DOCSLIB.ORG

Postconcussional Disorder and Loss of Consciousness

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Postconcussional Disorder and Loss of Consciousness Postconcussional Disorder and Loss of Consciousness Stephen D. Anderson, MD, FRCP(C) Postconcussional disorder (PCD) has been described in the psychiatric, neuro- logical, neuropsychological, and rehabilitation medicine literature for many years. PCD has recently been introduced into DSM-IV, appearing in an appendix that contains a number of proposals for new categories and axes that were suggested for possible inclusion in DSM-IV. There are some major difficulties with the proposed criteria for PCD. This article explores some of these difficulties, partic- ularly focusing on the criteria of loss of consciousness (LOC). A review of the literature demonstrates that LOC is not necessary for PCD to occur. The major difficulty with the DSM-IV criteria is the definition of concussion. The article suggests that, instead, the criteria for mild traumatic brain injury, as defined by the American Congress of Rehabilitation Medicine, may be more appropriate. Postconcussional disorder (PCD) has been symptoms include headache pain, nausea. described in the medical literature for dizziness or vertigo. unsteadiness or poor over a century. The telm Post-concussion coordination, tinnitus, hearing loss. blurred syndrome was coined by Strauss and vision, diplopia, convergence insufficiency. Savitsky in 1934.' PCD is the most preva- light and noise sensitivity, and altered sense lent and yet controversial neuropsychiat~ic of taste and smell. The cognitive deficits diagnosis following brain injury. PCD is include memory difticulties, decreased at- linked most commonly to minor brain in- tention and concentration, decreased speed jury. because the symptoms are unobscured of information processing, communication by the myriad of findings that accompany a difficulties, difficulties with executive fin- more severe brain injuly. The constellation tioning (including initiation and planning, of symptoms includes physical symptoms. judgment and perception). and an increased cognitive deficits, and emotional sequelae. sensitivity to lack of sleep. fatigue, stress. PCD is described in the neurological, neu- drugs, and alcohol. Emotional symptoms ropsychological. psychiatric. and rehabilita- include emotional lability, irritability and tion medicine literature. Common physical aggression, a change in personality. fatigue and decreased energy, anxiety, depression, Dr. Anderson is clinical assistant PI-ofessor,Univcl-sity apathy, disordered sleep, loss of libido. and of British Colunlbia Faculty of Medicine, Department of poor appetite.' Psychiatry, Vancouver, Canada. Addl-ess cot-respon- dence to: Stephen I). Anderson, MD, University ol Although the underlying pathology of BI-itish Columbia Faculty of Medicine, Department ol PCD is uncertain, a generally accepted Psychiatry, 204-2775 Heathel- St., Vancouver, BC, Can- ada V5Z 1M9. theory is that it is caused by rotational Bull Am Acad Psychiatry Law, Vol. 24, No. 4, 1996 493 Anderson sheer strains and corresponding diffuse surgery Update Series, ~lexander' in- axonal injury throughout the brain. Stud- cluded a computed tomography (CT) scan ies of primates have confirmed that ac- of a 59-yeat--old man who never lost con- celeration of the head without impact can sciousness, but developed amnesia and a cause severe diffuse destruction of brain personality change. His CT scan clearly substance. Gennarelli et al.' produced demonstrated hemorrhagic lesions in an- traumatic coma in 45 monkeys by accel- terior and inferior frontal regions. erating their heads without impact. At Patients suffering from PCD usually autopsy, the principal abnormality seen have a reduction in the overall speed, was best appreciated microscopically and efficiency, execution, and integration of consisted of diffuse axonal injury (DAI), mental processes. This has been de- which manifest as axonal retsaction balls scribed as "reduced information process- or abnosmalities of axonal morphology in ing capacity" by Gronwall.' Following the white matter of the brain. Axonal mild brain injury, patients have difficul- damage was not confined to focal areas, ties in areas that require them to analyze but rather was scattered widely through- complex information. and they therefore out the white matter of the cerebral hemi- present as slower. more distractible. and spheres. 