Lenticulostriate infarction

Abstract

Lenticulostriate infarcts result from ischemia within the territory supplied by the deep perforating branches of the middle cerebral artery (MCA). They are too often associated with infarctions of the deep perforating branches of the internal carotid artery. Lenticulostriate arteries usually arise from the main trunk of the MCA, but can emerge from the cortical branches. The clinical aspects of lenticulostriate infarction should be properly differentiated from those of other anterior circulation infarcts. Clinical signs include motor deficit, sensory deficit and cognitive dysfunction. The principal mechanism for lenticulostriate infarction seems to be an embolism of cardiac origin. The concept of lacunar infarctions relating to lipohyalinosis is perhaps too often proposed without evidence. The prognosis is dependent primarily on the intensity of damage to the upper part of the posterior limb of the internal capsule. They are terminal arteries without anastomoses, making them more susceptible to ischemia and resulting in a greater risk of arteriolar necrosis and hemorrhagic transformation.