Advances in Psychiatric Treatment (1999), vol. 5, pp. 250-260

Psychiatric sequelae of acquired 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 . 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 , 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 , 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 . 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 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 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 illness may also Restlessness is the most common problematic confuse theclinical picture and post-injury delirium symptom in post-injury delirium and, although it sometimesevolves into a manic orparanoid state. may settle within hours, can cause major problems Behaviour disorders in the phase following coma in a surgical or medical environment. Relatives are presenta major problem for neurosurgical staffand understandably apprehensive about having the person home owing to the need for 24-hour observation. Removal from that environment to a more domestic one with trained mental health care 80 1. As e ing people with psychiatric staff can have beneficial effects and avoid the need problem following acquired brain injury to prescribe neuroleptics which may impede recovery (Feeney et ai, 1982). These problems are Look for evidence of: undoubtedly acute and psychiatric in nature, yet Organic delu ional, affective disorder or many acute psychiatric services are reluctant to take adjustment disorder such patients because their problem is 'organic' or Organic per onality di order or less severe because they are considered 'at risk' in an acute per onality change (in particular, ward. Neither reason is valid as in the absence of a and impulsive behaviours includingaggre • local specialist neuropsychiatry service such sion, bizarre or eccentric behaviours) problems are within general adultpsychiatry. That Significant risk of deliberate or accidental said, it is also common for relatives to beresistant to elf-harm or harm to other transfer to psychiatric care. ignificant motor (weaknes, pa ticity, ata ia) or ensory/perceptual (visual, auditory, somatosensory, taste and smell, neglect or inattention) deficit 80 2. ICD-I0 cla ification: equelae of Impairment in verbal communication (expres• acquired brain injury sive and receptive dysphasias, dysle ia• particularly as ociated with left-sided Organic hallucinosis brain damage) Organic catatonic disorder Impairment in non-verbal communication Organic delusional (including schizophre- (inabiHty to u e or interpret emotional tone nia-like) disorder of voice and facial expression; inability to Organic mood (affective) disorder under tand humour, irony, arcasm• Organic dis ociative disorder particularly a sociated with right-sided Organic labile disorder brain dysfunction) Organic personality disorder Cognitive dysfunction (attention and concen• Mild cognitive di order tration, visual, verbal, procedunl and Po t-encephalitic syndrome epi odic memory, equencing, planning, Po t-concussional syndrome problem-solving/cognitive slowing or Other organic personality and behaviour inability to carry out everal ta k simul• disorder due to brain damage taneously) Delirium, not induced by alcohol and other Problems pre-injury (in mental health, psychoactive sub tance learning, personality traits, social skills, Dementia in other pecified di eases cIa • relation hip and employment) ified elsewhere SignHicant relation hip problems (spou e, Un pecified dementia parent, children) Organic amne ic syndrome, not induced by Social welfare need (hou ing, finance, alcohol and other psychoactive ub lance tran port, home aid and adaptation , Otherspecified mental disorders due to brain home care, day care or respite care) damage ....cll"dIlC 01 Ilc/II/ircd 1m/ill il/;I/I"II \ I'1 (/999), ,'0/. ',p. 2,1

