cva

1. PSYCHIATRIC ASPECTS OF CVA
MODERATOR: DR. VISHAL SINHA
PRESENTATOR: DR. RAMASHANKAR

2. STROKE
 It is 3rd commonest cause of death
 Annually, 15 million people worldwide suffer a stroke (WHO)
 Most frequent cause of disability in community
 CAUSE: hypertension, atherosclerosis
 PREDISPOSING FACTOR: heart disease, raised lipid profile, smoking,
diabetes etc.

3.  Mainly divided in to 2 type
 A) Infraction (ischaemia)
 B) Haemorrhage
 I: H 4:1
 Hypertension is a risk factor for both
type.
 However risk is more for haemorrhage
 DIAGNOSIS:
 No any cause except vascular origin +
Table
Box -Criteria for diagnosing stroke (Warlow et al.1996)
A stroke should be suspected when:
• there is a sudden onset of symptoms
• focal symptoms and signs are present that can be explained by
a single lesion of the brain
• there is loss of function
• symptoms and signs are maximal at onset, then remain stable
or improve over time
However, on occasion
-symptoms may develop over a few minutes . .. .
-symptoms may not be explained by a single lesion, e.g. there
has; been previous stroke
-symptoms may be 'positive'; e.g. jerking, paraesthesiae, visual
hallucinations
-symptoms may have a sudden onset and then worsen over
minutes: or hours

4. CEREBRAL HAEMORRHAGE
 15% of stokes
 May be divided into :
 1) Intracerebral haemorrhage (10%)
 1) Subarachnoid haemorrhage (2-3%)
 HAEMORRHAGE
 Most common between 60-80years of age
 Onset is often during exertion and rarely during sleep
 Headache, vomiting , loss of consciousness are more common
 Focal neurological sign present in intracerebral haemorrhage
 Sign of meningeal irritation is common in SAH

5. CEREBRAL INFARCTION
 CLASSIFICATION OF
CEREBRAL INFARCTS
By cause (Adams et al.1993)
 Large-artery atherosclerosis (25%)
 Cardioembolism
 Small-artery occlusion (50%)
 lacunar infarcts (20%)
 Stroke of other aetiology
 Stroke of undetermined aetiology
 By location (Bamford et al.1991)
 Total anterior circulation infarcts
 Partial anterior circulation infarcts
 Posterior circulation infarcts
 Lacunar infarcts

6.  PARADOXICAL EMBOLISM: in which a congenital cardiac malformation allows material
from the veins of the legs to reach the brain by bypassing the pulmonary circulation.
 Onset is often during sleep
 The neurological deficit is typically maximal from the outset, often with
rapid resolution over the first few hours thereafter. Regardless of the
cause of the cerebral infarction,
 Headache may be present in the early stages but is often absent
throughout.
 Some degree of mental confusion is common, but consciousness may be
little if at all impaired.

7.  Prognosis for cerebral infarction is much better than for cerebral
haemorrhage
 Approximately 20% of patients die in the acute stage, 20% recover
completely and 60% are left with residual disability.

8. Transient ischaemic attacks
 ‘A brief episode of neurologic dysfunction caused by focal brain or retinal
ischemia, with clinical symptoms typically lasting less than one hour,
and without evidence of acute infarction’ (Albers et al. 2002)
 Atherothromboembolism, cardiogenic embolism and intracranial small
vessel disease probably accounting for 95% of cases (Bamford
2001)
 10% of patients will have a stroke within 90 days and 25% within 5years;
 20% will have had a stroke or myocardial infarct or be dead by 1 year.

9.  Those at greatest risk of later stroke have
 longer-lasting TIAs,
 Repeated TIAs while receiving antiplatelet therapy, or have crescendo TIAs,
 Over 60 years of age, and having diabetes mellitus or hypertension.
 Weakness or speech impairment during the episode also increases the risk
(Shah & Edlow 2004).

