Adult Personality and Behaviour 115 course over the years. Earlier, it was believed to pre- Treatment dispose to the development of schizophrenia, but later The response to treatment is usually poor, except for studies have failed to replicate the fi ndings. brief psychotic episodes. Treatment 1. Psychoanalysis or psychoanalytical psycho- 1. Individual psychotherapy. therapy. 2. Psychoanalysis or psychoanalytical psycho- 2. Individual psychotherapy. therapy. 3. Drug therapy: Antipsychotics have been used with- 3. Gradual involvement in group psycho therapy. out much benefi t. The role of antipsychotics in the The patients often do not seek treatment on their treatment is limited to brief psychotic episodes. own. The response to treatment is usually not good. Drug treatment clearly has a very limited role. Antisocial or Dissocial Personality Disorder According to ICD-10, the diagnostic guidelines for Schizotypal (Personality) Disorder dissocial (antisocial) personality disorder include the According to ICD-10, this disorder is not classifi ed following clinical features. Clear evidence is usually under specifi c personality disorders but instead along required of the presence of at least three of six traits with schizophrenia. However, in DSM-IV-TR, it is or behaviours given in the clinical description. This considered to be a personality disorder. disorder is synonymous with previously used terms The diagnostic guidelines for schizotypal (per- such as psychopathy and sociopathy, but does not sonality) disorder include the following features. A always mean criminal behaviour. These traits include disorder characterised by eccentric behaviour, and callous unconcern for the feelings of others, gross and anomalies of thinking and affect, which resemble persistent attitude of irresponsi bility and disregard those seen in schizophrenia, though no defi nite and for social norms, rules and obligations, incapacity to characteristic schizo phrenic anomalies have occurred maintain enduring relation ships, very low tolerance at any stage. At least three or four out of nine should to frustration and a low threshold for discharge of be present continuously or episodically for a period of aggression, incapacity to experience guilt and to profi t at least 2 years. These include inappropriate or con- from experience, particularly punishment, and marked stricted affect, odd, eccentric, or peculiar behaviour, proneness to blame others. poor rapport with others and social withdrawal, odd There may also be persistent irritability as an beliefs or magical thinking, suspiciousness or paranoid associated feature. History of conduct disorder in ideas, obsessive ruminations without inner resistance, childhood and adolescence, though not invaria bly unusual perceptual experiences, vague, circumstantial, present, may further support the diagnosis. There are metaphorical, or stereotyped thinking, and occasional no psychotic features in this dis order. transient quasi-psychotic episodes (with intense illu- Earlier antisocial personality disorder or psycho- sions, hallu cinations, and delusion-like ideas). pathy was divided into four clinical types, namely: This disorder lies between schizoid personality 1. Aggressive psychopath, disorder and schizophrenia on a schizo phrenic con- 2. Inadequate psychopath, tinuum. Differentiation from simple schizophrenia, 3. Creative psychopath, and schizoid personality disorder, and paranoid person- 4. Sexual psychopath. ality disorder is not clearly demarcated. It is more As these are not discrete groups and their charac- commonly seen in indivi duals related to patients teristic symptoms merge with one another, they are with schizophrenia and is believed to be a part of no longer classifi ed in this manner. Although no clear the genetic ‘spectrum’ of schizophrenia. However, aetiology is known, several genetic, environmental its onset, evolution and course are usually those of a and biological factors are associated with this disorder. personality disorder. It usually runs a chronic course. These factors include more than a ‘normal’ prevalence 116 A Short Textbook of Psychiatry of anti social personality disorder in father; presence of speech and motor behaviour are present. There is of impulsive and inconsistent parents; presence of soft an attempt to look charming, beautiful and seductive. neurological signs, nonspecifi c EEG abnormalities; Suicidal ges tures may be made at times. Interpersonal and presence of conduct and/or attention defi cit dis- relation ships are often stormy and ungratifying. order in childhood. This disorder is more common in female gender. This disorder is diagnosed more commonly in Hysteria (conversion and dissociation disorder) was males. The course is usually chronic; however, there previously thought to be more common in the presence is some decrease in the symptoms after the fi fth decade of histrionic personality disorder, but recent studies of life in some patients. have failed to prove this relationship. Psychodynami- Treatment cally, there are usually intense dependency needs. The Patients often do not seek psychiatric help and if they defense mechanisms used most often are acting out do, it is usually under pressure from the legal authori- and dissociation. ties. The therapeutic alliance is often not sustained. Treatment The treatment methods include: Psychoanalysis and psychoanalytic psychotherapy are 1. Individual psychotherapy. the modes of treatment which are most successful. 2. Psychoanalysis or psychoanalytical psychotherapy. Narcissistic Personality Disorder 3. Group psychotherapy and self-help groups. A relatively new concept in classifi cation, this disorder 4. Drug therapy: Pharmacotherapy is of little help. is charac terised by: Earlier claims of benefi cial effect of pericyazine 1. Ideas of grandiosity and infl ated sense of self- (an antipsychotic drug) in certain behaviour importance. patterns of antisocial personality disorder have 2. Preoccupation with fantasies of unlimited not been substantiated. success. 3. Attention seeking, dramatic behaviour, needs Histrionic Personality Disorder constant praise, and unable to face criticism. According to ICD-10, the dia gnostic guidelines for 4. Lack of empathy with others, with exploitative histrionic personality disorder include the following behaviour. clinical features. Clear evidence is usually required 5. Shaky self-esteem, underlying sense of inferiority, of the presence of at least three of six traits or behav- easily depressed by minor events. iours given in the clinical description. These include Treatment self-dramatisation and exaggerated expression of Psychodynamic/psychoanalytical psychotherapy is emotions, suggestibility (easily infl uenced by others), the treatment of choice in a psychologically-minded shallow and labile affectivity, continual attention- patient. seeking attitude, inappropriate seductiveness, and over-concern with physical attractiveness. Associated Emotionally Unstable Personality Disorder features may include egocentricity, self-indulgence, According to ICD-10, emotionally unstable personal- continuous longing for appreciation, feelings that are ity disorder is described as a disorder in which there easily hurt, and persistent manipulative behaviour to is a marked tendency to act impulsively without con- achieve own needs. sideration of the consequences, together with affective Tantrums or anger outbursts are common. The ac- instability. This disorder is further classifi ed into two tions are not planned for any long-term goals; instead types: Impulsive type and borderline type. they seek instant satisfaction and approval. Exhibition- The impulsive type is characterised by emotional istic traits such as dressing fl amboyantly, mannerisms instability and lack of impulse control. Out bursts of Disorders of Adult Personality and Behaviour 117 violence or threatening behaviour are common, par- 3. Cognitive behaviour therapy (CBT) or dialectical ticularly in response to criticism by others. behaviour therapy (DBT) approaches or principles The borderline type is characterised by emotional have been used with some success in treatment. instability. In addition, patient’s own self-image, aims, 4. Drug therapy: Antidepressants have been used and internal preferences (including sexual) are often with success in certain patients with depression. unclear or disturbed. There are usually chronic feel- Major depressive episode, if occurs, necessitates ings of emptiness. A liability to become involved in antidepressant therapy. Occasionally antipsychot- intense and unstable relationships may cause repeated ics, lithium, valproate or carbamazepine have emotional crises and may be associated with excessive been used when aggres sion or impulsivity are efforts to avoid abandonment and a series of suicidal prominent. threats or acts of self-harm, (although these may occur Drug therapy is not the treatment of fi rst choice without obvious precipitants). in borderline personality disorder. The borderline type is also known as border line personality disorder (DSM-IV-TR), the characteristic Anxious (Avoidant) Personality Disorder features of which include the following: According to ICD-10, the diag nostic guidelines 1. Signifi cant and persistent disturbance of identity of for anxious (avoidant) per sonality disorder include self, e.g. ‘who am I’. There is marked uncertainty the following features. Clear evidence is usually about major issues in life. required of the presence of at least three of six traits 2. Unstable and intense interpersonal relation ship or behaviours given in the clinical description. patterns. These include persistent and pervasive feelings of 3. Impulsivity. tension and apprehension, belief that one is socially 4. Unstable emotional responses, with rapid shifts. inept, personally unappealing, or inferior to others, Anger outbursts may occur. excessive preoccupation with being criticised or re- 5. Chronic feelings of boredom or emptiness with jected in social situations, unwillingness to become inability to stay alone. involved with people unless certain of being liked, 6. Deliberate self-harm is common in the form of restrictions in lifestyle because of need to have self-mutilation, suicidal gestures, or accident- physical security, and avoidance of social or occupa- proneness. tional acti vities that involve signifi cant inter-personal The term borderline personality disorder currently contact because of fear of criticism, disapproval, or includes ambulatory schizophrenia and pseudoneu- rejection. rotic schizophrenia, which were earlier thought to Associated features may include hyper sensitivity be subtypes of schizophrenia. Psychodynamically, to rejection and criticism. These patients do not enter splitting is the primary defense mechanism employed into inter personal relationships unless they are very in borderline perso nality disorder. sure of uncritical approval. This disorder is an epitome There is a considerable overlap between border- of what is often called as inferiority complex. Under- line, narcissistic and antisocial (dissocial) personality standably, secondary depression is very com mon. disorders (they belong to the same Cluster of per- Treatment sonality disorders, i.e. Cluster B). Major depressive 1. Individual psychotherapy. episodes occur commonly in this disorder. 2. Group psychotherapy. Treatment 3. Behaviour therapy: In particular, social skills 1. Psychoanalysis or psychoanalytical psycho- training and assertiveness training are useful. therapy. 4. CBT: The focus is on negative thoughts and nega- 2. Supportive psychotherapy. tive self-appraisal. 118 A Short Textbook of Psychiatry

Dependent Personality Disorder others submit to exactly their way of doing things, According to ICD-10, the diag nostic guidelines for and intrusion of insistent and unwelcome thoughts dependent personality disorder include the following or impulses. features. Clear evidence is usually required of the pres- This disorder is more often diagnosed in males, ence of at least three of six traits or behaviours given in and is common in premorbid personality of patients the clinical description. These include allowing others with obsessive compulsive disorder. Major depres- to make decisions for them, subordination of one’s sive episodes are frequent. Psychodynamically, this own needs to those of others and undue compliance disorder is believed to result from fi xation at the anal with their wishes, unwillingness to make even reason- sadistic phase, with the employment of reaction for- able demands on the people one depends on, feeling mation as a defense mechanism. uncomfortable or helpless when alone, preoccupation Treatment with fears of being abandoned by a person with whom These patients usually retain insight, and hence seek one has a close relationship, and limited capacity to psychiatric help on their own. make everyday decisions without an excessive amount 1. Psychoanalysis or psychoanalytical psychotherapy. of advice and reassurance from others. 2. Group psychotherapy. Associated features may include perceiving oneself as helpless, incompetent, and lacking stamina. Passive-Aggressive Personality Disorder There may be an overlap with avoidant and passive- This disorder is not listed as a personality disorder in aggressive personality disorders. Some patients both ICD-10 and DSM-IV-TR, though it is listed in exhibit masochistic character. They repetitively DSM-IV-TR under the section on ‘Criteria provided establish close interpersonal relationships which result for further study’. It is characterised by the following in punishment. clinical features: Treatment 1. Signifi cant and persistent passive resistance to 1. Individual psychotherapy. demands for adequate social and occupa tional 2. Group psychotherapy. performance. 3. Behaviour therapy (such as asserti veness training 2. Stubbornness, intentional ineffi ciency, pro cras ti- and social skills training) is often useful. nation, unjustifi ed protests, ‘forget fulness’ and/or 4. CBT: The focus is on negative thoughts and nega- dawdling are used to achieve the purpose. tive self-appraisal. Passive resistance is viewed as an expression of ‘covert anger’ or ‘ retrofl exed anger’. This behaviour Obsessive-Compulsive (Anankastic) is often ‘chosen’ in spite of the fact that a more direct Personality Disorder and active way of showing an opinion and/or resisting According to ICD-10, the dia gnostic guidelines for was possible. An overlap with dependent personality anankastic personality disorder include the following disorder is common. Secondary depression may clinical features. Clear evidence is usually required develop. of the presence of at least three of eight traits or Treatment behaviours given in the clinical description. These 1. Supportive psychotherapy. include feelings of excessive doubt, preoccupation 2. Behaviour therapy: Social skills training and with details, perfectionism that interferes with task assertiveness training are helpful. com pletion, excessive conscientiousness, excessive 3. Group therapy. pedantry and adherence to social conventions, rigid- 4. Drug therapy: Antidepressants may be needed for ity and stubbornness, unreasonable insistence that secondary depression. Disorders of Adult Personality and Behaviour 119

ENDURING PERSONALITY CHANGES, Trichotillomania (compulsive hair-pulling) is NOT ATTRIBUTABLE TO BRAIN characterised by noticeable hair loss caused by per- DAMAGE AND DISEASE son’s persistent and recurrent failure to resist impulses This new category in ICD-10 includes disorders of to pullout hair. There is an intense urge to pull out hair adult personality and behaviour which develop fol- with mounting tension before the act and a sense of lowing catastrophic or excessive prolonged stress, or relief afterwards. There is no pre-existent skin lesion following a severe psychiatric illness, in people with or infl ammation, and hair pulling is not secondary to no personality disorder. The presence of brain damage any delusion or hallucination. or disease which may cause similar clinical features The management of impulse control disorders should be ruled out. consists of behaviour therapy (e.g. aversion therapy), cognitive behaviour therapy (CBT), individual psy- HABIT AND IMPULSE DISORDERS chotherapy, and occasionally pharmacotherapy (e.g. carbamazepine for intermittent explosive disorder; This category includes disorders such as patholo gical fl uoxetine for trichotillo mania). gambling, pyromania, kleptomania, tricho tillomania, and intermittent explosive disorder. The disorders GENDER IDENTITY DISORDERS in this heterogeneous group are characterised by impulsive behaviour which the patient cannot resist or These disorders of adult personality and behaviour control. There may be a feeling of release of tension by are discussed in detail in Chapter 10. doing the act and a feeling of guilt after the act is over. Pathological gambling is characterised by two or DISORDERS OF SEXUAL PREFERENCE more episodes of gambling per year which have no profi table outcome, but are continued despite personal These disorders of adult personality and behaviour distress and interference with personal functioning in are discussed in detail in Chapter 10. daily living. The person has an intense urge to gamble which is diffi cult to control and cannot stop gambling PSYCHOLOGICAL AND BEHAVIOURAL by effort of will. Preoccupation with thoughts or DISORDERS ASSOCIATED WITH SEXUAL mental images of gambling and situations surrounding DEVELOPMENT AND ORIENTATION gambling is often present. Pyromania (pathological fi re-setting) is charac- These disorders of adult personality and behaviour terised by two or more acts of fi re-setting without an are discussed in detail in Chapter 10. apparent motive. There is an intense urge to set fi re to objects, with a feeling of tension before the act and a FACTITIOUS DISORDER sense of relief afterwards. There is often a preoccupa- (MUNCHAUSEN SYNDROME) tion with thoughts or mental images of fi re-setting and situations surrounding fi re-setting. Munchausen syndrome (also known variously Kleptomania (pathological stealing) is charac- as hos pital addiction, hospital hoboes, or profes- terised by two or more thefts, in which there is stealing sional patients) is used for those patients who without apparent motive of personal gain or gain for repeatedly simulate or fake diseases for the sole another person. There is an intense urge to steal, with purpose of obtaining medical attention. There is no a feeling of tension before the act and a sense of relief other recogni sable motive (hence, it is different from afterwards. malingering). 120 A Short Textbook of Psychiatry

Factitious disorders can present with predomi- The cause is not clear. Probably these patients are nantly physical signs and symptoms, or psychological masochistic, seek dependency from a father-fi gure signs and symptoms, or combined signs and symptoms. (e.g. the physician), attempt to manoeuvre control The patients distort their clinical histories, laboratory over the father-fi gure and see the surgical procedure tests’ reports, and even facts about other aspects of as partial suicide. The early childhood of these patients is characterised by deprivation and neglect. their lives ( pseudologia fantastica). Sometimes, they The prognosis is usually poor and treatment often distort physical signs by self-infl icted injuries and unsuccessful. secondary infections. Drug abuse, especially abuse Certain points must be kept in mind by the physi- of prescription drugs, is common. cian (or surgeon), after the diagnosis has been made. These patients often have a detailed though These include: superfi cial knowledge of many medical terms and 1. Avoid the feelings of anger, hostility and ridicule procedures. Evidence of earlier treatment, usually which are aroused by the discovery of factitious surgical procedures, is often available in the form i llness. of multiple scars (e.g. ‘grid-iron abdomen’). These 2. Patients should not be confronted or labelled as liars. Instead, a psychiatric or psychological con- patients are often manipulative and convincingly tell sultation should be sought, as these patients may lies, create problems in the inpatient setting and often need help. leave against medical advice, usually after the surgical 3. Of course, the unnecessary surgical proce dure(s) procedure has been performed. should not be carried out. 10 Sexual Disorders

The sexual disorders can be classiﬁ ed into four main 1. Normal anatomic sex. types: 2. Persistent and signiﬁ cant sense of discomfort 1. Gender identity disorders. regarding one’s anatomic sex and a feeling that it 2. Psychological and behavioural disorders asso- is inappropriate to one’s perceived-gender. ciated with sexual development and matura tion. 3. Marked preoccupation with the wish to get rid of 3. Paraphilias (disorders of sexual prefe rence). one’s genitals and secondary sex characteristics, 4. Sexual dysfunctions. and to adopt sex characteristics of the other sex In ICD-10, gender identity disorders, disorders of (perceived-gender). sexual preference, and sexual development and orien- 4. Diagnosis is made after puberty. tation disorders are listed under the disorders of adult Transexualism is of two main types: Primary and persona lity and behaviour, while sexual dysfunctions secondary. (not caused by organic disorder or disease) are listed under the behavioural syndromes associated with Primary Transexualism physiolo gical disturbances and physical factors. This condition has an onset in early childhood and has a stable course over time. This is a rela tively GENDER IDENTITY DISORDERS homogeneous category. Primary transexuals, more than secondary tran se xuals, are pre oc cupied with These disorders are characterised by disturbance in sex-change or sex-reassign ment surgery. There are gender identity, i.e. the sense of one’s masculinity or two main types: femininity is disturbed. This group includes: i. Male (or, male-to-female) primary transexua- 1. Transexualism: Male and female; primary and lism. secondary. ii. Female (or, female-to-male) primary transexua- 2. Gender identity disorder of childhood. lism. 3. Dual-role transvestism. 4. Intersexuality. Secondary Transexualism In contrast to the primary type, secondary transexu- Transexualism alism usually has an onset later in life. This is a Transexualism, the severest form of gender iden tity less severe and more heterogeneous category. The disorders, is characterised by the following clinical only common feature is a wish to change the ana- features: tomic sex. 122 A Short Textbook of Psychiatry

This category includes effeminate homo sexuals, The methods include: transvestites who secondarily become transexuals i. Psychotherapy. and others. A majority of these patients are male ii. Behaviour therapy. (or, male-to-female) transexuals. The prevalence of Sex-change to the Desired Gender transexualism is 1:100,000 in males and 1:400,000 This procedure is known as sex reassignment in females. surgery (SRS). The first procedure was done in 1951 (Denmark) on an American soldier, George Differential Diagnosis Jorgensen who become Christine Jorgensen after Differential diagnosis is from the following condi- SRS. The fi rst female-to-male SRS was performed tions: in 1956. Transvestism (Fetishistic Transvestism) The procedures include hormonal treat ment, phal- Transvestism (or fetishistic cross-dressing) is the loplasty, castration, mastectomy, and hys terectomy wearing or using of clothes traditionally of the other with salpingo-ophorectomy, which have been used in gender (cross-dressing), for the purpose of sexual different combinations. The proce dure is performed excitement. This is almost exclusively seen in males. more often in primary tran sexuals. In contrast, transexuals wear clothes of other sex, As SRS is an almost irreversible process, the fol- because they feel a part of the other sex and, not for lowing steps are taken before assigning a patient to sexual excitement. surgery: Cross-gender Homosexuality 1. The diagnosis of primary, stable, long-stan ding Effeminate male homosexuals and masculine female transexualism is confi rmed. homosexuals sometimes cross-dress and occasionally 2. A possibility of stress-induced transexua lism is want a sex-change (called pseudo-transexualism ). But considered and eliminated. unlike true primary transexualism, these patients do 3. The patient has to undergo psychotherapy for at not feel a part of the other sex and always acknowl- least 3-6 months preoperatively. edge them selves as homosexuals (This is in contrast 4. Experimental trial in the new gender role pre- to tran sexualism. For example, a male transexual operatively, to assess patient’s ability to adjust in who feels like a female, even if he has a homo sexual the ‘new’ role. relationship with another male, justifi es it as hetero- 5. The limitations of SRS should be explained, e.g. sexual because ‘he himself feels like a female’), and infer tility, nonfunctional testes, etc. seek sex-change only rarely, to rationalise or justify The success rate in carefully planned SRS can their primary homosexual behaviour. be up to 80-90%. Postoperative psycho therapy is of utmost importance in prevention of psychiatric mor- Treatment bidity. The treatment can aim at two opposite ends by either making the person reconcile with the anatomic sex, Dual-role Transvestism or arrange sex-change to the desired gender. Dual-role transvestism is characterised by wearing Reconciliation with the Anatomic Sex of clothes of the opposite sex in order to enjoy the There are only occasional reports of achieving this temporary experience of membership of the opposite purpose in primary transexuals. How ever, in second- sex, but without any desire for a more permanent sex ary transexuals, this method may be more effective change (unlike tran sexualism). No sexual excitement and should be employed fi rst if possible though this accompanies the cross-dressing (unlike in fetishis tic decision is best made by the patient. trans vestism). Sexual Disorders 123

Gender-identity Disorder of Childhood homosexual, or bisexual) causes signifi cant distress This is a disorder similar to transexualism, with a very to the individual or distur bances in the relationships. early age of onset (2-4 years of age). This is charac- It is important to remember that any type of sexual terised by the following clinical features: orientation by itself is not a disorder unless it causes 1. Persistent and signifi cant desire to be of the other distress or disability. gender, or insistence on being of the other gender. 2. Marked distress regarding the anatomic sex, with Sexual Maturation Disorder strong denial of anatomic sex (in contrast, there This disorder usually begins in adolescence and is is no denial of anatomic sex in transexualism). characterised by uncertainty regarding the gender 3. Involvement in traditional activities, games and identity or sexual orientation (heterosexual, homo- clothing pattern of the perceived gender. sexual, or bisexual). This uncer tainty often leads to 4. Onset before puberty. anxiety and depression. Sometimes, this disorder Although a majority of primary transexuals have arises for the time in an individual after a period of gender-identity disorder of childhood in their past apparently stable sexual orientation. history, only a very few of the children with gender- identity disorder, in prospective studies, actually Egodystonic Sexual Orientation develop transexualism. In this disorder, the sexual orientation is clear. How- Treatment ever, the individual wishes to change the orientation Treatment of gender identity disorders is similar to because of the associated distress and/or psychological transexualism. When the anatomic sex and the gender- symptoms. This dis or der is seen most commonly in identity are opposing, decision on treatment should be homosexuality. based on the gender-identity of the patient. Homosexuality Inter-sexuality Homosexuality, in contrast to hetero sexuality, is the The patients with this disorder have gross anatomical sexual relationship between persons of the same sex. and/or physiological aspects of the other sex. These This is a disorder only when it is the predominant, aspects can be in: signifi cant and persistent mode of sexual relationship 1. External genitals, e.g. pseudo-hermaphroditism. for that person and it is ego-dystonic (causes signifi - 2. Gonads, e.g. ovotestes. cant distress to the individual). 3. Internal sex organs, e.g. true hermaphro dite. It is obviously of two types: Male homo sexuality, 4. Hormonal disturbances, e.g. testicular femi- and female homosexuality. Female homosexuals are nisation syndrome, congenital adrenal hypo- also called as lesbians or sapphic after Sappho, a plasia. female homosexual who lived on the Isle of Lesbos 5. Chromosomes, e.g. Turner’s syndrome, in ancient Greece, while male homosexuals are called Klinefelter’s syndrome. gay. The prevalence of homosexuality (in USA) is PSYCHOLOGICAL AND BEHAVIOURAL 4-6% of males and 1-2% of females. Another 5-10% DISORDERS ASSOCIATED WITH SEXUAL may show bisexual orientation. Homosexual behav- DEVELOPMENT AND MATURATION iour can be divided into the following types: 1. Obligatory homosexuality Disorders of sexual development and maturation in- • Only homosexuality clude disorders where sexual orientation (heterosexual, • No heterosexuality. 124 A Short Textbook of Psychiatry

2. Preferred homosexuality 1. For seeking a Change in Sexual Orientation • Predominant homosexuality The methods employed include: • Occasional heterosexuality. i. Psychoanalytic psychotherapy (espe cially when 3. Bisexuality associated with personality issues). • Almost equal homosexuality and hetero- ii. Behaviour therapy: Aversion therapy (rarely sexuality. used), covert sensitisation, systematic desen- 4. Situational homosexuality sitisation (especially if there is a phobia of • Predominant heterosexuality hetero sexual relationship). • Occasional homosexuality. iii. Supportive psychotherapy. 5. Latent homosexuality iv. Androgen therapy (occasionally). • Only heterosexuality 2. For Seeking Removal of Distress Only • Fantasies of homosexuality. The following methods may be useful: Last few decades have seen a raging controversy i. Psychotherapy: Psychoanalytic and suppor tive, on whether homosexuality is a normal phenomenon depending on the personality character. or a psychiatric disorder. At fi rst, homosexuality was ii. Drug therapy: Antidepressants and/or benzodi- divided into two types (DSM-III, 1980): azepines can be used for treatment of associated 1. Ego-syntonic homosexuality (no distress about depression and anxiety. homosexual behaviour). 3. Referred by Others 2. Ego-dystonic homosexuality (associated with The decision regarding treatment for this group is marked distress), and only ego-dystonic type was highly debatable. The opinions range from ‘no treat- called abnormal. ment at all’ to ‘treatment as early as possible’. The fi nal Later (DSM-III-R, 1987), homosexuality was approach depends on the sociocultural background of completely dropped from the psychiatric nomencla- the patient and the viewpoint of the therapist. ture, under social and political pressure. DSM-IV- The current viewpoint is that the individuals TR does not list homo sexuality as a disorder, while should be informed regarding sexuality and sexual ICD-10 only mentions homosexuality under ego- orientation in as much detail as they wish and the fi nal dystonic sexual orien tation. decision of choosing the sexual orientation should be Treatment left to the individual. Obviously, further treatment Some people with homosexual orientation, who have would depend on that fi nal choice. The individual’s signifi cant distress about their homo sexual orientation motivation and presence of signifi cant distress are and themselves seek psychiatric help, should be important factors in therapy. offered treatment. At present, the treatment is generally offered under Sexual Relationship Disorder the following conditions only. The gender identity disorder or disorder of sexual 1. Self-referral by a person with homosexual orienta- preference leads to diffi culties in estab lishing and/or tion, for seeking a change in the sexual orientation maintaining sexual relation ships. In such a case, both towards heterosexuality. diagnoses should be made. 2. Self-referral by a person with homosexual orientation, for remo val of distress associated with PARAPHILIAS ( DISORDERS OF SEXUAL homosexuality but not for a change in sexual PREFERENCE) orientation. 3. Referred by parents, relatives or signifi cant others. Paraphilias ( sexual deviations; perversions) are However, treatment can generally be offered only disorders of sexual preference in which sexual arousal if the individual seeks help. occurs persistently and signifi cantly in response to Sexual Disorders 125 objects which are not a part of normal sexual arousal although this is not essential. The methods used range (e.g. nonhuman objects; suffering or humiliation of from restraining by tying, beating, burning, cutting, self and/or sexual partner; children or nonconsenting stabbing, to rape and even killing. person). These disorders include: Fetishism; fetishis tic Sexual Masochism transvestism; sexual sadism; sexual maso chism; This is just the reverse of sexual sadism. Here the per- exhibitionism; voyeurism; frotteurism; pedo philia; son (the ‘masochist’) is sexually aroused by phy sical zoophilia ( bestiality); and others. and/or psychological humiliation, suffering or injury infl icted on self by others (usually ‘sadists’). Most Fetishism often the masochist is a female though any pattern is In fetishism, the sexual arousal occurs either solely possible. The methods used are the same as the ones or predominantly with a nonliving object, which is used in sexual sadism. Only there is a role reversal. usually intimately associated with the human body. To be called a disorder, this should be a persistent The word fetish means magical, i.e. the nonliving and signifi cant mode of sexual arousal in the person. object ‘magically’ becomes phallic for that person. Sexual sadism and sexual masochism are often seen This disorder is almost exclusively seen in males. in the same individual and are on a conti nuum; there- The fetish object may include shoes, gloves, bras, fore they are classifi ed together as sadomasochism in underpants, stockings, etc. ICD-10. Fetishism is not diagnosed if the sexual object is the wearing of clothes of opposite sex (fetishistic Exhibitionism transvestism), the use of a human body part (mastur- Exhibitionism is a persistent (or recurrent) and bation), or the use of a genital-stimulating object (e.g. signifi cant method of sexual arousal by the exposure vibrator). Fetishism is very often associated with of one’s genitalia to an unsuspecting stranger. mastur bation. This is often followed by masturbation to achieve orgasm. The disorder is almost exclusively seen in Fetishistic Transvestism males, and the ‘unsuspecting stranger’ is usually a This disorder occurs exclusively in heterosexual female (child or adult). males. The person actually or in fantasy wears clothes of the opposite sex (cross-dres sing) for sexual arousal. Voyeurism This disorder should be differentiated from dual-role This is a persistent or recurrent tendency to observe transvestism and transexualism. unsuspecting persons (usually of the other sex) naked, This disorder may be associated with fantasies of disrobing or engaged in sexual activity. other males approaching the person who is in a female This is often followed by masturba tion to achieve dress. Masturbation or rarely coitus is associated orgasm without the observed person(s) being aware. with cross-dressing to achieve orgasm. To be called This is almost always seen in males. Watching por- a disorder, this should be a per sistent and signifi cant nography is not included here. mode of sexual arousal in the person. Frotteurism Sexual Sadism This is a persistent or recurrent involvement in the In this disorder, the person (the ‘sadist’) is sexually act of touching and rubbing against an unsuspecting, aroused by physical and/or psycho logical humiliation, nonconsenting person (usually of the other sex). suffering or injury of the sexual partner (the ‘victim’). Frottage is often employed in crowded places, e.g. Most often the person infl icting the suffering is male, buses, where the victim does not protest because she 126 A Short Textbook of Psychiatry cannot suspect that frottage can be com mitted there. 4. Other treatments: Castration and psychosurgery This is often seen in adolescent males. are extremely rare choices these days.

Paedophilia SEXUAL DYSFUNCTIONS Paedophilia is a persistent or recurrent involvement of an adult (age >16 years and at least 5 years older than Sexual dysfunction is a signiﬁ cant disturbance in the the child) in sexual activity with prepubertal children, sexual response cycle, which is not due to an underly- either heterosexual or homosexual. ing organic cause. This may be associated with sexual sadism. To understand sexual dysfunction, a brief outline The paedophilic behaviour may be either limited to of normal human sexual response cycle is in order incest or may spread to children outside the family. (Table 10.1). In the light of normal human sexual In most civilised societies, paedophilia is a serious response cycle, it is easier to understand sexual dys- offense and the convicted paedophile’s name remains functions. on a sex offenders’ register in order to protect the The common dysfunctions include the following: society. Disorders of Appetitive Phase Zoophilia ( Bestiality) (Sexual Desire Disorders) Zoophilia as a persistent and signiﬁ cant involvement Hypoactive sexual desire disorder in sexual activity with animals is rare. Occasio nal or This disorder is characterised by an absence of fanta- situational zoophilia is much more common. sies and desire for sexual activity which is not secondary to other sexual dysfunctions, such as premature Other Paraphilias ejaculation or dyspareunia. Lack or diminution of These include sexual arousal with urine ( urophi lia); sexual desire does not imply an inability to experience faeces (coprophilia); enemas (klismaphilia); corpses sexual pleasure; it makes the initiation of sexual act ( necrophilia), among many others. less likely. This disorder is many times more common in Treatment females (previously called as frigidity) and its preva- 1. Psychoanalysis and psychoanalytic psycho- lence increases with age. The contributing factors may therapy: This is of particular help if the patient is include fear of pregnancy, unsatisfactory past sexual psychologically minded and has good ego strength experiences, marital disharmony, or fatigue. If the dis- for therapy. order is secondary to biological factors (such as drugs, 2. Behaviour therapy: Aversion therapy is the treat- chronic medical illnesses), it should be listed under ment of choice in severe, distressing paraphilia, ‘sexual disorders due to a general medical condition’. with the patient’s consent. Sexual aversion disorder and lack of sexual 3. Drug therapy: Antipsychotics have sometimes enjoyment disorder been used for severe or dangerous aggression In the sexual aversion disorder, there is an aversion associated with paraphilias. Benperidol was earlier to and avoidance of all sexual activity with a sexual believed to be particularly useful but the claim partner. The thought of sexual interaction is associ- has not been substantiated, and the drug is not ated with negative feelings and causes anxiety. The available in the market. Antiandrogens ( cyprot- contributing factors may include history of sexual erone acetate or medroxy-progesterone acetate) abuse/molestation (especially in childhood), unsatis- can be used in paraphilias with excessive sexual factory past sexual experiences, or culturally induced activity. negative feelings towards sexual matters. Sexual Disorders 127

Table 10.1: Normal Human Sexual Response Cycle A normal human sexual response cycle can be divided The duration of this phase may last from half to into fi ve phases: several minutes. 1. Appetitive Phase: The phase before the actual sexual 4. Orgasmic Phase: The phase with peak of sexual ex- response cycle. This consists of sexual fantasies and citement followed by release of sexual tension, and a desire to have sexual activity. rhythmic contractions of pelvic reproductive organs. 2. Excitement Phase: The fi rst true phase of the cycle, The important changes are as follows: which starts with physical stimulation and/or by Males: 4-10 contractions of penile urethra, prostate, appetitive phase. The major changes during this vas, and seminal vesicles; at about 0.8 sec intervals; phase are: autonomic excitement becomes marked in this Males: Penile erection, due to vasocongestion of phase. Doubling of pulse rate and respiratory rate, corpus cavernosa; elevation of testes with scrotal sac. and 10-40 mm increase in systolic and diastolic BP Females: Lubrication of vagina by a transudate; erec- occur; ejaculatory inevitability precedes orgasm; tion of nipples (in most women); erection of clitoris; Ejaculatory spurt (30-60 cm; decreases with age); thickening of labia minora. contractions of external and internal sphincters. The duration of this phase is highly variable and may Females: 3-15 contractions of lower 1/3rd of vagina, last for several minutes (or longer). cervix and uterus; at about 0.8 sec intervals. No 3. Plateau Phase: The intermediate phase just before contractions occur in clitoris; autonomic excitement actual orgasm, at the height of excitement. It is often becomes marked in this phase. Doubling of pulse diffi cult to differentiate the plateau phase from the rate and respiratory rate, and 10-40 mm increase excitement phase. The following important changes in systolic and diastolic BP occur; contractions of occur during this phase: external and internal sphincters. Males: Sexual fl ush (inconsistent); autonomic hy- The duration of this phase may last from 3-15 sec- peractivity; erection and engorgement of penis to onds. full size; elevation and enlargement of testes; dew 5. Resolution Phase: This phase is characterised by the drops on glans penis (2-3 drops of mucoid fl uid with following common features in both sexes: A general spermatozoa). sense of relaxation and well-being, after the slight Females: Sexual fl ush (inconsistent); Autonomic hy- clouding of consciousness during the orgasmic phase; peractivity; retraction of clitoris behind the prepuce; disappearance of sexual fl ush followed by fi ne per- development of orgasmic platform in the lower 1/3rd spiration; gradual decrease in vasocongestion from of vagina, with lengthening and ballooning of vagina; sexual organs and rest of the body; refractory period enlargement of breasts and labia minora; increased for further orgasm in males varies from few minutes vaginal transudate. to many hours; there is usually no refractory period in females.

In the lack of sexual enjoyment disorder ( sexual Disorders of Excitement and Plateau anhedonia), the sexual response is usually normal Phase ( Sexual Arousal Disorders or (which may include a normal orgasm). However, there Failure of Genital Response) is a feeling of lack of subjective sexual pleasure. This Male erectile disorder ( Impotence; Erectile disorder is more common in females. dysfunction) Excessive sexual drive This disorder is characterised by an inability to have Rarely, both men ( satyriasis) and women ( nympho- or sustain penile erection till the completion of sat- mania) may complain of excessive sexual drive as a isfactory sexual activity. It is a relatively common problem. disorder. 128 A Short Textbook of Psychiatry

Table 10.2: Physical Causes of Male Erectile Although a large number of physical disorders Disorder/Impotence have been aetiologically incriminated in the causation of male erectile disorder, some important ones I. Local Genital Pathology are mentioned below. If the disorder is secondary to 1. Priapism biological factors (such as drugs, chronic medical 2. Congenital malformations illnesses), it should be listed under ‘sexual disorders 3. Surgical procedures on pelvic region, e.g. peri- due to a general medical condition’ (Table 10.2). neal prostatectomy Since many drugs impair the normal sexual 4. Mumps functioning and often cause more than one sexual 5. Elephantiasis dysfunction, these are listed separately in Table 6. Hydrocele or varicocele. II. Endocrine Disorders 10.3. The secondary sexual dysfun ction is usually 1. Diabetes mellitus more profound in males. In cases of male erectile 2. Dysfunction of pituitary-adrenal-testis axis dysfunction where bio logical causes have been ruled 3. Testicular atrophy, e.g. secondary to cirrhosis, out, psy cho logical factors should be considered in dystrophia myotonica, haemochromatosis causation. 4. Thyroid dysfunction. Psy cho logical impotence usually occurs acutely. III. Neurological Disorders The early morning erections and erec tions during 1. Autonomic neuropathy, e.g. in diabetes mellitus REM sleep (nocturnal penile tumescence; NPT) are 2. Spinal cord lesions, e.g. transverse myelitis usually preserved. These psychological factors may 3. 3rd ventricle tumours include one of the following conditions. 4. Brain damage, especially in temporal lobe 1. Ignorance regarding the sexual act. 5. Multiple sclerosis. 2. Fear of failure and performance anxiety (e.g. dur- IV. Cardiovascular Disorders ing ‘honeymoon’). 1. Leriche syndrome. 3. Interpersonal diffi culties between the sexual part- V. Any Severe or Debilitating Systemic Illness ners (e.g. marital confl ict). VI. Alcohol and Drugs. 4. Anxiety disorder. 5. Mood disorder. Female sexual arousal disorder 6. Masturbatory anxiety (and ‘dhat syndrome’ in This disorder is characterised by subjective as well as India). objective lack of sexual arousal in the form of lack of 7. Fatigue (e.g. after the day’s hard work). lubrication or vaginal dry ness. 8. Fear of pregnancy, or sexually transmit ted disease. The causes can be biological (e.g. postmeno- 9. Fear of ‘damaging’ the sexual partner or one-self. pausal) or psychological (uncommon). 10. Certain environmental factors (e.g. lack of pri- vacy). Disorders of Orgasmic Phase 11. Lack of a consistent sexual partner. (Orgasmic Disorders/Dysfunctions) 12. Fear of commitment (in premarital and extra- Male orgasmic disorder (Male a norgasmia) marital sexual relationships). Failure or marked diffi culty to have orgasm, despite 13. Poor self-image or ‘inferiority complex’. normal sexual excitement, during coitus. An uncom- 14. Sexual abuse in childhood. mon disorder, it often presents as retarded ejacula- In many cases of erectile dysfunction, aetiology tion. The causes can be biological (e.g. post-prostate can be mixed (i.e. both organic as well as psychogenic surgery, drug-induced) or psychological (e.g. marital factors can be present). confl icts). Sexual Disorders 129

Table 10.3: Sexual Dysfunctions Caused by Drugs Drugs Effect on Effect on Effect on Sexual Desire Erectile Function Ejaculation I. Antihypertensives 1. Methyldopa Inhibited Impaired Impaired 2. Clonidine — Impaired Impaired 3. Propranolol Inhibited Impaired — 4. Thiazide diuretics — Impaired — 5. Spironolactone Inhibited Impaired Impaired 6. Guanethidine — Impaired Impaired; Retrograde ejaculation 7. Hexamethonium — Impaired Impaired; Retrograde ejaculation II. Hormonal Preparations 1. Corticosteroids Inhibited Impaired Impaired 2. Oestrogens Inhibited (in males) Impaired Impaired 3. Androgens Increased (in both sexes) III. Psychotropic Medications 1. Tricyclic antidepressants +/– Impaired Impaired and MAO inhibitors 2. SSRI antidepressants +/– Impaired Delayed ejaculation (e.g. paroxetine, fl uoxetine) 3. Thioridazine Inhibited Impaired Retrograde and Delayed ejaculation 4. Chlorpromazine Inhibited Impaired — 5. Haloperidol — Impaired — 6. Trazodone — Priapism — 7. Barbiturates and Increased (with low dose, Impaired (with Impaired (with high benzodiazepines due to decrease in anxiety) high dose) dose) Decreased (with high dose) 8. Lithium — Impaired — 9. Disulfi ram — — Delayed ejaculation IV. Psychoactive Substance Use 1. Alcohol Increased (with low dose) Impaired Impaired 2. Opiates and cocaine Inhibited Impaired (with Impaired high dose) V. Others 1. Anti-infl ammatory drugs Inhibited Impaired — (e.g. indomethacin) 2. L-dopa Inhibited — — 3. Anticholinergic drugs — Impaired Impaired (e.g. trihexiphenidyl) 130 A Short Textbook of Psychiatry

Female orgasmic disorder (Female anorgasmia) being inadequate either in focus, intensity or dura- Failure or marked diffi culty to have orgasm, despite tion, a diagnosis of excitement and orgasmic phase normal sexual excitement, during coitus. This is a very disorders is not made. common disorder. Anorgasmia can be either primary or secondary. Diagnosis and Differential Diagnosis Although the disorder causes marked distress, it is Before making a diagnosis of sexual dysfunction, it rarely complained of in the clinical setting, particularly is of paramount importance to rule out an underlying in India. This is probably due to cultural factors. physical cause, which would need treatment. The causes can be biological (e.g. endocrinal Although the diagnosis is clinical, a detailed physi- disorders such as hypothyroidism, drug-indu ced) or cal examination and laboratory investiga tions (e.g. psychological (e.g. marital confl icts). blood counts, blood sugar, liver function tests, thyroid Premature ejaculation function tests, hormonal profi le, and rarely, routine This disorder is defi ned as ejaculation before the examination and culture of prostatic fl uid) coupled completion of satisfactory sexual activity for both with a good history is a must in every patient to rule partners. In severe cases, it is characterised by ejacu- out an underlying physical cause. lation either before penile entry into vagina or soon Certain laboratory techniques (e.g. penile plethys- after penetration. It is a very common disorder in the mograph, penile tumescence moni toring during sleep) clinical setting. may help in differentia ting organic and nonorganic The causes can be biological (relatively uncom- sexual dysfunc tions. If NPT ( nocturnal penile mon) or psychological (e.g. performance anxiety). tumescence) is abnormal, then ancillary investigations such as penile vascular investigations (e.g. penile pulse Sexual Pain Disorders pressure, penile Doppler, duplex ultrasono graphy, Nonorganic vaginismus diagnostic intracavernosal vasoactive substance-papa- This disorder is characterised by an involuntary spasm verine injection test, arteriography, DICC-dynamic of the lower 1/3rd of vagina, interfering with coitus. infusion cavernosomatogram and cavernosogram, Penile entry is either painful or impos sible. and cavernosography) and penile neurological inves- Before a presumption of nonorganic vagi nis mus, tigations (e.g. penile sensory threshold test or penile it is important to rule out organic factors (e.g. local biothesiometry) may be employed. pathology causing pain). Though searching for an organic factor responsible Nonorganic dyspareunia for the sexual dysfunction is very important, a large This disorder is characterised by pain in the genital majority of dysfunctions are psychosexual in nature. area of either male or female, during coitus. Before a A detailed sexual and personal history is important presumption of nonorganic dyspareunia, it is particu- in fi nding out the underlying causes. The common larly important to rule out organic factors (e.g. local psychological causes of sexual dysfunction have been pathology causing pain) in both males and females. discussed earlier. It should be specifi ed whether the sexual dysfunc- Sexual Disorders Due to a General tion is psychogenic alone or biogenic factors co-exist; Medical Condition whether the dysfunction is life-long or acquired; and The disorders listed above may occur secondary to a whether the dys function is situational or generalised. general medical condition; they should then be coded here. These dysfunctions are called disorders only Treatment when they occur recurrently and persistently. Also if The treatment usually consists of one or more of the the sexual dysfunction is due to sexual stimulation following methods: Sexual Disorders 131

1. Treatment of the underlying physical or psychiatric ii. Round-table discussions aiming at: disorder, if present. a. Education about normal sexuality. 2. Psychoanalysis: This is particularly indicated when b. Understanding of the couple’s current sexual the dysfunc tion is more pervasive and involves person- problem(s). ality diffi culties. The goal is not symptom removal but c. Enhancing communication between the part- is resolution of the underlying unconscious confl icts. ners regarding sexual matters. 3. Hypnosis : Hypnosis can be used either alone or in iii. Behaviour modifi cation steps, depending on the con junction with other therapies aiming at symp tom type of psychosexual dysfunction. removal. However, only suggestible patients can be Brief examples of the techniques used are: hypnotised. a. Sensate focus technique: This is used particularly 4. Group psychotherapy : Patients of same sex with for treatment of impotence, although it is also different sexual problems or of both sexes with similar useful in management of other dysfunctions as sexual pro blems can be treated in group therapy well. The aim is to ‘discover’ on body (exclud- sessions. The focus is usually on providing education ing genital area) ‘sensate focuses’ (body areas regarding normal sexuality and to remove anxiety where manipulation leads to sexual arousal). or guilt by sharing viewpoints in a group setting. This is usually a general exercise before any Although occasionally used alone, it is more helpful sex therapy. as an adjunct to other methods of treatment. b. Squeeze technique ( Seman’s technique): This 5. Behaviour therapy: The methods commonly em- has been used in treatment of premature ejacu- ployed include the following: lation. The female partner is asked to manually i. Relaxation training, e.g. Jacobson’s pro gressive stimulate the penis causing erection. When the relaxation technique. male partner experiences ‘ ejaculatory inevita- ii. Assertiveness training. bility’, the female partner ‘squeezes’ the penis iii. Systematic desensitisation, aimed at reducing on the coronal ridge thus delaying ejaculation. the phobic anxiety related to the sexual act, e.g. There are similar simple techniques (such as in sexual aversion disorder. orgasmic conditioning, desensitisation) for treatment iv. Biofeedback, using a penile plethysmo graph. of other psychosexual dysfunc tions. The response 6. Masters’ and Johnson’s technique: This is one of the rate is close to 80%, with maximum success in the most popular and successful methods of treatment for treatment of premature ejaculation. psychosexual dysfunctions. The patient is not treated 7. Oral drug therapy: Till very recently, this was rarely alone, but both the partners are treated together. This a treatment of fi rst choice in sexual dysfunctions. is called as dual-sex therapy, where both the sexual Current indications of drug treatment include: partners are treated by a team of therapists (one male i. Treatment of underlying psychiatric disorder. and one female), although later modifi cations of this ii. Intense anxiety related to sexual activity may technique use only one therapist. require use of low dose benzodia zepines (such The goal of the treatment is symptom removal, as alprazolam) for a very limited period (to using simple behavioural techniques. The couple is prevent benzodiazepine misuse or dependence). usually seen on a weekly basis; however, the sessions iii. Premature ejaculation may sometimes require can be more frequent if the couple is encountering treatment with fl uoxetine, trazodone, or tricyclic particular diffi culties during treatment. Some common antidepressants such as clomipramine (to retard steps before starting therapy include: ejaculation). i. Detailed history taking (sexual history) from each iv. Several drugs have been used in the treat ment partner separately. of impotence with varying degrees of effi cacy, 132 A Short Textbook of Psychiatry

e.g. alpha-blockers (such as yohim bine, with poor cardio vas cular status, with anatomi- idazoxan), opiate antago nists (such as naltre- cal deformation of penis, with conditions that xone), dopamine agonists (such as bromocrip- predispose to priapism, and especially those on tine, apomorphine), pento xi fylline, and topical nitrates. drugs (glyceryl trinitrate, minoxidyl, papaverine Other similar drugs include tadalaﬁ l and verde-

and PgE1 and E2). nafi l. v. Sildenafi l citrate has been used for treatment vi. Hormonal treatment (e.g. androgens) should of erectile dysfunction. Rapidly absorbed af- not be employed unless there is an evidence of ter oral administration, the maxi mum plasma hormonal dysfunction. concentration is reached in 30-120 minutes. It It should always be remembered that prescription is metabolised in liver (mainly by cytochrome of the non-essential drugs may worsen sexual dysfunc- P450 3A4) and is converted to an active metabo- tion. lite. Sildenafi l has a terminal half life of about 8. Intracavernosal Injection of Vasoactive Drugs 4 hours. It is highly bound to plasma proteins (IIVD): Papaverine, an alkaloid and a vasoactive and is not dialysable. It is a competitive and substance, has been used as an intracaver nosal in- selective inhibitor of cGMP (cyclic guanos- jection in the differential diagnosis of organic and ine monophosphate)-specific PDE-5 (phos- non-organic impotence and also for treatment of phodiesterase type 5). It prevents the rate of impotence (either alone; or along with phento lamine,

breakdown of cGMP causing enhanced relaxa- phenoxy-benzamine, alprostadil or prostaglandin E1, tion of cavernosal smooth muscle, increase in ar- and/or atropine). terial fl ow in to corpus cavernosa, compression 9. Physical devices: Various suction devices (for of subtunical veins, and hence penile erection. producing artifi cial penile tumescence) and penile The typical dose is 50 mg (25-100 mg), 1 hour prosthetic implants are available. Their use, however, before sexual activity. The maximum recom- should be limited to only those patients who suffer mended dosing frequency is once a day. The from organic sexual disorder or in whom a suffi cient drug acts only in the presence of sexual stimula- and regular trial of psychological management has tion. The adverse effects include transient and been completing, with distress persisting. mild headache, fl ushing, dyspepsia, and nasal 10. Vascular surgery: Rarely, vascular surgery may congestion. Caution needs to be exercised in be needed for some patients with underlying vascular patients with known history of hypersensitivity, insuffi ciency (organic sexual disorder). 11 Sleep Disorders

