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Neuropsychiatry matic amnesia (PTA) – the period from those in the absence of injury but injury to the return of continuous there is often more evidence of lability of day-to-day memory. Those with a PTA mood and apathy. Simon Fleminger PhD MRCP MRCPsych , duration of longer than one month are Stroke is a significant risk factor for Consultant Neuropsychiatrist unlikely to return to work. suicide. After TBI, the standardised Mike Dilley BSc MB, Senior House Officer in Table 1 illustrates the range of neuro- mortality rate for suicide is increased Psychiatry psychiatric sequelae observed after stroke. threefold so that about 1% will commit Maudsley Hospital, London Similar problems, with similar prevalence suicide over a 15-year follow-up, the risk rates, are observed after TBI. TBI is asso- remaining fairly constant over this ciated with higher rates of manic- period4. Clin Med JRCPL 2002;2:516–20 depressive illness, and may be particularly A recent systematic review suggests associated with ‘ rapid-cycling’ manic- that there is no relationship between depressive illness (ie periodicity of days lesion location and after Stroke and traumatic brain 5 injury rather than weeks). stroke . Significant depressive symptoms Agitation and aggression, relatively should be treated vigorously (T able2). Neurological symptoms (eg hemiparesis infrequent after stroke, are often seen The fact that they are ‘understandable’ or or dysphasia) are the main cause of dis- after TBI and partly reflect the pre- consist of symptoms that may be a direct ability after stroke. Neuropsychiatric morbid personalit y characteristics of consequence of brain injury (egapathy) complications are likely to make disability those who suffer TBI. Agitation is should not prevent a trial of an anti- worse and possibly increase mortality. common in associatio n with the depressant. Several antidepressants have Most (TBI) is post-traumatic confusional state (see been shown to be effective in post-stroke caused by closed head injury and often section on delirium). Early agitation depression7. Selective serotonin reuptake complicated by alcohol. The vulnera- predicts long-term aggressive behaviour, inhibitors (SSRIs), which have fewer side bility to contusions of areas of the brain which typically is explosive. There is no effects, are a reasonable first choice for involved in social behaviour, cognition evidence that aggression differs from depression after stroke or TBI (Table3). and regulation of mood (medial orbital agitation in terms of its response to If all else fails, ECT is safe for the treat- frontal and anterior temporal lobes 1) medication3. ment of depression after both stroke and partly explains why the neuropsychiatric TBI. sequelae of TBI usually outstrip the Mood disorders Antidepressants are useful in treating neurological sequelae as predictors of emotionalism (lability of mood, emo- outcome. The best predictor of outcome Mood disorders are common in both tional incontinence). Cognitive behav- after TBI is the duration of post-trau- stroke and TBI. They are usually like iour may improve adjustment tostroke. Early educational inter-ven- tions after TBI may prevent later Table 1. Psychiatric syndromes associated with stroke 2. symptoms. Syndrome Prevalence Clinical features (mean % from prevalence studies) Other neuropsychiatric sequelae

Depression: Feeling miserable or hopeless, . TBI probably increases two-to major 20 tearfulness, demotivation, decreased threefold the risk of developing a schizo- minor/subthreshold 21 appetite, weight loss, reduced phreniform psychosis. Olanzapine or interactions quetiapine are reasonable antipsychotics Mania Rare Elevated mood, decreased , to use because they have fewer extra- thought disorder, grandiosity pyramidal side effects. Bipolar affective disorderRare Alternating symptoms of depression and mania Personality changes. Thoughtlessness, Anxiety disorder 25 Uncontrollable fear or apprehension, impulsiveness and irritability are partic- restlessness, somatic anxiety symptoms ularly troublesome changes in person- Apathy without depression 20 Avolition, anhedonia, demotivation ality after TBI. They are common causes Psychosis Rare Delusions, of distress for family and carers, the Emotionalism 20 Impairment in the control of crying problems often being compounded by and, more rarely, laughing apathy and poor motivation. Catastrophic reaction 20 Bursts of aggressive behaviour, anxiety, crying Dysexecutive syndrome . Personality Cognitive impairment 25 Visuospatial neglect, apraxia, impaired learning, reduced attention change is often associated with the dysex- ecutive syndrome in which there is

