NEURO-PSYCHIATRIC ASPECTS

OF STROKE

Dr. B. DIVYA
(ASST. PROFESSOR)
DEPT. OF PSYCHIATRY,
NRI MEDICAL COLLEGE.
• INTRODUCTION
• RELEVANT NEUROANATOMY
• PATHOPHYSIOLOGY OF STROKE
• NEUROPSYCHIATRIC SEQUELAE
OF STROKE
• Stroke is defined as the sudden loss of blood supply
to the brain leading to permanent tissue damage.

• An ischemic deficit that resolves rapidly without

radiologic evidence of an infarction is termed
a transient ischemic attack (TIA)

• 24 h is a commonly used boundary between TIA and

stroke, although most TIAs last between 5 and 15
min.

• Stroke is a leading cause of neurologic disability in

adults – 3rd most common cause of death
PREVALENCE
POST STROKE NEUROPSYCHIATRIC DISORDERS
DEPRESSION -35%
DEMENTIA-30%
ANXIETY DISORDER-25%
APATHY-20% Most common are
PATHOLOGICAL AFFECT-20% anxiety,depression,
CATASTROPHIC REACTION-20% emotional incontinence
DELIRIUM-13-48%
MANIA-RARE
BIPOLAR DISORDER –RARE
PSYCHOSIS-RARE
NEUROPSYCHIATRIC
CONSEQUENCES OF STROKE

 Location and Size of stroke

 Preexisting Brain pathology
 Baseline Intellectual capacity and
functioning
 Age
 Premorbid Psychiatric H/o
NEUROPSYCHIATRIC SYMPTOMS AND CORRESPONDING NEUROANATOMY

Symptom Neuroanatomical regioneuroanatomical

region

Depression Frontal lobe, Left anterior frontal cortex, Ant

cingulate gyrus, sub genu of Corpus
callosum, Basal ganglia, Left caudate

Mania Infero-medial and Ventro-medial Frontal

cortex, Right inferomedial Frontal cortex,
Anterior cingulate, Caudate nucleus,,
Thalamus.
 r Anterior cingulate gyrus, Nucleus
tAPATHY accumbens, Globus pallidus,
Thalamus
Orbital or medial frontal cortex,
OCD Caudate nucleus, Globus pallidus.

DISINHIBITION Orbito frontal cortex,

Hypothalamus,
PSYCHOSIS Frontal lobes, Left temporal cortex,
Right hemisphere.
PAPARAPHILIA Medial temporal cortex,
Hypothalamus,, Rostral Brain stem
POST STROKE DEPRESSION
• EPIDEMIOLOGY : Most common 35%
• Most develop within first month.
• If untreated duration of major PSD is 9months -1yr , whereas the duration
of minor depression is several yrs.

• ETIOLOGY : Risk factors

Consistent Controversial
• Past psych history • Age
• Dysphasia • Gender
• Poor social support • Impaired ADLs
• Lesion location
• Lesion volume
POST STROKE DEPRESSION AND LESION
LOCATION
• Most with left anterior lesions.

• Especially near the left frontal pole or left caudate

nucleus.

• Left prefrontal lesions are more associated with

acute depression & maybe complicated by aphasia
resulting in patients inability to express the
symptoms.

• Most recent review articles have not supported a

relationship between lesion location and depression
in post stroke patients ( Bhogal et al. 2004).
 EARLY POST STROKE MAJOR DEPRESSSION :

• More strongly related to interruption of networks ( especially in the left

hemisphere in proximity to the frontal pole) regulating emotion associated
with larger lesion volumes.

• More severe (i.e. vegetative & psychological symptoms).

• More functionally impairing.

LATE POST STROKE DEPRESSION :

• Appears to be more reactive to stroke related disability.

COURSE AND PROGNOSIS

• Most impaired patients in ADLs have the most severe depression.

• Recovery in ADLs is significantly worse if a patient has depression following

their acute stroke.

• Between 12 -24 months following stroke, cognitive functions tend to

improve.

• By 2yrs follow up , no difference exists in the severity of cognitive

impairment , regardless of lesion location (Rt vs Lt hemisphere) or
depression status.
• Depression within 3months of
stroke – poor clinical outcomes.

• 3- 4 fold increase in mortality at

10yr follow up.
DIAGNOSIS OF PSD IS DIFFICULT

• Language disorders – Difficulty in expressing or comprehending.

• Cognitive impairment – Lack of insight of depressive symptoms.

• Overlap between symptoms of depression & medical condition secondary

to medication, hospital stay & other medical conditions or stroke itself.
QUANTIFYING DEPRESSIVE SYMPTOMS
• Beck Depressive Inventory (BDI).

• Geriatric Depression Scale (GDS).

• Hamilton rating scale for Depression (HAM –D).

• Hospital Anxiety and Depression Scale (HADS).

• Post Stroke Depression Rating Scale (PSDRS).