SLEEP ii. K-complexes: High voltage spikes present intermittently. Nearly one third of human life is spent in sleep, an Stage 3, NREM-sleep shows appearance of high easily reversible state of relative unres pon siveness voltage, 75 μV, δ-waves of 0.5-3.0 cycles/sec. and serenity which occurs more or less regularly and Stage 4, NREM-sleep shows predominant repetitively each day. The EEG recordings show typi- δ-activity in EEG. cal features of sleep which is broadly divided into two NREM-sleep is followed by REM-sleep, which broadly different phases: is a light phase of sleep. The EEG is characterised 1. D-sleep (desynchronised or dreaming sleep), also by a return of α-waves (α-wave sleep); other changes called as REM-sleep (rapid eye movement sleep), are similar to stage 1 NREM-sleep. One of the most active sleep, or paradoxical sleep. characteristic features of the REM-sleep is presence 2. S-sleep (synchronised sleep), also called as of REM or rapid (conjugate) eye move ments. The NREM-sleep (non-REM sleep), quiet sleep, or other features include generalised muscular atony, orthodox sleep. S-sleep or NREM-sleep is further penile erection, autonomic hyperac tivity (increase in divided into four stages, ranging from stages 1 to pulse rate, respiratory rate and blood pressure), and 4. As the person falls asleep, the person fi rst passes movements of small muscle groups, occurring intermi- through these stages of NREM-sleep. ttently. Although it is a light stage of sleep, arousal is The EEG recording during the waking state shows diffi cult. alpha waves of 8-12 cycles/sec. frequency. The onset These stages occur regularly throughout the whole of sleep is characterised by a disappearance of the duration of sleep. The fi rst REM period occurs typi- alpha-activity. cally after 90 minutes of the onset of sleep, although it Stage 1, NREM-sleep is the fi rst and the lightest can start as early as 7 minutes after going-off to sleep, stage of sleep characterised by an absence of alpha- e.g. in narcolepsy, in major depression, and after sleep waves, and low voltage, predominantly theta activity. deprivation. Stage 2, NREM-sleep follows the stage 1 within a The important time periods of the various sleep few minutes and is characterised by two typical EEG stages are summarised below: changes: 1. In an 8 hour sleep, usually 6-6½ hours are spent i. Sleep spindles: Regular spindle shaped waves in the NREM-sleep while 1½-2 hours are in the of 13-15 cycles/sec. frequency, lasting 0.5-2.0 REM-sleep. seconds, with a characteristic waxing and wan- 2. Out of 6-6½ hours NREM-sleep period, only about ing amplitude. 70-80 minutes are spent in Stage 4 sleep. 134 A Short Textbook of Psychiatry

Fig. 11.1: Stages of Sleep

3. The maximum Stage 4 sleep occurs in the ﬁ rst hallucinations (both visual and audi tory), jerky muscle one-third of the night. In the later part, the REM- movements involving small muscle groups, and deper- sleep follows the Stage 3 NREM-sleep directly. sonalisation and derealisation. Some of the methods 4. The REM-sleep occurs maximally in the last of sleep study are listed in Table 11.1. one-third of the night. The REM-sleep occurs Depending on the duration of total sleep, two regularly after every 90-100 minutes, with pro- extremes of ‘normal’ sleeping patterns have been gressive lengthening of each REM period. The described. ﬁ rst REM period typically lasts for less than 10 1. Long-sleepers: These persons regularly and minutes. Usually, there are 4-5 REM periods in habitually sleep for more than 9 hours/night, and the whole night of sleep. this pattern of sleep does not cause any symptoms 5. A younger person may typically need more sleep. or dysfunction. The usual sleep duration in newborn children is 2. Short-sleepers: These persons regularly and 16-18 hours/day, with nearly 8-10 hours spent in habitually sleep for less than 6 hours/night, and the REM-sleep. As the age advances, the sleep this pattern of sleep does not cause any symptoms duration tends to reduce. or dysfunction. Certain phenomena are common just before On comparing long-sleepers and short-sleepers, going-off to sleep (hypnagogic phenomena) and just it has been found that the time spent in stage 3 and 4 after waking-up ( hypnopompic pheno mena). These of NREM-sleep is the same in both. The maximum phenomena include a variety of illusions and simple difference is in the duration of the REM-sleep. The Sleep Disorders 135

Table 11.1: Methods of Sleep Study behaviour, persecutory ideation or delusions, and mild To study sleep and its associated pheno mena, the fol- disorientation and confusion. lowing techniques can be used. As time progresses, frank delirium may occur. 1. Observation of a sleeping person for exter nally visible Whether this type of psychosis can occur in previously changes. normal individuals is doubtful, mainly due to lack of 2. EEG. suffi cient research data. Clearly, ethical considerations 3. Polysomnography (This is usually the preferred prevent this kind of research. method in the sleep research cent ers). It consists of: Recovery after sleep deprivation is charac terised i. Continuous EEG recording, parti cularly from by an increase in total sleep duration, usually lasting occipital and parietal leads. for 15-16 hours. There is also a rebound increase in ii. EOG (electro-oculography) to record the eye the stages 3 and 4 of the NREM-sleep in the fi rst few movements. hours and an increase in the REM-sleep later. iii. EMG (electromyography) for muscle potential and activities. FUNCTIONS OF SLEEP iv. ECG for changes in cardiac status. v. In certain cases, respiratory tracings of various Despite accumulation of vast amount of research data kinds are used, such as oxymetry, expired CO , 2 regarding physiology and biochemistry of sleep, func- O saturation. 2 tions of sleep are still far from clear. vi. MSLT (Multiple sleep latency test): It involves It has been observed that persons sleeping for 7-9 repeated measures of the sleep latency (i.e. time to onset of sleep). hours per day have signifi cantly lower rates of illness. vii. Penile tumescence, body temperature, GSR On the other hand, certain disorders carry a higher (galvanic skin response), and body movements mortality when present during sleep (especially during are also sometimes studied. early hours of morning), for example, coronary artery The recordings are made throughout the night sleep. disease, nocturnal asthma, sudden nocturnal death (in south-east Asian men), and sleep apnoea. long-sleeper, on an average, has almost double the It has been observed that there is a 5-25% decrease duration of REM-sleep as compared to a short-sleeper. in metabolic rate during night sleep. Conservation of energy therefore appears to be one of the important SLEEP DEPRIVATION functions of sleep. It also serves a resto rative function for the whole body (particularly during NREM-sleep) Experimental deprivation of sleep is an important and for the brain (cognitive functions; especially dur- method of studying the functions of sleep. After a ing REM-sleep). Further research is likely to clarify few days of sleep deprivation, EEG recordings show exact functions of various components of the sleep a gradual diminishing of α activity, with an increase cycle. in the lower frequency activity. After 4-5 days of sleep deprivation, psycho- SLEEP DISORDERS logical symptoms become prominent. Initially, there is a decrease in attention span, with easy distractibil- There are several types of sleep disorders known. The ity, drowsiness, decreased initiative to perform and ASDC (Association for Sleep Disorders Centre) has ‘ micro-sleeps’ lasting but a few seconds. In predis- done a lot of work in classifying the various sleep disposed individuals, psychotic symptoms may appear orders and their classifi cation has been adapted for use on the fi fth night, characterised by break with reality, both by DSM-IV-TR and ICD-10. The sleep disorders illusions and hallucinations, grossly disorganised are known as non-organic sleep disorders in ICD-10. 136 A Short Textbook of Psychiatry

The various sleep disorders are divided in 2 sub- Table 11.2: Common Causes of Insomnia types: 1. Medical illnesses I. Dyssomnias i. Any painful or uncomfortable condition 1. Insomnia ii. Heart diseases 2. Hypersomnia iii. Respiratory diseases 3. Disorders of sleep-wake schedule. iv. Rheumatic and musculo-skeletal disease II. Parasomnias v. Old age 1. Stage 4 sleep disorders vi. Brain stem or hypothalamic lesions 2. Other sleep disorders. vii. Delirium viii. PMS ( Periodic movements in sleep) Dyssomnias 2. Alcohol and drug use Dyssomnias are sleep disorders that are characterised i. Drug or alcohol withdrawal syndrome by disturbances in the amount, quality or timing of ii. Delirium tremens sleep. These are the commonest disorders of sleep. iii. Amphetamine or other stimulants, e.g. caffeine iv. Chronic alcoholism Insomnia 3. Current medication, e.g. fl uoxetine, steroids, theo- Insomnia is also known as the Disorder of Initiation phylline, propranolol and/or Maintenance of Sleep ( DIMS). Inso mnia means 4. Psychiatric disorders i. Mania (may not complain of decrease in sleep, one or more of the following: as there is often a decreased need for sleep) 1. Diffi culty in initiating sleep (going-off to sleep). ii. Major depression (diffi culty in maintenance of 2. Diffi culty in maintaining sleep (remaining asleep). sleep is more prominent, although diffi culty in This can include both: initiating sleep is also present) a. Frequent awakenings during the night, and iii. Dysthymia (diffi culty in initiating sleep is char- b. Early morning awakening. acteristic) 3. Non-restorative sleep where despite an adequate iv. Anxiety disorder (diffi culty in initiating sleep is duration of sleep, there is a feeling of not having common) rested fully (poor quality sleep). v. Stressful life situation (may cause temporary Insomnia is very common, with nearly 15-30% insomnia). of general population complaining of a period of 5. Idiopathic insomnia insomnia per year requiring treatment. It is required for diagnosis that sleep disturbance occurs at least three One cause of insomnia, PMS ( periodic move- times a week for at least 1 month, and that it causes ments in sleep) needs further mention. PMS actually either marked distress or interferes with social and consists of two different syndromes, which often occur occupational functioning. together: Aetiology 1. Periodic Limb Movement Disorder (PLMD), and The common causes of insomnia are listed in 2. ‘Restless Legs’ Syndrome (RLS or Ekbom synd- Table 11.2. rome). A person suffering from insomnia should be dif- Periodic Limb Movement Disorder (PLMD) ferentiated from a short-sleeper, who needs less than It is characterised by sudden, repeated contrac tion of 6 hours of sleep per night and has no symptoms or one or more of muscle groups (usually of the legs) dysfunction. A short-sleeper does not need any treat- during sleep. Often occurring bilaterally, it is followed ment. by partial (most commonly) or complete arousal. Since Sleep Disorders 137 each individual contrac tion lasts for a few seconds and Table 11.3: Sleep Hygiene is repeated at an interval of 20-60sec. during a long Some basic components of sleep hygiene are: sleep-period, partial or complete awaken ings occur 1. Regular, daily physical exercises (preferably not in many times in one night sleep. the evening). The patient is usually not aware of the myoclonus 2. Minimise daytime napping. and usually complains of non-restorative sleep or of 3. Avoid fl uid intake and heavy meals just before bed- frequent awakenings. The myoclonus is observed, if time. at all, by the bed partner. This is commonly seen in 4. Avoid caffeine intake (e.g. tea, coffee, cola drinks) middle-aged and elderly people. Due to night-time before sleeping hours. insomnia, daytime hypersomnia can occur and, at 5. Avoid regular use of alcohol (especially avoid use of times, may be the only presenting symptom. alcohol as a hypnotic for promoting sleep). ‘Restless Legs’ Syndrome (Ekbom syndrome) 6. Avoid reading or watching television while in bed. RLS is a condition in which the person expe riences, 7. Sleep in a dark, quiet, and comfortable environment. during waking, an extremely uncomfortable feeling 8. Regular times for going to sleep and waking-up in the leg muscles. Sometimes, it may resemble pain- 9. Try relaxation techniques ful creeping sensations deep inside the calf muscles. Classically, these abnormal sensations occur while If the diffi culty in initiating sleep is the main sitting or lying down and cause an irresistible urge to symptom, then a benzodiazepine with shorter half- move the legs. Moving about or standing provides life should be used, such as temazepam, oxa zepam immediate, tempo rary relief. This is often associated or lorazepam. with periodic limb movement disorder (PLMD) dur- If the diffi culty in maintaining sleep is the ing night sleep. Daily, regular exercises can lead to predominant symp tom, then a longer acting ben- marked improvement in certain cases. zodiazepine, such as nitra zepam, fl uraze pam or Treatment even diazepam, should be used (see Chapter 15 1. A thorough medical and psychiatric assess ment. for details). 2. Polysomnography (see Table 11.1) may be needed Physicians should be careful to avoid benzo - in some patients to reach a diagnosis. diazepine abuse or dependence in patients present- 3. Treatment of the underlying physical and/or psy- ing with insomnia. Non-benzodiazepine hypnotics chiatric disorder, if present. (e.g. zopiclone, zolpidem, zalpelon and trazodone) 4. Withdrawal of current medications, if any. are useful alterna tives (see Chapter 15). 5. Relaxation techniques before sleep time and edu - 8. L-tryptophan, an amino-acid present in many ca tion regarding sleep hygiene (see Table 11.3). vegetables, is an apparently non-dependence pro- Sleep hygiene consists of general guidelines for ducing hypnotic. The usual dose is 0.5g at night promoting good sleep. In itself, it is not a treatment time. for insomnia. 6. Psychotherapy, if indicated. Hypersomnia 7. Benzodiazepines may be used, either alone, e.g. Hypersomnia is also known as Disorder of excessive in primary insomnia, or may be used with the somnolence (DOES). Hypersomnia means one or treatment of underlying physical or psychiatric more of the following: disorder(s). The use of benzo dia zepines should 1. Excessive day time sleepiness. only be for short-term periods, not more than for 2. ‘Sleep attacks’ during day time (falling asleep 4-6 weeks at one time. unintentionally). 138 A Short Textbook of Psychiatry

3. ‘ Sleep drunkenness’ (person needs much more Table 11.4: Causes of Hypersomnia time to awaken; and during this period is confused 1. Medical illnesses or disoriented). i. Narcolepsy (in about 25% of all patients with Hypersomnia is seen in about 1-2% of general hypersomnia) population at any given time. As insomnia and hyper- ii. Sleep apnoea (in about 50% of all patients with somnia may be present at the same time, the underly- hypersomnia) ing causes may be common to both. It is required for iii. Kleine-Levin syndrome the diagnosis that the sleep disturbance occurs daily iv. Menstrual-associated somnolence for at least 1 month or for recurrent periods of shorter v. Sleep deprivation duration, and that it causes either marked distress or vi. Following or with insomnia interferes with social and occupational functioning. vii. Encephalitis Aetiology viii. Hypothyroidism The common causes of hypersomnia are listed in ix. Head Injury Table 11.4. x. Cerebral tumours in the region of mid-brain A person suffering from hypersomnia should be xi. Hypothalamic lesions differentiated from a long-sleeper, who needs more xii. Trypanosomiasis than 9 hours of sleep per night and has no symptoms xiii. PMS ( Periodic movements in sleep); in about or dysfunction. A long-sleeper does not need any 10% of all patients with hypersomnia. treatment. 2. Alcohol and drug use A few important causes of hypersomnia are dis- i. Stimulant withdrawal cussed below: ii. Alcohol intoxication 1. Narcolepsy iii. Use of CNS depressant medications. This is a disorder characterised by excessive day- 3. Psychiatric disorders time sleepiness, often disturbed night-time sleep and i. Dysthymia ii. Atypical depression disturbances in the REM-sleep. The hallmark of this iii. Seasonal mood disorder. disorder is decreased REM latency, i.e. decreased 4. Idiopathic hypersomnia. latent period before the ﬁ rst REM period occurs. Nor- mal REM latency is 90-100 minutes. In narcolepsy, REM-sleep usually occurs within 10 minutes of the drop, or paresis of all skeletal muscles of body onset of sleep. resulting in a fall. This may be precipitated by The common age of onset is 15-25 years, with sudden emotion. The consciousness is usually usually a stable course throughout life. The prevalence clear and memory is normal, unless sleep attacks rate of narcolepsy is about 4 per 10,000. supervene. The classical tetrad of symptoms is: iii. Hypnagogic hallucinations: These are vivid per- i. Sleep attacks (most common): The person is ceptions, usually dream-like, which occur at the unable to resist a sleep attack or ‘nap’, from onset of sleep and are asso ciated with fearfulness. which he or she awakens refreshed. These ‘at- When these occur at awa ke ning, they are called tacks’ can occur during any time of the day, hypno pompic hallu cinations. even whilst driving. Usually, there is a gap of iv. Sleep paralysis (least common): This occurs 2-3 hours between the two attacks. either at awakening in the morning (usually) ii. Cataplexy: This is characterised by a loss of or at sleep onset. The person is conscious but muscle tone in the various parts of body, e.g. jaw unable to move his body. The episode may last Sleep Disorders 139

from 30 seconds to a few minutes and may cause 3. Kleine-Levin Syndrome signifi cant distress. This is a rare syndrome characterised by: Not all symptoms of the tetrad are present in one 1. Hypersomnia (always present), occurring recur- person. The other associated symptoms are fugue rently for long periods of time. states, blackouts and blurring of vision. Poly somno- 2. Hyperphagia (usually present), with a voracious graphy helps in making a diagnosis in doubtful cases, appetite. showing a decreased REM latency. 3. Hypersexuality (associated at times), consis ting of The treatment consists of forced naps at regu- sexual disinhibition, masturbatory activity, exhi- lar times in the day, stimulant medication (such as bitionism, and/or inap pro priate sexual advances. amphetamines) or modafi nil in some patients, and/ The associated features include apathy, irri table or antidepressants (particularly when cata plexy is a behaviour, confusion, social withdrawal, bizarre prominent symptom). behaviour, psychotic symptoms (such as delu sions 2. Sleep Apnoea and hallucinations), and disorien tation. One or more This condition is characterised by presence of repeated of these symptoms may occur during the episode. episodes of apnoea during sleep. In this context, EEG abnormalities, usually showing intermittent non- apnoea is defi ned as the cessation of airfl ow at the nos- specifi c slowing, are common but are not diagnostic. trils (and mouth) for 10 seconds or longer. The apnoea A typical episode lasts for one to several weeks, can be of central type, obstructive type or mixed type. followed usually by a complete remission. The It is commoner in elderly and obese (Pick wickian common age of onset is the second decade of life. syndrome). Typically, there are 5 or more apnoeic Apparently this disorder has a fi nite course with a large episodes per hour of sleep and the total number of majority of patients recovering completely before the apnoeic episodes exceeds 30 during one night’s fi fth decade of life. The disorder is almost always seen sleep. In severe cases, the number of episodes may in males. be in hundreds. The patients are usually not aware of No specifi c treatment is available but Lithium and the occurrence of apnoea. Instead, they complain of occasionally Carbamazepine have been reported to be an inability to stay awake in the day time and non- successful. restorative sleep at night. The bed part ner may report Treatment of loud snoring, rest less sleep or of periodic absences 1. A thorough physical and psychiatric assess ment. of breathing. 2. Treatment of the underlying cause is the most The diagnosis can be established in doubtful cases important method. using polysomnography, with the respi ratory tracings 3. Associated or underlying insomnia should be included. Sleep apnoea can be a dangerous condition. looked for and treated. It can cause cardiac arrhythmias, pulmonary and sys- 4. Withdrawal of current medication causing hyper- temic hypertension, and death. somnia, especially depressant medi cation. The treatment consists of avoidance of alcohol 5. Benzodiazepines at night may paradoxi cally and depressant medications, use of stimulants such decrease hypersomnia by correcting night time as caffeine, regular exercises, losing excess weight, insomnia. teaching correct sleeping posture, and corrective procedures for obs tructive sleep apnoea (e.g. mechanical Disorders of Sleep-wake Schedule tongue retaining device). Very severe obstructive sleep These are characterised by a disturbance in the timing apnoea may necessitate tracheostomy (functional only of sleep. The person with this disorder is not able to at night), CPAP (continuous positive airway pressure) sleep when he wishes to, although at other times he through nasal mesh, or even pharyngoplasty. is able to sleep adequately. This is due to a mismatch 140 A Short Textbook of Psychiatry between person’s circadian rhythm and the normal simple to complex. He may leave the bed, walk sleep-wake schedule demanded by the environment. about or leave the house. Arousal is diffi cult and Aetiology accidents may occur during sleep-walking. The common causes of disorders of sleep-wake sched- 2. Sleep-terrors or night terrors (pavor nocturnus): ule are listed below: The patient suddenly gets up screaming with 1. ‘Jet lag’ or rapid change of time zone: This typi- auto nomic arousal (tachycardia, sweating and cally occurs during international fl ights crossing hyperventilation). He may be diffi cult to arouse many ‘time zones’. At the new place, the person’s and rarely recalls the episode on awakening. In internal time of sleep and the sleep time of sur- contrast, nightmares (which occur during REM- roundings are different, leading to insomnia during sleep) are clearly remembered in the morning. the new sleep time and somnolescence in the new 3. Sleep-related enuresis (bedwetting): This is dis- daytime, thus causing impairment of functioning. cussed in detail in Chapter 14. 2. ‘ Work-shift’ from day to night or vice-versa. 4. Bruxism (teeth-grinding): The patient has an 3. Unusual sleep phases: Some persons are unable involuntary and forceful grinding of teeth during to sleep early. They typically sleep late at night sleep. Though the bed partner reports loud sounds and get up late in the morning. They are called produced by grinding of teeth and destruction of as ‘ owls’. Others are similarly unable to remain the tooth enamel is obvious, the patient remains awake at night. They typically sleep early at night completely unaware of the episode(s). and get up early in the morning. They are called 5. Sleep-talking (somniloquy ): The patient talks as ‘larks’. Some others have a longer-than 24 hour during stages 3 and 4 of sleep but does not sleep-wake cycle (usually of 25 hours). remember anything about it in the morning on Treatment awakening. No specific treatment is usually needed. Benzo- These disorders are often co-existent. As they diazepines may be needed for short-term correction occur during stage 4 (and 3) of NREM-sleep, they of insomnia. Changes in ‘work-shifts’ may be needed are more common during the fi rst one-third of the for persons with unusual sleep phases. Exposure to night (There is more NREM-sleep in the fi rst third of sunlight during outdoor activity (instead of stay- the night while the last third has more REM-sleep). ing indoors) and adopting the local (new) hours Arousal is diffi cult and on waking-up, there is a comfor sleeping (and working) can help in combating plete amnesia for the event(s). jet lag. Treatment Since benzodiazepines suppress stage 4 of NREM- Parasomnias sleep, a single dose at bedtime usually provides relief Parasomnias are dysfunctions or episodic noc turnal from stage 4 parasomnias. events occurring with sleep, sleep stages or partial arousals. Most parasomnias are common in childhood Other Sleep Disorders though they may persist into adulthood. Nightmares (dream anxiety disorder) occur during the REM-sleep. They are characterised by fearful dreams Stage 4 Sleep Disorders occurring most commonly in the last one-third of These disorders occur during deep sleep, i.e. Stages night sleep. The person wakes up very frightened and 3 and 4 of NREM-sleep. remembers the dream vividly. The common Stage 4 parasomnias are: This is in contrast to night terrors which occur 1. Sleep-walking ( somnambulism): The patient car- early in the night, are a stage 4 NREM disorder, and ries out automatic motor activities that range from are characterised by complete amnesia. In both the Sleep Disorders 141 conditions, the observer fi nds the person frightened Treatment There is no specific treatment. Treatment of the during the episode. underlying condition is the most important step. The Other sleep disorders include nocturnal angina, treatment of nightmares is by suppression of REM- nocturnal asthma, nocturnal seizures, paroxys mal sleep, e.g. by bedtime dose of a benzodiazepine. nocturnal haemoglobinuria, nocturnal head banging, However, on stopping the drug, a rebound increase and familial sleep paralysis. in symptoms may occur. Behavioural Syndromes Associated with Psychological Disturbances 12 and Physiological Factors

The disorders can broadly be classifi ed into the fol- 2. There is an intense fear of becoming obese. This lowing categories: fear does not decrease even if body becomes very 1. Eating Disorders thin and underweight. 2. Sleep disorders 3. There is often a body-image disturbance. The per- 3. Sexual disorder and dysfunctions son is unable to perceive own body size accurately. 4. Postpartum psychiatric disorders However, body image disturbance may sometimes 5. Psychosomatic disorders not be seen in patients from non-Western cultural In addition to these, the chapter also describes settings and several such cases have been de- briefl y consultation liaison psychiatry and psychiatric scribed from India. aspects of grief and bereavement. 4. There is a refusal to maintain the body weight above a minimum normal weight for that age, sex EATING DISORDERS and height. 5. Signifi cant weight loss occurs, usually more than Eating disorders are characterised by clinical presen- 25% of the original weight. The fi nal weight is usu- tation primary focused on eating behaviour. The fol- ally 15% less than the minimum limit of normal lowing disorders are briefl y discussed in the chapter: weight (for that age, sex and height) or a Quetelet’s 1. Anorexia nervosa body-mass index (BMI) of 17.5 or less (Quetelet’s 2. Bulimia nervosa body-mass index = weight in kg divided by square 3. Obesity (associated with other psychological of height in meters). disturbances) 6. No known medical illness, which can account for 4. Binge-eating disorder the weight loss, is present. 5. Psychogenic vomiting 7. Absence of any other primary psychiatric disorder. 8. Amenorrhoea, primary or secondary, is often Anorexia Nervosa present in females. Anorexia nervosa is an eating disorder characterised In addition to these typical clinical features, other by the following prominent clinical features: associated features are often present. The patient im- 1. It occurs much more often in females as compared poses dietary restrictions on self; can have peculiar to the males. The common age of onset is adoles- patterns of handling food, such as brea king food into cence (13-19 years of age). small bits, hiding food; and can engage in vigorous Behavioural Syndromes Associated with Psychological Disturbances and Physiological Factors 143 exercises. ‘Anorexia’ is actually a misnomer as there • Short-term treatment, to encourage weight gain is never really a decrease in appetite, initially; in fact and correct nutritional defi ciencies, if any. patient is often preoccupied with food. A lot of time • Long-term treatment, aimed at maintaining the may be spent in collecting recipes and cooking food near normal weight achieved in short-term treat- for signifi cant others. ment and preventing relapses. Depressive symptoms are common and so are The various treatment modalities used can include: obsessive-compulsive personality traits. Psychomo- 1. Behaviour therapy (BT): Behavioural treatments tor activity is usually increased. In severe cases, fi ne are based on providing positive reinforcements lanugo hair may develop all over the body. Women (and at times, negative reinforcements) contingent with anorexia nervosa can present with poor sexual on weight gain by the patient. See Chapter 18 for adjustment, with confl icts about being a woman and further details for BT. fear of pregnancy. Many patients are unconsciously A too rapid weight gain is not desirable or safe. unable to accept a ‘ female role’. The weight gain should not exceed 1.5 to 2 kg in A large number (up to 50%) of patients with ano- a fortnight. As patients are usually unable to eat rexia nervosa also have bulimic episodes. These are a large meal, especially in the initial part of treat- characterised by rapid consumption of large amounts ment, it is advisable to suggest more number of of food in a relatively short period of time, occurring meals (about six) per day. Occasionally, forceful usually when alone. This is known as eating binges Ryle’s tube feeding may be needed initially, in or binge-eating. These binges are followed by intense resistant patients. guilt and attempts to remove eaten food, for example, 2. Individual psychotherapy is often helpful in addi- by self-induced vomiting, laxative abuse, and/or diu- tion to supportive physical treatment. This could retic abuse. involve psychotherapy with a focus on cognitive If untreated, the weight loss can become behaviour therapy, psychodynamic principles or marked. Death may occur due to hypokalaemia supportive measures. See Chapter 17 and 18 for (caused by self-induced vomiting), dehydration, more details. malnutri tion or congestive cardiac failure (caused by 3. Hospitalisation, with adequate nursing care for anaemia). food intake and weight gain, can be helpful in Anorexia nervosa should be differentiated from short-term treatment as well as prevention and/ other conditions capable of causing signifi cant weight or treatment of complications. However, hospi- loss. These include medical illnesses (such as hypopi- talisation does not necessarily ensure long-term tuitarism, lateral hypothalamic lesion and debilitating improve ment. It is important to keep a close eye systemic illnesses, e.g. dissemi nated tuberculosis) and on water and electrolyte balance, need for supple- psychia tric disorders (such as depressive disorder and mentation with vitamins and minerals, and prevent schizophrenia). osteoporosis. Another important differential diagnosis is bulimia 4. Drugs are an important adjunct to other modes of nervosa. Although bulimic episodes are common in therapy. The drugs used can include: anorexia nervosa (binge eating followed by vomit- i. Antipsychotics: Chlorpromazine is rarely used ing), patients of bulimia nervosa usually maintain a these days. Olanzapine has effi cacy in improv- near normal body weight (or are overweight), in sharp ing weight gain but it is important to be aware of contrast to the patients with anorexia nervosa. possibility of prolongation of QTc particularly in patients with low BMI. Treatment ii. Antidepressants (such as fluoxetine, clomi- The treatment of anorexia nervosa can be considered pramine) for treatment of anorexia nervosa and/ in two phases, which often merge into each other. or asso ciated depression. 144 A Short Textbook of Psychiatry

iii. Cyproheptadine: This is particularly helpful in 6. No known medical illness is present which can inducing weight gain, decreasing depressive account for the disorder. symptoms and increasing appetite, if anorexia 7. Absence of any other primary psychiatric disorder. is actually present. The usual dose is 8-32 mg/ day, in divided doses. However, co-prescription Treatment with SSRIs can interfere with their effectiveness The various treatment modalities that can be used as Cyproheptadine is a serotonin antagonist. include: 5. Group therapy and family therapy can be helpful 1. Behaviou r therapy: This is based on providing in psycho-education for the patient and carers/ positive reinforcements (and at times negative family about nature of anorexia nervosa and its reinforcements) contingent on the control of binge treatment. Psycho-education may also include eating by the patient. See Chapter 18 for further discussion of current social norms of slimming details for BT. and fi tness, since there is evidence to suggest that 2. Individual psychotherapy: See Chapters 17 and anorexia nervosa is far more common in countries 18 for further details. with social pressures for slimming, such as USA 3. Antidepressant drugs are an important adjunct and UK. India is indeed quite fast catching up with to other modes of therapy. A Selective serotonin similar social pressures. uptake inhibitor (SSRI) such as Fluoxe tine (in The prognosis is generally better if diagnosis doses of 20-60 mg) is particularly useful as it can is made early, absence of previous hospitalisations cause loss of appetite at least in the initial phase and absence of bulimic episodes. Weight gain and of treatment, along with its antidepressant effect. improvement in mental outlook often precede return The drugs used in the past have included tricy clic of menstrual function. antidepressants such as imipramine, though they are currently not widely used. Bulimia Nervosa 4. Group therapy and family therapy: These methods Bulimia nervosa is an eating disorder charac terised are used for psycho-education of patient and by the following clinical features: carers/family about nature of bulimia nervosa and 1. Bulimia nervosa usually has an onset in early teens its treatment. or adolescence. 2. There is an intense fear of becoming obese. There Obesity (Overeating Associated with Other may be an earlier history of anorexia nervosa. Psychological Disturbances) 3. There is usually body-image disturbance and the Obesity caused by a reaction to distressing events is person is unable to perceive own body size ac- included here. Obesity caused by drugs or endocrinal curately. factors, or due to constitutional factors is not consid- 4. There is a persistent preoccupation with eating, ered a psychiatric disorder. and an irresistible craving for food. There are Treatment options depend on the underlying cause; episodes of overeating in which large amounts of for example, psychotherapy (for present or past psy- food are consumed within short periods of time chological distress), antidepressants (for depression), ( eating binges). advice from dietician, drug treatment, or even bariatric 5. There are attempts to ‘counteract’ the effects of surgery. overeating by one or more of the following: self- induced vomiting, purgative abuse, periods of Binge Eating Disorders starvation, and/or use of drugs such as appetite In binge eating disorder, large amounts of food are suppressants. consumed in a relatively short period, followed by Behavioural Syndromes Associated with Psychological Disturbances and Physiological Factors 145 severe discomfort and feelings of self-denigration. NON-ORGANIC SLEEP DISORDERS There is a sense of lack of control over eating during the episode. Additionally, there also may be eating Non-organic sleep disorders are discus sed in of large amounts of food throughout the day with no Chapter 11. planned meal times, eating alone because of being embarrassed, and/or feeling guilty and depressed SEXUAL DYSFUNCTIONS, NOT CAUSED after overeating. BY ORGANIC DISORDERS OR DISEASE The disorder is not listed separately in ICD-10 and symptoms of binge eating are also seen in bulimia Non-organic sexual dysfunctions are discussed in nervosa. Chapter 10. Treatment is similar to bulimia nervosa, though the role of drug treatment in binge eating disorder is POSTPARTUM PSYCHIATRIC not so clear. DISORDERS (MENTAL AND BEHAVIOURAL DISORDERS Psychogenic Vomiting ASSOCIATED WITH PUERPERIUM, This is a clinical syndrome in which biopsychosocial NOT CLASSIFIED ELSEWHERE) factors interact to produce symp toms which are often mistaken for upper gastrointestinal tract disease, Pregnancy and puerperium are highly stressful periods anorexia nervosa, dissociative (conversion) disorder, in a woman’s life. The person is threatened by: somatization disorder, or malingering. 1. Physical, physiological and endocrinal changes The characteristic clinical features include: occurring in one’s body, 1. Repeated vomiting, which typically occurs soon 2. Reorganisation of psyche in accordance with the after a meal has begun or just after it has been new ‘ mother-role’ (in the fi rst pregnancy), completed. 3. Body image changes, and 2. Vomiting often occurs in complete absence of 4. Unconscious intrapsychic confl icts relating to nausea or retching (Patients say that food just pregnancy, childbirth and motherhood may be- seems to come back up). come activated. 3. Vomiting is often self-induced and can be sup- It is no surprise then that 25-50% of all women pressed, if necessary. can develop psychological symptoms in the puerperal 4. Despite repeated vomiting, weight loss is not usu- period. The commonest type of presentation is mild ally signifi cant. depression and irritability, often known as post-natal 5. The course of illness is usually chronic with fre- blues. These ‘blues’ pass-off within a few days and quent remissions and relapses. usually need no active manage ment except monitoring and support. Treatment However, in 1.5-4.6/1,000 deliveries (average 1. The fi rst and most important step is correct di- 2/1000 deliveries), the mother can develop severe agnosis and exclusion of other physical and/or psychiatric symptoms including psychotic symptoms. psychiatric causes. This is known as postpartum psychosis. 2. Identifi cation of psychosocial stressor. The postpartum psychosis can present with: 3. Environmental manipulation and encouragement 1. Depressive episode with psychotic symptoms of coping strategies to deal with stress. (most common), or 4. Psychotherapy of either cognitive behavioural or 2. Schizophrenia-like symptoms, or psychodynamic nature (see Chapters 17 and 18 3. Manic episode, or for further details). 4. Delirium (least common). 146 A Short Textbook of Psychiatry

Typically, the onset of symptoms occurs 3-7 days the duration of psychiatric disorder and may make it after delivery. An onset before the 3rd day postpartum chronic. is rare. The symptoms usually peak by the end of 4th week, and may necessitate admission to a hospital set- Treatment ting. As the puerperium lasts for 6 weeks, the relevant 1. Treatment of the type of postpartum psychiatric postpartum period for psychiatric symptomatology to disorder, such as antidepressants and/or ECTs appear is 6 weeks (according to ICD-10). Hence, any for the depressive episode; antipsychotics and/or psychiatric symptoms appearing within 6-week period mood stabilisers for the manic episode; antipsy- after delivery are called as postpartum psychiatric chotics for the psychotic symptomatology. disorder(s), if they do not fulfi l the criteria of the major 2. Psychotherapy for psychological issues, especially psychiatric disorders. after recovery from psychosis has occurred. It was earlier believed that schizophreniform 3. General supportive care during the puerperium. disorder is the commonest postpartum psychiatric 4. Lithium, antipsychotics and antidepres sants are disorder in developing countries (such as India), in excreted in milk and may be dangerous to the contrast to developed countries where depression is infant. A judicious decision has to be made regard- usually more common. However, recent studies negate ing feeding of the infant, depending on the dose this hypo thesis. Even in India, depressive episode is prescribed, social support available and risks of the most common type of postpartum psychiatric dis- keeping the infant and mother separate. order encountered in routine clinical practice though 5. As patients can lack insight, have poor judgement, psychotic symptoms are frequently present. may be unable to care for themselves and the baby, The factors involved in causation are both bio- and are receiving psycho tropic medication, it is logical (changes in endocrine status especially steroid not uncommon that the baby receives ‘top feeds’ withdrawal, sleep disturbances, amine disturbances) (supple mentary feeds). In that case, it may be nec- and psychosocial (intra psy chic confl icts relating to essary to extract milk from breast daily (or more motherhood, family and interpersonal confl icts in light often) either manually or with a breast-pump. It is of the new ‘role’). more practical to give oral Stilboestrol, Pyridoxine Presently, it is believed that postpartum psycho- (100 mg/day) or very rarely Bromocriptine to sis is not a special or separate category, but only a inhibit lactation. It is important to remember the resi dual category in ICD-10. Depressive episode or risk of psychosis with Bromocriptine. schizophreniform disorder occurring separately or as a part of postpartum psychiatric disorder are very PSYCHOSOMATIC DISORDERS similar, except the presence of confusion as a promi- (PSYCHOLOGICAL OR BEHAVIOURAL nent and common symptom in postpartum psychiatric FACTORS ASSOCIATED WITH disorders. Childbirth merely acts as a stressful event DISORDERS OR DISEASES CLASSIFIED precipitating the illness. ELSEWHERE) Postpartum psychoses have a better prognosis as compared to similar disorders occurring in a non- Psychosomatic disorders (a term coined by Heinroth postpartum setting; however 15-25% of these patients in 1918) are those disorders in which psychosocial have a recurrence, usually of the same type, during factors are very important in causation. Broadly the next puerperium. Patients with a history of post- applied, this term can encompass all physical ill- partum or postnatal depression are also considered nesses. A narrow but more practical defi ni tion would high risk for development of bipolar disorder. During include those physical disorders which are either an episode, presence of folate defi ciency can prolong initiated or exacerbated by the presence of meaningful Behavioural Syndromes Associated with Psychological Disturbances and Physiological Factors 147 psychosocial envi ronmental stressors. ICD-10 lists in a psychosomatic illness. This viewpoint has become these disorders under the category of Psychological very popular and is now almost integral to psychiatric or behavioural factors associated with disorders or teaching and practice throughout the World. It can be diseases classifi ed elsewhere. depicted in a diagram (Fig. 12.1). Franz Alexander, the Father of Psycho s omatic Beginning from seven classical psychoso matic Medicine, initially described the seven classical illnesses of Alexander, number of these illnesses psychosomatic illnesses (Table 12.1). His speci fi city continued to increase as their biopsychosocial causa- hypothesis stated that if a specifi c environmental stres- tion became more evident and clear. At present, the sor or emotional confl ict occurs, it results in a specifi c list of psychosomatic illnesses is virtually endless illness in a genetically predetermined organ. as it is not diffi cult to imagine the effect of psycho- George Engel in 1977, described a biopsychosocial social factors on most illnesses. The important and model to explain the complex interaction between common psychosomatic illnesses are mentioned in biological, psychological and social spheres resulting Table 12.2. It is not the purpose of this book to go into the Table 12.1: Classical Psychosomatic Disorders details of these physical disorders. How ever, certain The 7 classical psychosomatic disorders are: important aspects and conditions are described, which 1. Bronchial asthma are often not available in detail in most medical text- 2. Ulcerative colitis books. 3. Peptic ulcer Type A Personality 4. Neurodermatitis When personality characteristics of a patient with 5. Thyrotoxicosis coro nary artery disease (CAD) are exa mined, there 6. Rheumatoid arthritis may be preponderance of a certain type of personal- 7. Essential hypertension. ity traits, collectively described as coronary prone

Fig. 12.1: A Biopsychosocial Model for Psychosomatic Illness 148 A Short Textbook of Psychiatry

Table 12.2: Common Examples of Psychosomatic Type A behaviour by Friedman and Rosenman. This Disorders Type A behaviour is characterised by following fea- I. Cardiovascular disorders tures: 1. Essential hypertension Time Urgency 2. Coronary artery disease 3. CCU delirium or post-cardiac surgery delirium There is always a hurry to ﬁ nish the task at hand. This 4. Migraine is extended even to day-to-day routine activities such 5. Cerebrovascular disease as eating, bathing. Speech is usually hurried and the 6. Mitral valve prolapse syndrome (MVPS) psychomotor activity is often increased. II. Endocrine disorders 1. Diabetes mellitus Excessive Competitiveness and Hostility 2. Hyperthyroidism 3. Cushing’s syndrome There is a need to always win, with mistrust for other 4. Peri-menopausal syndrome people’s motives. Rage ensues, if the person is inter- 5. Amenorrhoea rup ted from achieving an objective. 6. Menorrhagia Overall, there is a chronic struggle to achieve (or III. Gastro-intestinal disorders complete) a large number of tasks, working against the 1. Oesophageal reﬂ ux limits of time available and/or other people in the sur- 2. Peptic ulcer rounding environment. In contrast, Type B behaviour 3. Ulcerative colitis is just the opposite, characterised by a relaxed unhur- 4. Crohn’s disease ried atti tude and less vigorous attempts to achieve a IV. Immune disorders (These overlap with other goal. disorders mentioned in this table) Some studies report that per sons with Type B 1. Auto-immune disorders such as Ulcerative colitis, Systemic lupus erythematosus (SLE) personality are paradoxically more successful than 2. Allergic disorders such as Bronchial asthma, those with Type A personality. It is important to note Hay fever that not all patients with CAD present with Type A 3. Viral infections personality traits. V. Musculo-skeletal disorders 1. Rheumatoid arthritis Treatment 2. Systemic lupus erythematosus (SLE) As persons with Type A behaviour are usually aware VI. Respiratory disorders of presence of these personality traits, they may come 1. Bronchial asthma for treatment on their own, or may need treatment 2. Hay fever after CAD has occurred. One or more of the following 3. Vasomotor (allergic) rhinitis VII. Skin disorders methods may be used. 1. Psoriasis 1. Relaxation techniques: This is one of the most 2. Pruritus important methods aimed at reducing the basal 3. Urticaria generalised anxiety or inner sense of restlessness. 4. Alopecia areata The common techniques include: 5. Acne vulgaris i. Jacobson’s progressive muscular relaxation 6. Psychogenic purpura (PMR) techni que 7. Trichotillomania ii. Yoga 8. Dermatitis artifacta iii. Autohypnosis 9. Lichen planus iv. Transcendental meditation 10. Warts. v. Biofeedback. Behavioural Syndromes Associated with Psychological Disturbances and Physiological Factors 149

2. Behaviour modifi cation techniques. Anticholinergic medication should not routinely 3. Individual psychotherapy, usually cognitive be added to antipsychotics, as it may actually worsen behaviour therapy. the delirium. However, it may be needed if there 4. Group therapy. are any signifi cant extrapyramidal adverse effects present. Post-cardiac Surgery Delirium This is a condition similar to ICU (Intensive care unit) PSYCHIATRY IN MEDICINE syndrome. A fairly common disorder, its onset typically occurs after 24-48 hours of surgery. The patients, About one-third to two-third of medical outpatients who develop post-surgery delirium, can sometimes may have primary or associated psychiatric disorders. be the ones who are most fearful before the surgery. If minor psychological and social problems are also Many causes have been attributed for delirium, taken into consi deration, this number would be even which include: larger. Since these patients may benefi t from a psychia- 1. Cardiac status. tric referral, psychiatrists are becoming increasingly 2. Presence of preoperative, subclinical organic brain involved in treatment of medical and surgical patients. disease. In fact a whole new branch of consultation-liaison 3. Restrictive environment of the ICU/CCU, with psychiatry has sprung up in the last few decades. isolation. Consultation-liaison psychiatry is an area of clini- 4. Electrolyte imbalance. cal psychiatry which includes diagnos tic, therapeutic, 5. Preoperative anxiety, fearfulness, depres sion or teaching and research activities of psychiatrists in the denial. non-psychiatric parts of the hospital. Probably the condition is aetiologically multi- The common reasons for a psychiatric referral factorial and should be treated as a type of delirium include: (see Chapter 4). 1. Suicidal attempt, ideation or threat. 2. Grossly ‘abnormal’ behaviour disturbing the Treatment inpatient setting. 1. Preoperative measures. 3. Presence of disorders related to alcohol or sub- i. Allaying the anxiety and fears of the patient. stance abuse/dependence such as severe with- ii. Treatment of depression, if present. drawal symptoms. iii. Easy access to clocks and windows in ICU/ 4. Organic brain syndromes. CCU, to keep the patient oriented in time. 5. Psychosomatic disorders. iv. Allowing a family member to stay near the 6. Psychological reaction to medical illness. patient. 7. Uncertain diagnosis (No medical illness can be 2. Treatment of delirium as described in Chapter 4. found despite the presence of signifi cant symp- Since delirium can be life threatening, as patients toms). can take out IV lines, catheters or other ‘life-lines’ and 8. Manipulative or diffi cult or hostile patient. can jump down from balcony or window, urgent treat- 9. Psychiatric side-effects of drugs. ment is often needed. Small doses of benzodiazepines 10. Patient is unable to manage his or her own affairs. (such as Diazepam or Lorazepam) or antipsychotics 11. Presence of severe primary psychiatric disorder(s). (such as Haloperidol or Risperidone) can be used A large number of medical illnesses can present orally or parenterally. Later the patient can be switched with psychiatric symptomatology. It is important to to low dose oral haloperidol or risperidone till recov- keep in mind the possibility of a secondary mental ery from delirium occurs. disorder, i.e. a psychiatric disorder which is caused 150 A Short Textbook of Psychiatry

