Lacunar Infarction and Small Vessel Disease: Pathology and Pathophysiology.
- Author:
Louis R CAPLAN
1
Author Information
- Publication Type:Review
- Keywords: Cerebral small vessel diseases; CADASIL; Cerebral amyloid angiopathy; Pathophysiology
- MeSH: Adventitia; Amyloid; Arteries; Arterioles; Atrophy; Basal Ganglia; Brain; Brain Ischemia; CADASIL; Cerebral Amyloid Angiopathy; Cerebral Small Vessel Diseases; Connective Tissue; Edema; Gliosis; Humans; Hypertension; Hypertrophy; Metalloproteases; Muscle, Smooth; Parents; Pathology*; Pons; Stroke, Lacunar*; Tunica Media
- From:Journal of Stroke 2015;17(1):2-6
- CountryRepublic of Korea
- Language:English
- Abstract: Two major vascular pathologies underlie brain damage in patients with disease of small size penetrating brain arteries and arterioles; 1) thickening of the arterial media and 2) obstruction of the origins of penetrating arteries by parent artery intimal plaques. The media of these small vessels may be thickened by fibrinoid deposition and hypertrophy of smooth muscle and other connective tissue elements that accompanies degenerative changes in patients with hypertension and or diabetes or can contain foreign deposits as in amyloid angiopathy and genetically mediated conditions such as cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy. These pathological changes lead to 2 different pathophysiologies: 1) brain ischemia in regions supplied by the affected arteries. The resultant lesions are deep small infarcts, most often involving the basal ganglia, pons, thalami and cerebral white matter. And 2) leakage of fluid causing edema and later gliosis in white matter tracts. The changes in the media and adventitia effect metalloproteinases and other substances within the matrix of the vessels and lead to abnormal blood/brain barriers in these small vessels. and chronic gliosis and atrophy of cerebral white matter.
