Post stroke psychiatric symptoms
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This document discusses post-stroke psychiatric disorders. It describes five frontosubcortical circuits that are involved in cognition, behavior and movement. Common post-stroke psychiatric conditions include depression, anxiety, apathy, psychosis and pathological laughing/crying. Lesion location can impact the type of psychiatric disorder, such as left anterior lesions increasing risk of depression. Treatment involves pharmacotherapy, such as antidepressants, and psychotherapy. Screening and ongoing monitoring of symptoms is important after a stroke to identify and manage post-stroke psychiatric complications.
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Post stroke psychiatric symptoms
- 2. Frontosubcortical Networks • Five frontosubcortical circuits • subserve cognition, behavior, and movement • Neurotransmitters involved - Dopamine (DA), Glutamate, γ-aminobutyric Acid (GABA), Acetylcholine, Norepinephrine, & Serotonin
- 3. Frontosubcortical Networks 1. Motor circuit 2. Oculomotor circuit 3. Dorsolateral prefrontal circuit 4. Orbitofrontal circuit 5. Anterior cingulate circuit
- 4. Motor circuit • Subserves somatic motor function • Originating in the supplementary motor area Oculomotor circuit • Originating in the frontal eye fields • Subserves oculomotor function
- 5. Dorsolateral Prefrontal Circuit Executive functions, including • Ability to plan and maintain Deficits •Slowed information attention • Problem solve processing • Learn, retrieve remote memories •Memory retrieval deficits • Sequence the temporal order of •Mood and behavioral events • Shift cognitive and behavioral sets • Generate motor programs changes •Gait disturbance •Dysarthria Involved in subcortical dementias •Other motor impairments
- 6. Orbitofrontal Circuit • connects frontal monitoring functions to the limbic system • governs appropriate responses to social cues, empathy, social judgment, and interpersonal sensitivity • pairs thoughts, memories, and experiences with corresponding visceral and emotional states • heavily involved in the process of decision making and evaluating the costs and benefits of specific behavioral responses to the environment
- 7. Orbitofrontal Circuit Medial OFC Evaluates reward Monitors and decodes punishment Lateral OFC Anterior OFC Reward value for more abstract and complex secondary reinforcing factors such as money Posterior OFC Reward value for more concrete factors such as touch and taste Evaluating the emotional significance of stimuli
- 8. Orbitofrontal Circuit Dysfunction • Disinhibition • Irritability • Aggressive outbursts • Inappropriate social responses • Impulsive decision making
- 9. Anterior Cingulate Circuit • nucleus accumbens with both afferent and efferent connections to the dorsolateral prefrontal cortex (DLPFC) and amygdale • involved in motivated behavior Lesions • apathy, abulia, and akinetic mutism
- 10. Prevalence of Post Stroke Neuropsychiatric Disorders • Depression: 35% • Mania: rare • Bipolar disorder: rare • Anxiety disorder: 25% • Apathy : 20% • Psychosis: rare • Pathologic affect 20% • Catastrophic reaction: 20% Most common are: depression, anxiety, emotional incontinence and catastrophic reactions
- 11. Neuropsychiatric consequences of stroke depend on • Location and size of the stroke • Preexisting brain pathology • Baseline intellectual capacity and functioning • Age • Premorbid psychiatric history
- 12. Post Stroke Neuropsychiatric Disorders • period of high risk for psychiatric complications is first 6 months following a stroke • In general, interruption of bilateral frontotemporal lobe function is associated with an increased risk of depressive and psychotic symptoms
- 13. Post Stroke Depression • In 30% to 40% of patients within the first year • most develop within the first month (Ballard and O’Brien, 2002) • 30% to 50% of survivors at 1 year • About half will meet criteria for a major depressive episode
- 14. Post Stroke Depression • Prevalence varies over time with an apparent peak at 3-6 months after stroke and a subsequent decline to about 50% of initial rates at 1 year • Duration of major PSD is about 9 months to 1 year whereas the duration of minor depression is several years • Spontaneous remission can occur 1-2 year poststroke. (Robinson et al, 1987)
- 15. Risk factors for post stroke depression Consistent Controversial Past Psych history Age Dysphasia Gender Poor Social Support Impaired ADLs Lesion Location Lesion Volume Premorbid diagnosis of depression (5 to 6 times more likely) (Ried et al., 2010)
