To the Editor: The complex connectivity of basal ganglia with other cortical and thalamic circuits that guide our behavior, cognition, and movement is still a matter of controversy. However, the past decade brought about the increased insight into the synchronized oscillations between basal ganglia-cortical and thalamo-cortical circuits, as well as the awareness about the potential detrimental effect that any interruptions (including brain infarction) of these oscillations may instigate.1,2 Small infarctions in the subcortical white- and gray-matter areas are sometimes clinically overlooked and only inadvertently reported on post-hoc neuroimaging.3–8 Furthermore, even those subcortical lesions that appear to be strategically placed are sometimes without overt clinical signs and with symptoms that come and go despite the presence of fixed cavities on the neuroimaging. (as reviewed in4). Consequently, a certain incredulity on the part of investigating clinicians, when assessing the retrospective reports by patients and their families about associated symptoms, is common, and their putative impact on cognition and behavior is not always easily argued.3,4 The converging evidence, however, suggests that such infarcts could affect distant areas/neuronal circuits via a combination of local and remote chemical and electrophysiological effects.3,4,9–11 We present here the case of intermittent behavioral and cognitive changes associated with the striatocapsular lesion due to infarction. It is hoped that this and similar case reports that detail the plethora of paroxysmal neuropsychiatric symptomatology resulting from lesions in this area will aid improved clinical recognition of subcortical “silent” infarcts.