NSP of cardio vascular Attack psychiatry .pptx

CVA stroke

1. NEUROPSYCHIATRIC ASPECTS OF STROKE Dr Hemil Mehta (R3) Psychiatry department

2. INTRODUCTION Cerebrovascular disorders are divided into two etiologies Ischemic (i.e., absence of blood flow) and Hemorrhagic (i.e., bleeding in or around the coverings of the brain) Classified according to the size of the affected blood vessel Large artery disease produces large lesions of the brain, while Small artery (arteriolar) disease results in small lacunar or hyperintensity lesions on MRI.

3. STROKE A stroke is defined as the sudden loss of blood supply to the brain leading to permanent tissue damage. Nearly 90 percent of strokes are due to ischemia while the remaining 10 percent are caused by hemorrhagic events. While less common, hemorrhagic strokes tend to be more severe and are associated with greater mortality than ischemic strokes Stroke is the fourth-leading cause of death in the United States and the second-leading cause of death globally

4. nosology DSM-5 defines poststroke psychotic, mood, and anxiety disorders as disorders due to another medical condition, stroke

5. NEUROPSYCHIATRIC aspects OF STROKE Vascular neurocognitive disorder Depression Mania Anxiety Psychosis Apathy Catastrophic reaction Pathological laughter & crying Anosognosia

6. epidemiology The age standardized prevalence was 6.4 percent for all-cause dementia and 1.6 percent for vascular dementia Pooled prevalence of depression observed at any time point was 29 percent Mania after stroke is a rare When anxiety symptoms were assessed by a rating scale, the prevalence of anxiety was 25 percent

7. epidemiology 49 percent met criteria for GAD without comorbid depression 14 percent had comorbid GAD and major depression patients who had a stroke or transient ischemic attack (TIA) and found that 18 percent likely had PTSD 5. The reported frequency of psychotic disorders was 0.4 percent 6. Prevalence of apathy of 34.6 percent

8. epidemiology 7. Based on a survey 19 percent patient with acute stroke lesions were found to have catastrophic reactions 8. In a recent cohort study patients with ischemic stroke, 9.4 percent of patients had evidence of pathological emotions during their admission for care of acute stroke 9. Frequency of anosognosia for hemiplegia to range from 20 to 44 percent

9. 1. Vascular Neurocognitive Disorder types DSM-5 identifies two forms of cognitive impairment due to vascular disease: major and minor vascular neurocognitive disorders. ‘ Major neurocognitive disorder due to vascular disease ’ replaces ‘Vascular dementia’ used in DSM-IV. ‘ Minor vascular neurocognitive disorder ’ replaces ‘Mild cognitive impairment’.

10. major neurocognitive disorder DSM-5 criteria Acquired impairment in one or more cognitive domains and significant impairment in activities of daily living not better explained by another medical condition Clinical features are consistent with a vascular aetiology 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); 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.

11. Vascular Neurocognitive Disorder TREATMENT Risk factors for stroke can be effectively treated, hypertension is the biggest risk factor for stroke Antihypertensive medications had a reduced risk of vascular dementia Acetylsalicylic acid (ASA) and other antiplatelet drugs have been shown to be effective in the secondary prevention of stroke Carotid endarterectomy , when carotid stenosis ranges from 70 to 99 percent, may be indicated to minimize the risk of future strokes After cardioembolic stroke, anticoagulation is an effective treatment to reduce the risk of stroke recurrence

12. Vascular Neurocognitive Disorder TREATMENT Therapeutic measures aimed at 1. Reducing vascular risk factors include antihypertensives (e.g., beta-blockers or calcium channel blockers), 2. Lipid-lowering agents such as statins , 3. smoking cessation , and 4. prevention or careful management of diabetes mellitus Treatment may also include antidepressant agents , cholinergic agonists (e.g., donepezil) and neurotrophic factors.

13. 2. POST-STROKE DEPRESSION DIAGNOSIS AND CLINICAL FEATURES According to DSM-5, two types of poststroke depressive disorders are recognized: 1. Depressive disorder due to stroke with major depression-like episode 2. Depressive disorder due to stroke with depressive symptoms (i.e., sub- syndromal depression) The diagnostic criteria require : mood disorder is the direct physiological consequence of the stroke. If this judgment is made, then the patient is diagnosed with “depression due to stroke with major depressive-like episode.”

