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Additional recommended knowledge
Lacunes are caused by occlusion of a single deep penetrating artery. The deep penetrating arteries are small nonbranching end arteries (usually smaller than 500 micrometers in diameter), which arise directly from much larger arteries (eg, the middle cerebral artery, anterior choroidal artery, anterior cerebral artery, posterior cerebral artery, posterior communicating artery, cerebellar arteries, basilar artery). Their small size and proximal position predisposes them to the development of microatheroma and lipohyalinosis.
At the beginning, lipohyalinosis was thought to be the main small vessel pathology of lacunes; however, 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).
A hemodynamic (hypoperfusion) mechanism is suggested when there is a stenosis (and not occlusion) 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.
The Clinical Picture
It is estimated that lacunar infarcts account for 25% of all strokes that are due to infarction.
If there is enough white matter disease from lacunar pathology, one can see a subcortical dementia such as Binswanger disease.
|This article is licensed under the GNU Free Documentation License. It uses material from the Wikipedia article "Lacunar_stroke". A list of authors is available in Wikipedia.|