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Dr. Manu Sharma Chairperson: Dr.


What is stroke?
85%-ischemic, 12%-hemorrhagic The association of neuropsychiatric disorders with

cerebrovascular disease has been recognized by clinicians for over 100 years, but it is only within the past 30 years that systematic studies have been conducted.









Adolf Meyer -identified several disorders such as

delirium, dementia, and aphasia that were the direct result of brain injury Bleuler - after stroke melancholic moods lasting for months and sometimes longer appear frequently. Kraepelin concluded that cerebrovascular disorder may be an accompanying phenomenon of manic depressive disease or may itself produce depressive disorder.

In 1956, Redvers- pathological crying
Derek Denny-Brown- the indifference reaction Kurt Goldstein- the catastrophic reaction

(DSM-IV-TR) defines: Poststroke psychotic disorder, mood disorders, and

anxiety disorders as disorders due to cerebral vascular disease or stroke . The only disorder that is specific for cerebrovascular disease is vascular dementia that may be uncomplicated or occur with delirium, delusions, or depressed mood. The other DSM-IV-TR defined disorder that is commonly seen in patients with cerebrovascular disease is minor depression.

inclusive approach in which depressive diagnostic

symptoms are counted regardless of whether they may be related to physical illness etiological approach in which a depressive symptom is counted only if the diagnostician feels that it is not caused by the physical illness substitutive approach in which other psychological symptoms of depression replace the vegetative symptoms exclusive approach in which symptoms are removed from the diagnostic criteria if they are not found to be more frequent in depressed than non-depressed pts.

Post- stroke depression

Epidemiology In community samples mean prevalence for major depression is 14.1 % and for minor depression is 9.1%. For hospitalized patients, major depression is 21.6% and minor depression is 20.0%. The similar data for outpatient studies are 24.0%major depression and 23.9 %minor depression.

Post- stroke depression

Etiology Patients with left anterior lesions developed poststroke depression during the acute stroke period compared with other lesion locations. A previous personal history or a family history of psychiatric disorders Frequency of poststroke depression was 25% in women and 18% in men High neuroticism personality traits and negative life events. 5HT2 receptor binding in the left temporal cortex. Proinflammatory cytokines such as IL-1 activate enzymes such IDO. Lateral orbital frontal circuit abnormalities

Relationship to lesion location

Schematic axial slice of the brain at the level of the body of lateral ventricles. The brain is shown divided into four quadrants, and the number indicates the percentage of patients who had major depression during the acute poststroke period following a lesion whose anterior border lay within that quadrant. Patients with left anterior legions had significantly higher frequency of depression than patients with any other lesion location.

Bilateral injury: left anterior lesions significantly associated

with depression. Physical impairment: relationship strong in the first 6 months. Cognitive impairment: does not directly produce depression, but the two are significantly associated due to common biochemical (serotonergic) mechanisms Aphasia: does not play a causal role, but depression may affect recovery from aphasia Social functioning: relationship between poor social support and depression strong in the first 6 months (especially spousal) Premorbid: subcortical atrophy, female gender and family/personal history of affective/anxiety disorder, high neuroticism, more severe impairment in ADL, negative life event in the 6 months prior to stroke (Morris, 1992; Hirschfield, 1989; Krause, 1986)

Post- stroke depression

RCOP, 2005 An emotional response to sudden onset disability & its assoc changes Altered biochemical balance within the brain producing changes in mood Preceding tendency for/history of depression

Post- stroke depression

A study of growth-hormone response to desipramine

found that growth-hormone responses were significantly blunted in patients with poststroke depression, Suggesting diminished 2-adrenergic activity. The sensitivity of the test was 100%, and the specificity was 75%. Future studies may further examine the validity of endocrine responses as markers of poststroke depression.

Lipsey et al, 1986: n=43 PSD vs primary depression

slowness was higher in frequency among the stroke patients. loss of concentration and interest in primary depression.
Gainotti et al, 1999; PSDS- higher scores on

hyperemotionalism, diurnal mood variation

Paradiso et al 1997: morning depression and anergia thru

out 2 yr follow up loss of libido in early follow up early morning awakening in late follow up.

Post- stroke depression

Course & Prognosis There appear to be a minority of patients with either major or minor depression who develop depressions following stroke that may last for more than 3 years. Depression severity was an independent predictor of severity of ADL impairment. Pts with poststroke depression who responded to treatment with citalopram showed significantly better improvement in ADLs. Major depression following acute stroke is associated with more severe cognitive impairment if the stroke occurred in the left hemisphere.

