Lacunar infarct

Lacunar infarcts are small (<20 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 are due to fibrinoid degeneration.

Clinical presentation

Patients without diagnostic imaging who present with symptoms of a lacunar stroke may be described as suffering from a lacunar stroke syndrome (LACS), one of five distinct syndromes.

Pathology

They are caused by occlusion of one of the small penetrating end-arteries at the base of the brain, thought to result primarily from in situ microatheroma formation, or lipohyalinosis ² (c.f. cortical infarcts where embolisation of distal thrombus is the primary aetiology).

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

Radiographic features

CT / MRI

• small discrete foci of hypodensity / diffusion restriction
• 3-20 mm in diameter, most commonly 10 mm
• may enhance in the late acute or early subacute stage
• unilateral pontine infarcts have a sharp demarcation at the midline
• higher signal intensity than CSF (marginal gliosis)

History and etymology

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

Differential diagnosis

• enlarged Virchow-Robin spaces
• neurocysticercosis
• choroid fissure cysts
• striatocapsular infarct