post stroke psychiatric disorders

8/12/2019 Post Stroke Psychiatric Disorders

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Dr. Manu Sharma

Chairperson: Dr. Krishnamurthy


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IntroductionWhat is stroke?

85%-ischemic, 12%-hemorrhagic

The association of neuropsychiatric disorders withcerebrovascular disease has been recognized byclinicians for over 100 years, but it is only within thepast 30 years that systematic studies have been

conducted.


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HOLISTIC APPROACH

STROKEGMC

PSYCHIATRICDISORDER

ADL

COGNITIVEDEFICITS

LIFE STYLE

QOL, DISABILITY, REHABILITATION,CARE GIVERS BURDEN.


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HistoryAdolf Meyer -identified several disorders such as

delirium, dementia, and aphasia that were the directresult of brain injury

Bleuler- after stroke melancholic moods lasting formonths and sometimes longer appear frequently.

Kraepelinconcluded that cerebrovascular disorder

may be an accompanying phenomenon of manicdepressive disease or may itself produce depressivedisorder.


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History In 1956, Redvers- pathological crying

Derek Denny-Brown- the indifference reaction

Kurt Goldstein- the catastrophic reaction


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Nosology (DSM-IV-TR) defines:

Poststroke psychotic disorder, mood disorders, andanxiety disorders as disorders due to cerebral vascular

disease or stroke . The only disorder that is specific for cerebrovascular

disease isvascular dementia that may beuncomplicated or occur with delirium, delusions, or

depressed mood. The other DSM-IV-TR defined disorder that is

commonly seen in patients with cerebrovasculardisease is minor depression.


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Nosology inclusive approach in which depressive diagnostic

symptoms are counted regardless of whether they may berelated to physical illness

etiological approach in which a depressive symptom iscounted only if the diagnostician feels that it is not causedby 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 bemore frequent in depressed than non-depressed pts.


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Post- stroke depressionEpidemiology

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.


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Post- stroke depressionEtiology Patients with left anterior lesions developed poststroke

depression during the acute stroke period compared withother lesion locations.

A previous personal history or a family history ofpsychiatric disorders Frequency of poststroke depression was 25% in women and

18% in men High neuroticism personality traits and negative life

events. 5HT2receptor binding in the left temporal cortex. Proinflammatory cytokines such as IL-1 activate enzymes

such IDO. Lateral orbital frontal circuit abnormalities


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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 thepercentage of patients who had major depression during the acute poststrokeperiod 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.


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Bilateral injury: left anterior lesions significantly associatedwith 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 commonbiochemical (serotonergic) mechanisms

Aphasia: does not play a causal role, but depression may affectrecovery from aphasia

Social functioning: relationship between poor social supportand depression strong in the first 6 months (especially spousal)

Premorbid: subcortical atrophy, female gender andfamily/personal history of affective/anxiety disorder, highneuroticism, more severe impairment in ADL, negative life eventin the 6 months prior to stroke (Morris, 1992; Hirschfield, 1989;

Krause, 1986)


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Post- stroke depressionRCOP, 2005

An emotional response to sudden onset disability & its

assoc changesAltered biochemical balance within the brain

producing changes in mood

Preceding tendency for/history of depression


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Post- stroke depressionA study of growth-hormone response to desipramine

found that growth-hormone responses weresignificantly blunted in patients with poststrokedepression,

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 poststrokedepression.


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PHENOMENOLOGY of PSD

Lipsey et al, 1986: n=43 PSD vs primary depressionslowness was higher in frequency among

the stroke patients.

loss of concentration and interest in

primary depression.

Gainotti et al, 1999; PSDS- higher scores onhyperemotionalism, diurnal mood variation

Paradiso et al 1997: morning depression and anergia thruout 2 yr follow up

loss of libido in early follow up

early morning awakening in late follow up.


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Post- stroke depressionCourse & Prognosis

There appear to be a minority of patients with either majoror 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 totreatment with citalopram showed significantly betterimprovement in ADLs.

Major depression following acute stroke is associated withmore severe cognitive impairment if the stroke occurred inthe left hemisphere.