Table 12.3: Physical Illness and Psychopathology Physical Illness Psychiatric Symptomatology (Not all symptoms are present in one patient) 1. Hyperthyroidism ( Thyrotoxicosis) Anxiety, depression (with apathetic hyperthyroidism), impairment of higher mental functions, paranoid disorder, delirium (with thyroid storm), mania, schizophreniform disorder, organic mental disorder 2. Hypothyroidism ( Myxoedema) Apathy and lethargy, memory impairment, slow thinking, poor attention span, irritable mood, paranoid ideation, severe depressive episode, dementia, myxoedema madness 3. Hyperadrenalism ( Cushing’s Depression, with paranoid ideation, generalised anxiety, psychosis with syndrome) somatic delusions 4. Adrenal cortical defi ciency Depression, with paranoid defi ciency ideation, delirium (toxic psycho- ( Addison’s disease) sis), stupor 5. Hyperpituitarism ( Acromegaly) Apathy, depression, anxiety 6. Hypopituitarism ( Simmond’s Depression with memory disturbances, hypersomnia, delirium, stupor disease) or coma 7. Hyperparathyroidism Depression, delirium (with parathyroid crises), coma (following recurrent seizures), early dementia 8. Hypoparathyroidism Delirium (particularly in postoperative cases), dementia (in idiopathic hypoparathyroidism), depression (with partial parathyroid insuffi ciency), mental retardation (especially in pseudo-hypoparathyroidism and pseudo-pseudo-hypoparathyroidism), ‘pseudoneurosis’ 9. Phaeochromocytoma Anxiety and panic attacks 10. Acute intermittent porphyria Acute anxiety, severe excitement or psychomotor withdrawal, conversion symptoms, schizophreniform disorder (rare), stupor or coma (rare) 11. AIDS (Acquired immunodefi - Anxiety, depression, delirium, dementia (AIDS-dementia complex), ciency syndrome) organic catatonia, adjustment disorder, suicidal behaviour, delusional disorder 12. Systemic lupus erythematosus Depression, delirium (toxic psychosis), steroid psychosis (iatrogenic), ( SLE) schizophreniform disorder (uncommon) 13. Hepatolenticular degeneration Personality changes (slow and insidious), mental retardation (in early ( Wilson’s disease) onset), dementia (in late onset), schizophreniform disorder (can become chronic), antisocial behaviour, with rapid mood swings, poor impulse control and aggressive behaviour 14. Multiple sclerosis Euphoria or depression, histrionic personality traits, conversion and/or dissociation symptoms, dementia (if of long duration) 15. Parkinsonism Depression, dementia, paranoid features 16. Pancreatic carcinoma Severe depression 17. Progressive supra-nuclear palsy Depression, dementia (PSP) by an underlying physical disease. Some important In addition, a large number of physical dis orders physical illnesses with their commonly presenting such as auto-immune disorders; infections; nutritional psy chia tric symptoms are listed in Table 12.3. defi ciencies (particularly pellagra, pernicious anaemia, Behavioural Syndromes Associated with Psychological Disturbances and Physiological Factors 151 beriberi); malignancies; alcohol and drug abuse; side- deceased (often ignoring negative qualities). These effects or toxicity of many medications; metabolic preoccupations are usually of a comfor ting nature. and water and electrolyte disturbances (and many This may be associa ted with a ‘ sense of presence’ of others) may present with psychiatric symptomatology the deceased in the surroun dings and a misinterpreta- either alone (especially in initial stages) or with other tion of voices and faces of others as that of the lost physical signs and symptoms. Some of these have person. Rarely, fl eeting hallucinations may occur. been mentioned under the causes of organic mental The grieved person often becomes depressed disorders. (Table 12.4) and may become somewhat withdrawn socially. Guilt feelings, hostility towards others, panic GRIEF attacks, sense of futility, tiredness, neglect of work and self, insomnia and suicidal ideas may occur. The Grief is the normal response of an individual to the loss person may identify with the deceased, sometimes of a loved object. An “object” (psychological speak- even taking on the deceased’s qualities, mannerisms ing) can include a close relative or a friend, material and charac teristics. Finally, a period of reorganisation values or non-material things such as reputation and sets in and readjustment to the environment occurs. self-esteem. Grief has been classifi ed by Gurmeet Singh in Grief is a universal phenomenon which is usually to normal grief and morbid grief reaction. Morbid transient and self-limiting. Uncomplicated grief is not grief has been further divided in to pathological and a psychiatric disorder and does not usually require complicated grief reactions. any psychiatric treat ment. How ever, as physicians (and psychia trists) are sometimes called to intervene Pathological Grief Reaction in severe cases with complications, the condition is When there is an exaggeration of one or more discussed under this chapter. symptoms of normal grief, or the duration becomes Bowlby (1961) described three phases of the prolonged beyond 6 months without spontaneous behaviour response to loss of a loved object: recovery, grief becomes morbid. i. protest, ii. despair, and Table 12.4: Grief and Depression iii. detachment. Following the loss, there is often a state of shock. Features Grief Severe Depression The grieved person feels a sense of bewilderment or 1. Identifi cation with Normal Abnormal numbness, or may completely deny the loss. Although the deceased most commonly this state lasts for a few hours, some- 2. Ambivalence Less More times it may extend up to 2 weeks. This period may 3. Suicidal ideas Rare Common depend on individual characteristics such as mean- 4. Global worthlessness Rare Common ing of loss, personality factors and suddenness of 5. Self-blame for loss Limited Global loss. When the full extent of loss is realised, various 6. Response evoked Empathy; Annoyance; physical and mental symptoms appear. These include from others Sympathy Irritation repeated sighing and crying, diffi culty in breathing, 7. Self-limited Usually May not be choking sensation, weakness, poor concentration and 8. Response to Usually Usually poor appetite. These symptoms usually last for 4-6 assurance good Not as good weeks but may some times extend up to 6 months. 9. Vulnerability to Increased Increased Preoccupation with the memory of the deceased is physical illness 10. Response to a characteristic feature. This is associated with vivid Antidepressants Poor Good mental images, vivid dreams and idealisation of the 152 A Short Textbook of Psychiatry

The various subtypes are: 2. In morbid and (especially) complicated grief, i. chronic grief (dura tion more than 6 months); medication may be needed depending on the ii. delayed grief (onset after 2 weeks of loss); presenting clinical features. iii. inhibited grief (denial of loss); 3. The emphasis should be on: iv. excessive anxiety, guilt, anger or religiosity i. Helping the person face the loss by counter- grief; acting denial. v. identifi cation with the deceased; ii. Ventilation of feelings ( catharsis). vi. over-idealisation of the deceased; and iii. Encouraging presence of signifi cant others. vii. anniversary reactions (grief reaction on death iv. Bringing together similarly grieved persons, anniversary). to encourage communication, share experi- Complicated Grief Reaction ences of the loss and to offer com panionship, and social and emotional support. In some Here, the grief is complicated by specifi c neurotic countries (such as UK), referral to CRUSE or psychotic illness, in addition to grief reaction counselling is often helpful. There are now symptoms. The various subtypes described include hysterical, phobic, obsessive-compulsive, manic or some organisations providing help in some acute psychotic episode. parts of India, for example, Sangath Bereave- ment Service (in Goa); Courage-India and Treatment Can-Support (for cancer related bereavement 1. Normal grief does not require any psychiatric treat- counselling). ment. Occasionally, mild anxiolytic or hypnotic v. Encouragement of goal-directed activities, in a may be needed for short-term use. supportive manner. 13 Mental Retardation

NORMAL CHILD DEVELOPMENT INTELLECTUAL DEVELOPMENT

For understanding behavioural and psychological Intellectual development goes hand-in-hand with the problems of childhood, it is essential to know the development of physical and behavioural character- normal patterns of child develop ment. Although no istics. According to Jean Piaget, it can be divided into two children are alike, there are general similarities the following stages. in the mental and physical development of all normal children. A newborn human infant is probably the most Sensori-Motor Stage helpless of all mammalian infants, and needs much This stage extends from birth to 2 years of age, and more time to become self-dependent. is characterised by: The normal development of a child can be divided i. Actions related to sucking, orality and assimila- into four major areas (these are modiﬁ ed after the tion of objects. Denver Development Screening Test, DDST). ii. Ability to think of only one thought at a time. 1. Motor behaviour. iii. Inanimate objects are given human qualities. 2. Adaptive behaviour. iv. ‘Out of sight’ means ceasing to exist. 3. Language, and 4. Personal and social behaviour. Concrete Thinking Stage As normal children cross these milestones or This stage lasts from 2 years to 7 years of life, and is developmental levels at nearly expected age limits characterised by: (within a few months’ range) it is best to describe i. Egocentric thought with a unique logic of its these developmental changes as milestones. In addi- own, involving a limited point of view and tion to these milestones, there are other developmental lacking introspection. parameters such as height, weight, activity level and ii. Inability to generalise from speciﬁ c events and general health which have an important bearing on to specify from general events. the development of a child. These milestones should not be seen as rigid set of dates and slight delays from Abstract or Conceptual Thinking Stage these milestone dates is not abnormal. Statistically This stage begins at 7 years of age and lasts till 11 years only those values, which are outside two standard of age, although it may be said to continue throughout deviations from the population mean are considered life. This is characterised by: abnormal. However, statistical abnormality is not i. Ability to focus on several dimensions of a always the same as clinical abnormality. problem at one time, mentally. 154 A Short Textbook of Psychiatry

Table 13.1: Normal Developmental Milestones Age Developmental Milestones Age Developmental Milestones 1. Motor Behaviour 1½ years Makes a tower of 3-4 cubes; Scribbles < 4 weeks Moves head laterally in prone position spontaneously, imitating writing; Some- 4 weeks Momentarily lifts head when prone times may draw a vertical line 3 months Head-holding; Lifts head to 90° when 2 years Turns one page of a book at one time; prone Makes a tower of 6-7 cubes; 5 months Sits with support; Rolls over Draws (copies) a horizontal line 6 months Lifts head and upper chest with support 3 years Makes a tower of 9-10 cubes; Makes a of extended arms 3-cube bridge; Draws (copies) a circle. 8 months Sits steadily with straight back; Crawls; 4 years Draws (copies) a cross. Early stepping movements when feet are 5 years Draws (copies) a square; Draws (copies) placed on ground, with support a recognisable man 10 months Pulls from supine to sitting and sitting 6 years Draws (copies) a triangle to standing; Stands holding furniture; 7 years Draws (copies) a diamond (Fig. 13.1) Cruises around; Stands without support 8 years Draws (copies) the following figures momentarily; Creeps on ground without (Figs 13.2 and 13.3) support of abdomen 9 years Draws (copies) the following figure 14-15 months Walks well without support; Walks (Fig. 13.4) backwards and sideways 3. Language 2 years Runs well; Climbs stairs alone; Kicks a 4 weeks Turns head and responds to sound of a large ball; Throws a ball overhead bell; Vocalises (apart from crying) 2½ years Walks on tip-toes 3 months Laughs aloud 3 years Climbs stairs in a coordinated manner, with alternate feet going up the staircase; Rides a tricycle; Makes a broad jump; Jumps in place 4 years Stands on one foot for 5 seconds 5 years Heel-to-toe walk; Jumps on one foot 2. Adaptive Behaviour (includes ﬁ ne motor movements) 4 weeks Momentarily regards close moving objects, close to mid-line Fig. 13.1 Fig. 13.2 3 months Follows the moving objects, even away from mid-line; converges and focuses 4-5 months Grasps objects crudely; Reaches to grasp 6 months Transfer objects from one hand to other 9-10 months Claps hands and matches two hand-held objects in mid line; Thumb-ﬁ nger grasp 1 year Gives hand-held objects to mother, when asked; Turns 2-3 pages of a book at one Fig. 13.3 Fig. 13.4 time

Contd... Mental Retardation 155

Contd... 9 months Speaks mama, dada, m-m-m, ah (and 3 months Recognises mother other vowel sounds); Responds to name 6 months Takes foot to mouth; Smiles back at 10 months Understands spoken speech to some mirror-image of self extent, e.g. where is ‘mama’? 9 months Responds to social play; Resists pulling 1-1¼ years Uses 3-5 words meaningfully away of toy and tries to reach for it; 18 months About 10 words spoken including name Holds milk-bottle and eats a biscuit all 2 years Combines 2 different words; Names by oneself at least one object in picture; Points to 1½ years Feeds oneself with a spoon, with little at least one named body part; Simple spilling; Mimics actions of others; Pulls sentences made a toy with a string; Toilet training started 3 years Uses plurals; Has a fairly good vocabu- 2 years Wears simple garments, socks and shoes lary 3 years Unbuttons buttons; Buckles shoes; Can 5 years Colour naming accurately (primary dress and undress, with help colours); Deﬁ nes words 4 years Buttons the dress well; Washes own face; 4. Personal and Social Behaviour Plays with other children easily; Sepa- 4 weeks Regards face intently rates from mother with little difﬁ culty. 2-3 months Social smile 5 years Dresses without supervision.

ii. The thought process is fl exible and rever sible. the word learning disability is used instead to avoid iii. Ability of abstraction, i.e. ability to generalise the pejorative connotations associated with the word from specifi c and ability to fi nd simi larities and mental retardation. However, in this book, the term differences among specifi c objects. mental retardation is retained as it is the preferred term in both ICD-10 and DSM-IV-TR. Adolescent Th inking or Formal Mental retardation is defined as significantly Operational Stage sub-average general intellectual func tioning, as- This stage begins at 11 years of age and continues sociated with significant deficit or impairment life-long. This is characterised by: in adaptive functioning, which manifests dur- i. Ability to imagine the possibilities inherent in a ing the developmental period (before 18 years of situation, thus making the thought comprehen- age). General intellectual functio n ing is usually as- sive. sessed on a standardised intelligence test with sig- ii. Ability to develop complete abstract hypotheses nifi cantly sub -ave rage intelligence as two standard and to test them. deviations below the mean (usually an IQ of below By the end of adolescence, the individual’s 70), whilst adaptive behaviour is the person’s ability to intellec tual ability is nearly completely developed, meet responsibilities of social, personal, occupational although learning and intellectual growth go-on and interpersonal areas of life, appropriate to age, throughout the lifespan of individual. sociocultural and educational background. Adaptive behaviour is measured by clinical interview and MENTAL RETARDATION standardised assessment scales. Very often, it is assumed that the persons with One to three percent of the general population has mental retardation constitute a homogenous group. mental retardation. In some countries (such as UK), This is however not true. Persons with mental 156 A Short Textbook of Psychiatry retardation vary in their behavioural, psychological, Table 13.2: Classifi cation of Mental Retardation by IQ physical and social charac teris tics as much as the so- Mental Retardation Level IQ Range called ‘normal’ general population does. Another common error is taking the IQ score as 1. Mild 50-70* the measure of someone’s intelligence. It should be re- 2. Moderate 35-50* membered that a person with mental retardation must 3. Severe 20-35* have a defi cit in both general intellectual functioning 4. Profound <20* and adaptive behaviour. (*As intelligence tests employed to measure IQ generally A classifi cation of mental retardation on the basis have an error of measurement of about 5 points, each of IQ (Intelligence Quotient, which is equal to mental fi gure means ± 5 points, e.g. IQ of 50 means an IQ of age, i.e. MA, divided by chronological age, i.e. CA, 50 ± 5, depending on the adaptive behaviour). multiplied by 100; i.e. IQ = MA/CA × 100), is provided in Table 13.2. Severe Mental Retardation Severe mental retardation is often recognised early Mild Mental Retardation in life with poor motor development (signifi cantly This is the commonest type of mental retar dation, delayed developmental milestones) and absent or accounting for 85-90% of all cases. The diagnosis markedly delayed speech and other communication is made usually later than in other types of mental skills. retardation. Later in life, elementary training in personal health In the preschool period (before 5 years of age), care can be given and they can be taught to talk. At these children often develop like other normal children, best, they can perform simple tasks under close super- with very little defi cit. Later, they often progress up to vision. In the earlier educational classifi cation, they the 6th class (grade) in school and can achieve voca- were called as ‘dependent’. tional and social self-suffi ciency with a little support. Only under stressful conditions or in the presence of Profound Mental Retardation an associated disease, supervised care may be needed. This group accounts for about 1-2% of all persons with This group has been referred to as ‘educable’ in a mental retardation. The associated physical disorders, previous educational classifi cation of mental retarda- which often contribute to mental retardation, are com- tion . mon in this subtype. The achievement of developmental milestones is Moderate Mental Retardation markedly delayed. They often need nursing care or About 10% of all persons with mental retardation have ‘life support’ under a carefully planned and structured an IQ between 35 and 50. In the educational classi- environment (such as group homes or residential fi cation, this group was earlier called as ‘trainable’, placements). although many of these persons can also be educated. In the early years, despite a poor social awareness, Aetiology these children can learn to speak. Often, they drop Mental retardation is a condition which is caused not out of school after the 2nd class (grade). They can be only by biological factors but also by psychosocial trained to support themselves by performing semi- factors. In more than one third of cases, no cause can skilled or unskilled work under supervision. A mild be found despite an extensive search. stress may destabilise them from their adaptation; thus Some of the common causes of mental retarda- they work best in supervised occupational settings. tion are listed in Table 13.3. There appears to be a Mental Retardation 157

Table 13.3: Some Causes of Mental Retardation 1. Genetic (probably in 5% of cases) iii. Birth trauma i. Chromosomal abnormalities (such as Down’s iv. Hypoxia syndrome, Fragile-X syndrome, Turner’s syn- v. Intrauterine growth retardation (IUGR) drome, Klinefelter’s syndrome) vi. Kernicterus ii. Inborn errors of metabolism, involving amino- vii. Placental abnormalities acids (phenylketonuria, homo-cystinuria, viii. Drugs during fi rst trimester. Hartnup’s disease), lipids (Tay-Sachs disease, 3. Acquired physical disorders in childhood (prob- Gaucher’s disease, Niemann-Pick disease), ably in 2-5% of cases) carbohydrates (galactosaemia, glycogen storage i. Infections, especially encephalopathies diseases), purines (Lesch-Nyhan syndrome), ii. Cretinism and mucopolysaccharides (Hurler’s disease, iii. Trauma Hunter’s disease, Sanfi llipo’s disease). iv. Lead poisoning iii. Single-gene disorders (such as tuberous sclero- v. Cerebral palsy. sis, neurofi bromatosis, dystrophia myotonica) 4. Sociocultural causes (probably in 15% of cases) iv. Cranial anomalies (such as microcephaly) i. Deprivation of sociocultural stimulation. 2. Perinatal causes (probably in 10% of cases) 5. Psychiatric disorders (probably in 1-2% of cases) i. Infections (such as rubella, syphilis, toxoplas- i. Pervasive developmental disorders (such as mosis, cytomegalo-inclusion body disease) Infantile autism) ii. Prematurity ii. Childhood onset schizophrenia. preponderance of males among people with mental However, the physical appearance may be normal retardation. Some important causes of mental retar- and diagnosis made only after investigations, which dation are discussed below. include:

1. Ferric chloride test: Addition of FeCl3 to urine Phenylketonuria gives a green colour in patients with phenylketon- An inborn error of metabolism, it accounts for about uria. This results from the presence of phenylpy- 0.5-1% of all cases of mental retardation. It is an ruvic acid in urine. This test may be positive in autosomal recessive (AR) disorder, most prevalent other aminoacidurias as well. in North Europe. The basic defect is absence or 2. Guthrie’s test: This involves a bacteriological pro- inactivity of phenylalanine hydroxylase, a hepatic cedure for measurement of phenylalanine levels enzyme, responsible for catalysis of phenyl alanine in blood. to paratyrosine conversion (Fig. 13.5). It results in 3. Chromatography: An early diagnosis is clearly of marked increase in blood phenyl alanine levels and its paramount importance, since mental retar dation metabolites. There is also a decrease in 5-HT, epine- of phenylketonuria is preventable, if diagnosis is phrine and norepi nephrine levels in brain. made early in life. The treatment consists of a low The majority of patients with phenylketonuria phenyl ala nine diet, best started before the age of have severe mental retardation. The associated 6 months and usually continued up to 5-6 years features may include short stature, fair com plexion of age. The diet should not be completely devoid with coarse features, widely spaced upper incisors, of phenyla lanine, as it is an essential amino-acid eczematous dermatitis, epilepsy, hyperactivity, poor and its absence may itself be hazardous. communication skills and poor motor coordination. Other disorders which cause mental retar dation EEG may be abnormal in up to 80% of cases. and are preventable by dietary treatment, include: 158 A Short Textbook of Psychiatry

Fig. 13.5: Metabolic Pathways of Phenylalanine: Normal and Abnormal

1. Homocystinuria: The treatment is with methio- 3. Translocation between chromosome 21 and 15. nine-free diet. Thus, the total number of chromosomes is 46, in 2. Galactosaemia: The treatment is with lactose and spite of 3 chromosomes at 21. The translocation is galactose-free diet. inherited, with asymptomatic carriers containing 3. Maple syrup urine disease (Menkes’ disease): The only 45 chromo somes. treatment is with a diet low in leucine, iso-leucine The most important risk factor is higher maternal and valine. age (>35 years), with a risk of 1:50 after the age of 4. Hyperprolinaemia: The treatment is with low 45. The clinical features may include genera lised proline diet. hypotonia, hyperflexibility, round face, oblique 5. Leucine-sensitive hypoglycaemia: The treatment palpebral fi ssures, a fl at nasal bridge, short ears, loose is with low-protein, leucine-defi cient diet. skin folds at the nape of neck, persistent epicanthic 6. Fructose intolerance: Fructose, sucrose and other folds, single palmar crease, high arched palate, thick sugars should be replaced in diet. tongue, incurved little fi ngers and Brushfi eld spots on irides. Down’s syndrome Congenital heart disease (in about 35% of cases), Down’s syndrome or mongolism occurs in 1 out of gastrointestinal anomalies (in about 10%), chronic every 700 births. It accounts for about 10% of children serous otitis media (in >50%), hypothyroidism and with moderate to severe mental retardation. Alzheimer’s disease (in 30’s and 40’s), epilepsy (in There are three types of chromosomal aberra tions about 10%), ocular disorders, reduced fertility and in Down’s syndrome: reduced life span (often due to antecedent complica- 1. Trisomy-21 is the commonest where karyotype of tions like infections) are common. mother is normal. The diagnosis is made by clinical assessment and 2. Mosaicism, with both normal and trisomic cells chromosomal studies. At present, there is no effective present. pharmacological treatment available. Mental Retardation 159

Tuberous Sclerosis voice, large tongue, subnormal temperature, pot belly, This is an autosomal dominant disorder, also known as anaemia, hypotonia of muscles, hypertelorism and epiloia. It occurs in about 1:15,000 persons in general mental retardation, which may be severe to profound. population. The characteristic clinical features are known as Vogt’s triad, which consist of: Cerebral Palsy i. Mental retardation, ranging from mild to severe. This is a syndrome consisting of a conglomeration of ii. Convulsions. perinatal disorders of various aetiologies, presenting iii. Adenoma sebaceum, present on the face (usually with a common feature of paralysis of limbs. The red) and also on the rest of the body (usually paralysis may be monoplegia, hemiplegia, paraplegia, brownish white). The distribution on the face triplegia or quadriplegia. It is usually of upper motor is usually of butterfl y type. neuron type, presen ting with spasticity. Multiple glial nodules appear throughout the cer- The extrapyramidal symptoms may be pre sent ebral cortex and cerebellum. Tumours in the various and seizures may occur often. Mental retardation is other parts of the body (e.g. rhabdomyoma of heart, present in about 70% of all cases, and ranges from mixed tumours of kidney, retinal nerve tumours) may mild to severe. occur. In addition, periosteal thickening, pulmonary fi brosis, renal failure and cardiac failure can be mani- Diagnosis fested. The diagnosis is made by the following steps: There is no effective treatment at present except 1. History. symptomatic management of seizures and other sys- 2. General physical examination. temic manifestations. 3. Detailed neurological examination. 4. Mental status examination, for the assessment of Fragile-X Syndrome associated psychiatric disorders and the clinical This is second commonest chromosomal aberration assessment of the level of intelligence. causing mental retardation. Occurring in about 1 out 5. Investigations. of 1000 live births, it is diagnosed on chromosomal i. Routine investigations. studies. The characteristic presence of a fragile site ii. Urine test, e.g. for phenylketonuria, maple syrup at the tip of the long arm of X-chromosome appears urine disease. as a constriction. iii. EEG, especially in presence of seizures. Clinically, the person may have a short stature, iv. Blood levels, for inborn errors of meta bolism. large head, large ‘bat’ ears, long face and big sized v. Chromosomal studies, e.g. in Down’s syndrome, testes (in males after puberty). The associated psy- prenatal (by amniocentesis or chorionic villus chiatric disorders, like attention defi cit disorder, may biopsy) and post natal. be present. vi. CT scan or MRI scan of brain, e.g. in tuberous sclero sis, focal seizures, unexplained neurologi- Cretinism cal syndromes, anomalies of skull confi guration, Goitrous cretinism is a common cause of mental retar- severe or profound mental retardation without dation in India. It is endemic in iodine-defi cient areas any appa rent cause, toxoplasmosis. such as the goitrous Himalayan belt. Early recognition vii. Thyroid function tests, particularly when cretin- and treatment is essential, as it is a preventable cause ism is suspected. of mental retardation. viii. Liver function tests, e.g. in mucopolysacc- The clinical features include goitre, dwarfi sm, haridosis. coarse skin, ossifi cation delays, apathy, hoarseness of 6. Psychological tests 160 A Short Textbook of Psychiatry

The commonly used tests for measurement of Primary Prevention intelligence include: This consists of: i. Seguin form board test. 1. Improvement in socioeconomic condition ii. Stanford-Binet, Binet-Simon or Binet-Kamath of society at large, aiming at elimination of tests. under-stimulation, malnutrition, prema tu rity iii. Wechsler Intelligence Scale for Children and perinatal factors. (WISC) for 6½ to 16 years of age. 2. Education of lay public, aiming at remo val of the iv. Wechsler’s Preschool and Primary Scale of misconceptions about individuals with mental Intelligence (WPPSI) for 4 to 6½ years of retardation. age. 3. Medical measures for good perinatal medical v. Bhatia’s battery of performance tests. care to prevent infections, trauma, excessive vi. Raven’s progressive matrices (coloured, stand- use of medications, malnutrition, obstetric ard and advanced). complications, and diseases of pregnancy. The tests used for the assessment of adaptive 4. Universal immunisation of children with BCG, behaviour include: polio, DPT, and MMR. i. Vineland Social Maturity Scale (VSMS). 5. Facilitating research activities to study the ii. Denver Development Screening Test (DDST). causes of mental retardation and their treatment. iii. Gessell’s Development Scale. 6. Genetic counselling in at-risk parents, e.g. in phenylketonuria, Down’s syndrome. Differential Diagnosis The diagnosis of mental retardation is usually simple. Secondary Prevention However, while making this diagno sis, the following 1. Early detection and treatment of preven table dis- conditions must be kept in mind, as they can be and orders, e.g. phenylketon uria (low phenylalanine are many times mistaken for mental retardation, with diet), maple syrup urine disease (low branched disastrous results. amino-acid diet) and others as discussed earlier; 1. Deaf and dumb (This possibility must always be hypo thy roidism (thyroxine). ruled out either by clinical examination and/or by 2. Early detection of handicaps in sensory, motor or audiometry). behavioural areas with early remedial measures 2. Deprived children, with inadequate social stimula- and treatment. tion (Although this can also cause mental retarda- 3. Early treatment of correctable dis orders, e.g. tion, many children become ‘normal’ intellectually infections (antibiotics), skull configuration on providing adequate stimulation). anomalies (surgical correc tion). 3. Isolated speech defects. 4. Early recognition of presence of mental retarda- 4. Psychiatric disorders (such as infantile autism, tion. A delay in diagnosis may cause unfortunate childhood onset schizophrenia). delay in rehabilita tion. 5. Systemic disorders (without mental retarda tion 5. As far as possible, individuals with mental but with physical debilitation). retardation should be integrated with normal 6. Epilepsy. individuals in society, and any kind of seg- regation or discrimination should be actively Management avoided. They should be provided with facilities The management of mental retardation can be dis- to enable them to reach their own full potential. cussed under prevention at primary, secon dary and However, there is a role of special schools for tertiary levels. those with more severe mental retardation. Mental Retardation 161

Tertiary Prevention 6. Legislation: In 1995, the ‘Persons with Dis- 1. Adequate treatment of psychological and be- ability Act’ came in to being in India. This act havioural problems. envisages mandatory support for prevention, 2. Behaviour modiﬁ cation, using the principles of early detection, educa tion, employment, and positive and negative reinforcement. other facilities for the welfare of persons with 3. Rehabilitation in vocational, physical, and social disabilities in general, and mental retardation areas, commensurate with the level of handicap. in parti cular. This Act provides for afﬁ rmative 4. Parental counselling is extremely important action and non-discrimination of persons with to lessen the levels of stress, teaching them to disabilities. adapt to the situation, enlisting them (especially In 1999, the ‘National Trust Act’ came in to parents) as co-therapists, and encouraging for- force. This Act proposes to involve the parents mation of parents’ or carers’ organisation (s) and of mentally challenged persons and voluntary self-help groups. 5. Institutionalisation or residential care may be organisations in setting up and running a variety needed for individuals with pro found mental of services and facilities with govern mental retardation. funding. 14 Child Psychiatry

CLASSIFICATION IN CHILD PSYCHIATRY The defi cit in functioning may be in scho lastic skills, speech and language, and motor skills. These The various psychiatric disorders seen in child- may include reading (develop mental reading disor- hood (‘disorders of psychological develop ment’ and der), language (developmental language disorder), ‘behavioural and emotional disorders with onset arithmetic or mathematics (developmental arithmetic usually occurring in childhood and adolescence’) are or mathematics disorder), articulation (developmental discussed under the following headings: articula tion disorder or phonological disorder), or 1. Mental retardation coordination (developmental coordination disorder ). 2. Specifi c developmental disorders Sometimes, more than one developmental disorder is 3. Pervasive developmental disorders present. 4. Hyperkinetic disorders All developmental disorders either cause impair- 5. Conduct disorders ment in academic functioning at school, especially 6. Tic disorders when language is affected, or impairment in the daily 7. Enuresis and encopresis activities. A large majority of these children have an 8. Speech disorders underlying cerebral disorder. Boys are usually more 9. Habit disorders affected than girls. 10. Other disorders. Before making a diagnosis of specifi c developmental disorder, it is impor tant to keep in mind the MENTAL RETARDATION mental age, IQ, sociocultural background, schooling, impairment(s) in vision and hearing, or any neurologi- Mental retardation (or learning disability) has been cal defi cit. discussed in Chapter 13. Specifi c Reading Disorder SPECIFIC DEVELOPMENTAL DISORDERS It is also called as developmental reading disorder or dyslexia. Mental retardation is a generalised impairment in The child presents with a serious delay in learn- nearly all areas of functioning. In contrast, spe- ing to read which is evident from the early years. cifi c developmental disorders are characterised by an The problems may include omissions, distortions, or inadequate development in usually one specifi c area substitutions of words, long hesitations, reversal of of functioning. words, or simply slow reading. Child Psychiatry 163

Writing and spelling are also impaired. It is im- tions; it is obviously important to rule out deafness portant to differentiate the disorder from scholastic and pervasive developmental disorder. backwardness; therefore a proper assessment is mandatory. Specifi c Developmental Disorder of Motor Function Specifi c Arithmetic Disorder It is also called as motor skills disorder, developmen- It is also called as developmental arithmetic dis- tal coordination disorder, clumsy child syndrome or order or developmental mathematic disorder or motor dyspraxia. It is characterised by poor coordina- dyscalculia. tion in daily activities of life, e.g. in dressing, walking, The child presents with arithmetic abilities well feeding, and playing. There is an inability to perform below the level expected for the mental age (below fi ne or gross motor tasks. par). The problems may include failure to understand simple mathematical concepts, failure to recognise Treatment mathematical signs or numerical symbols, diffi culty The treatment of specifi c developmental dis orders is in carrying out mathematical manipulations, and dif- based on learning theory principles and is behavioural fi culty in learning mathematical tables. in approach. It involves use of special remedial teaching, focusing on the underlying defi cit (for example, Specifi c Developmental Disorder of per cep tual motor training in motor skills disorder). Speech and Language The treatment of common co-morbid emotional It is also called as developmental language disor- problems is often necessary. Parental education and der, developmental communication disorder, or counselling are important components of good man- dysphasia. agement. There are three main types: i. Phonological disorder: Also called as dyslalia , it PERVASIVE DEVELOPMENTAL is characterised by below par accuracy in the use DISORDERS of speech sounds despite normal language skills. The problems include severe articula tion errors Infantile autism was described for the fi rst time by Leo that make it diffi cult for others to understand the Kanner in 1943 as ‘autistic disturbance of affective speech. Speech sounds or phonemes are omitted, contact’. This syndrome has variously been descri bed distorted or substituted (e.g. wabbit for rabbit, ca as autistic disorder, pervasive developmental disorder, for car, bu for blue). childhood autism, childhood psychosis and pseudo- ii. Expressive language disorder: It is characterised defective psychosis. by a below par ability of using expressive speech. This syndrome is more common (3-4 times) in The problems include restricted voca bu lary, diffi - males and has a prevalence rate of 0.4-0.5 per 1000 culty in selecting appropriate words, and immature population. Although earlier it was thought to be com- grammatical usage. Cluttering of speech may also moner in upper socioeconomic classes, recent studies be present. have failed to confi rm this fi nding. iii. Receptive language disorder: The disorder often Typically, the onset occurs before the age of 2½ presents as a receptive-expressive language disor- years though in some cases, the onset may occur later der and both receptive and expressive impairments in childhood. Such cases are called as childhood onset are present together. The disorder is characterised autism or childhood onset pervasive developmental by a below par understanding of language. Prob- disorder. Autism occur ring before or after 2½ years lems include failure to respond to simple instruc- of age is not clinically very different. 164 A Short Textbook of Psychiatry

Clinical Features profound mental retardation. There appears to be a The characteristic features are: correlation between severity of mental retardation, 1. Autism (marked impairment in reci procal social absence of speech and epilepsy in autism. and interpersonal interaction): 5. Other features i. Absent social smile. i. Many children with autism particularly enjoy ii. Lack of eye-to-eye-contact. music. iii. Lack of awareness of others’ existence or feel- ii. In spite of the pervasive impairment of func- ings; treats people as furniture. tions, certain islets of precocity or splinter iv. Lack of attachment to parents and absence of functions may remain (called as Idiot savant separation anxiety. syndrome). Examples of such splinter functions v. No or abnormal social play; prefers solitary are prodigious rote memory or cal cula ting abil- games. ity, and musical abilities. vi. Marked impairment in making friends. iii. Epilepsy is common in children with an IQ of vii. Lack of imitative behaviour. less than 50. viii. Absence of fear in presence of danger. The course of infantile autism is usually chronic 2. Marked impairment in language and non-verbal and only 1-2% become near normal in marital, social communication and occupational function ing. A large majority (about i. Lack of verbal or facial response to sounds or 70%) lead dependent lives. voices; might be thought as deaf ini tially. ii. In infancy, absence of communicative sounds Aetiology like babbling. Presently, the cause of infantile autism seems to be pre- iii. Absent or delayed speech (about half of autistic dominantly biological. Earlier reports of cold, ‘refrig- children never develop useful speech). erator’ mothers causing autism in their children have iv. Abnormal speech patterns and content. Presence not been substantiated and have unnecessarily lead of echolalia, perseveration, poor articulation and to undue distress to parents of children with autism. pronominal reversal (I-You) is common. The evidence for biological causation inclu des a v. Rote memory is usually good. higher than average history of perinatal CNS insult, vi. Abstract thinking is impaired. EEG abnormalities, epilepsy, ven t ri cular dilatation 3. Abnormal behavioural characteristics on brain imaging, increased serotonin (5-HT) levels i. Mannerisms. in brain and/or neurophysiological abnormalities in ii. Stereotyped behaviours such as head-bang ing, some patients. body-spinning, hand-ﬂ icking, lining-up objects, rocking, clapping, twirling, etc. Treatment iii. Ritualistic and compulsive behaviour. The treatment consists of three modes of intervention iv. Resistance to even the slightest change in the which are often used together. environment. 1. Behaviour Therapy v. Attachment may develop to inanimate objects. i. Development of a regular routine with as few vi. Hyperkinesis is commonly associated. changes as possible. 4. Mental retardation ii. Structured class room training, aiming at learn- Only about 25% of all children with autism have ing new material and maintenance of acquired an IQ of more than 70. A large majority (more learning. than 50%) of these children have moderate to iii. Positive reinforcements to teach self-care skills. Child Psychiatry 165

iv. Speech therapy and/or sign language teaching. Schizophrenia, mood disorders and organic v. Behavioural techniques to encourage interper- psychiatric disorders have a nearly similar picture in sonal interactions. children as in adulthood. Sometimes, childhood onset 2. Psychotherapy schizophrenia may be mistaken for autism. The most Paren tal counselling and supportive psychotherapy important differentiating features are: can be very useful in allaying parental anxiety 1. Delusions, formal thought disorder and hallucina- and guilt, and helping their active involve ment in tions may be present in childhood-onset schizo- therapy. However, overstimulation of child should phrenia while they are always absent in infantile be avoided during treatment. autism. 3. Pharmacotherapy 2. Typical age of onset of symptoms is before 2½ Drug treatment can be used for treatment of autism years in infantile autism while it is after 5-6 years as well as for treatment of co-morbid epilepsy. in childhood onset schizophrenia. i. Haloperidol decreases dopamine levels in brain. 3. Moderate to severe mental retardation and epilepsy It is believed to decrease hyper activity and are common in infantile autism while they are rare behavioural symptoms. Risperidone, an atypi- in childhood-onset schizoph renia. Mental retarda- cal antipsychotic, is helpful in some patients tion, if ever present, is usually of mild type. and is licensed in some countries for treatment Another type of childhood psychosis, called of autism in children aged 5 and above. Both Heller’s syndrome or disintegrative psychosis, has haloperidol and risperidone can cause extra- often been described in literature. Typically, the age pyramidal side-effects (EPSE), though usually of onset is between 3 to 5 years and the syndrome is more with haloperidol. characterised by a rapid downhill course, leading to The starting dose for Risperidone is usually deterioration and development of neurological defi cits. 0.25-0.5 mg (based on body weight), with a This is really a ‘rag-bag’ category containing diverse dose range of 0.02-0.06 mg/kg/day. organic brain syndromes of varying aetiologies (For ii. Other drugs such as SSRIs, chlorpromazine, example, some are caused by lipoid degeneration of amphetamines, methysergide, imipra mine, ganglia in central nervous system). Prognosis is usu- multi-vitamins and triiodothy ronine have been ally poor in this condition. tried with limited success and should be used Two other syndromes with autistic features have only by the experts in the fi eld. been described; namely, Asperger’s syndrome and iii. Anticonvulsant medication is used for the treat- Rett’s syndrome. ment of generalised or other seizures, if present. Asperger’s syndrome is characterised by autism without any signifi cant delay in language or cognitive OTHER PERVASIVE DEVELOPMENTAL development (including intelligence). This syndrome DISORDERS occurs predominantly in boys (male : female ratio = 8:1). It probably represents mild cases of autism and Childhood psychosis is a vague term which includes has been also called as high functioning autism. all psychotic illnesses occurring in childhood, such Rett’s syndrome is a disorder which is only as infantile and childhood onset autism, childhood reported in girls so far. After an apparently normal schizophrenia, mood disorders, and organic psychiat- early development and normal head circumference at ric disorders. This term has frequently been misused in birth, there is a deceleration of head growth between the past, also meaning at times infantile autism alone. the age of 5 months and 30 months. There is also a loss This is a term which is probably best dispensed with. of purposive hand movements and acquired fi ne motor 166 A Short Textbook of Psychiatry manipulative skills between the same ages, with the 2. Attention defi cit disorder without hyperac- subsequent development of stereotyped movements tivity: It is a rare disorder with similar clinical of hands (e.g. hand-wringing). Later, other movement features, except hyperactivity. disorders also develop and severe mental handicap is 3. Residual type: It is usually diagnosed in a patient invariable. in adulthood, with a past history of ADD and presence of a few residual features in adult life. ATTENTION DEFICIT DISORDER 4. Hyperkinetic disorder with conduct disorder (HYPERKINETIC DISORDER) (Hyperkinetic conduct disorder).

This is a syndrome fi rst described by Heinrich Hoff Diagnosis in 1854. Since then, it has been known by a variety The diagnosis can be made on the basis of: of names such as minimal brain dysfunction (MBD), 1. Teacher’s school report (often the most reliable). hyperkinetic syndrome, Strauss syndrome, organic 2. Parent’s report. drivenness and minimal brain damage. 3. Clinical examination (many children with hyper- A relatively common disorder, it occurs in about activity may be able to sit still in the new setting 3% of school age children. Males are 6-8 times more of the hospital and thus the diagnosis may be often affected. The onset occurs before the age of missed). 7 years and a large majority of patients exhibit symp- Hyperactivity is also a common clinical symptom toms by the 4th year of age. in mental retardation. Thus, mental retardation should Attention defi cit disorder (ADD) is of four clini- always be excluded, before making a diagnosis of cal types: with hyperactivity, without hyperacti vity, ADD. residual type, and with conduct disorder. 1. Attention defi cit disorder with hyperactivity Aetiology (Hyperkinetic disorder): This is the commonest Many factors, such as minimal brain damage, matura- type. The characteristic clinical features are: tional lag, genetics, neurotransmitters (norepinephrine Poor attention span with distractibility and dopamine) and early developmental psychody- i. Fails to fi nish the things started. namic factors have been incriminated. The cause is ii. Shifts from one uncompleted activity to not yet known but it is more likely to be a biological another. factor than a purely psychosocial one, though a focus iii. Doesn’t seem to listen. on both factors is important in the management of an iv. Easily distracted by external stimuli. individual patient. v. Often loses things. Hyperactivity Course i. Fidgety. A large majority (about 80%) of patients improve ii. Diffi culty in sitting still at one place for long. on their own by the time of puberty, though a few iii. Moving about here and there. (15-20%) may have persistent symptoms even in iv. Talks excessively. adulthood. Impulsivity and inattention are usually the v. Interference in other people’s activities. most common residual features after puberty while Impulsivity hyperactivity often tends to remit. i. Acts before thinking, on the spur of the mo- ADD can also present in adulthood and Adult ment. ADD is recognised by both ICD-10 and DSM-IV-TR. ii. Diffi culty in waiting for turn at work or These includes graduates of childhood onset ADD play. which continue to have symptoms in adulthood and Child Psychiatry 167 those who begin with symptoms for the fi rst time in CONDUCT DISORDERS adulthood. Conduct disorder is characterised by a persistent and Treatment signifi cant pattern of conduct, in which the basic rights The management of ADD consists of the following of others are violated or rules of society are not fol- methods: lowed. The diagnosis is only made when the conduct is far in excess of the routine mischief of children and Pharmacotherapy adolescents. The onset occurs much before 18 years 1. Stimulant medication: Dextro-amphetamine or of age, usually even before puberty. dexamphetamine (2.5-20 mg/day) and methyl- The disorder is much more (about 5-10 times) phenidate (5-60 mg/day) have been traditionally common in males. In United States of America, about used. Currently, Methylphenidate is the drug 10% of all male children under the age of 18 have of choice in the treatment of ADD, with a high conduct disorder. response rate. Methylphenidate is also available According to ICD-10, there are four subtypes of in sustained release formulations which are pref- conduct disorder: erable due to improved treatment concordance 1. Conduct disorder confi ned to the family context. and convenience of once a day dose. 2. Unsocialised conduct disorder. Both dexamphetamine and methylphenidate 3. Socialised conduct disorder. act on the reticular activating system, causing 4. Oppositional defi ant disorder. stimulation of the inhibitory infl uences on the The characteristic clinical features include: cerebral cortex, thus decreasing hyperactivity 1. Frequent lying. and/or distracti bility. 2. Stealing or robbery. 2. Others: When stimulant medication is not avail- 3. Running away from home and school. able or is not effective, other drugs can be used 4. Physical violence such as rape, fi re-setting, assault after careful individual consideration of the risks or breaking-in, use of weapons. and benefi ts in the individual patient. These 5. Cruelty towards other people and animals. include clonidine, tricyclic antidepressants In the more common socialised (group) type of (such as imipramine), bupro pion, venlafaxine, conduct disorder, the person claims loyalty to his or chlorproma zine, thiorida zine, and lithium her group. The unsocialised (solitary) type is a more carbo nate. serious disorder with usually a severe underlying Atomoxetine, a norepinephrine reuptake inhibitor, psychopathology. Earlier, the patients with conduct may be an alternative for children who do not respond disorder were called as juvenile delinquents. to stimulants. The usual dose range is 0.5-1.2 mg/kg/ Many patients of conduct disorder, especially day. Atomoxetine appears to be the drug of choice in socialised (group) type, go on to improve mark- adult ADD. edly and may lead well adjusted lives. Some others, Barbiturates are contraindicated in ADD as they especially those with severe symptoma tology, have increase hyperactivity. a more chronic course and may be diagno sed with antisocial personality disorder (or traits) after 18 Behaviour Modifi cation years of age. In addition to the typical symptoms of conduct Counselling and Supportive Psychotherapy disorder, secondary complications often develop Behaviour modifi cation and counselling are very such as substance misuse or dependence, unwanted important in the successful management of ADD and pregnancies, criminal record, suicidal and homicidal can be used along with drug therapy. behaviour. 168 A Short Textbook of Psychiatry