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Table 2. Management of depression : (National Clinical Guidelines for Stroke 6). brain at the time of injury. A single stroke may be the precursor of • Provide information, advice and the opportunity to talk about the impact of illness multi-infarct dementia. • Assess psychosocial needs Screen for depression and anxiety within the first month of stroke and monitor Parkinson’s disease • mood • Use standardised questionnaires for screening in those who can respond Several neural circuits which link frontal Emotionalism after stroke should be confirmed by a few simple questions at cortex, thalamus and basal ganglia are • interview involved in movement, attention, • In the presence of one syndrome assess for other mood disorders memory and reward processes. This Severe, persistent or troublesome tearfulness (emotionalism) should be treated explains why disorders of the basal • with antidepressants, monitoring the frequency of crying to check effectiveness ganglia, including Parkinson’ s disease • Consider a trial of antidepressant medication in those with persistently depressed (PD), are characterised by abnormalities mood of at least one month duration. If there is a good response, antidepressants of movement, mental state and cognitive should be continued for at least sixmonths function (Fig 1, Table 4) 8. • Consider seeking advice from, or co-managing patients with, liaison professionals in cases of persistent distress or worsening disability Depression

Depression is common in PD. It is asso- Table 3. Factors influencing choice of psychotropic medication . ciated with faster disease progression, more rapid decline in cognitive function • Side effects, particularly cognitive due to anticholinergic medication and activities of daily living, and is a risk • Whether the drug is generally sedative, useful in agitation or anxiety, or alerting factor for developing dementia. It is Drug interactions, particularly with anticoagulant, cardiac and antiparkinsonian probable that both biological and psy- • medications chological factors explain depression in • Drug efficacy in the population of interest PD: • Potential for reducing seizure threshold • Biological: loss of monoaminergic neurones, hypometabolism in caudate, inferior orbitofrontal and impaired problem-solving due to diffi- Cognitive decline . Brain injury may be medial frontal regions on positron culties in planning, prioritisi ng and followed by cognitive decline. Dementia emission tomography. monitoring tasks, and multitasking. pugilistica may develop years after • Psychological: chronic disabling Impairments of concentration and repeated blows to the head, usually in illness, psychosocial stress. memory and psychomotor slowing are boxers. Severe head injuries, particularly also common cognitive symptoms after in men, may predispose to the develop- Treatment of depression . Tricyclic antide- brain injury. Specialist rehabilitat ion ment of Alzheimer’s disease, presumably pressant drugs are effective and may also may be needed. due to deposition of beta-amyloid in the improve motor symptoms by virtue of

Post-concussion syndrome . The relative contributions of brain injury and psy- Key Points chological responses may be difficult to Neuropsychiatric sequelae may exacerbate disability, therefore psychosocial disentangle in the post-concussion syn- problems should be identified early drome. Symptoms include double and blurred vision, noise sensitivity, dizzi- Always search for physical causes for symptoms, particularly in delirium and agitation, and consider drug effects, both prescribed and abused ness, difficulties concentrating, fatigue, head and neck . Anxiety and Always start drug on low dosage and go slowly when prescribing psychotropics; depression tend to occur later after avoid cocktails injury. Similar non-specific symptoms Do not leave depressive symptoms untreated. Selective serotonin reuptake are seen in somatisati on disorders, inhibitors are usually a safe first-choice antidepressant including chronic fatigue syndrome. Interventions such as graded exercises When choosing an antipsychotic for patients after brain injury or with Parkinson’s and cognitive behaviour therapy are disease, choose one with the least extrapyramidal sideeffects if possible appropriate. As in whiplash, being When prescribing psychotropics in epilepsy, monitor anticonvulsant levels involved in a compensation claim may increase symptoms, particularly after KEY WORDS: CPD, delirium, depression, epilepsy, neuropsychiatry, Parkinson’s mild injury. disease, , psychosis, stroke, traumatic brain injury

