Vascular dementia: an obsolete concept. Commentary.
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Biomedical subjects
Publications and source records attributed to V Hachinski.
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Experimentally, focal and global cerebral ischemia are markedly affected by small changes in brain temperature. Mild hypothermia greatly ameliorates and mild hyperthermia markedly exacerbates ischemic-induced neuronal injury. Mild hypothermia not only protects against neuronal injury but also improves clinical outcome. This effect depends on the temperature of the brain both during and after the ischemic episode. Clinical and laboratory evidence concerning the value of hypothermia and the danger of hyperthermia in acute ischemia are presented. Potential mechanisms of action of hypo- and hyperthermia in ischemic injury are also addressed. The need to treat fever in acute cerebral ischemia, even if evidence is only empiric, and the intriguing possibility of using mild hypothermia to treat acute cerebral infarction are discussed.
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We obtained a topographic computer analysis of the electroencephalogram in 53 normal elderly subjects. Normal aging was not associated with an increase in slow (delta) activity. However, cognitive performance correlated positively with fast (beta) activity particularly in frontal leads, even after controlling for age, education, occupation, and medication. Five subjects who showed early signs of cognitive decline, had all a marked reduction in beta activity suggesting that this may be an early indication of intellectual loss.
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PURPOSE: The prevalence of the antiphospholipid syndrome was determined prospectively in patients presenting with stroke and transient ischemic attacks. An attempt was made to define a subset of stroke patients at risk for this syndrome on the basis of their clinical features. PATIENTS AND METHODS: Fifty-one consecutive patients with stroke and transient ischemic attacks were assessed. Tests used for the laboratory diagnosis of the antiphospholipid syndrome included four phospholipid-dependent coagulation tests for detection of the lupus anticoagulant, and two enzyme-linked immunosorbent assays for antibodies to phospholipid. RESULTS: Three of 51 patients (6%, 95% confidence intervals 0% to 12.0%) had a lupus anticoagulant and the clinical features of the antiphospholipid syndrome. Seven patients had clinical features suggestive of the syndrome but negative laboratory tests. Those patients who were clinically unlikely to have this syndrome also had negative laboratory tests. CONCLUSION: In a series of 51 unselected patients presenting with stroke and transient ischemic attacks, three had the antiphospholipid syndrome. The clinical features of this syndrome are helpful in identifying this group of patients. The role of the lupus anticoagulant in the pathogenesis of stroke remains to be defined.