Update on cerebral small vessel disease: a dynamic whole-brain disease

Four possible mechanisms that cause a lacunar infarct (from bottom to top): (A) an embolus from the big arteries or cardiac sources goes up to MCA and ends up entering and occluding lenticulostriate arteries, resulting in a lacunar lesion in basal ganglia; (B) if the atheroma in the parent artery (ie, MCA) is positioned at the opening of its penetrating branches, it could lead to an acute occlusion of one or several penetrating arteries, hence causing a lacunar infarct; (C) a lacunar infarct could also be due to atheroma in the perforating artery if an acute occlusion happens; (D) intrinsic small vessel disease may lead to diffused disrupted blood–brain barrier. If this happens at an arteriolar level, plasma fluid components would enter and deposit in the vessel wall, resulting in narrowing of the arteriolar lumen, vessel wall thickening and eventually a secondary luminal occlusion and traditional infarct. MCA, middle cerebral arteries.

Example of MRIs of a lacune from a haemorrhagic source (A,B), and from a lacunar infarct (C, D). D (the DWI) is from the acute presentation (i.e. within a few days of the stroke), and C (the FlAIR) is weeks to months later when the lesion has cavitated. DWI, diffusion-weighted imaging; FLAIR, fluid-attenuated inversion recovery; SWI, susceptibility-weighted imaging.