Lacunar infarct

Last revised by Rohit Sharma on 21 Jan 2024

Lacunar infarcts are small (<15 mm) infarcts in the distal distribution of deep penetrating vessels (lenticulostriate, thalamoperforating, and pontine perforating arteries, recurrent artery of Heubner). They result from occlusion of one of the small penetrating end arteries at the base of the brain and have traditionally been thought to occur due to fibrinoid degeneration. However, there is debate in the literature that the etiology of lacunar infarction also includes embolism 5.

Most lacunar infarcts are clinically silent, but repeated episodes are associated with vascular dementia. Symptomatic patients may present with lacunar stroke syndrome, one of five distinct syndromes.

Lacunar infarcts, by definition, are caused by occlusion of small penetrating end-arteries and must be smaller than 15 mm. Although they are thought to result primarily from in situ microatheroma formation or lipohyalinosis 2, they are also described as being caused by embolism 5. Some argue that it is important to investigate lacunar infarction for underlying embolism even though this may only be present in a minority of patients 6.

Pathologically, they are small holes of encephalomalacia and are traversed by a cobweb-like mesh of fibrous strands.

In the acute setting, lacunar infarcts appear as ill-defined hypodensities.

Chronic lesions appear as hypodense foci (similar to CSF).

In an acute setting, the following signal changes are seen:

  • T1: slightly hypointense

  • T2/FLAIR: hyperintense

  • DWI: restricted diffusion

    • may demonstrate acute lesions not visible on other sequences

  • T1 C+ (Gd): may enhance if acute (or early subacute)

Chronic lesions are isointense to CSF on all sequences but may demonstrate a peripheral T2/FLAIR hyperintense rim of marginal gliosis.

The term was penned by Charles Miller Fisher (1913-2012) 4, a Canadian neurologist, who described "lacunes" (Latin: lake) of empty fluid within the brains of stroke victims post-mortem.

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