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 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 51-yearold man with moderate intermittent hypertension had a rapidly progressive, profound dementia in the absence of significant localizing neurological signs. Postmortem examination disclosed the vascular alterations and diffuse white matter degeneration which characterize subcortical arteriosclerotic encephalopathy (SAE) or Binswanger's disease. The case underscores the need to consider vascular disease as an etiology of dementia -- even in the absence of focal neurological deficit.
Stroke
PMID:Subcortical arteriosclerotic encephalopathy (Binswanger's disease). A vascular etiology of dementia. 100 40

Dementia is in addition to cerebral haemorrhage major symptom of cerebral amyloid angiopathy (CAa). In order to explore the pathological basis for dementia in CAa-related conditions, we made a clinicopathological analysis of CAa, with special attention to dementia. Among 150 patients (mean age 78.6 years) with autopsy-proven intracranial haemorrhage in Tokyo Metropolitan Geriatric Medical Center, CAa with cerebral haemorrhage accounted for 8.0% (12 cases), associated with hypertension and metastatic brain tumour. Among 38 patients with lobar haemorrhage, CAa represented the second most common cause (21.1%) of intracranial haemorrhage after hypertension. A total of 20 patients with CAa (mean age 82.5 years) were studies clinically and pathologically. Hypertension was present in 50%. Thirteen had a history of stroke and others had either ill-defined or no strokes. The average number of strokes 2.9. Fifteen patients (75%) had dementia. Based on the clinicopathological grounds for dementia, CAa-related conditions could be divided into three subtypes: "haemorrhagic", "dementia-haemorrhagic" and "dementia" type. Haemorrhagic type (30%, 6 cases) showed multiple recurrent lobar haemorrhages caused by CAa. Hypertension was present in only 1 patient. The incidence of senile plaques and neurofibrillary tangles was generally correlated with age. Only 1 patient had dementia. The dementia-haemorrhagic type (40%, 8 patients) had recurrent strokes with cerebral haemorrhage after preceding dementia. There were two different neuropathological subsets: CAa with atypical senile dementia of Alzheimer type (SDAT) and CAa with diffuse leucoencephalopathy. Patients with CAa with atypical SDAT had multiple cerebral haemorrhages caused by CAa combined with atypical Alzheimer-type pathology. Patients with CAa with diffuse leucoencephalopathy had cerebral haemorrhages in combination with diffuse white matter damage like Binswanger's subcortical vascular encephalopathy (BSVE). The incidence of senile changes correlated with age. Patients with the dementia type (30%, 6 patients) showed progressive dementia with or without haemorrhage. All had hypertension. They had a combined condition of Alzheimer-type pathology with conspicuous CAa with BSVE. Dementia in CAa-related conditions may be responsible for multiple factors including not Alzheimer-type degeneration, but also diffuse leucoencephalopathy like Binswanger's disease. We also found an asymptomatic type, an ischaemic type, a vasculitis type and an hereditary type in this condition.
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PMID:Dementia in cerebral amyloid angiopathy: a clinicopathological study. 144 72

In 1898, Alzheimer wrote an exhaustive update on psychogeriatric issues. He discussed paralytic dementia, involutional melancholia, senile dementia, presenile dementia, arteriosclerotic dementia, Binswanger disease, stroke-induced dementia, and other dementias of vascular origin. In this paper, he appeared to describe his very first case of Alzheimer disease, he anticipated the ischemic score, and outlined his opinion about numerous issues of dementia research that are of current interest.
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PMID:Recent studies on dementia senilis and brain disorders caused by atheromatous vascular disease: by A. Alzheimer, 1898. 178 68

Hypertensive vascular lesions in the brain include increased formation of atheroma, lacunae and lacunar infarctions, atherothrombotic brain infarction and vascular dementias such as multi-infarct dementia and Binswanger's disease. Hypertension is also associated with an increased risk of intracerebral and subarachnoid hemorrhage. Reduction of arterial pressure with antihypertensive agents can prevent the occurrence and limit the extent of stroke.
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PMID:[Cerebral vascular damage in hypertension]. 184 89

We examined sclerotic changes of the medullary arteries in 110 nonneuropsychiatric patients ranging in age from the second to the ninth decades, in 20 patients with subcortical arteriosclerotic encephalopathy (Binswanger's disease), and in 20 patients with dementia of the Alzheimer type. The principal sclerotic change was fibrohyaline thickening of the wall, which began to appear during the late fourth decade, increased in incidence gradually with age, and was most severe in patients with subcortical arteriosclerotic encephalopathy. Morphometry showed that the sclerotic changes of the medullary arteries were most prominent in the frontal lobe, followed by the parietal, occipital, and temporal lobes, in both the nonneuropsychiatric and demented groups. The sclerotic rate in the frontal lobe of patients with dementia of the Alzheimer type was slightly higher than that in the nonneuropsychiatric patients (p less than 0.05) but far less than that in the patients with subcortical arteriosclerotic encephalopathy (p less than 0.001). The sclerotic rate correlated well with the degree of ischemic white matter changes as well as with blood pressure.
Stroke 1991 Apr
PMID:Medullary arteries in aging and dementia. 202 72

