sign in sign up
<<
Home , Emotional conflict, Psychogenic amnesia

J7ournal ofNeurology, Neurosurgery, and 1993;56: 1149-1156 1149 J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.56.11.1149 on 1 November 1993. Downloaded from

NEUROLOGICAL EMERGENCY

Acute behaviour disturbances

GG Lloyd

Psychiatric disorders are commonly encoun- Affective disorders tered in neurological practice and most neu- The fundamental disturbance is a change of rologists accept the need to assess and mood (or ), either or elation. manage behavioural problems. The more However, mood disturbance is not necessarily complicated cases require expert psychiatric the most prominent symptom and it may be intervention and, for optimum care, it is masked by a wide range of other abnormali- essential that there is close collaboration ties which at first sight suggest the presence of between neurologist and psychiatrist. organic disease. Affective disorders have a Many neurological conditions, particularly tendency to recur. When the recurrences those with cerebral involvement, increase the always take the same form, the condition is risk of developing a psychiatric disorder. referred to as unipolar affective disorder; Furthermore psychiatric disorders can be when the mood change varies between associated with symptoms such as headache, depression or elation it is described as bipolar dizziness and weakness which suggest neuro- affective disorder. logical disease but for which no organic explanation can be found. This phenomenon, DEPRESSIVE DISORDER known as somatisation, is being increasingly Depression not associated with organic dis- recognised and accounts for a substantial pro- ease usually presents to the neurologist with portion of patients who are referred to neuro- symptoms such as headache, dizziness, dis- logical departments. turbance of higher mental function and facial Schiffer' evaluated a consecutive series of or bodily .4 Psychological symptoms, 241 patients attending an American neurol- emotional conflicts, and life stresses may not ogy service and found that 101 (41.9%) had be volunteered and are only elicited by tact- symptoms sufficient to warrant a psychiatric ful, direct questioning on the part of the diagnosis according to DSM-III criteria. Of examining doctor. Fitzpatrick and Hopkins5 57 inpatients, 10 were considered to have a assessed a series of patients referred to a neu-

primary psychiatric disorder and five of these rologist with headaches not due to structural http://jnnp.bmj.com/ had no neurological illness. Among 184 out- disease and found that 37% had an affective patients, 32 had a primary psychiatric disor- disorder of at least mild severity. The preoc- der and 30 of these had no neurological cupation with pain may dominate the clinical illness. Kirk and Saunders2 had previously picture to such an extent that the patient does described a retrospective survey from a neu- not appear depressed and does not readily rological clinic in northeast England and admit to depressed. This has been reported that, during a four year period, 358 described in relation to facial pain6; the cogni- (13-2%) of 2716 patients had a psychiatric tive features of depression such as self on September 28, 2021 by guest. Protected copyright. disorder with no evidence of neurological ill- reproach, suicidal thinking and psychomotor ness. retardation were uncommon but, in addition If the psychiatric disorder underlying the to pain, the patients complained of , neurological symptoms is not recognised, fatigue, , and agitation. patients can be subjected to unnecessary and Depression also complicates existing neu- expensive investigations3. They may receive rological disease. In some cases-for exam- symptomatic treatment which fails to alleviate ple, spinal cord injuries,78 depression appears their condition and they will become dissatis- to result largely from the personal and social fied with the result of their treatment and try implications of the neurological disability. to consult other specialists in the of In diseases in which there is cerebral in- finding a more effective remedy. volvement, the aetiology of depression is Some of the psychological symptoms and more complex. The mood disturbance may behavioural disturbances which the neurolo- be triggered by the emotional impact of the Department of gist encounters are of sudden onset and disease but may also result from structural Psychiatry, Royal require urgent . This review pathology, possibly through interference Free Hospital, describes the clinical features and manage- with neurotransmitter pathways within the London, UK G GLloyd ment of those disorders which are most likely . Depressive disorders with cerebral in- Correspondence to: to give rise to acute behavioural problems in volvement are classified as the organic mood Dr Uloyd neurological practice. disorders by the International Classification 1150 Lloyd J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.56.11.1149 on 1 November 1993. Downloaded from of Disease (ICD-10).9 One of the most signif- should evaluate the patient as soon as icant features of these disorders is that the possible. A number of management options, mood disturbance, either depression or including outpatient or day hospital treat- , may be the first manifestation of ment, are available according to the perceived underlying neurological pathology. 