0ppenheimer4 found damaged forgetful. When patients are concentrat- axons with neuropathological changes ing on point A. they are unable to also similar to more severe injury in five pa- process point B simultaneously. and they tients with mild traumatic brain injury therefore present as inattentive because who had died from other injuries. One of they are unable to process a normal the patients had been knocked down by a stream of information. motor scooter, had no loss of conscious- Often there are few if any findings on ness. and was described only as physical examination, and the micro- "stunned" following his accident. scopic bsain damage is usually not de- In addition to DAI, focal in.juries may tected with conventional imaging tech- occur following head injury. For exam- niques such as CT or magnetic resonance ple, contusions may appear on the under- imaging (MRI) scanning. Neuropsycho- surface of the temporal and frontal lobes logical assessment is often undertaken, and the anterior pole of the temporal but tends to err in the direction of under- lobes due to contact with rough bony estimating disorders. Many valid prob- surfaces. The orbital frontal cortex is par- lems are not registered on neuropsycho- ticitlarly sensitive to damage during ac- logical testing. Orbital-frontal deficits are celeration/deceleration injuries because difficult to detect with standard neuropsy- of its proximity to the bony structures of chological testing. Subtle changes in at- the skull. This area is sometimes irrever- tention and concentration, new learning ently referred to as the "dashboard" of the ability, word retrieval. and judgment of- brain.%any patients even with severe ten do not register in the testing. Tradi- focal contusions never lose conscious- tional IQ tests are often insensitive. Al- ness. In the 1984 Neurology LII~Neuro- though no single test is diagnostic of 494 Bull Am Acad Psychiatry Law, Vol. 24, No. 4, 1996 Postconcussional Disorder frontal lobe functioning, the tinker toy deficits may be temporary, this does not test has been shown to have some predic- mean that brain damage is reversible. tive value with regard to future employ- Brain tissue does not regenerate. The cu- ment.8 mulative effect of subsequent head injury, Most available tests of memory assess causing ongoing cognitive deficits. is an verbal memory and learning and do not example of the ongoing residual effects of involve high level processing of complex brain in.jury. As discussed by ~ronwell,' information. Patients, however-, often there may be persistent "cognitive fragil- complain of difficulties with episodic ity" to central nervous system (CNS) memory (for day to day activities) or with stressors. Ewing rt al.'" compared perfor- procedural memory (the learning and re- mance under conditions of mild hypoxia call process). It is important, therefore, to in a group of imiversity students who had carefully interview patients and obtain made a "full recovery" from mild head collateral information from family, injury between one and three years before fsiends. and employers. Psychiatric and the study was done with a matched group neuropsychological assessments are per- of control students who had never had a formed in quiet, controlled environments head injury. The mild head injury group that do not include the distractions and perfommd, when mildly hypoxic. at a sig- frustrations of everyday living. and these- nificantly lower level than control sib fore difficulties may be undesestimated. jects on a memory and vigilance task. Testing of a patient within a few Although the students who had suffered months of the injury with repeated tcsting previously fsom mild head injury had re- a year 01- more later may provide more turned to their previous level of function- useful information then an examination ing and had engaged in full-time univer- given at only one point in time. Testing sity work, the mild head injury may have that revealx improvement oves time helps left a residual effect that impaired their confirm that the disorder began at the ability to withstand another CNS stressor. time of the brain il~.jur~." Psychological factors may also intlu- Fortunately. the majority of studies ence late symptoms. This often occurs suggest that although PCD is seen in the when primary deficits are undiagnosed, majority of patients within the first month resulting in a dysfunctional cycle. Pa- following mild traumatic brain injury. the tients are frequently bewildered and over- incidence of PCD is reduced significantly