Psychosomatic medicine in relation to stroke

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Psychosomatic medicine in relation to stroke

  1. 1. Psychosomatic Medicine in Relation toSTROKE<br />13th April, 2010<br />:: Speaker ::Dr. SantanuGhoshPostgraduate Student<br /> :: Moderator ::Dr. D. J. Bhuyan<br />AssistantProfessor<br />Assam Medical College & Hospital<br />
  2. 2. Layout of presentation<br />Introduction<br />What is stroke?<br />Classification of stroke<br />Epidemiology<br />Psychiatric sequelae of stroke<br />Biological basis of neuropsychiatric consequences<br />Psychiatric conditions mimicking stroke<br />Psychological factors increasing the risk of stroke<br />Role of psychiatrist in management of post stroke sequelae<br />Comparative nosology<br />Prognosis <br />Management<br />Summary<br />Bibliography<br />2<br />
  3. 3. Introduction<br />Disease of vascular system contribute greatly to the sum total of psychiatric disability, chiefly in the elderly population & mainly as a result of stroke. CVA & subarachnoid hemorrhage therefore considered first, with emphasis on their psychiatric sequelae & problems encountered in rehabilitation. The psychiatric components of such illness have gained increasing recognition & appear to be attributable in part to involvement of the cerebral vasculature.<br />3<br />
  4. 4. What is Stroke?<br />4<br />
  5. 5. WHO defined stroke as a rapidly developing clinical signs of local (at times focal) disturbance of cerebral function lasting more than 24 hours or leading to death, with no apparent cause other than that of vascular origin<br />5<br />
  6. 6. Epidemiology<br />World<br />India<br />Prevalence<br />200 /100000 persons<br /> Incidence<br />2 /1000 population<br />80%= Cerebral infarction<br />Prevalence<br />5/1000 population<br />10% = Intracerebral hemorrhage<br />10% = Subarachnoid hemorrhage<br />Asia<br />Intracranial hemorrhage = 25 - 35%<br />Source:<br />IJPMR April 2006; 17 (1): 8-10<br />
  7. 7. Types of stroke<br />Hemorrhagic (SAH, ICH, SDH)<br /> Ischemic <br />AtherothomboticCardioembolic<br /> 80% of all strokes are ischemic<br />7<br />
  8. 8. Psychiatric conditions mimicking stroke<br /><ul><li> Catatonia
  9. 9. Conversion disorder
  10. 10. Delirium
  11. 11. Seizures and postictal states
  12. 12. Familial hemiplegic migraine
  13. 13. Malingering or factitious hemiparesis</li></ul>8<br />
  14. 14. Psychological factors increasing the risk of stroke<br />Type A Personality<br /> Substance abuse disorder<br /> Patient on 2nd generation antipsychotics<br />Clozapine>olanzepine>risperidone<br /> Preexisting MDD<br /> Unhealthy food habit<br />9<br />
  15. 15. Psychiatric sequelae of stroke<br />10<br />
  16. 16. Cognitive Disorders<br />Delirium <br />It occurs in 30% to 40% of patients during the first week after a stroke<br />It occurs especially after a hemorrhagic stroke. (Gustafson et al 1993)<br /> It is associated with poorer prognosis, longer hospital stays, and increased risk of dementia.<br />11<br />
  17. 17. Cognitive Disorders contd…<br />B. Dementia<br />It occurs in approximately 25% of patients at 3 months after stroke. (Desmond et al 2000)<br />Vascular dementia (subcortical ischemic dementia, multi-infarct dementia, and dementia due to focal strategic infarction)<br /> Critical brain areas which are commonly affected are:<br /> Thalamus,<br /> Internal capsule<br /> Basal ganglia.<br />12<br />
  18. 18. Cognitive Disorders contd…<br />Most common difficulty is learning new information<br />Memory is not a single skill affected; different aspects can be affected selectively<br /> Recognition vs. recall<br /> Verbal vs. non-verbal<br />13<br />
  19. 19. Psychiatric Issues that May Present After Stroke<br />Aphasia<br />Anosognosia<br />Dysprosody<br />Apathy<br />Depression<br />Anxiety<br />Mania<br />Emotional Incontinence<br />Catastrophic Reactions<br />Psychosis<br />Obsessive-Compulsive Disorder<br />Hyposexuality<br />14<br />M. Conversion Disorder<br />N. . Personality or behavioral changes<br />