10. Post-Stroke Neuropsychiatric Problems
 Neuro cognitive disorder
 Depression
 Major
 Minor
 Mania and Bipolar Disorder
 Anxiety Disorders
 Pathological Laughing and
Crying (PLC)
 Apathy
 Aggression
 Psychosis

11. Neuro cognitive disorder
 The only DSM-5 disorders that are specific for cerebrovascular disease
are the major or minor vascular neurocognitive disorders.
 In DSM-IV it was described as vascular dementia
 Prevalence varies from 6-32%
 Lifetime prevalence of vascular dementia increase with advancing age
 Cognitive impairment due to vascular disease is expected to occur in the
presence of multifocal motor and/or sensory deficits (Jacova et al 2012)
 Vascular dementia is the second most common type of dementia,
accounting for 15 to 20% of all cases of dementia*
*Ruitenberg A, Ott A, van Swieten JC, Hofman A, Breteler MMB. Incidence of dementia: does gender make a
difference? Neurobiology of Aging. 2001;22(4):575–580.

12. DSM-5 criteria for Vascular
Neurocognitive Disorders
1. Criteria are met for major neurocognitive disorder (i.e., the presence of
acquired impairment in one or more cognitive domains and significant
impairment in activities of daily living not better explained by another
medical condition);
2. The clinical features are consistent with a vascular etiology as suggested
by either
 (a) cognitive deficits that are temporally related to one or more
cerebrovascular events or
 (b) presence of prominent executive dysfunction (e.g., inattentiveness or
slow processing speed);
3. The patient’s history, physical examination, and/or neuroimaging findings
are consistent with cerebrovascular disease of sufficient severity to account
for patient’s cognitive impairment.

13. COURSE AND PROGNOSIS
 Temporal relationship between stroke occurrence and deterioration of
cognitive function
 Framingham Heart Study (2014) reported after prospective follow-up
of 132 new-onset, dementia-free stroke patients.
 At 6 months after stroke, a significantly greater impairment in the
following cognitive domains was seen: immediate recall of logical and
visual memory, verbal learning, naming, executive function, visuospatial,
and motor skills.
 These deficits were independent of prestroke cognitive function and
vascular risk factors

14.  Meta-analysis* of data from several studies yielded estimates
 1-in-10 patients being demented prior to a first stroke,
 1-in-10 developing new dementia soon after a first stroke,
 over 1-in-3 being demented after a recurrent stroke
 The incidence of dementia in older people with a longer follow-up time
increases from 10% at 1 year to 32% after 5 years
Leys D., Henon H., Mackowiak-Cordoliani M.A., Pasquier F. Poststroke dementia. Lancet Neurol. 2005;4:752–759.)
*Pendlebury S.T. Stroke-related dementia: rates, risk factors and implications for future research. Maturitas. 2009;64:165–171.
*Pendlebury S.T., Rothwell P.M. Prevalence, incidence, and factors associated with pre-stroke and post-stroke dementia: a
systematic review and meta-analysis. Lancet Neurol. 2009;8:1006–1018

15.  Hypertension has been shown to be the most common modifiable risk
factor for stroke worldwide (CTP-10th ed)
 Recurrent stroke, pre-stroke dependency, pre-stroke cognitive
impairment, development of apathy or quality of life with lower
educational status and history of diabetes mellitus
 Baseline stroke severity, greater severity of WM changes and medial
temporal lobe atrophy appear the strongest contributors of subsequent
impairment
(Chaudhari et al 2014, Jacquin et al 2014, Ihle-Hansen et al 2011, Brodaty et al. 2013, Park et al. 2013)

16.  Treatment with antiplatelet aggregate drugs has reduced the number of
repeated ischemic vascular episodes in patients with TIAs
 The United Kingdom-TIA Aspirin Trial, with 2,435 patients using two different dosages of
ASA, found that there were 21.7 and 25.1 percent reductions, based on dosage, in the
risk of nonfatal strokes, myocardial infarction, or death compared with placebo treatment.