10 risk and availability of social support. When of unrecognised physical illness the risk is high and the patient has little in the should be particularly high if there is no clear way of support, admission to a psychiatric psychosocial precipitant, if the ward should be advised; this may have to first presents in middle or late life and if there involve invoking the Act if the is no family or personal disposition to psychi- patient cannot be persuaded to accept volun- atric illness." tary admission. Depression has been described as a presenting feature of cerebral tumours,12 Stupor multiple sclerosis,"3 14 Parkinson's disease'5 16 Stupor is another serious complication of and Huntington's chorea17 18 but most atten- depression. It is a term that leads to disagree- tion has been given to its association with ment between neurologists and psychiatrists, cerebrovascular disease. Eastwood et al 19 re- who use it in different ways. It is sometimes ported that 10% of patients in a stroke reha- used to describe an intermediate stage on the bilitation inpatient unit had a major spectrum of impaired consciousness that depressive disorder, while 40% had symp- eventually leads to coma. Lishman29 argues toms of minor depression. Robinson et al 20 that this is an incorrect use of the concept studied patients admitted to hospital after an which he believes is more appropriately acute stroke and found that 27% demon- defined as a syndrome in which the patient is strated symptoms of major depression, while conscious but makes no spontaneous move- 20% had symptoms of minor depression. The ment and shows little response to external association between mood disturbance and stimuli; in the most advanced form of stupor severity of physical impairment is not a strong the patient is completely mute and immobile. one and it has been proposed that the site of Consciousness is inferred by the fact that the vascular lesion is important in determin- there may be purposeful eye movements, fol- ing post-stroke depression. Left-sided lesions lowing the actions of other people in the in the frontal lobe or basal ganglia have been vicinity, and also by the patient's of particularly implicated.2' Other reports have events once recovery has occurred. In psychi- not confirmed this hypothesis and have found atric practice, depression and a lower prevalence of depressive illness, espe- are the commonest causes of stupor.30"3 The cially when the survey has included patients diagnosis depends on eliciting a history of the not admitted to hospital.22 relevant symptoms during the weeks before Some patients with cerebrovascular disease the onset of stupor. In the case of depression experience mood disturbances that are too there is a history of progressive psychomotor brief to justify the diagnosis of a depressive retardation in addition to the psychological illness.2' This phenomenon, known as patho- symptoms of low mood, and self logical emotionalism, is manifest by rapid reproach. A full neurological evaluation, in- changes of mood, sudden episodes of crying, cluding CT of the brain, is essential before a can be made with and inappropriate and uncontrollable laugh- diagnosis . http://jnnp.bmj.com/ ter. This type of mood change has been Cerebral disorders that can give rise to the observed more commonly in patients with clinical picture of stupor include , lesions in the left frontal and temporal areas. encephalitis, and cerebral tumour or cyst in the upper midbrain or posterior diencephalon Assessment ofsuicide risk causing increased intracranial pressure. The risk of is one of the reasons why depression can become an acute medical Management ofdepressive disorder problem and it must be considered when Depression usually responds to a combined on September 28, 2021 by guest. Protected copyright. assessing any patient who is thought to be approach of antidepressant medication and depressed. The risk is increased in several cognitive therapy. Tricyclic antidepressants neurological disorders,2425 particularly multi- (amitriptyline, imipramine) are still the main- ple sclerosis, epilepsy, head injury, and spinal stay of treatment but are poorly tolerated in cord lesions. association with physical illness and prescrib- The most important consideration is ing practice is slowly changing in favour of whether the patient is expressing active suici- the selective serotonin re-uptake inhibitors dal intent, either spontaneously or in (SSRIs) (fluoxetine, paroxetine) because of Table 1 Risk factorsfor response to direct questioning. Table 1 shows their lower risk of side effects. Monoamine suicide in depressed the profile of demographic factors that oxidase inhibitors (phenelzine, tranylcypro- patients increase the risk of suicide, which has mine) are also effective in depressive illness. Previous suicide emerged from various studies of people who They are used by some psychiatrists as the attempts * Male sex have attempted suicide; a knowledge of these preferred drug when depression is accom- * Increasing age is important when assessing a depressed panied by , phobic symptoms, weight * Living alone * Social patient.2S25 gain, , and fatigue. For many * Recent bereavement If the risk of a suicide attempt is consid- years they have been underused because of * Unemployment Drug and alcohol ered to be significant, or if there is of their interaction with tyramine- misuse about this, the neurologist should consult containing foods, potentially resulting in a * urgently with a psychiatrist colleague who catastrophic rise in blood pressure. Various Acute behaviour disturbances 1 151 J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.56.11.1149 on 1 November 1993. Downloaded from foods, alcoholic drinks, and drugs have had to has been reported to complicate cerebro- be avoided by patients taking monoamine vascular disease, brain tumour, and head oxidase inhibitors. This problem has been injury. Most reported cases have had lesions overcome by the introduction of reversible involving the limbic or related areas of the and selective inhibitors of monoamine oxi- right hemisphere; there is also an increased dase subtype A, such as moclobemide. prevalence of a family history of affective dis- All antidepressants take up to two to three order suggesting that both genetic and weeks to produce a clinical effect. In some anatomical factors are important in the devel- clinical situations this delay may be danger- opment of mania secondary to neurological ous and a speedier response to treatment is disease.'2 A study of mania following closed required. Electroconvulsive therapy (ECT) is head injury reported that six of 66 patients the preferred treatment in these situations, (9%) had features of mania at some stage particularly when the risk of suicide is high, during a 12-month