The lenticulostriate arteries are a group of six to twelve small perforating arteries arising from the proximal M1 segment of the middle cerebral artery. They ascend through the anterior perforated substance to supply the putamen, caudate nucleus, internal capsule (posterior limb and genu), and part of the thalamus. They are end-arteries with no collateral anastomoses, making the territory they supply highly vulnerable to both ischaemia and hypertensive haemorrhage.
The lenticulostriate arteries are the most common site of hypertensive intracerebral haemorrhage (putaminal haemorrhage), accounting for approximately 35% of all spontaneous intracerebral haemorrhages. Small vessel disease affecting these penetrating arteries causes lacunar infarcts, which are small infarcts in the basal ganglia, internal capsule, and thalamus producing classic lacunar syndromes: pure motor hemiplegia, pure sensory stroke, sensorimotor stroke, ataxic hemiparesis, and dysarthria-clumsy hand syndrome.
Rupture of a lenticulostriate artery from chronic hypertension produces an intracerebral haematoma in the putamen and internal capsule, causing contralateral hemiplegia, conjugate gaze deviation, and altered consciousness with characteristic CT appearances, managed with blood pressure control and surgical evacuation when haematoma volume exceeds 30 mL.
Lipohyalinosis and microatheroma of lenticulostriate arteries causes small subcortical infarcts producing stereotyped lacunar syndromes, particularly pure motor hemiplegia from posterior limb internal capsule lacunae, managed with risk factor control and antiplatelet therapy.