 Main strategy is to modify risk factor for further chance of CVA
 Use of antihypertensives , lipid lowering agents such as statins, smoking cessation, and
prevention or careful management of diabetes mellitus
(Sally Sharp et al 2011)
 Treatment may also include antidepressant agents, cholinergic agonists
(e.g., donepezil), antiplatelet aggregation agents, statins, and
neurotrophic factors (CTP- 10th ed)

17. Post-Stroke Depression
 DSM-5 defines post stroke psychotic, mood, and anxiety disorders as
disorders due to another medical condition, stroke.
 In the most recent studies including 20,293 patients found the pooled
prevalence of depression observed at any time point was 29% (Ayerbe L et al. 2013)
 Various other studies prevalence varies from 9-33%
 May be due to abnormalities in biomarkers, dysregulation such as the
serotonin transporter gene and certain inflammatory cytokines,
particularly interleukin 6 and 18. Elevated levels of glucocorticoids, which
affect glutamate transmission,
 (Robinson et al. 1997; Robinson 2003; Desmond et al. 2003; Lincoln et al. 2003; Aben et al. 2002)

18.  3 to 12 months after stroke, the prevalence of PSD is similar in those
with left- and right-hemispheric lesions
 In the first few months after stroke
 Left anterior stroke > posterior lesion.
 Left anterior lesion > right anterior
 Disability after stroke showed a positive and significant association with
PSD
 Cognitive deterioration is maximum in left hemispheric stroke
 Personal history or a family history of psychiatric disorders and poor
social support are important risk factor for PSD
(Vataja et al. 2001; Narushima et al. 2003; Spalletta et al. 2002; Kimura et al. 2000; Vataja et al. 2004)

19.  Early and late post-stroke depression may not be the same
– Early post-stroke major depression:
• 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 and psychological symptoms)
• more functionally impairing than late post-stroke depression
– Late post-stroke depression appears to be more reactive to
stroke-related disability
(Robinson 2003; Narushima et al. 2003; Bhogal et al. 2004; Tateno et al. 2002; Robinson et al.
1996; Williams et al. 1986)

20.  The severity or existence of PSD is proportional to severity of
impairment in ADL ( Robinson R G 2006).
 Risk of depression is proportional to duration
 Severity of depression directly affect the outcome (Parikh et al 1990)
 According to DSM-5, two types of PSD disorders are recognized:
 Depressive disorder due to stroke with major depression-like episode
 Depressive disorder due to stroke with depressive symptoms (i.e., sub-
syndromal depression).

21.  Parikh et al compared a consecutive series of 33 patients with major or
minor depression during the acute stroke period with 30 non-depressed
stroke patients and examined their recovery at 2-year follow-up and
found that the depressed patients had significantly less improvement at
the 2-year follow-up than the non-depressed patients.
 Similar results were reported by Pohjasvaara et al who found that
among 256 patients, depression at 3 months was associated with,
significant residual motor impairment at 15 months, compared with non-
depressed patients.
 Parikh RM, Robinson RG, Lipsey JR, et al. The impact of poststroke depression on recovery in activities of daily living over two-year follow-up. Arch Neurol.
1990;47:785–789
 Pohjasvaara T, Vataja R, Leppavuori A, et al. Depression is an independent predictor of poor longterm functional outcome post-stroke. Eur J Neurol.
2001;8(4):315–319.

22. EFFECT OF TREATMENT
 Narushima and Robinson assessed 34 patients who received
antidepressant treatment with either nortriptyline (100 mg/day) or
fluoxetine (40 mg/day) for 12 weeks beginning 19 days of post stroke,
compared with 28 patients who received the same antidepressant but
began at 140 days post stroke.. During the period from 6 to 24 months
following stroke, when the 2 groups were matched. The early treatment
group continued to show gradual recovery in ADL during 2 years,
whereas the late-treatment group showed gradual deterioration between
12- and 24-month follow-up.
Thus antidepressant treatment of depression appears to significantly
influence recovery in ADL
Narushima K, Robinson RG. The effect of early versus late antidepressant treatment on physical impairment associated with poststroke depression: is
there a time-related therapeutic window? J Nerv Ment Dis. 2003;191(10):645–652.