follow-up period, this fig- or when the patient is stuporose and is not ure being higher than has been reported in maintaining adequate nutrition or fluid other brain-injured people. In this study intake. ECT may have to be given under the mania was associated with temporal basal terms of the Mental Health Act if the patient polar lesions; no links were established with is incapable of giving informed consent to the severity of brain injury or previous per- treatment; in England and Wales this involves sonal or family history of psychiatric obtaining a second opinion from a psychia- disorder." trist appointed by the Mental Health Act Commission. Table 2 shows the main indica- Management of acute mania tions for ECT in depressive disorder. Treatment is best carried out in hospital; if the patient is already in a neurology ward, Table 2 Indications for electroconvulsive therapy in transfer to a psychiatric ward is desirable. depressive disorder Because of the lack of insight which is charac- teristic of mania compulsory admission may * Severe depression with high risk of suicide * Depressive stupor have to be arranged. The three groups of * Depressive disorder with psychotic symptoms drugs which are used regularly in acute mania * Failure to respond to an adequate course of an antidepressant are phenothiazines (such as chlorpromazine), * Inability to tolerate side effects of antidepressants butyrophenones (for example, haloperidol) * If physical illness makes antidepressants less safe than ECT and lithium. Chlorpromazine can be given orally starting at a dose of 25-50 mg eight hourly, increasing to a maximum daily dose of 1500 mg according to the clinical re- There are no absolute contraindications to sponse. When oral treatment is not accepted ECT. A decision on treatment should be an intramuscular injection of up to 150 mg taken after careful consideration of the risks can be given but this should not be repeated of the various treatment options weighed because of its irritant effect on muscle tissue. against the risks of continuation of the Haloperidol can be started at an oral dose of depressive disorder. 5 mg eight hourly increasing to a maximum daily dose of 100 mg. When speedier control

MANIA of symptoms is required, an intramuscular http://jnnp.bmj.com/ The symptoms of mania are in many ways the injection of 10-20 mg can be given. Lithium opposite of those of depression. There is ele- carbonate, in a daily dose of 800-1200 mg, is vation of mood accompanied by an enhanced well tolerated but has a slower onset of effect sense of well being, physical and mental over- than the other drugs. It is most effective when activity, pressure of speech, flight of ideas, given in combination with chlorpromazine in increased self confidence, and a loss of social acute mania but its main use is as a long term inhibitions. Some manic patients are predom- prophylactic drug in recurrent affective inantly irritable rather than elated, particu- disorder. on September 28, 2021 by guest. Protected copyright. larly when other people do not share their Phenothiazines and butyrophenones are views of their own abilities. In severe forms of likely to produce a variety of extrapyramidal mania, the inflated self esteem may develop side effects, especially in patients with exist- into of a grandiose or religious ing brain damage. Akathisia, Parkinsonism, nature and there may be auditory or visual acute dystonia and tardive dyskinesia are well hallucinations in keeping with the prevailing established complications. Akathisia, a sub- mood. Lesser degrees of mania are referred to jective sense of motor restlessness, leads to as hypomanic episodes when the severity of hyperactivity and an inability to relax. It can symptoms does not lead to severe disruption be wrongly attributed to a worsening of the of work or . Mania is a serious manic condition, so an inexperienced clini- condition if the symptoms are not treated cian may increase the dose of neuroleptic adequately. Impaired judgement can lead to rather than reduce it and consequently the accidents, catastrophic overspending, and akathisia symptoms worsen. A fl-adrenergic promiscuity with its attendant risks of infec- blocking drug such as propranolol is an effec- tion. Sustained overactivity eventually leads tive remedy once the condition is diagnosed. to exhaustion or cardiovascular collapse. Acute dystonias can also give rise to diagnos- Mania is a much rarer problem than tic . They can present with tongue depression in neurological practice and only protrusion, torticollis, oculogyric crisis or small series of cases have been described. It opisthotonos and these are often wrongly 1152 Lloyd J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.56.11.1149 on 1 November 1993. Downloaded from diagnosed as dissociative (hysterical) reac- injuries actually sustained may be quite triv- tions. Rapid relief of symptoms can be ial. The experiences which evoke the response achieved with an intravenous dose of 5-10 include natural disaster, road traffic acci- mg of procyclidine. dents, military or terrorist activity and being If manic symptoms do not respond to the victim of torture or rape. The disorder medication, ECT can prove to be a quick and has been estimated to occur in 10% of effective treatment. patients who sustain multiple injuries after road traffic accidents.34 There is a delay between the traumatic Anxiety and -related disorders event and the onset of symptoms which Patients with anxiety and allied conditions ranges from a few weeks up to six months. may present to neurologists if their symptoms The typical symptoms include recurrent are intermittent and of sudden onset. intrusive of the event ('flashbacks'), disturbed sleep, of the event, PHOBIC ANXIETY DISORDERS emotional blunting, avoidance of cues that A is an abnormal, disproportionate evoke memories of the original trauma, of an object or situation which leads to depression, irritability, and autonomic avoidance of the object or situation that pre- . cipitates it. is the commonest phobia encountered clinically and symptoms