European neurology
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To gain insight of the underlying mechanisms of astroglial response to Alzheimer's disease (AD), the level of glial fibrillary acidic protein (GFAP) in cerebrospinal fluid (CSF) from controls and AD subjects were immunochemically determined, and the correlation between that level and dementia severity of AD patients was evaluated. Means and SD of CSF levels of GFAP for the young control group (from 1 to 25 years, mean +/- SD 14.2 +/- 5.0, n = 13) adult control (from 26 to 55 years, 41.6 +/- 10.1, n = 9) and senescent control (older than 56 years, 65.4 +/- 8.0, n = 8) were 2.96 +/- 1.04, 2.80 +/- 1.46 and 3.99 +/- 1.55 ng/ml, respectively, and the CSF level of GFAP was not dependent on age (ANOVA, p = 0.17). ⋯ The CSF level of GFAP in the moderately to severely demented patients (MMSE /= 18, 6.85 +/- 5.76 ng/ml, n = 18; ANOVA, p < 0.05). These findings together with our previous report on an increase in the CSF level of apolipoprotein E suggest that degeneration and stimulation of astrocytes takes place concurrently in the AD brain.
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It is generally believed that a homonymous defect of macular vision (HMV) is caused by a small lesion restricted to the occipital lobe tip and rarely results from ischemic stroke. The incidence of HMV was studied retrospectively in 54 patients with infarction of the posterior cerebral artery territory who underwent Goldmann's visual field test. ⋯ All had a relatively large infarction extending from the occipital lobe tip to the posterior part of the calcarine cortex and/or the neighboring subcortical regions. Stroke-induced HMV can be caused by a large lesion involving the occipital pole and may not be so rare as generally considered.
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Restless legs syndrome (RLS) is a common sleep disorder. In 1995, clinical criteria for the diagnosis of RLS were defined. ⋯ RLS is a clinically pleomorphic syndrome, reflecting the contribution of multiple genetic and acquired factors in the pathogenesis of RLS.
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'Iatrogenic' Wernicke's encephalopathy has appeared to occur more frequently in Japan, probably induced by the change of our Japanese national health insurance policy in 1992. We report 4 nonalcoholic patients with such Wernicke's encephalopathy, which occurred during the early postoperative oral food intake period following intravenous nutrition without vitamin supplements. We analyzed the medical records of 4 patients, 3 men and 1 woman, aged between 55 and 71 years, who were admitted to our hospital between 1992 and 1995. ⋯ We speculated that the body vitamin B(1) stores had been decreasing in our patients who did not receive any vitamin supplements during intravenous hyperalimentation or hydration. Subsequent administration of high calorie and high carbohydrate oral diets increased the demand for vitamin B(1), further depleting the vitamin stores, thereby causing 'iatrogenic' Wernicke's encephalopathy. The change of our national health insurance policy in 1992 discouraged the routine administration of vitamins, probably causing Wernicke's encephalopathy in our patients.