23.  Better prognosis in left hemispheric lesion
as compared to right (Morris et al 1990, Downhill et
al 1994, and Spalletta et al 2002)
 Treatment of early post-stroke depression
with either fluoxetine or nortriptyline
decreases mortality for up to 9 years post-
stroke
 – Interestingly, treatment of non-depressed stroke
survivors with these agents also decreased mortality
over this period of study
Robinson RG. The Clinical Neuropsychiatry of Stroke
. Cambridge, UK: Cambridge University Press; 2006:155

24. •Prophylactic treatment with sertraline, citalopram, fluoxetine, and
nortriptyline has been demonstrated to decrease the incidence of post-
stroke depression in the first 3 months after stroke
However, prophylactic treatment of stroke survivors with antidepressants for
either depression or long-term post-stroke mortality is not presently supported by
large RCTs or meta-analyses of smaller studies
(Jorge et al. 2003; Rasmussen et al. 2003; Anderson et al. 2004 )

25.  Double-blind placebo controlled studies:
– Nortriptyline: effective as assessed by Ham-D scores, but 20% incidence of delirium and
agitation
– Nortriptyline: improvement in depression, and associated improvements in ADLs in
treatment responders
– Nortriptyline vs. fluoxetine vs. placebo: nortriptyline wins
– Fluoxetine: improved outcome at 18 months post-stroke
– Fluoxetine: improves MADRS scores at 6 weeks post-stroke
– Trazodone: improves Zung Depression Scale and ADL scores
– Sertraline: decreased Ham-D scores
– Citalopram: effective as assessed by Ham-D scores, no significant adverse events
– Methylphenidate: improved MDRS scores over 3 weeks in acute rehab
 Open-label studies
– Sertaline improved depressive symptoms at 4 and 12 weeks, with a low
rate (3%) of side-effect mediated treatment discontinuations
Rasmussen et al. 2003; Chemerinski et al. 2001; Robinson et al. 2000; Fruehwald et al. 2003; Wiart et al. 2000; Reding et al. 1986; Van de Meent et al. 2003;
Rampello et al. 2004; Lazarus et al. 1992; Spalletta and Caltagirone 2003; Zifko et al. 2002;

26.  ECT is safe and effective
 rTMS may also be effective
 Group and family therapy
 Psychotherapy
(Weintraub and Lippman 2000; Currier et al. 1992; DeQuardo and Tandon 1988; Murray et
al. 1986; Jorge et al. 2004; Lincoln and Flannaghan 2003)

27. Stroke and Suicide
 Teasdale et al. (2001) studied the relationship between stroke and
suicide in Demark from 1979-1993
– Database of 114,098 patients with stroke discharged from the hospital
during the study period with a registry of causes of death over the same
time period
– Identified 359 suicides in this population
– The annual rate of suicide among persons with stoke was nearly
twice that of the general population
 Suicide risk was greatest among stroke patients 50 years or younger
 Duration of hospitalization was inversely associated with suicide risk, being lowest
among those hospitalized longer than three months post stroke and highest among
those hospitalized less than two weeks post stroke
 The risk for suicide appeared to be greatest in the first five years following stroke

28. Mania and Bipolar Disorder
 Compared to PSD, mania after stroke is a rare (Starkstein et al. 2000, Vuilleumier et al 1998)
 Etiology of mania remains unknown
 The frequency of right hemispheric lesions was significantly higher
 Lesions associated with mania were either cortical (basotemporal or
orbitofrontal cortices) or subcortical (frontal white matter, basal ganglia,
or thalamus)
 genetic predisposition to affective disorders and brain atrophy may be
Independent risk factors for post stroke mania
Santos C O, Caeiro L, Ferro J M, Figueira M L. Mania and Stroke: A Systematic Review. Cerebrovasc Dis
2011;32:11–21

29.  DSM-5 classified PSM with specifier as mania with poststroke onset.
 Treatment
– Largely unknown
• Case reports and expert opinion suggest that valproate, carbamazepine,
lithium, typical and atypical antipsychotics, and clonidine may be useful
in some cases
– Use caution when prescribing any of these agents in a person with
stroke
• May impair cognition and motor function
• Other problems?