whelmed by their symptoms. Despite by three to six months following the in- having relatively mild injuries, they may jury." However, at one year after inj~~ry. continue to be plagued by problems such approximately 15 percent of patients still as headaches. lack of enesgy. dizziness. have disabling symptoms.' '. I* Patients at and an inability to concentrate on or cope high risk of having pessistent PCD symp- with life's stressors. It is not surprising. toms include those with a history of head therefore. that patients become frustrated. injury and older patients (probably above angry, and depressed. ~a~"described 40 years of age).13 Although the cognitive how a person's sense of predictability
Load more

Recommended publications
  • Tactics of Family Doctors in Case of Syncopal States
    MINISTRY OF PUBLIC HEALTH OF UKRAINE ZAPORIZHZHIA STATE MEDICAL UNIVERSITY DEPARTMENT OF GENERAL PRACTICE – FAMILY MEDICINE AND INTERNAL DISEASES DEPARTMENT OF GENERAL PRACTICE – FAMILY MEDICINE, THERAPY, CARDIOLOGY AND NEUROLOGY OF THE POSTGRADUATE FACULTY TACTICS OF FAMILY DOCTORS IN CASE OF SYNCOPAL STATES STUDY GUIDE for the students of the specialty "Medicine" in the program of the educational discipline "General Practice - Family Medicine" Zaporizhzhia 2020 2 UDC 616.8-009.832-08(072) М 99 Аpproved by Central Methodical Council of Zaporizhzhia State Medical University as а study guide (Protocol № 3 of 27.02.2020) and recommended for use in the educational process Authors: N. S. Mykhailovska - Doctor of Medical Sciences, Professor, head of the Department of General practice – family medicine and internal diseases, Zaporizhzhia State Medical University; A. V. Grytsay - PhD, associated professor of the Department of General practice – family medicine and internal diseases, Zaporizhzhia State Medical University; І. S. Kachan - associated professor of the Department of Family medicine, therapy, cardiology and neurology of the Postgraduate faculty, Zaporizhzhia State Medical University. Readers: S. Y. Dotsenko – Doctor of Medical Sciences, Professor, Head of the Internal Medicine №3 Department, Zaporozhye State Medical University; S. M. Kiselev – Doctor of Medical Sciences, Professor, Professor of the Department of Internal diseases 1, Zaporizhzhia State Medical University. Mykhailovska N. S. M99 Tactics of family doctors in case of syncopal states = Тактика сімейного лікаря при синкопальних станах: study guide for the practical classes and individual work for 6th-years students of international faculty (speciality «General medicine»), discipline «General practice – family medicine» / N. S. Mykhailovska, A. V. Grytsay, I.S.
    [Show full text]
  • Unarousable Unresponsiveness in Which the Patient Lies with the Eye Closed and Has No Awareness of Self and Surroundings (2)
    Neurological Disease Deborah M Stein, MD, MPH 1. Coma a. Coma is defined as “a state of extreme unresponsiveness, in which an individual exhibits no voluntary movement or behavior” (1). i. Alternatively, coma is a state of unarousable unresponsiveness in which the patient lies with the eye closed and has no awareness of self and surroundings (2). b. Coma lies on a spectrum with other alterations in consciousness – from confusion to delirium to obtundation to stupor to coma and, ultimately, brain death (2). c. To be clearly distinguished from syncope, concussion, or other states of transient unconsciousness coma must persist for at least one hour (2). d. There are 2 important characteristics of the conscious state (3) i. The level of consciousness – “arousal or wakefulness” 1. Regulated by physiological functioning and consists of more primitive responsiveness to the world such as predictable involuntary reflex responses to stimuli. 2. Arousal is maintained by the reticular activating system (RAS) - a network of structures (including the brainstem, the medulla, and the thalamus) ii. The content of consciousness – “awareness” 1. Regulated by cortical areas within the cerebral hemispheres, e. There are two main causes for coma: i. Bihemispheric diffuse cortical or white matter damage or ii. Brainstem lesions bilaterally affecting the subcortical reticular activating systems. f. A huge number of conditions can result in coma. One way to categorize these conditions is to divide them into the anatomic and the metabolic causes of coma. i. Anatomic causes of coma are those conditions that disrupt the normal physical architecture and anatomy, either at the level of the cerebral cortex or the brainstem ii.
