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Lacunar infarction and small vessel disease: pathology and pathophysiology.

Caplan LR - J Stroke (2015)

Bottom Line: These pathological changes lead to 2 different pathophysiologies: 1) brain ischemia in regions supplied by the affected arteries.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.

View Article: PubMed Central - PubMed

Affiliation: Division of Cerebrovascular Disease, Department of Neurology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.

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.

No MeSH data available.


Related in: MedlinePlus

A necropsy specimen showing a cavity due to an old lacunar infarct that is located in and the medial basal ganglia (mostly the globus pallidus) and extends through the internal capsule in a patient with a pure motor hemiplegia during life.
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Figure 4: A necropsy specimen showing a cavity due to an old lacunar infarct that is located in and the medial basal ganglia (mostly the globus pallidus) and extends through the internal capsule in a patient with a pure motor hemiplegia during life.

Mentions: The major related pathology in the brain are small deep infarcts and degenerative abnormalities in the cerebral and cerebellar white matter. Lacunar infarcts are small, discrete, often irregular lesions, ranging from 1 to 15 mm in size. Inspection of these small cavities usually shows fine strands of connective tissue resembling cobwebs. The most common locations of these lacunar infarcts are the putamen and the pallidum, followed by the pons, thalamus, caudate nucleus, internal capsule, and corona radiata. Figure 4 shows a typical bold basal ganglia lacune. Rarer are lacunes in the cerebral peduncles, pyramids, and subcortical white matter. These lesions are not found in the cerebral or cerebellar cortices.


Lacunar infarction and small vessel disease: pathology and pathophysiology.

Caplan LR - J Stroke (2015)

A necropsy specimen showing a cavity due to an old lacunar infarct that is located in and the medial basal ganglia (mostly the globus pallidus) and extends through the internal capsule in a patient with a pure motor hemiplegia during life.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4325635&req=5

Figure 4: A necropsy specimen showing a cavity due to an old lacunar infarct that is located in and the medial basal ganglia (mostly the globus pallidus) and extends through the internal capsule in a patient with a pure motor hemiplegia during life.
Mentions: The major related pathology in the brain are small deep infarcts and degenerative abnormalities in the cerebral and cerebellar white matter. Lacunar infarcts are small, discrete, often irregular lesions, ranging from 1 to 15 mm in size. Inspection of these small cavities usually shows fine strands of connective tissue resembling cobwebs. The most common locations of these lacunar infarcts are the putamen and the pallidum, followed by the pons, thalamus, caudate nucleus, internal capsule, and corona radiata. Figure 4 shows a typical bold basal ganglia lacune. Rarer are lacunes in the cerebral peduncles, pyramids, and subcortical white matter. These lesions are not found in the cerebral or cerebellar cortices.

Bottom Line: These pathological changes lead to 2 different pathophysiologies: 1) brain ischemia in regions supplied by the affected arteries.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.

View Article: PubMed Central - PubMed

Affiliation: Division of Cerebrovascular Disease, Department of Neurology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.

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.

No MeSH data available.


Related in: MedlinePlus