“…The hypothetical mechanisms considered by those au thors supporting the role of lesion location are based on the observation of a higher incidence of familial psychiat ric disorders in patients with a right posterior lesion, which might suggest differential vulnerability to depres sion for right and left lesions [ 15], Both PET studies show ing a possible compensatory upregulation of 5-HT2 (sero tonin) receptors in the RH after stroke, which is not seen after left-sided lesions [42], and animal studies showing a lateralized biochemical response to ischemia, suggesting asymmetry in the human biological response to injury, support this view [43], However, the finding of temporolimbic hypoperfusion in patients with depression and sub cortical stroke suggests that alternative mechanisms might be involved [44], Treatment Nortriptyline, trazodone and serotonin re-uptake in hibitors [19][20][21] were shown to be effective in randomized placebo-controlled studies of poststroke depression. Be cause of the high frequency of their contraindication and adverse effects (orthostatic hypotension, atrioventricular block), tricyclic antidepressives are not the first choice in cerebrovascular patients [45], Serotonin re-uptake inhibi tors may be the best choice [20,21]; however, adverse reactions such as fluoxetine-induced mania in a patient with poststroke depression can occur [46], Open trials have suggested the potential benefit of psychostimulants (methylphenidate), but further controlled studies are re quired to reach a conclusion [45], Imipramine and mianserine have been effective in trials, and imipramine proba bly has a combined action on the noradrenergic and espe cially the serotonergic systems [45], The potential benefit of electroconvulsive therapy may warrant confirmation [45,47], Treatment against spasticity, psychological assis tance and social support should not be neglected [48].…”