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Post- stroke depressionDuring the first 6 months following strokedepressed patient

has more disability/poor QOL

Which Impairs the following area

Help seeking behavior

Compliance

Life style modification

Rehabilitation process

Recovery


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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


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Post- stroke depressionStroke patients with major depression were

eight times

more likely to die than the thannon-depressed stroke patients.

(Morris et al. 1993ANJP, Ricardo et al 2003 AJP)


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Post- stroke depressionTreatment- current evidence

9 placebo-controlled, randomized, double-blindtreatment studies on the efficacy of antidepressanttreatment of poststroke depression.

Nortriptyline, SSRIs

There are now 3 studies that have found f luoxetine to

be no better than placebo in the treatment ofpoststroke depression.

Transcranial magnetic stimulation


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Post-stroke ManiaEpidemiology

There are no epidemiological studies that documentthe incidence or prevalence of this condition.

About half of the reported cases involve single orrepeated manic episodes without major depression.

Bipolar disorder

Significantly more cognitive deficits as measured byMMSE scores with p


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Post-stroke ManiaEtiology

The frequency of right-hemisphere lesions wassignificantly higher .

Lesions associated with mania were either cortical(basotemporal cortex or orbitofrontal cortex) orsubcortical (frontal white matter, basal ganglia, orthalamus).

PET- focal hypometabolic deficiency in the rightbasotemporal cortex.

Higher frequency of a positive family history of mooddisorders.


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Post-stroke Mania The mechanism of secondary mania remains

unknown.

The right basotemporal cortex may play an importantrole.

The basotemporal cortex has strong efferentconnections 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 orbitalfrontalthalamic circuit may lead to the production of

mania.


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Lesion location


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Post-stroke ManiaDiagnosis

The symptoms of mania that occurred after braindamage (secondary mania) appeared to be the same asthose found in mania without brain damage (primarymania).

As with depression, although the current diagnosis is

mood disorder due to stroke with manic features, abetter diagnostic classification might be mania withpoststroke onset.


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Post-stroke ManiaCourse & Prognosis

The course of mania following stroke has not beensystematically examined.

Anecdotal cases have been reported indicating thatrecurrent episodes of mania or depression may occurin these patients.

Most patients, however, have spontaneous remissionof their mania within 3 to 4 months.


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Post-stroke ManiaTreatment- current evidence

There are no RCTs of the treatment of mania.

Data on individual patients with single or recurrentepisodes of mania suggest that they respond tolithium.

Some may fail to respond to Li or CBZ.


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Post-stroke AnxietyAmong community samples, the rate of GAD alone

was 2% and GAD with depression was 8%.

Hospital and OP samples found that GAD aloneoccurred in 5.5% and GAD with depression in 15.2%.

The major confound, however, is that the majority ofpatients with poststroke anxiety disorder also have

depression. There have been no systematic studies of panic

disorder or other forms of anxiety disorder.


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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 followingstroke had a significantly higher frequency of all

diagnostic Sx compared to similar stroke patientswithout GAD.

A study of pts with acute stroke lesions for the presenceof anxiety and depressive sx found that GAD

(excluding the 6 month duration criteria) wasassociated with a prior h/o alcohol abuse.

GAD particularly with comorbid depression impacts onphysical and social recovery from stroke.


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

comorbid depression are stable at about 20% over 3years 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 meanduration of depression.


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Post-stroke AnxietyTreatment- current evidence

BZDs

3 randomized double-blind treatment studies weremerged to evaluate nortriptylinevs placebo in thetreatment of patients with comorbid GAD anddepression following stroke.

Buspirone less adverse effects, less risk ofdevelopment of tolerance.


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

history and later age at onset of OCD symptoms thanpatients with idiopathic OCD.

Relatively similar clinical phenomenology, severity ofOC symptoms, and profile of neuropsychologicaldeficits.

Cognitive deficits +

Frontal-limbic-subcortical circuits(Berthier et al, Neurology, 1996)

Case reports suggest that both antidepressants andbehavior therapy can be effective.


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Post-stroke Psychoses Rare case reports

No epidemiological study

3 factors may be important in the mechanism of organichallucinations:

a right-hemisphere lesion involving thetemporoparietal cortex,

seizures, and/or subcortical brain atrophy.


