The neuropsychiatry of stroke John O’Donovan

Stroke Third most common cause of death post MI and cancer 11% of deaths in UK and Wales 20% of acute beds and 25% of long term beds occupied by stroke patients Acute focal neurological deficit resulting from vascular disease. TIA not very accurate really, concept of less then 24 hours, note TIA with risks can suggest a 30% chance of a full stroke happening. Be cautious with these patients!

Types of stroke Nearly all arterial, less then 1% is venous. 85% are infarctions 15% are haemorrhagic, which can be intercranial or subarachnoid 3 mechanisms of ischemic stroke, thrombosis, embolism or hypoperfusion.

Risk factors Age: incidence doubles each decade post 55 Hypertension: 25% of adult population 140/90 Smoking Diabetes: 2 fold increase A fib: 5% of over 60s, 4% per year risk of stroke Dyslipidemia Alcohol Obesity Carotid stenosis Drug misuse

Lacunar Stroke Small discrete lesion, generally deep tissue and associated with hypertension/ischemia. 5 classical types 1: pure motor hemiparesis 2: sensorimotor 3: pure sensory 4: ataxic hemiparesis 5: dysarthria/clumsy Hand

Lacunar Stroke 2 Can be associated with cognitive impairment Can be associated with depression Can be silent Can be associated with unusual sub types such as antiphospholipid AB syndrome and CADASIL No cortical signs No neglect DWI test of choice. If pronnounced may cause leucoaraiosis

Large Vessel Disease Cortical signs Note: amarosis fugax Generally large vessel occlusion, embolic Tends to be MCA territory ACA is less common Lesion site is obviously important for presentation

Haemorrhage Much less common, 10-15% Much worse outcome Big risk is hypertension

SAH Nearly always rupture of an aneurysm Mortality of 50% 10/100,000 incidence Risks: genetics, connective tissue problems, smoking, hypertension, female sex Also AVM Cavernous angiomas

Rare causes of stroke CADASIL Venous Shunting, PFO Moya moya disease Carotid dissection Vasculitis Thrombophilias Mitochondrial Farby’s disease

Psychiatry and stroke Psychiatric patients Medical patients Risk factors Smoking Increased mortality Insulin resistance Poor compliance with medical therapy Common problem Post stroke depression or mood changes Post stroke emotionalism Post stroke cognitive impairment Stroke risk and development of dementia

Stroke and psychiatric effects Basic ideas Certain stroke syndromes are likely to cause specific presentations. Stroke may not always be apparent. As patients get older the odds of having cerebrovascular disease increases. Stroke is very common and should be considered in atypical depression, cognitive impairment or any unusual psychiatric presentation.

Prevalence of psychiatric disorders post stroke • Depression:  35%
• Mania: rare
• Bipolar disorder: rare
• Anxiety disorder: 25%
• Apathy : 20%
• Psychosis: rare
• Pathologic affect 20%
• Catastrophic reaction: 20%

Depression post stroke Prevalence studies vary from 10-79% depending on location of study, time of study and case ascertainment. In general hospital studies report higher rates. Interesting clinical point is that depression more or less immediately post stroke does not predict further problem Depression at six months, suggests ongoing problems for another year.

Risk factors for depression post stroke Definite Argued Prior psychiatric illness Dysphasia Poor social support Age Gender Lesion location Lesion volume Impaired ADLs

Clinical features Core psychopathology Stroke related depression Core features of sustained low mood and anhedonia need to be distinguished from common medical problems such as fatigue and sleep disturbance. Concentrate on cognitive features. Some authors argue in favor of a more somatic approach Peak at 3-6 months post event. Generally prevalence reduces by up to half at one year.

Mechanism Psychological Physical Weak evidence of lesion location High rates in many medical illnesses Treatment effects, are not very convincing Loss and obvious psychological mechanisms Loss of role, independence, future effects High prevalence of depression in stroke Frontal striatal mechanism Lesion location, head of caudate, frontal akinesis etc Differential response to noradrenergic anti depressants Occurs in anosognosia

Post stroke depression treatment Psychological Pharmacological Firstly depression post stroke is clearly both psychological and biological Rehabilitation is crucial Pain management Social supports Encourage independence again, sense of future hope Good evidence for SSRIs post stroke Suggestion that they may prevent depression post stroke and improve rehabilitation outcomes. Cochrane database reviews do not give clear outlines for any intervention

Post stroke mania Rare 1-5% prevalence Classically non dominant temporal lobe However this is a non robust finding Increased rate in BPAD patients Concept of manic defence for exams Treatment with antipsychotics/mood stabilisers (note increased risk of CVA with anti psychotics and dementia)

Post stroke apathy Apathy Depression Absence of concern about the environment and self Little interest in doing things Frontal type initiation, not uncommon in stroke Look at lesion location, frontal? Trial of ADTs anyway? Some suggest that noradrenergic and or stimulants more effective nearly always has features of apathy Distinction difficult Generally core cognitions will distinguish

Post stroke anxiety disorders 20% of post stroke patients. GAD and panic No clear evidence about what treatments are best. Frequently interlinked with depression

Post stroke catastrophic reactions Up to 19% post stroke Associated with basal ganglia lesions and frontal lesions Outbreak of severe distress when unable to perform simple tasks secondary to new disability. Release phenomena commonly

Hyperemotionalism Pathological affect Emotional lability Inability to control affect in response to emotional or other stimuli Frequently seen as part of a pseudobulbar affect. Some evidence for SSRIs (weak-case series data)

Psychosis post stroke Allegedly very rare in longitudinal case series with prevalence below 1% I doubt this and would suggest that it depends on how long the psychosis must last to be identified, certainly stroke is not uncommonly associated with delirium and this frequently is associated with psychosis.

ACAM anuerysm Can cause a WKS Same structures as affected in Wernick’e anatomically Patients can end up profoundly amnestic, with a degree of confabulation from disruption of thalamic connections. Generally seen post SAH/neurosurgery.

Hypoxic ischemic encephalopathy Any age Most commonly describe in children Also adults how suffer pump failure/global hypoperfusion/hpoxia/CO poisoning Selective hippocampal loss and watershed infarcts, vulnerable areas Global cognitive problems but classically amnestic due to hippocampal damage.

Head of the caudate lesion In this example bilateral Classically associated with outflow problems from basal ganglia to frontal cortices “akinetic mutism” Can mimic catatonia but acuity of onset is classical.

Bilateral thalamic damage Can occur in general from embolic causes (rare) When it does occur, prominent psychiatric features can result of disorientation, impaired memory, visual hallucinosis and longer term amnestic type state. Diencaphalic amnesia Can also be similar to bilateral caudate problems.

Bilateral occipital/parietal stroke In general hospital, most commonly seen post CABG Hypoperfusion injury or embolic Can have a very odd presentation and frequently the team seek psychiatric opinion. Generally has features of cortical blindness and visuospatial integration problems

Conclusion Stroke is very common Significantly complicated by psychiatric disturbance Need to consider physical rehab, psychiatric and psychological aspects Sometimes a trial of treatment when things are not clear is a valid option. Remember language disturbance may make diagnosis difficult