  20. 20. A. Aphasia<br />Global aphasia occurs when all linguistic abilities have been lost, making communication extremely limited, <br /> In expressive (Broca’s) aphasia, intense emotional frustration is common due to the difficulties in patients’ making themselves understood and problems is in social interaction.<br /> In receptive (Wernicke’s) aphasia, patients manifest irritability and rage because they do not understand what others are saying, and therefore lack insight. <br />15<br />
  21. 21. 16<br />Types of aphasia:<br />Pure word deafness<br /> Pure word blindness( Alexia without agraphia)<br /> Pure word dumbness<br /> Pure agraphia (agraphia without alexia)<br /> Primary sensory (Wernicke’s) dysphasia<br /> Primary motor (Broca’s) dysphasia<br /> Nominal dysphasia<br /> Conduction dysphasia<br /> Isolation syndrome<br />Transcortical motor dysphasia<br />Transcortical sensory dysphasia<br /> Alexia with agraphia<br />
  22. 22. B. Anosognosia<br />It refers to partial or complete unawareness of a deficit.<br /> In extreme cases, patients may deny that a limb or an entire side of their body belongs to them, attributing it to someone else. <br />It occurs more frequently with nondominant parietal lobe strokes.<br /> <br />17<br />
  23. 23. C. Affective Dysprosodia<br />It is impairment of the production of those aspects of speech that communicate emotions<br /> It is characterized by alterations in intensity, timing, rhythm, melody, and intonation of words. <br />It is a deficit in the ability to communicate emotions, but is not associated with an actual deficit in the ability to experience emotions. <br />The speech sounds flat and robotic. <br />Others must infer the patient’s emotional state from the content of the patient’s speech and facial expressions.<br /> <br />18<br />
  24. 24. D. Apathy<br />Epidemiology<br />It is significantly associated with major, but not minor depression. <br />Approximately 27% of stroke survivors have an apathy syndrome. <br />Etiology and lesion correlates<br />Apathy in post-stroke patients may result from dysfunction of cortico-subcortical circuits involving the prefrontral cortex, basal ganglia, and thalamus.<br />
  25. 25. Apathy contd…<br />Patients show absence of passion, emotion, or excitement.<br /> They lack interest in or concern for things that others find moving or exciting. <br />These patients produce little spontaneous action or speech. <br />20<br />
  26. 26. E. Depression<br />Epidemiology(based on world pooled data)<br />Hospitalized acute stroke patients (N = 2178): mean prevalence was 22% for major depression and 17% for minor depression <br />Outpatient populations (N = 2191): mean prevalence was 24% for major depression, and 24% for minor depression <br />Community samples (N = 2108): mean prevalence for major depression was 14% and minor depression was 9% <br />Source: Blumenfeld<br />
  27. 27. Depression cont…<br />Etiology and lesion correlates<br />Strategic lesions of the brain appear to provoke Post Stroke Depression <br />Depletion of serotonin and/or catecholaminergic transmission in structures could lead to dysfunction in cortico-thalamic circuits<br />
  28. 28. Depression in stroke (Royal college of physician 2005)<br />Why depression after stroke? <br /> An emotional response to sudden onset of disability & its associated changes<br /> Direct result of the brain injury leading to altered biochemical balance within the brain producing changes in mood<br />Preceding tendency to depression or history of depression<br />23<br />
  29. 29. Depression cont… <br />Patients with major depression frequently had:<br />past personal and family history of depression <br />greater degree of cognitive impairment <br />left anterior lesions <br />Patients with minor depression frequently had left posterior lesions.<br />
  30. 30. Depression cont… <br /> Duration: based on longitudinal studies<br />Mean duration of untreated major depression was 9.0 months, with 26% still having major depression at 1-year follow-up.<br />In-hospital minor depression had a less predictable duration, but an average of 41% were still depressed at 1-year follow-up. <br />Source: Blumenfeld<br />