Management ofanxiety and stress-related attributed to neurological disease are particu- disorders larly prominent; these include headache, Behaviour therapy, involving and impaired concentration, dizziness, and a fear gradual exposure to the precipitating situa- of falling. The clue to the diagnosis comes tion, is of proven value in phobic disorders from eliciting a link between the symptoms and in disorder when there is avoidance and specific situations which invariably pre- behaviour. A clinical psychologist should cipitate them. In the case of agoraphobia the assess the patient and organise treatment if commonest triggers are open spaces, crowded behaviour or cognitive therapy are considered streets, supermarkets, and public transport. appropriate. Phenelzine is a useful adjunct to psychological methods of treatment. Drug treatment is more important in spontaneous The characteristic features are recurrent panic attacks; both phenelzine and episodes of overwhelming anxiety which are imipramine have been shown to be effective. unpredictable and not confined to a particu- There has been considerable in the lar situation. The somatic symptoms of anxi- psychological treatment of people who have ety, notably palpitations, chest pain, been involved in accidents or disasters and hyperventilation, and dizziness, usually domi- who are at risk of developing post-traumatic nate the picture but there is also intense psy- stress and other psychiatric disorders.35 Early chological anxiety, often involving a fear of intervention is believed to be important.'6 going mad or dying from a heart attack or Various techniques have been used including brain tumour. This may be accompanied by psychotherapy and cognitive therapy. The depersonalisation which the patient describes essence of treatment is to allow the patient to

as an altered sensation in his body which feels relive the experience and ventilate the emo- http://jnnp.bmj.com/ lifeless or unreal as if he has lost his tional response in a cathartic manner and to and is observing himself from the outside. prevent the development of avoidance behav- Panic attacks may be mistaken for the aura of iour. If symptoms have become established, temporal lobe epilepsy, vestibular disease or either tricyclic antidepressants or monoamine the early manifestation of multiple sclerosis. oxidase inhibitors can provide symptomatic Non-neurological conditions that need to be relief.37 considered in the differential diagnoses are hyperthyroidism, phaeochromocytoma, hypo- on September 28, 2021 by guest. Protected copyright. glycaemia, and supraventricular tachycardias. Dissociative (conversion) disorder A typical attack lasts only a few minutes This group of disorders is also known as con- but tends to recur. Patients become appre- version . The term hysteria is a con- hensive of recurrent episodes and some learn troversial one and is used in several different to avoid certain places where an attack would ways; as a result it has been omitted from be particularly embarrassing, such as a public both DSM-III and ICD-10 but it is still place far from home from which there is no widely used as a diagnostic category in clini- easy escape route. Thus panic attacks come cal practice. to be associated with agoraphobic behaviour Dissociative disorders are characterised by in some patients. symptoms that suggest lesions in the motor or sensory pathways of the voluntary nervous POST-TRAUMATIC STRESS DISORDER system. There is loss or distortion of neuro- This syndrome is a delayed response follow- logical function which cannot be adequately ing exposure to a stressful experience of an accounted for by organic disease.38 Psy- exceptionally threatening nature which is chiatrists would also want to establish positive quite outside the range of everyday experi- evidence that the symptom is linked to psy- ence and which is likely to cause distress to chological factors,39 either previous severe almost everyone. There is a perceived danger stress, emotional conflict, or an associated of death or severe physical trauma but the psychiatric disorder. It is assumed that the Acute behaviour disturbances 1153 J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.56.11.1149 on 1 November 1993. Downloaded from symptoms are not intentionally produced, and not when the patient is alone or asleep. as in , but are a result of Some episodes simulate partial motor seizures unconscious motives. This, however, is a or simple faints. Others occur in rapid succes- notoriously difficult distinction to make and it sion without recovery of consciousness and often appears that the degree of insight into they may be accompanied by deliberate the nature of the disability varies from time to tongue biting or incontinence so the clinical time. picture mimics status epilepticus. In addition Dissociative disorders are thought to be to the clinical features of the attacks, certain declining in incidence. A survey at the demographic characteristics help to distin- National Hospital, London, indicated that guish pseudoseizures from true epilepsy. the diagnosis was made in approximately 1% Patients with pseudoseizures are more likely of inpatients.40 The commonest symptoms, to have a family history of psychiatric illness, which are usually of acute onset, are motor a personal history of psychiatric illness, previ- weakness, altered sensation, gait disturbance, ous suicide attempts, sexual maladjustment, and pseudoseizures.4' The neurological exam- and current affective disorder.44 ination reveals characteristic abnormalities Dissociative, or psychogenic, can that enable the experienced neurologist to also create diagnostic problems.45 There is a make a confident diagnosis in most cases.42 sudden loss of , usually in relation to Weakness usually involves whole movements a markedly stressful event. The amnesia is rather than muscle groups and it affects the selective and predominantly involves the extremities much more often than ocular, inability to recall emotionally charged memo- facial, or cervical movements. Various clinical ries. The