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Psychiatric Sequelae of Acquired Brain Injury Ken Barrett

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Psychiatric Sequelae of Acquired Brain Injury Ken Barrett Advances in Psychiatric Treatment (1999), vol. 5, pp. 250-260 Psychiatric sequelae of acquired brain injury Ken Barrett Improvements over recent decades in acute care of when the head strikes a hard objectwhichbreaches the brain-injured now ensure that all but the most the skull and meninges and penetrates the brain. severely injured survive. The legacy ofthatsurvival This type of injury carries the highest risk of post­ is an increasing number of people with enduring traumatic epilepsy. Relatively small areas of brain organic mental disorders. Here, I will focus upon damage in the brain stem, usually arising from thepsychiatricsequelaeoffive types ofseveresingle­ extreme flexion orextension injuries oftheneck, can insult brain injury: head trauma, subarachnoid result in very prolonged periods ofcoma followed haemorrhage, and hypoxic, hypoglycaemic and bya range ofenduringsensory, pyramidalandbulbar postencephalitic injury. Thrombotic stroke is a problems, but higher cortical functions may be common and important cause of brain injury but intact. Head trauma sets in train a range ofphysio­ the psychiatric consequences have been more logical processes which can be and often are more extensively studied and are fairly well-known damaging than theimmediate traumaticinjury. This (Robinson & Price, 1982; Starkstein et aI, 1987). includes cerebral haemorrhage and oedema, with Damage due toalcohol and associated malnutrition the risk of coning and respiratory arrest. Massive is also well-docwnented Oacobson & Lishman, 1987, release ofneurotransmitters, particularlyglutamate, 1990). Neither will be specifically addressed here, leads to an opening ofcalcium channelswithcyto­ thoughsomeofthe consequencesofbrain injury are toxic consequences. There are now a variety of similar, regardless ofcause. strategies for limiting the damage caused by these processes and this has lead to higher rates of survival, though with ever new patterns of severe and lasting damage. Repeated minorhead trauma, Five causes of brain injury as occurs in boxing, can also lead to brain damage, particularly in the basal ganglia (Corsellis, 1989). Head trauma The contribution of brain damage to chronic post­ concussive syndromes following a single minorhead injury remains uncertain (King, 1997). About1 in10 000 peopleeach year (Medical Disabil­ itySociety, 1988) sufferssevereandpersistentdisability as a result ofhead trauma. Head trauma can lead to Subarachnoid haemorrhage varying patterns of brain injury. Diffuse axonal injury is most likely to occur when there is rapid Subarachnoid heamorrhage (SAH) can occur as a deceleration, leading to oscillating compression consequence ofhead injury butalsooccursspontan­ waves within thebrainsubstance. This type ofinjury eously due to rupture of an arterial aneurysm, is common during road traffic accidents in which leakage ofan arterio-venous malformationorother the head itself may appear relatively unmarked. cerebral pathology. The annualincidence is about6 Penetrating injury can occur due to a missile such per 100000 of the population (Storey, 1972). as a gunshot, but in the UK occurs morecommonly Aneurysmscanoccurin manylocationsbutthemost Ken Barrett has been a consultant neuropsychiatrist for 10 years and is also Senior Clinical Lecturer in the Department of Psychiatry, Keele University. His main interest is in chronic neuropsychiatric disorders. The Neurobehavioural Unit in Stoke (Haywood Hospital, High Lane, Burslem, Stoke-on-Trent ST6 7AG) is one of few NHS units specialising in psychiatric problems following brain injury. He also chairs the UK Psychiatrists Brain Injury Group. Seqllellle of Ilcquired lmlill ill;/lry ,\PT(1999), "0/. ;, p. 2;1 common is at the junction ofarteries in the circle of Willis which sits below the frontal lobes. Brain injury Psychiatric disorders occurs following aneurysm in a number of ways: for example, a large volumeofblood can cause local following brain injury pressure, midline shiftor coning; orarterial spasm can result in hypoperfusion for several hours There are a numberofreasons whybraininjury may resulting in hypoxic damage. The inferior and increase the risk ofdeveloping mental illness. Brain medial frontal lobes and medial temporal structures injury may: increase the constitutional vulnerability are most commonly damaged and for this reason to major mental illnesses; impair the ability to adjust psychiatric sequelae are relatively common, partic­ and adapt to life change; lead to a loss of role and ularly personality change and depression. In employment, break-up relationships and produce addition, a wide range of physical disabilities can financial hardship. There may also be persistent