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good evidence that low-dose clozapine can improve psychosis without worsen- ing Parkinsonism 10 but careful moni- Cortex toring is needed, particular ly in the

Caudate and elderly. putamen Epilepsy and non-epileptic Globus seizures ext pallidus Depression is the commonest neuro- int psychiatric disorder associated with Thalamus epilepsy11 (Table 5). Post-ictal confu- sional states can be associated with psy- chosis and violence. Interictal psychosis resembles schizophren ia. Personality change has been described, but has been pc Subthalamic nucleus pr poorly validated. It is important to identify the relation- Substantia nigra ship of the psychiatric disturbance to ictal events, the role of antiepileptic Fig 1. Basal ganglia and their connections (ext = external; int = internal; pc = pars drugs in the aetiology of symptoms, and compacta; pr = pars reticulata). the importance of psychosocial factors including stigma. For symptoms directly 9 their anticholinergic activity , but their ment medication, particularly subcuta- related to the seizure itself, optimisation sideeffects, including cognitive impair- neous apomorphine, despite dyskinetic of seizure control is the treatment of ment, may limit their use. Although adverse effects. They also show hypersex- choice. SSRIs generally have fewer side effects, uality, hypomanic symptoms and patho- the evidence that they work is not as logical gambling. Psychotropic medication strong, and some have extrapyramidal effects which exacerbate motor symp- Psychosis When considering psychotropic medica- toms. Psychologica l treatments for tion for patients with epilepsy there is depression in PD have not been fully Psychosis in PD, often with visual hallu- always the worry that it will decrease evaluated. cinations and persecutory delusions, is seizure threshold. However, a recent associated with cognitive impairment retrospective study suggests that psy- and recent increases in antiparkinsonian Hedonistic homeostatic chotropic medication does not increase medication. Consideration should be 12 dysregulation mean seizure frequency . It is important given to decreasing or stopping these to start psychotropic medications at low In a condition known as hedonistic drugs. Antipsychotic medication should dose and increase slowly. It has been sug- homeostatic dysregulation, patients take always be used with caution because of gested that SSRIs are less likely to reduce increasingly more dopamine replace- the extrapyramidal sideeffects. There is seizure threshold than tricyclic anti-

Table 4. Neuropsychiatric complications of Parkinson’s disease (PD).

Psychiatric manifestation Frequency (%) Associations

All psychiatric symptoms 70 Depression 50 Female; younger onset; bradykinesia and gait disturbance. ?Correlated with disease progression. cognitive status and ADL Hypomania/ 2/10 Levodopa and DA agonist treatment especially in pre-existing BPAD Anxiety 40 Depression; younger patients Apathy common Executive impairment Psychosis 40 (drug related) Dopaminergic/anticholinergic medications; hallucinations 20% (esp. visual); delusions 3–30% Cognitive impairment 19 with no dementia Older patients, late onset PD; low SES and education; severe EPS 15–40 with dementia

ADL = activities of daily living; DA = dopamine; BPAD = bipolar affective disorder; EPS = extrapyramidal signs; SES = socio-economic status.