ability to learn new information is techniques can be employed to show that relatively preserved as are cognitive skills such weakness of a limb is associated with simulta- as reading and writing. A characteristic fea- neous contraction of opposing muscle groups. ture is a loss of personal identity; the patient There is discontinuous resistance during test- is unable to recall his name, age, address, ing of power ("give way weakness"), muscle occupation, and family details and may fail to wasting is absent, and reflexes are normal. recognise his relatives when they visit. Sensory loss or distortion is often inconsistent Recovery is usually rapid and complete. In when tested on more than one occasion and some cases, however, dissociative amnesia incompatible with peripheral nerve or root lasts for several days or weeks and is accom- distribution. There may be discrete patches of panied by an apparently purposeful wander- anaesthesia or hemisensory loss that stops ing away from home or place of work. During abruptly in the midline. Visual symptoms this condition, known as a dissociative fugue, include monocular diplopia, triplopia, field a new name and identity may be assumed. defects, tunnel vision, and bilateral blindness Self care is maintained and the patient's associated with normal pupillary reflexes. behaviour may appear completely normal to Dissociative gait disturbance, astasia-abasia, people who do not know him. Recovery is recognised by its bizarre character and occurs abruptly and there is amnesia for the intermittent pattern; the patient walks nor- period of the fugue. Organic conditions that mally if he thinks he is not being observed. In need to be considered in the differential diag- some cases, when being observed, the patient nosis of dissociative amnesia included head

actively attempts to fall and this contrasts injury, , epileptic fit, Wernicke's http://jnnp.bmj.com/ with the patient with organic disease who encephalopathy, alcoholic blackout, and tran- tries to support himself. sient global amnesia. Pseudoseizures are more difficult to evalu- Any patient suspected of having dissocia- ate because they are episodic and often co- tive symptoms should be examined carefully exist with true epilepsy. An account from a by a neurologist and psychiatrist. Special reliable observer is invaluable but it is essen- investigations, such as an MRI and EEG tial for the clinician to witness an attack telemetry, are required in some cases before a before making a firm diagnosis. The clinical confident diagnosis can be made and, in a on September 28, 2021 by guest. Protected copyright. features, which simulate epilepsy to a varying few, a decision has to be deferred until the degree, have been described in detail.43 symptoms can be reviewed after a suitable During an attack there is marked involvement time interval. The presence of organic disease of the truncal muscles with opisthotonos and does not rule out a diagnosis of dissociative lateral rolling or jerking of the head or body. disorder. Indeed it is now recognised that All four limbs may exhibit random thrashing neurological lesions and dissociative symp- movements which increase in amplitude if toms occur together more frequently than can restraint is applied. Cyanosis is rare unless be explained by chance. Although the neuro- there is deliberate breath holding. Corneal logical lesion cannot explain the presenting and pupillary reflexes are retained although symptom, coexisting disease of the nervous they may be difficult to elicit because the eye- system may facilitate the emergence of disso- lids are kept firmly closed. Tongue biting and ciative mechanisms and provide a model for urinary micontimence are uncommon unless the symptom.39 This may explain the frequent the patient has some degree of medical occurrence of pseudoseizures in patients who knowledge and has learned from experience also have genuine epilepsy. that they are characteristic features of epilepsy. Management ofdissociative disorder In contrast to true epilepsy, pseudoseizures Once the diagnosis of usually occur in the presence of other people has been established, the results of the clinical 1154 Lloyd J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.56.11.1149 on 1 November 1993. Downloaded from examination and special investigations should illnesses. In most cases they are due to delir- be discussed with the patient together with ium and represent the acute effects on mental reasons for considering the symptoms to have functioning of intracranial lesions, or meta- a psychological basis. This should not be bolic or toxic disturbance elsewhere in the conducted in a confrontational manner. It is body. The characteristic features are alter- best to explain that the symptoms are due to ations of consciousness, muddled thinking, stress, that they are familiar to the clinician, mood change, psychomotor abnormalities- that serious disease has been excluded and either retardation or excitability-and percep- that full recovery can be expected. Requests tual disturbances in the visual or tactile for further investigations should be resisted. senses. In severe cases there are florid visual A reassuring and encouraging approach is and tactile hallucinations. The aetiology and beneficial. Any associated psychiatric disorder management of delirium have already been such as depression should be treated appro- reviewed in this series.48 priately and interpersonal conflicts discussed Delirium arising during treatment of with the patient and key relatives. These Parkinson's disease can often lead to diagnos- patients are often highly suggestible so they tic problems because psychological symptoms respond well to predictions of recovery. may be due to the disease itself or to pre- Given that they are preoccupied with physical scribed drugs. Anticholinergic drugs such as complaints, their recovery can be assisted by benzhexol, procyclidine, and orphenadrine providing a physical framework for improve- can precipitate acute delirium which resolves ment. Physiotherapy is particularly effective when the