Following a stroke, the onset of depression is acute, usually occurring within 1 day or a few days of the cerebrovascular accident (CVA).[1]
Approximately 33% of stroke survivors develop PSD at some point, with the frequency being highest in the first year of stroke (and declines thereafter).
Pathophysiology
The pathophysiology of PSD involves both biological and psychosocial factors, but certain stroke lesions and locations are associated with a higher risk for post-stroke depression.[2]
Localization
Historically, left-sided strokes were thought to place patients at greater risk for PSD, but newer studies show mixed findings (i.e. - outpatient clinics actually see depression more commonly in right-sided strokes).[3]
PSD can be longer lasting compared to non-stroke depression due its multifactorial nature, and is more difficult to treat with antidepressants.
Prophylaxis
The prophylactic use of SSRIs in post-stroke neurological recovery is debated, with an argument to be made that some studies have shown reduced depression post-stroke.[4]
Two recent randomized control trials demonstrated no difference from placebo, and in fact, an increased risk of fractures, falls, and seizures.[5][6][7]
There is some debate about whether or not the study population is representative of typical stroke populations (e.g., most enrolled individuals had milder forms of stroke)[8]
Thus, the use of antidepressants as prophylaxis for post-stroke depression has not been routinely recommended.
A comprehensive risk-benefit analysis should be considered along with a personalized approach to treatment, with monitoring of side effects if antidepressant therapy is pursued.