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 CADASILNo cortical signs No neglectDWI test of choice. If pronnounced may cause leucoaraiosis

Large Vessel Disease

Cortical signs Note: amarosis fugax Generally large vessel occlusion, embolicTends to be MCA territoryACA is less common Lesion site is obviously important for presentation

Haemorrhage

Much less common, 10-15%Much worse outcomeBig 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 AVMCavernous 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• Risk factors • Smoking • Increased mortality • Insulin resistance • Poor compliance with

medical therapy • Common problem

Medical patients• 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• Prior psychiatric illness • Dysphasia • Poor social support

Argued• Age • Gender • Lesion location • Lesion volume • Impaired ADLs

Clinical features

Core psychopathology• 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

Stroke related depression• Peak at 3-6 months post

event. • Generally prevalence

reduces by up to half at one year.

Mechanism

Psychological • 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

Physical• 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 • Firstly depression post

stroke is clearly both psychological and biological

• Rehabilitation is crucial• Pain management • Social supports• Encourage independence

again, sense of future hope

Pharmacological• 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 • 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

Depression• 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 WKSSame 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 encephalopathyAny 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