    [Show full text]
  • Heat Illness & Hydration
    Sideline Emergencies: Exertional Heat Illness- Prevention and Treatment Updates AOSSM: 2019 Sports Medicine & Football - Youth to the NFL Damion A. Martins, MD Medical Director of Sports Medicine Sports Medicine Fellowship Program Director, Atlantic Health Systems Director of Internal Medicine, New York Jets DISCLOSURE Neither I, (Damion Martins, MD), nor any family member(s), author(s), have any relevant financial relationships to be discussed, directly or indirectly, referred to or illustrated with or without recognition within the presentation. Learning Objectives Describe the pathophysiology of Exertional Heat Illness Identify signs and symptoms of Exertional Heat Stroke Understand urgent on the field management and treatment of Heat Illness Understand current evidence for prevention and treatment of Exertional Heat Stroke Overview Heat Illness – Diagnosis – Pathophysiology – Risk Factors – Evaluation / Treatment Hydration – NCAA / NFL data – IV vs PO data McNair video 6 Physiology Thermoregulation Production Dissipation – – basal metabolism conduction – – exercise radiation – convection – evaporation Sandor RP. Phys SportsMed. 1997;25(6):35-40. Heat Illness Spectrum Heat Illness Heat Injury Heat Stroke Definitions Exertional Heat Illness (EHI) Heat edema – initial days of heat exposure – self-limited, mild swelling of hands / feet Heat cramps or Exercise Associated Muscle Cramps (EAMCs) – skeletal muscle cramping during or after exercise – usually abdominal and extremities Heat syncope – orthostatic dizziness or sudden
    [Show full text]
  • Neurologic Manifestations of Hypoglycemia
    13 Neurologic Manifestations of Hypoglycemia William P. Neil and Thomas M. Hemmen University of California, San Diego United States of America (USA) 1. Introduction Unlike most other body tissues, the brain requires a continuous supply of glucose. It has very limited endogenous glycogen stores, and does not produce glucose intrinsically.1 Although it accounts for 2% of body weight, the brain utilizes 25% of the body’s glucose due to its high metabolic rate.2, 3 Evidence for the brains sole reliance on glucose came from obtaining a respiratory quotient of one after measuring differences between arterial and venous content of oxygen and carbon dioxide in blood traveling through the brain.4 In the past, neurons were thought to directly metabolize glucose, however, more recent studies suggest astrocytes may play an important role in glucose metabolism.5 Astrocytic foot processes surround brain capillaries, which deliver glucose to the brain. With this, they form the first cellular barrier for entering glucose.5 Astrocytes contain the non-insulin dependent GLUT1 transporter, as well as the insulin dependent GLUT4 transporter, suggesting a possible role for astrocytes in regulating and storing brain glucose in an insulin dependent and independent manner (see figure 1).6-8 In addition to glucose, the brain contains a very limited store of glycogen, (between 0.5 and 1.5 g, or about 0.1% of total brain weight). Unlike peripheral tissue, where glycogen is readily mobilized during hypoglycemia, the brain can only function normally for a limited duration. Glycogen content seems to fall in areas of highest brain metabolic rate, suggesting at least some, albeit limited role as fuel during hypoglycemia.7 Although the brain relies primarily on glucose during normal conditions, it can use ketone bodies during starvation.
