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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

Diagram showing the relationship of a lacune in the pons to the causative penetrating artery vascular lesion. The artery beyond the region of arterial disorganization is thrombosed and thrombus has also formed in a retrograde manner extending toward the parent basilar artery (Reproduced with permission from C Miller Fisher.).
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Figure 6: Diagram showing the relationship of a lacune in the pons to the causative penetrating artery vascular lesion. The artery beyond the region of arterial disorganization is thrombosed and thrombus has also formed in a retrograde manner extending toward the parent basilar artery (Reproduced with permission from C Miller Fisher.).

Mentions: Deep small infarcts are caused by decreased perfusion in the territory of penetrating arteries. Intrinsic disease of a penetrator (lipohyalinosis, CAA, CADASIL or other occlusive diseases within the course of the penetrating artery) causes a small infarct in the center of the penetrating artery supply. Figure 6 is a cartoon which illustrates this pathophysiology. Collateral circulatory capacity is very limited in the territory of these deep penetrators and occlusive changes in the adjoining penetrators can lead to infarcts that are larger than the territory of the acutely compromised penetrating vessel.


Lacunar infarction and small vessel disease: pathology and pathophysiology.

Caplan LR - J Stroke (2015)

Diagram showing the relationship of a lacune in the pons to the causative penetrating artery vascular lesion. The artery beyond the region of arterial disorganization is thrombosed and thrombus has also formed in a retrograde manner extending toward the parent basilar artery (Reproduced with permission from C Miller Fisher.).
© Copyright Policy - open-access
Related In: Results  -  Collection

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

Figure 6: Diagram showing the relationship of a lacune in the pons to the causative penetrating artery vascular lesion. The artery beyond the region of arterial disorganization is thrombosed and thrombus has also formed in a retrograde manner extending toward the parent basilar artery (Reproduced with permission from C Miller Fisher.).
Mentions: Deep small infarcts are caused by decreased perfusion in the territory of penetrating arteries. Intrinsic disease of a penetrator (lipohyalinosis, CAA, CADASIL or other occlusive diseases within the course of the penetrating artery) causes a small infarct in the center of the penetrating artery supply. Figure 6 is a cartoon which illustrates this pathophysiology. Collateral circulatory capacity is very limited in the territory of these deep penetrators and occlusive changes in the adjoining penetrators can lead to infarcts that are larger than the territory of the acutely compromised penetrating vessel.

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