Abstract

Post-stroke depression has been well-researched over the last few decades. Despite advances, it remains a poorly understood entity and till now, a replicable and valid model explaining the etiology of post-stroke depression remains elusive. This is alarming considering the fact that the prevalence of post-stroke depression has been estimated to be around 18 to 33% of patients suffering from stroke in various studies.1 Post-stroke depression is often associated with changes in the expression of the monoamine receptors and alteration in the receptor sensitivity.2 A number of studies have attempted to recognize clinical and neuro-anatomical correlates that can predict the development of post-stroke depression in patients suffering from stroke.3–5 The most replicated risk factor that has been postulated for post-stroke depression include a history of mental disorder, higher stroke severity, higher post-stroke physical disability, higher cognitive impairment, and poorer social support.3,4 However, here we present a case of post-stroke depression with few of the predictive factors being present.

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