Mechanismcally, it may due to Lipohyalinosis
The two proposed mechanisms are microatheroma and lipohyalinosis.[5] At the beginning, lipohyalinosis was thought to be the main small vessel pathology, but microatheroma now is thought to be the most common mechanism of arterial occlusion (or stenosis). Occasionally, atheroma in the parent artery blocks the orifice of the penetrating artery (luminal atheroma), or atheroma involves the origin of the penetrating artery (junctional atheroma). Alternatively, hypoperfusion is believed to be the mechanism when there is stenosis of the penetrating artery. When no evidence of small vessel disease is found on histologic examination, an embolic cause is assumed, either artery-to-artery embolism or cardioembolism. In one recent series, 25% of patients with clinical radiologically defined lacunes had a potential cardiac cause for their strokes.
Pathophysiology of small vessel occlusion and lipohyalinosis
it is characterized by vessel wall thickening and a resultant reduction in luminal diameter. Fisher considered this small vessel disease to be the result of hypertension, induced in the acute stage by fibrinoid necrosis that would lead to occlusion and hence lacunar stroke.
The Trial of Org 10172 in Acute Stroke Treatment (TOAST).
Stroke Subtype
1. Large artery atherosclerosis
2. Cardioembolism
3. Small vessel occlusion
4. Undetermined etiology
