Perivascular anoxia‐ischemia lesions in the human brain

Hart, Michael N.; Galloway, Gregg M.; Dunn, Martin

doi:10.1212/wnl.25.5.477

Cited by 5 publications

(3 citation statements)

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“…Although the neuronal loss could be induced by recurrent hypoxic-ischemic episodes owing to respiratory depression during the intoxicated state, the reduction of GFAP-positive astrocytes argues against such a phenomenon as the sole cause. Furthermore, CNS lesions after global hypoxic-ischemic damage are predominantly seen in the Purkinje cell layer of the cerebellum and the hippocampal formation (13). Because the nerve cell density in these regions was not significantly changed between both groups, other factors must be of pathogenetic significance.…”

Section: Discussionmentioning

confidence: 98%

Neuropathological Alterations in Drug Abusers: The Involvement of Neurons, Glial, and Vascular Systems

Büttner

Weis

2006

FSMP

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Because the effects of drug abuse on the cellular elements of the human brain have not been studied systematically, an investigation was performed using histology, immunohistochemistry, and morphometry. The main cortical and subcortical brain areas of 50 polydrug deaths were analyzed as compared with controls.In the brains of drug abusers, a significant neuronal loss was present. Interestingly, the number of glial fibrillary acidic protein (GFAP)-positive astrocytes was reduced. the numerical density of perivascular and parenchymal microglia was increased in the white matter and in most subcortical regions. In the white matter there were widespread β-amyloid precursor protein deposits. Furthermore, there was a prominent vascular hyalinosis, endothelial cell proliferation, and a loss of immunoreactivity for collagen type IV within the vascular basal lamina.The neuronal loss seems to be the result of a direct impairment of nerve cells and, indirectly, to a damage of astrocytes, axons, and the microvasculature. The reduction of GFAP-positive astrocytes is also indicative of a drug-induced damage. The axonal injury suggests a toxic-metabolic drug effect, whereas the concomitant activation of microglia is indicative of a long-standing progressive process. The noninflammatory vasculopathy can be considered as the morphological substrate of a disturbed blood-brain barrier. Our findings demonstrate that drugs of abuse initiate a cascade of interacting toxic, vascular, and hypoxic factors that finally result in widespread disturbances within the complex network of central nervous system cell-cell interactions.

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Section: Discussionmentioning

confidence: 98%

Neuropathological Alterations in Drug Abusers: The Involvement of Neurons, Glial, and Vascular Systems

Büttner

Weis

2006

FSMP

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“…Second, the perivascular lesions seen in humans following circulatory arrest combined with hyperosmolality are predominantly situated around penetrating cortical vessels and not associated with capillaries. 8 The further possibility that larger vessel occlusion might be caused by spasm is suggested by Wade and associates 13 who have demonstrated increased concentrations of potassium in rat brain interstitial fluid following ischemia and have postulated that the no-reflow state which they observed might possibly be due to vascular contraction since it is known that high potassium concentrations can cause contractions of vascular smooth muscle. 14 Zervas et a/.…”

Section: Discussionmentioning

confidence: 99%

“…However, we have observed perivascular patterns of necrosis in human cerebral cortices following ischemia combined with serum hyperosmolality. 8 Upon reexamination of that material we concluded that the focal ischemic areas were associated with penetrating vessels large enough to contain significant amounts of smooth muscle in their walls. This observation raised the question of whether spasm of intraparenchymal cerebral vessels could occur and if it could be contributory to post-ischemic no-reflow in the cerebral cortex.…”

Section: S U M M a R Y The Reaction Of Brain Parenchymal Vessels In Amentioning

confidence: 97%

Vascular spasm in cat cerebral cortex following ischemia.

Hart¹,

Sokoll²,

Davies³

et al. 1978

Stroke

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The reaction of brain parenchymal vessels in areas of no-reflow following ischemia in cats was evaluated. A method was devised by which brain biopsies following ischemia were quickly frozen at -170 degrees C, sections were cut and stained and vessel internal and external diameter measured. Vessels in the no-reflow areas had smaller internal and external diameters and thicker walls when compared to adjacent reflow areas as well as to normal control animals. By utilizing a 2-way analysis of variance in which reflow versus no-reflow vessel diameters were compared by region the differences were found to be statistically significant (p less than 0.05). The data raise the possibility that there may exist normal regional differences in the size of cerebral vessels.

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Neuropathologie

Peiffer¹

1984

Pathologie

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Perivascular anoxia‐ischemia lesions in the human brain

Cited by 5 publications

References 0 publications

Neuropathological Alterations in Drug Abusers: The Involvement of Neurons, Glial, and Vascular Systems

Neuropathological Alterations in Drug Abusers: The Involvement of Neurons, Glial, and Vascular Systems

Vascular spasm in cat cerebral cortex following ischemia.

Neuropathologie

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