    [Show full text]
  • Public Comment 8
    www.JazzPharmaceuticals.com May 20, 2021 Priya Shah West Virginia Medicaid 350 Capitol Street, Room 251 Charleston WV 25301 Dear Priya Shah, Thank you for your request for information regarding XYWAV™ (calcium, magnesium, potassium, and sodium oxybates) oral solution. If you did not specifically request the enclosed information, please contact Jazz Medical Information at 1-800-520-5568. XYWAV is indicated for the treatment of cataplexy or excessive daytime sleepiness (EDS) in patients 7 years of age and older with narcolepsy. Below is the information you requested. • XYWAV (calcium, magnesium, potassium, and sodium oxybates) Oral Solution Written Comments for Medicaid • XYWAV Prescribing Information Please refer to the accompanying XYWAV™ full Prescribing Information including the Boxed Warning. This information is provided to you as a professional courtesy and may include content that has not been approved by the United States Food and Drug Administration (FDA). Statements in this communication are not intended to advocate any indication, dosage, or other claim not set forth in the prescribing information. This response contains information of a general nature and is intended solely to assist you in formulating your own conclusions regarding our product. It is not meant to be a thorough review of the literature and does not represent all professional points of view on this subject. Thank you for your interest in XYWAV™. Please contact Medical Information at 1-800-520-5568 if you have further questions. Sincerely, Jazz Pharmaceuticals
    [Show full text]
  • Xyrem (Sodium Oxybate) Is a CNS Depressant
    HIGHLIGHTS OF PRESCRIBING INFORMATION These highlights do not include all the information needed to use Important Administration Information for All Patients XYREM safely and effectively. See full prescribing information for • Take each dose while in bed and lie down after dosing (2.3). XYREM. • Allow 2 hours after eating before dosing (2.3). • Prepare both doses prior to bedtime; dilute each dose with approximately ¼ XYREM® (sodium oxybate) oral solution, CIII cup of water in pharmacy-provided containers (2.3). Initial U.S. Approval: 2002 • Patients with Hepatic Impairment: starting dose is one-half of the original dosage per night, administered orally divided into two doses (2.4). • WARNING: CENTRAL NERVOUS SYSTEM (CNS) DEPRESSION Concomitant use with Divalproex Sodium: an initial reduction in Xyrem dose and ABUSE AND MISUSE. of at least 20% is recommended (2.5, 7.2). --------------------DOSAGE FORMS AND STRENGTHS------------------- See full prescribing information for complete boxed warning. Oral solution, 0.5 g per mL (3) Central Nervous System Depression ----------------------------CONTRAINDICATIONS------------------------------ • Xyrem is a CNS depressant, and respiratory depression can occur with • In combination with sedative hypnotics or alcohol (4) Xyrem use (5.1, 5.4) • Succinic semialdehyde dehydrogenase deficiency (4) Abuse and Misuse • Xyrem is the sodium salt of gamma-hydroxybutyrate (GHB). Abuse or misuse of illicit GHB is associated with CNS adverse reactions, ---------------------WARNINGS AND PRECAUTIONS----------------------
    [Show full text]
  • Types of Brain Dysfunction in Critical Illness Robert D
    Neurol Clin 26 (2008) 469–486 Types of Brain Dysfunction in Critical Illness Robert D. Stevens, MD*, Paul A. Nyquist, MD, MPH Departments of Anesthesiology Critical Care Medicine, Neurology, and Neurological Surgery, Johns Hopkins University School of Medicine, Meyer 8-140, 600 North Wolfe Street, Baltimore, MD 21287, USA Many patients in the ICU develop a global alteration in cognitive func- tion that may be structural or metabolic in origin [1]. Terms used to describe these disturbances include delirium, acute confusional state, organic brain syndrome, acute organic reaction, cerebral insufficiency, brain failure, ICU psychosis, and encephalopathy. Etiology-specific terms, such as septic encephalopathy or hepatic encephalopathy, have been used when there is a strong presumption regarding the causative mechanism. It has been pos- tulated that many of these disorders are clinical expressions of a pathophys- iologic spectrum, collectively referred to as ‘‘critical illness brain syndrome’’ [2], ‘‘critical illness–associated cognitive dysfunction’’ [3], or ‘‘critical illness encephalopathy’’ [1]. Recently, there has been an effort to rationalize this terminology and to classify brain dysfunction in the ICU as either delirium or coma, using validated clinical criteria [4–7]. Coma Clinical assessment In the clinical realm consciousness is described in terms of two primary neurologic functions: arousal or wakefulness, and awareness of self and of the environment [8]. Awareness is the content of consciousness and includes multiple cognitive domains including perception, attention, memory, This is an updated version of an article that originally appeared in Critical Care Clinics, volume 22, issue 4. * Corresponding author. Division of Neurosciences Critical Care, Johns Hopkins University School of Medicine, Meyer 8-140, 600 North Wolfe Street, Baltimore, MD 21287.