drug is withdrawn. Quicker resolu- in restoring the power to a paralysed or weak- tion can be achieved by parenteral adminis- ened limb. Using such an approach with tration of the anticholinesterase, physostig- patients with hysterical gait disorders, about mine. Delirium also occurs during treatment half recovered completely during a three to with levodopa but other acute psychological four day hospital stay.46 reactions can develop with this drug includ- In resistant cases an abreaction interview ing depression, hypomania, , under intravenous sedation is useful. Several delusions and hallucinations in clear con- drugs can be used to provide the required sciousness. Clozapine has been recommen- level of sedation but most experience has ded as an effective treatment for psychotic been gained with sodium amytal.47 The pro- disorders associated with levodopa therapy.49 cedure involves slow intravenous injection at This drug is currently available for the treat- a rate of no more than 50 mg per minute ment of resistant schizophrenia; its use is until the sedation threshold is achieved as restricted because of the appreciable risk of judged by drowsiness, slurred speech, and agranulocytosis which occurs in at least 1 % of rapid horizontal nystagmus. This usually cases. The white cell count has to be moni- occurs with a dose of 150-350 mg after tored weekly for the first 18 weeks of treat- which the level of sedation should be main- ment and fortnightly thereafter. Other side tained by further slower injection to a maxi- effects of clozapine include convulsions and mum total dose of 500 mg. During the hypersalivation. interview the patient is encouraged to explore Occasionally transient psychotic disorders and ventilate any emotional problems that develop in clear consciousness in the absence have hitherto not been discussed. This can of other features of delirium. The most strik- have a cathartic effect and is often followed ing clinical symptom is a well developed delu- http://jnnp.bmj.com/ by dramatic improvement which is facilitated sional system, nearly always of a paranoid if the interviewer predicts recovery before and nature. These psychotic disorders are seen during the interview. An interview using amy- most commonly in patients who have been tal can also be useful to clarify the diagnosis admitted acutely to hospital and who have and gain access to undisclosed psychopathol- been treated in intensive care or coronary ogy. It appears particularly useful for disso- care units which they perceive as bewildering

ciative amnesia and should be used if the and threatening. The delusions typically on September 28, 2021 by guest. Protected copyright. memory impairment does not begin to involve the nursing or medical staff treating improve within a few days of its onset. the patient who may accuse them of trying to can be employed as an alternative poison-or even kill him. In response to these procedure if the clinician has sufficient expe- delusions there may be sudden outbursts of rience of the technique. aggression towards members of staff or attempts to leave hospital against medical Somatoform disorders and advice. Psychoses of this nature are probably These disorders tend to be chronic and are precipitated by the emotional impact of the associated with repeated consultations for illness and by the disruption it causes to the physical symptoms and requests for medical patient's familiar environment. investigations despite previous negative find- Acute psychoses without features of delir- ings. They are unlikely to present as emergen- ium or dementia can occur in association cies but as part of a lengthy history, at times with a wide range of cerebral disorders, exceeding 30 years, of chronic ill health and notably epileptic foci, cerebral tumour, cere- contact with medical services. bral trauma, Wilson's disease, Parkinson's disease, and Huntington's chorea. The psy- Acute psychotic disorders chosis can take the form of a schizophrenic or Psychotic symptoms are common compli- affective disorder. The site of the lesion has cations of neurological and other medical been considered to influence the pattern of Acute behaviour disturbances 1155 J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.56.11.1149 on 1 November 1993. Downloaded from

symptoms. A schizophrenic presentation has being upset by minor changes in routine been particularly associated with temporal (38%) 53 lobe lesions in the dominant hemisphere, Brain injury can produce an exaggeration whereas affective disorders have been linked of premorbid personality traits so that a per- with lesions in the non-dominant hemisphere. son with an obsessional personality becomes Not all studies have demonstrated such an even more meticulous and preoccupied with association with laterality.50 detail, whereas someone with a psychopathic personality becomes more impulsive and irre- Management of acute sponsible. Among a group of patients with When the psychosis is believed to be triggered Wilson's disease, psychopathic personality by the perceived stress of the treatment envi- traits were significantly related to the severity ronment it is advisable to transfer the patient of neurological symptoms, particularly as soon as possible to a less intimidating envi- dysarthria, bradykinesia, and rigidity.54 If the ronment-for example, from an intensive damage is localised to particular parts of the care unit to a general ward or from a general brain, the personality changes tend to be ward to the patient's home, if care is available more specific.55 56 Frontal lobe damage is there. Medication may be needed if there is associated with , lack of initiative, tact- aggressive or disruptive behaviour. Chlorpro- lessness, irritability, , and disinhibi- mazine or haloperidol may be given in doses tion. Although the patient's demeanour is similar to those used in acute mania. If very predominantly listless there may be unpre- rapid control of symptoms is required, dictable outbursts of aggression or sexually droperidol can be given intravenously in a disinhibited behaviour. Social