The concept of poststroke depression as a nosological entity, despite decades of research, remains controversial. Neither its biological nor psychopathological specificity has never been unambiguously confirmed. Although some correlates between clinical characteristics of poststroke depression and some patient-related (age and gender) and stroke-related (localization) variables have been proposed, it seems reasonable to treat stroke as a pathoplastic than a causative factor. Effective treatment of poststroke depression affects the outcomes of rehabilitation, in particular patients functional abilities and activities of daily living.
No standard or generally recommended treatments exist for poststroke depression and welldesigned clinical studies are sparse. Nortriptyline has been proved to be effective, though its use (the same is true for other tricyclics) is limited by side effects. Citalopram, trazodone and reboxetine have also been evaluated in controlled trials and evaluated as helpful. The results of one study suggest that citalopram might be of choice when depression is accompanied by significant anxiety while reboxetine when apathy and withdrawal are prevailing.
Psychological interventions have not been so far systematically evaluated, still behavioralcognitive therapy is often indicated.
A small number of pharmacological prevention of poststroke depression trials have been conducted showing conflicting and rather discouraging results.