  31. 31. Depression cont… <br />Outcome in activities of daily living(ADL) Parikh et al<br />Patients with either major or minor depression showed the same amount of recovery in ADL when their depression improved.<br />Outcome in cognitive impairment<br />Major depression contributes to the degree of cognitive impairment among patients with stroke.<br />
  32. 32. Depression cont… <br /> Outcome in mortality<br />major or minor depression during in-hospital evaluation was significantly associated with an increased mortality rate at 1, 2, and 10 years follow-up<br />
  33. 33. Early Predictors of PSDCarota, et al. (2005)<br />Age <68 years<br />Crying in first few days<br />Pathological crying (not associated with PSD)<br />Emotionalism (41% developed PSD)<br />Catastrophic reaction (63% developed PSD)<br />
  34. 34. Course of PSD<br />About 40% of those with PSD will develop symptoms within 3 months.<br />30% of nondepressed patients become depressed upon discharge from the hospital.<br />At 6 months, a majority of patients with PSD continued to have symptoms. <br />Course of PSD different for major and minor depression<br />
  35. 35. Major PSD<br />Recovery significantly better in major PSD than minor PSD with nearly 75% resolution in symptoms after two years. <br />Chemerinski & Robinson, 2000.<br />
  36. 36. Minor PSD<br /> Prognosis worse in patients with minor depression.<br />Chemerinski& Robinson, 2000<br />
  37. 37. PSD and mortality Morris, et al., 1993<br />Patients with either Major or Minor PSD are 3.4 times more likely to die during a 10 year period poststroke than nondepressed patients.<br />Patients with PSD and few social contacts have an even increased mortality rate: 90% died in Morris et al cohort. <br />
  38. 38. Diagnosis of PSD<br />Difficult to reliably diagnose<br />Post-stroke depression under-diagnosed by non-psychiatric physicians in 50-80% of cases. Shuebert, et al. 1992<br />Widespread belief that depression is simply an understandable psychological reaction or grief response.<br />
  39. 39. F. Mania<br />Etiology and lesion correlates<br /> Right hemisphere either cortical (basotemporal cortex or orbitofrontal cortex) or subcortical (frontal white matter, basal ganglia, or thalamus). <br />
  40. 40. G. Anxiety Disorder<br /> Epidemiology<br />Generalized Anxiety Disorder (GAD) without depression occurs in approximately 10% of patients with acute stroke.<br />Approximately 75% of patients with post-stroke GAD have co-morbid major or minor depression. <br />
  41. 41. Anxiety Disorder cont… <br /> Etiology and lesion correlates<br />Anxious-depressed patients had a significantly higher frequency of cortical lesions.<br />Depression-only group showed a significantly higher frequency of lesions of the basal ganglia.<br />
  42. 42. H. Emotional Incontinence<br />Synonyms: pathological crying or laughing, emotional diarrhea, emotional lability, pseudobulbar affect, involuntary emotional expression disorder <br /> It is characterized by episodes of crying or laughing that are unrelated to or out of proportion to the eliciting stimulus. <br />The crying or laughing are disinhibited and experienced by the patient as unwanted and a struggle to stop. <br /> Found in stroke, patients with frontal lobe lesions due to traumatic brain injury, multiple sclerosis, pseudobulbar palsy, and amyotrophic lateral sclerosis.<br />37<br />
  43. 43. Emotional Incontinence cotd…<br />Pathological crying or laughing can have a significant impact on individuals’ social functioning and their relationships with others.<br /> Unpredictable and uncontrollable outbursts of affect often cause severe embarrassment and avoidance of social interactions and may result in subsequent agoraphobia.<br />38<br />