- 16. Diagnosis of PSD is difficult sometimes because of • Language disorders - difficulty in expressing or comprehending • Cognitive impairment - anosognosia or lack of insight or lack of awareness of depressive symptoms • Overlap between symptoms of depression & medical condition - several symptoms of depression such as loss of energy, decreased appetite, insomnia are found among non- depressed stroke patients secondary to hospital environment, use of medications, other medical conditions and stroke itself
- 17. Causes of PSD Probably due to a combination of biological, psychological and social factors. • Biological: disruption of neural circuits & neurochemicals. Genetic cause. • Psychological: presence of poor coping skills • Social: disability, limited social support, loss of independence may overwhelm coping skills Psychological stressors can overwhelm anyone, and in the setting of biological vulnerability, can cause depression
- 18. Biology of Depression Dysfunction in • Orbitofrontal–basal ganglia– thalamic circuit • Basotemporal limbic circuit that links the orbitofrontal cortex and the anterior temporal cortex by the uncinate fasciculus
- 19. Four interconnected functional compartments • Mood regulation (medial frontal, medial orbital-frontal and pregenu anterior cingulate cortex) • Mood monitoring (ventral striatum-caudate, amygdale, dorsomedial thalamus, midbrain-ventral tegmental area) • Interoception (subcallosal cingulated, ventral-anterior hippocampus, anterior insula, brain stem, hypothalamus) • Exteroception (prefrontal, premotor, parietal, mid- cingulate and posterior cingulate cortices with dorsalposterior hippocampus)
- 20. Consequences of post stroke depression • Longer hospital stays – affect rehabilitation • Poorer recovery of activities of daily living • Increased morbidity ( more with presence of executive dysfunction) • Poorer quality of life, even when neurological symptoms and disability are held constant
- 21. Depression and Lesion Location • more with left anterior lesions • esp nearer the left frontal pole or left caudate nucleus More recent review articles have not supported a relationship between lesion location and depression in poststroke patients (Bhogal et al., 2004)
- 22. Depression and Lesion Location • with left sided lesions in hospital samples, whereas with right-sided lesions in community samples • with left-sided lesions in first month following stroke • with right-sided lesions in more than 6 months after the stroke (Bhogal et al., 2004)
- 23. Depression and Lesion Location Left prefrontal lesions are more apt to be associated with acute depression and may be complicated by aphasia, resulting in the patient’s inability to express the symptoms
- 24. Screening for depression SIGECAPS • Sleep, Interest level, Guilt, Energy level, Concentration, Appetite, Psychomotor activity level, and Suicidal thoughts • presence of 5 or more of these symptoms (one of which must be depressed mood or decreased interest level) for 2 weeks is the threshold for a diagnosis of major depression
- 25. Quantifing depressive symptoms • self-administered Beck Depression Inventory (BDI) and clinician-administered Hamilton Rating Scale for Depression (HDS) • clinician-administered Post-Stroke Depression Rating Scale (PSDRS) addresses the "major" and "minor" forms of PSD
- 26. Treatment of PSD • Supportive psychotherapy and pharmacotherapy • Antidepressants are well tolerated • 60% respond to medications
- 27. Psychopharmacologic treatment • Tricyclic antidepressants (TCAs) • Selective serotonin reuptake inhibitors (SSRIs • Psychostimulants (eg, methylphenidate) No particular class has an advantage over the other
- 28. SSRIs • first-line treatment In the acute phase • cause fewer serious side effects, such as delirium and sedation, than do TCAs • may increase bleeding risk in some patients because of their effects on platelet function • recent major review found no causal relationship between SSRIs and bleeding in post-stroke patients
- 29. Dosing of Antidepressants • "start low and go slow," • Consider starting at half the typical adult starting dose • allow 1 to 2 weeks between dose increases • best to conduct an adequate trial: minimally, a trial of 6 weeks' duration at the usual adult therapeutic dose
- 30. Follow up at least monthly repeating the cognitive examination and depression inventory to monitor treatment response Clinical remission No clinical response despite demonstrated adherence Initial antidepressant is poorly tolerated Continue treatment for up to 12 months at the full effective dose Switch to a different antidepressant class and/or augment the therapy with a psychostimulant (eg, methylphenidate, dextroamphetamine)
- 31. Psychostimulants • safe, well tolerated and efficacious • no definitive conclusions can be made given lack of randomization • Risk of seizure and/or cardiac side effects • If history of seizures, consideration of antiseizure medication, along with psychostimulants, appears reasonable