The treatment of conduct disorder is usually dif- i. Simple motor tics: These may include eye- fi cult. The most frequent mode of management is blinking, grimacing, shrugging of shoulders, placement in a corrective institution, often after the tongue protrusion. child has had legal diffi culties. Behavioural, educa- ii. Complex motor tics: These are facial gestures, tional and psycho therapeutic measures are usually stamping, jumping, hitting self, squatting, twirl- emp loyed for the behaviour modifi cation. ing, echokinesis (repetition of observed acts), Drug treatment may be needed in presence of copropraxia (obscene acts). epilepsy (anticonvulsants), hyperactivity (sti mu lant Motor tics are often the earliest to appear, begin- medication), impulse control disorder and episodic ning in the head region and then progressing down- aggressive behaviour (lithium, carbamazepine), and wards. These are later followed by the vocal tics. psychotic symptoms (antipsy chotics). Vocal Tics TIC DISORDERS The vocal tics in Tourette’s disorder can also be simple or complex. Tic disorders are characterised by the presence of i. Simple vocal tics: Simple vocal tics include tics. Tic is an abnormal involuntary movement (AIM) coughing, barking, throat-clearing, sniffi ng, and which occurs suddenly, repetitively, rapidly and is clicking. purposeless in nature. It is of two types: ii. Complex vocal tics: These include some very 1. Motor tic, characterised by repetitive motor move- characteristic, though not always present, ments. symptoms of Tourette syndrome; for exam ple, 2. Vocal tic, characterised by repetitive vocalisations. echolalia (repetition of heard phrases), palilalia Tic disorders can be either transient or chronic. (repetition of heard words), coprolalia (use of Transient tic disorders are more common in boys obscene words), and mental coprolalia (thinking and can occur in 5-20% of children. Tics are easily of obscene words). worsened by stressful life situations, fatigue and/or Obsessions and Compulsions are often the associ- use stimulants such as caffeine and nicotine. A vast ated symptoms. These are usually the last symptoms majority of these disappear by adulthood. to appear. A special type of chronic tic disorder is Gilles de la Tourette’s syndrome or Tourette’s disorder. Aetiology The aetiology of Tourette syndrome is not known but Tourette’s Disorder the presence of learning diffi culties, neurological soft Tourette’s disorder is typically characterised by: signs, hyperactivity, abnormal EEG record, abnormal 1. Multiple motor tics. evoked potentials, and abnor mal CT Brain fi ndings in 2. Multiple vocal tics. some patients, point towards a biological basis. 3. Duration of more than 1 year. There is some evidence to suggest that Tourette 4. Onset usually before 11 years of age and almost syndrome may be inherited as autosomal dominant always before 21 years of age. disorder with variable penetrance. The disorder is usually more common (about three times) in males and has a prevalence rate of about 0.5 Treatment per 1000 people. Pharmacotherapy is usually the preferred mode of treatment though there is lack of clear evidence of Motor Tics effi cacy. Antipsychotics are often helpful in small The motor tics in Tourette’s disorder can be simple doses and several drugs have been tried including or complex. haloperidol, risperidone, olanzapine, aripiprazole, Child Psychiatry 169 ziprasidone, quetiapine, and sulpiride. Treatment tation, spina bifi da, neurogenic bladder, urinary tract options are often chosen based on adverse effect infection, diabetes mellitus, and seizure disorder. profi le of each drug (which adverse effects to avoid). In secondary enuresis, the age of onset is usually SSRIs (such as fl uoxetine) have been used for the 5-8 years. Enuresis tends to remit spontaneously and treatment of co-morbid obsessive compulsive symp- only 1% of children with enuresis continue to have toms. the disorder in adulthood. In the resistant cases or in case of severe side- effects, pimozide or clonidine can be used under Treatment expert supervision. Behaviour therapy can sometimes The management consists of one or more of the fol- be used, as an adjunct. lowing measures: 1. Restriction of fl uid intake after 8 PM, in nocturnal NON-ORGANIC ENURESIS enuresis. 2. Bladder training during daytime, aimed at increas- Enuresis is repetitive voiding of urine, either during ing the holding-time of bladder. This is carried out the day or night, at inappropriate places. This state of in a step-by-step manner using positive reinforce- affairs is normal in infancy. ments. Most children achieve bladder control by the age 3. Interruption of sleep before the expected time of of three years. By the age of 5 years, there are still bed wetting. The child should be fully woken up about 7% of children who wet their bed. Technically, and made aware of passing of urine. enuresis is diagnosed only after 5 years of age (and 4. Conditioning devices, which cause an alarm to at least 4 years of mental age). sound as soon as the voided urine touches the bed- Enuresis can be either of: sheet. It is important to check the child’s hearing 1. Primary type, where bladder control has never before starting treatment. The alarm causes inhibi- been achieved, or tion of further micturition and the child awakens. If 2. Secondary type, where enuresis emerges after a properly used, it is an effective method of therapy. period of bladder control (at least one year). 5. Supportive psychotherapy for the child, parents The majority (about 80%) of children with enuresis and the whole family is often needed. have nocturnal bed wetting only. Non-organic enuresis 6. Pharmacotherapy: Drug treatment is usually not is more common (about two times) in males. a preferred option for the treatment of enuresis. The drug of choice in those who need pharma- Aetiology cotherapy has traditionally been a tricyclic antide- The exact cause of enuresis is not known. A variety pressant, usually imipramine (25-75 mg/day). It of factors, which are implicated in its causation, are probably acts by its anti cho linergic effect as well as largely biopsychosocial. About 75% of children with by decreasing the deep sleep (stage 4 NREM-sleep) enuresis have a fi rst degree relative with history of period. However, there is a risk of sudden death in enuresis. some children with the use of tricyclic antidepressants. The most commonly occurring factors, however, It should never be used for children under the age of are psychosocial, such as emotional disturbances, in- 6 years. security, sibling rivalry, death of a parent. An organic Intranasal desmopressin has been found useful cause must be looked for in children with diurnal in some patients and is a good alternative. The other enuresis (15% of all cases of diurnal enu resis) and drugs that have been used for this purpose include adolescents with enuresis. The organic causes are diazepam, anticholinergics, ampheta mines, placebos, present in about 5% of cases and include worm infes- but none have shown a good therapeutic response. 170 A Short Textbook of Psychiatry

NON-ORGANIC ENCOPRESIS warm and understanding. The emo tional disturbances of the child should not be ignored and should be dealt Encopresis is repetitive passage of faeces at inap- with at the earliest. The communication between the propriate time and/or place, after bowel control is family members should be direct. physiologically possible. This is not due to the pres- After encopresis has developed, the treatment of ence of any organic cause, which is called as faecal choice is behaviour therapy, using reinforcements incontinence. Normally, toilet training is achieved (both positive and negative). The other treat ments between the ages of 2 and 3. Encopresis is defi ned as include psychotherapy, biofeedback and imipramine occurring after the age of 4 years. (in non-retentive encopresis). Encopresis can be either of: SPEECH DISORDERS 1. Primary type, where toilet training has never been achieved, or Stuttering is a disorder of speech, characterised by the 2. Secondary type, where encopresis emerges after following features: a period of faecal continence. This type typically 1. Disturbed fl uency and rhythm of speech. occurs between the ages of 4 and 8. 2. Intermittent blocking. Encopresis is more common (about 3-4 times) in 3. Repetition of words rapidly. males. By the age of 5 years, 1-1.5% of children suffer 4. Prolongation of sounds. from encopresis. It tends to remit spontaneously with 5. Associated anxiety or distress. increasing age and by the age of 16 there are virtually Earlier stammering and stuttering were differen- no adolescents with encopresis. About 25% of these tiated on the basis of minor differences. At present, patients have associated enuresis. they are thought to be synonymous. The disorder is a fairly common one, affecting 2-5% of all children Aetiology and 0.5-1% of all adults. Males are more commonly The factors implicated in causation of enco presis (about three times) affected. include: Differential diagnosis is from cluttering, which is 1. Inadequate, inconsistent toilet training. characterised by an erratic and dysarrhythmic pattern 2. Sibling rivalry. of speech, with jerky and rapid spurting of words. 3. Maturational lag. Unlike in stuttering where the person is aware of the 4. Underlying hyperkinetic disorder. diffi culty in speech, the affected person in cluttering 5. Emotional disturbances. is usually unaware of the abnormal speech pattern. 6. Mental retardation. 7. Childhood schizophrenia. Treatment 8. Autistic disorder. The treatment is by behaviour modifi cation techniques Whenever presented with a patient of enco pre sis, such as desensitisation, biofeedback and stammer organic causes (faecal incontinence) must be ruled out suppresser; and by techniques to diminish anxiety (such as Hirschsprung’s disease, over fl ow diarrhoea like relaxation therapy, drug therapy, or individual or with constipation, hypothy roi dism, inflammatory group psychotherapy. bowel disease and neuro logical lesions). HABIT DISORDERS Treatment The best treatment of encopresis is preventive. The These are stereotyped disorders which are intention- toilet training period should be made as consistent and ally and repetitively produced but serve no construc- smooth as possible. The family environ ment should be tive or socially acceptable function. Child Psychiatry 171

The common habit disorders include thumb sucking, despite the presence of language competence in ing, nail biting, pulling out of hair (trichotillomania), at least some situations. head banging, masturbation, teeth grinding, picking Typically, it is fi rst manifested in early child- of nose, biting parts of the body, skin-scratching, hood and is seen more often in girls. It is estimated body rocking, breath-holding, and swallowing of air to be present in 3-8/10,000 chil dren. It may be as- (aerophagia). sociated with tempera mental traits involving social These habits range from normal to abnor mal, anxiety, withdrawal, sensitivity or resistance. The depending on the severity of occurrence and the time child is often mute in front of strangers or at school. of presentation during the developmental period Other socio-emotional disturbances may also be (what is normal in infancy, may be abnormal in later present. childhood). Many of habit disorders, particularly Elective mutism should be differentiated from shy- those which are self-stimulating in nature, are called ness in normal children, mental retar dation, pervasive as gratifi cation habits. These have been considered developmental disorder, expressive language disorder, by some as masturbatory equivalents. These habit and conversion disorder. Most cases improve with the disorders tend to be commoner in individuals with passage of time, though some children may require mental retardation or learning disability. pharma cotherapy (such as with fl uoxetine) and/or psychosocial manage ment. Treatment The treatment is by behaviour modifi cation techniques OTHER DISORDERS and treatment of underlying psychopathology, if present. The other childhood psychiatric disorders include separation anxiety disorder, phobic anxiety disorder ELECTIVE (SELECTIVE) MUTISM of childhood, social anxiety disorder of childhood, sibling rivalry disorder, mixed disorders of conduct Elective mutism is characterised by the presence of and emotions, and reactive attachment disorder of marked, emotionally determined, selectivity in speak- childhood. 15 Psychopharmacology

HISTORY OF TREATMENT IN 8. Miscellaneous drugs, such as stimulants, drugs PSYCHIATRY used in treatment of eating disorders, drugs used in treatment of alcohol and drug dependence, The treatment of psychiatric disorders in past had often anaesthetics, drugs used in treatment of demen tia, constituted of merely institu tio na lisation (i.e. admis- drugs used in child psychiatry, vitamins, calcium sion in an asylum or mental hospital), sometimes along channel blockers, and other drugs. with the use of treatment which now seems either ridiculous or fantastic or mostly both. The advent An Ideal Psychotropic Drug of psychopharmacology in the last six decades has An ideal psychotropic drug should have the following brought treatment of psychia tric disorders within the characteristics (modifi ed after Hollister, 1983): realm of scientifi c medicine. 1. It should cure the underlying pathology causing Some important milestones in the treat ment of the disorder or symptom(s) under focus, so that psychiatric disorders are summarised in Table 15.1. the drug can be stopped after sometime. 2. It should benefi t all the patients suffering from that CLASSIFICATION OF PSYCHOTROPIC disorder. DRUGS 3. It should have no side-effects or toxicity in the therapeutic range. The drugs which have a signifi cant effect on higher 4. It should have rapid onset of action. mental functions are called as psychoactive or psycho- 5. There should be no dependence on the drug and tropic drugs. These psychotropic drugs can be broadly no withdrawal symptoms on stopping the drug. classifi ed as follows: 6. There should be no tolerance to the drug so that 1. Antipsychotics same dose is effective for long duration of time. 2. Antidepressants 7. It should not be lethal in overdoses. 3. Mood stabilising drugs (or drugs for maintenance 8. It can be given in both inpatient and out patient treatment of bipolar disorder) settings. 4. Anti-anxiety and hypnosedatives Although psychotropic drugs available at present 5. Anticonvulsants (or anti-epileptics) are far from ideal, they are still helpful in alleviation 6. Alcohol and drugs of dependence (discussed in of symptoms and suffering of patients. With increasing Chapter 4) research, new emerging products appear to be better in 7. Antiparkinsonian drugs effi cacy and have fewer, though newer, side-effects. Psychopharmacology 173

Table 15.1: A Brief History of Psychopharmacology <4000 BC Ayurveda describes treatment of psychiatric patients with sympathy and kind ness. The methods of treatment inclu ded dhatura and roots of serpentina plant mixed with oil (ghee). 1853 Bromide used as a sedative-hypnotic. 1869 Chloral hydrate used in the treatment of melancholia and mania. 1882 Paraldehyde used as a hypnotic. 1883 Phenothiazines synthe sised during synthesis of methylene blue (Bernthsen). 1903 Barbiturates ( barbital) used for seda tion in 1903; phenobarbital introduced in 1912. 1917 Malarial treatment for General Paralysis of Insane (GPI) received a Nobel prize (Julius von Wagner Jauregg). 1922 Barbiturate-induced coma introduced for the treatment of psychoses (Jacob Klaesi). 1927 Insulin-shock treatment introduced for schizophrenia (Manfred Sakel). 1931 First report of successful treatment of psychoses (Ganesh Sen and Kartik Bose from India); using Rauwolfi a serpentina extract ( reser pine). Report ignored till Nathan Kline (1958) confi rmed the fi nding. 1934 Metrazol-induced con vulsions used for the treatment of psycho ses (Laszlo von Meduna). 1936 Frontal lobotomy advocated for treatment of psychiatric disorders (Egas Moniz and Almenda Lima). 1937 Amphetamines used in the treatment of behaviour disorders of children (C Bradley). 1938 Electroconvulsive therapy used for the treatment of psycho ses (Ugo Cerletti and Lucio Bini). 1940 Phenytoin used as an anticon vulsant (Tracy Putnam). 1943 LSD synthesised (Albert Hofmann). 1949 Lithium used in mania (John F Cade); did not receive much attention even in Australia. 1950 Chlorpromazine synthesised while making a better antihis taminic than promethazine (Charpentier). 1950 Methylphenidate used in treatment of ADHD, then known as Minimal Brain Dysfunc tion (MBD). 1951 Lytic cocktail used (Laborit); Chlorpromazine earlier used (as ‘456 ORP’) in artifi cial hibernation. 1951 Isoniazid (INH) found to have mood elevating properties in patients with tuberculosis. Iproniazid, a MAOI and a derivative of INH, was later (1958) introduced for treatment of depression. 1952 The revolution in psychopharmacology came with intro duction of chlorpromazine (Jean Delay and Pierre Deniker). The number of admissions in mental hospitals show a sudden decrease after introduction of chlorpromazine. 1955 Meprobamate was introduced as an anti-anxiety agent. 1958 Imipramine, a tricyclic anti depressant (TCA) synthesised by Hafl inger and Schindler in the late 1940’s, was introduced for treatment of depression in 1958 (Thomas Kuhn). 1958 MAOIs (e.g. iproniazid) introduced for treatment of depression (Nathan Kline). 1958 Haloperidol synthesised in Belgium (Janssen). 1960 Chlordiazepoxide used as an anti-anxiety agent in 1960-1961 (Sternbach; Synthesised in 1957). 1966 Valpromide (Valproate) used in bipolar disorder (Lambert). 1968 Pimozide used for treatment of schizophrenia (Janssen). 1967 Clomipramine used in OCD (Fernandez and Lopez-Ibor). 1971 Carbamazepine used in bipolar disorder (Takezaki and Hanoaka) (Synthesized in 1953 by Schindler). 1986 Buspirone introduced in US market as a non-benzodiazepine anti-anxiety agent. 1988 Clozapine re-discovered in US as an effective treatment for refractory schizophrenia (Kane et al) (Syn the sised in 1959). Approved by US FDA in 1990 and introduced in Indian market in 1995. 1990s Second Generation Antipsychotics introduced in market starting with Risperidone. 174 A Short Textbook of Psychiatry

The information in this chapter is necessarily very 4. Mania (with or without mood stabilisers) brief and introductory in nature. A much more detailed 5. Maintenance treatment of bipolar disorders reading is defi nitely recommended before prescrib- (e.g. olanzapine, quetiapine) ing any psychotropic medication to a patient with 6. Major depression (for psychotic features, consultation of local formularies and guidelines. This agita tion, and melancholic features; along with information should not be used to make any treatment antidepressants) decisions without further reading. 7. Delusional disorders Neurotic and Other Psychiatric Disorders ANTIPSYCHOTIC DRUGS 1. Severe, intractable, and disabling anxiety (rarely used and not recommended) Antipsychotics are psychotropic drugs which are 2. Treatment refractory obsessive compulsive used in the treatment of psychotic disorders and disorder (as an adjunct) psychotic symptoms. These are also known as major 3. Anorexia nervosa (rarely used and not widely tranquilisers, neuro leptics, ataractics, anti-schizo- recommended) phrenic drugs and D2-receptor ( dopa mine receptor) Medical Disorders blockers; however, the term antipsychotic appears 1. Huntington’s chorea (e.g. haloperidol) to be the most appropriate and the most widely used 2. Intractable hiccups (e.g. chlorpromazine in low term. doses) (rarely used) 3. Nausea and vomiting (rarely, in low doses); Indications ondansetron, an anti-emetic drug, is a weak Antipsychotics have previously been used as urinary antipsychotic antiseptics and anti-helminthic; however, their use 4. Tic disorders, e.g. Gilles de la Tourette synd- stopped was due to toxicity and lack of effi cacy. rome (e.g. haloperidol, risperidone) Although they have been used in a wide variety of conditions in the past their current use includes the Pharmacokinetics following conditions. The orally administered antipsychotics are absorbed Organic Psychiatric Disorders erratically and variably from gastro intestinal tract, 1. Delirium (in small doses; e.g. haloperidol, with uneven blood levels. Intramuscular and intra- risperidone) venous admini s tration provides much more reliable 2. Dementia (careful and considered use for psy- blood levels. On an average, the oral liquid dose pro- chotic features, and severe agitation) duces a peak level at 1½ hours and the intramuscular 3. Delirium tremens (and psychoses occurring dose peaks at 30 minutes. in drug and alcohol withdrawal states; e.g. The antipsychotics are highly lipophilic and haloperidol, risperidone) highly protein-bound. They easily enter areas with 4. Drug induced psychosis (e.g. haloperidol in good blood supply such as brain, lung, kidneys and amphetamine-induced psychosis) foetus, and accumulate there. They are not dialys- 5. Other organic mental disorders (e.g. organic able. The half-lives of most antipsychotics are long hallucinosis; organic delusional disorder; sec- and theoretically a single daily dose is suffi cient to ondary mania) produce sustained thera peutic blood levels. However Non-organic Psychotic Disorders in practice, divided doses are administered, at least 1. Schizophrenia initially, to decrease adverse effects. Later an attempt 2. Schizo-affective disorder can be made to give the whole dose or a major part of 3. Acute psychoses total daily dose at night. Psychopharmacology 175

Steady state plasma levels are usually reached in blockade which is usually highest for drugs such as 5-10 days. Once the drug is withdrawn, it may remain chlorpromazine and thioridazine. in body for many days to many months. The main metabolic pathway is through liver (hepatic microsomal Second Generation Antipsychotics enzymes). Oxidation and conjugation are the most A search for an antipsychotic drug which acts only important methods of metabolism for phenothiazines. on the mesolimbic system but has no effect on nigro- Many of the meta bolites, such as mesoridazine (for striatal or tubero-infundibular systems, has led to the thioridazine), reduced haloperidol (for haloperidol) development of a heterogeneous group of drugs col- and 9-hydroxy-risperidone (for risperidone), are also lectively known as atypical or newer antipsychotics. active compounds. Chlorpromazine has more than 150 These are also known as second generation anti- metabolites, some of which are active. The excretion psychotics (SGAs) or serotonin-dopamine antagonists of the metabolites is through kidneys and liver (entero- or (SDAs). These include risperidone, quetiapine, hepatic circulation). olanzapine, amisulpride, paliperidone, zotepine, Most of the antipsychotics tend to have a therapeu- ziprasidone and aripiprazole. tic window. If the blood level is below this ‘window’, By defi nition these drugs are effective antipsy- the drug is ineffective. If the blood level is higher than chotics without theoretically producing undesirable the upper limit of the ‘window’, there is toxicity or extrapyramidal side-effects (i.e. antipsychotics with- the drug is again ineffective. out neuroleptic effect), or causing elevation of serum prolactin levels. These are characterised by a selective Classifi cation limbic dopamine blockade, D4-receptor blockade, or A classifi cation of currently available antipsychotic a combination of potent 5-HT 2 and weak D2 antago- drugs is presented in Table 15.2. nism. These drugs should theoretically be safer with lesser incidence of serious side-effects such as tardive Mechanism of Action dyskinesia and neuroleptic malignant syndrome. The exact mechanism of action of antipsy chotics is Clozapine is one such drug but it can cause unknown. However, one of the major mechanisms agranulocytosis and seizures. Risperidone, olanzapine, appears to be antidopaminergic activity of these drugs. quetiapine, aripiprazole, amisulpride and ziprasi done

Antipsychotic drugs block D 2-receptors, which are are currently being used widely as atypical antipsy- mainly present in mesolimbic-mesocortical system chotics, while paliperidone and zotepine are also ( mesolimbic system is concerned with emotional reac- available in the international market. tions), nigro-striatal system and tubero-infundibular Atypical antipsychotics, in addition to their effect system. The relative potencies of these drugs in com- on positive symptoms, are believed to be effective peting for D2-receptors parallel quite closely their in treatment of negative symptoms (such as apathy, clinical potencies. decreased sociality, anhedo nia) of chronic schizophre- It is currently believed that antipsy chotic drugs nia. Cloza pine in particular is effective in mana gement are effective in treating psychosis due to their ac- of treatment-resistant schizophrenia. However, there tion on the D2-receptors located in the mesolimbic is need for close haematological monitoring for system whilst extrapyramidal side-effects (EPSE) neutropenia or agranulocytosis as suggested in SPC are caused by blockade of D2-receptors situated in of the drug. nigro-striatal system and hyperprolactinaemia is Side Effects caused by D2-blockade in tubero-infundibular system. However, other neurotransmitters (such as 5-HT, ace- The antipsychotics are safe drugs with a high thera- tylcholine) are clearly implicated (see below; atypical peutic index and wide margin of safety in routine antipsychotics). Sedation is caused by histaminergic clinical dosages. In spite of this safety, a wide range 176 A Short Textbook of Psychiatry

Table 15.2: Clas sifi cation and Properties of Antipsychotics Drugs Oral Dose Parenteral #Some Common Adverse Effects** (mg/d) Dose (mg) Sedation Hypotension EPSE* Weight Increased Gain Prolactin I. Phenothiazines A. Aliphatics 1. Chlorpromazine 300-1000 50-100 IM +++ +++ + ++ ++ (CPZ) 2. Trifl upromazine 100-400 30-60 IM ++ ++ ++ ++ ++ B. Piperidines 1. Mesoridazine 100-400 ____ ++ + + ++ + 2. Thioridazine 300-600 ____ +++ ++ + ++ + C. Piperazines 1. Fluphenazine 2-20 ____ + + +++ + +++ 2. Prochlorperazine 45-150 40-80 IM + + +++ + +++ 3. Trifl uoperazine 15-50 1-5 IM + + +++ + +++ II. Thioxanthenes A. Aliphatics 1. Chlorprothixene 75-600 25-75 IM +++ ++ ++ ++ ++ B. Piperazines 1. Flupentixol 3-18 ____ + + ++ ++ ++ 2. Thiothixene 6-60 2-6 IM + ++ ++ ++ ++ 3. Zuclopenthixol 25-150 50-100 IM ++ ++ ++ ++ +++ III. Butyrophenones 1. Haloperidol 5-30 5-10 IM + + +++ + +++ 2. Trifl uperidol 0.5-8.0 2.5-5.0 IM ± ± +++ + ++ IV. Diphenylbutylpiperidines 1. Penfl uridol 20-60 mg ____ + + ++ + ++ weekly 2. Pimozide 4-20 ____ + + ++ + +++ V. Indolic Derivatives (Dihydroindolones) 1. Molindone 50-225 ____ ++ 0 + ± ± VI. Dibenzoxapines 1. Loxapine 25-250 ____ ++ ++ ++ + +++ VII. Atypical or Second Generation Antipsychotics A. Dibenzodiazepines 1. Clozapine 50-900 ____ +++ +++ 0 +++ 0 B. Substituted Benzamides 1. Amisulpride 400-1200 ____ ± + + + +++ 2. Sulpiride (not 400-2400 ____ ± + + + +++ called atypical usually) Contd... Psychopharmacology 177

Contd... Drugs Oral Dose Parenteral #Some Common Adverse Effects** (mg/d) Dose (mg) Sedation Hypotension EPSE* Weight Increased Gain Prolactin C. Benzisoxales 1. Iloperidone 4-24 ____ 0+ +++0 2. Paliperidone 3-12 ____ + ++ + ++ +++ 3. Risperidone 2-8 ____ + ++ + ++ +++ D. Benzisothiazolyl 1. Ziprasidone 40-160 ____ ±+ 0±± E. Thienobenzodiazepine 1. Olanzapine 5-20 2.5-10 IM ++ + ± +++ + F. Dibenzothiazepine 1. Quetiapine 150-750 ____ ++ ± 0 ++ 0 G. Partial Agonists 1. Aripiprazole 5-30 ____ 00 0±0 2. Bifeprunox 20 ____ 00 0±0 H. Dibenzothiepin 1. Zotepine 75-300 ____ ++ ± + ++ ++ I. Dibenzooxepinopyrrole 1. Asenapine 5-10 ____ 0± 0±0 # The estimate of common adverse effects in this table is a very rough and empirical guideline to the clinical use of antipsychotics. The drug dosage in each patient needs to be individualised based on the clinical symptoms, their severity, response to treatment and several other clinical factors. * EPSE means Extrapyramidal side effects. ** 0 = Absent; ± = Probable/Very little; + = Mild; ++ = Moderate; +++ = Severe of side-effects do occur with the use of antipsychotics After 1 month: Weight, BMI, Blood pressure, Waist even in the therapeutic doses. circumference, and Fasting blood sugar. The common side-effects are listed in Table 15.3 After 3 months: Weight, BMI, Blood pressure, Waist with their mechanisms of causation and management. circumference, and Fasting blood sugar. Some of newer antipsychotics appear to have a higher After 6 months: Weight, BMI, Blood pressure, Waist association with metabolic syndrome (see Chapter 5 circumference, Fasting blood sugar, Serum lipids, and Table 15.3). and LFTs. It is important to monitor physical health whilst After 12 months: Weight, BMI, Blood pressure, Waist prescribing antipsychotics and the following are the circumference, Fasting blood sugar, and Serum lipids. most commonly recommended minimum suggestions. Several antipsychotics can increase QTc interval Other investigations may also be indicated (such as (QT interval corrected for heart rate). These include

ECG, HbA1c) based on clinical opinion. sertindole, haloperidol, pimozide, ziprasidone, zo- Baseline (before prescribing): Obtaining detailed tepine, quetiapine, or any intravenously administered personal and family history, Weight, BMI, Waist antipsychotic. A similar effect is seen with administra- circumference, Blood pressure, WBC and Neutrophil tion of TCAs. QTc prolongation can be made worse count, Fasting blood sugar, Serum lipids, and LFTs. with co-prescribed medications (e.g. anti-arrhythmics 178 A Short Textbook of Psychiatry

Table 15.3: Side Effects of Antipsychotics Category and Probable Cause Maximum with Minimum with Management Side Effect (For example) (For example) A. Autonomic Side Effects 1. Dry mouth Muscarinic Choliner- Chlorpromazine Haloperidol Usually none; Tolerance gic blockade Risperidone develops; Occasionally Pilocarpine 2% 2. Constipation –do– Chlorpromazine Haloperidol Usually none; Tolerance Risperidone develops; Bulk (or sometimes other) laxatives 3. Cycloplegia –do– Chlorpromazine Haloperidol Usually none; Tolerance Risperidone develops; Occasionally Pilocarpine 2% 4. Mydriasis –do– Thioridazine; Haloperidol Usually none; Tolerance miosis with Risperidone develops; Occasionally Chlorpromazine) Pilocarpine 2% 5. Urinary –do– Chlorpromazine Haloperidol Usually none if only hesi- Retention Risperidone tancy occurs. Tolerance develops; Rule out BHP; Bethanethol or catheteri- sation for retention 6. Delirium (central –do– Chlorpromazine Haloperidol Physostigmine (neostig- anticholinergic Risperidone mine does not enter syndrome) CNS); Diazepam sometimes supportive care

7. Orthostatic α1 Adrenergic Chlorpromazine Haloperidol Usually none; Tolerance hypotension blockade Aripiprazole develops; change in posture slowly. When severe, use plasma expanders, raise leg, supportive measures. 8. Impotence –do– Chlorpromazine Haloperidol Decrease dose. If severe, change medication. 9. Impaired –do– Thioridazine Haloperidol Decrease dose. If severe, ejaculation change medication. B. Extra-pyramidal Side Effects (EPSE)

1. Parkinsonian Dopaminergic (D2) Haloperidol Clozapine Antiparkisonian medica- syndrome receptor blockade in Quetiapine tion for treatment; also (esp. tremor) striatal areas Aripiprazole for prevention if needed. 2. Akathisia (motor –do– –do– Clozapine Change of medication or restlessness) Quetiapine reduction; Beta-blockers such as Propranolol; Ben- zodiazepines Contd... Psychopharmacology 179

Contd... Category and Probable Cause Maximum with Minimum with Management Side Effect (For example) (For example) 3. Acute Dystonia —do— —do— —do— Antiparkinsonian medication; Rule out hypercalcaemia 4. Rabbit Syndrome —do— —do— —do— Antiparkinsonian (Peri-oral tremor) medication

5. Tardive Dopaminergic (D2) Not known Clozapine Treatment unsatisfactory, Dyskinesia (late receptor though several drugs are onset oro-facial super-sensitivity available. Prevention dyskinesia) best. 6. Neuroleptic Not known Probably Not known Bromocriptine, Dantro- Malignant haloperidol lene, Baclofen, General Syndrome supportive care. Add-on (Fever, EPS, lorazepam, Occasionally High CPK, ECT catatonic symptoms and autonomic dysfunction) C. Other Central Nervous System Effects 1. Seizures Decreased seizure Clozapine Triﬂ uoperazine Decrease dose. Change threshold Chlorpromazine to a safer antipsychotic (High doses) 2. Sedation Histaminergic —do— Haloperidol This side effect may be blockade Aripiprazole beneﬁ cial. Otherwise decrease dose. Change drug. Give single dose only at night 3. Depression or Decreased catecho- Not known SDAs Decrease dose. Change Pseudo- lamine levels in (e.g. Ziprasidone) drug. Occasionally anti- depression brain depressants or ECT. D. Metabolic and Endocrine Side Effects

1. Weight gain H1 blockade Almost all Aripiprazole Change drug. Dietary antipsychotics esp. Haloperidol control. Exercises. Clozapine and Olanzapine 2. Diabetes Not known Clozapine Ziprasidone Change drug. Dietary Olanzapine Aripiprazole control. 3. Galactorrhoea Increased Prolactin Haloperidol Aripiprazole None. Change drug. with/without released due to Risperidone Quetiapine amenorrhoea dopaminergic blockade in hypothalamus Contd... 180 A Short Textbook of Psychiatry

Contd... Category and Probable Cause Maximum with Minimum with Management Side Effect (For example) (For example) E. Allergic Side Effects 1. Cholestatic Hypersensitivity Chlorpromazine Haloperidol Change drug. Benign Jaundice reaction course. Supportive care. 2. Agranulocytosis —do— Clozapine —do— Stop drug immediately. (very rare) Treat infection. Isolation. General supportive care. Figastrim may be useful F. Cardiac Side Effects 1. ECG Changes Anticholinergic Thioridazine Aripiprazole Change drug, if severe. (e.g. QTc effect Pimozide prolongation) Calcium channel blocking effect 2. Sudden Death Probably ventricular Not known Not known None (very rare) ﬁ brillation G. Ocular Side Effects 1. Granular Not known Chlorpromazine Haloperidol Change drug. deposits in (Probably (High doses for cornea and lens photosensitivity long duration) 2. Pigmentary Not known Thioridazine only All other antipsy- Never give more than retinopathy (Dose-related) chotics 800 mg/day of thiori- resembling dazine. Prevention only retinitis pigmentosa H. Dermatological Side Effects 1. Contact Allergic Chlorpromazine —do— Avoid handling. dermatitis (By handling) Symptomatic treatment 2. Photosensitive Probably —do— (High doses) —do— Avoid sunlight. reaction photosensitive Use sunscreen. 3. Blue-gray —do— —do— (High doses —do— Change drug. metallic for long duration) discolouration such as quinidine, anti-malarials such as quinine, Treatment Adherence and antibiotics such as erythromycin) and/or medical conditions (such as ischaemic heart disease, extremes Many patients with schizophrenia can be unco- of ages). operative, with a poor treatment adherence (see This list of side-effects is necessarily incomplete Table 15.4). Therefore, it may at times be difﬁ cult to and it is important to read the SPC of any drug before ensure adequate admi ni s tration of antipsychotics on prescribing it in a patient. an outpatient basis. Psychopharmacology 181

Table 15.4: Some Factors in Poor Drug Concordance Since discontinuation of antipsychotic medication 1. Drug Related Factors often leads to relapse, long-acting prepara tions of i. Adverse effects (particularly their early appear- antipsychotics are valu able in the treatment. They ance and persistence) may be given in a depot form, either intramuscularly ii. Slow onset of desirable effects or administered orally. There are several different iii. Complexity of regimen (e.g. several doses/day) preparations available in the international market but iv. Route of administration (IM/IV as opposed to the preparations summarised in Table 15.5 are used oral) most often. 2. Patient Related Factors i. Poor education regarding illness and medication Clinical Use ii. Denial of illness/absent insight Some general principles regarding routine clinical use iii. Perceived stigma of mental disorder, medica- of antipsychotics include: tion, or visible side effects (e.g. dystonia) 1. Although atypical antipsychotics are usually iv. Treatment access problems (e.g. poverty, cost preferred, the choice of antipsychotic medication of medications, distance from hospital) should be individualised in a particular patient. v. Low IQ and/or low educational level The recent evidence shows more differences in vi. Poor social support adverse effect profi les but not in effi cacy between vii. Specifi c psychopathology, e.g. persecutory idea- older and newer antipsychotics. tion, hopelessness 2. Whenever possible the lowest effective dose viii. Poor doctor-patient relationship. should be used. 3. Routinely only one antipsychotic should be used Table 15.5: Some Antipsychotic Depot Preparations* at one time. Rational polypharmacy should be reserved only for judicious treatment after non- 1. Flupentixol decanoate 20-300 mg IM every 2-4 response to single antipsy chotics. weeks (40 mg IM every 2 weeks roughly equivalent to 4. High doses of antipsychotics should be avoided. 25 mg of fl uphenazine decanoate IM every 2 weeks) 5. Whenever appropriate, psychosocial mana ge ment 2. Fluphenazine decanoate 12.5-100 mg IM every 2-4 should be combined with antipsychotic treatment. weeks (25 mg IM every 2 weeks roughly equivalent to 300 mg of oral Chlorpromazine per day) 6. It is really important to monitor physical health 3. Haloperidol decanoate 25-250 mg IM every 4 weeks on a regular basis whilst the patient receives an- (100 mg IM every 4 weeks roughly equivalent to 5 tipsychotic medication (see above). mg/day of oral haloperidol) 7. Do not use rapid neuroleptisation (parenteral use 4. Olanzapine pamoate 150-300 mg IM every 2 weeks of a loading dose of antipsychotic medication), if or 300-405 mg IM every 4 weeks (Note risk of post- possible. injection syndrome; Also note dose escalation chart in SPC) ANTIDEPRESSANT DRUGS 5. Pipotiazine palmitate 25-100 mg IM every 4 weeks 6. Risperidone Consta 25-50 mg IM every 2 weeks Antidepressants are those psychotropic drugs which (Note delay in onset of action by 2-3 weeks and need are used for treatment of depres sive disorders. These for refrigeration) have also been called as mood-elevators and thy- 7. Zuclopenthixol decanoate 200-400 mg IM every 2-4 moleptics. weeks (200 mg IM every 2 weeks roughly equivalent Isoniazid (INH) was found to have mood elevating to 25 mg/day of oral Zuclopenthixol) properties in some patients suffering from tuberculosis * Check SPC (Summary of Product Characteristics) before in 1951. Iproniazid, a MAO inhibitor and a derivative prescribing any medicines of INH, was later (1958) introduced for the treatment 182 A Short Textbook of Psychiatry of depression. The fi rst tricyclic antidepressant (TCA) 4. Cataplexy (associated with narcolepsy) imipramine was used in 1958 by Thomas Kuhn. It was 5. Aggression in elderly (e.g. trazodone) different from phenothiazines by only a replacement 6. Eating disorders (e.g. fl uoxetine in bulimia ner- of sulphur with an ethylene linkage. With this small vosa) structural difference (discovered by chance), imi- 7. Borderline personality disorder (for treatment of pramine was found not effective as an antipsychotic dep res sive symptoms) but instead quite benefi cial in depressed patients. 8. Trichotillomania (e.g. clomipramine; fl uoxetine) Since 1958, the number of antidepressants has been 9. Depersonalisation syndrome gradually increasing. 10. Post-traumatic stress disorder (PTSD) Antidepressants have no euphoriant effect when 11. Generalised anxiety disorder (e.g. SSRIs) administered to normal, non-depressed individuals. 12. Nicotine dependence (e.g. bupropion is used for treatment of craving) Indications 13. Alcohol dependence (e.g. fl uoxetine sometimes Presently, the indications for the use of anti depressants used for treatment of craving) include: Medical Disorders Depression 1. Chronic pain (in low doses, e.g. amitri ptyline, 1. Depressive episode (also called major depression, duloxetine) endo genous depression) 2. Migraine (as an adjuvant) 2. Depressive episode with melancholia (with or without ECTs) Classifi cation 3. Depressive episode with psychotic fea tures (with Classification and properties of antidepressants antipsychotics or ECTs) (Table 15.6). 4. Dysthymia (with psycho the rapy) 5. Reactive depression (with psychotherapy) Pharmacokinetics 6. Dep ressive equivalents and masked depression The oral dose of TCAs is incompletely though ad- (sometimes) equately absorbed. As they are highly anticholinergic 7. Atypical depression (e.g. MAO inhibitors) in nature, they delay gastric emptying and slow gastro- 8. Secondary depression (e.g. in hypothyroidism, intestinal motility. SSRIs are well absorbed from the Cushing’s syndrome) gastrointestinal tract. 9. Abnormal grief reaction These antidepressants, much like antipsychot- Child Psychiatric Disorders ics, are highly lipophilic and are highly protein 1. Enu resis (with or without behaviour therapy) bound. Thus they have a large volume of distribu- 2. Attention defi cit disorder with hyperactivity (in tion and tend to accumulate in areas with good blood low doses, after 6 years of age, when stimulant supply. Like antipsychotics, they are also not dialysable. medication is not avai lable) Their other pharmacokinetic properties of TCAs 3. School phobia (sometimes, in low doses) are similar to those of phenothiazines. The half-life 4. Separation anxiety disorder (in children) is long, usually more than 24 hours. Although TCAs 5. Somnambulism can be administered in a single night-time dose, the 6. Night terrors routine clinical practice is to prescribe divided doses, Other Psychiatric Disorders at least in the initial days of treat ment, to prevent 1. Panic attacks (e.g. SSRIs) accumulated side-effects. The metabolism of TCAs is 2. Agoraphobia and social phobia by oxidation (hepatic microsomal enzymes) followed 3. Obsessive compulsive disorder with or without by conjugation (glucoronic acid). The major metabo- depression (e.g. clomipramine, SSRIs) lites of imipramine and amitripty line (desipramine and Psychopharmacology 183

Table 15.6: Classiﬁ cation and Properties of Antidepressants Drugs Oral Dose Some Common Adverse Effects# (mg/d) Sedation* Orthostatic Hypotension* Anticholinergic* I. Cyclic Antidepressants A. Tricyclic Tertiary Amines 1. Amitriptyline 75-300 +++ +++ +++ 2. Clomipramine 75-250 ++ ++ ++ 3. Dosulepin (Dotheipin) 75-300 +++ +++ ++ 4. Doxepine 75-300 +++ +++ + 5. Imipramine 75-300 ++ ++ ++ 6. Lofepramine 70-210 + + + 7. Tri-imipramine 75-300 +++ ++ ++ B. Tricyclic Secondary Amines 1. Desipramine 75-300 ± + ++ 2. Nortriptyline 75-200 + ++ + 3. Protriptyline 15-60 0 ++ ++ C. Tetracyclic Antidepressants 1. Amoxapine 150-400 + + ++ 2. Maprotiline 75-225 ++ ++ ++ 3. Mianserin 30-120 +++ ± ± D. Bicyclic Antidepressants 1. Viloxazine 100-300 ± ± ± II. Selective Serotonin Reuptake Inhibitors (SSRIs) 1. Citalopram 20-40 ± ± 0 2. Escitalopram 10-20 ± ± 0 3. Fluoxetine 20-60 ± 0 0 4. Fluvoxamine 50-300 ± ± ± 5. Paroxetine 20-40 + 0 ± 6. Sertraline 50-200 ± ± 0 III. Serotonin Norepinephrine Reuptake Inhibitors (SNRIs) 1. Duloxetine 60 ± ± ± 2. Venlafaxine 75-375 + ± ±

IV. Norepinephrine Serotonin Reuptake Enhancers (NSREs) 1. Tianeptin 37.5 + 0 ± V. Noradrenergic and Speciﬁ c Serotonergic Antagonists (NaSSAs) 1. Mirtazapine 15-45 +++ + ± VI. Norepinephrine Dopamine Reuptake Inhibitors (NDRIs) 1. Bupropion 150-450 Activating 0 0 VII. Serotonin Antagonists and Reuptake Inhibitors (SARIs) 1. Nefazodone 200-600 ++ + ± (withdrawn from market) 2. Trazodone 150-400 +++ ± ± Contd... 184 A Short Textbook of Psychiatry

Contd... Drugs Oral Dose Some Common Adverse Effects# (mg/d) Sedation* Orthostatic Hypotension* Anticholinergic* VIII. Noradrenergic Reuptake Inhibitors (NARIs) 1. Reboxetine 8-10 ± ± ± IX. Mono-amine Oxidase Inhibitors (MAOIs) A. Irreversible Non-selective and Selective MAOIs Not available in India B. Reversible Selective MAO-B Inhibitors 1. Selegiline 5-10 Useful in Parkinsonism C. Reversible Selective MAO-A Inhibitors (RIMAs) 1. Moclobemide 300-600 Activating 0 0

X. Melatonin receptor agonist and 5-HT2C antagonist 1. Agomelatin 25-50 + 0 0 # The estimate of common adverse effects in this table is a very rough and empirical guideline to the clinical use of antidepressants. The drug dosage in each patient needs to be individualised based on the clinical symptoms, their severity, response to treatment and several other clinical factors. * 0 = Absent; ± = Probable/Very little; + = Mild; ++ = Moderate; +++ = Severe

nortriptyline respectively) are active antidepressants 1. Blocking reuptake of norepinephrine (NE), sero- themselves. Fluoxetine is demethylated in liver to tonin (5HT) and/or dopamine (DA) at the nerve norfl uoxetine. terminals, thus increasing NE, 5HT and/or DA With the regular administration of TCAs, a con- levels at the receptor site. stant blood level is achieved usually by the end of 2. Down-regulation of the β-adrenergic recep tors. two weeks. Although routine monitoring of blood The Mono-amine oxidase inhibitors (MAOIs) levels is not indicated, it may become important in instead act on mono-amine oxidase (MAO) which cases of toxicity. Also, some antidepressants such is responsible for degradation of catecho lamines fol- as nortriptyline and protriptyline have a therapeutic lowing their reuptake. The fi nal effect is the same, i.e. window. a functional increase in the NE and/or 5HT levels at Antidepressants (especially SSRIs, e.g. fl uo xe tine) receptor site. also cause inhibition of cytochrome P450 enzymes in Another important clinical point is that it takes liver (e.g. CYP P450 2D6 and CYP P450 3A4). 5-10 days before a MAOI, and 2-3 weeks before a The MAO inhibitors are absorbed well by oral non-MAOI antidepressant, has any evident action on route, and are predominantly metabolised in liver by depression (although sleep, anxiety and agitation may acetylation. respond earlier). The reason for this is not fully clear though an increase in brain amine levels is possibly Mechanism of Action responsible for antidepressant action. However, post- The exact mechanism of action is not clearly known. synaptic events (such as down-regulation of postsyn- It appears from clinical studies that the predo minant aptic receptors) are probably more important and they action of antidepressants is to increase the catecho- take longer than an increase in amine levels. Therefore, lamine levels in brain (Amine hypo thesis). it is of no benefi t to prescribe antidepressants on an Tricyclic antidepressants are also called as Mono- SOS or PRN (as needed) basis. They must be admin- amine reuptake inhibitors (MARIs). Their main modes istered regularly in appropriate doses to achieve the of action include: desired effect. Psychopharmacology 185

It is essential to continue the antidepressant for a activity. These include anxiety, agitation, confusion, period of further 6 months after reaching remission, in clonus (e.g. ankle clonus, ocular clonus), hyperrefl ex- the fi rst episode of depressive disorder (and for longer ia, myoclonus, rigidity, increased heart rate, tremor, duration in subsequent episodes) to prevent recur- fl ushing, hyperthermia and excessive sweating. Death rence of symptoms. It is important to prescribe the can occur in severe serotonin syndrome. antidepressant in the same dose as used for treatment Treatment includes discontinuation of the offend- unless there are adverse effects requiring a decrease ing drug(s), supportive management and (sometimes) in dose. use of serotonin and histamine antagonist cyprohep- Only when adequate doses (150-300 mg tadine. imipramine equivalent) have been administered for an adequate period (at least 6 weeks) without a clini- Refractory Depression cal response then the drug can be called ineffective About 20-35% of patients do not respond to the for that patient. Another drug, usually from a different antidepressant therapy. The chief reasons for this class or group, or ECT may then be used. non-response include: 1. Poor drug concordance. Side Effects and Toxicity 2. Inadequate dosage. The common side effects of antidepressants with their 3. Insuffi cient treatment duration. manage ment are summarised in Table 15.7. 4. Low plasma antidepressant levels. TCAs are dangerous in overdose; amitriptyline 5. Incorrect diagnosis. and dosulepin (dotheipin) are particularly cardiotoxic Even when these important reasons are excluded, whilst lofepramine is the safest amongst TCAs. Clini- there still remains a group (15-20%) of depres sed cal features of overdose include agitation, delirium, patients who are non-respon ders or poor-responders. paralytic ileus, urinary retention, coma, respiratory Such patients should receive a trial of another antide- depression, seizures, hyperpyrexia, cardiac arrhyth- pressant preferably from a different group (e.g. SNRI) mias, conduction defects, mydriasis, and death. The for adequate duration. In case the patient still does not lethal dose of imipramine is 1-2 g. (40-80 tabs. of respond, the treatment of choice of refractory depres- 25 mg imipramine equivalence). sion is electroconvulsive therapy (ECT), though other The treatment options in overdose include gastric treatment choices (such as lithium augmentation) are lavage/induction of vomiting, activated charcoal for also available. adsorption, cardio-respiratory resuscitation, treatment of seizures (if they occur), general supportive care MOOD STABILISING DRUGS and symptomatic management. Quinidine-like drugs (DRUGS USED IN PROPHYLAXIS are contraindicated whilst antiarrhythmics such as OF BIPOLAR DISORDER) lignocaine can be helpful. Physostigmine 0.5 mg IV/IM bolus repeated to a total of 3-4 mg/day may These drugs are usually effective in treatment of ma- be used under careful supervision. Coma often reverts nia and therefore the word antimanic is often used to in less than 24 hours, although toxicity lasts for describe them. But as they are effective in preventing 5-6 days. mood swings in bipolar disorder, the better term is Co-prescription of serotonergic drugs (such as mood-stabilising agent or a prophylactic agent. The SSRIs) with other serotonergic agents and especially most commonly used mood-stabilising agents include MAOIs can lead to serotonin syndrome. It is char- lithium, valproate, carbamazepine, and lamotrigine, acterised by a classic triad of mental status changes, though there are several other experimental mood neuromuscular abnormalities and autonomic hyper- stabilisers such as oxcarbaze pine. 186 A Short Textbook of Psychiatry

Table 15.7: Side Effects of Antidepressants Category and Probable Cause Maximum with Minimum with Management Side Effect (For example) (For example) A. Autonomic Side Effects 1. Dry mouth Muscarinic Amitriptyline Fluoxetine See table for side effects of Cholinergic antipsychotics (Table 15.3) blockade 2. Constipation –do– Amitriptyline Fluoxetine 3. Cycloplegia –do– Amitriptyline Fluoxetine 4. Mydriasis –do– Amitriptyline Fluoxetine 5. Urinary retention –do– Amitriptyline Fluoxetine 6. Delirium –do– Amitriptyline Fluoxetine 7. Aggravation of –do– Amitriptyline Fluoxetine Do not use in elderly and in narrow angle patients with past history. glaucoma Change or stop drug.