Post- stroke depression

During the first 6 months following stroke depressed patient has more disability/poor QOL Which Impairs the following area
Help seeking behavior Compliance Life style modification Rehabilitation process Recovery

Post- stroke depression

Delayed onset depression:

(After the first months following an acute stroke) Robinson et al, 1986: - Has similar relation to lesion location as acute depression - No relation to intellectual impairment - Less impairment in ADLs - Higher social functioning - May be related more to perception of poor social support than to disability

Post- stroke depression

Stroke patients with major depression were eight times more likely to die than the than non-depressed stroke patients.
(Morris et al. 1993 ANJP, Ricardo et al 2003 AJP )

Post- stroke depression

Course & Prognosis Mortality Pts with depression, assessed at 3 weeks poststroke, had 50% higher mortality at 1 year compared to nondepressed patients. A 9 year follow-up of patients who had been treated for poststroke depression found that active treatment with nortriptyline or fluoxetine vs. placebo over 12 weeks resulted in increased probability of survival at 6 years follow-up .

Post- stroke depression

Treatment- current evidence 9 placebo-controlled, randomized, double-blind treatment studies on the efficacy of antidepressant treatment of poststroke depression. Nortriptyline, SSRIs There are now 3 studies that have found fluoxetine to be no better than placebo in the treatment of poststroke depression. Transcranial magnetic stimulation

Post-stroke Mania
Epidemiology There are no epidemiological studies that document the incidence or prevalence of this condition. About half of the reported cases involve single or repeated manic episodes without major depression.
Bipolar disorder
Significantly more cognitive deficits as measured by

MMSE scores with p<0.05

Related to subcortical lesions which cause

hypometabolic effects in bilateral brain regions

Post-stroke Mania
Etiology The frequency of right-hemisphere lesions was significantly higher . Lesions associated with mania were either cortical (basotemporal cortex or orbitofrontal cortex) or subcortical (frontal white matter, basal ganglia, or thalamus). PET- focal hypometabolic deficiency in the right basotemporal cortex. Higher frequency of a positive family history of mood disorders.

Post-stroke Mania
The mechanism of secondary mania remains

unknown. The right basotemporal cortex may play an important role. The basotemporal cortex has strong efferent connections to the orbital frontal cortex. The lateral orbital frontal circuit in the right hemisphere may play a role in the etiology of mania. A combination of biogenic amine system dysfunction and release of tonic inhibitory input to the orbital frontalthalamic circuit may lead to the production of mania.

Lesion location

Post-stroke Mania
Diagnosis The symptoms of mania that occurred after brain damage (secondary mania) appeared to be the same as those found in mania without brain damage (primary mania). As with depression, although the current diagnosis is mood disorder due to stroke with manic features, a better diagnostic classification might be mania with poststroke onset.

Post-stroke Mania
Course & Prognosis The course of mania following stroke has not been systematically examined. Anecdotal cases have been reported indicating that recurrent episodes of mania or depression may occur in these patients. Most patients, however, have spontaneous remission of their mania within 3 to 4 months.

Post-stroke Mania
Treatment- current evidence There are no RCTs of the treatment of mania. Data on individual patients with single or recurrent episodes of mania suggest that they respond to lithium. Some may fail to respond to Li or CBZ.

Post-stroke Anxiety
Among community samples, the rate of GAD alone

was 2% and GAD with depression was 8%. Hospital and OP samples found that GAD alone occurred in 5.5% and GAD with depression in 15.2%. The major confound, however, is that the majority of patients with poststroke anxiety disorder also have depression. There have been no systematic studies of panic disorder or other forms of anxiety disorder.

Post-stroke Anxiety
The diagnosis of GAD based on DSM-IV-TR criteria is

termed anxiety disorder due to stroke with GAD. Over the course of 2 years, pts with GAD following stroke had a significantly higher frequency of all diagnostic Sx compared to similar stroke patients without GAD. A study of pts with acute stroke lesions for the presence of anxiety and depressive sx found that GAD (excluding the 6 month duration criteria) was associated with a prior h/o alcohol abuse. GAD particularly with comorbid depression impacts on physical and social recovery from stroke.

Post-stroke Anxiety
The prevalence rates of GAD with and without

comorbid depression are stable at about 20% over 3 years poststroke. (Schultz et al; Astrom et al.) Early onset- assoc with prior h/o psychiatric disorder, including alcohol abuse; mean duration 1.5 months Delayed onset-mean duration of 3.0 months. Pts with GAD and major depression had a longer mean duration of depression.

Post-stroke Anxiety
Treatment- current evidence BZDs 3 randomized double-blind treatment studies were merged to evaluate nortriptyline vs placebo in the treatment of patients with comorbid GAD and depression following stroke. Buspirone less adverse effects, less risk of development of tolerance.

Post-stroke OCD
Patients with acquired OCD had a negative familial

history and later age at onset of OCD symptoms than patients with idiopathic OCD. Relatively similar clinical phenomenology, severity of OC symptoms, and profile of neuropsychological deficits. Cognitive deficits + Frontal-limbic-subcortical circuits (Berthier et al, Neurology, 1996) Case reports suggest that both antidepressants and behavior therapy can be effective.

Post-stroke Psychoses
Rare case reports
No epidemiological study

3 factors may be important in the mechanism of organic hallucinations: a right-hemisphere lesion involving the temporoparietal cortex, seizures, and/or subcortical brain atrophy.

Lesion location

A schematic template of lesion location in post-stroke psychosis.

