Lacunar infarcts are caused by Cerebral small vessel disease (cSVD). They result from occlusion of one of the small penetrating lenticulostriate end arteries at the base of the brain. Most lacunar infarcts are asymptomatic due to small size.
Acute occlusion of an intracranial vessel causes reduction in blood flow to the brain region it supplies causing infarction. Occlusion of the small perforating lenticulostriate arteries leads to ‘lacunar’ infarction’ or lacunar stroke. These occur in older patients with sporadic or genetic small vessel diseases or due to spontaneous cervical artery dissection in younger people.
Lacunar infarcts are small infarcts (2–20 mm in diameter) in the deep cerebral white matter, basal ganglia, or pons. Lacunar stroke is a well-known ischemic stroke. It contributes significantly to morbidity and mortality worldwide.
The occlusion of small, deep penetrating branches of the middle cerebral artery, anterior cerebral artery, posterior cerebral artery, or basilar artery cause lacunar infarcts. These penetrating arteries are end arteries because they have no collaterals.
About 20% to 50% of the elderly population have asymptomatic lacunar strokes on imaging due to the involvement of small vessels causing small-sized infarcts. Lacunar infarcts mostly affect the elderly with long-standing hypertension.
Lacunar strokes do not affect memory, language, and judgment. The most common clinical features are contralateral hemiparesis of the face, arm, and leg; dysarthria; impaired or abnormal sensation of the contralateral of the face, arm, and leg or a combination of contralateral sensory and motor loss.
Lacunar strokes present as ill-defined hypodensities on CT. CT scans may not identify lacunar ischemic infarcts within the first 24 hours due to their small size. Early signs of infarct on non-contrast CT are loss of grey-white differentiation and focal hypoattenuation of brain parenchyma. These details are difficult to appreciate in small subcortical strokes. Chronic lesions appear as hypodense foci.
In the acute stage, the MRI diffusion-weighted image (DWI) has the highest sensitivity to detect a lacunar infarct. It is positive within half an hour of stroke onset.
The initial treatment is to achieve medical stability and thrombolysis with tissue plasminogen activator (tPA) within 4.5 hours of symptom onset in appropriate candidates.
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