8. Orthostatic α1 Adrenergic Amitriptyline Fluoxetine See table for side effects of hypotension blockade antipsychotics (Table 15.3) B. Sexual Side Effects

1. Impotence α1 Adrenergic Amitriptyline Mirtazapine blockade Bupropion

2. Impaired/ α1 Adrenergic Amitriptyline Mirtazapine Cyproheptadine given 1 hour retarded blockade Paroxetine Bupropion before, can reverse anorgas- ejaculation mia and retarded ejaculation caused by SSRIs. 3. Anorgasmia 5-HT blockade SSRIs Mirtazapine TCAs Bupropion 4. Priapism Not known Trazodone Not known Stop drug; muscular relaxation; sometimes surgical procedure needed C. CNS Effects 1. Sedation α Adrenergic Amitriptyline Protriptyline This side effect may be ben- blockade Fluoxetine efi cial; Otherwise decrease dose. Change drug. Give single dose only at night. 2. Tremor and Serotonergic Amoxapine Not known Decrease dose. Change drug. Other EPSE 3. Jitteriness Adrenergic; Imipramine MAOI This is very common in syndrome Serotonergic Fluoxetine fi rst week of therapy. Add diazepam for fi rst 1-2 weeks. Tolerance occurs. 4. Withdrawal Dependence Imipramine Protriptyline Slow withdrawal of drug. syndrome (mild) Paroxetine Fluoxetine 5. Seizures Decreased Bupropion Nomifensine Decrease dose. Change drug. threshold Amitriptyline Fluoxetine Contd... Psychopharmacology 187

Contd... Category and Probable Cause Maximum with Minimum with Management Side Effect (For example) (For example) 6. Aggravation of Sympathomimetic Not known Amoxapine Stop drug. Re-evaluate. psychosis 7. Precipitation of Sympathomimetic Tricyclics Not known Stop drug. Use mood mania stabilisers. D. Cardiac Side Effects 1. Tachycardia Anticholinergic Amitriptyline Trazodone Decrease dosage. Use safer 2. Quinidine-like Cardiotoxic Amitriptyline Fluoxetine drugs in elderly and those action (decreased with past history or co-exist- conduction time) ing heart disease 3. ECG changes Cardiotoxic Amitriptyline Fluoxetine 4. Arrhythmias Cardiotoxic Dosulepin Fluoxetine (in overdoses) Amitriptyline 5. Direct myocardial Cardiotoxic Amitriptyline Fluoxetine depression (in overdoses) 6. Hypertension Noradrenegic Venlafaxine SSRIs Close monitoring; ECG and Duloxetine BP check before start (especially on higher doses); treat hypertension E. Allergic Side Effects 1. Agranulocytosis Hypersensitivity Mianserin Not known See table for side effects of (very rare) Mirtazapine antipsychotics (Table 15.3) 2. Cholestatic Hypersensitivity Not known Not known jaundice (very rare) 3. Skin rashes Hypersensitivity Not known Not known 4. Systemic vasculitis Not known Not known Not known F. Metabolic and Endocrine Side Effects 1. Weight gain Not known Mirtazapine Bupropion Change drug. Exercise. Diet Amitriptyline Fluoxetine can control. cause weight loss G. Miscellaneous Side Effects 1. Hypertensive Interaction with Tranylcypromine Non-MAOIsPrevent use of such agents crises tyramine in foods with MAOI. Carry ‘warning (cheese, red wine, cards’. When crisis occurs, chicken liver) use alpha (α) blockers like and /or sympatho- phentolamine. mimetic drugs (e.g. amphetamine) Contd... 188 A Short Textbook of Psychiatry

Contd... Category and Probable Cause Maximum with Minimum with Management Side Effect (For example) (For example) 2. Severe hepatic Toxic or Iproniazid Tranylcypromine Stop/change drug. Supportive necrosis (rare) Hypersensitive care; Death rate high. 3. Hyperpyrexia Interaction with Not known Not known Stop drug. Keep a gap of tricyclics or 1 week between imipramine meperidine and MAOI. Supportive care. 4. Bleeding Decreased SSRIs Not known Change drug. Do not co- platelet serotonin prescribe other drugs that increase risk of bleeding; Gastro-protective drugs such as PPIs can decrease risk to some extent in high-risk patients 5. Hyponatraemia Probably SIADH SSRIs Not known; Risk higher in elderly; Avoid SNRIs Probably MAOIs co-prescribing other drugs that cause hyponatraemia (such as diuretics); monitor closely

Recently, several atypical antipsychotics such as The element was discovered in 1817 by Arfuedson. olanzapine, quetiapine and aripiprazole have been Since then, it has been used for treatment of gout and added to list of drugs used in maintenance treatment for salt replacement in cardiac disease, but its use was of bipolar disorder. In addition, other antipsychotics restricted due to fatal toxicity. such as risperidone (and the others mentioned above) It was rediscovered in 1949 by John Cade, for use are also used as antimanic agents. in treatment of mania but its potential went unrecog- Lamotrigine and Quetiapine (and its metabolite nised as it was discovered in Australia. Mogen Schou norquetiapine) appear to have particular efﬁ cacy for in 1957, had to rediscover it yet again before it became treatment of bipolar depression. There is a risk of skin popular as a treatment of mania. rash with lamotrigine particularly early in treatment and the risk appears higher with faster escalation of Indications dose as well as with co-prescription of valproate. It is Although lithium salts are used in treatment of a therefore important to increase the dose of lamotrigine myriad of psychiatric and non-psychiatric disorders, very gradually as suggested in the summary of product the established indications are only the following characteristics (SPC) and the dose prescribed depends ones: on other co-prescribed drugs (such as carbamazepine 1. Treatment of acute mania and valproate). 2. Prophylaxis of bipolar mood disorder. In addition, the following may also constitute LITHIUM possible clinical indications of lithium use: 3. Treatment of schizo-affective disorder Lithium (Li) is an element (Atomic number 3 and 4. Prophylaxis of unipolar mood disorder Atomic weight 7) which is the smallest alkali ion. 5. Treatment of cyclothymia Psychopharmacology 189

6. Treatment of acute depression (as an adjuvant for 8. It interferes with the phosphatidyl-inositol cycle refractory depression) by blocking the conversion of IMP (inositol mono- 7. Treatment of chronic alcoholism (in pre sence of phosphate) to inositol, by inositol monophosphate signifi cant depressive symptoms) and psy cho- phosphatase. The muscarinic acetylcholine (Ach) active use disorders (e.g. cocaine depen dence) receptor is among one of the neurotransmitter 8. Treatment of impulsive aggression recep tors linked to this system in brain. The 9. Treatment of Kleine-Levin syndrome. antimanic effects of lithium may be attributed to this effect on Ach, thus affecting the cholinergic- Pharmacokinetics adrenergic balance. Lithium is very rapidly absorbed from the gastro- All these actions result in a decreased catecho- intestinal tract. The peak serum levels occur between la mine activity, thus ameliorating mania. How ever, 30 minutes to 3 hours. The absorption is virtually these mechanisms do not explain the anti depressant complete in about 8 hours. effect and the prophylactic effect in bipolar mood dis- The distribution is in total body water with a slow order. It is also described to possess NMDA (n-methyl entry into the intracellular compartment. Lith ium is d-aspartate) mediated neuroprotective properties. not protein bound. The maximum levels occur in There is a lag period of 7-10 days before the onset thyroid (3-5 times serum level), saliva (two times), of action occurs, which is probably due to the time milk (0.3-1.0 times) and CSF (0.4 times). The steady taken to achieve steady state levels. state levels are achieved in about 7 days. There is no metabolism of lithium in body and it is excreted Clinical Use almost entirely by the kidneys. Proxi mal reabsorption Lithium is available in market in the form of the fol- is infl uenced by the sodium balance, and depletion lowing preparations. of sodium results in reten tion, causing higher blood 1. Lithium carbonate (300 mg tablets; 400 mg levels of lithium. sustained-release tablets) 2. Lithium citrate (300 mg/5 ml liquid; not available Mechanism of Action in India) Lithium’s mechanism of action is not known; however, Before starting treatment, it is essential to ensure the following mechanisms have been hypothesised: normal functioning of kidneys (one of the most im- 1. It affects the Na+-K+ ATP-ase and accumu lates portant), thyroid, heart and central ner vous system. intracellularly as a substitute of Na+. After starting lithium, it is necessary to investigate 2. It inhibits the adenylate cyclase and thus decreases these systems at repeated intervals. cAMP ( II messenger) intracellu larly. The usual profi le of inves tigations is as follows: 3. It accelerates the presynaptic reuptake and des- 1. Routine general and systemic physical examina- truc tion of catecholamines, like norepinep h rine. tion. 4. It inhibits the release of catecholamines at the 2. Routine blood counts (Hb, TC, DC). synapse. 3. Urine: routine and microscopic examination.

5. It decreases the postsynaptic serotonin 5-HT 2 4. ECG. receptor sensitivity. 5. Renal function tests (blood urea, serum creatinine, 6. It stabilizes the cell membrane, along with Ca++ 24 hour urine volume, urine speciﬁ c gravity). and Mg++. eGFR with creatinine clearance test, if indicated. ++ 7. It decreases the Ca mobilisation from the intra- 6. Thyroid function tests (TSH, T3, T4). cellular pools by ITP (inositol-triphos phate)- The initial daily starting dose of lithium for treat- dependent Ca++ channels (II messenger system). ment of acute mania is usually 900-2100 mg/day, 190 A Short Textbook of Psychiatry

Table 15.8: Blood Lithium Levels by decreasing the dose of lithium or by adding (in treatment of bipolar disorder) propranolol. 2. Muscular weakness. • Therapeutic levels = 0.6-1.2 mEq/L (For the treat- 3. Cogwheel rigidity (mild). ment of acute mania) 4. Seizures (decreased threshold). • Prophylactic levels = 0.6-1.0 mEq/L (For relapse 5. Neurotoxicity: The important features include prevention in bipolar disorder) delirium, cerebellar signs, abnormal invo luntary • Toxic lithium levels > 2.0 mEq/L movements, seizures, and later coma. In some individuals, toxicity may occur even within the given in 1-3 doses. Ideally, the treatment is started therapeutic range. The treatment of choice for after serial lithium estimation, conducted after a loa- acute toxicity is haemo dialysis. ding dose of 600 mg or 900 mg of lithium carbo nate, II. Renal to determine pharma cokinetics. However, this method The renal side effects occur in about 10-50% of all is much less frequently practiced these days. patients on maintenance lithium therapy. Some of the During treatment it is essential to esti mate blood features include: lithium levels at regular intervals (usually 3 monthly) 1. Polyuria, polydipsia. (Table 15.8). The blood sample for estimation is 2. Tubular changes. taken 12 hours after the last lithium dose. If any 3. Nephrogenic diabetes insipidus. changes are made in lithium dosage, the next blood 4. Nephrotic syndrome. level is estimated after at least 5-7 days of the last III. Cardiovascular change. The effects on heart are similar to those of hypokalaemia. When stopping lithium treatment (except in cases The commonest ECG change is T-wave depression. of lithium toxicity), it is desirable to gradually taper IV. Endocrine the dose of lithium over several days or weeks in order 1. Goitre. to minimise the risk of early relapse on discontinua- 2. Hypothyroidism. tion. 3. Abnormal thyroid function (30-40%). There is evidence from several studies that lithium 4. Weight gain (pedal oedema is also common). substantially reduces the risk of suicide in bipolar V. Gastrointestinal disorder; however, it has a narrow margin of safety These side effects include nausea, vomiting, diarrhoea, and it is important to remember this particularly in metallic taste and abdominal pain. patient with active ideas or plans of suicide. VI. Dermatological These dermatological side effects include acneiform Side Effects eruptions, papular eruptions and exacerbation of Adverse effects are common and toxicity can occur psoriasis. easily, if blood levels reach about 2.0 mEq/L; life- VII. Side effects during pregnancy and lactation threatening intoxication occurs, if levels reach about 1. Teratogenic (possibly). 3.5 mEq/L. In acute admi nistration, toxicity is prima- 2. Increased incidence of Ebstein’s anomaly (dis- rily neurological whilst during maintenance therapy tortion and downward displacement of tricuspid renal side effects are the commonest. valve in the right ventricle), when taken in the ﬁ rst The common side effects are listed below: trimester. I. Neurological 3. Secreted in milk with 30-100% of the maternal 1. Tremor: This is the commonest side effect, blood lithium levels. Lithium can therefore cause occurring in up to 50% of patients. Treatment is toxicity in the infant. Psychopharmacology 191

Contraindications of Lithium Use It is rapidly and completely absorbed after oral 1. Presence of clear evidence of cardiac, renal, thy- administration. The peak plasma levels are reached roid or neurological dysfunction at 1-4 hours after a single oral dose. The half-life of 2. Presence of blood dyscrasia valproate is 8-17 hours. 3. During pregnancy and lactation The usual dose of valproate is 1000-3000 mg/day 4. Concomitant administration of thiazide diu retics, orally in divided doses. The therapeutic blood level is tetracyclines or anaesthetics 50-125 mg/ml. Oral loading stra tegies (20-30 mg/kg/ ACE inhibitors (such as captopril), Angiotensin day) are rapidly effective in the management of acute II receptor antagonists (such as losartan), NSAIDs mania. (nonsteroidal anti-infl ammatory drugs) and COX-2 inhibitors (such as celecoxib) can increase the risk of Indications lithium toxicity in an unpredictable manner, especially In addition to its primary indication as an anti con- in elderly. vulsant, Valproate has several other indications in various psychiatric and neuropsy chiatric disorders. VALPROATE Bipolar Disorders Valproate and lithium have been widely used as Acute Mania (as a fi rst-line agent for the treatment fi rst line drugs for treatment of mania as well as for of acute mania in oral and IV forms): Several factors prophylaxis of bipolar mood disorder. associated with a favourable antimanic response to Valproic acid was fi rst synthesised by Burton valproate (as well as carbama zepine) include: and used as an organic solvent. In 1963, Meunier a. Co-morbid substance abuse or other psychiatric serendipitously discovered the antiepi leptic proper- disorders ties of valproic acid, while Lambert reported in 1966 b. Later age at onset and/or shorter duration of illness that valpromide (a valproic acid analogue) might be c. History of poor response to lithium effective as an antimanic. It was approved by the US d. Dysphoric mania, mixed affective episodes, or FDA as an antiepileptic drug for absence seizures in rapid cycling 1978 and for the treatment of acute mania (and for e. Organic/complicated mania associated with sei- migraine headache prophylaxis) in 1996. zure disorder, history of head trauma, or EEG Although its mechanism of action is not clearly abnormalities understood, it increases GABA though other non- f. D-M-I (Depression-Mania-Well Interval) pattern GABAergic mechanisms have been proposed. of illness, as opposed to the M-D-I pattern The term valproate is often used to denote all There is some suggestion that patients non- commercial preparations, since the common entity responsive to valproate may respond well to in blood is valproic acid. The following preparations carbamazepine. of valproate are available in India: Prophylaxis: Valproate is probably less effective in i. Valproate sodium maintenance treatment of bipolar disorder than in ii. Divalproex (Enteric-coated stable coor dination treatment of acute mania. It has been used alone, as compound composed of sodium valproate and well as along with lithium and other mood stabilisers valproic acid in a 1:1 molar relationship) in the maintenance treat ment. iii. Chrono preparations (Enteric-coated compound The addition of valproate to lithium has been composed of sodium valproate and valproic acid recognised as a useful treatment for mania refractory in a 3:2 ratio). to lithium mono therapy. 192 A Short Textbook of Psychiatry

Rapid cycling bipolar disorder and mixed (or dys- The use of valproate in pregnancy and lactation phoric) mania: The patients with rapid cycling, mixed should be best avoided. The NICE guidelines for treat- affective episodes, or dysphoric mania are often ment of bipolar disorder recommend that valproate is resistant to lithium treatment and respond better to best avoided in women of childbearing potential (see valproate. Valproate is also effective in management Further Reading List). of ultra-rapid cycling mood disorders. In overdose, the amount of drug, that is not protein Bipolar depression: Valproate appears to be generally bound, is high. Therefore, dialysis is useful in the more effective in the treatment of acute mania than in management of an overdose with valproate. bipolar depression. Drug Interactions Neurological Disorders Certain drug may increase (such as aspirin, cimeti dine, Migraine and Pain syndromes: Valproate has been ibuprofen, erythromycin, fl uoxetine, fl uvo xa mine, used for prophylaxis of migraine headaches, as well phenothiazines) or decrease (such as carbamazepine, as for aborting an acute attack (IV route). Valproate phenytoin, phenobarbital, ethosuximide, rifampicin, has also been used in treatment of trigeminal neuralgia mefl oquine) the serum levels of valproate. and neuropathic pain. In addition, valproate increases serum levels of Seizure disorders: Valproate is primarily indicated for other drugs (such as lamotrigine, tricyclic antidepres- treatment of absence seizures (both simple and com- sants, zidovudine, tolbutamide). plex), complex partial seizures, myoclonic seizures, and generalised tonic-clonic seizures, as monotherapy CARBAMAZEPINE as well as adjunct therapy. Like lithium and valproate, carbamazepine too has Other Disorders been used as an antimanic and for prophylaxis of bi- Valproate has also been used at times in several other polar disorder. It is a tricyclic compound synthesised conditions, including behavioural agitation in demen- in 1953 by Schindler. It has a structure similar to tia, severe behavioural symptoms in mental retarda- TCAs. The onset of action can be faster as compared tion, ADHD and conduct disorder, schizoaffective to lithium, but slower compared to valproate. disorder (bipolar type), alcohol withdrawal, tardive The usual dose is 600-1600 mg/day orally, in dyskinesia, impulse control disorder, panic disorder divided doses. The treatment is best monitored with and borderline personality disorder. repeated blood levels. The therapeutic blood levels are 4-12 μg/ml and the toxic blood levels are usually Side Effects reached at >15 μg/ml. Adverse effects are more common with valproate concentrations above 100 mg/ml. Indications The common side effects are nausea, seda- The indications for use of carbamazepine include: tion, tremor, flushing, weight gain, thrombo- 1. Seizures cytopenia, menstrual disturbances (in women) and hair i. Complex partial seizures (CPS) loss. There are some reports of polycystic ovaries ii. Generalised tonic clonic seizures and hyperandrogenism in young women with iii. Alcohol withdrawal seizures (rum fi ts), if per- epilepsy. sistent (also used sometimes for treatment of The most serious, though relatively uncommon, simple alcohol withdrawal synd rome) side effects include hepatic toxicity (espe cially in 2. Psychiatric disorders young children), acute haemorrhagic pancreatitis, and i. Bipolar mood disorder (especially for rapid Steven-Johnson syndrome. cyclers; lithium-refractory patients; lithium- Psychopharmacology 193

intolerant patients; for prophylaxis in some Intermediate Acting patients; for treatment of acute mania, especially The duration of action is 5-8 hours. Examples include severe and dys phoric mania) amobarbital and pentobarbital. ii. Impulse control disorder and aggres sion (in Short Acting some cases) The duration of action is 1-5 hours. Examples include iii. Psychosis (especially mania) with epilepsy secobarbital. iv. Borderline personality disorder (for treatment Ultra-Short Acting of mood swings) The duration of action is less than 1 hour. Examples v. Cocaine withdrawal syndrome include thiopentone and methohexital. 3. Paroxysmal pain syndromes Barbiturates are no longer used or recommended as i. Trigeminal neuralgia anti-anxiety agents. They produce multiple side effects ii. Phantom limb pain such as excessive sedation, respiratory and circulatory iii. Other paroxysmal pain syndromes (neu ral gias). depression, hepa tic enzyme induction, dependence, with drawal symptoms, rebound increase in REM- sleep Side Effects on withdrawal, and potential for use in suicide. The major side effects include diplopia, drow si- ness, dizziness, nausea, vomiting, ataxia, skin rash, Non-barbiturate, Non-benzodiazepine Steven-Johnson syndrome (ery thema multiforme Anti-anxiety Agents major), photosensitivity, cholestatic jaundice, acute These can be further divided into the following cat- oliguria with hypertension, leucopenia and thrombo- egories: cytopenic purpura. The most dangerous side effects Carbamates include bone marrow depression (causing aplas- The common examples are meprobamate, tybamate tic anaemia), agranulocytosis and cardiovascular and carisoprodol. These are not used commonly due collapse. to the potential for abuse and dependence. Therefore, it is essential to monitor cardiac, renal, Piperidinediones hepa tic and bone-marrow functions during carba- An example is glutethimide. This drug too is not used mazepine treatment. The use of carbamazepine in now-a-days due to its dependence potential. pregnancy and lactation should be best avoided. Alcohols The use of carbamazepine in management of The examples include ethanol, chloral hydrate and bipolar disorder appears to be recently declining. ethchlorvynol. These drugs are highly depen dence producing and clearly not recommended. ANTI-ANXIETY DRUGS Quinazoline Derivatives An example is methaqualone. Methaqua lone had Anti-anxiety drugs, also known as minor tranquilisers become a street drug (i.e. a drug of abuse) and its and anxiolytics, can be classiﬁ ed as follows: use was discontinued as an anti-anxiety agent and a hypnotic. Classiﬁ cation Anti-histaminics The common examples include diphenhydramine, Barbiturates hydroxy zine and promethazine. In past, diphenhy- Barbiturates can be divided into four main types: dramine was usually combined with methaqualone or Long Acting diazepam. They may be used as hypnotic-sedatives, The duration of action is more than 8 hours. Examples but their use as anti-anxiety agents is minimal and include phenobarbital. probably not safe. 194 A Short Textbook of Psychiatry

Cyclic Ethers Indications An example is paraldehyde. It is not used commonly The indications for use of benzodiazepines include as it is not very effective and is also dependence the following: producing. 1. Generalised anxiety disorder; adjust ment disorder Others with anxious mood (Short-term use) Antipsychotics (such as thioridazine, fl upentixol, 2. Panic disorder, agoraphobia, and school pho- olanzapine, quetiapine) and anti depressants (such as bia (particularly alprazolam and clo na zepam; doxepine) have sometimes been used for the treatment short-term use, along with antidepressants) of severe, intractable anxiety. However, antipsychotics 3. Agitated depression (short-term use, along with are not the drugs of fi rst choice and should be used antidepressants, for fi rst 1-2 weeks) with extreme discretion (with balancing of risks and 4. Short-term treatment of insomnia benefi ts) when all other drugs have failed to benefi t. 5. Stage 4 NREM- sleep disorders such as enu resis, Antidepressants (such as SSRIs, SNRIs and Mirta- somnambulism ( diazepam reduces dura tion of zapine) have recently emerged as treatments of choice Stage 4 NREM-sleep) in several anxiety disorders including generalised 6. Nightmares (diazepam also reduces the REM- anxiety disorder, obsessive compulsive disorder, panic sleep duration). disorder and obsessive compulsive disorder. There is 7. Pre-medication in anaesthesia (intravenous some data to support that smaller starting doses are lorazepam, midazolam, or diazepam) better as anxiety symptoms may worsen initially in 8. Anticonvulsant use (drugs of choice for status epi- treatment. lepticus, myoclonic seizures and certain infantile Beta (β) Blockers spasms) An example is propranolol which is particularly effec- 9. To produce skeletal muscle relaxation (e.g. in tive in treatment of peripheral somatic manifestations tetanus, cerebral palsy) of anxiety. It is also helpful in treatment of anticipa- 10. Treatment of alcohol and other drug withdrawal tory anxiety and situational anxiety. Propranolol can syndromes be used either alone or along with benzodiazepines. 11. For minor surgical, endoscopic or obs tetric pro- β-blockers are not treatments of fi rst choice in the cedures treatment of psy chic or psychological manifestations 12. Acute mania (lorazepam, usually with lithium or of anxiety. atypical antipsychotics). Propranolol is contraindicated in patients with 13. Antipsychotic-induced akathisia bronchial asthma and cardiac conditions. It should be 14. Emergency management of acute psycho ses used with caution in patients of age 40 and above. The (IV lorazepam, along with parenteral anti psy- usual dose is 40-240 mg/day, administered in divided chotics). doses. 15. Narcoanalysis or abreaction (IV diaze pam) Whenever administered, benzodiazepines should Benzodiazepines not be ordinarily used for more than 2-4 weeks at a Since the discovery of chlordiazepoxide in 1957 by time; otherwise risk of dependence is quite high and Sternbach, benzodiazepines have replaced other anti- tolerance occurs. anxiety drugs and hypnotics though SSRIs are now Mechanism of Action gradually becoming drugs of fi rst choice in manage- The exact mechanism of action of benzodiaze pines is ment of anxiety disorders. not clear. The discovery of the benzo diazepine recep- The benzodiazepines can be classifi ed accor ding tors in 1977 shed some light on the mode of action to their elimination half-lives (Table 15.9). (Fig. 15.1). Psychopharmacology 195

Table 15.9: Classiﬁ cation and Properties of Benzodiazepines Class and Drug Elimination Usual Oral Dose Parenteral Active Other Comments Half-life Hypnotic (mg/day) Dose (mg) Metabolites (Hours) Dose (mg HS/Nocte) I. Very Short Acting Drugs 1. Midazolam 2-5 hours ______Used for anaesthesia 2. Triazolam 2-5 hours 0.125-0.25 ______α-hydroxy- Rapid oral absorp- mg triazolam tion; Marketed as hypnotic II. Short Acting Drugs 1. Alprazolam 6-20 hours ___ 0.5-6.0 mg ___ α-hydroxy- ___ alprazolam 2. Estazolam 8-24 hours 1-2 mg 1-2 mg ______3. Loprazolam 6-12 hours 1-2 mg ______Piperazine ___ N-oxide 4. Lormetazepam 10-12 hours 0.5-1.5 mg ______Lorazepam ___ 5. Lorazepam 10-20 hours 0.5-2.0 mg 2-6 mg 2-4 mg None High dependence potential 6. Oxazepam 5-15 hours 15-30 mg 15-120 mg ___ None Slow oral absorption 7. Temazepam 10-20 hours 10-20 mg 10-20 mg ___ Oxazepam Slow oral absorption III. Long Acting Drugs 1. Chlorazepate 30-100 7.5-30 mg 7.5-60 mg ___ Nordiazepam Hydrolysed to hours active form in stomach 2. Chlordiazepoxide 25-48 hours 10-25 mg 15-100 mg 50-100 mg Desmethyl- Erratic absorption demoxepam after IM injection 3. Clonazepam 20-40 hours ___ 0.5-20 mg 2-5 mg ___ Also used in treatment of epilepsy 4. Diazepam 14-90 hours 2-10 mg 2-30 mg 2-20 mg Nordiazepam Erratic absorption after IM injection 5. Flurazepam 30-100 15-30 mg 15-60 mg ___ Desmethyl- Marketed as a hours hydroxy-ethyl- hypnotic ﬂ urazepam 6. Halazepam 30-60 hours 20-40 mg 40-160 mg ___ Nordiazepam ___ 7. Nitrazepam 20-60 hours 5-10 mg 5-20 mg ___ Nordiazepam Marketed as a hypnotic Contd... 196 A Short Textbook of Psychiatry

Contd... Class and Drug Elimination Usual Oral Dose Parenteral Active Other Comments Half-life Hypnotic (mg/day) Dose (mg) Metabolites (Hours) Dose (mg HS/Nocte) 8. Prazepam 30-60 hours 10-20 mg 20-60 mg ___ Nordiazepam Slow oral and Diazepam absorption 9. Quazepam 40-160 7.5-15 mg 7.5-30 mg ___ Probably selective hours for benzodiazepine receptor I; may cause less cognitive/motor disturbances. Each drug is described under the headings of elimination half-life (hours); usual hypnotic dose (mg nocte/HS); usual oral dose (mg/day; if applicable); usual parenteral dose (mg; if applicable); active metabolites and other comments.

Fig. 15.1: Probable Mechanism of Action of Benzodiazepines (BDZ)

There are, presently, two known benzodia z epine Benzodiazepine receptor antagonists (such as (BDZ) receptors. fl uma zenil) are anxiety-provoking agents. Fluma- 1. BDZ Receptor I, which is linked with the GABA zenil has a half-life of 60 minutes and administered (Gamma-Aminobutyric acid) rece p tor and is in- in a parenteral dose of 0.2-1.0 mg IV given over 1-2 volved in mediation of sleep. minutes in treatment of benzodiazepine toxicity. 2. BDZ Receptor II, which is alone and is involved in cognition and motor control. Classifi cation of Benzodiazepines Thus, benzodiazepines act by enhan cing GABA Each drug is described in Table 15.9 under the head- transmission in the brain. ings of elimination half-life (hours); usual hypnotic Psychopharmacology 197 dose (mg nocte/HS); usual oral dose (mg/day; if ap- 2. Zopiclone plicable); usual parenteral dose (mg; if applicable); Zopiclone belongs to a new class of non-benzo- active metabolites and other comments. diazepine drugs, the cyclopyrrolones. Cyclopyrrolone Side Effects derivatives also act on the GABA receptors, but at a The side effects of benzodiazepines include nausea, site distinct from that of benzodiazepines. Zopiclone vomiting, weakness, epigastric pain, diarrhoea, ver- has a short duration of action as well as shorter onset. tigo, blurring of vision, body aches, urinary inconti- After oral admini stration, it is absorbed rapidly, with nence (rare), impotence, sedation, lassitude, increased peak plasma concentra tion occurring in about 60 reaction time, ataxia (in high doses), dry mouth, minute. The elimination half-life is 4-6 hours. retrograde amnesia (rare), impairment of driving The usual dose of zopiclone is 3.75-7.5 mg skills, severe effects when administered with alco hol, at bedtime (lower dose in elderly patients and in irritability, disinhibited behaviour, dependence and patients with severe hepatic failure). The side effects withdrawal symptoms (on stopping the drug). include bitter taste, dry mouth, drowsi ness, nausea Cross-tolerance occurs with barbiturates, meth- and headache. Its safety in children, in pregnancy aqualone and ethyl alcohol. A worsening of depres- and lactation is not proven. It is clinically superior sion and pre-existing psychosis with use of benzodi- to benzodiazepines in subjective awakening quality, azepines has been reported. well-being, and attention span in the morning. Since withdrawal symptoms usually occur after 3. Zolpidem long-term use, benzodiazepines should be withdrawn Zolpidem is an imidazopyridine derivative which slowly. is marketed as a hypnotic. It is administered in a dose of 5-10 mg for hypnotic use. It has a half-life Newer Drugs of 2-3 hours; therefore it is useful in the treatment 1. Buspirone of diffi culty in initiation of sleep (ini tial insomnia). Buspirone is a non-benzodiazepine, anti-anxiety drug. The side effects include drowsi ness, dizziness, It is an azaspiro decanedione (azapirone) derivative. headache, depression, nausea, dry mouth, and myalgia. Buspirone is a 5-HT1A partial agonist and a selective It should not be used for more than two weeks at one DA auto receptor antagonist. It also inhibits the spon- time. Its safety in children, in pregnancy and lactation ta neous fi ring of 5-HT neurons. is not proven. It does not seem to act on the benzodiazepine re- 4. Zalpelon ceptors. It is anxioselective, with no sedative action, Zalpelon is a pyrazolo-pyrimidine deri vative which and no anticonvul sant or muscle-relaxant properties. is marketed as a hypnotic. Although a non-benzodi- It is administered in a dose of 15-30 mg/day, in a azepine drug, it acts on the omega-1 benzodiazepine thrice daily schedule due to a short half-life. As it has receptor located on the alpha sub-unit of the GABA-A a slower and more gradual onset of action, it usually receptor complex (causing sedation), with very little takes about two weeks before its anti-anxiety effects effect on omega-2 and omega-3 receptors. are evident. Buspirone is not useful in treatment of It is administered in a dose of 5-10 mg for panic disorder. The common side effects include diz- hypnotic use. It has a half-life of one hour with a rapid ziness, headache, lightheadedness and diarrhoea. onset of effect. Therefore, it is useful in treatment As it is an anxio-selective and lacks any risk of of diffi culty in initiation of sleep (initial insomnia). dependence, it was hoped that it might replace the It can be taken again at night if there is more than benzo dia zepines as the drug of choice in treatment 4 hours of sleep time remaining. Because of the very of generalised anxiety disorders. However, it is not short half-life, there is virtually no hangover in the as widely used as it was once expected. morning. 198 A Short Textbook of Psychiatry

The side effects include headache, drowsi ness, diz- benzodiazepine agonists; anxiolytic without seda- ziness, nausea, and myalgia. It should not be used for tion; rapid onset of action), abecarnil (β-carboline more than 2 weeks at one time. Its safety in children, partial agonist at benzodiazepine receptor; anxiolytic in pregnancy and lactation is not proven. and anticonvulsant), tiagabine, riluzole, and alpidem (anxiolytic). 5. Other Drugs Pregabalin is licensed for treatment of anxiety in The other newer hypnosedative and anti-anxiety some countries. Cognitive behaviour therapy with or drugs include suriclone (a cyclopyr rolone deriva- without medication is helpful in treatment of several tive; a hypnotic), bretazenil and imidazenil (partial anxiety disorders. Other Biological 16 Methods of Treatment

The last 75 years have seen the development of sev- A much safer form of convulsive therapy was used by eral biological methods of treatment for treatment of Cerletti and Bini in 1938 (Table 16.1). They called it psychiatric disorders. The earlier modes of treatment, EST or electroshock therapy. Later, this method of such as malarial treat ment for general paralysis of treatment came to be known as ECT or electroconvul- insane (GPI), insulin coma therapy, atropine coma sive therapy. The 1970s saw widespread criticism of therapy, continuous sleep treatment, sub-convulsive ECT, with many legislations passed in the US states ECT, chemical convulsive therapy, sleep deprivation, (e.g. in California, 1975), restricting the use of ECT. mega-vitamin therapy and hallucinogens (to name a Following this, widespread modifi cations in the ECT few important methods) are no longer used in routine technique made it even safer mode of treatment. clinical practice. In 1974, the American Psychiatric Association’s Although there are other new biological methods (APA’s) Council on Research and Develop ment recently introduced for the treatment of psychiatric appointed a Task Force on ECT. The APA Task Force disorders, such as vagal nerve stimulation (VNS), on ECT, in 1976, gave its report which provided clear transcranial magnetic stimulation (TMS) and deep guidelines for use of ECT and declared it to be a safe brain stimulation (DBS), these are not discussed in and effective method of treatment when used by this book. professionals trained in the technique. The 1990 APA There are two methods which though introduced Task Force Report on ECT redefi ned the indications, at the same time have been revised extensively and gave guidelines for obtaining consent and set standards are still in use presently. These methods are electro- for training, treatment and privileging of ECT. The convulsive therapy and psychosurgery. most recent version of this task force report became available in 2001. ELECTROCONVULSIVE THERAPY Indications Brief History The indications for electroconvulsive therapy are: 1. Major severe depression Von Meduna, in 1934, used 25% camphor in oil intra- i. With suicidal risk (This is the fi rst and most muscularly to produce convulsions for the fi rst time for important indication for ECT) therapeutic purposes. Later, he used pentylenetetrazol ii. With stupor ( metrazol) for the same purpose. iii. With poor intake of food and fl uids 200 A Short Textbook of Psychiatry

Table 16.1: A Brief Early History of Biological Treatments in Psychiatry Year Treatment Started by 1785 Camphor-induced seizures W Oliver 1917 Malarial treatment of GPI Julius Wagner von Jauregg 1922 Barbiturate coma therapy Jacob Klaesi 1931 Reserpine (1st drug treatment in psychosis) Ganesh Sen, Kartik Bose 1933 Insulin coma therapy Manfred Sakel 1934 Cardiazol (metrazol) induced seizures LLJ von Meduna 1936 Psychosurgery (prefrontal leucotomy) Egas Moniz, Almenda Lima 1938 Electroshock (electroconvulsive therapy) Ugo Cerletti, Lucio Bini 1949 Lithium (for mania) John F Cade 1952 Chlorpromazine (1st antipsychotic) Jean PL Delay, Pierre Deniker 1954 Meprobamate FM Berger 1958 Iproniazid (1st MAO inhibitor) Nathan Kline 1958 Imipramine (1st tricyclic antidepressant) Thomas Kuhn 1958 Haloperidol (1st non-phenothiazine antipsychotic) Janssen 1960 Chlordiazepoxide (1st benzodiazepine) Hugo Sternbach

iv. With melancholia response with ECT and patient preference for ECT v. With psychotic features also determine the use of ECT. vi. With unsatisfactory response to drug therapy The 1990 APA Task Force on ECT also defi ned vii. Where drugs are contraindicated, or have as suggestive indications (for occasional use) the fol- serious side effects lowing disorders: viii. Where speedier recovery is needed. 1. Organic mental disorders (e.g. organic mood syn- 2. Severe catatonia (non-organic) drome, organic hallucinosis, organic delusional i. With stupor disorder, and delirium). ii. With poor intake of food and fl uids 2. Medical disorders (e.g. organic catatonia, neuro- iii. With unsatisfactory response to drug therapy leptic malignant syndrome and parkin sonism). iv. Where drugs are contraindicated, or have serious side-effects. Pre-treatment Evaluation v. Where speedier recovery is needed. The pre-treatment evaluation consists of the follow- 3. Severe psychoses ( schizophrenia or mania) ing steps: i. With risk of suicide, homicide or danger of 1. An informed consent, taken from the patient. If the physical assault patient does not have capacity or competence to ii. With unsatisfactory response to drug therapy give consent, consideration must be given to the iii. Where drugs are contraindicated, or have most recent legal guidelines and local procedures serious side effects which can include the best interest decision with iv. With very prominent depressive features (e.g. consent of guardian/family and additional opinion schizo-affective disorder). from another professional. The use of ECT in mania and schizophrenia is 2. Detailed medical and psychiatric history taking, not a treatment of fi rst choice and is employed only which includes the current and past treatment his- in the above-mentioned conditions. A history of good tory. Other Biological Methods of Treatment 201

3. General and systemic physical examina tion. the day, the patient should be empty stomach for at 4. Routine laboratory investigations, such as Hb, TC, least 4 hours. No oral medication should be given DC, ESR, urinary examination, ECG, X-ray chest, in the morning. The bladder (and bowel) should be and any other investigations in the light of history emptied just before the treatment, as incontinence can and examination. Other optional investigations, occur during the induced seizure. Dentures, if present, which are not done routinely, include EEG and should be removed, and the presence of loose teeth estimation of plasma pseudocholinesterase activity should be ruled out. Tight clothing, and metallic and (for patients who would receive succinylcho line sharp objects (if any) should be removed from the for general anaesthesia). person’s body. 5. Examination of fundus oculi to rule out papil- The usual anaesthetic precautions are taken. The loedema. patient is placed on a hard bed which is well insulated. A slow intravenous drip may be started (though not Contraindications needed in all patients). Atropine (0.6 mg) is given IV just before the treatment or else is given IM or Absolute SC 30 minutes before treatment. Atropine is given The only absolute contraindication is the presence of to decrease the oral secretions and to pre vent vagal raised intracranial tension (so an examination of the stimulation during E CT which can cause cardiac fundus oculi is an essential step). However, the APA arrest. However, this method is not followed at many Task Force Report on ECT recognises this too as a centres these days. relative contraindication. This step is followed by administration of an anaesthetic agent such as propofol (0.75–2.5 mg/kg) Relative or thiopentone (2-5 mg/kg, usually indivi dualised These include: dose for each patient) and a muscle relaxant like 1. Recent myocardial infarction (MI) succinylcholine (0.5-1.5 mg/kg). An anaesthetic mask 2. Severe hypertension is placed on the face and ventilation with 100% oxygen 3. Cerebrovascular accident (CVA) is given. As succinylcholine is a depolarising block- 4. Severe pulmonary disease ing agent, its administration is followed by muscular 5. Retinal detachment, and fasciculations which move from above down wards. 6. Pheochromocytoma. When the fi ne twitching movements disappear from the lower extre mities, it is the time of complete mus- Technique cular relaxation. The techniques used for ECT administration are of Now a mouth gag is inserted between teeth, to two types: prevent tongue bite during convul sion and pressure is i. Direct ECT is administered in the absence of applied on man dible to approximate upper and lower muscular relaxation and general anaesthesia. teeth till convulsions stop. The electrodes (usually All the other steps are the same as in modifi ed U-shaped) are moistened with saline or 25% bicar- ECT. This method of treatment is nowadays bonate solution and are applied on head. According very infrequently used and not understandably to the position of application of electrodes, ECT is of encouraged by most guidelines. two types: ii. Modifi ed ECT is modifi ed by drug-induced i. Bilateral ECT: This is the standard form of ECT muscular relaxation and general anaesthesia used most commonly. Each elec trode is placed administered by an anaes thetist. 2.5-4.0 cm (1-1½") above the midpoint, on a ECT is usually administered in the morning after line joining the tragus of the ear and the lateral an overnight fast. If given at any other time during canthus of the eye. 202 A Short Textbook of Psychiatry

ii. Unilateral ECT: In this type, electrodes are The usual dose for obtaining an adequate seizure placed only on one side of head, usually the response is 90-150 volts (average 110 volts) for 0.1-1.0 non-dominant side (right side of head in right- seconds (average 0.6 seconds). The usual amount of handed individual). There are various positions current passed in an ECT session is 200-1600 mA. described for the electrode placement. Earlier, the ECT machines used a sine wave to The unilateral ECT is safer, with much fewer side deliver the current (with a positive and a negative wave effects, particularly those of memory impairment. constituting a cycle). However, with sine wave, unnec- However, according to the APA ECT Task Force essarily excessive and ineffi cient electrical stimulus Report, bilateral ECT is superior to unilateral ECT in is delivered. The newer ECT machines instead use effectiveness. a brief pulse wave form that delivers the electrical The electrode placement sites are cleaned with stimulus, usually in a 1-2 msec time period at a rate normal saline or 25% bicarbonate solution, or a con- of 30-100 pulses/second. There fore, the brief pulse ducting gel is applied. One attendant places one hand current is more effi ca cious and safer than the sine wave each on both thighs near the knee joint, while another current. There are clear guidelines available regarding attendant holds the shoulders. This is usually a must the procedure with the new machines. in direct ECT, but may also be done in modifi ed ECT. The stimulus dosing protocols have two principles, This is to prevent falls from the bed and causation of namely calculation of the seizure threshold (the mini- fracture or dislocation due to muscular contractions mum stimulus that induces an adequate seizure) and (which may occasionally occur even in modifi ed ECT). calculation of the treatment stimulus (usually 1.5 times The therapeutic adequacy of the treatment is supra-threshold for the bilateral and 2.5 times for the usually gauzed by the occurrence of a gene ralized unilateral ECT). So, the patient is stimulated at higher tonic-clonic seizure lasting for not less than 25-30 stimulus levels during the treatment than the seizure seconds. This is ensured by: threshold (therefore, suprathreshold). 1. Observing the seizure (in direct ECT). After seizure has occurred, the mouth gag is 2. EEG recording during ECT (in modifi ed ECT). removed, secretions are removed by a suction machine 3. Occluding the circulation of one extremity with from the oral cavity, and oxygen mask is applied. Till a BP apparatus cuff, before giving succi nyl- consciousness is regained, the patient is turned to one choline. Thus, the whole body is paralyzed but side to prevent aspiration. The vital parameters are one extremity convulses and can be directly constantly monitored till recovery occurs. The patient observed. is made to rest, for about 30 minutes to 1 hour, on bed 4. Observing plantar extension and eyelid cont rac- after the treatment is over. tions which may be seen despite the muscular relaxation (not a very reliable method). Duration of Therapy Most guidelines recommended that seizure activity The total duration and number of treatments given by EEG of at least 25 seconds and observed convul- depends on the diagnosis, presence of side effects, and sion of at least 15 seconds was needed for the seizure the response to treatment. Usually 6-10 treatments are to be classifi ed as adequate. However, the recent suffi cient, although up to 15 treatments can be given (Third) Report of the Royal College of Psychiatrists’ if needed. The treatments should be spaced, so that Special Committee on ECT (2004) recommended no more than 3 ECTs are given per week. that there is not enough evidence to suggest that the Although ECT is very effective in severe depres- observed seizure duration is important. According sive disorder (for example), the benefi t lasts only to this report, a bilateral generalized seizure is more till the ECTs are given. There is no residual benefi t important. after the treatment is over. Hence, the patient needs Other Biological Methods of Treatment 203

antidepressants (for example) during and after the PSYCHOSURGERY ECTs are over. Defi nition Mechanism of Action Psychosurgery is defi ned (by APA’s Task Force) as, a The effi cacy of ECT is linked with production of surgical intervention, to sever fi bres connec ting one generalised tonic-clonic seizures though, as stated part of brain with another, or to remove, destroy or above, there is some recent doubt about the need for stimulate brain tissue, with the intent of modifying a seizure duration of 25-30 sec. Although the exact behaviour, thought or mood disturbances, for which mechanism is unclear, one hypothesis states that ECT there is no underlying organic pathology (i.e. the possibly affects the catecholamine pathways between disturbance is ‘functional’). diencep halon (from where seizure generalisation occurs) and limbic system (which may be responsible Brief History for mood disorders), also involving hypothala mus. Although surgery on skull (such as trephining) was As ECT increases the threshold for further seizu- done for mental illnesses even in ‘primitive’ times, res, it may paradoxically act as an anticonvulsant. ECT psychosurgery was introduced as leucotomy by Egas also causes down-regulation of β1 receptors in cortex Moniz and Almenda Lima in 1936. Egaz Moniz later and hippocampus. even received a Noble prize. Freeman and Watts later introduced prefrontal lobotomy in 1937, while Side Effects in India, Govindaswami and Rao performed the fi rst 1. Side effects associated with general anaesthesia: leucotomies in 1944. Deaths during ECT are usually due to the gene- Psychosurgery came in for a severe public criti- ral anaesthesia, succinylcholine (in patients with cism in the 1950s when its use decreased substantially. deficiency of pseudo-cholinesterase) or drug- In the last few decades, several better methods of interactions. According to the APA Task Force treatment have been developed which are safer and Report (2001), the approximate mortality rate is more specifi c. In addition, careful guidelines for the 1:10,000 patients (or 1:80,000 treatments), which use of psychosurgery have also been laid down. is similar to any operative procedure under anaesthesia. Anatomical Basis 2. Memory disturbances (both anterograde and retro- It is believed that limbic system is closely linked grade) are very common. These are usually mild with normal and abnormal emotional reactions. The and recovery occurs within 1-6 months after treat- limbic system (Fig. 16.1) consists mainly of cingulum ment. Unilateral ECTs cause much less memory (cingu late gyrus and cingulate bundle), hippo campus, disturbance than bilateral ECTs. parahippo cam pal gyri, fornix, amyg dala, parts of 3. Confusion may occur in the postictal period. Like thala mus, parts of hypothalamus and posterior part memory disturbances, confusion is much com- of orbital frontal cortex. moner with bilateral ECTs. Usually, no treatment The limbic system is closely connected with the is needed. Paren teral diazepam may be given for frontal and temporal lobes, midbrain and other parts excitement during this period. of brain, by many connecting fi bres. The aim of psy- 4. Other side effects include headache, prolonged chosurgery is to produce surgical lesions in carefully apnoea, prolonged seizure, cardiovascular dys- selected parts of limbic system and/or its connecting function, emergent mania, muscle aches and fi bres. One major part of limbic system, believed to be apprehension. important in emotional experiences, is Papez circuit. ECT does not cause any brain damage. This important circuit, which lies within the limbic 204 A Short Textbook of Psychiatry

Techniques Before any procedure, an informed consent must be obtained by the neurosurgeon and the treating team. Currently, all techniques use stereotactic methods so that the lesion made is precise and side effects produced are few. The available procedures include bimedial leuco tomy, orbital undercutting, rostral leucotomy, prefrontal leucotomy, anterior or posterior cingulumectomy and stereotactic tractotomy (in addition to those mentioned below). The lesion is produced by electrocoagula tion, Fig. 16.1: Papez Circuit freezing, thermocoagulation, ultrasonic method, Yttrium-90 seeds, or laser. The currently employed procedures include: system, connects cingulate bun dle, hippocampus, 1. Stereotactic Subcaudate Tractotomy: A large anterior thalamus, mammillary bodies, fornix and subcaudate lesion is produced. It is recommended septum (Fig. 16.1). for severe depression, severe anxiety, severe ob- Indications sessive-compulsive disorder and schizo-affective disorder. The current indications for psychosurgery include 2. Stereotactic Limbic Leucotomy: A small sub- the following: caudate lesion is made, in addition to a lesion 1. Chronic, severe, incapacitating depression, which in cingulate bundle. It is used for treatment of has not responded to all available treatments. intractable obsessive-compulsive disorder and 2. Chronic, severe, incapacitating obsessive-compul- schizophrenia. sive disorder (OCD), which has not responded to 3. Amygdalotomy: This is used for severe, patho- all available treatments. logical, uncontrolled and intractable aggression 3. Chronic, severe, incapacitating anxiety dis order, associated with neuropsychiatric disorders. which has not responded to all available treat- Side Effects ments. With the use of stereotactic procedures, side effects 4. Schizophrenia with severe depressive compo nent, are very rare. These include a less than 1% risk of which has not responded to all available treat- seizures, a very uncommon risk of personality change ments. (which used to be frequent with earlier procedures) 5. Severe, pathological and uncontrolled aggres sive and a 1:1,000 to 1:10,000 mortality risk. behaviour associated with a psychiatric or neurological illness (e.g. temporal lobe epilepsy). Comments It is believed that the maximum improvement It must be remembered that at present, psychosurgery occurs in distress, tension, anxiety and agitation is an extremely uncommon procedure in the routine rather than in other symptoms. An intact, well- psychiatric practice in India and most of the world. maintained premorbid personality is a good prognostic Most psychiatrists would have never referred any sign. patient for the procedure. 17 Psychoanalysis

