Traveling for Care?
Whether you're crossing the country or the globe, we make it easy to access world-class care at Johns Hopkins.
by Vani Rao, M.D.
The definition of a Stroke (WHO Stroke, 1989) is as follows:
Over the last decade there has been a decrease in incidence and mortality probably secondary to improved measures to treat hypertension, less smoking and better management of heart disease factors. However, it is still the 3rd leading cause of death with an incidence of 500,000/yr, 1/3 of who die each year. Additional epidemiologic factors include:
Pathophysiology of a Stroke
Ischemic strokes are caused by interruption of blood supply to the brain. Atherosclerosis causes narrowing of blood vessels and vascular occlusion can occur by thrombosis or embolism, which lead to infarcts.
Risk factors for stroke include:
|Prevalence of Post Stroke Neuropsychiatric Disorders|
Neuropsychiatric (NS) disorders are common after stroke. The entire spectrum of psychiatric illness can be seen. Most common are: depression, anxiety, emotional incontinence and catastrophic reactions.
|Post Stroke Depression|
The most important message is that there is conflicting evidence regarding risk factors for post stroke depression. The table below outlines these factors, although those listed as consistent are not 100%.
DSV IV Minor Depression Criteria requires the presence of more than 2 but less than 5 depressive symptoms including either a depressed mood or loss of interest. However, the DSM IV Major Depression Criteria can be reliably used to diagnose major PSD.
The duration of major PSD is about 9 months to 1 year whereas the duration of minor depression is several years.
In a study done by Robinson et al in the 1990s on comparison of depressed to non-depressed, most depressed folks had these neuro-vegetative and psychological symptoms of depression compared to the non-depressed folds. In 1991, Fedoroff et al, examined frequency of depressive symptoms among both depressed and non-depressed patients with stroke. With the exception of early morning awakening, all neuro-vegetative and psychological symptoms of depression were significantly more frequent among patients with depressed mood compared to those without depressed mood. Even when the frequency of nonspecific symptoms among the non-depressed patients was taken into account, the frequency of major depression decreased by only 2% from 23 to 21.
Little is known about the course of major depression after stroke. 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. Spontaneous remission can occur 1-2 year post-stroke. (Robinson et al, 1987)
A significant number of stroke survivors develop depression hours to days after stroke following the pattern of what is classically called reactive depression.
Etiopathogenesis of PSD
Instead of debating biological vs psychological, the best way to look at the etiology of PSD is from the biopsychosocial perspective. PSD is probably due to a combination of biological, psychological and social factors.
Psychological stressors such as loss of independence and poor physical functioning can overwhelm anyone, and in the setting of biological vulnerability, can cause depression
Because there is so much debate over Lesion location (LL) and PSD, let’s examine a great article by Bhogal et al 2004, who conducted an extensive literature review and looked at different studies that had examined the association between PSD and lesion location. This is what they found.
The Robinson study was controversial. It began with 3 arms: Prozac, NTP and placebo. After the first phase, only 2 arms remained. The majority of the Prozac group had people from the placebo group, i.e. people with more resistant depression.
Seven studies (either no standardized depression criteria or no randomized controls) indicate:
There is a widespread belief that PSD is psychological reaction. Severity of side-effects of psychotropics account for the resistance of many physicians to prescribe antidepressants.
Patients with NTP compared to placebo did better on HAM D and Zung self-rating depression scale; 3 of the 14 treated with NTP dropped out, 2 patients developed delirium and 1 died suddenly of unknown cause.
Three reports on use of psychostimulants - 2 retrospective chart reviews & 1 open label study using Ritalin (Johnson et al 1992; Masand et al, 1991Lazarus et al 1994). They were found to be safe, well tolerated and efficacious. However, no definitive conclusions can be made given lack of randomization.
ECT was found useful in 2 retrospective chart reviews (Murray et al 1986; Currier et al 1992). Currier et al, found 19/20 elderly PSD “markedly or moderately” improved. None of the pts developed exacerbations of stroke or new neuro deficits.
Treatment with Fluoxetine or NTP during the first 6 months post-stroke is associated with significant increase in survival in both depressed and non-depressed patients (68% on antidepressant vs. 36% on placebo) (Jorge et al 2003). Three reasons are:
However, caution is needed when using antidepressants in stroke patients. These studies are intriguing, but have limitations (uncertain how statistically significant results can be translated into real-life outcomes). Antidepressants have side-effects such as falls, increased bleeding, seizures, and sedation. There is a pressing need for further research to better define role of antidepressants in stroke prevention.
|Post Stroke Anxiety|
The Prevalence of PSA is about 20%, with a majority of PSA patients also having PSD.
Study of 288 patients (Castillo, Robinson et al 1995), found that Anxiety Depression (AD) was associated with left cortical lesions and anxiety alone with right hemisphere lesions
PSA Risk Factors:
In the Shimoda and Robinson study of 142 pts with GAD and Depression, 18 had more significant impairment in ADL compared to PSD alone at the end of 2 years. The comorbidity of PSD and GAD produced longer duration of PSD than PSD alone and this prolonged depression might lead to poorer physical and social outcomes.
|Post-Stroke Catastrophic Reactions|
Catastrophic reaction is an outburst of emotion, such as anxiety, agitation, or crying, that occurs when unable to perform simple tasks that were possible before. This is not uncommon in stroke patients. 19% in a series of 62 consecutive acute stroke patients were found to display CR (Starkstein et al, 1993).
Catastrophic Reaction is associated with PSD & Basal Ganglia lesions and may be a release phenomenon due to subcortical damage. It is often associated with expressive aphasia.
Treatment consists of prophylactic and supportive measures.
Other names: Emotional Incontinence; post-stroke emotionalism
Treatment: Antidepressants and mood stabilizers have been used to treat pathological laughter and pathological crying. However, more research in this area is necessary.
|Post Stroke Psychosis|
Psychosis is a rare complication post-stroke. Rabins et al screened all stroke individuals > 60 over a 9-year period (n=1191). Only 5 patients identified with psychosis. All had right frontoparietal lesions and subcortical atrophy compared to 5 matched controls. 3 of the 5 had post-stroke seizures. None of the 5 non-psychotic controls had seizures.
Treatment consists of neuroleptics or anticonvulsants.