518 Clinical Medicine Vol 2No 6November/December 2002 CME Psychiatry depressants. Anticonvulsant drug levels distractable. Attention and concentra- diagnosis of the agitation is . should be closely monitored because tion are impaired (egas demonstrated by Poor sleep, , constipation and sys- there may be an interaction between psy- poor performance on a digit span). They temic illness may be contributory factors. chotropics and anticonvulsant drug are neither alert nor oriented and likely levels, for example fluoxetine may to be agitated and frightened. Psychotic Management of agitation. Some patients increase blood levels of carbamazepine. symptoms with hallucinati ons, often will settle with reassurance and explana- Haloperidol and sulpiride may be less visual, and fleeting delusions may be tion. Relatives may be able to help. epileptogenic than other antipsychotics, elicited. Delirium may also present as a Haloperidol and lorazepam may be used and are therefore the treatment of choice hypoactive withdrawn state akin to to produce rapid sedation. The patient for epileptic psychoses. stupor. should be placed on regular nursing observation, monitoring respiration and Non-epileptic seizures Management of delirium neurological state. If sedation is required for more than one or two days, atypical An important differential diagnosis of After making the patient safe, an attempt antipsychotic medication should be used epilepsy is non-epileptic seizures. These should be made to find the cause. (egolanzapine or quetiapine ) w ith come under the rubric of conversion dis- Numerous physical problems, including which there is less chance of producing orders or dissociative states; they can drugs and drug withdrawal, may be extrapyramidal side effects. V alproate, co-exist with epilepsy and are associated responsible. Nursing should be in a calm carbamazepine and beta-blockers may with sexual abuse and female sex. Recent environment in a sideroom with oppor- be helpful3. Drug combinations should unpublished work suggests that cognitive tunities for undisturbed sleep, consistent be avoided as these may increase agita- behaviour therapy may be effective. staff and plenty of light and things to tion and aggression by increasing confu- occupy the patient 13. sion. Delirium Agitation Delirium, often called an acute confu- References sional state, is characterised by a distur- Agitation is often present in delirium. If bance of the level of consciousness. The the patient has been treated with anti- 1Tranel D, Bechara A, Damasio AR. Decision patient is obtunded, drowsy or highly psychotics, an important differential making and the somatic marker hypothesis. In: Gazzaniga MS (ed). The new cognitive . Cambridge, MA: MIT Press, Table 5. Neuropsychiatric associations with epilepsy. 2000:1047–61. 2Chemerinski E, Robinson RG. The neuro- Symptoms/syndromesFrequency and associations psychiatry of stroke. Review. Psychosomatics 2000;41:5–14. Depression 30–50% 3Fleminger S, Oliver DL, Greenwood RJ. Possible relationship with lesion location (eg TLE) Pharmacological management for agitation Demoralisation and stigma and aggression in people with acquired Increased mortality secondary to suicide brain injury. In: Cochrane Library , Issue 1, Panic disorder Lifetime prevalence 21% 2002. Oxford: Update Software. Can be interictal and peri-ictal 4Teasdale TW, Engberg AW. Suicide after Need for differentiation of panic from seizure activity traumatic brain injury: a population study. JNeurol Neurosurg Psychiatry 2001;71: Psychosis Prevalence 3–7% but failed to use operationalised 436–40. criteria for SCZ or differentiating SLPE/episodic psychosis 5Carson AJ, MacHale S, Allen K, Lawrie SM More common in partial epilepsies et al. Depression after stroke and lesion Possible role of mesial temporal and extratemporal location: a systematic review. Lancet damage as risk factor 2000;356:122–6. Episodic Most commonly post-ictal or drug-induced 6The Intercollegiate Working Party for Affective, psychotic and confusional phenomena lasting Stroke. National clinical guidelines for stroke . up to a week Section 9.1. Psychological impairment. Chronic Debate as to whether chance association or separate London: RCP, 2000. interictal/(SLPE) disorder 7Turner-Stokes L, Hassan N. Depression Inconclusive evidence of increased risk of psychosis in after stroke: a review of the evidence base to TLE or with left-sided focus inform the development of an integrated Non-epileptic seizuresAbnormal illness behaviour care pathway. Part 2: Treatment alternatives. Generally lack features of epileptic seizures but can be Clin Rehabil 2002;16:248–60. difficult to differentiate 8Ring HA, Serra-Mestres J. Neuropsychiatry Can co-exist with epilepsy of the basal ganglia. Review. J Neurol Possible physical and sexual abuse in childhood Neurosurg Psychiatry 2002;72:12–21. 9Rascol O, Goetz C, Koller W, Poewe W , SCZ = ; SLPE = schizophrenia-like psychoses of epilepsy; TLE = epilepsy. Sampaio C. Treatment interventions for Parkinson’s disease: an evidence based

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