The term psychoanalysis can denote one or more of Although it was later almost replaced by the structural the following: theory, it is still useful in understanding the mental 1. A psychological theory of mind and personality mechanisms. development based primarily on the concept of The tripartite division of mind included the un- intrapsychic ‘confl ict’. conscious, the preconscious and the conscious. 2. A procedure for investigation of unconscious psychical processes, otherwise inacces sible. The Unconscious 3. A therapeutic technique of treating psychiatric Much of the mental activity lies outside the sphere disorders by psychological means. of consciousness. However, this uncons cious mental activity infl uences the conscious thought and behav- HISTORICAL OVERVIEW iour even if it is not available to voluntary recall. The unconscious contains those ideas and affects Although the credit for ‘invention’ of psycho ana lysis which have been repressed (by the censor, as repres- belongs to Sigmund Freud (1856-1939), he drew heav- sion is known). This repres sed material can only reach ily from the work of several prominent researchers consciousness through preconscious when the censor including Jean-Martin Charcot (hypnosis), Theodor is rela xed (for example, in dreams or abreaction) or Meynert (neuroanatomy and psychiatry), Ernst Brucke overpowe red (for example, in slips of tongue or free (physiology and phy siochemistry), Hippolyte Bern- association). heim (hypno sis) and Josef Breuer (hysteria), among The unconscious mental activity is charac terised others. by primary process thinking which is typically found Although there were several changes in psycho- in young children, severe psychosis, mental retarda- analysis, some of them even fundamental, as Freud’s tion and dreams. It is different from normal thinking thinking evolved over the years, an attempt is made ( secondary process thinking) in that it strives for here to illustrate the basic concepts of psychoanalysis immediate discharge of drive energy, lacks contact as it existed near the end of Freud’s career. with reality, is full of contradictions, lacks organisation and logical connections, and is based on the pleasure BASIC CONCEPTS principle. Topographic Theory of Mind The Preconscious This theory was advanced by Freud in the year 1900, This region of mind lies between the unconscious and in the book called The Interpretation of Dreams. the conscious, with access to both. The uncons cious 206 A Short Textbook of Psychiatry mental contents can reach the conscious only through maintains a balance between the id and the super-ego the preconscious. It is not present at birth but develops on one hand and the reality on the other. in childhood, paralleling the ego development. The For example, the individual observes a pleasurable censor lies here, main tain ing the repres sive barrier. object surrounded by a barrier. The id wants immediate The preconscious mental contents can easily be- gratifi cation by obtaining the object, without seeing come conscious with focusing of attention. the reality of a barrier around it. The super-ego, on the other hand, proclaims that it is sinful to derive The Conscious pleasure from an object surrounded by barrier. The ego If mind can be divided in portions, the conscious strikes a balance between the two, as well as the real constitutes only a tiny part of it. Freud conceptualised world, and decides to wait and fi nd a way to ‘climb’ conscious as a type of special sense organ of atten- the barrier and derive pleasure. Although simplistic, tion concerned with registration of stimuli from both the example illustrates the ego’s function of delaying within and without. The conscious mental contents are gratifi cation in view of the reality. characterised by secondary process thinking based on The ego is the seat of conscious, intellectual, the reality principle. self-preservative and defensive functions of mental In addition to the topographic m odel of mind, apparatus. Freud also theorised the concept of psychic determinism which means that all mental activity is meaningful The Super-ego and purposeful, though uncons cious, and is linked The super-ego is predominantly an unconscious sub- with the previous life experiences. Hence, according division of mental apparatus that develops from the to this principle, no mental activity can be accidental ego. It is especially concerned with moral standards or pur poseless. and has two parts: a punitive conscience and a non- punitive ego ideal. Structural Theory of Mind Both derive from the effect of parental infl uence In 1923, in ‘The Ego and The Id’, Freud divided the on the ego. This parental infl uence not only includes mental apparatus into three dynamic structures: the the effect of actual parents but also of the important id, the ego and the super-ego (Fig. 17.1). family members, religion and important people in the surrounding environment (such as celebrities). The The Id criticisms, prohibitions, guilt-arousing statements and The id is theorised to be the original state of human punish ments are introjected as conscience. mental apparatus with which a newborn baby is born. On the other hand, the approvals and rewards It is totally unconscious, containing the basic drives become introjected as the ego ideal. The ego ideal and instincts concerned with survival, sexual drive is later involved in the setting of personal goals and and aggression. It is characterised by primary process aspirations. thinking and is based on pleasure principle, lacking any direct link with reality. The only urge of these drives is imme diate gratifi cation. The Ego The ego is primarily determined by the expe rience of reality and is, therefore, guided by the reality principle. It is predominantly conscious though some parts (such as ego defense mecha nisms) are unconscious. Ego Fig. 17.1: Structural Theory of Mind Psychoanalysis 207

Ego Defense Mechanisms nisms are listed in Table 17.1, along with defi nitions, The term ego defense mechanism refers to the auto- clinical illustra tions and examples in normal situa- matic, involuntary, and uncon s ciously instituted psy- tions. chological activity by which the unacceptable urges or No ego defense mechanism is by itself psychotic, impulses are excluded from the conscious awareness. neurotic, immature, mature or normal. Almost all These defense mechanisms are a function of ego. mechanisms of defense can be used in normal indi- The defense mechanisms usually operate on an viduals. It is an exclusive or abnormally excessive unconscious level (except, for example, suppres sion use that makes a defense mechanism neurotic or which is a voluntary defense mechanism). In contrast, psychotic. coping mechanisms are voluntary and conscious mechanisms of defense which an individual employs The Theory of Psychosexual Development to deal with day-to-day external and conscious fears In 1905, in ‘Three essays on the theory of sexuality’, and confl icts. Freud enunciated his theory of infantile sexuality and There is no ‘standard’ list of defense mecha nisms; described the psychosexual stages of development however, a few commonly used ego defense mecha- (Table 17.2 for a very brief summary). Table 17.1: Commonly used Ego Defense Mechanisms Defense Mechanism Defi nition Example(s) in Normal life Illustration(s) from Clinical Situations A. Primary 1. Repression Unconsciously excluding 1. ‘Forgetting’ Psychogenic amnesia from conscious awareness 2. Slips of the tongue of anxiety provoking ideas and/or feelings B. Psychotic/Narcissistic 1. Regression Reversion to modes of 1. Dreams 1. Neuroses (mild regres- psychological functioning 2. Regression in the service sion) that are characteristic of of ego (ability of a mature 2. Psychoses (more perva- earlier life stages, especially adult to appropriately in- sive regression) childhood years dulge periodically in playful 3. Severe, prolonged physi- childlike activities) cal illness 2. Denial Involuntary exclusion of 1. Grief 1. Psychoses unpleasant or painful reality 2. Children (3-6 year olds) 2. Alcohol dependence from conscious awareness 3. Projection Unconscious attribution A universal phenomenon Persecutory delusions and of one’s own attitudes and though occurs more com- hallucinations urges to other person(s), monly in children because of intolerance or painful affect aroused by those attitudes and urges 4. Distortion Unconscious gross ‘reshap- — 1. Hallucinations ing’ of external reality to 2. Delusions, especially of satisfy inner needs grandiosity Contd... 208 A Short Textbook of Psychiatry

Contd... Defense Mechanism Deﬁ nition Example(s) in Normal life Illustration(s) from Clinical Situations C. Neurotic/Immature 1. Conversion A repressed, forbidden Sometimes seen in normal Conversion disorder urge is simultaneously kept individuals when exposed (Hysteria) out of awareness and also to catastrophic stress; expressed in symbolic/ otherwise presence always disguised form of some implies psychopathology somatic conversion ‘reaction’ (usually either motor or sensory) 2. Dissociation Involuntary splitting or sup- Near death experience Dissociative disorders, pression of a mental func- e.g. psychogenic amnesia, tion or a group of mental psychogenic fugue, multiple functions from rest of the personality, somnambulism, personality in a manner that possession syndrome allows expression of forbidden unconscious impulses without having any sense of responsibility for actions 3. Displacement Unconscious shifting of Normal, day-to-day deﬂ ec- 1. Phobia (especially in emotions, usually aroused tion of ‘anger’ on a substi- children) by perceived threat, from tute target 2. OCD an unconscious impulse to a less threatening external object which is then felt to be the source of threat 4. Isolation ( Isolation of Separation of the idea of an 1. Grief Obsessional thoughts affect) unconscious impulse from 2. Ability to discuss trau- its appropriate affect, thus matic events without the allowing only the idea and associated disturbing emo- not the associated affect to tions, with passage of time enter awareness 5. Reaction formation Unconscious transformation Normal character formation Obsessive compulsive per- of unacceptable impulses in childhood (from 3 years sonality traits and into exactly opposite onwards) disorder attitudes, impulses, feelings or behaviours 6. Undoing Unconsciously motivated 1. Checking of gas knobs or 1. Compulsive acts in OCD acts which magically/sym- locks to ensure safety 2. Compulsive rituals bolically counteract unac- 2. Automatically saying ‘I ceptable thoughts, impulses am sorry’ on bumping into or acts somebody Contd... Psychoanalysis 209

Contd... Defense Mechanism Defi nition Example(s) in Normal life Illustration(s) from Clinical Situations 7. Rationalisation Providing ‘logical’ explana- A universal phenomenon Usually used to explain tions for irrational behav- behaviours resulting from iour motivated by unaccept- other defense mechanisms able unconscious wishes 8. Intellectualisation Excessive use of intellectual When faced with stressful — processes (logic) to avoid af- situation, use of logic to fective expression (emotion) focus closely on external reality and avoiding expression of inner feelings (e.g. fear) 9. Acting out Expression of an uncon- Destruction of any object in Impulse control disorders scious impulse, through a ‘fi t of rage’ action, thereby gratifying the impulse 10. Schizoid fantasy Withdrawal into self to Seen in adolescence (wish Schizoid and schizotypal gratify frustrated wishes by fulfi lling daydreams) personality disorder fantasy 11. Turning against the Unconscious defl ection of 1. Head banging in chil- 1. Suicide self ( Retrofl exion) hostility towards another dren 2. Severe depression person onto oneself result- 2. Destruction of property 3. Any form of deliberate ing in lowered self-esteem, or self in a fi t of rage self harm (DSH) self-criticism and at times injury to self 12. Introjection Unconscious internalisation 1. Identifi cation with the Depression of the qualities of an object aggressor (e.g. sometimes or person seen in victims kidnapped by terrorists; also known as Stockholm syndrome) 2. Grief reaction 13. Hypochondriasis Unconscious transformation Abnormal illness behaviour Hypochondriasis of unacceptable impulses in physically disordered or into inappropriate somatic normal individuals concern 14. Inhibition Involuntary decrease or loss 1. Writing ‘blocks’ or work 1. OCD of motivation to engage in ‘blocks’ 2. Phobias some goal-directed activity ’2. Social shyness to prevent anxiety arising out of confl icts with unacceptable impulses Contd... 210 A Short Textbook of Psychiatry

Contd... Defense Mechanism Deﬁ nition Example(s) in Normal life Illustration(s) from Clinical Situations 15. Compensation Unconscious tendency to 1. Involvement in dare-devil 1. Nymphomania (to ( Counter-phobic defense) deal with a fear or conﬂ ict activities (e.g. sky diving to counter a sense of sexual by unusual degree of effort counter fear of heights) inadequacy) in the opposite direction 2. Excessive pre-occupation 2. Keeping excessive details with body building to coun- in a diary in patients suffer- ter feelings of inferiority ing from dementia

16. Splitting Unconscious viewing of self Believing personalities to Borderline personality or others as either good or be either ‘black’ or ‘white’ disorder bad without considering the without the shades of ‘grey’ whole range of qualities (e.g. in a ‘typical’ Bolly- wood movie, the Hero often is all good and the Villain all bad)

D. Mature

1. Sublimation Unconscious gradual chan- Channelisation of sexual — nelisation of unacceptable or aggressive impulses infantile impulses into into creative activities (e.g. personally satisfying and diverting forbidden sexual socially valuable behaviour impulses into artistic paint- patterns ings)

2. Suppression Voluntary postponement of Voluntary decision not to — (Voluntary) focusing of attention on an think about an argument impulse which has reached with a close friend while conscious awareness going for an interview

3. Anticipation Realistic thinking and plan- Anticipation is a universal — ning about future unpleas- phenomenon occurring in urable events all intelligent individuals

4. Humour Overt expression of unac- A universal phenomenon — ceptable impulses using humour in a manner which does not produce unpleas- antness in self or others

No ego defense mechanism is psychotic, neurotic, immature, mature or normal per se. Almost all mechanisms of defense are sometimes used in normal individuals. It is an exclusive or abnormally excessive use that makes a defense mechanism neurotic or psychotic. Psychoanalysis 211

Table 17.2: Psychosexual Stages of Development (Sigmund Freud) Phase Age Range Normal Development Psychiatric syndromes theorised to result from fi xation (and regression) to this stage 1 Oral phase Birth to Major site of gratifi cation is the oral region. It 1. Dependent personality 1-1½ consists of 2 phases: traits and disorder years i. Oral erotic phase (sucking) 2. Schizophrenia (oral and ii. Oral sadistic phase (biting) pre-oral phase) 3. Severe mood disorder 4. Alcohol dependence syndrome and drug dependence 2 Anal phase 1-1½ Major site of gratifi cation is the anal and perianal 1. Obsessive compulsive years to area; major achievement is toilet training (sphinc- personality traits and 3 years ter control). disorder It consists of 2 phases: 2. OCD (Anal sadistic phase) i. Anal erotic phase (excretion) ii. Anal sadistic phase (‘holding’ and ‘letting go’ at will) 3 Phallic (Oedipal) 3 to 5 Major site of gratifi cation is the genital area; 1. Sexual deviations phase years genital masturbation is common at this stage. 2. Sexual dysfunctions According to Freud, this development is different 3. Neurotic disorders in both sexes. Male development The boy develops castration anxiety (fear of castration at the hand of his father in retaliation for the boy’s desire to replace his father in his mother’s affections). This leads to formation of the Oedipus complex (aggressive impulses directed towards the father; named after the Greek tragedy Oedipus rex in which Oedipus unknow- ingly kills his father and marries his mother, unaware of their true identities). Oedipus complex is usually resolves by identifi cation with father, attempting to adopt his characteristics. Female development The girl develops penis envy (discontent with female genitalia following a fantasy that they result from loss of penis). This is theorised by Freud to lead to a wish to ‘receive’ the penis and to bear a child. Resolution occurs by identifi cation with the mother. This phase has been called as Electra complex. Contd... 212 A Short Textbook of Psychiatry

Contd... Phase Age Range Normal Development Psychiatric syndromes theorised to result from fi xation (and regression) to this stage 4 Latency phase 5-6 years Oedipus (and Electra) complex is usually Neurotic disorders to 12 resolved at the beginning of this stage. This is a years stage of relative sexual quiescence. Super-ego is formed at this stage. Sexual drive is channelised into socially appropriate goals such as development of interpersonal relationships, sports, school, work, etc. 5 Genital phase 12 years Adult sexuality develops with capacity for Neurotic disorders onwards) intimacy (during puberty) and respect for others. Gradual release from parental controls with more infl uence of peer group. True self-identity develops. The normal development described here is a simplifi ed account of Sigmund Freud’s theory of psychosexual development. Till date, it remains a theory; there is no empirical evidence for, say, Oedipus complex or contribution of these stages to development of psychiatric symptoms or syndromes.

Theory of Dreams According to this theory, the dream work consists of the following mechanisms: Dream interpretation has been a major component of 1. Symbolism psychoanalysis. Beginning with his own dream expe- 2. Displacement riences, Freud analysed dreams as “the royal road to 3. Condensation the unconscious”. He believed dreams to be conscious 4. Projection expression of unconscious fantasies or impulses which 5. Secondary elaboration (since dream content are not accessible to the individual in wakefulness, consists of primary process thinking, secondary thereby providing gratifi cation by wish fulfi lment. elaboration is used to introduce logical thinking or Since expression of unconscious forbidden fanta- secondary process thinking in the dream content). sies can evoke considerable anxiety, these fantasies are In addition to the unconscious impulses, wishes considerably modifi ed so as to preserve sleep on the and fantasies, the dream content is also infl uenced by: one hand and provide gratifi cation of the fantasies on 1. Nocturnal sensory stimuli (e.g. thirst, hunger, full the other. This modifi cation is known as dream work. bladder). Here the unconscious forbidden fantasies or wishes 2. Day residue (residue of day experiences of previ- which threaten to break sleep constitute the latent ous one or several days). dream content, whereas the dream content modifi ed by dream work constitutes the manifest dream content. Psychoanalysis and Psychoanalytical According to Freud, the aim of dream interpretation is Psychotherapy to get to the latent dream content from manifest dream Psychoanalysis and psychoanalytical psycho- content, via free association, in order to understand the therapy as treatment methods are briefl y discussed ‘real meaning’ of the dream experience. in Chapter 18. 18 Psychological Treatments

PSYCHOTHERAPY Table 18.1: Psychosocial Therapies Therapy/School Proponent(s) Psychotherapy can be defi ned (modifi ed from Wol- 1. Psychoanalysis Sigmund Freud berg) as, the treatment by psychological means, of the 2. Analytical psychology Carl Gustav Jung problems of an emotional nature, in which a therapist 3. Behaviourism John Broadus Watson deliberately establishes a professional relationship 4. Character analysis Wilhelm Reich with the patient to, 5. Classical conditioning Ivan Petrovich Pavlov 1. Remove, modify or retard existing symptoms, 6. Client-centred Carl R Rogers 2. Mediate disturbed patterns of behaviour, and/or psychotherapy 3. Promote positive personality growth and develop- 7. Cognitive behaviour Donald Meichenbaum ment. therapy Psychotherapy can be conducted by either verbal 8. Cognitive therapy Aaron T Beck or non-verbal means. There are several different kinds 9. Dual sex therapy William Masters and of psychotherapies. The important types include the Virginia Johnson following (Table 18.1). 10. Existential logotherapy Victor E Frankl Psychoanalysis and Psychoanalytical 11. Gestalt therapy Frederich Perls Psychotherapy 12. Group therapy Joseph Pratt 13. Hypnosis James Braid These psychotherapeutic methods are based primarily 14. Operant conditioning Burrhus Frederic on Sigmund Freud’s work, although many other tech- Skinner niques developed by other important workers (such as 15. Primal therapy Arthur Janov Carl Jung, Alfred Adler, Erich Fromm, Harry Stack 16. Progressive muscular E. Jacobson Sullivan, Karen Horney, Melanie Klein, Otto Rank, relaxation Wilhelm Reich and many others) are also in use. 17. Psychodrama Jacob L Moreno A detailed discussion of Freudian psychoanalysis 18. Rational emotive therapy Albert Ellis is not attempted here (see Chapter 17) and a very brief 19. Reciprocal inhibition Joseph Wolpe outline of therapy is presented. 20. Therapeutic community Maxwell Jones Classical Psychoanalysis 21. Token economy Ayllon and Azrin 22. Transactional analysis Eric Berne Freudian psychoanalysis typically needs 2-5 visits/ 23. Will therapy Otto Rank week by the patient for a period of 3-5 years (even 214 A Short Textbook of Psychiatry longer). No detailed history taking, mental status aims at modifying maladaptive behaviour and substi- examination, or formalised psychiatric diagnosis is tuting it with adaptive behaviour. attempted. The patient is allowed to communicate Although there are many theories of learn ing, unguided, by using ‘free association’. majority of behaviour therapy techniques are based The therapist remains passive with a non-directive on operant conditioning model (Skinner) and classi- approach; however, the therapist constantly challen ges cal conditioning model (Pavlov). Many of the ideas the existing defenses and interprets resis tance (dur- actually seem like (and are) common sense principles. ing the therapy) and transference (patient’s feelings, The learning theories assume that all behaviour is behaviours and relationship with the therapist). learned behaviour. The behaviour that is followed No direct advice is ever given to the patient. The by a reward is more likely to occur again (operant crux of the therapy is on interpretation. During the model), and that behaviour is learned more easily if therapy, the patient typically lies on the couch, with taught in small steps. the therapist sitting just out of vision. No other therapy Behaviour therapy is typically a short duration is usually used as adjunct. therapy; therapists are easy to train and it is usually cost-effective. The total duration of therapy is usually Psychoanalytically-oriented 6-8 weeks. Initial sessions are scheduled daily but (Psychodynamic) Psychotherapy the later sessions are more spaced out. A behavioural Psychoanalytically-oriented, psychodynamic psychoanalysis is usually carried out before planning behav- therapy is a much more direct form of psychoanalysis. iour therapy. One of the simplest methods of behaviour The duration of therapy is much briefer and advice is analysis is called as ABC charting, which involves a given to the patient occasionally. The patient and the close look at the: therapist may sit face-to-face or else couch is used. The i. Antecedent (e.g. circumstances under which rest of technique is nearly the same as psychoanalysis. the behaviour began; who, if any, were present; However, additional modes of treatment, including other details), drug therapy can be used. ii. Behaviour (description of the behaviour in The indications for both psychoanalysis and detail), and psychoanalytically-oriented psychotherapy are not iii. Consequence (what happened afterwards; what usually based on any psychiatric diagnoses. The most factors helped to maintain behaviour). important indication is the pre sence of long-standing Some of the important behavioural techniques are mental confl icts which, although are unconscious, described briefl y. produce signifi cant symptomatology. The prerequisites of therapy are that the patient Systematic Desensitisation should be motivated for therapy, should have strong Systematic desensitisation (SD) is based on the prin- ‘ego-structure’ (which can bear frustrations of ciple of reciprocal inhibition, described by Wolpe. impulses during the therapy), should be psychologi- The principle states that if a response incompatible cally-minded and should not have recent signifi cant with anxiety is made to occur at the same time as an life stressors. anxiety-provoking stimulus, anxiety is reduced by It is usually used for the treatment of neuro tic dis- reciprocal inhibition. orders and personality disorders (or charac tero logical This consists of three main steps: diffi culties). i. Relaxation training (described later). ii. Hierarchy construction: Here the patient is Behaviour Therapy asked to list all the con ditions which provoke Behaviour therapy is a type of psychotherapy (broadly anxiety. Then, he is asked to list them in a des- defi ned) which is based on theories of learning, and cending order of anxiety provocation. Thus, Psychological Treatments 215

a hierarchy of anxiety-producing stimuli is ii. Negative reinforcement: Here, on performance prepared. of the desirable behaviour, punishment can be iii. Systematic desensitisation proper: This can avoided. be done either in imagery (SD-I) or in real- iii. Modelling : The person is exposed to ‘model’ ity/in vivo (SD-R). At ﬁ rst, the lowest item in behaviour and is induced to copy it. This can hierarchy is con fronted (in reality or in image- also be used to avoid certain behaviours. ry). The patient is advised to signal whenever anxiety occurs. With each signal, he is asked Flooding to relax (Step-I). After a few trials, patient is This is usually the method used in the treatment of able to control his anxiety. Thus, gradually the phobias. Here, the person is directly exposed to the hierarchy is climbed till the maximum anxiety- phobic stimulus, but escape is made impos sible. By provoking stimulus can be faced in the absence prolonged contact with the phobic stimulus, therapist’s of anxiety. guidance and encouragement, and therapist’s model- SD is a treatment of choice in phobias and obses- ling behaviour, anxiety decreases and the phobic sive-compulsive disorders. behaviour diminishes. Aversion Therapy Operant Conditioning Procedures for Aversion therapy is used for the treatment of condi- Decreasing Behaviour tions which are pleasant but felt unde sirable by the These methods include: patient, e.g. alcohol dependence, transvestism, ego i. Time-out : Here, the reinforcement is withdrawn dystonic homosexuality, other sexual deviations. for some time, contingent upon the undesired The underlying principle is pairing of the pleasant response. Time-out is often used in therapy with stimulus (such as alcohol) with an unplea sant response children. (such as brief electrical stimulus), so that even in ii. Punishment : Aversive stimulus is here absence of unpleasant response (after the therapy is presented, contingent upon undesired response over), the pleasant stimulus becomes unpleasant by (i.e. whenever undesired response occurs, pun- association. The unpleasant aversion can be produced ishment is given). by electric stimulus (low voltage), drugs (such as apo- iii. Satiation : The undesired response is positively morphine and disul ﬁ ram) or even by fantasy (when it reinforced, so that tiring occurs. A simi lar tech- is called as covert sensitisation). nique is negative practice procedure. Typically, 20-40 sessions are needed, with each session lasting about 1 hour. After comp letion of treat- Other Behavioural Techniques ment, booster sessions may be given. The current use Many other techniques such as token economy (for of aversion therapy has declined sharply in the Western hospitalised patients), social-skills training (for world (and also elsewhere) as it is felt by many that it patients with social difficulties), family therapy, may violate the human rights of the patient. marital therapy, and cognitive behavioural therapy are available. The interested reader is referred to the Operant Conditioning Procedures for Reading List. Increasing Behaviour The common methods for augmenting an adaptive Cognitive Therapy or Cognitive behaviour include: Behaviour Therapy i. Positive reinforcement: Here, the desirable Cognitive behaviour therapy (CBT) is a type of psy- behaviour is reinforced by a reward, either chotherapy which aims at correcting the maladaptive mate rial or symbolic. methods of thinking, thus providing relief from con- 216 A Short Textbook of Psychiatry

Fig. 18.1: Cognitive Behaviour Therapy Model sequent symptoms. The thera pist plays an active role, tivity in perspectives, identifying and testing unlike in psychoanalysis. mala daptive assumptions, and decentering, Developed separately by Beck and Meichen baum, ii. Behavioural techniques such as activity it is used for treatment of depres sion, anxiety disorder, scheduling, homework assignments, graded task panic disorder, phobias, eating disorders, anticipatory assignment, behavioural rehearsal, role playing, anxiety, and also for teaching problem-solving meth- and diversion techniques, and ods. Some centres also use CBT for management of iii. Teaching problem-solving skills. psychotic symptoms such as delusions and hallucina- iv. Mindfulness, originally a Buddhist technique, tions. can also be combined with CBT. Figure 18.1 illustrates the hot cross bun model of cognitive behaviour therapy. Supportive Psychotherapy A typical cognitive therapy schedule consists This is a very directive method of psycho therapy, with of about 15 visits over a three-month period. Some the focus clearly on existing symptoms and/or current important techniques in CBT are: life situations. The aims of the therapy are: i. Cognitive techniques such as recognising and i. Correction of the situational problem. correcting negative automatic thoughts, teach- ii. Symptom rectiﬁ cation. ing reattribution techniques, increasing objec- iii. Restoring or strengthening defenses. Psychological Treatments 217

iv. Prevention of emotional breakdown. utilize psychoanalytic, supportive, transactional or v. Teaching new coping skills. behavioural app roaches. The aim is achieved by a conglomeration of Over the years, many types of group therapies have techniques which include guidance, sug gestion, emerged such as self-help groups (Alcoholics Anony- environmental manipulation, reassurance, persuasion, mous for alcoholics, Weight Watchers for obese, development of a doctor-patient relationship, diver- Phoenix-House for opiate dependent individuals), sion, and even hospitalisation and medication. This is Trans actional Analysis groups (Eric Berne), Training a highly skilled method of psycho therapy which can groups (Kurt Lewin), Psycho drama (Jacob Moreno) provide excellent results when used judiciously. and the like. Family and Marital Therapy Suggestion In family therapy and marital therapy (also called as Although an integral part of supportive psycho- couples therapy), the focus of intervention is not on therapy, it is often used alone. It is used by nearly all the individual but is instead on the family as a unit or medical practitioners, without realising or naming the marital unit. it as such. It is suggestion, which is in part respon- There are several varieties of family and marital sible for the placebo response. A placebo prescribed therapies, such as those based on psychody namic, confi dently by an ‘impressive’ physician can lead to behavioural or systemic principles. Whenever there some improvement in about 33% of patients with are relational problems within a family or marital unit most conditions. (either primarily or secondary to a psychiatric disorder), family and/or marital therapy is indicated. For Hypnosis example, in a behavioural marital therapy, components Hypnosis is a state of artifi cially induced (by self or of therapy may include problem solving, training in others) increased suggestibility. There is a constric- communication skills, writing a behavioural marital tion in the peripheral awareness with increased focal contract, and home-work assignments. concentration on task at hand. Trance phenomena were routinely utili zed by Group Therapy Anton Mesmer in 1775 who called ‘this force’ as Group therapy (or group psychotherapy) is a animal magnetism. The word hypnotism was fi rst used less time-consuming procedure, in which usually by James Braid in the 19th century. 8-10 people can be treated at one time. This was fi rst Not everyone can be hypnotised. The capacity used by Joseph Pratt (an internist) in 1905, for patients for hypnosis is called hypnotisability, which can be suffering from tuberculosis. measured in a person by using tests such as the eye Now, it is known that group therapy is not only roll sign or hand levitation test. Basically, these tests time-saving but also especially benefi cial for certain measure suggestibility. group of patients. Group therapy offers patients (and About 60% of the general population can be hyp- their relatives) an opport unity to realise that many notised but only 5-10% reach deep hypnotic trance. others have and share problems which are very similar A wide variety of techniques are available for the to their own problems, and that they are not alone in induction of hypnosis. their suffering. Following changes occur commonly during the Typically, sessions are held once or twice a hypnotic trance: week, with each session lasting 1-2 hours (often 1½ i. The person under hypnosis becomes highly hours). The patients usually sit in a circle, with equal suggestible to commands of hypnotist, without opportunities for interaction. Group therapy may understanding their nature. 218 A Short Textbook of Psychiatry

ii. Dissociation of a part of body or emo tions from longer commonly used in clinical practice, due to risk the remainder may occur. of dependence (in case of amphetamines and LSD) iii. There is a partial or complete amnesia for the and/or side effects. events occurring during the hypnotic trance. Another method is the use of 5% solution of iv. There is an ability to produce or remove symp- sodium amobarbital (amytal) or thiopen tone sodium toms, perceptions and/or movements. (pentothal), infused at a rate no faster than 1 cc/min to v. Post-hypnotic suggestion can be given just after prevent sleep as well as respiratory depression. This the trance and it is followed by the hypnotised procedure must always be done very carefully with person. support from an anaesthetist who should be physically Persons who are hypnotisable are in no way present. abnormal as compared to the rest of the popu lation. The abreactive procedure is begun with neutral topics at fi rst, gradually approaching area(s) of con- Indications in Psychiatry fl icts. Usually about 150-350 mg (3-7 cc.) of amytal i. As an adjunct to psychotherapy. is suffi cient for the purpose. In elderly and patients ii. To abreact past experiences. with organic brain disorder, even 75 mg of amytal The conditions in which hypnosis can help in may produce exces sive drowsiness. treatment are many. The most important ones are listed The indications of amytal interview include: below. i. Abreaction (mainly) e.g. in hysteria. i. Psychosomatic disorders ii. Interview with a mute patient. ii. Conversion disorder ( hysteria) iii. Diagnostic test in catatonic syndrome. iii. Dissociative disorder (hysteria) iv. Differentiating test in stupor (for diffe rential iv. Eating disorders (anorexia nervosa, buli mia diagnosis of depression, schizophrenia, hysteria nervosa and obesity) and organic brain disorder). v. Habit disorders (smoking) There are certain contraindications for the use of vi. Pain amytal interview: vii. Anxiety disorder. i. Airway disease including upper respiratory tract infection. Abreaction ii. Severe renal or hepatic disease. Abreaction is an important procedure which brings to iii. History of porphyria. conscious awareness, for the fi rst time, unconscious iv. Hypotension. confl icts and associated emotions. v. Dependence on barbiturates. The release of emotions is therapeutic. Although vi. Psychosis (except for catatonia or stupor). abreaction is an integral part of psycho analysis and The other medications which have been used hypnosis, it can be used independently also. Abreac- successfully for abreaction include diazepam and tion can be done with or without the use of medication. ketamine. The use of abreaction has declined considerably in the last three decades and the cur- Abreaction with Medication rent practice and guidelines do not encourage its Earlier amphetamines, ether, nitrous oxide and routine use. lysergic acid diethylamide (LSD) have been used for abreaction. Particularly, intra venous amphe tamines Relaxation Therapies were very successful as they lead to a marked increase The aim of these therapies is to induce muscular in pro ductivity of speech, thus facilitating release of relaxation. Since anxiety produces muscular tension, unconscious ideas and emotions. These agents are no which in turn reinforces (and thus increases) anxiety, Psychological Treatments 219 any relaxation technique would decrease both anxiety A large number of patients with psychiatric disor- and muscular tension. ders (such as schizophrenia) may have a poor quality Relaxation techniques are an integral part of a of life, residual symptoms, and long-term disability. majority of behaviour therapies, such as systematic Although early recognition and treatment is the corner- desensitisation. There are many methods which can stone of preven ting long-term disability, a substantial be used to induce relaxation and these include: number of patients may need rehabilitation. A. Jacobson’s progressive muscular relaxation: There are several components and methods avail- This is the most frequently used technique. The able for rehabilitation, depending on the type and/or patient fi rst tenses and then relaxes major muscle stage of disorder and the type of support available groups of the body in a prefi xed and systematic to the patient. Necessarily, a comprehensive assess- order, usually beginning at the top of the body and ment is needed before deciding on the individualized progressing downwards. rehabilitation for a particular patient. B. Hypnosis Some of the methods used for psychiatric reha- C. Transcendental meditation (TM) or Yoga bilitation include housing placement (such as half D. ‘Shavasna’ (‘The corpse posture’): Similar to pro- way homes, supervised housing), vocational training gressive relaxation but the sequence of progression and rehabilitation (such as activity therapy, sheltered is below upwards. workshop, transitional or supported employment, E. Yog Nindra, Pranayama and Vipasna are other vocational guidance, occupational therapy), and treat- Indian methods. ment (such as ensuring compliance with medication, F. Biofeedback. social skills therapy, family therapy, cognitive reme- diation). Biofeedback There is an acute shortage of psychiatric rehabili- Biofeedback (introduced for the fi rst time in 1969) is tation facilities in most parts of India. The Persons the use of an instrument (usually electronic), which with Disabilities (Equal Opportunities, Protection of provides immediate feedback to the patient regarding Rights, and Full Participation) Act (PDA), 1995 is a his physiological activities normally not available to step forward, as it includes psychiatric disorders and the conscious mind, such as ECG, EEG, pulse rate, mental retardation. blood pressure, EMG, and galvanic skin response (GSR). Indian Perspective The feedback helps the patient, apparently to con- Just about the time Freud was practicing psycho- trol these responses. Relaxation is easily achieved by analysis, Girindra Shekhar Bose was using his own this method. A simpler form (relaxometer ) uses only version of psychoanalysis in Calcutta. However, one parameter, the GSR. currently psychoanalysis is not widely used in India. The other uses of biofeedback include treatment It is believed by some that most Indian patients, of enuresis, migraine headaches, tension headache, as compared to patients in western, developed coun- idiopathic hypertension, inconti nence, car diac arrhyth- tries, are not psychologically minded and are unable mias, uncontrolled generalised tonic clonic seizures, to introspect. They lack verbal fl uency and have more and also for neuromuscular rehabilitation. physical symptoms. The Indian patients have difficulty in main- Rehabilitation taining one-to-one relationship with the physi cian- Psychiatric rehabilitation is defi ned as resto ration of psychiatrist, as they believe him to be a healer who is the fullest physical, mental, social, vocational, and of higher status than them (some thing like a Guru). economic usefulness of which the person suffering The Guru-Chela relationship in the patient-doctor from psychiatric disorder is capable. interaction was fi rst described by JS Neki. 220 A Short Textbook of Psychiatry

Psychoanalysis (which avoids giving direct majority of Indian patients should be preferably brief, advice) is difﬁ cult, as patients expect the therapist to direct, crisis-orien ted, with the therapist playing an guide them and make decisions for them. The patients active role. However, in psychologically minded and are also often fatalistic (‘this had to happen’; ‘it is educated Indian patients, western models can be used the result of destiny and past karma’) and often have with or without modiﬁ cation. magical expectations of cure. The commonest type of psychotherapy used in Most psychotherapists in India agree that West- India is probably supportive psychotherapy though ern models of psychotherapy cannot be directly use of CBT has increased substantially over the last transplanted in the Indian setting. Psycho therapy in a few years. 19 Emergency Psychiatry

An emergency is defi ned as an unforeseen combination EXAMINATION of circumstances which calls for an imme diate action. A medical emergency is defi ned as a medical When faced with a psychiatric emergency, it is often condition which endangers life and/or causes great important to combine speed with obtaining of ‘compre- suffering to the individual. A psychiatric emergency hensive’ or ‘adequate’ information. A scheme for the typi- is a disturbance in thought, mood and/or action which cal emergency psychiatric evaluation is presented here: causes sudden distress to the individual (or to signifi cant others) and/or sudden disability, thus requiring Psychiatric History immediate management. A similar term crisis means It is important to ‘always’ obtain history from both a situation that presents a challenge to the patient, the the patient and the informant(s). Informant(s) may be family and/or the community. more coherent and may provide more relevant information in emergency situation(s). TYPES OF PSYCHIATRIC EMERGENCIES i. Chief complaint: elaborate, with emphasis on dating of onset and progression. A psychiatric emergency can be one or more of the ii. Recent life-changes, such as any losses (real or following: imagined); any physical illnesses. 1. A new psychiatric disorder with an acute onset. iii. Level of adjustment, prior to the psychiatric 2. A chronic psychiatric disorder with a relapse. emergency. 3. An organic psychiatric disorder. iv. Past history (briefl y) of any physical or psy- 4. An abnormal response to a stressful situa tion. chiatric disorder(s). 5. Iatrogenic emergencies. v. Family history (briefl y) of any physical or psy- i. Side effects or toxicity of psychotropic medi- chiatric dis order(s). cation(s). vi. Drug and alcohol history, prescription drugs, ii. Psychiatric symptomatology as a side effect or street drug(s) or alcohol dependence/abuse. toxicity of other medication(s). 6. Alcohol or drug dependence. Detailed General Physical and i. Withdrawal syndrome. Neurological Examination ii. Intoxication or overdose. It is essential to rule out (or diagnose) secondary iii. Complications. psychiatric disorders, with particular emphasis on the 7. Deliberate harm to self or others. presence of any head injury. 222 A Short Textbook of Psychiatry

Mental Status Examination Table 19.1: Some Common Themes in Suicide i. Screen for organicity (most important). Test for 1. A crisis that causes intense suffering with feelings of higher mental (or cognitive) functions, such as hopelessness and helplessness consciousness, orientation, atten tion, concentra- 2. Confl ict between unbearable stress and survival tion, memory, intel li gence, abstract thinking, 3. Narrowing of the person’s perceived options insight and judgement. 4. Wish to escape (it can often be an escape, rather ii. Brief mental status examination, to diagnose or than a going-towards) rule out any psychiatric dis order(s). 5. Often a wish to punish self and/or punish signifi cant iii. Particular emphasis should be placed on the others with guilt presence of ideas of self-harm or suicide, or of harming others. suicidal behaviour, the probable suicide rate per year in India would be around 15/100,000 popu lation. COMMON PSYCHIATRIC EMERGENCIES According to the National Crime Records Bureau (NCRB), there were 125,017 suicides in India in 2008, Suicide which is an increase of 1.95 over the previous year. Suicide is the model of psychiatric emer gencies and In 2003, there were about 300 suicides per day or is also the commonest cause of death among the psy- one suicide every 5 minutes. The comparable period chiatric patients. Some common themes in suicide are prevalence rate for suicide throughout world ranges listed in Table 19.1. from 5/100,000 population/year to 30/100,000 popula- Suicide is a type of deliberate self-harm (DSH) tion/year. The World Health Report, 2001, estimates and is defi ned as a human act of self-intentioned and that every year one million people worldwide com- self-infl icted cessation (death). It ends with a fatal out- mit suicide (100,000 suicides per year in India out of come. DSH is an act of intentionally injuring oneself, 1 million suicides in the world every year), while irrespective of the actual outcome. 10-20 million people attempt suicide. Thus, the ratio An attempted suicide is an unsuc cessful suicidal of attempted suicide to completed suicide is 10-20:1. act with a nonfatal outcome. It is believed that 2-10% In India, the highest suicide rate is in the age group of all persons who attempt suicide, eventually com- of 15-29 years. Some of the highest numbers of suicide plete suicide in the next 10 years. in India are reported from West Bengal (11.9% of all A suicidal gesture, on the other hand, is an cases), Tamil Nadu, Maharashtra, Andhra Pradesh and attempted suicide where the person performing the Karnataka. These fi ve states account for 56.2% of all action never intends to die by the act. How ever, some suicides in the country (NCRB 2008). There are some of these persons may acci dentally die during the act. recent reports of high rates of suicide in teenage girls Attempted suicide is more common in women while (15-19 years old) in some parts of Tamil Nadu and completed suicide is 2-4 times commoner in men. farmers in some areas of Andhra Pradesh. However, suicide rate per 100,000 population (as Epidemiology opposed to number of suicides) was highest in Sikkim Suicide is among the top 10 causes of death in India (48.2 as compared to national average of 10.7/100,000 and most other countries. The offi cial suicide rate in population/year) and followed by Pondicherry (46.9) India in 2008 was 10.8/100,000 population/year (9.7 (NCRB 2008). in 1995; 6.3 in 1980). In 2000, the rate in men was Some important risk factors are summarised in 12.2/100,000 and in women 9.1/100,000) with an Table 19.2. Table 19.3 lists an example of biopsy- overall male to female ratio of 64:36 in 2008 (NCRB). chosocial summary of risk and protective factors for However, as there is considerable under-reporting of suicide in a given case. Emergency Psychiatry 223

Aetiology 1. Depression Some of the common causes of suicide include: i. Major depression. Psychiatric Disorders ii. Depression secondary to a serious physi cal ill- Psychiatric disorders are a major cause of suicide; ness. for example: iii. Reactive depression, secondary to life stressors, e.g. family and/or marital disputes, failure in Table 19.2: Risk Factors for Suicide goal achievement, occupa tional and fi nancial The presence of following factors increases the risk of diffi culties, and death of signifi cant others. completed suicide: 2. Alcoholism and drug dependence. 1. Age>40 years 3. Schizophrenia. 2. Male gender Genetic factors (a concordance rate of 18% in 3. Staying single monozygotic twins) and biochemical factors (low 4. Previous suicidal attempt(s) levels of 5-HIAA) are important in some cases of 5. Depression (risk about 25 times more than usual) i. Presence of guilt, self-accusation, agitation, ni- suicide. hilistic ideation, worthlessness, hypochon driacal Physical Disorders delusions and/or severe insomnia Patients with incurable or painful physical disorders, ii. Risk is usually higher at the beginning or such as cancer and AIDS, often commit suicide (21.9% towards the end of a depressive episode of all suicides in India; NCRB 2008). iii. Risk can often be higher soon after response to Psychosocial Factors treatment rather at the peak of depression; this Psychosocial factors are a very important cause of applies to all forms of treatment but particularly suicide. Some of the examples are failure in an exami- so with antidepressant treatment nation, love affairs (3%), dowry diffi culties (2.4%), iv. There is a higher risk of suicide in the week marital diffi cul ties, ‘illegitimate’ preg nancy, family after discharge from a psychiatric inpatient unit problems (23.8% of all suicides in India) or family 6. Suicidal preoccupation (for example, a written ‘suicide note’ and/or detailed plans are made for psychopathology, loss of a loved object by death committing suicide) or otherwise, occupational and fi nancial diffi culties 7. Alcohol or drug dependence (bankruptcy 2.4%; poverty 2.4%), and social isola- 8. Severe, disabling, painful or untreatable physical tion (data from NCRB 2008). In about 16% cases, no illness obvious causes were found (NCRB 2008). 9. Recent serious loss or major stressful life event 10. Social isolation Methods Used 11. Higher degree of impulsivity In India (NCRB 2008), the commonest modes of committing suicide are ingestion of poison (34.8%) Table 19.3: An Example of Summary of Risks and Protective Factors for Suicide Factors Biological Psychological Social Predisposing Genetic factors Early childhood trauma Poor social support Male gender Personality traits Unemployment Older age Precipitating Discontinuation of antidepressant Separation from spouse Financial diffi culties Psychiatric diagnosis Hopelessness Easy availability of lethal means Worthlessness Perpetuating Alcohol and drug misuse Poor self-esteem Poor social support Protective Children; elderly parents; religious and moral values; good engagement with treatment 224 A Short Textbook of Psychiatry followed by hanging (32.2%), burning (about 8.8%), in preventing the act. This can be done at suicide drowning (about 6.7%), jumping in front of a train or prevention centres, crisis intervention centres (both of another vehicle (3%) and ‘alcoholism’ (1.2%). There these are not available as yet on a large scale in India), were also about 3038 ‘dowry deaths’ in a year in 2008. psychiatric emergency services, medical emergency Men often tend to use more violent methods for suicide services, social welfare centres (such as Samaritans, as compared with women. Sanjivini, Maitri, Sumaitri, Befrienders International) or even at home of the patient. Medicolegal Aspects There are several misconceptions about suicide Under the Indian law, suicide and attempted suicide and these are briefl y enumerated in Table 19.4. are punishable offenses. Section 309 of IPC (Indian Some important steps for preventing suicide Penal Court) states that “whoever attempts to commit include: suicide and does any act towards the commission 1. Take all the suicidal threats, gestures and/or of such offense, shall be punishable with simple attempts seriously and notify a psychiatrist or a imprisonment for a term which may extend to one mental health professional. year and shall also be liable to fi ne”. 2. Psychiatrist (or a mental health professional) It was argued that the law esteems the lives of should quantify the serious ness of the situation men as not only valuable to their own possessors (a proper risk assessment) and take remedial but also valuable to the State which protects them precautio nary measures. and for the protection of which the State exists. The i. Inspect physical surroundings and remove all State, therefore, had the right to prevent persons from means of committing suicide, such as sharp taking their own lives. However, it compounded the objects, ropes, drugs, fi rearms, etc. Also, search sufferings of a person who survived after a suicide the patient thoroughly. attempt by making him/her a puni shable offender. ii. Surveillance, depending on the severity of risk. The Section 309 of IPC was repealed by the 3. Acute psychiatric emergency interview. Supreme Court of India in 1994. However, in March 4. Counselling and guidance 1996, a fi ve judge Constitution Bench of the Supreme i. to deal with the desire to attempt suicide. Court again made the ‘attempt to suicide’ a punishable ii. to deal with on-going life stressors, and teaching offense. So, the Section 309 IPC continues to be valid coping skills and interpersonal skills. at present. 5. Treatment of the psychiatric disorder(s) with medication, psychotherapy and/or ECT. Management ECT is the treatment of choice for patients with Once suicide is committed, it is obviously no longer major depression with suicidal risk. It should also treatable. The management of suicide, therefore, lies be used for the treatment of suicidal risk associated

Table 19.4: Common Misconceptions about Suicide (Modiﬁ ed after Shneidman and Farberow, 1961) Misconceptions Facts 1. People who talk about suicide, do not commit Nearly 80% of persons who commit suicide, give deﬁ nite suicide warnings and/or clues about their suicidal intentions 2. Suicide happens without warning 3. Suicidal persons are fully intent on dying Most suicidal persons are undecided about dying or living 4. Once a person is suicidal, he/she is suicidal Suicidal person is usually suicidal only for a limited forever period of time 5. All suicidal persons are mentally ill or psychotic Although a suicidal person is often extremely unhappy, he/she is not necessarily mentally ill Emergency Psychiatry 225