30. Anxiety Disorders
 Prevalence varies from 2-40%
 Phobic disorders and GAD were the most common
 More common in female
 Most have comorbid depression
 both depression and anxiety are associated with poor recovery
 A 2013 study looked at long-term outcomes of post stroke anxiety in
220 patients followed longitudinally.
 At 5 years post stroke, 64 (29 percent) of patients were deemed anxious
and 73 (33 percent) were depressed, with anxiety and depression
comorbidity in 43 (20 percent).
 Higher anxiety scores at 6 months following stroke were associated with
anxiety at 5 year
Lincoln NB, Brinkmann N, Cunningham S, et al. Anxiety and depression after stroke: a 5 year follow-up. Disabil Rehabil.
2013;35(2):140–145.

31.  Cortical right hemisphere lesions are most common associated with
anxiety-only (Tang et al 2012)
 Depression-anxiety is more commonly associated with cortical left
hemisphere lesions (Castillo, Robinson et al 1995)
 In sum,
 Anxiety is common after stroke
 Its prevalence remains elevated even several years out from the stroke
 Depression and anxiety after stroke are strongly associated
 Both depression and anxiety are associated with poor recovery
 Regular assessments for PSD and anxiety are warranted (CTP-10th ed)

32.  In meta-analysis (Kimura et al. 2003), nortriptyline appears to improve
comorbid poststroke anxiety disorder and depression
 SSRIs as first line treatment
 Benzodiazepines should be avoided. However, if used, should be time
limited
 Campbell et al 2011, evaluate 175 patients in two trials of paroxetine or
buspirone and found significant improvent in anxiety symptom
 Half of the participants receiving paroxetine experienced adverse events
that included nausea, vomiting or dizziness; however, 14% of those
receiving buspirone experienced nausea or palpitation
Campbell Burton CA1, Holmes J, Murray J, Gillespie D, Lightbody CE, Watkins CL, Knapp P. Interventions for treating anxiety after stroke. Cochrane
Database Syst Rev. 2011 Dec 7;(12)

33. Pathological Laughing and Crying (PLC)
 Prevalence varies from 6.3-16.9%
 Characterized by the sudden onset of crying, or more rarely, laughing,
which is out of proportion to the conversation or situation in which the
emotional reaction occurred
 May last from a few seconds to a few minutes with no residual feelings
of sadness or happiness

34.  It is important to consider the presence of a depressive episode in
people who present with excessive emotionality
 Most people with PLC do not have a diagnosable mood disorder, and
many do not manifest depressive symptoms at all.
 The etiology of PLC is unknown
 Evidence suggest that monoaminergic neurotransmission is altered
(Giacobbe P, Flint A. Pharmacological treatment of post-stroke pathological laughing and crying. J
Psychiatry Neurosci. 2007 Sep; 32(5): 384.)

35.  Antidepressant treatment, including both tricyclic and SSRI/selective
serotonin–norepinephrine reuptake inhibitors (SNRIs),
 EFFECTIVE DOSE (fluoxetine 20 mg, sertraline 50 mg and citalopram
10–20 mg)
 Case reports suggest that bupropion, mirtazapine, venlafaxine and
lamotrigine may be effective for PLC
Giacobbe P, Flint A. Pharmacological treatment of post-stroke pathological laughing and crying. J
Psychiatry Neurosci. 2007 Sep; 32(5): 384.
 FDA-approved combination drug consisting of dextromethorphan and
quinidine
Dynela G B, Thomas M. Johnson, Wagner J. Therapeutic Approach of a High Functioning Individual With
Traumatic Brain Injury and Subsequent Emotional Volatility With Features of Pathological Laughter and Crying
With Dextromethorphan/Quinidine. Medicine (Baltimore) 2016 Mar; 95(12): e2886.