skills tend to be dose of 5-15 mg and repeated every four to lost with a failure to consider the feelings of six hours. other people and the impact of tactless These neuroleptic drugs are well recog- remarks. The ability to plan ahead is nised as having unpleasant extrapyramidal impaired with the result that irresponsible side effects. The most dangerous of these, but decisions may be taken with little concern fortunately the least frequent, is the neurolep- about their outcome. tic malignant syndrome in which extrapyra- Irritability and aggressive outbursts are midal rigidity and akinesia develop abruptly especially associated with temporal lobe or within a few days.5' Pyrexia is always pre- pathology. Herpes simplex encephalitis has sent, together with autonomic disturbances an affinity for the temporal lobes, so behav- including profuse sweating, increased saliva- ioural manifestations are common during the tion, hyperventilation, tachycardia, and labile acute stages of the illness and after recovery if blood pressure. Laboratory investigations there is residual brain damage. Patients who show a leucocytosis and a raised creatinine survive temporal lobe damage may manifest kinase. The incidence of the condition is not the features of the Kluver-Bucy syndrome known but is probably well under 1% of all which include hypersexuality, aggressive out- cases treated with neuroleptics if strict diag- bursts, excessive oral behaviour and visual nostic criteria are applied.52 Neuroleptics agnosia. should be stopped immediately once the con- dition is diagnosed. Rapid improvement is Management of aggressive behaviour

seen if a dopamine agonist, such as Table 3 summarises the conditions in which http://jnnp.bmj.com/ bromocriptine, is administered and the mor- unpredictable outbursts of aggression may tality rate has been considerably reduced by occur. this treatment. Patients who are potentially violent should not be interviewed in an isolated room; when the risk is particularly high the doctor should Personality change due to cerebral not be alone with such patients. Adequate disease staff should be available nearby. The immedi- A change in personality is likely to follow dif- ate aims are to control the risk of violence, to on September 28, 2021 by guest. Protected copyright. fuse, severe damage to the brain of the sort diagnose the underlying disorder and to that is commonly seen after major head injury administer specific treatment. A detailed his- but which can also occur in association with tory and full physical and mental state assess- cerebral tumours, cerebrovascular disease, ment are rarely possible; immediate treatment , and encephalitis. The changes in has to be arranged before complete informa- behaviour are persistent and often develop tion is available. gradually but they may lead to sudden out- bursts of impulsivity which create acute prob- lems. A survey of patients who had survived a severe head injury reported that the preva- lence of personality change increased with Table 3 Neurological and psychiatric disorders associated time; at five years after the injury, 74% of with aggression patients were described by their relatives as * Acute delirium having undergone a personality change. * Brain damage-especially to frontal and temporal lobes * Epilepsy Threats or gestures of violence had occurred * Functional psychoses-schizophrenia, bipolar affective in 54% while there had been an actual assault disorder * Alcohol abuse-intoxication, withdrawal on a relative in 20% of cases. Other problems * Drug abuse-intoxication, withdrawal, threatening which had occurred included trouble with behaviour to obtain drugs the law (31%), childishness (38%) and * Personality disorder 1156 Lloyd J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.56.11.1149 on 1 November 1993. Downloaded from

Every effort should be made to calm findings during the initial evaluation. Stroke 1983;14: 736-41. patients by sympathetic understanding and 21 Starkstein SE, Robinson RG. Affective disorders and cere- reassurance. Violence is often a response to brovascular disease. BrJ Psychiatry 1989;154: 170-82. 22 House A, Dennis M, Mogridge L, Warlow C, Hawton K, paranoid experiences and patients can be Jones L. Mood disorders in the first year after stroke. pacified if they believe that the doctor appre- BrJ Psychiatry 1992;158:83-92. 23 House A, Dennis M, Molyneux A, Warlow C, Hawton K. ciates the reasons for their behaviour. If this Emotionalism after stroke. Br MedJ 1989;298:991-4. can be achieved medication may be accepted 24 Stenager EN, Stenager E. Suicide and patients with neu- rologic diseases: methodological problems. Arch Neurol voluntarily; otherwise compulsory treatment 1992;49: 1296-303. becomes unavoidable if patients are endan- 25 Stenager EN, Stenager E, Koch-Henderson N, et al. Suicide and multiple sclerosis: an epidemiological inves- gering themselves or others. Physical restraint tigation. Jf Neurol Neurosurg Psychiatry 1992;55:542-5. should be applied with the assistance of secu- 26 Nordentoft M, Breum L, Munck LK, Nordestgaartd AG, Hunding A, Bjaeldager PAL. High mortality by natural rity staff; the safety of all involved is best and unnatural causes: a 10 year follow up study of ensured by having more than a sufficient patients admitted to a poisoning treatment centre after suicide attempts. BrMedJ 1993;306:1637-41. number of staff available. At least one person 27 Hawton K, Fagg J, Platt S, Hawkins M. Factors asso- should restrain each limb while another ciated with suicide after parasuicide in young people. Br MedJ7 1993;306:1641-4. administers medication.5758 Haloperidol 28 Kreitman N. Suicide and parasuicide. In: Kendell RE, 10-20 mg intramuscularly or droperiodol Zealley AK, eds. Companion to Psychiatric Studies, 5th edn. Edinburgh: Churchill Livingstone, 1993;743-60. 5-15 mg intravenously are the preferred 29 Lishman WA. Organic psychiatry: the psychological conse- drugs, except for cases of alcohol or mis- quences of cerebral disorder, 2nd edn. Oxford: Blackwell, drug 1987. use or patients with serious physical illness. 