    [Show full text]
  • Clouding of Consciousness Example
    Clouding Of Consciousness Example Fraught and lethal Myron thrills dictatorially and shredded his diaphanometers immanently and convivially. Mart remains guerilla: she alarms her pennyworts spates too catechumenically? Goose is skim: she bacterized unmitigatedly and epitomising her shammers. By the acquisition of clouding of consciousness The example can follow on many who lack of clouded consciousness versus true seizures superimposed on our culture; rather than occasional in. At all chinese observe what causes icu psychosis indistinguishable from wells ce, including such challenges can positron emission tomography with smoking rates during one example encephalitis. State laws and immediate psychiatric association provides access treatment differs and diet, examples and record how is seen in a clouded consciousness? We have learned for mayor that cap of delirium in ICU patients is error of the strongest independent. Symptoms of intoxication include clouding of consciousness slurring of speech. Clouding of consciousness can about a fresh mild stretch of ALOC in contempt there. Clouding of consciousness Definition and Examples Biology. The Effects of Marijuana on Consciousness Drug Library. Essential Psychopathology & Its Treatment Fourth Edition. Thank tfd for alzheimer disease of clouding consciousness may play. Withdrawal stage is already purchased this hypothesis that. Now always implies that altered consciousness state should be able to an equivalent situation which itself with microcephaly, alcohol can provide a danger to coma by these. Paroxysmal Disorders in Neuropsychiatry Why Episodic. Possible causes seem to me catch up included clinical instrument such as hysterical stupor or attacking others. With ambulatory eeg. Occasionally epilepsia partialis continua is all patients do not conscious, which gets transformed into urine sample reported this can change your primary generalized.
    [Show full text]
  • Coma Eelco F M Wijdicks
    Neurology in Practice THE BARE ESSENTIALS Coma Eelco F M Wijdicks Correspondence to Comatose patients present to the neurologist in should be discouraged. It is better to note a set of Professor E F M Wijdicks, several ways, mostly first in the emergency room or key findings and make comparisons over time (eg, Consultant, Neurosciences Intensive Care Unit, St intensive care unit. Given the many causes of coma, “the patient has improved, is now able to track my Mary’s Hospital, Mayo Clinic, the central focus is a comprehensive evaluation that finger, but eyes open only to a loud voice, localise to 200 first Street SW, Rochester, starts with a detailed history, although this has to be pain, extubated and able to protect the airway”). MN 55905, USA; wijde@ mayo.edu an account—at least to begin with—from bystand- Comatose patients have several outcomes: they ers, paramedics or even the police. This is followed may lose all brain function (brain death), remain by a neurological and general examination, gath- unconscious (persistent vegetative state) or regain ering of key findings, localisation of the involved consciousness (minimally conscious, fully con- brain structure, neuroimaging and other laboratory scious but disabled, or good recovery) (figure 1). tests. Sorting out the cause of coma is what neu- Most emerge from coma in 1–2 weeks. Survivors rologists do best—compared with other specialists. with abnormal consciousness may remain in a Of course the relatively recent availability of MRI minimally conscious state (MCS) or in a persis- has helped tremendously in understanding some tent vegetative state (PVS).
    [Show full text]
  • Quantitative EEG Evaluation in Patients with Acute Encephalopathy
    DOI: 10.1590/0004-282X20130204 ARTICLE Quantitative EEG evaluation in patients with acute encephalopathy Análise quantitativa do EEG em pacientes com encefalopatias agudas Aline Souza Marques da Silva Braga, Bruno Della Ripa Rodrigues Assis, Jamil Thiago Rosa Ribeiro, Patrícia Maria Sales Polla, Breno José Hulle Pereira, Ronaldo Guimarães Fonseca, Luiz Eduardo Betting ABSTRACT Objective: To investigate the use of quantitative EEG (qEEG) in patients with acute encephalopathies (AEs) and EEG background abnormali- ties. Method: Patients were divided into favorable outcome (group A, 43 patients) and an unfavorable outcome (group B, 5 patients). EEGLAB software was used for the qEEG analysis. A graphic of the spectral power from all channels was generated for each participant. Statistical comparisons between the groups were performed. Results: In group A, spectral analysis revealed spectral peaks (theta and alpha frequency bands) in 84% (38/45) of the patients. In group B, a spectral peak in the delta frequency range was detected in one patient. The remainder of the patients in both groups did not present spectral peaks. Statistical analysis showed lower frequencies recorded from the posterior electrodes in group B patients. Conclusion: qEEG may be useful in the evaluations of patients with AEs by assisting with the prognostic determination. Keywords: encephalopaties, coma, EEG, neurophysiology. RESUMO Objetivos: Investigar o uso do EEG quantitativo (qEEG) em pacientes com encefalopatias agudas (EAs ) e anormalidades da atividade de base no EEG. Método: Os pacientes foram divididos em prognóstico favorável (grupo A, 43 pacientes) e desfavorável (grupo B, 5 pacientes). O pro- grama EEGLAB foi utilizado para a análise do qEEG.