Deliriumoften only lastsa few hoursor daysand application ofstandardised psychiatric criteria may reduction ofagitation and related behaviours may be misleading. None the less, depression is an be achieved with sedative medication alone. importantcontributor to disability after injury and Chlormethiazole and clonazepam canbe useful for should be considered, particularly when there is a up to 3-4 days in this context. Porcher et al (1994) deterioration in function in an injured patient who reported that buspirone in combination with had beenimproving. Inthe longer terma numberof carbamazepine was effective in reducing agitation factors can make it difficult for professionals and in four patients in post-injurydelirium. Carbamaz• family members to recognise the presence of epine alone may also be effective. Major tran• depressive disorder. The expression of emotion in quillizers mustbe seen as a last resort and used for facial expressionand toneofvoice may beimpaired asa shortperiodoftimeaspossible. Butyrophenones by right hemisphere, basal ganglia and thalamic rather than phenothiazines are indicated. damage. Dysphasia and dysarthria can make it difficult to understand what is reported, and affective features of depressive disorder can be Organic affective disorder misidentified as nothing more than understandable unhappiness in the face ofhardship. Persistent low Depression mood, , irritability and poormotivation, A 39-year-old teacher suffered a severe head injury withorwithoutotherfeatures ofdepressivedisorder, in a road traffic accident. He was in coma and ventil• should lead to the consideration of a trial of ated for seven days and suffered a severe and nearly treatmentwithanantidepressant, particularly when fatal chest infection. He recovered consciousness after the mental stateorsocial function has deteriorated. 10 days and emerged from delirium at three weeks. A pre-injury history of depressive disorder and He had no focal motor or sensory deficits but had a poorsocial function appear tobe the mostimportant range of cognitive impairments which gradually risk factors for post-injurydepression (Robinson & improved in the months after injury. Previously Jorge, 1994) and brain injury not infrequentlyarises confident and flamboyant, he had become timid and as a resultofself-harm in thecontextofdepression. reserved. The location of focal brain lesions may also be a He returned to teaching after a year, although with a reduced load and a greatly increased dependence factor inthedevelopmentofdepressionbutseparate upon notes and cues. He coped less well with staff studies have implicated lesions in the right frontal interactions and meetings and became more socially (Grafmanet ai, 1986) and leftfrontal Oorgeet ai, 1993) withdrawn. By half-term he was persistently low in areas. Inpractice, mostcivilianbraininjury is diffuse mood, irritable, gloomy about the future and and the neurotransmitter changes that underlie sleeping 12 hours out of 24 at weekends. He was clinicallySignificant depressivedisordersarelikely referred for psychiatric opinion by his general prac• tobe modulated by many factors. titioner and was initially treated with supportive Response to is often satisfactory counselling, without benefit. His mood significantly and the choice of medication should be guided by improved two weeks after commencing antidepres• thedesiretoavoidside-effects. Brain injury increases sant medication but he remained off work for several sensitivity tosedativeeffects, anticholinergic effects months and eventually decided to retire from teaching. may impairconcentration, and there is an increased risk ofepilepsy. Hence itis besttoavoid tricyclics in The frequency of depressive disorder after head the first instance and a selectiveserotonin reuptake trauma has been reported to be as high as 50% inhibitoris the treatmentofchoice. Itis worth noting (Gualtieri & Cox, 1991), and up to 25% following thatlow-dosesedativetricyclics, particularlyamitrip• SAH (Storey, 1972) but the findings of different tyline (10-25 mg) can be valuable in post-injury investigatorsvary widely depending upon sample headacheand sleep-wakecycle problems(i.e. where size, diagnosticcriteria, severity of, and time since, thecycleofsleepis delayed orirregular). Treatment• injury. Nofigures areavailable for the prevalenceof resistant depression should be treated as in non• depression in post-encephalitic, hypoxic and injured people. Althoughelectroconvulsivetherapy hypoglycaemicdamage.Jorgeet al (1993), employing (ECT) is not contraindicated there are few data on standardised assessments and DSM-ill-R criteria, effects ofECT in peoplewithseverebraininjuryand found 23% of a sample of severely head-injured it is best avoided in the first six months after injury. patients met criteria for major depression at three In the aftermath of a severe brain injury many months post-injury, and the rate fell only slightly aspectsofthe injured person's life are affected. The through the first year. However, in the first three ability toengageinemploymentandleisurepursuits monthsafter trauma, sleep, appetite, vitality, temper may be impaired and personality change can lead and otherareasoffunction arecommonly impaired to the breakdown of relationships and social as a direct result of neuronal damage and so the networks, withincreased dependence upon parents /lPT(1999), vol. 5, p. 254 BIl,-rcttIEIlIIICS or spouse. Levels of carer distress, anxiety and Organic delusional and depression are high