  44. 44. I. Catastrophic Reaction<br />Epidemiology<br />Starkstein et al. reported that a catastrophic reaction was present in 19% of a consecutive series of 62 patients with acute stroke. <br />Etiology and lesion correlates<br />Starkstein et al. found that catastrophic reactions were significantly associated with basal ganglia lesions. <br />
  45. 45. Catastrophic Reaction contd…<br />These are outbursts of frustration, dysphoria, and anger when confronted with a frustrating (usually cognitive) task, often appearing suddenly and unexpectedly, startling caregivers and relatives. <br />These are emotional incontinence, and poststroke depression share some symptoms in common and often co-occur but are distinct clinical syndromes. <br />40<br />
  46. 46. Catastrophic Reaction contd…<br />One prospective study of patients with a first stroke identified catastrophic reactions in 12 of 326 patients within 48 hours from onset of the stroke, and were associated with nonfluent aphasias.<br />Another study - after acute stroke were significantly associated with depression, a personal and family history of psychiatric disorder, and subcortical lesions which were mostly located in the basal ganglia.<br />41<br />
  47. 47. J. Psychosis<br />Epidemiology<br /> - Incidence 1% Starkstein et al 1987<br />Delusions or hallucinations are rare complications of stroke–no prevalence studies have been done.<br />Etiology and lesion correlates<br /> Right hemisphere lesion and either seizure disorder or pre-stroke subcortical atrophy. <br />
  48. 48. Psychosis contd…<br />Release visual hallucinations are visual hallucinations associated with loss of vision, arising if there is any defect in the afferent visual pathway. <br />Proposed mechanisms - release of inhibition in the higher visual cortex or release of previously recorded percepts due to sensory deprivation in the defective field of vision.<br />43<br />
  49. 49. Psychosis contd…<br />There is usually a delay of days to weeks between the ischemic event and the onset of hallucinations. <br />The patient reported here first experienced release visual hallucinations almost two weeks after his initial symptoms. <br />44<br />
  50. 50. Psychosis contd…<br />The complexity of hallucinations in this setting have no localizing value.<br />Release visual hallucinations are usually within the defective field of vision, continuous, non-stereotyped and increased in the dark.<br />There is a report in which visual hallucinations in a patient with left occipital infarction exacerbated on exposure to light<br />The hallucinations are usually transient, lasting days or weeks,<br />They may be more persistent.<br />45<br />
  51. 51. K. Hyposexuality<br />Decline in sexual interest and activity is common after stroke, with greater declines in those who are older or disabled. <br />Psychological rather than physical aspects account for most of the decline in sexual activity in stroke survivors. <br />Patients’ partners play a substantial role in the decline of sexual activity, related to their own anguish and anxiety over risk for recurrence of stroke.<br />46<br />
  52. 52. Hyposexuality contd…<br /> Patients and their partners can be counseled that sexual intercourse does not increase risk for stroke. <br />Sexual dysfunction after stroke frequently occurs alongside depression. <br />May also have major medical comorbidities contributing to sexual dysfunction, including diabetes mellitus, peripheral vascular disease, and hypertension.<br />47<br />
  53. 53. L. Hypersexuality.<br /> Lesion: Bilateral infarction of amygdala<br /> Features:<br /> Patient is not afraid of anything.<br /> Extreme curiosity.<br /> Forgets rapidly.<br /> Tendency to place anything in mouth.<br /> Hypersexuality.<br />48<br />
  54. 54. M. Obsessive-Compulsive Disorder<br />Most often those affecting the basal ganglia or brainstem.<br />Case reports suggest that both antidepressants and behavior therapy can be effective.<br />49<br />
  55. 55. N. Conversion Disorder and Stroke<br />conversion disorder Patients presents with acute onset of neurologic symptoms, they may be misdiagnosed as having transient ischemic attacks or strokes. <br /> <br />Careful neurologic examination and imaging studies permit distinguishing which patients really have strokes. <br />The older the patient, the less likely it is that the diagnosis is conversion disorder<br />50<br />
