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Abstract
Over the last 50 years there has been a steady decline in stroke incidence and mortality. Improved control of hypertension and acute management of stroke patients are important factors contributing to this decline. The American Heart Association nevertheless estimates that 500,000 new cases of stroke appear in the United States per year. Also, although stroke ranks in the top three leading causes of death, accounting for 150,000 fatalities per year, a population of around 3 million stroke survivors exists at any given time. Of the survivors, two-thirds have some degree of permanent disability that requires rehabilitation care. Recent studies have concluded that neuropsychiatric complications (i.e., emotional, behavioral, and cognitive disorders) may have a negative effect not only on the social functioning and overall quality of life of stroke survivors, but also on the recovery of their motor functioning,
Depression after stroke has long been recognized as a common condition with many negative effects in the post-stroke period. Because effective treatments exist but are likely underutilized for depression, this is an important example of an evidence-practice gap to which increased efforts to improve care should be made. Such efforts would likely improve not only patient symptoms but may also decrease stroke risk, influence stroke functional recovery, decrease mortality, and reduce post-stroke health care utilization.
Researchers are split into 2 groups with opposing views about the etiology of psd. Some propose purely biological mechanisms and while other propose psychological mechanisms. An integrated bio-psycho-social model including both biological and psychosocial aspects of post stroke depression seems warranted.
Other post stroke psychiatric disorders are likely to occur but in lesser frequency than PSD. These disorders are mania, personality changes, anxiety, psychosis, sexual dysfunction and cognitive impairment.
Despite high prevalence (30% to 50%) and serious sequels, (PSD) remains undetected and untreated. Early diagnosis and successful intervention may improve clinical outcome and should be considered a key for better stroke care, so antidepressants have been used as prophylaxis to prevent PSD.
National clinical guidelines for the management of mood disturbance after stroke (Dilley et al, 2006):
• Provide information, advice and the opportunity to talk about the impact of the stroke.
• Assess psychosocial needs.
• Screen for depression and anxiety within the first month of stroke and monitor mood.
• With those who can respond use standardised questionnaires for screening.
• Confirm emotionalism by a few simple questions at interview.
• If one mood disorder is present assess for the others.
• Severe, persistent or troublesome tearfulness (emotionalism) should be treated with anti-depressants; the frequency of crying should be monitored to check effectiveness.
• Consider a trial of antidepressant medication in those with persistently depressed mood of at least 1 month’s duration.
• If there is a good response, antidepressants should be continued for at least 6 months after.
To diagnose PSD, since there may be an overlap between symptoms of depression and signs associated with the neurologic disease. The best approach is to assess the presence of depressive symptoms using semi-structured or structured psychiatric interviews such as the Present State Exam, the Structured Clinical Interview for DSM-IV, or the Schedules for Clinical Assessment in Neuropsychiatry. The diagnosis of a depressive syndrome should be made using standardized diagnostic criteria for mood disorders due to neurological disease such as in the DSM-IV or the ICD-10.
Patients with new-onset mania require an evaluation that includes a thorough history, a neurologic examination, neuroimaging, and other selected tests. The management of patients with neurologic mania involving correcting the underlying disorder when possible and the judicious use of drugs such as the anticonvulsant medications.
Persons with post-stroke psychosis should be referred for psychiatric care, with subsequent comanagement from the psychiatrist. Treatment includes:
• Psychiatry referral is recommended to assess the need for psychiatric hospitalization
• Begin treatment with atypical antipsychotic medication
• Schedule follow-up examinations every 2 weeks and titrate the drug dose to effect
• Reassess for psychosis and repeat the cognitive examination and depression inventory at each visit
• Cotreatment of the patient with the psychiatrist may be required.
An adaptation of the Cambridge Cognitive Examination (CAMCOG), the Rotterdam-CAMCOG, had excellent sensitivity and specificity for detecting post-stroke dementia in a clinical setting. Clinical cognitive examinations such as the Folstein Mini-Mental State Examination should be used even in cognitively asymptomatic patients post-stroke and can be repeated serially to monitor progression and/or treatment response. The therapeutic efficacy of the serotonin norepinephrine reuptake inhibitor (SNRI) on both cognitive impairment and depression in post-stroke depression (PSD) patients was effective in improving cognitive dysfunction.