even five years after injury schizophrenia-like disorders (Brooks, 1990). Psychological supportfor the injured person and their family, and practical help with A 23-year-old accountant suffered a severe head finances and other needs are also important injury in a road traffic accident. He was in coma for components of treatment. Cognitive-behavioural three weeks and in post-traumatic delirium for three and other psychological therapies have been months. Computed tomography brain scan showed reported to be effective in individual cases (Miller, extensive inferior bi-frontal damage. Thereafter, he 1991; Prigatano, 1991). made a remarkable physical recovery although had a moderate a global reduction in intellect, a mild Mania dysarthria and flattened voice intonation, personality change and limited insight into his disabilities. He A 48-year-old engineer fell while rock climbing and expressed doubt about ever suffering a head injury suffered a blow to his right temple. He was only and began to accuse family members of cheating him briefly unconscious but subsequently developed a in various ways. subdural haematoma which required surgical He was referred to a clinical psychologist by a drainage. A computed tomography scan revealed medical rehabilitationist who sought to help him right temporo-parietal damage. He recovered accept and adjust to his disabilities. However, he consciousness rapidly after surgery and was oriented maintained that he would return to his old job and within three days but was restless, had pressure of became increasingly irritable, talking of little else but talk and flight of ideas, was over-familiar, elated and the wrongs he believed had been done to him, at times irritable, and had impaired sleep. He had no particularly by his brother. Heeventually threatened previous history of psychiatric disorder. He settled his brother with a knife, was arrested and subse• quickly on carbamazepine 400 mg/day and the quently detained under the Mental Health Act 1983. medication was reduced and withdrawn a month after He was considered to be suffering from paranoid injury without recurrence of mania. delusions, and he improved greatly over a period of six weeks on sulpiride but was over-sedated and so Brain injury in childhood has been reported in 5% this was replaced with risperidone. He later admitted of people with adult-onset mania (Wilcox & that he had been hearing voices telling him that he Nasrallah, 1987). However, the term 'organic mania' had been 'ripped off' for at least two years and that is usually applied to manic states which follow brain he often heard people in the street or pubs talking injury inadulthood. Thereareover30 cases ofmania about him. These experiences had stopped after three following brain injury in the literature, including weeks on the medication and he then recognised that manic states that merge with resolving post• they were abnormal, although his insight into his limit• traumatic delirium (e.g. Bracken, 1987; Starkstein, ations with regard to employment did not improve. 1988). Organic mania usually develops in the He remained stable after two years on3 mg risperid• one daily, although attempts to reduce the dosage presence of right hemisphere lesions, particularly have been followed by a return of paranoid ideation. when the basal temporal region is injured. The diagnosis is complicated in the early post-injury Several studies have shownhigh rates ofpsychosis period by the fact that restlessness and inattention in people who have suffered brain injury. Davison are common in delirium, and in later stages by & Bagley (1969) after an extensive literature review disinhibition and fatuousness due to frontal injury. concluded that brain injury increased the risk two• Organic mania can be more confidently diagnosed to three-fold, and subsequent research has not when the injured person has regained orientation altered this figure convincingly. While there is also buttheir mental state has altered to include elation, evidence that left temporalleionsare morelikely to irritability, flight of ideas and pressure of talk. be associated with schizophreniform disorders Several treatment approaches are reported in the (Buckley et ai, 1993), most causes ofbrain injury do literature, all on a single case, open trial basis. not restrict damage to a single lobe. A number of Carbamazepine is probably the treatment of first factors cancomplicate theassessment anddiagnosis choice but a more rapid titration may be necessary of psychosis in brain-injured people. In psychosis than in the treatmentofepilepsy (200-400 mg start there is an abnormality in individuals' ability to dose). Valproate, lithium and major tranquillizers correctly interpret what is happening within them have also been reported to be effective. There is no and in the world around them. Brain injury canalter literature on the longer-term prognosis in organic their appraisal of the world in a variety ofways that mania, but in the first instance it is appropriate to are listed in Box 3, and this should bebornein mind assume the episode is a one-off, and gradually when assessing such patients for possible psychosis. withdraw medication. When mania immediately The identification ofdelusional disorders may also follows delirium a gradual reduction can be be impaired by acceptance ofaberrantbehaviouras attempted after only a few weeks. due to injury-induced eccentricity of personality. Seql/dae o!l1cql/imf braill i/ljl/lY APT(1999), vol. 5, p. 255