• Stroke Aphasic Depression Questionnaire (SADQ

10 ).
CONSEQUENCES OF POST STROKE DEPRESSION

• Longer hospital stays- affect rehabilitation.

• Poorer recovery of activities of daily living.

• Increased morbidity ( more executive

dysfunction).

• Poorer quality of life, even when neurological

symptoms & disability are held constant.
TREATMENT OF POST STROKE DEPRESSION
• Supportive psychotherapy & pharmacotherapy.

• Antidepressants are well tolerated.

• 60% respond to medication.

• PHARAMACOLOGICAL TREATMENT –

• TCAs - Nortriptyline
• SSRIs – Escitalopram, Fluoxetine, Sertraline.
• Psychostimulants – Methylphenidate.
CONSIDER ECT

• Depression -related emergencies , such as repeated suicide

attempts and severe melancholic PSD.

• Refractory to maximal medication management.

• Psychopharmacologic agents cause intolerable side effects.

Electroconvulsive therapy for post-stroke depressed
geriatric patients.
Currier MB 1, Murray GB , Welch CC

These findings indicate that ECT is a generally well tolerated

and effective treatment for depressed, medically ill post-stroke
geriatric patients.
 Prophylactic treatment with an antidepressant
• High incidence of depression after stroke makes
prophylaxis worthy of consideration.

• Specially if patients has

- Prior episodes of depression.

- Left sided lesions.
- History of psychiatric illness.
- Family history.
 ADVANTAGES

• Have effect on serotonin mediated platelet activation.

• Increase compliance with vascular disease medication.

Antidepressants have side effects such as falls, increase

bleeding, seizures and sedation so must be considered while
prescribing to patients.
 NEUROCOGNITIVE IMPAIRMENT
• EPIDEMIOLOGY –
• Vascular dementia -2nd most common.

• Prevalence – 6- 36%

• Post stroke dementia 10% at 1yr & 32% after 5yrs.

• Temporal relationship between stroke and onset of dementia.

• Step-wise progression of cognitive decline.

• Evidence of cerebrovascular disease , Clinical examination and

neuroimaging.
 RISK FACTORS FOR POST STROKE DEMENTIA
Demographic factors Age (>65yrs),
Female
Index stroke factors Haemorrhagic stroke
Dominant hemisphere
Recurrent.
Post stroke factors Infection
Delirium
Seizures
Neuroimaging factors Cerebral small vessel disease.
Cortical atrophy
Medial temporal lobe atrophy.
Post stroke factors Physical impairment
Cognitive decline.
 ASSESSMENT SCALES

• ACE – R ( Addenbrookes Cognitive Evaluation- Revised).

• IQCODE (Informant Questionnaire for Cognitive Decline in

Elderly).

• MMSE ( Mini Mental State Examination).

• MoCA (Montreal Cognitive Assessment).

 TREATMENT

• Treat risk factors of stroke with Anti-platelets, Anti-hypertensives

and Lipid lowering agents.

• AcetylCholinesterase inhibitor agonists ( Donepezil).

• SSRIs for agitation.

• Cognitive remediation therapy.

 ANXIETY DISORDERS

Predictors Protective factors

• EPIDEMIOLOGY –
• Prevalence – 25-30% Low income Older age
• Phobic disorders & GAD are most History of recurrent Social support
common. stroke or TIA

• Comorbid with depression 50%.

More disability Emotional support
• PSTD 18%.
• 20% - within 1month , 23% within 1- Medical comorbidity
5months , 24% at >= 6months.
• 26% & 39 % in men and women respectively.

• More common in cortical & subcortical stroke.

• Anxiety & depression was associated with left cortical lesions and anxiety
alone with right hemisphere lesions.

MANAGEMENT :

• SSRIs , NDRIs.
• Avoid benzodiazepines – cognitive decline.
• Buspirone , Pregabalin.
 Post Stroke Mania
• Rare.
• Risk Factors:
Male gender
Rt Cerebral infarct

• Associated with right-sided stroke.

• LESIONS
• Cortical-Basotemporal or Orbitofrontal
• Subcortical-Frontal white matter,Basal ganglia,Thalamus
 Post Stroke Mania
• CLINICAL FEATURES:

• Expansive/irritable mood, decreased need for sleep, increased goal directed

activity, recklessness, disregard for social constraints, excessive
talkativeness, racing thoughts, excessive laughter and poor judgement

Management
Mood stabiliser and/or atypical antipsychotic
 Post Stroke Psychosis
• Rare complication

• Include Delusions, Hallucinations (which may affect various sensory

modalities; auditory and visual hallucinations are the most common),
Ideas of reference, Thought disorganization, and Regressed motor
behavior

• More prone to have comorbid epilepsy

• Psychotic episodes can also be a manifestation of complex partial

seizures secondary to stroke
• Correlate with right-sided lesions and cortical/subcortical atrophy
TREATMENT:

Atypical antipsychotic - Risperidone or

Olanzapine

Close follow up every 2 weeks, and titration

of antipsychotic dose is recommended.
EPIDEMIOLOGY:

• Apathy is typified by the absence or lack of feeling,

emotion, interest, concern, or motivation and has
been reported frequently among patients with
brain injury, including stroke.

