Lacunar Infarction

LACUNAR INFARCTS

Lacunar infarcts are miniature, discrete lesions, ranging from 1 to 20 mm in size. The most common locations are the putamen and the pallidum, followed by the pons, thalamus, caudate nucleus, internal capsule, and corona radiata. Rarer are lacunes in the cerebral peduncles, pyramids, and subcortical white matter. Lacunes are not found in the cerebral or cerebellar cortices.

The two most common pathologies that affect penetrating arteries are lipohyalinosis and atheromatous branch disease. Serial sections of penetrating arteries that supply the territory of lacunar infarcts often have focal enlargements and small hemorrhagic extravasations through the walls of the arteries. Subintimal foam cells sometimes obliterate the lumens, and pink-staining fibrinoid material lies within vessel walls. Arterial segments are often replaced by whorls, tangles, and wisps of connective tissue that obliterate the usual vascular layers. This vascular pathology has been called segmental arterial disorganization, fibrinoid degeneration, and lipohyalinosis. Hypertension is the predominant pathophysiologic mechanism. The distribution of deep hypertensive hemorrhages is the same as the locations of lacunes (putamen, capsule, thalamus, and pons). Lipohyalinotic arteries could occlude, causing lacunar infarction, or rupture, causing intracerebral hemorrhage.

Intracerebral branch atheromatous disease also effects brain tissue supplied by penetrating arteries. In this condition, the orifices of penetrating arteries are blocked by atheroma in the parent artery. Atheroma could originate in the parent artery and extend into the branch, or microatheroma could arise at the origin of the branch itself. Thrombus is sometimes superimposed on the atheromas. This vasculopathy is sometimes referred to as microatheromatous disease. Pontine infarcts are the most frequent neuropathologic lesion found in necropsies of diabetics and, in most cases, are caused by atheromatous branch disease.

Two genetic conditions are also known to predominantly affect these small penetrating vessels: cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) and COL 4, A1 mutations. In CADASIL, penetrating arteries contain a granular material in the media that extends into the adventitia. Smooth muscle cells in the media are swollen and often degenerated, and the endothelium may be absent and replaced by collagen fibers. This hereditary condition causes lacunar infarcts in the basal ganglia and cerebral white matter similar to those found in hypertensive patients.

A hereditary angiopathic condition associated with mutations in a gene encoding procollagen type IV alpha 1 (COL 4, A1) effects small brain arteries as well as larger retinal and cerebral arteries. The clinical findings include perinatal hemorrhages and porencephaly, tendency to brain hemorrhage after trauma, retinal artery tortuosity, cerebral aneurysms, penetrating artery related infarcts, white matter gliosis, and kidney disease.

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