There is almost no literature addressing the and adverse effects have been conducted in brain• efficacy of antipsychotic treatment in organic injured people. When psychosis fails to respond to delusional disorder, and brain-injured people are antipsychotics a trial ofcarbamazepineorvalproate often rejected from clinical trials ofnewdrugs. While may be worthwhile. No information is available on there have been several single and multiple case the frequency of treatment resistance or the long• reportsofpost-injury psychosis in the past30 years term prognosis in post-injury psychosis. only three included detail ofresponse to treatment. Two cases responded well to neuroleptics (Nasrallah Organic personality disorder et aI, 1981; Vedie et aI, 1993 ) and one did not but responded to carbamazepine (Ritchie et aI, 1989). Based upon his extensive clinical experience One of the mostcommon complaints voiced by rel• Lishman (1998) maintains that most post-injury atives ofbrain injured peopleis that theirloved one's psychoses respond to antipsychotic drugs and this is certainly my experience, but optimum manage• mentshould includea care programme that addres• ses the wide range of problems that can arise as a Bo 3. Factor contributing to impaired result of brain-injury and psychosis. In addition, appraisal of the world after brain injury people withbrain injuryare atincreased risk ofdrug side-effects includingearlyand lateextrapyramidal Memory impainnent may include not only effects, sedation, reduced motivation, and epileptic the ability to learn new information, but seizures. Whenhemiparesishasoccurred,• also the ability to recall old information. blocking drugscan produceorexacerbate spacticity This can include autobiographical detail as well as impairing gait and coordination. Anti• and everal year in an individual' life cholinergic drugs used to treat side-effects are also may be forgotten. Hence, for e ample, more likely to impairconcentration and memory in retirement from work or remarriage may brain-injured people. Sulpiride or risperidone are have been forgotten, with predictable in myexperience usually effective but these are not results. Problems with autobiograpical entirelyfree from extrapyramidaleffects andtheremay memory are particularly common after be a case for considering newer 'atypical' agents right dor o-Iateral injury such as olanzapine and quetiapine as a first line. Perceptual and en ory problems can impair the ability to ee, hear etc., but there may A43-year-old male lorry driver suffered a compound also be sensory neglect, inattention or depressed fracture of the right temporo-parietal anosagnosia - denial of illness region. Several bony fragments were removed from the underlying brain and he was left with a large Impaired elf-awarene and under tanding skull defect. He recovered consciousness after three of other' reactions can occur, particularly days and was immediately very restless and following basal frontal lobe lesions assaultive, and this state only settled with major In receptive apha ia inability to under tand tranquillizers. He became oriented after six weeks what i being aid i often put down to a and insisted on being discharged from hospital. fault in the person speaking. The affected Several attempts to withdraw neuroleptics led to individual may also be unaware that they anxiety, agitation and irritability, but they were them elves are talking nonsen e eventually withdrawn follOWing the development of In receptive apro odia the ability to under• an oral dyskinesia two years after his injury. stand changes infacial expression and voice He subsequently became depressed, anxious and intonation (non-verbal communication) i avoidant, and was inclined to stay in bedwhen at home. Respite and review admissions occurred and during impaired or lost 0 what is said i taken these he appeared quickly to brighten up, participated literall . Hence loss of understanding of in ward activities and denied feeling depressed. His humour, arca m, irony etc. Right pari to• behaviour at home remained the same and after some temporal Ie ions can cau e the e problem time he talked of suicide and appeared threatening In agno ia objects and their purpose cannot to his wife and adult step-sons. He agreed to admis• be correctly identified and this can lead to sion and on this occasion confessed that he believed a wide range apparently odd behaviours his wife and step-sons were planning to kill him, and Compie partial seizures can produce a wide had felt this since his injury. He responded rapidly to range of hort-lived but disturbing en ory olanzapine 20 mg daily, was discharged after three and emotional e periences including weeks and did not revert to his previous behaviour. stereotyped hallucinations and comple Firm recommendations regarding these newer dream-like e periences agents cannotbegiven until studiesoftheir positive APT(1999), i'ol. 5,p. 256 Bal'l'cttlEamcs