• The estimated relative risk of depression among

apathetic patients was 1.8.
ETIOLOGY: Apathy is a/w PSD and greater cognitive impairment.

• Lesions along the anterior cingulate subcortical circuit (including

cingulate gyrus, frontal cortex, ventral striatum, ventral pallidum,
and magnocellular dorsomedial thalamus)

Poststroke Apathy
• DIAGNOSIS & CLINICAL FEATURES:

• Screening- Apathy rating scale.

• LOSS OF MOTIVATION OR DRIVE which is the required symptom for the diagnosis of
apathy
A/w Older age, depression, and cognitive impairment.

No difference : gender, stroke type, lesion location & measures of ADLs

were examined.

Apathy was a stronger predictor of than

depression.
TREATMENT:

• Post stroke Apathy has been treated with Nortriptyline, Bromocriptine,

Methylphenidate, Amantadine, Selegiline, and Tacrine with some success.

• NEFIRACETAM (900 mg/day) - was significantly better in reducing scores on

the Apathy Rating Scale.

• ?Escitalopram may prove helpful for the prevention of post-stroke apathy.

EPIDEMIOLOGY: Catastrophic reactions are characterized by anxiety,
tears, aggressive behavior, swearing, displacement, refusal,
renouncement, and/or sometimes compensatory boasting.

Prevalence -19%

Comorbidity: 75% - Major depression; 1.24% - Minor depression; 7.44%

- Anxiety
• ETIOLOGY:

• Lesions involving the basal ganglia, anterior lesions.

• Neurophysiological dysfunction rather than intellectual impairment.

• Subcortical damage has also been hypothesized to underlie the

“release” of emotional display by removing inhibitory input to limbic
areas of the cortex.
• DIAGNOSIS AND CLINICAL FEATURES:

• Patients typically present with sudden outbursts of refusal, swearing,

tears and sometimes aggressive behavior.

• This intense emotional reaction is usually provoked by stressful

situations and typically subsides within a few minutes.

• Higher frequency of familial and personal history of psychiatric

disorders- depression.
Catastrophic Reaction Scale (CRS)

LAB DIAGNOSIS , COURSE AND PROGNOSIS & TREATMENT:

Not established.
EPIDEMIOLOGY:

9-10% of patients — Pathological emotions during their admission for care of

acute stroke.

3 months later—7-18%.

ETIOLOGY:

Bilateral interruption of descending neocortical upper motor neuron innervation of

Bulbar motor nuclei.

Crying episodes - Large bilateral pontine lesions.

ETIOLOGY:

Hypothesis - Pathological emotions may arise from partial destruction

of raphe serotonergic neurons or their projections.

Lesions are located along fronto-ponto-cerebellar pathways.

DIAGNOSIS & CLINICAL FEATURES:

Sudden onset of crying, or more rarely laughing, which is out of proportion to the conversation
or situation in which the emotional reaction occurred.

The emotion may last from a few seconds to a few minutes with no residual feelings of sadness
or happiness.

The hallmark features of PLAC are as follows:

> Inability to control crying or laughter;

> Increased frequency of such emotional display;
> Recognition by the patient that the emotional display is inconsistent or excessive to his or
her underlying emotional feelings.
• DIFFERENTIAL DIAGNOSIS: MOOD DISORDER.

• TREATMENT:

• Antidepressant treatment, including both tricyclic and SSRIs, SNRIs significantly

reduce the frequency and severity of PLAC.

• FDA-approved combination drug consisting of dextromethorphan and quinidine

(Nuedexta) is now available with a specific indication for the treatment of PLAC.
POST - STROKE FATIGUE

• Frequency ranges from 29% to 77%.

• Managed with antidepressants and psychostimulants , particularly those

with effects on noradrenergic and/or dopaminergic activity ( bupropion,
venlafaxine and mirtazapine)
POST STROKE SUICIDE

• Two times increased risk of suicide.

• Recurrent strokes, depressive symptoms, more disabiling stroke and right

sided stroke correlated to suicidal ideas.
WITZELSUCHT SYNDROME

• German word witzeln means joke

• Rare syndrome
• Set of pure and rare neurological symptoms characterized by a tendency
to make puns, or tell inappropriate jokes or pointless stories in socially
inappropriate situations
• Most commonly seen in patients with Frontal Lobe disease(Tumor,Stroke)
• Frontal-subcortical circuit dysfunction-pathological joking as compulsion
 SUMMARY

• Depression & anxiety are the 2 most common post stroke syndromes.

• Both depression & anxiety increase morbidity and delay rehabilitation.

• Identification of risk factors & early intervention helps in preventing

morbidity related to neuropsychiatric sequalae.

• Treatment of neuropsychiatric post stroke disorders have the greatest

potential in improving quality of life.