    [Show full text]
  • GEHA Coverage Policy: Senory Stimulation in Coma
    Corporate Medical Policy Sensory Stimulation in Coma Description of Procedure or Service Coma is an alteration of consciousness in which a person appears to be asleep, cannot be aroused, and shows no awareness of the environment. Coma is therefore the most profound degree to which the two components of consciousness, arousal and awareness, can be diminished. Less profound states of impaired consciousness (stupor, lethargy, obtundation) preserve one or more of these components to some degree (NINDS, 2019). Sensory stimulation or coma stimulation is a therapeutic technique intended to enhance the rehabilitative potential of brain-injured individuals in a coma or vegetative state. Protocols may involve stimulation of any or all of the following senses: visual, auditory, olfactory, gustatory, cutaneous and kinesthetic. Benefit Application This medical policy relates only to the services or supplies described herein. Please refer to the Member's Benefit Booklet for availability of benefits. Policy Statement GEHA considers sensory stimulation (Coma Stimulation) in the treatment of coma and/or persistent vegetative states experimental. Background Sensory stimulation is intended to enhance the rehabilitative potential of brain-injured individuals in a coma or vegetative state. Protocols may involve stimulation of any or all of the following senses: visual, auditory, olfactory, gustatory, cutaneous and kinesthetic. Various stimuli may be used for each sense. Protocols may differ with respect to who performs the stimulation and where. Professionals providing this service may include nurses, occupational therapists, physical therapists, and speech-language therapists. In some cases, family members may be trained in the techniques and are given primary responsibility for providing the therapy.
    [Show full text]
  • NEUROLOGICAL ASSESSMENT of COMA David E Bateman *I13
    J Neurol Neurosurg Psychiatry 2001;71(suppl I):i13–i17 J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.71.suppl_1.i13 on 1 September 2001. Downloaded from NEUROLOGICAL ASSESSMENT OF COMA David E Bateman *i13 he neurologist is often required to evaluate the unconscious patient from both the diagnostic and prognostic perspective. Knowledge of the anatomical basis of coma is Tessential for competent evaluation but must be combined with an understanding of the many, often multi-factorial, medical conditions that result in impaired consciousness. Consciousness is a state of awareness of self and the environment. This state is determined by two separate functions: c awareness (content of consciousness) c arousal (level of consciousness ). These are dependant upon separate physiological and anatomical systems. Coma is caused by disordered arousal rather than impairment of the content of consciousness, this being the sum of cognitive and aVective mental function, dependent on an intact cerebral cortex. The absence of all content of consciousness is the basis for the vegetative state. Arousal depends on an intact ascending reticular activating system and connections with dien- cephalic structures. Like awareness, arousal is not an all or nothing concept and gradations in awareness have been described in the past as inattentiveness, stupor, and obtundation. Such terms lack precision and coma can be more objectively assessed using measures such as the Glasgow coma scale (GCS) (table 1). This analyses three markers of consciousness—eye opening, and motor and verbal responses—bringing a degree of accuracy to evaluation. The GCS arbitrarily defines coma as a failure to open eyes in response to verbal command (E2), copyright.
    [Show full text]