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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Subcortical arteriosclerotic encephalopathy, a chronic vascular dementia with hydrocephalus, was characterized pathologically in five patients by severe thickening of small vessels and by diffuse regions of white matter loss with gliosis. Lacunar infarcts were also present. The clinical picture in 11 patients was characterized by: (1) persistent hypertension and systemic vascular disease; (2) acute strokes; (3) subacute accumulation of focal neurologic symptoms and signs over weeks to months; (4) long plateau periods; (5) lengthy clinical course; (6) dementia; (7) prominent motor signs and pseudobulbar palsy and; (8) hydrocephalus. The pathogenesis of subcortical arteriosclerotic encephalopathy is unknown; possible mechanisms include diffuse ischemia and fluid transudation with subsequent gliosis related to subacute hypertensive encephalopathy.
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PMID:Clinical features of subcortical arteriosclerotic encephalopathy (Binswanger disease). 56 79

With 60 million Americans meeting criteria for either essential or secondary hypertension, elevated arterial pressures remain a major health problem. While efforts to find etiologies for essential hypertension continue, clinicians battle its effects on organ systems, including the nervous system. Hypertensive changes in the nervous system may be acute, chronic, or both. The intracerebral vasculature is commonly affected. Not infrequently, acute changes including hemorrhage, encephalopathy, and cerebral edema are superimposed on chronic changes of hyaline and fibrinoid arteriolosclerosis. Chronic vascular changes sacrifice vascular lumina. The resulting ischemia is responsible for cystic (lacunar) lesions and subcortical ischemic white matter lesions consistent with Binswanger's disease.
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PMID:The effects of hypertension on the nervous system. 206 1

Oxygen affinity of hemoglobin, erythrocyte 2,3-diphosphoglycerate (DPG) and adenosine triphosphate (ATP) concentrations were compared before and after oral administration of vinpocetine (TCV-3B) (15 mg/d), a primarily vasodilating agent, for three weeks in eight patients with vascular dementia of the Biswanger type which is characterized by diffuse myelin pallor and multiple lacunes in the cerebral white matter. After vinpocetine administration, oxygen affinity of hemoglobin (P50) was significantly increased (26.5 +/- 0.55 to 27.6 +/- 0.62 mmHg; mean and standard deviation, p less than 0.05), red blood cell (RBC) ATP concentrations were significantly increased (846 +/- 168 to 1,158 +/- 130 mumol/l RBC, p less than 0.05), while DPG concentrations were unaltered (4.46 +/- 0.48 to 4.59 +/- 0.57 mmol/l RBC). There was a significant positive correlation between the increase of P50 and the increase of erythrocyte ATP concentrations (r = 0.67, p less than 0.05). The effect of vinpocetine of enhancing oxygen release of hemoglobin may offer an additional benefit to its primary vasodilating action in the treatment of vascular dementia of the Binswanger type due to chronic ischemia.
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PMID:Effect of vinpocetine on oxygen release of hemoglobin and erythrocyte organic polyphosphate concentrations in patients with vascular dementia of the Binswanger type. 239 97

Computed tomography is often insensitive to such lesions as atrophic demyelination, enlarged perivascular spaces and infarction in the periventricular white matter. In attempt to better understand the discrepancy between the pathologic and X-CT findings, the author correlated areas that had focal, patchy on X-CT and brains with gross and microscopic findings. Patients with cerebral strokes had larger volume infarcts characterized centrally by necrosis, axonal loss, and demyelination. The progressive subcortical vascular encephalopathy (Binswanger's disease) is characterized by ischemic demyelinization of white matter provoked by hypertensive vascular changes in small vessels and is usually accompanied by multiple lacunar infarcts in a periventricular area and the basal ganglia. Small, deep hemispheric infarcts may be of no clinical significance unless a sufficient aggregate of these occurs. It should be pointed out that many small infarcts are clinically silent, and chronic multifocal ischemia may be responsible for observed senescent changes in cerebral tissue. The extension of the infarcted area might be most important in the development of cerebrovascular dementia. Mixed forms of degenerative dementia and any type of cerebral vascular disease are common and account for 10-20% of all dementias.
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PMID:[Cerebrovascular dementia; correlation of computed and histopathologic findings]. 260 Oct 93

To investigate the relationship between middle cerebral artery (MCA) trunk lesions and the etiology of Binswanger type (B type) infarction, which was demonstrated as a diffuse subcortical low density area/high intensity area by CT/MRI, patients with both MCA lesions and B type infarction were studied clinically. Eighteen patients with B type infarction were diagnosed among 224 patients with MCA occlusion/stenosis on angiography accounting for 8%. The incidence was as high as 25% in M2 stenosis. The mean age of B type infarction patients was 64 years and 16 of them were men. Chronologically stepwize/slowly-progressive deterioration of clinical manifestations were observed in 14. All patients had hemiplegia, though half of them were mild or moderate in severity. Furthermore, aphasia, Gerstmann syndrome and dementia were present in 10, 1 and 2 patients, respectively. Twelve had a history of hypertension, while 11 showed transient decreases with marked changes (more than 31 mmHg in mean arterial blood pressure) in arterial blood pressure during their clinical course. Out of 9 patients in whom cerebral blood flow (CBF) was measured by 133Xe injection method/inhalation method, 7 demonstrated mild to moderate decreases in mean CBF (more than 30 ml/100 g/min) with no relation to the severity of MCA lesions. These findings suggested that hemodynamic mechanisms associated with hypoperfusion due to marked fluctuations in blood pressure are accelerating factors of B type infarction and MCA lesions, even though ischemia in the subcortical area due to leptomeningeal anastomosis may be mild or moderate.
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PMID:[Clinical study on the relationship between middle cerebral artery lesions and Binswanger type infarction]. 260 75

