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Biomedical subjects

V Hachinski

Publications and source records attributed to V Hachinski.

At least 127 records · Page 7Linked to original sources
PubMed1986

H.J.M. Barnett.

Explore the source record for details and available documents.

History, 20th Century↗
PubMed1986

The significance of white matter lucencies on CT scan in relation to cognitive impairment.

As part of a prospective clinicopathological study a cohort of "normal" elderly volunteers (n = 110) has been investigated with CT scans, psychometric testing (Extended Scale for Dementia) and neurological examination. CT scans were evaluated by a neuroradiologist for the presence or absence of white matter lucencies (WML). WML were defined as patchy or diffuse areas of decreased attenuation involving only white matter and with no change in adjacent ventricles or sulci. The 12 subjects with WML had lower scores on the ESD than the 98 subjects without WML (mean ESD with WML 229.5 +/- 14; without WML 236.7 +/- 8.6, t-test p less than .01) and the difference remains significant even after adjusting for the possible confounding effects of age (ANCOVA, P less than .043).

Aged↗
PubMed1986

The EEG in Alzheimer type dementia: lack of progression with sequential studies.

Our findings dispel the commonly held belief that the EEG always worsens progressively in dementia of the Alzheimer's type. In a continuing cohort analytical study of dementia, 139 patients with Alzheimer's disease and 148 controls were studied for EEG abnormalities and progression. EEGs were read without knowledge of the previous EEGs or clinical condition, and classified according to the presence of diffuse delta or theta, bisynchronous spikes, projected activity, and focal activity. EEGs were significantly different in the two groups. EEG scores generally worsened over 1-4 years, but most of the subjects showed no alteration in their EEG scores. A few patients with Alzheimer's disease showed improvement of EEG findings.

Alzheimer Disease↗
PubMed1985

A new definition of Alzheimer's disease: a hippocampal dementia.

Preliminary data support the hypothesis that the decline of all higher cognitive functions in senile dementia of the Alzheimer type is attributable to histopathological changes in the hippocampal formation, with or without neocortical neuronal lesions. Previous literature amply supports the critical role of this "locus minoris resistentiae" in memory processing and cognitive physiology. New observations include quantitative morphometric evaluations of the hippocampal formation from a longitudinal study of prospectively tested patients and histological and neurochemical data from patients with a clinical presentation consistent with typical Alzheimer's disease, in whom the only neuropathological abnormality was devastating nerve cell loss and gliosis in the hippocampi.

Aged↗
PubMed1983

Multi-infarct dementia.

Arteriosclerosis causes damage by strokes. No evidence exists for continuous ischemia in the brain. Decreased cerebral blood flow and metabolism are the result not the cause of dementia so the use of cerebral vasodilators and "activators" lacks a scientific basis. Instead, the treatment and prevention of multi-infarct dementia consist in the treatment and prevention of stroke.

Alzheimer Disease↗