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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

Small penetrating artery showing lipohyalinosis and fibrinoid necrosis (white arrow); lumen is considerably compromised (upper black arrow). The thickened media contains lipohyalinotic material (Lower black arrow) (Supplied by Dr. C. Miller Fisher.).
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Figure 1: Small penetrating artery showing lipohyalinosis and fibrinoid necrosis (white arrow); lumen is considerably compromised (upper black arrow). The thickened media contains lipohyalinotic material (Lower black arrow) (Supplied by Dr. C. Miller Fisher.).

Mentions: Miller Fisher, nearly a half century ago, analyzed the arterial pathology that caused small deep infarcts by carefully assessing serial sections of vessels at necropsy.1 He observed that the penetrating arteries that supplied the territory of lacunar infarcts showed a characteristic vascular pathology. These tiny vessels often contained focal enlargements and small hemorrhagic extravasations through the walls of these arteries. Subintimal foam cells sometimes obliterated the lumens, and pink-staining fibrinoid material was present within the vessel walls. The arteries in some regions were often replaced by whorls, tangles, and wisps of connective tissue that obliterated the usual vascular layers. Fisher called these processes segmental arterial disorganization, fibrinoid degeneration, and lipohyalinosis.1Figure 1, given to me by Fisher, shows a severely narrowed penetrating artery in a patient with severe hypertension. The media is hypertrophied and contains fibrinoid material.


Lacunar infarction and small vessel disease: pathology and pathophysiology.

Caplan LR - J Stroke (2015)

Small penetrating artery showing lipohyalinosis and fibrinoid necrosis (white arrow); lumen is considerably compromised (upper black arrow). The thickened media contains lipohyalinotic material (Lower black arrow) (Supplied by Dr. C. Miller Fisher.).
© Copyright Policy - open-access
Related In: Results  -  Collection

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

Figure 1: Small penetrating artery showing lipohyalinosis and fibrinoid necrosis (white arrow); lumen is considerably compromised (upper black arrow). The thickened media contains lipohyalinotic material (Lower black arrow) (Supplied by Dr. C. Miller Fisher.).
Mentions: Miller Fisher, nearly a half century ago, analyzed the arterial pathology that caused small deep infarcts by carefully assessing serial sections of vessels at necropsy.1 He observed that the penetrating arteries that supplied the territory of lacunar infarcts showed a characteristic vascular pathology. These tiny vessels often contained focal enlargements and small hemorrhagic extravasations through the walls of these arteries. Subintimal foam cells sometimes obliterated the lumens, and pink-staining fibrinoid material was present within the vessel walls. The arteries in some regions were often replaced by whorls, tangles, and wisps of connective tissue that obliterated the usual vascular layers. Fisher called these processes segmental arterial disorganization, fibrinoid degeneration, and lipohyalinosis.1Figure 1, given to me by Fisher, shows a severely narrowed penetrating artery in a patient with severe hypertension. The media is hypertrophied and contains fibrinoid material.

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