Circulation to the brain is greatly affected by hypertension and by its treatment. Neurologic dysfunction is prominent among the complications of increased arterial pressure and is also most susceptible to preventive antihypertensive therapy. The upward resetting of the limits of autoregulation of cerebral blood flow in hypertension is probably due largely to structural thickening of the walls (hyaline arteriosclerosis) of the resistance vessels. Other consequences of hypertensive vascular lesions in the brain include increased formation of atheroma, lacunae and lacunar infarction, cerebral infarction, multi-infarct dementia and Binswanger's disease. There is also an association between hypertension and hemorrhagic strokes, namely, subarachnoid and intracerebral hemorrhage. Brain lesions are also prominent in malignant hypertension and hypertensive encephalopathy. Antihypertensive treatment, especially if intensive, can result in boundary zone ischemia in the brain if arterial pressure decreases steeply.
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PMID:Morphologic changes during hypertension. 264 56

Binswanger's encephalopathy is reviewed in respect to history, computed tomography, magnetic resonance imaging, epidemiology, pathology, clinical picture, laboratory findings, differential diagnosis, and treatment. The various viewpoints on the pathogenesis of the process are discussed, in particular the role of ischemia, vascular disease, high blood pressure, lacunar infarction, hypoxia, edema, and hydrocephalus. The white matter hypomyelination of congophilic angiopathy and Alzheimer's disease should provide clues. A unifying hypothesis has not been attained.
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PMID:Binswanger's encephalopathy: a review. 265 69

Subcortical arteriosclerotic encephalopathy (SAE) is a common though infrequently recognized dementia of the elderly. The unique vascular anatomy of the subcortical white matter and central brain stem probably predisposes those regions to chronic ischemia and incomplete infarction in the presence of various cardiovascular and hemodynamic insults. Recent studies have begun to define the risk factors for SAE, and others have shown it to be a condition frequently comorbid with the dementias of Alzheimer's disease, the multi-infarct state, and normal pressure hydrocephalus. Recent research into the etiologies of these disorders suggest certain pathogenetic links between them, strongly implying that they are not neatly distinct disease entities, as is commonly believed, and accounting for some of the overlap between these dementing illnesses seen clinically.
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PMID:Binswanger's disease (Part II): Pathogenesis of subcortical arteriosclerotic encephalopathy and its relation to other dementing processes. 269 55

The pathological changes in the brains of seven patients who had been clinically diagnosed as normal pressure hydrocephalus (NPH) are described and the possible etiological mechanisms are discussed. The pathological findings in all cases consisted of demyelination akin to Binswanger's type of encephalopathy, especially in the frontal lobes. Arteriosclerosis accompanied by occasional organized thrombi and scattered microinfarcts in the periventricular white matter were seen. Focal leptomeningeal fibrosis, diminution of arachnoidal granulations, and non-specific aging processes were noted. Among the above of particular interest, was the degeneration of both periventricular and deep white matters with microinfarcts, and moderate to severe arteriosclerosis. On the basis of these observations, we assume that the degeneration in the white matter is not merely a secondary change due to the result of enlargement of ventricle, but plays an important role in the development of NPH. The development of NPH requires not only the disturbance of cerebrospinal fluid, but also the pre- or coexisting vulnerability in the white matter caused by variables such as ischemia, hypoxia, and trauma.
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PMID:Normal pressure hydrocephalus. Neuropathological study. 357 65

White matter changes, which are noted in Binswanger's disease and which may be due to ischemia, have previously been explained mainly on the basis of the hemodynamic mechanism. To elucidate the etiopathophysiology of Binswanger's disease from the hemorheology viewpoint, platelet activation in the cerebral circulation was studied in 30 patients with Binswanger's disease, who satisfied the diagnostic criteria of Binswanger's disease proposed by Bennett et al. Plasma beta-thromboglobulin concentration gradients (delta BTG) between the jugular vein and the antecubital vein, as indicators of platelet activation in the cerebral circulation, were determined in these patients (Binswanger's disease group) compared with those of different stroke subtypes groups (lacunar, atherothrombotic, cardioembolic) in the chronic phase and 25 patients with various diseases other than stroke (non-stroke group). Among these groups, the elevation of delta BTG levels in the Binswanger's disease group (4.55 +/- 6.95) were so frequent and prominent that differences were significant, especially in comparison to those of the cardioembolic group, and the non-stroke group. The enhanced platelet activation in the cerebral circulation observed in Binswanger's disease indicated not only the widespread development of underlying vascular lesions, but also accelerated release reaction of vasoactive substances from platelets into the blood stream, which could biochemically injure the vascular wall and neurons downstream, resulting in Binswanger's disease.
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PMID:[The role of platelet in the etiology of Binswanger's disease]. 782 2


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