14. POST-STROKE DEPRESSION ETIOLOGY Many hypotheses about depression Abnormalities in biomarkers linked to mood dysregulation such as 1. serotonin transporter gene and 2. certain inflammatory cytokines (interleukin 6 and 18). Elevated levels of glucocorticoids , which affect glutamate transmission, and stroke location, which results in the interruption of biogenic amine transmission

15. POST-STROKE DEPRESSION ETIOLOGY In the first few months after stroke, lesion location does appear to increase the risk of PSD. Left anterior strokes > Left posterior strokes Left anterior strokes > Right anterior strokes 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

16. POST-STROKE DEPRESSION TREATMENT patients treated with nortriptyline (50 to 100 mg/day) and citalopram (20 mg/day under age 65; 10 mg/day over age 65) had significantly greater reduction in Hamilton Depression Scores over 6 weeks Escitalopram (5 mg/day over age 65; 10 mg/day under age 65) over 1 year problem solving therapy (PST)

17. 3. Post STROKE MANIA patients showed elation, pressured speech, flight of ideas, grandiose thoughts, insomnia, hallucinations, and paranoid delusions. the symptoms of mania that occurred after stroke diagnosed by DSM-5 as bipolar disorder due to stroke with manic-like episode if full criteria for mania are met bipolar disorder due to stroke with manic features if full criteria for mania are not met

18. Post STROKE MANIA etiology Etiology of mania remains unknown. Lesions associated with mania were either cortical ( basotemporal or orbitofrontal cortices) or subcortical (frontal white matter, basal ganglia, or thalamus) mania appears to be provoked by injury to specific right hemispheric structures that have connections to the limbic system A combination of biogenic amine system dysfunction and release of tonic inhibitory input to the orbitofrontal–thalamic circuit may lead to the production of mania secondary mania had a significantly greater degree of subcortical atrophy

19. Post STROKE MANIA treatment single or recurrent episodes of mania suggest that they respond to lithium But some fail to respond to either lithium or carbamazepine one longitudinal study of 23 patients showed that most patients’ mania remit within a few months .

20. 4.Post STROKE ANXIETY anxiety is common after stroke defined by a score of 8 or more on the Anxiety Section of the Hospital Anxiety Depression Scale depression and anxiety after stroke are strongly associated both depression and anxiety are associated with poor recovery

21. Post STROKE ANXIETY treatment Patients receiving nortriptyline treatment showed significantly more rapid improvement on the Hamilton anxiety scores compared with the Hamilton depression scores Suggesting that anxiety may respond more quickly to treatment than depression .

22. 5. Post STROKE PSYCHOSIS etiology patients had right-hemispheric lesions, primarily involving frontoparietal regions patients with secondary psychosis had significantly greater subcortical atrophy high frequency of seizures among patients with secondary psychosis seizures usually started after the brain lesion but before the onset of psychosis Overall, a righthemispheric lesion, seizures, and subcortical brain atrophy appear to be important factors in the pathogenesis of poststroke psychosis.

23. Post STROKE PSYCHOSIS treatment Anecdotal reports have suggested two basic approaches to treatment: anticonvulsant therapy or antipsychotic medication The use of anticonvulsants has its rationale in the frequent coexistence of seizures with psychotic disorders following stroke.

24. 6. Poststroke APATHY Essential symptom of apathy the loss of motivation or drive which is the required symptom for the diagnosis of apathy Lack of motivation may be manifested emotionally, cognitively, or behaviorally apathy was associated with older age, depression, and cognitive impairment apathy was a stronger predictor of poor functional recovery than depression

25. Poststroke APATHY etiology patients were also found to have lesions of the ventral putamen and globus pallidus, as well as dorsal thalamus and prefrontal cortex apathy patients associated with PSD and greater cognitive impairment. 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

26. Post stroke Apathy treatment treated with nortriptyline , bromocriptine , methylphenidate , amantadine , selegiline , and tacrine with some success nefiracetam (900 mg/day) for the treatment of comorbid apathy and depression d/t it was significantly better in reducing scores on the Apathy Rating Scale but has not been approved by FDA Escitalopram may prove helpful for the prevention of poststroke apathy

27. 7. PATHOLOGICAL LAUGHTER AND CRYING characterized by the sudden onset of crying or laughing, which is out of proportion to the conversation or situation in which the emotional reaction occurred emotion may last from a few seconds to a few minutes with no residual feelings of sadness or happiness Hallmark features are an inability to control crying or laughter; an increased frequency of such emotional display; and recognition by the patient that the emotional display is inconsistent or excessive to his or her underlying emotional feelings.

28. PATHOLOGICAL LAUGHTER AND CRYING etiology patients with frontal or temporal lesions in either hemisphere had a significantly increased frequency of pathological emotions most frequent crying episodes had relatively large bilateral pontine lesions hypothesis that pathological emotions may arise from partial destruction of raphe serotonergic neurons critical lesions eliciting PLAC are located along fronto - ponto -cerebellar pathways

29. PATHOLOGICAL LAUGHTER AND CRYING 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

30. 8. CATASTROPHIC REACTION characterized by emotional outburst involving various degrees of anger, frustration, depression, tearfulness, refusal, shouting, swearing, and sometimes aggressive behavior.

31. CATASTROPHIC REACTION etiology significantly higher frequency of lesions involving the basal ganglia Catastrophic reactions occurred predominantly in patients 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

32. 9. Anosognosia indicate a patient’s lack of awareness of his or her hemiplegia term has been extended to unawareness of other deficits after stroke, such as cortical blindness, hemianopia, and amnesia.

33. REFERENCES Kaplan & Sadock’s comprehensive textbook of psychiatry 10 th edition

34. THANK YOU