  56. 56. O. Personality or behavioral changes:<br />Associated with infarction to orbitofrontal lobe or anterior temporal lobe.<br /> Frontal lobe syndrome is characterized by disinhibition, impulsivity, irritability, aggressive outburst.<br /> Pseudo- depressed personality syndrome: apathy, blunted affect.<br /> Pseudo -psychopathic personality syndrome: disinhibition, egocentricity & sexual inappropriateness.<br />51<br />
  57. 57. Biological basis of neuropsychiatric consequences:<br />52<br />Source: CTP 8th edition<br />
  58. 58. Role of psychiatrist in management of post stroke sequelae <br />Treatment of post stroke axis I psychiatric disorder<br /> Counseling of family members<br /> Life style modification <br /> Management of rehabilitation<br />53<br />
  59. 59. Comparative nosology<br /> ICD 10<br /> Annex:<br /> Other conditions often associated with mental & behavioral disorder:<br /> Chapter IX: Disease of circulatory system<br />І60: Subarachnoid hemorrhage<br />І61: Intracerebral hemorrhage<br />І62: Other nontraumatic intracerebral hemorrhage<br />І63: Cerebral infarction <br />І65: Stroke not specified as hemorrhage or infarction<br /> F01: Vascular dementia <br />54<br />
  60. 60. Comparative nosology contd..<br />DSM- IV-TR<br /> Disorder due to cerebral vascular disease or stroke:<br /> Post stroke psychotic disorder<br /> With or without delusion<br /> With or without hallucination<br /> Post stroke mood disorder<br /> With depressive feature<br /> With major depressive-like episode<br /> With manic feature<br /> With mixed feature<br /> Post stroke anxiety disorder<br /> With GAD<br /> With panic attack<br /> With obsessive compulsive symptoms<br />55<br />
  61. 61. PROGNOSIS<br />56<br />
  62. 62. 57<br />Predictor of outcome:<br />Glasgow Coma Scale Scoring<br />Best Verbal Response (5)<br /><ul><li>No verbal response
  63. 63. Incomprehensible sounds.
  64. 64. Inappropriate words.
  65. 65. Confused
  66. 66. Orientated</li></ul>Best Eye Response (4)<br /><ul><li>No eye opening.
  67. 67. Eye opening to pain.
  68. 68. Eye opening to verbal command.
  69. 69. Eyes open spontaneously</li></ul> Best Motor Response (6)<br />No motor response.<br />Extension to pain.<br />Flexion to pain.<br />Withdrawal from pain.<br />Localizing pain.<br />Obeys Commands.<br />Total Score= E+ M+ V<br />
  70. 70. Predictor of outcome contd…<br />GCS score-<br /> - Mild : 13-15 <br /> - Moderate : 9-12 <br /> - Severe : 3-8<br />Coma is defined as: <br /> (1) not opening eyes, <br /> (2) not obeying commands<br /> (3) not uttering understandable words.<br />58<br />
  71. 71. Management<br />59<br />
  72. 72. Laboratory investigation<br />Vascular dementia:<br />Structural imaging studies: CT/ MRI, cerebral angiography<br />Blood chemistry – serum lipid profile, Vit. B12 , folate, thyroid profile<br />Neurophysiological studies: EEG, EEG with evoked responses<br />Post stroke depression: <br />Dexamethasone supressiontest : <br /> -Possible biological marker<br /> - Failure to suppress serum cortisol in response to administration of dexamethasone<br /> Growth hormone response to desipramine:<br /> - Blunted response<br /> - Diminished α2 adrenergic receptor function<br />60<br />
  73. 73. Psychological assessment<br /> Multifactor approach: different parts of the brain functions differently. Two widely known tests<br />1. Halstead-Reitan Neuropsychological Tests Battery<br />2. Luria-Nebraska Neuropsychological Battery<br />61<br />
  74. 74. Testing procedures developed in India:<br />PGI Battery of Brain Dysfunction<br />This battery includes five tests <br />Bhatia’s Short Scale<br /> Verbal Adult Intelligence Scale<br /> PGI Memory Scale<br /> Bender Visual Motor Gestalt Test <br />Nahor Benson Test of Perceptual Acuity. <br />62<br />
