Lacunar infarction

Differential diagnosis
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By Catalina Ionita MD

Lacunar syndromes may be caused by a large variety of pathologies, such as neurocysticercosis, tumors, demyelinating lesions, and small hemorrhages. Large cerebral infarcts are easily differentiated from lacunar infarcts. A pure motor monoparesis or a hemiparesis associated with “cortical” signs such as aphasia suggest a nonlacunar infarct. Restricted acral sensory syndromes or pseudothalamic sensory strokes can result from minor parietal strokes. A lacunar infarct must be differentiated from a deep cerebral watershed infarct. Deep watershed “low flow” infarcts tend to present with a combination of a lacunar syndrome and a “cortical” sign. Confluent low-flow white matter infarcts are larger than lacunar infarcts and have a worse prognosis (Fisher 1965). Symptomatic small centrum semiovale infarcts may be caused by large-vessel occlusive disease or cardioembolism and should be distinguished from lacunes and leukoaraiosis. The presence of retinal microangiopathy on retinography, leukoaraiosis on MRI, and increased carotid pulsatility index on ultrasound is a marker of lacunar infarcts not secondary to macrovascular lesion (Rodriguez 2010). Diffusion weighted-magnetic resonance imaging is more sensitive than conventional MRI and CT in detecting them. Multiple diffusion weighted imaging-hyperintense lesions raise the possibility of an embolic mechanism rather than microvascular disease (Ay 1999). A diffusion weighted-perfusion weighted imaging mismatch reliably distinguishes between a single perforating vessel occlusion and a large artery embolism for solitary small subcortical infarctions (Gerraty 2002).

In This Article

Historical note and nomenclature
Clinical manifestations
Pathogenesis and pathophysiology
Differential diagnosis
Diagnostic workup
Prognosis and complications
References cited