Striatocapsular infarcts involve the striatum (ie the caudate nucleus and putamen), without involvement of the cortex secondary to either a complete or partial proximal MCA occlusion limiting flow to the lenticulostriate arteries.

Classically patients exhibit both cortical (e.g. aphasia, sensory neglect or extinction, apraxia) and subcortical (e.g. upper limb hemiparesis, dysarthria) neurological signs.