Neuropathological Changes Late in Cerebral Edema: The Relationship to Trauma, Hypertensive Disease and Binswangerʼs Encephalopathy

Feigin, Irwin; Popoff, Nina

doi:10.1097/00005072-196307000-00011

Cited by 130 publications

(47 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Since the deep cerebral white matter belongs to the farthest territory from the heart in the central nervous system, this would result in disruption of the blood-brain barrier and edema-induced destruction of the myelin. 10 The pathological findings of the white matter of this case, such as the diffuse myelin loss and atrophy with mild gliosis and sparing of the subcortical U fibers and no evidence of leukodystrophy, are also compatible with this deduction. The significance of arterial SMC loss with respect to hemodynamic derangement in CADASIL is supported by the reduced cerebrovascular CO 2 reactivity associated with this disease 11 ; it has been shown that CO 2 reactivity is significantly lower in disabled than in nondisabled CADASIL individuals.…”

Section: Discussionsupporting

confidence: 66%

Arterial Changes in Cerebral Autosomal Dominant Arteriopathy With Subcortical Infarcts and Leukoencephalopathy (CADASIL) in Relation to Pathogenesis of Diffuse Myelin Loss of Cerebral White Matter

Okeda

Arima

Kawai

2002

Stroke

104

View full text Add to dashboard Cite

Background and Purpose-There is little information regarding the pathogenesis underlying diffuse myelin loss in the cerebral white matter and sparing of the U fibers in cerebral autosomal-dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL), in which the medial smooth muscle cells of systemic arteries are characteristically involved. We sought to examine the precise extent and severity of changes in the cerebral arteries in an autopsy case of CADASIL in relation to pathogenesis of the diffuse myelin loss. Methods-We reconstructed 1000 serial sections of the frontal cerebral medullary arteries of an autopsy subject, which was the first identified Japanese case of CADASIL, as confirmed by the presence of ultrastructural deposits of granular osmiophilic material in the media of some visceral arteries and by genetic analysis. Results-We reconstructed 11 medullary arteries of the frontal lobe showing diffuse myelin loss and atrophy of the white matter with sparing of the U fibers. All of these showed complete loss of medial smooth muscle cells over their entire length and severe adventitial fibrosis. Although intimal fibrosis or hyalinosis was present, luminal occlusion was scarce. These changes were also observed in the small and large arachnoidal arteries but were relatively mild in the latter and in the cortical and subcortical medullary arteries. Conclusions-These arterial changes resulted in transformation of the cerebral arteries, in particular almost all the medullary arteries, to a so-called earthen pipe state. This supports the reported findings of a reduction in vascular reactivity to fluctuations in CO 2 levels and systemic blood pressure in CADASIL.

show abstract

Section: Discussionsupporting

confidence: 66%

Arterial Changes in Cerebral Autosomal Dominant Arteriopathy With Subcortical Infarcts and Leukoencephalopathy (CADASIL) in Relation to Pathogenesis of Diffuse Myelin Loss of Cerebral White Matter

Okeda

Arima

Kawai

2002

Stroke

104

View full text Add to dashboard Cite

show abstract

“…18 Other authors have sustained that the white matter changes in BD might represent the late effect of chronic vasogenic edema secondary to hypertensive encephalopathy. 19 In our case the pathological study revealed severe hypertensive changes in the long penetrating arteries. Although no clear episodes of hypertensive encephalopathy occurred, the case history revealed poorly controlled long standing arterial hypertension as well as repeated episodes of hypotension.…”

Section: Pathologic Studysupporting

confidence: 48%

Computed Tomography, Magnetic Resonance Imaging and Pathological Correlations in a Case of Binswanger's Disease

Mascalchi

Inzitari²,

Pozzo³

et al. 1989

Can. j. neurol. sci.