result, including visual deficits and epilepsy. physical disabilities such as hemiparesis, ataxia, visual field or hearing loss, aphasia and epilepsy. Hypoglycaemic and hypoxic Because ofthe wide rangeofcomplex problems that injury follow brain injury the Care Programme Approach (CPA) provides a very useful management frame­ Hypoglycaemic brain damage occurs owing to work. Box 1 summarises the main questions to be accidental ordeliberate insulin overdose. Hypoxia considered in assessing people with brain injury. can have many causes including cardiac arrest, Box 2 presents the classification of the psychiatric drowning and choking, butnon-accidental injuries sequelae ofbrain injury according to lCD-tO. This includinghangingand carbon monoxide poisoning paper will concentrate upon organic affective arealso common. Hence, in many peoplewhohave disorder, organic delusional and schizophrenia-like hypoxic or hypoglycaemic injury the mental state disorders and organic personality disorder. First, immediately prior to injury is oftenoneofdepression coma and delirium will be discussed. withsuicidal features. The annual incidenceofthese forms ofinjury is not known. The areas ofbrain that Coma and delirium are most vulnerable to hypoxic/hypoglycaemic A 35-year-old man suffered a head injury in a road damage are those that have high metabolic rates. traffic accident and was in coma for three days. On The hippocampi and basal ganglia are particularly recovering consciousness he became restless and sensitive to damage and, while attention and aggressive. He did not believe he was in hospital, memoryproblemsarethe mostcommonafter-effects, said the nurses were trying to kill him and attempted manyoddbehaviouralsyndromescandevelop includ­ to leave. He was assessed bya psychiatrist who found ing bizarre dissociative disorders (Eames, 1992). him to be disoriented in time and place and acutely Cardiac arrest with subsequent resuscitation can anxious about the harm he believed was about to be lead to damage in areas of the brain with less rich done to him. He knew that he had suffered a head circulation (the 'watershed areas') and the conse­ injury but believed he was deliberately run down. quences includecomplex 'transcortical' dysphasias. He was detained in hospital under a section of the Mental Health Act 1983 and was transferred to an acute psychiatric ward. He appeared less anxious in Encephalitis that environment and received only two doses of a major tranquillizer. He settled quickly thereafter and after three days, had become fully oriented. There Herpessimplex encephalitishas anannual incidence were no psychotic features hence he was discharged ofabout 1per1 000 000 ofthe populationper yearand from his section. is oftenidentified and treated onlywhentheillness is well-established.lllness suggestive ofencephalitis in Coma is caused by dysfunction of the reticular whichnospecific pathogenisfound isprobably more activating system (RAS) in the brain stem. This can common. Herpes simplex can cause focal inflam­ occurasa resultoflocal compressionorfor metabolic mation and damage in any area of the brain but the reasons. The period ofcomaendswhenRAS function mostcommonarea tosuffer the mostsevere damageis resumes. In the transition to full alertness there will the medial temporal area. At its most severe this can be a period of drowsiness and inattention (i.e. lead toprofoundmemoryandconcentrationproblems, delirium). During this periodoftransitionsomepeople andeven 'Kluver-Bueysyndrome' includingagnosia, are quiet and docile but many are not and a wide hyperorality, agitation and altered sexual behaviour. range ofbehavioural, emotional, perceptual abnor­ This mixofsymptomsandsignsofvaryingseverityis malitiescanoccur. These includeelation, emotionality, referred to as the 'postencephaliticsyndrome' inleD­ irritability and aggression, feelings ofpersecution, 10 (World Health Organization, 1992). perceptual misinterpretations orhallucinations. The APT(1999), 1101. 5, p. 2S2 Barl'ett/Enmcs mental state during this period of post-traumatic psychiatric assistance is frequently sought. The delirium can change every few hours and the state psychiatrist's role is to establish whether or not may resolve quickly. The precise cause of the delir­ diagnoses other thandelirium are present (e.g. a pre­ ium is sometimes unclear and it is easy to miss a existing psychosis ormajordepressive disorder) and case of alcohol or tranquillizer withdrawal in the whether factors other than the brain injury may be aftermath of head or multiple injury. Electrolyte contributing (e.g. metabolic disturbance, alcohol or disturbance, particularly hyponatraemia, may con­ tranquillizer withdrawal), and to advise on or take tribute, although this is more common after neuro­ over the management of emotional sequelae. surgery. A pre-existing psychotic
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