Table 19.5: Some Causes of Catatonic Stupor with psychotic disorders. Follow-up care is very important to prevent future suicidal attempts or 1. Neurological Disorders suicide. i. Post-encephalitic parkinsonism ii. Limbic encephalitis Stupor and Catatonic Syndrome iii. Surgical procedures on basal ganglia Stupor is a common condition which presents at iv. Neoplasms in diencephalon, frontal lobe and limbic system the emergency services. It is deﬁ ned as a clinical v. Subacute sclerosing panencephalitis (SSPE) syndrome of akinesis and mutism but with relative vi. General paresis of insane (GPI) preservation of conscious awareness. vii. Petit mal status The term stupor, traditionally, has a psychia tric viii. Post-ictal phase of epilepsy connotation, but a careful analysis of the stuporous ix. Subdural haematoma patients shows that a large majority of them have x. Cerebral malaria an underlying organic cerebral cause. Stupor is xi. Cortical venous thrombosis often associated with catatonic signs and symptoms 2. Systemic and Metabolic Disorders (catatonic withdrawal or catatonic stupor). Catatonic i. Diabetic ketoacidosis syndrome is any disorder which presents with at least ii. Acute intermittent porphyria two catatonic signs. Catatonia can be either excited iii. Hyperparathyroidism causing hypercalcaemia or withdrawn (or mixed). Only catatonic withdrawal iv. Pellagra is associated with stupor. v. Hepatic encephalopathy vi. Systemic lupus erythematosis The various catatonic signs include mutism, nega- vii. Homocystinuria tivism, stupor, ambitendency, echolalia, echopraxia, viii. Membranous glomerulonephritis automatic obedience, posturing, mannerisms, stereo- 3. Drugs and Poisoning typies, excitement (not goal-directed), impulsiveness, i. Organic alkaloids combativeness or nudism. ii. Antipsychotics iii. ACTH (therapeutic doses) Aetiology iv. Aspirin A wide variety of disorders can cause catatonic stupor. v. Illuminating gas Some of the important causes are listed in Table 19.5. vi. Ethyl alcohol (large doses) vii. Levodopa Differential Diagnosis viii. Disulﬁ ram It is of foremost importance to differentiate between ix. CO poisoning x. Lithium toxicity organic stupor and psychogenic (or so called ‘func- xi. Methylphenidate tional’) stupor. This can be done on the basis of ante- xii. Phencyclidine (large doses) cedent medical and psychia tric history, mode of onset, xiii. Mescaline and detailed physical and neurological exami nation. 4. Psychiatric Disorders The important differentiating points between an i. Catatonic schizophrenia organic and a psychogenic stupor are tabulated in ii. Depressive stupor Table 19.6. If a diagnosis of organic catatonic stupor iii. Manic stupor is made, a search for underlying cause should be made. iv. Periodic catatonia On the other hand, if the pentothal/amytal/diazepam v. Conversion and dissociative disorder interview reveals psycho pathology, appropriate vi. Reactive psychosis treatment can be instituted. vii. During hypnosis. 226 A Short Textbook of Psychiatry

Table 19.6: Organic and Psychogenic Stupor Features Organic Stupor Psychogenic Stupor 1. Previous psychiatric illness Usually absent Usually present 2. Previous medical illness Usually present Usually absent 3. Previous history of stupor About 10% of cases 24-33% of cases 4. Precipitating stressor Usually absent Usually present 5. Frequency Much more common Not so common (3-5% of all stupor cases) 6. Onset Sudden or insidious Often sudden 7. Course Longer Shorter. Recovery usually within 7 days 8. Protective refl exes Absent Present (Blepharospasm, menace refl ex, protective response) 9. Resistance to eye opening Absent Usually present 10. Doll’s head eye phenomenon Usually present Absent (may avoid the gaze of ( Oculocephalic refl ex) examiner) 11. Meaningful posture and/or facial Absent May be present expressions 12. Urinary/faecal incontinence Usually present Unlikely 13. Neurological signs and defi cits May be present Absent 14. Abnormal EEG More often Less often 15. Oculovestibular refl ex Absent Present 16. Pentothal/amytal interview* Low dose (100-150 mg) increases High dose (300-400 mg) increases stupor and neurological signs alertness and a mental status exami- develop or increase nation can often be conducted 17. Mortality About 35% 0-3% *Pentothal/amytal interview is no longer carried out routinely in clinical practice is not routinely administered in clinical practice, Examination and the emphasis has recently shifted to making The examination consists of the following steps: this distinction on a clinical basis. 1. History and physical examination, with spe cial 4. Investigations: Blood glucose, blood urea, serum emphasis on neurological examination. creatinine, serum electrolytes, blood (arterial) gas 2. Level of consciousness should ideally be analysis, ECG, blood and urine examination for rated on the Glasgow Coma Scale. This scale drugs and poisons, blood and urine culture, and con sists of three main categories of activity, peripheral smear for malarial parasite. namely eye opening (1-4), motor response Also routine bloods including haemoglobin, (1-5) and verbal response (1-5). The rating is done total leucocyte count (TC), differential leuco cyte on a scale from 3 to 14. count (DC), ESR, urine (routine and microscopic) 3. Pentothal/amytal/diazepam interview is some- examina tion, thyroid and adrenal functions, liver times very helpful in differentiating organic and function tests, CSF examination, gastric lavage with psycho genic catatonic stupor. It should however examination of aspirate, EEG and CT scan/MRI scan be noted that pentothal/amytal/diazepam interview brain (if indicated). Emergency Psychiatry 227

Management some patients can indeed be aggressive especially Since psychogenic stupor may easily be mistaken for during the acute phase of the illness. organic stupor and coma, certain steps must be taken even before a detailed examination is undertaken, to Aetiology prevent irreversible brain damage and death which Some common causes of excited behaviour are listed may otherwise occur. These steps should be taken in below. the management of any uncons cious patient. I. Organic psychiatric disorders 1. Ensure the patency of airway; and provide 1. Delirium (acute organic brain syndrome), e.g. ventilatory support with oxygen (for possible delirium tremens. hypoxia). 2. Dementia, e.g. catastrophic reaction, loss of 2. Check cardiac rhythm and stabilise it (if needed). control. 3. Maintain circulation; insert IV (intravenous) line 3. Wernicke-Korsakoff’s psychosis. and give ﬂ uids (for possible ﬂ uid and electrolyte II. Nonorganic psychiatric disorders imbalance). 1. Schizophrenia and other psychoses. 4. Investigations; withdraw blood, CSF and urine i. Schizophreniform psychosis. samples, before instituting any treat ment. ii. Catatonic (excited) schizophrenia. 5. 50 ml of 50% dextrose (2 ml/kg body weight for iii. Paranoid schizophrenia. a child) should be given IV (for possible hypogly- iv. Acute psychotic disorder. caemia). 2. Mania. 6. Administer: Although excitement is common, violence Naloxone 0.4 mg IV (if morphine poisoning is occurs usually only when the patient is suspected); prevented from engaging in his activities, or Physostigmine 1-2 mg IV (if anticholinergic poi- when he is irritable. Similarly, patients with soning is suspected); dysphoric mania or mixed affective states may Thiamine 100 mg IV (if Wernicke’s encephalo- occasionally present similarly. pathy or delirium tremens is suspected); 3. Depression: Agitated depression may present Hydrocortisone 100 mg IV (if adrenal crisis is with excitement. Occasionally aggressive, suspected); violent behaviour may occur if the patient is L-Thyroxin 200-500 μg IV (if myxoedema coma irritable and agitated. is suspected); 4. Drug and alcohol dependence: Excitement and Flumazenil 0.2 mg IV (if benzodiazepine over- violence may occur in: dose is suspected). i. Intoxication. This should be followed by a detailed work-up. ii. Withdrawal syndrome. The underlying medical or psychiatric cause of stupor iii. Comorbid psychiatric disorder(s). should be searched for and treated. The importance 5. Epilepsy. of supportive care during the period of stupor cannot i. Complex partial seizures. be overemphasised. ii. Postictal confusion. iii. Epileptic furore. Excited Behaviour and Violence 6. Acute stress reaction. Excitement is a common reason for a referral to an 7. Neurotic disorders. emergency psychiatry setting. Although a large major- i. Panic disorder. ity of psychiatric patients are not dangerously violent, ii. Agoraphobia with panic attacks. 228 A Short Textbook of Psychiatry

Marked excitement can occur during a Other Psychiatric Emergencies panic attack but violent behaviour does not The list of possible psychiatric emergencies is usually occur. long. A few psychiatric emergencies are listed below, 8. Impulsive violent behaviour. some of which have already been discussed in the i. Borderline personality disorder. book. ii. Intermittent explosive disorder. 1. Severe depression (Chapter 6): Apart from 9. Reactive psychosis. presenting as a suicide/suicidal attempt and/or agitation, the depressed patient may come to Management casualty because of a refusal to eat and drink, The patient is examined according to the guidelines leading to dehydration or because of refusal to take suggested earlier in this chapter. The physician, medication (for example, secondary to hopeless- psychiatrist or another mental health professional, ness). examining an excited patient, must demonstrate an 2. Hyperventilation syndrome (Chapter 8). attitude of empathy but at the same time must be fi rm 3. Side effects of psychotropic medication, e.g. acute and should exude confi dence. dystonia (promptly relieved by promethazine The measures which can be adopted to handle 25-50 mg parenterally), akathisia, neuroleptic excited or violent behaviour include: malignant syndrome (Chapter 15). 1. Reassurance: In case of emergency, it rarely works 4. Psychiatric complications of medical and surgical alone but must be tried fi rst. diseases, procedures and medica tion (e.g. ICU 2. Sedation: Diazepam 5-10 mg parenterally slowly syndrome, hypomania caused by steroids). (or lorazepam 1-2 mg parenterally slowly) can be 5. Severe insomnia (Chapter 11). given. In the presence of psychosis, haloperidol 6. Pseudo seizures (conversion and/or dissociation 2-10 mg parenterally (with or without 5-10 mg hysteria) (Chapter 8). diazepam or 50 mg of promethazine) can be given. 7. Anorexia nervosa (usually presenting with dehy- It is really important to exercise care in adminis- dration and/or cachexia) (Chapter 12). tering parenteral antipsychotics to any patient, 8. Battered child syndrome or child abuse. but particularly one who is treatment (antipsy- 9. Grief and bereavement (Chapter 12). chotic) naïve. Oral antipsychotics are preferable to 10. Psychosocial crises (e.g. marital confl ict, occu- parenteral antipsychotic in routine clinical practice. pational and fi nancial diffi culties). 3. Restraint: Restraint should always be used as a last 11. Drug or alcohol use disorders (Chapter 4). resort, but when needed, it should not be delayed. 12. Panic disorder (Chapter 8). Restraint should always be done in a humane way, 13. Acute psychosis (Chapter 7). after taking (preferably) written consent from the Psychiatric patients, especially when exci ted or attendant relatives/carers. A second opinion from emotionally disturbed, often arouse anxiety in the another mental health professional is helpful. treating physicians as well as other patients in the Restraint is usually followed by compul sory casualty. So, it is necessary to have an ‘emergency hospitalisation and parenteral medication. It is psychiatry room’ or ‘psychiatric holding area’ near rarely ever necessary to continue restraint for more the casualty, where the patients can be interviewed than a few hours and restraint should be removed and treated. at the earliest possible time. An ideal place for treating psychiatric emergen cies Electroconvulsive therapy (ECT) is not a treatment is a separate ‘psychiatric intensive care unit’ (PICU) for excitement or violence per se. When used, there or ‘ crisis intervention centre’ (CIC) attached to a should be a clear indication for the use of ECT, which psychiatric unit in a general hospital or to a psychiatric should be clearly recorded in the case notes. hospital or nursing home. Legal and Ethical 20 Issues in Psychiatry

Forensic psychiatry deals with the legal aspects of of the act or that he is doing what is either wrong or psychiatry. Law comes in contact with psychiatry at contrary to law’. many points; for example, admission of a mentally So a mentally ill person is not protected ipso facto. ill person in a mental hospital, crime committed by a He must satisfy the above mentioned rule. A mentally mentally ill person, validity of marriage, witness, will, retarded person (called ‘ idiot’ in law) is not considered consent, right to vote, and drug depen dence. liable under Indian criminal law. The various legal aspects of psychiatry are briefl y The Law generally classifi es criminal lunatics discussed below. into three classes: an under-trial who cannot stand trial because of mental illness; guilty but insane; and CRIMINAL RESPONSIBILITY criminals who later become mentally ill. A Class II ‘criminal lunatic’ is acquitted under the law but is In January 1843, a young Scotsman, Daniel detained in a mental hospital (asylum) for further McNaughten shot dead Edward Drummond, the treatment. secretary to the British Prime Minister Sir Robert Peel. He had intended to kill the Prime Minister but CIVIL RESPONSIBILITY Drummond was assassinated by mistake. The Jury, after testifi cation by nine physi cians, There is usually a presumption in the favour of sanity found McNaughten not guilty by reasons of insanity. and the contrary must be proved. This applies both Queen Victoria, Sir Robert Peel and other prominent to the civil and criminal pro ceedings in the court of persons were outraged. Following this, 15 prominent law. judges were invited by the House of Lords. They were asked to respond to a series of questions on criminal Marriage responsibility. The answers, which are immortalised The Hindu Marriage Act (Act 25 of 1955) provides in the history of forensic psychiatry, have now come for conditions for a Hindu marriage under Section 5. to be known as McNaughten Rule(s). One of the conditions, i.e. Section 5 (ii) introduced The McNaughten Rule is used in a slightly modi- by Act 68 of 1976, states that ‘at the time of the mar- fi ed form in many countries even now. In India, Sec- riage, neither party, tion 84 of the Indian Penal Code (Act 45 of 1860) a. is incapable of giving a valid consent... (due to)... states that ‘nothing is an offense, which is done by a unsoundness of mind; or person, who at the time of doing it, by reason of un- b. though capable of giving consent, has been suf- soundness of mind, is incapable of knowing the nature fering from mental disorder of such a kind or to 230 A Short Textbook of Psychiatry

such an extent as to be unﬁ t for marriage and the Adoption pro creation of children; or Under the Hindu Adoptions and Maintenance Act c. has been subject to recurrent attacks of insanity (Act 78 of 1956), any Hindu male ‘who is of sound or epilepsy.’ mind and is not a minor’ can adopt a child, with the Any marriage solemnised in the contraven tion to consent of his wife unless ‘...(she) has been declared this condition shall be voidable and may be annulled by a court...to be of unsound mind’ (Section 7). by a decree of nullity under Section 12 of the Act. Similarly, any Hindu female ‘who is of sound Another ground of nullity under the same section is mind’, is not a minor, and is not married, can adopt a the fact that the consent for marriage was obtained child. If she is married, ‘then her husband is dead, or by ‘fraud’...‘as to any material fact or circum stance has ...renounced the world, or ...ceased to be a Hindu, concerning the respondent’, for example, the fact of or ...has been declared by a court ...to be of unsound mental illness or treat ment for the same. mind’ (Section 8). Divorce can be granted under Section 13 of the In addition, the person capable of giving in adop- Act on a petition presented by either spouse on the tion of a child should be of sound mind. ground that the other party ‘has been incu rably of unsound mind, or has been suffering continuously or Witness intermittently from mental disorder of such kind and Under the Indian Evidence Act 1872, a ‘lunatic’ is not to such an extent that the petitioner cannot reason ably competent to give evidence if he is prevented by virtue be expected to live with the respondent’ (Section 13 of his ‘lunacy’ from understanding the questions put to (iii) inserted by Act 68 of 1976). him and giving rational answers to them (Section 118). Here, the term mental disorder means ‘mental However, such a person can give evidence during a illness, arrested or incomplete development of mind, lucid interval on discretion of the judge (and the jury). psychopathic disorder or any other disorder or disability of mind and includes schizo phrenia’. The term Testamentary Capacity psycho pathic disorder means ‘a persistent disorder or Testamentary disposition is regulated by the Indian disability of mind (whether or not including subnor- Succession Act (Act 39 of 1925). Some of the sali- mality of intelli gence) which results in abnormally ent points regarding testamentary disposi tion are as aggressive or seriously irres ponsible conduct on the follows: part of the other party, and whether or not it requires 1. A will must be in writing, though it need not be or is susceptible to medical treatment’. registered. Under the dissolution of Muslim Marriages Act 2. It must be signed by testator in the presence of at 1939, a woman married under Muslim law is entitled least two witnesses. to obtain a decree for the dissolution of marriage on 3. A legatee cannot attest a will. the ground of her husband being insane for a period 4. An executor(s) is appointed under the will by the of 2 years. The husband under the Muslim law has testator to carry out its terms after his death. the power to pronounce divorce (talak) at anytime, 5. A will can be revoked or modiﬁ ed any time before anywhere, and without assigning any reason. the death of the testator. Any married person may be granted divorce, 6. A will comes into effect after the death of the under the Parsi Marriage and Divorce Act 1936, on testator. It is said to speak from grave and to be the ground that the other party had been of unsound ‘ambulatory’. mind at the time of marriage (and the petitioner was 7. The testator must be of a ‘sound and dis posing ignorant of the fact) and has been habitually so till the mind’. Section 59 of the Act states that ‘every date of petition, which should be within 3 years of the person of sound mind, not being a minor, may date of marriage. dispose of his property by will’. Legal and Ethical Issues in Psychiatry 231

Explanation 4 of this section states that ‘no person Transfer of Property can make a will while he is in such a state of mind, Under the Transfer of Property Act 1882 (Section 7), whether arising from intoxication or from illnesses only persons competent to contract, are authorised to or from any other cause, that he does not know transfer property. what he is doing’. If a medical practitioner is called to examine a Contract testator as to his fi tness to make a valid will, the fol- Under the Indian Contract Act 1872 (Section 11), lowing points must be kept in mind: every person to be competent to contract must be a 1. Testamentary capacity consists of: major and of sound mind. i. an understanding of the nature of the will, A person is said to be of sound mind for the pur- ii. a knowledge of the property to be disposed of, poses of a contract, if at the time of making a contract and he is capable of understanding it and of forming a iii. an ability to recognize those who may have rational judgement as to its effect upon his interests. justifi able claims on his property. 2. The testator should be tested on the above men- Driving tioned points by thorough questioning. It is important that advice be given regarding driving 3. If the testator is seriously ill, he must be made if there is likelihood that driving can be impaired by to read out aloud the will in the presence of the the nature of illness, prescribed medication and/or doctor. misuse of alcohol or drugs. 4. A will is invalid if it is executed under undue infl uence of any other person. If there is reason to INDIAN LUNACY ACT, 1912 suspect that such is the case, the testator should be questioned when he is alone. The Indian laws related to mental disorders were based 5. A will is invalid under the following conditions on British Acts. For example, the Indian Lunacy Act (for example): (ILA), Act 4 of 1912, was based largely on the earlier i. imbecility arising from advanced age or by English Lunacy Act of 1890 and replaced the existing excessive drinking. Indian Lunatic Asylums Act, Act 36 of 1858. ii. insane delusions making the testator incapable The ILA had 8 Chapters. Chapter 1 defi ned a of rational views and judge ment. lunatic as ‘an idiot or person of unsound mind’. 6. A will is valid under the following conditions (for Defectiveness of reasoning, whether partial or com- example): plete, was considered as unsound ness of mind. In i. deaf, dumb or blind persons who are not thereby Chapter 3, fi ve categories of admission methods were incapacitated for making a will and are able to mentioned, namely voluntary, reception order on know what they do by it. petition, reception order without petition, inquisition ii. lucid intervals. (judicial), and as a criminal lunatic. iii. if testator commits suicide imme diately after There was a ‘board of visitors’ appointed by making the will, in the absence of evidence of the Government which had a role in admission of mental disorder. voluntary patients, interfering with ongoing care and iv. presence of delusions not affecting in any way treatment and discharge (except in criminal cases). IG the disposal of the property or the persons (prisons) was an ex-offi cio member of this board. affected by the will. In 1950, three eminent psychiatrists appointed by 7. A will may be declared invalid if the testator dis- the Indian Psychiatric Society prepared a draft ‘Indian poses his property in a way which he would not Mental Health Act’ and forwarded it to Government have done under normal condi tions. of India. There was no action taken on the draft for 232 A Short Textbook of Psychiatry next ten years and it was only in 1978 that the Mental Chapter IV deals with the procedures of admis- Health Bill was intro duced in Parliament. The bill sion and detention in psychiatric hospitals or nursing had to be reintro duced in Lok Sabha in 1981 and was homes. In addition to the 5 methods allowed by the passed by Rajya Sabha in November 1986. Indian Lunacy Act of 1912, one more method has been incor porated. THE MENTAL HEALTH ACT, 1987 Hence, the admission in a psychiatric hospital or nursing home can be made in one of the following The Mental Health Bill became the Act 14 of 1987 on manners: 22nd May 1987. Later, the Govern ment of India issued 1. Voluntary Admission. orders that the Act came in force with effect from April i. By the patient’s request, if he is a major. 1, 1993 in all the states and Union territories of India. ii. By the guardian, if a minor (a new provision). The Act is divided into 10 chapters consisting of 2. Admission under Special Circumstances. 98 sections. Chapter I (Preliminary) deals with the This is an involuntary hospitalisation when the various defi nitions. The Act uses the term ‘ mentally ill mentally ill person does not or cannot express his person’ instead of ‘lunatic’ and defi nes it as ‘a person willingness for admission. Admis sion is made, who is in need of treatment by reason of any mental if a relative or a friend of the men tally ill person disorder other than mental retardation’. applies in writing for admission and the medical The term ‘mentally ill prisoner’ is used instead of offi cer in-charge of the hospital is satisfi ed that the ‘criminal lunatic’. Other new terms, which are defi ned admission will be in the interest of the mentally ill in the Chapter 1, are psy chiatric hospital (instead person. The duration of admission cannot exceed of mental hospital), psychiatric nursing home and 90 days. psychiatrist. 3. Reception order on application. Chapter II provides for establishment of Mental 4. Reception order without application, on produc- Health Authorities at Centre and State levels. These tion of mentally ill person (e.g. wan dering, danger- authorities will regulate and coordinate mental health ous, ill-treated or neglected mentally ill person) services under Central and State Government, respec- before the Magistrate. tively. 5. Admission as inpatient, after judicial inquisition. Chapter III lays down the guidelines for establish- 6. Admission as a mentally ill prisoner. ment and maintenance of psychiatric hospitals and In addition, the Magistrate can order detention of nursing homes. In addition, there is a provision for an alleged mentally ill person for short periods pend- a Licensing Authority who will process applications ing report by medical offi cer (for a period not exceed- for licenses. No private psychiatric hospital or nursing 10 days in aggregate) or pending his removal to ing home will be allowed to function without a valid psychiatric hospital or psychiatric nursing home (for license, which has to be renewed every 5 years. a period not exceeding 30 days). There is also a provision for an Inspecting Offi cer Chapter V deals with the inspection, discharge, who will inspect the psychiatric hospitals and nursing leave of absence and removal of mentally ill persons. homes to prevent any irregu larities. Chapter VI deals with the judicial inquisition regard- There is a provision for separate hospitals for: ing the alleged mentally ill person possessing property, 1. Those under the age of 16 years, custody of his person and management of his property. 2. Those addicted to alcohol or other drugs which If the court feels that the alleged mentally ill person lead to behavioural changes, is incapable of looking after both himself and his 3. Mentally ill prisoners, and property, an order can be issued for the appointment 4. Any other prescribed class or category. of a Guardian. If, however, it is felt that the person is Legal and Ethical Issues in Psychiatry 233 only incapable of looking after his property but can With the coming in force of the NDPSA, Act 61 of look after himself, a Manager can be appointed. 1985, on 16th September 1985, the above mentioned Chapter VII deals with the liability to meet the cost of acts have been repealed. The Act includes narcotic maintenance of mentally ill persons detained in psychi- drugs (cannabis, cocaine, coca leaf, opium, poppy atric hospitals or nursing homes. Chapter VIII is aimed straw and all manufactured ‘drugs’) and psychotropic at the protection of human rights of mentally ill persons. sub stances (76 drugs and their derivatives are listed This is a new chapter in the Act. It provides that: in the schedule, e.g. diazepam, pentazocine, pheno- 1. No mentally ill person shall be subjected, during barbital). treatment, to any indignity (whether physical or The authorities and offi cers have been sug gested mental) or cruelty. in Chapter 2. If any person produces, possesses, 2. No mentally ill person, under treatment, shall be trans ports, imports, exports, sells, purchases, or uses used for the purposes of research, unless any narcotic drug or psychotropic substance (except i. Such research is of direct benefi t to him. ‘ganja’), he shall be punishable with, ii. A consent has been obtained in writing from 1. Rigorous imprisonment (RI) for not less than 10 the person (if a voluntary patient) or from the years (which may extend to 20 years), and guardian/relative (if admitted involuntarily). 2. A fi ne of not less than 1 Lakh rupees (which may 3. No letters or communications sent by or to a extend to 2 Lakh rupees). mentally ill person shall be intercepted, detained Punishment for a repeat offense is a RI for not or destroyed. less than 15 years (which may extend to 30 years) Chapter IX deals with the penalties and the pro- and a fi ne of not less than 1.5 Lakh rupees (which ce dure, while Chapter X provides for mis cella neous may extend to 3 Lakh rupees). Punishment for sections. ganja handling is a RI for 5 years and/or a fi ne of In addition, the State Mental Health Rules, 1990 0.5 Lakh rupees. For a repeat offense, the imprison- (which also contains the nine important forms required ment may extend to 10 years and the fi ne to 1 Lakh by the Mental Health Act, 1987) and the Central Mental rupees. Health Authority Rules, 1990, have also been passed However, if a person is carrying ‘ small quantities’ by the Government of India on December 29, 1990. (e.g. 250 mg of heroin, 5 g of Charas, 5 g of opium, Currently consultations are in progress to consider 125 mg of cocaine) which were later specifi ed, then either modifying or updating the current Act. the punishment is a simple imprisonment which may extend to 1 year or a fi ne (unspecifi ed) or both. For THE NARCOTIC DRUGS AND ganja (<500 g), imprisonment is up to 6 months. PSYCHOTROPIC SUBSTANCES ACT There is also a provision for detoxifi cation under (NDPSA), 1985 court order. A later enactment, the Prevention of Illicit Traffi c in NDPS Act, 1988 has also been passed (Act The fi rst Act for drug abuse and dependence in India 46 of 1988). There is now a provision for preventive was The Opium Act of 1857. This was revised fi rst detention and seizure of property. The maximum in 1878 (The Opium Act, 1878) and then in 1950 punishment is death penalty, if a person is found to be (The Opium and Revenue Laws Act, 1950). Another traffi cking more than or equal to 1 kg of pure heroin relevant Act was the Dangerous Drug Act of 1930, (for example), twice (despite convic tion and warning which included among other drugs, Opium and its on the fi rst attempt). The Act was further amended alkaloids and Cocaine. This Act provided for a maxi- by the Narcotic Drugs and Psychotropic Substances mum punishment of 3 years. (Amendment) Act, 2001. 234 A Short Textbook of Psychiatry

A CODE OF ETHICS FOR PSYCHIATRISTS No psychiatrist should refuse to treat in an emergency. The Indian Psychiatric Society (IPS) has recom- 4. No gifts and gratiﬁ cations should be accepted from mended a code of ethics for psychiatrists (1989) which patients under treatment. is summarised here: 5. Any sexual advance towards any patient is unethical. Principles 6. In case of doubt and/or unconventional treatment 1. A psychiatrist has a clear social responsibility. procedures a second opinion must be obtained. 2. A psychiatrist must maintain high standards of 7. It is unethical to force a contract on a patient during professional competence and ensure continuing treatment. self-education. 8. Even if the patient is referred by legal or admin- 3. Benevolence and patient interest precede self istrative authority, patient’s welfare is paramount interest. and patient should be infor med of the purpose for 4. A psychiatrist must maintain high moral standards. which he is to be examined. 5. Patient welfare is of paramount concern to a psy- 9. The basic human rights of mentally retarded chiatrist. It includes not treating cases which are should not be unethically abridged. not in his domain, terminating treatment when 10. In the interest of the patient and the society, drug cannot help the patient, and treating with the best abusers who refuse to give consent may be treated of the ability. with the consent of their relatives. Effort has to be 6. Conﬁ dentiality of the patient records must be made to motivate them for accepting treatment meticulously maintained. voluntarily.

Recommendations ICMR GUIDELINES FOR RESEARCH, 1. Treatment should be given with patient’s consent. 2000 Every person who is a major and does not appear to have lost ability of reason is capable of consent. In 2000, the Indian Council of Medical Research If the patient cannot give consent due to mental ill- (ICMR) has released ‘Ethical guidelines for bio- ness, consent should be taken from a person close medical research in human subjects’. These guidelines to the patient who appears to be clearly interested are very similar to the GCP (Good Clinical Practice) in patient’s welfare. However, treatment can be guidelines and the prevalent international guidelines. given without consent in an emergency situation These guidelines regulate all biomedical research in involving immediate threat to the life or health of human subjects in India. patient or others. For research purposes, consent should be entirely MCI CODE OF MEDICAL ETHICS, 2002 voluntary. The patient can withdraw consent at any stage, without this affecting patient’s interest. All psychiatrists as doctors are also bound by the code 2. Hospitalisation should be for patient’s welfare, of medical ethics of Medical Council of India (MCI). keeping in view the legal and administrative con- Called as the Indian Medical Council (Professional straints, and social appropriateness. conduct, Etiquette and Ethics) Regulations, 2002, 3. Psychiatric treatment should be started only on the code came in to effect from 6th April, 2002. The clinical consideration for patient welfare and full code is available at the website of MCI, at http:// should be humane and never punitive. mohfw.nic.in/code.htm. 21 Community Psychiatry

Born in 1963, the community psychiatry movement ously at PGI, Chandigarh in 1975 ( Raipur Rani has been hailed as the third psychiatric revolution. The block of Ambala district, Haryana) and NIMHANS, fi rst revolution was the age of enlightenment follow- Bangalore in 1976 ( Sakalwara in Karnataka). ing the middle ages, when mental illness was viewed The basic model of community mental health was as a consequence of sin and witchcraft. The second defi ned by Gerald Caplan in 1967. The predominant revolution was the development of psycho analysis characteristics of com munity psychiatry are: which offered hope for a causative explanation of 1. Responsibility to a population for mental health psychiatric disorders. care delivery. How ever, the community psychiatry move ment 2. Treatment close to the patient in community based was made possible by another revolution, the one centres. ushered by the advent of psychopharma cology. There- 3. Provision of comprehensive services. fore, it may be more appropriate to refer to community 4. Multi-disciplinary team approach. psychiatry as the fourth psychiatric revolution. 5. Providing continuity of care. The community psychiatry concept has its an- 6. Emphasis on prevention as well as treat ment. tecedents in Clifford Beers’ (1908) mental hygiene 7. Avoidance of unnecessary hospitalisation. movement and Adolf Meyer’s recom mendation (1913) of establishment of treatment centres in the commu- NATIONAL MENTAL HEALTH nity. The period between 1955 and 1980 was an era PROGRAMME (INDIA) of deinstitutiona lisation in USA and other Western countries, consisting of discharging mentally ill Mental health is an integral component of health, patients from mental hospitals, to be cared for in the which is defi ned as a positive state of well-being community supported by community mental health (physical, mental and social) and not merely an ab- centres. This provided an impetus to the development sence of illness. With this aim in mind, an expert group of community psychiatry. was formed in 1980. The fi nal draft was submitted to In 1975, the World Health Organization strongly the Central Council of Health and Family Welfare (the recommended the delivery of mental health services highest policy making body for health in the country) through primary health care system as a policy for the on 18-20 August 1982, which recommended its imple- developing coun tries. In India, attempts to develop mentation. The National Mental Health Programme models of psychiatric services in the PHC (primary (NMHP) appeared almost simultaneously with the health centre) setting were made nearly simultane- National Health Policy (1993). 236 A Short Textbook of Psychiatry

The objectives of NMHP are: ii. Administration and supervision of maintenance 1. To ensure availability and accessibility of treatment for chronic psychiatric disorders. minimum mental health care for all in the iii. Diagnosis and management of grand mal epi- foreseeable future, particularly to the most lepsy, especially in children. vulnerable and underprivileged sections of popula- iv. Liaison with local school teacher and parents tion. regarding mental retardation and behaviour 2. To encourage application of mental health knowl- problems in children. edge in general health care and in social develop- v. Counselling in problems related to alcohol and ment. drug abuse. 3. To promote community participation in the mental B. Primary health centre (PHC): MO, aided by HS, health service development and to stimulate efforts to be trained for: towards self-help in the community. i. Supervision of MPW’s performance Three aims are specifi ed in the NMHP in planning ii. Elementary diagnosis mental health services for the country: iii. Treatment of functional psychosis 1. Prevention and treatment of mental and neurologi- iv. Treatment of uncomplicated cases of psychiatric cal disorders and their associated disabilities. disorders associated with physical diseases 2. Use of mental health technology to improve v. Management of uncomplicated psychosocial general health services. problems 3. Application of mental health principles in total vi. Epidemiological surveillance of mental morbid- national development to improve quality of life. ity. Two strategies, complementary to each other, were C. District hospital: It was recognized that there planned for immediate action: should be at least 1 psychiatrist attached to every 1. Centre to periphery strategy: Establishment and district hospital as an integral part of the district strengthening of psychiatric units in all district health services. The district hospital should have hospitals, with outpatient clinics and mobile teams 30-50 psychiatric beds. The psychiatrist in a reaching the population for mental health services. district hospital was envisaged to devote only a 2. Periphery to centre strategy: Training of an part of his time in clinical care and greater part in increasing number of different categories of training and supervision of non-specialist health health personnel in basic mental health skills, with workers. primary emphasis towards the poor and the under- D. Mental hospitals and teaching psychiatric units: privileged, directly benefi ting about 200 million The major activities of these higher centres of people. psychiatric care include: The mental health care service was envisaged to i. Help in care of ‘diffi cult’ cases. include three components or subprogrammes, namely ii. Teaching. treatment, rehabilitation and prevention. iii. Specialised facilities such as occupational 1. Treatment Subprogramme: Multiple levels were therapy units, psychotherapy, counselling and planned. behaviour therapy. A. Village and subcentre level: Multi-purpose 2. Rehabilitation Subprogramme: The components workers (MPW) and health supervisors (HS), of this subprogramme include maintenance treatment under the supervision of medical offi cer (MO), of epileptics and psycho tics at the community levels to be trained for: and development of rehabilitation centres at both the i. Management of psychiatric emergencies. district level and the higher referral centres. Community Psychiatry 237

3. Prevention Subprogramme: The prevention The District Mental Health Programme (DMHP) component is to be com mu nity-based, with the initial was started in 1995 as a component of NMHP. The focus on preven tion and control of alcohol-related prototype of the District Mental Health Programme problems. Later, problems such as addictions, juvenile was the Bellary District Programme (in Karnataka, delinquency and acute adjustment problems such as ~320 km from Bangalore). Started in 1985, it caters to suicidal attempts are to be addressed. a population of 1.5 million. District hospital psychiatry The other approaches designed to achieve the units have been opened in every district of Kerala and objectives of the NMHP include: Tamil Nadu. • Integration of basic mental health care into general Following the implementation of National Mental health services. Health Programme in India 1982, other neighbour- • Mental health training of general medical doctors ing countries soon followed the example by drawing and paramedical health workers. national programmes for mental health (Sri Lanka A plan of action was outlined in 1982, with the 1982; Bangladesh 1982; Pakistan 1986; Nepal fi rst opportunity to develop it in the 7th-fi ve-year plan 1987). starting from 1985, with a plan allocation of Rs. 100 The revised National Health Policy (NHP-2002) lakhs (10 million). A National Mental Health Advisory has been released in 2002. Its focus on mental health Group (NMHAG) was formed in August 1988 and “envisages a network of decentralised mental health a Mental Health Cell was opened in the Ministry of services for ameliorating the more common categories Health and Family Welfare under a Central Mental of disorders”. At the same time the NMHP 10th- Health Authority (MHA). fi ve-year plan was launched, with a plan to extend Various activities were planned under the action the DMHP to 100 districts. It also emphasizes the plan for implementation of national mental health need to broaden the scope of existing curriculum for programme in the 7th-fi ve-year plan, such as com- undergraduate training in psychiatry and to give more munity mental health programmes at primary health exposure to psychiatry in undergraduate years and care level in states and union territories; training of internship. An essential list of psychotropic drugs was existing PHC personnel for mental health care de- also being prepared. livery; development of a state level Mental Health The emphasis of NMHP-1982 was primarily on the Advisory Committee and state level programme rural sector. It is being realized that the urban mental offi cer; establishment of Regional Centers of com- health needs also need to be addressed under the ambit munity mental health; formation of National Advisory of NMHP. Group on Mental Health; development of task forces During the 11th-fi ve-year plan, an allocation of for mental hospitals and mental health education Rs 1000 crore (Rs 10 billion) has been made for the for undergraduate medical students; involvement of NMHP. The current focus (2009) is on establishing voluntary agencies in mental health care; identifi cation centres of excellence in mental health, increasing of priority areas (child mental health, public mental intake capacity and starting postgraduate courses in health education and drug dependence); mental health psychiatry, modernisation of mental hospitals and up- training of at least 1 doctor at every district hospital gradation of medical college psychiatry departments, during the next 5 years; establishment of a department focus on non-government organisations (NGOs) of psychia try in all medical colleges and strengthen ing and public sector partnerships, media campaign to the existing ones; and provision of at least 3-4 essential address stigma, a focus on research, and several other psychotropic drugs in adequate quantity, at the PHC measures (See http://india.gov.in/sectors/health_fam- level. ily/mental_health.php). 238 A Short Textbook of Psychiatry

Table 21.1: Extent of the Problem and Facilities Available in India The Problem Psychiatric beds in India Population = 1027 million (2001) Per 10,000 population = 0.25 (World = 1.69; Prevalence of psychiatric disorders = 58/1000 Median)* Severe mental illness Manpower Available in India Point prevalence = 10-20/1000 population Psychiatrists (qualiﬁ ed) in India Incidence = 35/100,000 population Numbers = ~3500 Neuroses and psychosomatic disorders Per 100,000 population = 0.2 (World = 4.15 Mean; Point prevalence = 2-3% 1.2 Median) Mental retardation Total qualiﬁ ed doctors in India = 503900 (1999) Point prevalence = 0.5-1.0% of all children Clinical psychologists in India Psychiatric disorders in children Numbers = ~1000 Point prevalence = 1-2% of all children Per 100,000 population = 0.03 (World = 0.6 Psychiatric OPD attendance in (1990 data) Median)* Govt. hospitals = 3.63 million/year Psychiatric social workers Private practice = 2.63 million/year Numbers = ~1000 Total OPD attendance = 6.29 million/year Per 100,000 population = 0.03 (World = 0.4 (~1% of population) Median)* Additionally, 15-20% of all help-seekers in the general Psychiatric nurses in India health services do so for emotional and psychosocial Numbers = 800-900 problems. Per 100,000 population = 0.05 (World = 2.0 Existing Mental Health Services Median)* No. of government mental hospitals = 37 Total nurses in India = 737000 (1999) No. of mental hospital beds = ~19000 Postgraduate centers = ~40 (very few of 140 medical Private psychiatric hospital beds = 2000-3000 colleges have a psychiatry department) General hospital psychiatry unit beds (GHPU beds) = MD/DPM seats (Psychiatrists/year) = ~200 (For com- 4000-5000 parison: Doctors/year = 13,000) (1990) Total health beds in India = 870161 (1994-95)

* Source: Atlas: Mental Health Resources in the World, 2005, WHO

The extent of mental health problems and facilities of life’. It points out that the psychiatric disorders are available in India are briefl y summarised in Table 21.1. estimated to account for 12% of the global burden of disease, yet the mental health budgets of the major- WORLD (MENTAL) HEALTH REPORT ity of countries constitute <1% of their total health 2001 expenditures. The WHR-2001 appears along with the Atlas, a This landmark publication of the WHO was published unique publication of WHO giving a comparative in 2001 (Editor-in-Chief: RS Murthy). The 2001 account of the mental health resources in the world. World Health Report focused on mental health (Men- The report identifi es that ‘mental disorders affect all tal Health: New Understanding, New Hope), with a people in all countries’, but the ‘people do not get slogan, Stop Exclusion: Dare to Care. the care they need...because of lack of resources,... The report identifi ed that ‘one person in every four because of fear of seeking help, ...and because of lack will be affected by a mental disorder at some stage of (mental health) policies’. Community Psychiatry 239

The WHR-2001makes ten recommendations for 6. Establish national policies, programmes and action: legislation. 1. Provide treatment in primary care. 7. Develop human resources. 2. Make psychotropic drugs available. 8. Link with other sectors. 3. Give care in the community. 9. Monitor community mental health. 4. Educate the public. 10. Support more research. 5. Involve communities, families and consumers.

Appendices

Appendix I: Nobel Prizes in Psychiatry and Allied Disciplines

Nobel Laureates Major Contributions Year of Award 1. Ivan Petrovich Pavlov (1849-1936; Russia) Classical conditioning 1904 Physiology of digestion 2. Camillo Golgi (1843-1926; Italy) Structure of CNS 1906 Santiago Ramon y Cajal (1852-1934; Spain) 3. Julius Wagner von Jauregg (1857-1940; Austria) Malarial treatment for GPI (First 1927 (First psychiatrist to receive a Nobel Prize in Physiol- successful treatment of a major ogy or Medicine) psychosis) 4. Antonio Caetano de Abreu Freire Egas Moniz Psychosurgery (prefrontal leu- 1949 (Egas Moniz) (1874-1955; Portugal) cotomy) Walter Rudolf Hess (1881-1973; Switzerland) Cerebral angiography 5. Konrad Lorenz (1903-1989; Austria) Ethology 1973 Karl Von Frisch (1886-1982; Germany) Nikolaas Tinbergen (1907-1988; UK) 6. Sir Godfrey Newbold Hounsﬁ eld (1919-2004; UK) Computerised Tomography Scan 1979 Allan Macleod Cormack (1924-1998; US) 7. Stanley B. Prusiner (1942b; US) Discovery of Prions 1997 8. Eric R. Kandel (1929b; US) Signal Transduction in CNS 2000 Arvid Carlsson (1923b; Sweden) Paul Greengard (1925b; US) 9. Paul C. Lauterbaur (1929-2007; US) Magnetic Resonance Imaging 2003 Sir Peter Mansﬁ eld (1933b; UK) 242 A Short Textbook of Psychiatry

Appendix II: Some Important Contributors in Psychiatry

Contributor Coined the Term Special Mention Adler, Alfred (1870-1937) Life style Founder of the school of individual Inferiority complex psychology Will to power Creative self Alexander, Franz (1891-1964) __ Sometimes known as the father of psychosomatic medicine Ayurveda (<4000 BC) __ Five types of constitution and 3 main types of personality were described. Modernistic descriptions of mental disorders were stated Beard, George Miller (1839-1883) Neurasthenia __ Berne, Eric (1910-1970) Games Founder of transactional analysis Transaction (TA). Wrote the book ‘Games People Play’ Binet, Alfred (1857-1911) __ Designed the 1st formal scale of intelligence Bleuler, Eugen (1857-1939) Schizophrenia Described ‘cardinal’ symptoms of schizophrenia Braid, James (1795-1860) Hypnosis __ Cicero (106-43 BC) Libido __ Cullen, William (1710-1790) Neurosis __ Delay, Jean PL (b 1907) Neuroleptic 1st antipsychotic treatment Neuroleptic malignant syndrome (chlorpromazine) of psychoses (NMS) Dendy, Walter Cooper (1794-1871) Psychotherapy (‘Psychotherapeia’) __ Deniker, Pierre (b 1917) ‘Hibernotherapie’ __ Erikson, Erik H (1902-1994) Psychohistory Described the stages of life Identity crisis Esquirol, Jean ED (1772-1840) Hallucination __ Monomania Falret, Jean-Pierre (1794-1870) Mental alienation Thus, psychiatrists came to be known as alienists Fechner, Gustav Theodore Psychophysics Founder of experimental and physi- (1801-1887) ological psychology Feuchtersleben, Ernst von Psychosis __ (1806-1849) Contd... Appendices 243

Contd... Contributor Coined the Term Special Mention Freud, Sigmund (1856-1939) Free association Founder of psychoanalysis; some Psychoanalysis of the signiﬁ cant contributions include: interpretation of dreams, Psychodynamics theory of infantile sexuality, struc- Oedipus complex tural and topographical model of Electra complex mind, theory of instincts, psychopa- Penis envy thology of everyday life and stages of psychosexual development Primal scene Ego defense mechanisms Repression Psychological determinism Pleasure principle Reality principle Gall, Franz Joseph (1758-1828) __ Founder of phrenology Gita Bhagavad (~4th Century BC) __ Probably the 1st recorded evidence of crisis-intervention psychotherapy Gockel (1547-1628) Psychology __ Griesinger, Wilhelm (1817-1868) Unitary psychosis Founder of the speciality of neuropsychiatry; 1st full time academic psychiatrist with a medical orientation Hecker, Ewald (1843-1909) Hebephrenia __ Heinroth, Johann C (1773-1843) Psychosomatic __ Horney, Karen (1885-1952) __ American psychoanalyst; Neo- Freudian; Described a theory of neurosis Janet, Pierre (1859-1947) Psychasthenia __ Jones, Maxwell (b 1907) Therapeutic community __ Jung, Carl Gustav (1875-1961) Collective and personal uncon- Founder of the school of analytical scious psychology Complex Introvert and extrovert Archetypes Persona Anima and animus Contd... 244 A Short Textbook of Psychiatry

Contd... Contributor Coined the Term Special Mention Kahlbaum, Karl (1828-1899) Catatonia __ Symptom complex Cyclothymia Kanner, Leo (1894-1981) __ Described infantile autism Klein, Melanie (1882-1960) Basic trust Child psychoanalyst Kraepelin, Emil (1856-1926) Dementia praecox Important work on psychiatric nosology and classiﬁ cation Krafft-Ebing, B Richard von Sadism Classic description of sexual (1840-1902) Masochism perversions Maslow, Abraham (1908-1970) Self-actualization Humanistic psychology; Described Self-realization hierarchy of needs Mesmer, Franz Anton (1734-1815) Animal magnetism __ Meyer, Adolf (1866-1950) __ Founder of psychobiology; Famous for ‘common sense psychiatry’ Morel, Benedict-Augustin Demence’ precoce’ __ (1809-1873) Pavlov, Ivan Petrovich (1849-1936) Classical conditioning Animal studies on conditioned reﬂ exes Piaget, Jean (1897-1980) __ Extensive studies on the nature of children’s intellectual development Pinel, Philippe (1745-1826) __ Famous for humane and ‘moral’ treatment of mentally ill Prichard, James (1786-1848) Moral insanity __ Rado, Sandor (1890-1972) Adaptational psychodynamics Hungarian psychoanalyst Rank, Otto (1884-1939) Birth trauma __ Will therapy Ray, Issac (1807-1881) __ Father of American forensic psychiatry Reil, Johann Christian (1759-1820) Psychiatry Founded the 1st psychiatric journal Rogers, Carl (1902-1987) Client-centred psychotherapy American psychologist; Non-directive psychotherapist Rush, Benjamin (1745-1828) __ Father of American psychiatry Skinner, Burrhus Frederic __ Founder of operant conditioning (1904-1990) model of learning Sullivan, Harry Stack (1892-1949) __ Founder of interpersonal school of psychiatry Tissot, Simon Andre (1728-1797) Onanism 1st medical description of masturbation Appendices 245

Contd... Contributor Coined the Term Special Mention Vives, Juan Louis (1492-1540) __ Wrote the 1st modern textbook of psychology Watson, John Broadus (1878-1958) __ Founder of behaviourism Weyer, Johann (1515-1588) __ Sometimes known as the father of modern psychiatry Zacchia, Paolo (1584-1659) __ Probably the 1st forensic psychiatrist 246 A Short Textbook of Psychiatry

