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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

Drawing showing the arterial pathology in atheromatous branch disease: (A) plaque in parent artery obstructing a branch, (B) junctional plaque extending into the branch, (C) microatheroma formed at the orifice of a branch.
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Figure 3: Drawing showing the arterial pathology in atheromatous branch disease: (A) plaque in parent artery obstructing a branch, (B) junctional plaque extending into the branch, (C) microatheroma formed at the orifice of a branch.

Mentions: The other type of pathology that causes small deep infarcts involves the large arteries that give rise to penetrating artery branches rather than intrinsic disease of the branches themselves. The orifices of these penetrating arterery branches could be obstructed by atherosclerotic plaque lesions. Fisher and Caplan,9 Fisher,10 and Caplan11 described the vascular pathology in these branches, and dubbed the condition intracranial branch atheromatous disease. Figure 3 contain cartoons that illustrate the location and mechanism of the pathology within the parent arteries. The orifices of the penetrating branches could be blocked by atheroma in the parent artery, atheroma could originate in the parent artery and extend into the branch (so-called junctional atheromatous plaques), or microatheromas could arise at the origin of the branch itself. Thrombus was sometimes superimposed on the atheromas and occasionally a microdissection developed in the parent artery and spread into the first millimeters of the branch.9


Lacunar infarction and small vessel disease: pathology and pathophysiology.

Caplan LR - J Stroke (2015)

Drawing showing the arterial pathology in atheromatous branch disease: (A) plaque in parent artery obstructing a branch, (B) junctional plaque extending into the branch, (C) microatheroma formed at the orifice of a branch.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

Figure 3: Drawing showing the arterial pathology in atheromatous branch disease: (A) plaque in parent artery obstructing a branch, (B) junctional plaque extending into the branch, (C) microatheroma formed at the orifice of a branch.
Mentions: The other type of pathology that causes small deep infarcts involves the large arteries that give rise to penetrating artery branches rather than intrinsic disease of the branches themselves. The orifices of these penetrating arterery branches could be obstructed by atherosclerotic plaque lesions. Fisher and Caplan,9 Fisher,10 and Caplan11 described the vascular pathology in these branches, and dubbed the condition intracranial branch atheromatous disease. Figure 3 contain cartoons that illustrate the location and mechanism of the pathology within the parent arteries. The orifices of the penetrating branches could be blocked by atheroma in the parent artery, atheroma could originate in the parent artery and extend into the branch (so-called junctional atheromatous plaques), or microatheromas could arise at the origin of the branch itself. Thrombus was sometimes superimposed on the atheromas and occasionally a microdissection developed in the parent artery and spread into the first millimeters of the branch.9

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