personality has changed. Sometimes this is an last ratherthan first resortinthe treatment oftemper exaggerationofprevious personality traits butoften disorders unless psychosis is presentorsuspected. the injured individual is described as being like a Disinhibitedbehaviours ofvarious sorts maybe different person. Occasionally this change is seen amenable to behavioural strategies but consistent as an improvement,butI have only seen this when management - and in severe cases, a specialist a previouslyanxious, worry-prone and obsessional residentialsetting- willbenecessary. Somecentres individual becomes more relaxed and laid back, report success with a combination of behavioural usuallyasa resultofpredominantlyfocal left frontal strategiesinassociationwithdrug treatment (Eames lobe damage. Althoughanyconstellation ofperson• & Wood, 1981) although generalisation to non• ality traits canarise afterbrain injury, three are most residential settings is difficult to achieve. A useful commonly complained of: disinhibited behaviour, review is providedbyCorrigen& Jakus (1994). explosive temper problems and abulia (impaired drive and motivation-literallyan absence ofwill). Abulia

Temperdisorders and disinhibition Abulia occurs when there is damage to the medial frontal lobe structures. This isbelieved tooccurbecause In recent times Blumer & Benson (1975) were the ofdamage toa dopaminergic systemwithits origin first to point out that subtypes could be identified inthe . Hence, damage to themidbrainand within thefrontal lobe syndrome. Orbitalfrontal and the lateral hypothalamus can have the same result anterior temporal damage results in a range of (Fisher, 1983). At its most severe the result of such disinhibited behaviour of various types, often damage is an organic catatonic state,butless severe associated with a reduction in emotional warmth abulic statesarecommonand often overlooked. The and lack of insight. In some cases disinhibition is first deSCription of drug treatment for abulia was confined to a temper disorder. Although temper providedbyOliverSacks (1973) inhisbookAmlkenings. disorders can occur primarily due to damage to L-dopa produced transient but dramatic improve• thesebrainstructures, theyare, inmostcases, multi• ments in drive in people with abulia as a result of factorial inoriginand canbecomplex to manage. In . Ross & Stewart (1981) pro• managing these disorders it is useful to identify if vided the first description ofthe use ofa dopamine there is a warning, trigger or precipitant. Is there , , in the treatment of severe recollection ofthe outburst,and remorse afterwards? abulia, and I (Barrett, 1991) described four cases of Manyfactors cancontribute to thedevelopmentand less severeabulia which were responsive tobromo• maintainance of temper problems including: criptineorlysuride. Therehavesincebeena number depressive disorder; misinterpretation of others' of other reports using this and other dopamine behaviour based upon aprosodia, psychosis or , and although not licensed for this indic• impaired cognition; psychosocial stressors includ• ation bromocriptine is now widely used in brain ing marital/family disharmony and financial injury rehabilitation. Therearea numberofpotential pressures; and physical factors including seizure problems with the use of dopamine agonists (see disorders, pain, alcohol and other drug use (minor Box 4), and these should be borne in mind. That tranquillizers such as diazepam may increase said, dopamine agonists can, when usedcautiously dyscontrol). Poorlycontrolled epilepsymayalso be and appropriately, dramatically reduce disability associated withtemper problems, presumably due in peoplewithno otherhope ofimprovement. to neurophysiological dysfunction intemporal and frontal lobe structures that are important for behavioural inhibition. References A number of drug treatments have been used to reduce aggression following braininjury. There have beencasereports ofcarbamazepineintemperdisorders Barrett, K. (1991) Treating organic abulia with bromcriptine and lisuride. Journal of Neurological and Neurosurgical following brain injury (e.g. Lewin & Sumners, 1992) Psychiatry, 54, 718-721. and a single case report using valproate (Geracioti, Blumer, D. & Benson, F. (1975) Personality change with 1994). It is not known if the anticonvulsant or frontal and temporal lobe lesions. In Psychiatric Aspects of Neurologic Disease (eds D. F. Benson & D. Blumer), pp. psychotropic properties of these drugs lead to their 151-171. New York: Grone & Stratton. beneficialeffects. Occasionally, wherecarbamazepine Bracken, P. (1987) Mania following head injury. British Journal producessedativeeffects, itcanimpairtemper control. of Psychiatry, 150, 69Q-692. British Medical Association & Royal Pharmaceutical Society Minortranquillizers mayalso worsendyscontrol. of Great Britain (1999) British National Formulary. London: Propranolol can be useful and may also reduce BMA and The Pharmaceutical Press. bothagitationand irritability ata widedosage range Brooke, M. M., Patterson, D. R., Questad, K, A., et al (1992) The treatment of agitation during initial hospitalisation from 40 mg daily upwards (Greendyke et ai, 1986; after traumatic brain injury. Archives of Physical Brookeet ai, 1992). Major tranquillizersshould be a and Rehabilitation, 73, 917-921. ~ctfllcltJc o(tJctf"ircd Imlilllll;lIry \Pr (1999),1'01. '), P. 2.')7