  75. 75. Testing procedures developed in India cond…<br />AIIMS Comprehensive Neuropsychological Battery in Hindi <br /> Based on Luria-Nebraska Neuropsychological Battery and potentially useful for both diagnosis and rehabilitation. It consists of thirteen basic scales<br />NIMHANS Neuropsychology Battery – 2004<br /> There are 19 tests in all, which measures 15 functions, in seven neuropsychological domains <br />63<br />
  76. 76. Risk factors for neuropsychiatric sequelae<br /><ul><li>Female > 60 yrs
  77. 77. History of depression
  78. 78. Dysphasia
  79. 79. Social isolation
  80. 80. Extent of impairment</li></ul>64<br />
  81. 81. Who should be admitted ?ABCD<br />Points<br />Age > 60 YEARS 1<br />Blood Pressure Systolic >140 <br /> +/ Diastolic > 90 1<br />Clinical Features Unilateral weakness 2<br /> Speech disturbance alone 1<br /> Other 0<br />Duration of symptom > 60 minutes 2<br /> 10-59 minute 1<br /> < 10 minutes 0<br />Diabetes present 1<br />A score of > 5 is highly predictive of 7 day risk of stroke and these patients should e admitted for further management<br />
  82. 82. Treatment:<br />Vascular dementia<br />Antiplatelet aggregate drugs: Aspirin<br /> Antihypertensive drugs<br /> Lipid lowering drugs: Statins<br /> Cholinergic agonist: Donepezil. Rivastigmine, Galantamine<br /> Smoking cessation<br /> Prevention & careful management of diabetes mellitus.<br />66<br />
  83. 83. Post-stroke Depression<br />Tricyclic antidepressants<br />SSRI and SSNRI Antidepressants <br />Psychostimulants<br />Counseling and Psychotherapy<br />
  84. 84. Effectiveness of antidepressant treatment of PSD<br />Meta-analysis of studies of antidepressant therapy conclude that this treatment modality may be beneficial to patients with PSD Chen, Y, et al, 20006 <br />Tricyclic antidepressants are as effective as newer generation selective serotonin reuptake inhibitors (SSRI) but with greater side effects reported..<br />
  85. 85. Effectiveness of antidepressant treatment of PSD contd…<br />SSRIs have been the most widely studied class of antidepressants<br />Citalopramis the single most widely studied agent in PSD<br />No evidence that one SSRI preferential over another.<br />Selective serotonin/norepinephrine reuptake inhibitors such as venlafaxine and duloxetine are also increasingly utilized.<br />
  86. 86. Considerations for treatment with antidepressant medication<br />Goal is to choose agent with least potential for side effects and titrate slowly to improve tolerability and compliance with treatment.<br />Some agents, such as mirtazapine, may be preferential to treat poor appetite or other vegetative symptoms in some patients.<br />In patients with apathy and significant psychomotor retardation, consider initiating treatment with psychostimulant and then convert to SSRI/SSNRI.<br />
  87. 87. Prophylactic treatment to prevent PSD<br />Mirtazapine has shown promise in as acute treatment for prevention of PSDNiedermaier et al., 2005<br />Sertraline has shown promise in the prevention of PSD as well as in treatment of PSD symptoms.Poulsen, et al, 2003<br />
  88. 88. Psychostimulant as treatment for PSD<br />Limited research regarding use of psychostimulants in PSD<br />Increasing clinical use reported, especially in patients with marked vegetative symptoms, apathy, and lethargy.<br />Masand, et al psychostimulant study results<br />Primary stimulants used were methylphenidate & Dextroamphetamine<br />82% of patients improved with 77% showing marked improvement<br />51% responded in one day, an additional 34% by the second day<br />Only 2% relapse during treatment<br />15% incidence of side effects<br />No cases of anorexia, appetite improved with mood.<br />
  89. 89. Treatment contd…<br /> Anxiety:<br />Benzodiazepines are the most commonly prescribed medications . -They tend to accumulate in older people. <br /> -should be used carefully in patients with stroke.<br />Buspirone, an anxiolytic medication with <br /> -partial serotonin agonist properties, <br /> -reported to have a similar efficacy as diazepam in the treatment of GAD <br /> - more tolerable side effect profile.<br />The utility of buspirone in the poststrokepopulation has not been examined. <br />73<br />
