Journal
BRAIN PATHOLOGY
Volume 22, Issue 5, Pages 583-591Publisher
WILEY
DOI: 10.1111/j.1750-3639.2012.00575.x
Keywords
cerebral small vessel disease; lacunar infarct; lacune; lipohyalinosis; pathology
Categories
Funding
- Medical Research Council
- Scottish Funding Council through the SINAPSE Collaboration (Scottish Imaging Network, A Platform for Scientific Excellence)
- Scottish Funding Council
- MRC [G1100616] Funding Source: UKRI
- Chief Scientist Office [CZB/4/517] Funding Source: researchfish
- Medical Research Council [G1100616, G0700704B] Funding Source: researchfish
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Twenty-five percent of ischemic strokes are lacunar in type, but the cause remains unclear. Pathological descriptions of lacunar lesions are available but have not been systematically assessed. We therefore systematically summarized studies describing lacunar lesions by extracting data on the number of patients and lesions, clinical details, pathological methods, brain regions and/or vessels examined, and both parenchymal and vascular findings. Among 39 papers describing >4000 lesions (>50% from one study), 15 papers examined patients with a clinical lacunar syndrome. Terminology varied, many studies only reported macroscopic pathology and many lesions were cavitated (ie, old). Aside from symptomatic lesions occurring more often in the internal capsule or caudate nucleus, we found no other differences between symptomatic and asymptomatic patients. Perivascular edema and thickening, inflammation and disintegration of the arteriolar wall were common, whereas vessel occlusion was rare. The causal mechanisms of lacunar stroke remain poorly defined because of methodological inconsistencies and challenges. Standardised pathological definitions based on well-characterized post-mortem derived material supported by detailed clinical and imaging data are needed.
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