Brooks, N. (1990) The head injured family. Journal of Clinical Jacobson, R. R. &: Lishman, W. A. (1987) Cortical and and Experimental Neuropsychology, 13, 1-34. diencephalic legions in Korsakoff's syndrome: a clinical Buckley, P., Stack, J. P., Madigan, c., et al (1993) Magnetic and CT scan study. Psychological Medicine, 20, 63-75. resonance imaging of schizophrenia-like psychoses Jorge, R., Robinson, R. G., Arndt, S. V., et al (1993) Depression associated with cerebral trauma: clinico pathological and traumatic brain injury: a longitudinal study. Affective correlates. American Journal of Psychiatry, 150, 146--148. Disorders, 27, 233-243. Corrigan, P. W. &: Jakus, M. R. (1994) Behavioural treatment. King, N. (1997) Mild head injury: neuropathology, sequelae, In Neuropsychiatry ofTraumJJtic Brain Injury (eds J. M. Silver, measurement and recovery. British Journal of Clinical S. C. Yudofsky &: R. E. Hales), pp. 733-769. Washington, Psychology, 36, 161-184. DC: American Psychiatric Press. Lewin, J. &: Sumners, D. (1992) Successful treatment of Corsellis, J. (1989) Boxing and the brain. British Medical episodic dyscontrol with carbamazepine. British Journal of Journal, 134, 105-109. Psychiatry, 161, 261-262. Davison, K &: Bagley, C. R. (1969) Schizophrenia-like psychoses Lishman, W. A. (1998) Organic Psychiatry (3rd edn). London: associated with organic disorders of the central nervous Blackwell Science. system: a review of the literature. In Current Problems in Medical Disability Society (1988) The Report of the Working Neuropsychiatry: Schizophrenia, Epilepsy, the Temporal Lobe (ed. Party on the Management of TraumJJtic Brain Injury. London: R. N. Herrington), pp. 113-184. British Journal of Psychiatry Medical Disability Society. special publication, no. 4. Ashford: Headley Brothers. Miller, I. (1991) Psychotherapy of the brain-injured patient: Eames, P. (1992) Hysteria following brain injury. Journal of principles and practices. Cognitive Rehabilitation, 9, 24-30. Neurological and Neurosurgical Psychiatry, 55, 1046-1053. Nasrallah, H. A., Fowler, R. C. &: Judd 1. 1. (1981) Schizophrenia• - &: Wood, R. (1981) Rehabilitation after severe brain like illness following head injury. Psychosomatics, 22, 359-396. injury: a follow-up study of a behaviour modification Porcher, E., Filteau, M. J., Bouchard, R. H., et al (1994) Efficacy approach. Journal of Neurological and Neurosurgical of the combination of buspirone and carbamazepine in Psychiatry, 48, 613-619. early posttraumatic delirium. American Journal of Feeney, Gonzales, A, Law, W. A, et al (1982) Amphetamine, Psychiatry, 151, 150-151. haloperidol and experience interact to affect rate of Prigatano, G. P. (1991) Disordered mind, wounded soul: the recovery after motor cortex injury. Science, 217, 855-857. emerging role of psychotherapy in rehabilitation after brain Fisher, C. M. (1983) Abulia monor vs agitated behaviour. injury. Journal of Head TraumJJ Rehabilitation, 64, 1-10. Clinical Neurosurgery, 31, 9-31. Ritchie, E. c., Primelo, R, Radke, A. Q. (1989) Bullet in the Geracioti, T. D. (1994) Valproic acid treatment of episodic brain: a case of organic psychosis. Journal ofNeuropsychiatry explosiveness related to brain injury. Journal of Clinical and Clinical Neurosciences, 1, 449-451. Psychiatry, 55, 416-417. Robinson, R G. &: Price, T. R (1982) Post stroke depressive Grafman, J., Vance, S. c., Swingartner, H., et al (1986) The disorders: a follow-up study of 103 patients. Stroke, 13, effects of lateralised frontal lesions on mood regulation. 635-641. Brain, 109, 1127-1148. Robinson, R. G. & Jorge, R. (1994) Mood disorders. In Greendyke, R. M., Shuster, D. B., Wooton, J. A, et al (1986) Neuropsychiatry of Traumatic Brain Injury (eds J. M. Silver, Propranolol in the treatment of assaultive patients with S. C. Yudofsky & R. E. Hale), pp. 219-250. Washington, organic brain disease. A double blind study. Journal of DC: American Psychiatric Press. Clinical Psychiatry, 8, 23-26. Ross, E. D. & Stewart, R M. (1981) Akinetic mutism from Gualtieri, C. T. &: Cox, D. R. (1991) The delayed neuro• hypothalamic damage: successful treatment with a behavioural sequalae of traumatic brain injury. Brain dopamine agonist. Neurology, 31, 1435-1439. Injury,S, 219-231. Sacks, O. (1973) Awakenings. London: Duckworth. Jacobson, R. R. &: Lishman, W. A. (1987) Selective memory Starkstein, S. E., Robinson, R G. & Price, T. R (1987) Compar• loss and global intellectual deficits in alcoholic Korsakoff's ison of cortical and subcortical lesions in the production of syndrome. Psychological Medicine, 17, 649-655. post-stroke mood disorders. Brain, 110, 1045-1059.