  90. 90. Treatment contd…<br /> Mania:<br /> Lithium<br /> Clonidine (an adrenergic agonist) rapidly reversed the manic symptoms<br />Valproate in combination with ziprasidone or aripiprazole<br />Apathy:<br />No controlled treatment studies of poststroke apathy have been conducted. <br />Marin et al. suggested the use of dopamine agonists for patients with basal ganglia and frontal lobe lesions<br />Multiple infarcts or with comorbid depression may obtain benefits from stimulant drugs or antidepressants with a stimulant profile such as bupropion.<br />74<br />
  91. 91. Emotional Incontinence<br /> 4 double-blind treatment trials which have shown that the following antidepressants are effective in treating this condition:<br />Nortriptyline<br />Citalopam<br />Escitalopam<br />Fluoxetine<br />Sertraline<br />
  92. 92. Psychosis<br />patients respond to treatment with typical neuroleptic medications <br />some treatment-resistant cases have been reported . In these treatment resistantcases, anticonvulsant medications have sometimes been reported to be useful . <br />Currently, there are no studies examining treatment response to the atypical antipsychotic medications. <br />76<br />
  93. 93. Management of rehabilitationBates et al 2005<br />Primary goals- <br /> - Prevent complication<br /> - Minimise impairments<br /> - Maximise functions<br /> Secondary prevention- fundamental to stroke prevention<br /> Early assessment & Intervention are critical to optimize rehabilitation.<br />Standardized evaluation & valid assessment tools mandatory for comprehensive treatment plan<br /> Evidence based interventions should be based on functional goals<br />77<br />
  94. 94. Management of rehabilitation contd…<br /> Every patient for rehab should have access to experienced & coordinated rehab team<br /> Patient, family member &/ or care giver are essential member in rehab team<br />Patient & family education improves the process of rehab.<br />Rehab team should utilize community resources for community reintegration<br /> Ongoing medical management of risk factors & comorbidities is essential to ensure survival<br />78<br />
  95. 95. Impact on family and care givers<br /><ul><li>Premorbid relationships crucial in determining subsequent coping
  96. 96. Anxiety/depression/guilt
  97. 97. Most difficult aspects are not physical but behavioural or personality changes</li></ul>79<br />
  98. 98. Summary:<br /> Common disorders following stroke:<br />Depression (15% in community, 20% in-hospital)<br />Anxiety Disorder (6% in-hospital)<br />Apathy (22% in-hospital)<br />Catastrophic reaction (19% in-hospital)<br />Pathological affect (15% in community)<br />Post-stroke psychosis (<1% in-hospital)<br />
  99. 99. Summary cont…<br />Pharmacological trials have demonstrated effective treatments for both post-stroke depression and post-stroke pathological laughing and crying.<br />Treatment trials for the other post-stroke disorders are urgently needed.<br />
  100. 100. Conclusion<br />82<br /> Post CVA patients are often having complications with psychiatric morbidity such as depression, anxiety disorders, adjustment problems and sexual dysfunction, etc. These complications hinder in the physical recovery of the patients. Therefore, such association of psychiatric morbidity in those patients should be recognized in time and appropriate treatment should be done along with management of neurological problems to improve their neuro-motor function.<br />
  101. 101. Bibliography<br />Lishman’s organic psychiatry,4thed, p 475-98<br /> Essentials of Psychosomatic Medicine , Levenson, P 701-05, American Psychiatric Publishing Textbook.<br />Psychosomatic Medicine, Blumenfield & Strain, P 254-74, Lippincott Williams & Wilkins.<br /> CTP, 8thed, Kaplan & Sadock, P 349-61<br /> Web:<br />www.pubmed.com<br />www.medscape.com<br />www.googlemage.com<br />83<br />
  102. 102. Thank you<br />84<br />

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