30 Joyston-Bechal MP. Clinical features and outcome of Benzodiazepines should then be given stupor. BrJPsychiatry 1966;112:967-81. 31 Johnson J. Stupor: a review of 25 cases. Acta Psychiat instead-for example, diazepam 10 mg by Scand 1984;70:370-77. slow intravenous injection or lorazepam 2 mg 32 Starkstein SE, Pearson GD, Boston J, Robinson RG. Mania after brain injury: a controlled study of causative intramuscularly. Once the risk of aggression factors. Arch Neurol 1988;44:1069-73. has been controlled it is nearly always neces- 33 Jorge RE, Robbinson RG, Starkstein SE, Arndt SV, Forrester AW, Geisler FH. Secondary mania following sary to arrange admission to an appropriate traumatic brain injury. Am J Psychiatry 1993;150: inpatient unit to begin a diagnostic evaluation 916-21. 34 Mayou R. Psychiatric aspects of road traffic accidents. Int and specific treatment for the underlying con- Rev Psychiatry 1992;4:45-54. dition when the has been clarified. 35 Rosser R, Dewer S. Therapeutic flexibility in post disaster diagnosis response. JRoy Soc Med 1991;84:2-3. 36 Ramsay R. Post traumatic stress disorder: a new clinical entity? Jf Psychosom Res 1990;34:355-65. 1 Schiffer RB. Psychiatric aspects of clinical neurology. Am 37 Davidson J. Drug therapy of post traumatic stress dis- J Psychiatry 1983;140:205-7. order. BrJ Psychiatry 1992;160:309-14. 2 Kirk C, Saunders M. Primary psychiatric illness in a 38 Marsden CD. Hysteria: a neurologist's view. Psychol Med neurological outpatient department in north-east 1986;16:277-88. England.J Psychosom Res 1977;21:1-5. 39 Lloyd GG. Hysteria: a case for conservation? Br Med Y 3 Lloyd G. Somatization: a psychiatrist's perspective. 1986;294: 1255-6. J Psychosom Res 1989;33:665-9. 40 Trimble MR. Neuropsychiatry. Chichester: John Wiley & 4 Kirk C, Saunders M. Primary psychiatric illness in a Sons, 1981. neurological outpatient department in North East 41 Ljunberg L. Hysteria: a clinical prognostic and genetic England: an assessment of symptomatology. Acta study. Acta Psychiat Scand 1957;32:Suppl 112. Psychiatr Scand 1977:56:294-302. 42 Pincus J. Hysteria presenting to the neurologist. In: Roy 5 Fitzpatrick R, Hopkins A. Referrals to neurologists for A, ed. Hysteria. Chichester: John Wiley & Sons, 1982. headaches not due to structural disease. 7 Neurol 43 Fenton GW. Epilepsy and hysteria. Br J Psychiatry 1986; Neurosurg Psychiatry 1981;44:1061-7. 149:28-37. 6 Lascelles RG. Atypical facial pain and depression Br Y 44 Roy A. Hysterical fits previously diagnosed as epilepsy Psychiatry 1966;112:651-9. Psychol Med 1977;7:271-3. 7 Fullerton DT, Harvey RF, Klein MH, Howell T. 45 Kopelman MD. Amnesia: organic and psychogenic. Br Y

Psychiatric disorders in patients with spinal cord Psychiatry 1987;150:428-42. http://jnnp.bmj.com/ injuries. Arch Gen Psychiatry 198 1;38: 1369-71. 46 Keane JR. Hysterical gait disorders: 60 cases. Neurology 8 Judd FK, Stone J, Weber JE, Brown DJ, Burrows GD. 1989;39:586-9. Depression following spinal cord injury: a prospective 47 Perry JC, Jacobs D. Clinical applications of the amytal inpatient study. BrJPsychiatry 1989;154:668-71. interview in psychiatric emergency settings. Am J 9 World Health Organization. The ICD-10 classification of Psychiatry 1982;139:552-9. mental and behavioural disorders: clinical descriptions 48 Taylor D, Lewis S. Delirium. J Neurol Neurosurg and diagnostic guidelines. WHO: Geneva, 1992. Psychiatry 1993;56:742-51. 10 Lloyd GG. Psychiatry in general medicine. In: Kendell 49 Friedman JH. The management of levodopa psychoses. RE, Zealley AK, eds. Companion to psychiatric studies. Clin Neuropharmacol 1991;14:283-95. Edinburgh: Churchill Livingstone, 1993; 779-92. 50 Feinstein A, Ron MA. Psychosis associated with demon- 11 Whitlock FA. Symptomatic affective disorders. London: strable brain diseases. Psychol Med 1990;20:793-803. Academic Press, 1982. 51 Kellam AMP. The neuroleptic malignant syndrome, so- on September 28, 2021 by guest. Protected copyright. 12 Ron MA. Psychiatric manifestations of frontal lobe called: a review of the world literature. Br J7 Psychiatry tumours. BrJtPsychiatry 1989;155:735-8. 1987;150:752-9. 13 Ron MA, Logsdail SJ. Psychiatric morbidity in multiple 52 Kellam AMP. The (frequentiy) neuroleptic (potentially) sclerosis: a clinical and MRI study. Psychol Med 1989; malignant syndrome. BrJ Psychiatry 1990;157: 169-73. 19:887-95. 53 Brooks N, Campsie L, Symington C, Beatty A, McKinlay 14 Berrios GE, Quemada JI. Depressive illness in multiple W. The five year outcome of severe blunt head injury: a sclerosis: clinical and theoretical aspects of the associa- relative's view. Y Neurol Neurosurg Psychiatry 1986;49: tion. Br_JPsychiatry 1990;156:10-6. 764-70. 15 Kearney TR. Parkinson's disease presenting as a depres- 54 Dening TR, Berrios GE. Wilson's disease: a prospective sive illness. J Irish MedAssoc 1964;54:117-9. study of in 31 cases. Br J Psychiatry 16 Mindham RHS. Psychiatric symptoms in Parkinsonism. 1989;155:206-13. J Neurol Neurosurg Pychiatry 1970;33: 188-91. 55 McClelland RJ. Psychosocial sequelae of head injury: 17 Lyon RL. Huntington's chorea in the Moray Firth area. anatomy of a relationship. Br J Psychiatry 1988;153: Br MedJ3 1962;1: 1301-6. 141-6. 18 Folstein SE, Abbott MH, Chase GA, Jenson BA, Folstein 56 Trimble MR. Behaviour and personality disturbances. In: MF. The association of affective disorder with Hunting- Bradley WG, Daroff RB, Fenichel GM, Marsden CD, ton's disease in a case series and in families. Psychol Med eds. Neurology in clinical practice, vol. 1. London: 1983;13:537-42._ _ Butterworth-Heinemann, 1991; 81-100. 19 Eastwood MR, Rifat SL, Nobbs H, Ruderman J. Mood 57 Sheard MH. Clinical pharmacology of aggressive behav- disorder following cerebrovascular accident. Br Jf iour. Clin Neuropharmacol 1988;11:483-92. Psychiatry 1989;154:195-200. 58 Goldberg RJ, Dubin WR, Fogel BS. Behavioural emer- 20 Robinson RG, Starr LB, Kubos Kbo et al. A two- gencies: assessment and psychopharmacologic manage- year longitudinal study of post-stroke mood disorder: ment. Clin Neuropharmacol 1989;12:233-48.