Abstract
Secondary mania after cerebral hemispherical dysfunction can be due to several causes [1]. Like Fenn and George [2] pointed out, mania following stroke is a rare entity compared with depression following stroke. Therefore, prospective studies on a cohort of post-stroke manic patients are extremely difficult. However, it is interesting to note that mania occurring in patients with traumatic brain injury are more common than post-stroke mania [3]. Therefore, studying the former patients will tell us more about the relationship between lesion location and development of secondary mania. Some studies have found no correlation between post-stroke depression and the hemisphere involved [4,5], although this is not supported by some other researchers. Starkstein and Robinson [6] have suggested that a number of other variables like time post-stroke, diagnosis of depression, prior brain injury, intrahemispheric lesion location can all influence the lateralised emotional response to brain injury. Extrapolating these findings, I think it is premature to assume that the mere chance finding of left-sided lesion or for that matter right-sided lesion can cause post-stroke mania. My own feeling is that the intrahemispheric lesion (frontal, temporal and sub-cortical, but not occipital) is more relevant than right or left hemisphere involvement. Only a prospective study of a cohort of a large number of patients with brain injury or stroke is going to unravel the mystery of lesion location and occurrence of secondary mania with some precision.