Appendix III: Glossary of Some Important Terms in Psychiatry

Abstract thinking: Abstract thinking is the ability Deja vu: A false sense of familiarity with unfamiliar to assume a mental set voluntarily, shift voluntarily circumstances or scenes. from one aspect of a situation to another, keep in mind Delusion: A false, unshakable belief which is not simultaneously the various aspects of a situation, grasp amenable to reasoning, and is not in keeping with the essentials of a ‘whole’ (e.g. situation or concept), the patient’s socio-cultural and educational back- and to break a ‘whole’ into its parts. ground. Affect: The outward expression of the immediate Delusional perception: Normal perception has a (cross-sectional) experience of emotion at a given private and illogical meaning. time. Depersonalization: An alteration in the perception Agitation: Presence of anxiety with severe motor of self, so that the feeling of one’s reality is (as if) restlessness. temporarily changed or lost. Akinesia: Absence of motor activity. Derealization: An alteration in the perception of Alexithymia: Inability to verbally describe one’s external world, so that the feeling of the reality of emotionally feelings. external world is (as if) temporarily changed or lost. Ambitendency: Due to ambivalence, tentative actions Disorientation: A disturbance in orientation in time, are made, but no goal directed action occurs. place and/or person. Ambivalence: Inability to decide for or against, due Distractibility: Inability to concentrate or focus to co-existence of two opposing impulses for the same attention. thing at the same time in the same person. Echolalia: Repetition, echo or mimicking of phrases Anergia: Lack of energy for day-to-day activities. or words heard. Anhedonia: Inability to experience pleasure in previ- Echopraxia: Repetition, echo or mimicking of actions ously pleasurable activities. observed. Anxiety: An unpleasurable emotional state, associated Ecstasy: Very severe elevation of mood (seen in with psycho-physiological changes in response to an delirious or stuporous mania); Intense sense of rapture intrapsychic confl ict. or blissfulness. Blunted affect: Severe reduction in the intensity of Elation: Moderate elevation of mood (seen in mania; affect. Stage II); Feeling of confi dence and enjoyment along Catalepsy: The person maintains body posture in to with increased psychomotor activity. which it is placed. Also see waxy fl exibility. Emotional incontinence: Complete loss of control Cataplexy: Abrupt loss of muscle tone without im- over affect (represents an extreme form of emotional pairment of consciousness. Often seen in Narcolepsy. lability). Circumstantiality: Digression in to unnecessary Euphoria: Mild elevation of mood (seen in hypo- details that distract from the central theme; however, mania); Increased sense of psychological well-being the patient returns back to the original theme after and happiness, not in keeping with on-going events. digression (unlike in tangentiality). Euthymia: Normal range of mood, with absence of Confabulation: A false memory that the patient depressed or elevated mood. believes to be true. Exaltation: Severe elevation of mood (seen in severe Coprolalia: Vocal tics characterised by shouting of mania; Stage III); Intense elation with delusions of obscene words. grandeur. Deja entendu: A false sense of familiarity when hear- Flight of ideas: Rapid speech with sudden shifts in ing something new. ideas, without loosing logical connection. Appendices 247

Folie å deux: Delusions shared between two closely Panic: An acute, intense, overwhelming episode of connected persons. Also known are folie å trios, folie anxiety, often associated with feelings of impending å quatre, and folie å famille. doom. Formication: A false sense of insects crawling on Perplexity: Puzzled bewilderment. one’s skin. Perseveration: Persistent repetition of words or Fugue: Physical and psychological fl ight (wandering) themes beyond the point of relevance. from one’s usual place. Phobia: An irrational fear of an object, situation or Grandiosity: Excessive and exaggerated feeling of activity. one’s importance. Posturing: Voluntary assumption of an inap propriate Hallucination: A perception that occurs in the absence and often bizarre posture for long periods of time. of a stimulus. Poverty of speech: Decreased speech production. Illusion: A misinterpretation of stimuli arising from Poverty of content of speech: The speech production external object(s). is adequate, but the content conveys little information. Incoherence: Thought process that is disconnected, Pressure of speech: Rapid production of speech disorganised, or incomprehensible. output, with a subjective feeling of racing thoughts. Insight: The ability to understand one’s own behaviour Rigidity (Catatonic): Maintenance of a rigid posture and emotions. In the context of psychiatric disorders, against efforts to be moved. it implies the degree of awareness and understanding Somatic passivity: Bodily sensations, especially that the patient has regarding his/her illness. sensory symptoms, are expe rienced as imposed on Intelligence: The ability to think logically, act ration- body by some external force. ally, and deal effectively with the environment. Somnolence: Inability to maintain a state of alertness Jamais entendu: A sense of unfamiliarity when hear- without constant stimulation. ing something familiar. Stereotypy: Odd, repetitive and non-goal directed Jamais vu: A sense of unfamiliarity with familiar movement (can also be verbal). circumstances or scenes. Stupor: A clinical syndrome of akinesis and mutism, Judgement: An ability to assess a situation correctly with relative preservation of conscious awareness. and act appropriately within that situation. Suicide: A human act of self-intentioned and self- Labile affect: Rapid and abrupt changes in affect, infl icted cessation (death). unrelated to external stimuli. Tangentiality: Sudden and oblique digression in to Loosening of associations: Thought process charac- unnecessary details that completely distract from the terised by a series of ideas without apparent logical central theme; however, the patient never returns connections. back to the original theme after digression (unlike in Mannerisms: Odd, repetitive and goal-directed circumstantiality). movements. Thinking: Normal thinking is a goal directed fl ow of Mood: The pervasive feeling tone which is sustained ideas, symbols and associations initiated by a prob- (lasts for some length of time) and colours the total lem or a task, characterised by rational connections experience of the person. between successive ideas or thoughts, and leading Mutism: Complete absence of speech. towards a reality oriented conclusion. Negativism: An apparently motiveless resis tance to Thought diffusion or Broadcasting: Subject experi- all commands and attempts to be moved, or doing ences that his thoughts are escaping the confi nes of just the oppo site. his self and are being experienced by others around. Neologisms: These are idiosyncratically formed new Thought echo: Voices speaking out thoughts aloud; words whose derivation cannot be understood easily. also called as echo de la pense. 248 A Short Textbook of Psychiatry

Thought insertion: Subject experiences thoughts Trance: A sleep like state of reduced consciousness imposed by some external force on his passive and suggestibility. mind. Verbigeration: Senseless repetition of same words Thought withdrawal: Thoughts cease and subject or phrases over and over again. experiences them as remo ved by external force. Waxy fl exibility: Parts of body can be placed in Tic: Involuntary, sudden, rapid, recurrent, non- positions that will be main tained for long periods of time, even if very uncomfortable; fl exible like wax. rhythmic and stereotyped movement (can also be The process is called as waxy fl exibility, while the end verbal). result is called as catalepsy. Suggested Further Reading

1. Abse DW. Hysteria and Related Mental Disor- 13. Benson FD. Aphasia, Alexia and Agraphia. ders: An Approach to Psychological Medicine. Churchill Livingstone, New York, 1979. 2nd edn, John Wright, Bristol, 1987. 14. Bleuler E. Dementia Precox: The Group of 2. Diagnostic and Statistical Manual of Mental Schizophrenias. International Universities Disorders. 4th edn, Text Revision. American Press, New York, 1950. Psychiatric Association, Washington DC, 2000. 15. Bowlby J. Processes of mourning. International 3. Task Force Report on Electroconvulsive Journal of Psycho-Analysis 1961; 42: 317-40. Therapy. American Psychiatric Association, 16. Brown GW, Birley JLT, Wing JK. Inﬂ uence of Washington DC, 1990. family life on the course of schizophrenic disor- 4. The Practice of Electroconvulsive Therapy: ders: A replication. British Journal of Psychiatry Recommendations for Treatment, Training 1972;121:241. and Privileging. Task Force Report on ECT, 17. Brown JAC. Freud and the Post-Freudians. American Psychiatric Association, Washington Penguin, New York, 1978. DC, 2001. 18. Cavenar JO, Brodie HKH. (Eds). Signs and 5. Arieti S. Interpretation of Schizophrenia. 2nd Symptoms in Psychiatry. JB Lippincott, Phila- edn, Basic Books, New York, 1974. delphia, 1983. 6. Ashton H. Benzodiazepines: How they work and 19. Chapman JP. The early symptoms of schizo- how to withdraw? The Ashton Manual. http:// phrenia. British Journal of Psychiatry 1966; benzo.org.uk/manual/index.htm 112: 225. 7. Bancroft J. Human Sexuality and its Problems. 20. Ciompi L. Catamnestic long-term studies on the 3rd edn, Churchill Livingstone Elsevier, Edin- course of life of schizophrenics. Schizophrenia burgh, 2009. Bulletin 1980;6:606-18. 8. Barlett J, Bridges P, Kelly D. Contemporary 21. Cleckley H. The Mask of Sanity. 4th edn, indications for psychosurgery. British Journal Mosby, St. Louis, 1964. of Psychiatry 1981;138:507. 22. Crow TJ. Molecular pathology of schizophrenia: 9. Beck AT, Rush AJ, Shaw BI, et al. Cognitive More than one disease process. British Medical Therapy of Depression. Guilford, New York, Journal 1980; 280: 66-68. 1979. 23. David A, Fleminger S, Kopelman M, Lovestone 10. Beck AT. Cognitive Therapy and the Emotional S, Mellors J. Lishman’s Organic Psychiatry: A Disorders. International Universities Press, New Textbook of Neuropsychiatry. 4th edn, Wiley- York, 1976. Blackwell, Oxford, 2009. 11. Bellack AS, Hersen M, Kazdin AE. Interna- 24. Dement WC. Some Must Watch While Some tional Handbook of Behavior Modiﬁ cation and Must Sleep. WH Freeman Co, San Francisco, Therapy. Plenum Press, New York, 1982. 1974. 12. Benson DF, Blumer D. (Eds). Psychiatric As- 25. Directorate General of Health Services. National pects of Neurologic Disease. Grune and Strat- Mental Health Programme for India. Directorate ton, New York Vol I, 1975 and Vol II, 1982. General of Health Services, New Delhi, 1982. 250 A Short Textbook of Psychiatry

26. Editorial. What next with Psychiatric illness? 43. Indian Council of Medical Research. Collabo- Nature 1988;336:95-96. rative Study on Phenomenology and Natural 27. Fenichel O. The Psychoanalytic Theory of History of Acute Psychosis. Report of an ICMR Neurosis. Norton, New York, 1945. Task Force Study. Indian Council of Medical 28. Fink M. Convulsive Therapy: Theory and Prac- Research, New Delhi, 1989. tice. Raven Press, New York, 1979. 44. Indian Council of Medical Research. Fac- 29. Folstein MF, Folstein SE, McHugh PR. Mini- tors Associated with Course and Outcome of Mental State: A practical method for grading Schizophrenia. Report of an ICMR Task Force the cognitive state of patients for the clinician. Study. Indian Council of Medical Research, Journal of Psychiatric Research 1975;12:189. New Delhi, 1989. 30. Freud A. The Ego and the Mechanisms of De- 45. Jefferson JW, Griest JH, Ackerman DL. Lithium fense. Hogarth Press, London, 1937. Encyclopedia for Clinical Practice. American 31. Freud S. The Psychopathology of Everyday Psychiatric Press, Washington DC, 1983. Life. In: Strachey J (Ed). The Standard Edition 46. Jellinek EM. The Disease Concept of Alcohol- of the Complete Psychological Works of Sig- ism. College and University Press, New Haven, mund Freud. Hogarth Press, London, 1960; 6. 1960. 32. Gelder M, Mayou R, Cowen P. Shorter Oxford 47. Jones E. The Life and Work of Sigmund Freud. Textbook of Psychiatry. 4th edn, Oxford Uni- Basic Books, New York, 1957. versity Press, New York, 2001. 48. Kraepelin E. Dementia Praecox and Paraphre- 33. Gelenberg AJ. The catatonic syndrome. Lancet nia. GM Robertson (Ed). Huntington. NY: 1976;1:1339. Krieger, 1971. 34. Gottesman II, Shields J. Schizophrenia: The 49. Kraepelin E. Manic-Depressive Insanity and Epigenetic Puzzle. Cambridge University Press, Paranoia. Livingstone, Edinburgh, 1921. New York, 1982. 50. Leff JP, Issacs AD. Psychiatric Examination in 35. Government of India. The Mental Health Act Clinical Practice. 2nd edn, Blackwell, Oxford, 14, 1987. 1981. 36. Government of India. The Narcotic Drugs 51. Lerer B, Weiner RD, Belmaker RH. ECT: Basic and Psychotropic Substances Act 61, 1985. Mechanisms. John Libbey, London, 1984. (Amended in 1989, Act 2 of 1989). 52. Marks IM. Fears, Phobias and Rituals. Aca- 37. Hall CS. A Primer of Freudian Psychology. demic Press, New York, 1988. World Publishing, Cleveland, 1954. 53. Masters WH, Johnson VE. Human Sexual In- 38. Hamilton M. Fish’s Clinical Psychopathology. adequacy, Little Brown, Boston, 1966. 3rd edn, John Wright, Bristol, 1983. 54. Masters WH, Johnson VE. Human Sexual Re- 39. Hamilton M. Fish’s Schizophrenia. 3rd edn, sponse. Little Brown, Boston, 1966. John Wright, Bristol, 1986. 55. Mellor CS. First rank symptoms of schizophre- 40. Heilman KM, Valenstein E (Eds). Clinical nia. British Journal of Psychiatry 1970;117:15. Neuro psychology. 2nd edn, Oxford University 56. Merksey H. The Analysis of Hysteria. Bailliére Press, New York, 1985. Tindall, London, 1979. 41. Hinsie LE, Campbell RJ. Psychiatric Dictionary. 57. Ministry of Health and Family Welfare. National 5th edn, Oxford University Press, New York, Mental Health Programme Booklet. DGHS, 1981. New Delhi, 1982. 42. Indian Council of Medical Research. Man- 58. Morgan C, Bhugra D (Eds). Principles of ual of Mental Health for Medical Officers. Social Psychiatry. 2nd edn, Chichester: Wiley- NIMHANS, Bengaluru, 1983. Blackwell, 2010. Suggested Further Reading 251

59. Murthy RS, Wig NN. The WHO Collabora- 72. Sadock BJ, Sadock VA, Ruiz P (Eds). Com- tive Study on Strategies for Extending Mental prehensive Textbook of Psychiatry. 9th edn, Health care. American Journal of Psychiatry Lippincott Williams and Wilkins, 2009. 1983;140:1486. 73. Sadock BJ, Sadock VA. Kaplan and Sadock’s 60. Murthy RS. National Mental Health Programme Synopsis of Psychiatry. 10th edn, Lippincott in India (1982-1989): Mid-point appraisal. In- Williams and Wilkins, 2007. dian Journal of Psychiatry 1989;31:267. 74. Schreiber FR. Sybil. New York: Warner Books, 61. National Collaborating Centre for Mental 1973. Health. Borderline Personality Disorder: The 75. Scott AIF (Ed). The ECT Handbook, 2nd edn, NICE Guideline on Treatment and Manage- Council Report CR128. Royal College of Psy- ment. National Clinical Practice Guideline No. chiatrists, 2004. 78. British Psychological Society and Royal 76. Sharma SD. Mental Hospitals in India. DGHS, College of Psychiatrists, 2009. New Delhi, 1990. 62. National Institute for Health and Clinical Ex- 77. Shneidman ES, Farberow NL. Some Facts about cellence. Core Interventions in the Treatment Suicide. PHS Publication No 852, US Govern- and Management of Schizophrenia in Adults ment. Printing Ofﬁ cem, Washington DC, 1961. in Primary and Secondary care. NICE Clinical 78. Singh G, Tewari SK. Morbid grief: Its clinical Guideline 82. National Collaborating Centre for manifestations and proposed classification. Mental Health, 2009. Indian Journal of Psychiatry 1980; 22: 74-80. 63. National Crime Records Bureau. 2008. Sui- 79. Slater E, Roth M. Clinical Psychiatry (Mayer- cides in 2008. http://ncrb.nic.in/ADSI2008/ Gross). 3rd edn, JPB Publishers, New Delhi, suicides-08.pdf 1986. 64. Neki JS. Guru-Chela relationship: The possibil- 80. Strub RL, Black FW. The Mental Status Ex- ity of a therapeutic paradigm. American Journal amination in Neurology. 2nd edn, FA Davis, of Orthopsychiatry 1973;3:755-66. 65. Noshpitz JD (Ed). Basic Handbook of Child Philadelphia, 1985, reprinted by JPB Publishers, Psychiatry. Vol I-IV. Basic Books, New York, New Delhi, 1991. 1979. 81. Taylor D, Paton C, Kapur S. The Maudsley Pre- 66. Oyebode F. Sims’s Symptoms in the Mind: An scribing Guidelines. 10th edn, Informa Health Introduction to Descriptive Psychopathology. care, London, 2009. 4th edn, Elsevier Saunders, 2008. 82. Thigpen CH, Cleckley HM. The Three Faces of 67. Padesky CA, Greenberger D. Mind over Mood: Eve. New York: McGraw Hill, 1957. Change How You Feel by Changing the Way 83. Varma VK. Psychotherapy in a Traditional You Think. Guilford Press, 1995. Society: Context, Concept and Practice. JPB 68. Perry JC, Jacobs D. Overview: Clinical appli- Publishers, New Delhi, 2008. cations of the amytal interview in psychiatric 84. Vaughn C, Leff J. The measurement of ex- emergency settings. American Journal of Psy- pressed emotion in the families of psychiatric chiatry 1982;139:552. patients. British Journal of Social and Clinical 69. Pincus J, Tucker GJ. Behavioral Neurology. 3rd Psychology 1976;15:157-65. edn, Oxford University Press, New York, 1985. 85. Watson JB, Rayner R. Conditioned emotional 70. Plum F, Posner C. The Diagnosis of Stupor and responses. Journal of Experimental Psychology Coma. 3rd edn, FA Davis, Philadelphia, 1980. 1920;3:1-14. 71. Sachdev PS, Keshavan MS (Eds). Secondary 86. Wolberg LR. The Technique of Psychotherapy. Schizophrenia. Cambridge University Press, Vol I and II. Secker and Warburg with Heine- Cambridge: 2010. mann, London, 1989. 252 A Short Textbook of Psychiatry

87. World Health Organization. The ICD-10 Clas- 91. The World Health Report: 2001. Mental Health: siﬁ cation of Mental and Behavioural Disorders: New Understanding, New Hope, World Health Clinical descriptions and diagnostic guidelines. Organization, Geneva, 2001. World Health Organization, Geneva, 1992. 92. Atlas: Mental Health Resources in the World. 88. World Health Organization. Definition of World Health Organization, Geneva, 2005. Health. Accessed May 2010. See http://www. http://www.who.int/mental_health/evidence/ who.int/about/deﬁ nition/en/print.html/ atlas/en/ 89. World Health Organization. Report of the Inter- national Pilot Study of Schizophrenia (IPSS). 93. Zilboorg GA, Henry GW. A History of Medical Geneva: WHO, 1973. Psychology. Norton, 1941. 90. World Health Organization. Schizophrenia: 94. Zubin J, Spring B. Vulnerability: A new view of An International Follow-up Study, Wiley, New schizophrenia. Journal of Abnormal Psychology York, 1979. 1977;86,103-26. Index

A Algophobia 93 Assertiveness training 131 Alogia 57, 62 Association disturbances 55 Abnormal illness behaviour 99, 209 Alprazolam 94, 98, 131 Astasia abasia 100 Abreaction 104, 218 Alzheimer’s Asterixis 20 Abstract thinking 14 dementia 23 Atenolol 92 Acamprosate 42 disease 26 Atomoxetine 167 Acetylcholine 64, 75 Amantadine 48 Attempted suicide 222 Acrophobia 93 Ambitendency 59, 225 Attention Acute Ambivalence 55, 56 defi cit disorder 166 and transient psychotic disorders 61, Ambulatory schizophrenia 117 seeking 103 76 Amine hypothesis 184 Atypical intoxication 33, 37, 46 Amisulpride 66 antipsychotics 29, 65 polymorphic psychotic disorder Amitriptyline 30 depression 81 with symptoms of schizophrenia Amok 110, 111 Audible thoughts 55, 56 86 Amotivational syndrome 46 Auditory hallucinations 13, 56 without symptoms of schizophre- Amphetamine 29, 48 Autism 55, 163, 164 nia 86 induced psychoses 61 Autistic psychosis 228 use disorder 48 disorder 163 schizophrenia-like psychotic disorder Amygdalotomy 204 thinking 55 60, 86 Amytal interview 218 Autochthonous delusions 56 stress reaction 111 Androgens 132 Automatic obedience 59, 225 Adenoma sebaceum 159 Anhedonia 12, 56, 57, 62 Aversion therapy 41, 103, 126, 215 Adjustment disorder 112 Anorexia nervosa 142 Ayurveda 54 with depressed mood 76 Antiandrogens 126 Admission under special circumstances Anti-anxiety drugs 193 B 232 Anticipation 210 Bad trip 50 Adolescent thinking 155 Anti-craving agents 42 Barbiturate 167, 193 Affective Antidepressant 30, 76, 82, 87, 92, 95, use disorder 50 disorders 69 105, 112, 144, 181 Battered child syndrome 228 fl attening 57, 62 Antimanic 185 Behaviour spectrum disorders 81 Antipsychotic 26, 30, 65, 67, 68, 78, 87, modifi cation 105, 131, 161, 167 Agitated depression 81 143, 168 therapy 41, 80, 94, 131, 143, 144, Agonist substitution therapy 44 depot preparations 181 214 Agoraphobia 92 dose in schizophrenia 66 Behavioural theory 91, 97 with panic disorder 93 drugs 174 Benperidol 126 without panic disorder 93 Antisocial personality disorder 167 Benzodiazepines 40, 87, 92, 98, 105, 112, AIDS dementia complex 25 Anxiety 71 137, 140, 194 Akathisia 228 disorder 89 receptor antagonist 51, 196 Akinesis 225 Anxious personality disorder 117 Beta blockers 194 Alcohol Apathy 56 Binge eating disorders 144 and substance history 10 Apomorphine 132 Biological sensitising drugs 41 Appetite 71 functions 72 use disorders 35, 228 Arctic hysteria 111 theories 63, 75, 91, 94 anonymous 41 Aripiprazole 29, 66, 168 Biopsychosocial model 17, 147 hallucinosis 28, 38 Ashton manual 51 Bipolar disorder 73, 75 seizures 38 Asperger’s syndrome 165 subtypes 73 254 A Short Textbook of Psychiatry

Blackouts 37 Childhood Comparison of delirium and dementia 22 Bladder training 169 history 9 Complex partial seizures 29, 31, 61, 227 Blocking 12 psychosis 165 Complicated grief reaction 152 Blood Chlordiazepoxide 40, 51 Complications of alcohol concentration 39 Chlorpromazine 66 alcohol dependence 39 lithium levels 190 Cholinesterase inhibitors 25, 26 chronic alcohol use 38 Blunted affect 58 Chromatography 157 Conceptual thinking stage 153 Borderline personality disorder 60, Chronic Concrete thinking stage 153 117, 228 depression 74, 77 Conditioning devices 169 Brain imaging 64, 75 fatigue syndrome 109 Conduct disorders 167 Brief Circumscribed amnesia 101 Conjugal paranoia 84 dissociative stupor 100 Citalopram 26 Consultation-liaison psychiatry 149 history of psychopharmacology 173 Citrated calcium carbimide 42 Continuous amnesia 101 pulse ECT 202 Civil responsibility 229 Contraindications of disulfi ram 42 Bromocriptine 48, 132 Classical Conversion Bruxism 140 conditioning model 214 disorder 99 Bulimia nervosa 144 psychoanalysis 213 release symptoms 102 Buprenorphine 44, 45 psychosomatic disorders 147 Coping Bupropion 52 Classifi cation in mechanisms 207 Buspirone 92, 98, 197 child psychiatry 162 skills training 112 psychiatry 2 Coprolalia 168 C Classifi cation of Cortical dementia 24 Caffeine 52, 53 alcoholism 37 Counselling 110 CAGE questionnaire 37, 39 benzodiazepines 196 Counter Cannabis mental retardation 156 phobic defense 210 preparations 45 psychotropic drugs 172 thoughts 96 use disorder 45 Claustrophobia 93 Covert sensitisation 41, 215 Capgras’ syndrome 87 Clerambault’s syndrome 84 CPAP 139 Carbamazepine 79, 192 Clomipramine 98, 131 Crack 47 Carphologia 20 Clonazepam 94, 98 Cretinism 159 Castration anxiety 211 Clonidine 44, 167, 169 Criminal lunatic 232 Cataplexy 138 Clozapine 52, 53, 66 Crisis 221 Catastrophic reaction 22 Cocaine 47 intervention 112 Catatonia 59 overdose 48 centre 228 Catatonic preparations 47 Critical behaviour 58 use disorder 46 comments 64 features 57 withdrawal syndrome 48 remarks 68 schizophrenia 59 Code of ethics for psychiatrists 234 Cross-gender homosexuality 122 signs 11, 225 Cognitive Culture bound syndromes 110 stupor 67, 225 behaviour therapy 68, 79, 94, 98, Cyclothymia 73 syndrome 225 112, 215, 216 Cyproheptadine 144 withdrawal 225 behavioural theory 91 Causes of therapy 215 D Combativeness 225 catatonic stupor 225 Dangerous Drug Act of 1930 233 hypersomnia 138 Command hallucinations 57 Deep brain stimulation 199 mental retardation 157 Common Defense mechanism 90 Censor 206 examples of psychosomatic disorders Defi nition of psychiatric disorder 1 Central mental health authority 233, 237 148 Deliberate self-harm 222 Cerebral palsy 159 psychiatric emergencies 222 Delirium 19, 21, 23 Chasing the dragon 43 themes in suicide 222 tremens 38, 41 Child Community Delusion of doubles 87 abuse 228 mental health 235 Delusional psychiatry 162 psychiatry 235 depression 77, 78 Index 255

disorder 58, 61, 76, 83, 84 perception 56 Electra complex 211 dysmorphophobia 84 sexual preference 124 Electroconvulsive therapy 29, 67, 77, halitosis 84 Disorganised 98, 199, 228 parasitosis 84 behaviour 62 Electroshock therapy 199 Delusions 58, 60, 62, 71 schizophrenia 58 Elementary auditory hallucinations 56 Delusions of symptoms 62 Elevated mood 70 control 56 Dissocial personality disorder 115 Emergency psychiatry 221 grandeur 56, 70, 83 Dissociative Emil Kraepelin 54 jealousy 83 amnesia 100, 101 Emotional nihilism 71 anaesthesia and sensory loss 100 blunting 56 persecution 56, 61, 70, 83 and conversion disorders 99 lability 22, 25 reference 56 convulsions 100, 101 over-involvement 64 Demence precoce 54 disorder 100 shallowness 56 Dementia 22, 23, 76 fugue 101 Emotionally unstable personality disor- praecox 54, 61 identity disorder 102 der 116 Denial 65, 207 motor disorders 99 Emotions 69 Dependence syndrome 34 Distortion 207 Encopresis 170 Dependent personality disorder 118 District mental health programme 237 English Lunacy Act of 1890 231 Depersonalisation 13, 46, 109 Disulﬁ ram 41, 42 Enuresis 169 derealisation syndrome 109 ethanol reaction 41 Environmental manipulation 26 disorder 109 Divalproex 191 Epidemiology 55, 222 Depot antipsychotic 67 Donepezil 25, 26 Epilepsy 28 Depressed mood 71 Dopamine 75 Epileptic seizures 101 Depression 61, 80, 95, 227 agonists 132 Epiloia 159 with psychotic features 77 Double depression 81 Erectile dysfunction 127 Depressive Down’s syndrome 158 Erotomania 84 episode 30, 71 Dream anxiety disorder 140 Erotomanic delusions 83 equivalent 81, 106 Drug 33, 228 Erythrophobia 93 ideation/cognition 71 and alcohol dependence 227 Eugen Bleuler 54, 55 pseudodementia 23 induced psychoses 61 Euphoria 70 stupor 71 Dual-role transvestism 122 Exaltation 70 Derealisation 13, 46, 109 Duration of Excessive sexual drive 127 Desmopressin 169 therapy 202 Excited Deterrent agents 41 untreated psychosis 63 behaviour 227 Detoxiﬁ cation 40, 41, 44 Dyslalia 163 catatonia 59 Developmental Dyssomnias 136 Expressed emotions 64, 65, 68 milestones 154 Dysthymia 73, 82 Expressive language disorder 163 reading disorder 162 Dysthymic disorder 80, 82 Dexamphetamine 167 F Dhat syndrome 110 E Factitious disorder 119 Diagnostic formulation 17 Eating disorders 142 Family Diazepam 40, 67, 87, 94, 112, 137, 149, Echolalia 56, 59, 168, 225 and marital therapy 80 218, 228 Echopraxia 59, 225 history 7 Digit Ecstasy 70 structure 7 backwards 14 Educational history 9 theories 64 span test 14 Ego 206 therapy 68, 144, 217 Dipsomania 34, 36 defense mechanisms 206, 207 tree 7 Disaster management 112 ideal 206 Fantasy life 10 Disintegrative psychosis 165 Egodystonic sexual orientation 123 Fatigability 72 Disorders of Ego-structure 214 Female adult personality and behaviour 113 Ekbom syndrome 136, 137 anorgasmia 130 affect 56 Elation 70 orgasmic disorder 130 excessive somnolence 137 Elective mutism 171 sexual arousal disorder 128 256 A Short Textbook of Psychiatry

Ferric chloride test 157 H Identiﬁ cation Fetishism 125 data 6 Fetishistic transvestism 122, 125 Habit with aggressor 209 First generation antipsychotics 66 and impulse disorders 119 Idiot savant syndrome 164 Flapping tremor 20 disorders 170 Imipramine 95, 167, 169, 182 Flashback phenomenon 46 Hallucinations 13, 28, 56, 58, 60-62, 71 Immediate retention and recall 14 Flight of ideas 12, 70 Hallucinatory behaviour 12 Impaired abstraction 56 Floccillation 20 Haloperidol 26, 28-30, 66, 149, 165, 228 Impairment of memory 27 Hangover 37 Flooding 94, 215 Impotence 127, 128 Hebephrenia 54 Flumazenil 51, 91, 196, 227 Indian Heller’s syndrome 165 Fluoxetine 42, 85, 95, 98, 131, 144, Contract Act 231 Hermaphrodite 123 Evidence Act 230 169, 171 Hierarchy construction 214 Lunacy Act, 1912 231, 232 Flupentixol 66 Higher mental functions 13 Lunatic Asylums Act 231 Flurazepam 137 Hindu Succession Act 230 Fluvoxamine 98 Adoptions and Maintenance Act 230 Induced delusional disorder 85 Forensic psychiatry 229 Marriage Act 229 Inferiority complex 117 Formal operational stage 155 History of Informants 6 Fragile-X syndrome 159 biological treatments in psychiatry Information processing hypothesis 65 Free association 214 200 Insomnia 38, 136 Free basing 47 present illness 6 Institutionalisation 161 Frontal lobe syndrome 31 Histrionic personality Insulin coma therapy 67 Frottage 125 disorder 116 Intellectual development 153 Frotteurism 125 traits 105 Intelligence 14 Functions of sleep 135 Homosexuality 123 Intermetamorphosis 87 Furore 59 Hopelessness 71 International Pilot Study on Schizophre- Hostility 64, 68, 148 nia 63 G Hyperkinesis 164 Inter-sexuality 123 Hyperkinetic disorder 166 Interview technique 5 GABA 64, 67, 75, 91 Hyperphagia 139 Intracranial space occupying lesions 28 benzodiazepine receptors 91 Hypersexuality 139 Introjection 75, 209 Galantamine 25, 26 Hypersomnia 137, 139 Investigations in psychiatry 15 Ganser’s syndrome 102 Hyperventilation syndrome 106, 228 Involutional melancholia 80 GCP guidelines 234 Hypnagogic Iproniazid 181 Gender identity disorders 121, 123 hallucinations 138 Irritable Generalised phenomena 134 bowel syndrome 107 amnesia 101 Hypnosis 131, 217, 219 mood 70 anxiety disorder 90 Hypnotisability 217 Isolation of affect 96, 208 Genetic hypothesis 63, 75 Hypoactive sexual desire disorder 126 Isoniazid 181 Genital phase 212 Hypochondriacal GGT 37 disorder 105 J Gilles de la Tourette’s syndrome 168 features 60, 72 Jacobson’s progressive 107 Glasgow coma scale 14, 226 paranoia 84 muscular relaxation 92, 131, 219 Globus hystericus 109 Hypochondriasis 105, 209 Jean Piaget 153 Hypomania 70 Glyceryl trinitrate 132 Jet lag 140 Hypothyroid dementia 25 Gratiﬁ cation habits 171 Judicial inquisition 232 Hysteria 99 Grid-iron abdomen 120 Juvenile delinquents 167 Grimacing 57 Hysterical pseudodementia 102 Group K psychotherapy 68, 131 I K-complexes 133 therapy 41, 80, 144, 217 ICD-10 2 Ketamine 52, 218 Guru-Chela relationship 219 Id 206 Kleine-Levin syndrome 139 Guthrie’s test 157 Idazoxan 132 Index 257

Kleptomania 119 Malignant syndrome 228 Monosymptomatic hypochondriacal Klismaphilia 126 Malingering 119 psychosis 84, 85 Koro 110, 111 Mania 61, 70, 80, 227 Mood 12, 69 Korsakoff’s Manic disorders 69, 76 psychosis 38, 39 depressive psychosis 73 stabiliser 30 syndrome 27 episode 30, 69 stabilising drugs 185 Kurt Schneider 54 stupor 70 Morbid grief 151 Mannerisms 57-59, 164 Motor activity 11 L MAOIs 81, 82 Multi-axial classiﬁ cation 4 LAAM 44, 45 Marchiafava-Bignami disease 40 Multifocal myoclonus 20 La-belle-indifférence 103 Marijuana 46 Multi-infarct dementia 25 Lack of Marital therapy 217 Multiple personality disorder 102 rapport 57 Masked depression 80, 105, 106 Munchausen syndrome 119 sexual enjoyment disorder 126 MCI code of medical ethics, 2002 234 Muslim Marriages Act 230 Lamotrigine 79, 188 McNaughten rule 229 Mutism 56, 59, 225, 171 Larks 140 Medical Latah 110, 111 emergency 221 N interview 5 Late paraphrenia 61 Naloxone 44, 227 Medicolegal aspects 224 Latency phase 212 challenge test 44 Megavitamin therapy 67 Latent schizophrenia 59 Naltrexone 42, 44, 132 Memantine 25, 26 Leaden paralysis 81 Narcolepsy 138 Memory disturbances 203 Learned behaviour 214 Narcotic Menstrual and obstetric history 9 Learning disability 155 anonymous 45 Mental Legal and ethical issues in psychiatry 229 antagonists 44 and behavioural disorders in ICD-10 Lethal catatonia 59 Drugs and Psychotropic Substances 3 Leucotomy 203 (Amendment) Act, 2001 233 disorders 19 Lewy body dementia 25 Drugs and Psychotropic Substances Health Licensing authority 232 Act (NDPSA), 1985 233 Act, 1987 232, 233 Life chart 7 National Authorities 232 Limbic system 203 Crime Records Bureau 222 retardation 153, 155, 162, 164 Lithium 78, 188 Health Policy 235, 237 status examination 10, 11, 222 Long-sleepers 134 Mental Health Mentally ill Loosening of associations 55, 58, 59, 62 Advisory Group 237 person 232 Lorazepam 26, 29, 87, 149, 228 Programme 235 prisoner 232 Loss of ego boundaries 57, 65 Trust Act 161 Metabolic syndrome 63 Loxapine 66 NDRI 52 Methadone 44 LSD use disorder 49 Necrophilia 126 maintenance 44 L-thyroxin 227 Negative Methylphenidate 167 L-tryptophan 137 reinforcement 215 Michigan alcoholism screening test 37 Lucid intervals 26 symptom 57, 58, 60-61 Migraine 28 Lunatic 232 Neurasthenia 109 Mild cognitive disorder 32 Neuroleptic M Milieu therapy 68 malignant syndrome 228 Mini mental state examination 13 Made sensitivity syndrome 26 Minimal brain dysfunction 166 feeling 55, 56 Neurosis 89 Minoxidyl 132 impulses 55, 56 Neurotic Mirror-gazing 58 volition 55, 56 depression 82 Mirtazapine 30 Maintenance therapy 44 traits 9 Misconceptions about suicide 224 Major depression 105 Nicotine 52 Mixed Male replacement therapy 52 affective 61, 73 anorgasmia 128 Night terrors 140 episode 73 erectile disorder 127 Nightmares 140 anxiety depressive disorder 80 orgasmic disorder 128 Nitrazepam 137 258 A Short Textbook of Psychiatry

NMDA 52 Orgasmic disorders/dysfunctions 128 Personality antagonist 26 Othello syndrome 84 disorders 113 NMHP 236 Other traits 113 NMS 87 acute predominantly delusional psy- Persons with Disability Act 161 Nonorganic chotic disorders 86 Pfropf schizophrenia 61 dyspareunia 130 biological methods of treatment 199 Phallic phase 211 vaginismus 130 organic mental disorders 28 Phencyclidine use disorder 52 Non-REM sleep 133 psychiatric emergencies 228 Phenelzine 95 Norepinephrine 75 Oxazepam 26 Phenylalanine 158 Normal Oxcarbazepine 79 Phenylketonuria 157 aging process 23 Phobia 92 child development 153 P Phobic mental health 1 anxiety-depersonalisation syndrome PAD syndrome 81 Nuclear schizophrenia 58 81 Paedophilia 126 Nymphomania 127 companion 93 Palilalia 168 disorder 92 O Paliperidone 66 Phonological disorder 163 Pananxiety 60 Phototherapy 82 Obesity 144 Panic disorder 90, 93, 228 Physical causes of male erectile disorder/ Obsessions 12, 95-97, 168 Pan-neurosis 60 impotence 128 Obsessive Pansexuality 60 Physiology of hyperventilation syndrome compulsive Papaverine 132 107 disorder 76, 95 Papez circuit 204 Physostigmine 227 personality disorder 118 Paranoid Piblokto 110, 111 symptoms 169 disorder 83, 84 Pickwickian syndrome 139 rumination 96 personality disorder 58, 84, 114 Pimozide 66, 85, 169 Occupational history 9 schizophrenia 58, 61, 84 Polysomnography 135, 137 Oculocephalic reﬂ ex 226 Paraphasias 56 Poor drug concordance 181 Oedipus complex 211 Paraphilias 124 Positive Olanzapine 28-30, 66, 168 Parental counselling 165 reinforcement 215 Oneiroid schizophrenia 60 Parkinsonian symptoms 26 symptoms 62 Operant conditioning 215 Parsi Marriage and Divorce Act 230 Possession hysteria 102 model 214 Passive-aggressive personality disorder Post-cardiac surgery delirium 149 Opiate antagonists 132 118 Post-natal blues 145 Postpartum Opioid Pathological psychiatric disorders 145 antagonists 45 grief reaction 151 psychosis 145 derivatives 43 intoxication 33, 37 Post-schizophrenic depression 60 use disorders 42 laughter and crying 30 Post-traumatic stress disorder 112 Opium and Revenue Laws Act, 1950 233 Pavor nocturnus 140 Poverty of Oppositional deﬁ ant disorder 167 Pedigree chart 7 ideation 56 Organic Peduncular hallucinosis 28 speech 56, 62 amnestic syndrome 27, 39 Penis envy 211 Pranayama 92, 219 anxiety 90 Pentothal/amytal/diazepam interview 225 Predisposing factors 6, 20 disorder 30, 91 Perinatal history 9 in delirium 21 catatonic disorder 29 Periodic limb movement disorder 136 Prefrontal lobotomy 203 delusional disorder 29 Pernicious catatonia 59 Pregabalin 198 dissociative disorder 32 Perpetuating and/or relieving factors 6 Premature ejaculation 130, 131 emotionally labile disorder 32 Perplexity 56 Premenstrual hallucinosis 28 Perseveration 56 syndrome 108 mood disorder 30, 72 Persistent tension 108 personality disorder 31 delusional disorders 83 Premorbid sexual disorder 132 mood disorder 73 histrionic personality traits 103 stupor 225, 226 somatoform pain disorder 109 personality 10 Index 259

Pressure of speech 59 Psychomotor activity 70, 71 Reversible dementias 26 Pre-treatment evaluation 200 Psychopath 115 Risperidone 26, 28-30, 66, 149, 165, 168 Prevention of Illicit Trafﬁ c in NDPS Act, Psychopharmacology 172-198 Rivastigmine 25, 26 1988 233 Psychosexual stages of development 211 Primary Psychosis 83, 89 S delusions 56 Psychosocial Satyriasis 127 process thinking 205, 206 crises 228 Schizoaffective disorder 61, 76, 87 transexualism 121 rehabilitation 42, 45, 68 Schizoid Problem-solving skills 216 therapies 75, 213 fantasy 209 Prochlorperazine 66 treatment 65, 67, 79 personality disorder 114 Prodromal symptoms of schizophrenia 59 Psychosomatic disorders 146 Schizophrenia 54, 76, 105 Prognostic factors in Psychosurgery 67, 79, 97, 98, 203 Schizophrenia—clinical types 58 mood disorders 74 Psychotherapy 41, 87, 91, 98, 104, 110, Schizophreniform disorder 60 schizophrenia 62 143, 144, 165, 213 Schizotypal disorder 115 Promethazine 67, 228 Psychotic Schneider’s ﬁ rst rank symptoms 54, 56 Propranolol 48, 67, 92, 194 disorders 83 Second generation antipsychotics 66, 175 Proverb testing 14 features 70-72 Secondary Pseudoseizures 228 Psychotropic drug 172 delusions 56 Pseudodementia 23 Punishment 215 depression 82 Pseudohallucination 13 Pyromania 119 gain 99 Pseudo-hermaphroditism 123 mania 82 Pseudologia fantastica 120 Q process thinking 205, 206 Pseudoneurotic schizophrenia 60, 117 Quetiapine 29, 66, 169, 188 transexualism 121 Pseudoseizures 100 Sedative-hypnotic use disorder 51 Pseudo-transexualism 122 R Selective Psychiatric amnesia 101 emergency 221 Rapid serotonin reuptake inhibitors 77 intensive care unit 228 cyclers 74 Seman’s technique 131 interview 5 cycling 73 Sensate focus technique 131 rehabilitation 219 Rapport 11 Sensory Psychiatry in medicine 149 Reaction to stress and adjustment disor- deprivation 28 Psychic determinism 206 ders 111 disorders 100 Psychoactive substances 35 Reactive psychosis 87 Serotonin 64 Psychoanalytic Reception order dopamine antagonists 67 psychotherapy 80, 98 on application 232 norepinephrine reuptake inhibitors theories 75 without application 232 77 Psychoanalytical psychotherapy 213 Receptive language disorder 163 syndrome 185 Psychoanalytically-oriented psycho- Recurrent depressive disorder 73 Sertraline 26, 30, 92, 95 therapy 214 Refractory depression 185 Severe depression 199, 228 Psychodynamic theory 90, 93, 96 Regression in service of ego 207 Sex reassignment surgery 122 Psychodynamic theory of Rejection sensitivity 81 Sexual dissociative disorder 103 Relaxation and marital history 9 obsessive compulsive disorder 97 techniques 91, 94, 107, 137, 148 anhedonia 127 Psychodynamically oriented psychotherapies 218 aversion disorder 126 therapy 94 training 214 desire disorders 126 Psychoeducation 67, 144 Release hallucinations 28 disorders 121, 130 Psychogenic Remote memory 14 dysfunctions 126, 129 pain disorder 109 REM-sleep 133 masochism 125 stupor 225, 226 Repression 90, 93, 205, 207 maturation disorder 123 vomiting 145 Reserpine 65 pain disorders 130 Psychological Residual schizophrenia 59 relationship disorder 124 theories 64 Restless legs’ syndrome 136, 137 response cycle 127 treatments 213 Rett’s syndrome 165 sadism 125 260 A Short Textbook of Psychiatry

Shavasna 219 Speech 12, 70 Theory of psychosexual development 207 Short-sleepers 134 disorders 170 Therapeutic Side effects of Splitting 117, 210 community 68 antidepressants 186 Squeeze technique 131 window 184 antipsychotics 178 SSRIs 26, 30, 81, 144, 169 Thiamine 27, 227 psychotropic medication 228 Stages of sleep 134 defi ciency 27 Sigmund Freud 205 Stammering 170 Thioridazine 66 Signal anxiety 90 Startle reaction 111 Third Sildenafi l 132 State person hallucinations 56 Simple anxiety 89 psychoses 83 dissociative disorder 100 Mental Health Rules, 1990 233 Thought schizophrenia 60 Stereotactic and speech disorders 55 Sleep 71 limbic leucotomy 79, 204 blocking 56 apnoea 139 subcaudate tractotomy 79, 204 broadcasting 56 attacks 137, 138 Stockholm syndrome 209 diffusion 55 deprivation 135 Stress disorder 58, 62 disorders 133, 135 management 112 echo 56 drunkenness 138 vulnerability hypothesis in schizo- insertion 55, 95 hygiene 137 phrenia 64 withdrawal 55, 56 paralysis 138 Structural theory of mind 206 Thymia 82 related enuresis 140 Stupor 29, 59, 199, 225 Thymoleptics 181 spindles 133 Stuporous catatonia 59 Tic disorders 168 studies 75 Subcortical dementia 24, 25 Token economy 215 terrors 140 Substance abuse 35 Topographic theory of mind 205 Social Substitution drugs 44 Tourette’s drift 65 Suction devices 132 disorder 168 history 9 Suicidal syndrome 168 judgement 15 gesture 222 Trait anxiety 89 manner 11 ideas 71 Trance and possession disorders 102 phobia 93 risk 72, 199 Transcendental meditation 92, 219 skills training 215 Suicide 57, 72, 222 Transcranial magnetic stimulation 199 package 68 Sulpiride 66, 169 Transexualism 121 withdrawal 60 Sun downing 20 Transfer of property 231 Sociocultural theories 65 Super-ego 206, 212 Transient global amnesia 27 Soft neurological signs 64 Supportive psychotherapy 82, 85, 98, Trazodone 131, 137 Somatic 105, 112, 167, 169, 220 Trichotillomania 119, 171 delusions 56, 83 Suppression 207, 210 Tricyclic antidepressants 77, 131 passivity 13, 55 Synaesthesias 46 Trifl uoperazine 66 Somatisation disorder 104, 105 Synanon 45 Trifl upromazine 66 Somatoform Syndrome of subjective doubles 87 Tuberous sclerosis 159 autonomic dysfunction 106 Systematic desensitisation 94, 131, 215 Type disorder 104 A Somnambulism 140 T behaviour 148 Somniloquy 140 personality 147 Tactile hallucinations 38 Specifi c I and Type II schizophrenia 61 Tadalafi l 132 arithmetic disorder 163 Types of psychiatric emergencies 221 developmental disorder of TCAs 81, 82, 184 motor function 163 Temporal U speech and language 163 arteritis 28 personality disorders 113 lobe epilepsy 31 Ultra-rapid cycling 74 phobia 93 Test judgement 15 Unconscious 205 reading disorder 162 Testamentary capacity 230, 231 Undifferentiated schizophrenia 60 Index 261

Unilateral ECT 202 Volatile solvent use disorder 51 Worthlessness 71 Unipolar depression 69, 75 Voluntary admission 232 Urophilia 126 Von Domarus law 55 X Vorbeireden 102 Xenophobia 93 V Voyeurism 125 Vagal nerve stimulation 199 Y Valproate 30, 79, 191 W Y-BOCS 96 Valproic acid 191 Waxy ﬂ exibility 59 Yog nindra 219 Valpromide 191 Wernicke’s encephalopathy 27, 38 Yoga 92, 107 Van Gogh syndrome 60 Wernicke-Korsakoff syndrome 27, 38 Yohimbine 132 Varenicline 52 Wihtigo 110, 111 Vascular surgery 132 Windigo 111 Z Verbigeration 56, 59 Withdrawal Verdenaﬁ l 132 Zalpelon 137, 197 state 33, 34 Violence 227 Ziprasidone 66, 169 Vipasna 219 symptoms 40 Zolpidem 137, 197 Visual hallucinations 29, 38, 56 syndrome 37, 46 Zoophilia 126 Vocal tics 168 Word approximations 56 Zoophobia 93 Voices Work-shift 140 Zopiclone 137, 197 commenting 55, 56 World (Mental) Health Report 2001 Zotepine 66 heard arguing 55, 56 238, 239 Zuclopenthixol 66