Using a noninvasive portable blood pressure recorder, we compared 24-hour variations of blood pressure among 1) 35 patients with Binswanger-type dementia, 2) 43 with lacunar-type dementia, 3) 26 with a single lacunar stroke, and 4) 30 controls. Each group was divided into antihypertensive-treated and -untreated subgroups. Among the untreated subgroups, patients with Binswanger-type dementia had significantly greater 24-hour mean systolic blood pressures, 24-hour systolic blood pressure standard deviations, and maximal systolic blood pressure variations than the controls (p less than 0.05). Among the treated patients, blood pressure variability increased similarly in all subgroups with cerebrovascular lesions compared with the controls (p less than 0.05). The nocturnal blood pressure decreases seen in the controls were absent among both untreated and treated patients with Binswanger- or lacunar-type dementia (p less than 0.05). Our results suggest the importance of hypertension, short-term variations in blood pressure, and a sustained nighttime elevation of blood pressure for the pathogenesis of both Binswanger-type and lacunar-type dementia in patients receiving antihypertensive medication.
Stroke 1991 May
PMID:Twenty-four-hour variation of blood pressure in vascular dementia of the Binswanger type. 202 89

Leuko-araiosis is a purely descriptive term indicating images of bilateral, patchy or diffuse areas of decreased density frequently observable in the deep white matter on brain CT scans of adults and elderly subjects. While in earlier studies these images were considered as the "in vivo" expression of leukoencephalopathy associated with Binswanger disease, subsequently they have been reported in a rather broad spectrum of clinical conditions, including healthy aging and dementia of different types. Evidence of arterial hypertension and lacunar stroke is found in only two-thirds of subjects with leuko-araiosis. The results of pathological studies are conflicting about the nature of leukoencephalopathy, and the type and severity of medullary artery involvements. Probably several mechanisms underlie leuko-araiosis. They might act separately or be combined in different cases. Classification by physiopathological mechanism may be a suitable aim of future research in this field.
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PMID:Leuko-araiosis: a reappraisal. I. CT studies. 220 63

We performed clinical and neuroradiologic studies, including positron emission tomography, in five patients with vascular dementia of the Binswanger type. The clinical features of these cases consisted of slowly progressive dementia, together with vascular risk factors such as hypertension and often a history of minor stroke, and characteristic white matter lesions on brain computed tomograms or magnetic resonance images. Digital subtraction angiography of the cervical and intracranial arteries demonstrated no occlusive lesion in any patient. Both cerebral blood flow and the cerebral metabolic rate for oxygen were markedly reduced in the white matter (54-77% of control values), and both were decreased in the parietal (73% of control), frontal (74-80%), and temporal (74-83%) cortices, where no abnormalities were detected by brain computed tomography or magnetic resonance imaging. We conclude that vascular dementia of the Binswanger type may be caused by disconnection between the cerebral cortex and subcortical structures due to ischemic damage in the white matter.
Stroke 1990 Dec
PMID:Cerebral blood flow and oxygen metabolism in patients with vascular dementia of the Binswanger type. 226 76

The literature regarding Binswanger's disease is reviewed. Emphasis is placed on reviewing the neuropsychological literature related to Binswanger's disease. In addition, a retrospective analysis was carried out among four groups of subjects (N = 61) who were divided according to the presence or absence of dementia and deep white-matter alterations. A main effect for deep white-matter alterations was found for almost all measures of diastolic and systolic blood pressure. Among the two nondemented groups there was an effect of deep white matter alteration on neuropsychological functioning. Subjects with deep white matter changes performed worse on tests of immediate and delayed recall of a prose passage. Among the two demented groups there were no differences on any of the neuropsychological measures, although subjects with deep white matter alterations exhibited a higher incidence of focal neurologic signs and stroke. We conclude that Binswanger's disease is probably more prevalent than currently appreciated. Also, among clinically nondemented individuals periventricular white-matter alterations may be associated with subtle but definable neuropsychological deficits, and these individuals may be at risk for developing a dementing illness.
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PMID:Binswanger's disease: some neuropsychological considerations. 234 85

Two more patients with triphasic waves (TW) on their EEGs in the absence of metabolic disturbances are described. One patient had coma associated with cerebellar hematoma, the other had mild dementia associated with idiopathic calcifications of the basal ganglia and normal auditory brainstem responses, subcortical and cortical somatosensory evoked potentials. Neurologic examination failed to show asterixis in both patients. The literature on nonmetabolic causes of TW was also reviewed, and the clinical and anatomic reports of 10 patients have been analyzed: 7 patients had focal brainstem-diencephalic lesions (craniopharyngioma: 2 patients; thalamic gliomas: 3 patients; pontine stroke: 2 patients), and 3 patients suffered from diffuse subcortical or multifocal encephalopathies (Binswanger's encephalopathy: 1 patient; cerebral carcinomatosis: 1 patient; multifocal cerebral lymphoma: 1 patient). From the clinical point of view, patients with nonmetabolic diseases causing TW presented either disturbance of higher cerebral functions with no asterixis or sudden onset of coma. It is concluded that TW may result from focal brainstem/diencephalic lesions or from diffuse subcortical or multifocal encephalopathies in the absence of concomitant metabolic abnormalities. Nonmetabolic causes of TW should be suspected in patients presenting with neurologic disturbances not associated with asterixis.
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PMID:Nonmetabolic causes of triphasic waves: a reappraisal. 236 53


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