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Lipohyalinosis is a small-vessel disease in the brain. Originally defined by Fisher as 'segmental arteriolar wall disorganisation', it is characterised 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. However, recent evidence suggests that endothelial dysfunction as a result of inflammation is a more likely cause for it. This may occur subsequent to blood–brain barrier failure, and lead to extravasation of serum components into the brain that are potentially toxic. Lacunar infarction could thus occur in this way, and the narrowing – the hallmark feature of lipohyalinosis – may merely be a feature of the swelling occurring around it that squeezes on the structure.

Hypertension is a strong causative factor. So-called deep-perforating arteries – relatively small arteries branching off of relatively large arteries (most commonly the lenticulostriate arteries from the middle cerebral artery) – are especially prone.[1] Uncontrolled hypertension and diabetes are risk factors for this condition. Lacunar infarcts are a result of atherosclerosis (microthrombi) and lipohyalinosis. These affect the deep structures of the brain and may leave small (~5mm) cavity lesions.

Chronic familial lipohyalinosis is a rare inherited variant.


  1. ^ Brenner D, Labreuche J, Pico F, et al. "The renin-angiotensin-aldosterone system in cerebral small vessel disease". J Neurol. May 2, 2000