- 32. Consider electroconvulsive therapy for • Depression-related emergencies, such as repeated suicide attempts and severe melancholic PSD • Refractory to maximal medication management • Complex psychopharmacologic regimens causing intolerable side effects
- 33. Prophylactic treatment with an antidepressant • prior episodes of depression • left-sided lesions • history of other psychiatric illness • strong family history of psychiatric illness
- 34. Prophylactic treatment with an antidepressant Advantages • antidepressants, neurotropic, stabilize the chemical imbalance; • increased compliance with vascular disease preventing regimens; • they may have an effect on serotonin mediated platelet activation. Antidepressants have side-effects such as falls, increased bleeding, seizures, and sedation
- 35. Pathological Laughing and Crying Other names: Emotional Incontinence; post-stroke emotionalism • Between 11% and 35% after stroke (Parvizi et al., 2009). • associated with brainstem and cerebellar lesions • sudden paroxysms of either laughter or crying, irrespective of the ambient mood state • can be triggered by nonspecific stimuli or by a low- threshold emotive stimulus
- 36. Pathological Laughing and Crying Management • Tricyclic and SSRI antidepressants • Lithium and anticonvulsants are alternatives
- 37. Post-Stroke Mania • Rare • associated with right-sided stroke • expansive and/or irritable mood, decreased need for sleep, increased goal-directed activity, recklessness, disregard for social constraints, talkativeness, racing thoughts, excessive laughter or giggling, and poor judgment
- 38. Post-Stroke Mania Management • mood stabilizer and/or an atypical antipsychotic • Observation for downward cycling of mood into an episode of PSD, using mood screening questions and/or depression inventories and clinical observation, is necessary
- 39. Post-Stroke Anxiety Disorders • Risks of 26% and 39% in men and women respectively • more common in cortical than subcortical stroke • discrete episodes of panic, tonic levels of increased anxiety, excessive sweating, worrying, and decreased sleep
- 40. Post-Stroke Anxiety Disorders • majority also having PSD • Anxiety Depression (AD) was associated with left cortical lesions and anxiety alone with right hemisphere lesions • comorbidity of PSD and AD produced longer duration of PSD than PSD alone and this prolonged depression might lead to poorer physical and social outcomes
- 41. Post-Stroke Anxiety Disorders Management • respond well to antidepressants (SSRIs ) • Avoidance of benzodiazepines is important; these agents may cause cognitive decline, verging on PSDem • Follow-up should be done in 1 month to assess response • If symptoms are incompletely responsive to antidepressant(s), consider buspirone, either with an antidepressant or as monotherapy
- 42. Post-Stroke Catastrophic Reactions • outburst of emotion, such as anxiety, agitation, or crying, that occurs when unable to perform simple tasks that were possible before • associated with PSD & Basal Ganglia lesions • may be a release phenomenon due to subcortical damage • often associated with expressive aphasia. • Treatment consists of prophylactic and supportive measures
- 43. Poststroke psychosis • rare complication • include paranoia, delusions, hallucinations (which may affect various sensory modalities; auditory and visual hallucinations are the most common), ideas of reference, thought disorganization, and regressed motor behavior
- 44. Poststroke psychosis • more prone to have comorbid epilepsy • Psychotic episodes can also be a manifestation of complex partial seizures secondary to stroke • correlate with right-sided lesions and cortical/subcortical atrophy
- 45. Paranoia Associated with lesions in a) left temporal strokes that result in Wernicke aphasia b) right temporoparietal region and the caudate nuclei
- 46. Visual hallucinations and delusions • Right hemispheric lesions Peduncular hallucinosis • well-formed and complex visual hallucinations • Lesions or infarcts of the ventral midbrain
- 47. Reduplicative paramnesia • patients claim that they are simultaneously in two or more locations • due to a) combined lesions of frontal and right temporal lobe b) temporal limbic- frontal dysfunction
- 48. Capgras syndrome • false belief that someone familiar, usually a family member or close friend, has been replaced by an identical appearing imposter • Right temporal-limbic-frontal disconnection disturbance in recognizing familiar people and places
- 49. Fregoli syndrome • patient believes a persecutor is able to take on a variety of faces, like an actor • Injury to the right frontal and left temporoparietal areas