36. Apathy
 Frequency of apathy 9- 50%. (Tang et al.(2014, Mayo et al. 2009)
 Depression occurred up to 40 percent of patients with apathy
 Apathy is typified by the absence or lack of feeling, emotion, interest,
concern or motivation
 Poor outcome in cognition of stroke patients
 Imaging studies have found that apathy is significantly associated with
lesions of the pons, frontal cortex, basal ganglia, dorsal thalamus,
posterior limb of the internal capsule, and temporal cortex
Hama et al. (2007), Murakami et al. (2013), Onoda et al. (2011), Tang et al. (2013)

37.  Rate of apathy was similar
 For left- and right-sided hemispheric stroke lesions and
 For ischemic and hemorrhagic stroke type
 Apathy rate is lower in patients without previous cerebrovascular disease
(Caeiro L, Ferro JM, Costa J. Apathy secondary to stroke: a systematic review and meta-analysis.
Cerebrovasc Dis. 2013;35(1):23-39.)

38.  Includes:
 Lack of Emotion
 Slowed Motor Activity
 Impaired Cognitive Activity
 Older age, cognitive impairment and functional disability were found to
be predictors of apathy after stroke.
 Overall, apathy secondary to stroke does not appear to have a negative
impact on clinical global outcome, except for apathetic patients with first-
ever stroke and for younger patients
 (Caeiro L, Ferro JM, Costa J. Apathy secondary to stroke: a systematic review and meta-analysis.
Cerebrovasc Dis. 2013;35(1):23-39.)

39. Mikami KI, Jorge RE, Moser DJ, Jang M, Robinson RG. Incident apathy during the first year after stroke and its effect
on physical and cognitiverecovery. Am J Geriatr Psychiatry. 2013;21(9):848

40.  Can be treated with nortriptyline, bromocriptine, methylphenidate,
amantadine, selegiline, and tacrine with some success (CTP-10th ed.)
 Administration of antidepressant medication such as escitalopram may
prove helpful for the prevention of poststroke apathy*
*Mikami K, Jorge RE, Moser DJ, Arndt S, Jang M, Solodkin A, Small SL, Fonzetti P, Hegel MT,
Robinson RG. Prevention of poststroke apathy using escitalopram or problem-solving therapy. Am J
Geriatr Psychiatry. 2013 Sep;21(9):855-62.

41. Psychosis
 Although rare, case reports and empirical
studies have documented
 Frequency of psychotic disorders was 0.4-
3.1%
 A right hemispheric lesion, seizures,
and subcortical brain atrophy appear to be
important factors in the pathogenesis of
post stroke psychosis.
 (Kumral & Ozturk 2004, Lampl et al 2005, Levine &
Finklestine 1882, Rabins et al 1991)

42.  Psychosis may be in form of delusion (Capgrass, persecutory),
hallucination( visual, auditory)
 Majority patients showed agitation, confusion.
 Anecdotal reports have suggested two basic approaches to treatment:
 utilization of anticonvulsant therapy
 antipsychotic medication

43. Catastrophic Reaction
 Characterized by anxiety, tears, aggressive behavior, swearing,
displacement, refusal, renouncement, and/or, sometimes, compensatory
boasting.
 Lesions involving the basal ganglia
 Catastrophic reactions occurred predominantly in patients with major
depression associated with anterior subcortical lesions.
 “release” of emotional display by removing inhibitory input to limbic areas
of the cortex.

44.  This intense emotional reaction is usually provoked by stressful
situations such as cognitive testing and typically subsides within a few
minutes.
 More common if familial and personal history of psychiatric disorders,
mostly depression
 Effective treatments have not been established for catastrophic reactions
(CTP.10th ed.)
 Treatment consists of prophylactic and supportive measures

45. Anosognosia
 Term introduce by Babinski to indicate a patient’s lack of awareness of
his or her hemiplegia.
 Later on this term has been extended to unawareness of other deficits
after stroke, such as cortical blindness, hemianopia, and amnesia.
 anosognosia is uncommon beyond 3 months post stroke