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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

Luxol fast blue (LFB) stained specimen of a cerebral hemisphere showing extensive loss of myelin staining.In a normal brain the entire white matter should stain uniformly blue.
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Figure 5: Luxol fast blue (LFB) stained specimen of a cerebral hemisphere showing extensive loss of myelin staining.In a normal brain the entire white matter should stain uniformly blue.

Mentions: At necropsy patients with chronic penetrating artery disease show extensive changes in white matter variously called leukoariosis and leukoencephalopathy. The combination of multiple small deep infarcts and extensive white matter abnormalities has been referred to as Binswanger disease,3,13,14 and the clinical findings are often classified as vascular dementia of the small artery type. Grossly visible in the cerebral white matter are confluent areas of soft, puckered, and granular tissue. These areas are patchy and emphasize the occipital lobes and periventricular white matter, especially anteriorly and close to the surface of the ventricles.3,13,14Figure 5 is a myelin stained section from the cerebral hemispheres that shows a large area of myelin loss in the cerebral white matter. The cerebellar white matter is also often involved. The ventricles are enlarged, and the corpus callosum is usually small. The volume of white matter is reduced, but the cortex is generally spared. The ventricles are enlarged as a result of atrophy of the white matter. The white-matter abnormalities surrounding the ventricles may reduce the strength of the supporting tissue and allow mechanically more ventricular distension.3,13,14 The white-matter abnormalities are nearly always accompanied by some lacunes. Microscopic examination shows myelin pallor. Usually, the myelin pallor is not homogeneous, but islands of decreased myelination are surrounded by normal tissue. At times, the white-matter abnormalities are so severe that necrosis and cavitation occur. Gliosis is prominent in zones of myelin pallor.


Lacunar infarction and small vessel disease: pathology and pathophysiology.

Caplan LR - J Stroke (2015)

Luxol fast blue (LFB) stained specimen of a cerebral hemisphere showing extensive loss of myelin staining.In a normal brain the entire white matter should stain uniformly blue.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

Figure 5: Luxol fast blue (LFB) stained specimen of a cerebral hemisphere showing extensive loss of myelin staining.In a normal brain the entire white matter should stain uniformly blue.
Mentions: At necropsy patients with chronic penetrating artery disease show extensive changes in white matter variously called leukoariosis and leukoencephalopathy. The combination of multiple small deep infarcts and extensive white matter abnormalities has been referred to as Binswanger disease,3,13,14 and the clinical findings are often classified as vascular dementia of the small artery type. Grossly visible in the cerebral white matter are confluent areas of soft, puckered, and granular tissue. These areas are patchy and emphasize the occipital lobes and periventricular white matter, especially anteriorly and close to the surface of the ventricles.3,13,14Figure 5 is a myelin stained section from the cerebral hemispheres that shows a large area of myelin loss in the cerebral white matter. The cerebellar white matter is also often involved. The ventricles are enlarged, and the corpus callosum is usually small. The volume of white matter is reduced, but the cortex is generally spared. The ventricles are enlarged as a result of atrophy of the white matter. The white-matter abnormalities surrounding the ventricles may reduce the strength of the supporting tissue and allow mechanically more ventricular distension.3,13,14 The white-matter abnormalities are nearly always accompanied by some lacunes. Microscopic examination shows myelin pallor. Usually, the myelin pallor is not homogeneous, but islands of decreased myelination are surrounded by normal tissue. At times, the white-matter abnormalities are so severe that necrosis and cavitation occur. Gliosis is prominent in zones of myelin pallor.

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