- 50. Treatment of Poststroke psychosis • Atypical antipsychotic, such as risperidone or olanzapine • Close follow-up every 2 weeks and titration of antipsychotic dose to effect is recommended • Reassessment for reemergence of psychosis, repeated cognitive examination, and depression inventory at each visit are recommended
- 51. Obsessive-compulsive features • due to dysfunction in the orbitofrontal-subcortical circuitry (Saxena et al., 1998)
- 52. Apathy • presents with profound lack of initiative without tearfulness, sleep/appetite disturbance, hopelessness, or suicidality • in the absence of depression may be difficult to appreciate • Treated with antidepressants and/or psychostimulants
- 53. Aggression • associated with increased motor dysfunction and dysarthria • Lesions in the area supplied by the subcortical middle cerebral artery → inability to control anger or aggression • Lesions nearer to the frontal pole → irritability and aggression
- 54. Aggression Management • Fluoxetine reduce levels of poststroke anger (Choi-Kwon et al., 2006) • Measures to reduce depression (Chan et al., 2006)
- 55. Post-stroke fatigue • Managed with Antidepressants and psychostimulants, particularly those with effects on noradrenergic and/or dopaminergic activity (eg, bupropion, venlafaxine, and mirtazapine) • Follow-up within 1 month is needed
- 56. Post-Stroke Dementia • A temporal relationship between a stroke and the onset of dementia • stepwise progression of cognitive decline • evidence of cerebrovascular disease on examination • Neuroimaging findings No specific neuroimaging profile exists that is diagnostic for pure cerebrovascular disease-related dementia.
- 57. Post-Stroke Dementia • Small vessel disease is the most frequently observed vascular pathology • series of deep white matter infarcts • present with prominent cortical, subcortical, or mixed features
- 58. Cortical vascular dementia • unilateral sensorimotor dysfunction • abrupt onset of cognitive dysfunction and aphasia • difficulties with planning, goal formation, organization, and abstraction
- 59. Subcortical vascular dementia • affects frontosubcortical circuitry • resulting in executive dysfunction, cognitive slowing, difficulties with abstraction, apathy, memory problems (recognition and cue recognition relatively intact), working memory impairment, and decreased ability to perform activities of daily living
- 60. Post-Stroke Dementia • Some cases of dementia diagnosed in the post-stroke period may represent previously unrecognized cases of AD • Memory difficulties tend to be less severe than in AD
- 61. Post-Stroke Dementia • changes in instrumental activities of daily living that require complex organizational and problem-solving skills (e.g., managing finances, following directions, “figuring things out”) are likely more prominent in a patient with VaD compared to one with AD • apathy is a hallmark symptom
- 62. Monitoring Post-Stroke Dementia • Folstein Mini-Mental State Examination or the cognitive portion of the Cambridge Examination for Mental Disorders of the Elderly • repeated serially to monitor progression and/or treatment response
- 63. Treatment for post-stroke dementia • low threshold for psychiatry referral for agitated behavior, persistent confusion, or cognitive inability to participate in treatment • An additional workup (vitamin B12, folate, and TSH analysis; toxicology screening; and rapid plasma reagent and HIV testing) for reversible causes of dementia should also be accomplished
- 64. Treatment for post-stroke dementia • may benefit from pharmacotherapy for AD (cholinesterase inhibitors and memantine) • dose increased at monthly intervals according to response • Initiate atypical antipsychotics and/or antidepressants for agitated behavior • followed up monthly, with reassessment of cognitive examination, repeated depression inventory, and screening for psychotic symptoms
- 65. Neuropsychiatric Symptoms and Corresponding Neuroanatomy
- 66. Neuropsychiatric Symptoms and Corresponding Neuroanatomy Symptom Neuroanatomical Region Anterior cingulate gyrus, nucleus Apathy accumbens, globus pallidus, thalamus Orbital or medial frontal cortex, caudate OCD nucleus, globus pallidus Orbitofrontal cortex, hypothalamus, Disinhibition septum Psychosis Frontal lobes, left temporal cortex
- 67. Neuropsychiatric Symptoms and Corresponding Neuroanatomy
- 68. Summary • Depression & anxiety are the 2 most common post- stroke syndromes. • Both depression and anxiety increase morbidity and delay rehabilitation. • Treatment of neuropsychiatric post-stroke disorders have the greatest potential for improving outcome and quality of life.