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Lesion location

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


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Post-stroke Psychoses Capgras/Fregoli right hemisphere infarcts

Hallucinosis can be caused by various lesions in thecalculi cortex, fusiform gyrus, midbrain/pons (LHermitte

peduncular hallucinosis)

Rx: one utilizing anticonvulsant therapy and the otherantipsychotic medication.


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ApathyThe 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 onlypsychiatric disorder while another 11% had bothapathy 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).


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ApathyApathetic 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 associatedwith severity of apathy than severity of depression

(Hama et al).


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ApathyTreatment- current evidence

Nortriptyline, apomorphine, and amphetamine.

Nefiracetam (900 mg/day) was significantly better inreducing scores on the Apathy Rating Scale comparedwith placebo. (not FDA approved)

Treatment trials are urgently needed to address a

problem that can be devastating to the recovery ofphysical and social activities following stroke.


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Catastrophic reaction Goldstein- anxiety, tears, aggressive behavior,

swearing, displacement, refusal, renouncement, and,sometimes, compensatory boasting,

which is attributed to an inability of the organism tocope when faced with physical or cognitive deficits.

19% with acute stroke lesions had catastrophic

reactions.


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Catastrophic reactionEtiology May result from neurophysiological dysfunction rather

than realization of intellectual impairment.

Predominantly in pts with major depression associatedwith anterior subcortical lesions.

Subcortical damage has also been hypothesized tounderlie the release of emotional display by

removing inhibitory input to limbic areas of thecortex.

Higher frequency of familial and personal history ofpsychiatric disorders (mostly depression)


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Pathological emotion Recently termed IEED, is characterized by episodes of

laughing and/or crying that are not appropriate to theunderlying emotion.

They may appear spontaneously or may be elicited bynon emotional events.

Frequencies of 18% in a rehabilitation hospital and

14% in a community-based study.


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Pathological emotion Secondary to the bilateral interruption of descending

neocortical upper motor neuron innervation of bulbarmotor nuclei.

Pts with pathological crying found that patients withthe most frequent crying episodes had relatively largebilateral pontine lesions.

It was hypothesized that pathological emotions mayarise from partial destruction of raphe serotonergicneurons or their projections.

Fronto-ponto-cerebellar pathways.


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Pathological emotions Pts with this condition acknowledge an inability to

control crying or laughter, an increased frequency ofemotional display,

and recognition that the emotional display isinconsistent or excessive to their underlying emotionalfeelings.

Citalopram & nortriptyline Poststroke depression and pathological laughing and

crying appear to be independent phenomena,although they may coexist.


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Aprosodia

Abnormalities in the affective components oflanguage or emotional gesturing.

Lesions in right frontal / temporoparietal lesionsand basal ganglia.


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AnosognosiaA term first used by Babinski to indicate the lack of

awareness of hemiplegia.

It has been used, however, to refer to unawareness ofother poststroke deficits, such as cortical blindness,hemianopia, and amnesia.

Among 80 acute stroke patients, 24 % had moderate or

severe anosognosia for motor impairment.


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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


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Post-stroke sexual dysfunction 57-75% of patients suffering some form of sexual

dysfunction (Korpelainen et al 1999; Monga, et al1986).

Erectile problems reported by 60%

Hyposexuality

Factors: physical, fatigue, psychological, other

illnesess, medications Hypersexuality

Sexual intercourse & risk of stroke


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Conversion Disorder and Stroke

Present with acute onset of neurologic symptoms,

Misdiagnosed as having TIA or strokes.

Careful neurologic examination and imaging studiespermit distinguishing which patients really havestrokes.

The older the patient, the less likely it is that the

diagnosis is conversion disorder.(Levenson, Primary Psychiatry, 2007)


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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 strategicinfarction.

Hachinskisischemia scale (>7-vascular etiology)


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Conclusion Depression, anxiety and dementia

Assoc. with particular lesion locations and adverselyaffect the physical recovery from cerebrovascularlesions.

Depression has been shown to respond to treatmentwith antidepressant medication.

Effective treatments have the potential for improvingthe outcome and quality of life of stroke survivors,additional studies are needed.


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post stroke psychiatric disorders

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