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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

Periodic acid Schiff (PAS) stain showing bright pink staining material within small cerebral arteries in a patient with CADASIL.
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Figure 2: Periodic acid Schiff (PAS) stain showing bright pink staining material within small cerebral arteries in a patient with CADASIL.

Mentions: The other major pathology that directly involves the walls of penetrating arteries is infiltration of the coats of these vessels with materials foreign to vessels. The penetrating arteries, arterioles and capillaries in a hereditary condition dubbed CADASIL contain a granular material in the media that extends into the adventitia. This disorder is caused by dominant mutations in the NOTCH3 gene that encodes a transmembrane receptor predominantly expressed in vascular smooth muscle and pericyte cells in adults.4,5 This receptor is needed for the structural and functional integrity of small vessels-small arteries, arterioles and capillaries. Periodic acid-Schiff (PAS) staining suggests the presence of glycoproteins, but staining for elastin and amyloid have been negative. Figure 2 is a PAS stained section that shows glycoprotein material within vessel walls in a CADASIL. The nature of the deposited material within the vessel wall and matrix remains unknown. Smooth muscle cells in the media are swollen and often degenerated. The endothelium may be absent and replaced by collagen fibers. At times abnormalities also found in hypertensive patients are also found, including duplication and splitting of the internal elastic lamina, adventitial fibrosis and hyaline change, and fibrosis and hypertrophy of the arterial media.


Lacunar infarction and small vessel disease: pathology and pathophysiology.

Caplan LR - J Stroke (2015)

Periodic acid Schiff (PAS) stain showing bright pink staining material within small cerebral arteries in a patient with CADASIL.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

Figure 2: Periodic acid Schiff (PAS) stain showing bright pink staining material within small cerebral arteries in a patient with CADASIL.
Mentions: The other major pathology that directly involves the walls of penetrating arteries is infiltration of the coats of these vessels with materials foreign to vessels. The penetrating arteries, arterioles and capillaries in a hereditary condition dubbed CADASIL contain a granular material in the media that extends into the adventitia. This disorder is caused by dominant mutations in the NOTCH3 gene that encodes a transmembrane receptor predominantly expressed in vascular smooth muscle and pericyte cells in adults.4,5 This receptor is needed for the structural and functional integrity of small vessels-small arteries, arterioles and capillaries. Periodic acid-Schiff (PAS) staining suggests the presence of glycoproteins, but staining for elastin and amyloid have been negative. Figure 2 is a PAS stained section that shows glycoprotein material within vessel walls in a CADASIL. The nature of the deposited material within the vessel wall and matrix remains unknown. Smooth muscle cells in the media are swollen and often degenerated. The endothelium may be absent and replaced by collagen fibers. At times abnormalities also found in hypertensive patients are also found, including duplication and splitting of the internal elastic lamina, adventitial fibrosis and hyaline change, and fibrosis and hypertrophy of the arterial media.

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