Bo 4. Potential problem with u e of dopamine agonists in brain injury rehabilitation

pathy and lack of pontaneity following brain injury mo t commonly occur within the context ofa depre ive di order. Hence other symptoms of a depressive d.i order hould be ought in the fir t in tance and antidepre ant medication con idered Dopamine agoni t can trigger a range of p ychotic phenomena and should be u ed onlywith careful monitoring, particularly wh re th re i a previou hi tory of P ycho i Although the drug are generally well-tolerated hypotension can occur and 0 a low do age

Starkstein, S. E., Boston, J. D. &: Robinson, R. G. (1988) 3. Temper disorders following braininjury: Mechanisms of mania after brain injury. 12 cases and a review of the literature. Journal of Nervous and Mental a are generally improved byminor tranqui1lizers Diseases, 176, 87-100. b are often caused by factors other than Storey, P. B. (1972) Emotional disturbances before and after malfunctioning brain subarachnoid haemorrhage. In Physiological, Emotional and Psychosomatic Illness (Ciba Foundation Symposium No. c should in the first instance betreated bymajor 8) (eds R. Porter &: J. Knight), pp. 337-343. Amsterdam: tranquillizers Associated Scientific Publishers. d may arise in as a result of psychosis or Wilcox, J. A. &: Nasrallah, H. A. (1987) Childhood head trauma and psychosis. Psychiatric Research, 21, 303-306. depression. World Health Organization (1992) The Tenth Revision of the International Classification of Diseases and Related Health 4. Hypoglycaemic and hypoxic braindamage: Problems (ICD-I0). Geneva: WHO. a often occur in someone who was depressed Vedie, c., Battoum, H. &: Katz, G. (1993) Schizophrenie post-traumatique. La Presse Medicale, 22, 1091-1094. atthe time ofinjury b generally lead to a uniform pattern of brain damage c often result in persistent memory problems Multiple choice questions d can result in bizarre dissociative disorders.

1. Depressive disorder following brain injury: a rarely responds to medication b can be easily identified by carers and professionals c may be the cause of a global deterioration in someone whowaspreviously improving d maybeobscured by extrapyramidal problems MCQanswer and aprosodia. 1 2 3 4 2. Abulia following brain injury: a F a F a F a T a is a form ofmovement disorder b F b T b T b F b mayoccurinthecontextofa depressivedisorder c T c F c F c T c is generally improved by major tranquillizers d T d T d T d T d may beimproved by dopamine agonists such asbromocriptine.

Cotntnentary Peter Eames

Causes of acquired brain injury of brain substance. It is remarkable how rarely psychiatric help is sought for those with this kind of injury. The other kind is found in the injuries It is helpful to consider two different kinds of discussed by Ken Barrett: non-penetrating trauma, acquired brain injury. The more common is stroke, subarachnoid haemorrhage, hypoxia, hypogly• which, like low-velocity penetratinginjury, produces caemia and encephalitis. What distinguishes these severe, often total destruction ofa circumscribed area is the combination of localised and diffuse insults,

Peter Eames is a consultant neuropsychiatrist at Grafton Manor Brain Injury Rehabilitation Unit (Grafton Regis, Towcester, Northants, NN12 75S). For 20 years, his main interests have been in acquired brain injury, in pursuit of which he helped develop the Kemsley Unit at St Andrew's Hospital and Grafton Manor, both units providing treatment and rehabilitation for those with severe behaviour disorders after brain injury. He has also worked in head injury follow-up clinics in district general hospitals.