View full text Add to dashboard Cite

The results of 3 computed tomography (CT) examinations carried out over a 7 year period and of a post-mortem magnetic resonance (MR) study showed aspects of a white matter disease in a hypertensive patient suffering from vascular dementia. Histopathology revealed the primary cause of dementia to be a white matter degeneration sparing the U fibers. Rarefaction of both the myelin sheaths and the axons was present together with severe thickening of the medullary arteries. These findings support the existence of Binswanger's disease (BD) as a distinct variety of arteriosclerotic dementia. CT and MR imaging are valuable aids for diagnosis. However, since there are many other causes of CT and MR demonstrated diffuse white matter degeneration in the elderly, a conclusive diagnosis of BD requires pathological confirmation. RESUME: Tomodensitometrie, imagerie par resonance magnetique nucleaire et correlations anatomopathologiques dans un cas de maladie de Binswanger Trois tomodensitometries faites sur une periode de sept ans et un examen par resonance magnetique nucleaire effectue en post-mortem ont mis en evidence des modifications compatibles avec une leuco-encephalopathie chez un patient hypertendu atteint d'une demence vasculaire. L'histopathologie a montre que la cause primaire de la demence etait une degSnerescence de la substance blanche epargnant les fibres en U. II existait une rarefaction des gaines de myeline et des axones ainsi qu'un epaississement important des arteres medullaires. Ces observations supportent la notion que la maladie de Binswanger (MB) est une variete distincte de d6mence arteriosclereuse. La tomodensitometrie et 1'imagerie par resonance magnetique nucleaire sont des aides precieuses pour le diagnostic. Cependant, comme il existe plusieurs autres causes de degenerescence de la substance blanche chez les sujets ages, qui sont evidentes a la tomodensitometrie et a l'imagerie par resonance magnetique nucleaire, une confirmation anatomopathologique du diagnostique de MB est essentielle.

show abstract

“…[6][7][8] It has also been reported that the oligodendrocyte is more easily impaired by ischemia than other cell types that constitute the white matter tissue.…”

Section: Discussionmentioning

confidence: 99%

White Matter Changes in the Gerbil Brain Under Chronic Cerebral Hypoperfusion

Kurumatani

Kudo

Ikura

et al. 1998

Stroke

View full text Add to dashboard Cite

Background and Purpose-An animal model of chronic cerebral hypoperfusion was developed with coiled clips applied to both carotid arteries of adult Mongolian gerbils for between 1 week and 2 months. In the brain of this animal model, rarefaction of white matter with dilatation of the ventricles was frequently observed. To better understand the mechanism of white matter alteration under cerebral hypoperfusion, the chronological sequence of molecular changes in the cerebral white matter of the animal model was determined. Methods-Specially designed coiled clips were placed around both carotid arteries of Mongolian gerbils to create stenosis without occlusion. Changes in levels of myelin basic protein (MBP) as a marker of myelin, neurofilament H (NFH) as a marker of axonal proteins, and glial fibrillary acidic protein (GFAP) in astroglia after 2 months of cerebral hypoperfusion were analyzed with Western blotting and enzyme-linked immunosorbent assay. Results-Western blotting of the white matter after 2 months of hypoperfusion showed that the levels of MBP and NFH decreased, whereas that of GFAP increased. The time course of MBP and NFH changes determined with enzyme-linked immunosorbent assay revealed that the change of MBP preceded that of NFH. Conclusions-In the present study it was shown that the damage to myelin precedes that to the axon in the white matter in a chronic cerebral hypoperfusion animal model, suggesting that the change in myelin is the primary pathological event in the cerebral white matter under chronic hypoperfusion. The present study may help in understanding the mechanisms of white matter pathology in leukoaraiosis.

show abstract

Neuropathological Changes Late in Cerebral Edema: The Relationship to Trauma, Hypertensive Disease and Binswangerʼs Encephalopathy

Cited by 130 publications

References 0 publications

Arterial Changes in Cerebral Autosomal Dominant Arteriopathy With Subcortical Infarcts and Leukoencephalopathy (CADASIL) in Relation to Pathogenesis of Diffuse Myelin Loss of Cerebral White Matter

Arterial Changes in Cerebral Autosomal Dominant Arteriopathy With Subcortical Infarcts and Leukoencephalopathy (CADASIL) in Relation to Pathogenesis of Diffuse Myelin Loss of Cerebral White Matter

Computed Tomography, Magnetic Resonance Imaging and Pathological Correlations in a Case of Binswanger's Disease

White Matter Changes in the Gerbil Brain Under Chronic Cerebral Hypoperfusion

Contact Info

Product

Resources

About