Post-stroke Psychoses
Capgras/Fregoli right hemisphere infarcts
Hallucinosis can be caused by various lesions in the

calculi cortex, fusiform gyrus, midbrain/pons (LHermitte peduncular hallucinosis) Rx: one utilizing anticonvulsant therapy and the other antipsychotic medication.

The absence or lack of feeling, emotion, interest, concern, or motivation. Using an apathy scale, in 80 consecutive patients with single stroke lesions, 9 showed apathy as their only psychiatric disorder while another 11% had both apathy and depression. Lesions involving the posterior limb of the internal capsule. Lesions along the anterior cingulate subcortical circuit (including cingulate gyrus, ventral striatum, ventral pallidum, and magnocellular dorsomedial thalamus).

Apathetic patients (with or without depression) were

significantly older. More severe deficits in ADLs. 50% meet criteria for both apathy and depression. Severity of impairment in ADL strongly associated with severity of apathy than severity of depression (Hama et al).

Treatment- current evidence Nortriptyline, apomorphine, and amphetamine. Nefiracetam (900 mg/day) was significantly better in reducing scores on the Apathy Rating Scale compared with placebo. (not FDA approved) Treatment trials are urgently needed to address a problem that can be devastating to the recovery of physical and social activities following stroke.

Catastrophic reaction
Goldstein- anxiety, tears, aggressive behavior,

swearing, displacement, refusal, renouncement, and, sometimes, compensatory boasting, which is attributed to an inability of the organism to cope when faced with physical or cognitive deficits. 19% with acute stroke lesions had catastrophic reactions.

Catastrophic reaction
Etiology May result from neurophysiological dysfunction rather than realization of intellectual impairment. Predominantly in pts with major depression associated with anterior subcortical lesions. Subcortical damage has also been hypothesized to underlie the release of emotional display by removing inhibitory input to limbic areas of the cortex. Higher frequency of familial and personal history of psychiatric disorders (mostly depression)

Pathological emotion
Recently termed IEED, is characterized by episodes of

laughing and/or crying that are not appropriate to the underlying emotion. They may appear spontaneously or may be elicited by non emotional events. Frequencies of 18% in a rehabilitation hospital and 14% in a community-based study.

Pathological emotion
Secondary to the bilateral interruption of descending

neocortical upper motor neuron innervation of bulbar motor nuclei. Pts with pathological crying found that patients with the most frequent crying episodes had relatively large bilateral pontine lesions. It was hypothesized that pathological emotions may arise from partial destruction of raphe serotonergic neurons or their projections. Fronto-ponto-cerebellar pathways.

Pathological emotions
Pts with this condition acknowledge an inability to

control crying or laughter, an increased frequency of emotional display, and recognition that the emotional display is inconsistent or excessive to their underlying emotional feelings. Citalopram & nortriptyline Poststroke depression and pathological laughing and crying appear to be independent phenomena, although they may coexist.

Abnormalities in the affective components of language or emotional gesturing.
Lesions in right frontal / temporoparietal lesions

and basal ganglia.

A term first used by Babinski to indicate the lack of

awareness of hemiplegia. It has been used, however, to refer to unawareness of other poststroke deficits, such as cortical blindness, hemianopia, and amnesia. Among 80 acute stroke patients, 24 % had moderate or severe anosognosia for motor impairment.

Personality change
One of the most troublesome sequelae.
May overshadow the intellectual deficits. Widespread vascular lesions are often responsible.

Personality change may progress even when the focal

sequelae of stroke improve Usually a prelude to a dementing illness. reduction of margins

Post-stroke sexual dysfunction

57-75% of patients suffering some form of sexual

dysfunction (Korpelainen et al 1999; Monga, et al 1986). Erectile problems reported by 60% Hyposexuality Factors: physical, fatigue, psychological, other illnesess, medications Hypersexuality Sexual intercourse & risk of stroke

Conversion Disorder and Stroke

Present with acute onset of neurologic symptoms,
Misdiagnosed as having TIA or strokes. Careful neurologic examination and imaging studies

permit distinguishing which patients really have strokes. The older the patient, the less likely it is that the diagnosis is conversion disorder. (Levenson, Primary Psychiatry, 2007)

Cognitive disorders
Delirium occurs in 30% to 40% of patients during the first

week after a stroke, especially after a hemorrhagic stroke. Delirium after a stroke is associated with poorer prognosis, longer hospital stays, and increased risk of dementia. Dementia is common following stroke, occurring in approximately 25% of patients at 3 months after stroke. Vascular dementia -subcortical ischemic dementia, multi-infarct dementia, and dementia due to focal strategic infarction. Hachinskis ischemia scale (>7-vascular etiology)

Depression, anxiety and dementia
Assoc. with particular lesion locations and adversely

affect the physical recovery from cerebrovascular lesions. Depression has been shown to respond to treatment with antidepressant medication. Effective treatments have the potential for improving the outcome and quality of life of stroke survivors, additional studies are needed.