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E Wagemann

Publications and source records attributed to E Wagemann.

4 recordsLinked to original sources

[Pellagra: diagnosis still valid].

Pellagra, caused by niacin deficiency, was described in 1730 by Casal in Spain and is specially frequent in alcoholics, subjects with malabsorption and mentally ill patients. We report three alcoholic patients (one female) aged 32, 57 and 26 years old, presenting with the typical desquamative and hyperpigmented lesions in exposed areas. One patient also had mental changes characterised by aggressiveness and clouding of consciousness. A diagnosis of pellagra was reached and treatment with nicotinic acid was started with good clinical response in all cases.

Adult↗

Altered pattern of immunohistochemical staining for glial fibrillary acidic protein (GFAP) in the forebrain and cerebellum of the mutant spastic rat.

The spastic rat is a neurological mutant of the Han-Wistar strain with prominent spasticity, tremor, and ataxia. Neurodegeneration is found in the CA3 sector of the hippocampus and in Purkinje cells of the cerebellum. We examined the forebrain and cerebellum of spastic rats for glial reactions by using immunolabelling for the astrocytic marker, glial fibrillary acidic protein (GFAP). First, a map of the GFAP-distribution was made representing a systematic series of frontal sections in controls. Reactive astrocytes with increased GFAP should occur in the areas with established neuronal degeneration, but they could also demarcate further regions with pathology in this rat strain. Since the baseline levels of GFAP-immunoreactivity differ between brain regions, control rats and clinically normal littermates served as controls to judge relative increases in major structures. In the CA3 sector and hilus of the dorsal hippocampus, a massive gliosis was detected. In the cerebellum, a patchy increase of GFAP labelling in Bergmann glia was found. Further increases of GFAP-labelling in reactive astrocytes occurred in fiber tracts, the ventral thalamic nuclei, medial geniculate nuclei, pontine region and optic layer of the superior colliculus. Inconsistent changes were noted in cortex and pallidum. No defects of glial labelling or malformations in glial architectonics were found. The reactive changes of astroglial cells in hippocampus and cerebellum are in proportion to the neuronal degeneration. The glial reactions in the other brain regions possibly reflect a reaction to fiber degeneration and incipient neuronal degeneration or functional alterations of glial cells in response to neuronal dysfunction.

Animals↗

Neuronal degeneration in hippocampus and cerebellum of mutant spastic Han-Wistar rats.

The neuropathology of the brain of mutant spastic Han-Wistar rats (Han-Wist SPA/SPA) was investigated using histological techniques. A surprising result was the detection of neuronal degeneration in the hippocampus and cerebellum of mutant spastic rat brains, whereas other regions, e.g. neocortex, isocortex, basal ganglia and thalamus, were overall normal. The CA3 sector in the septal third of the hippocampus including the cell band reaching into the hilus ('CA3c') showed a severe neuronal degeneration, whereas the granule cells of the dentate gyrus, several hilar neurons ('CA4') and the pyramidal cells in CA1 were found normal. In the cerebellum, a variable patchy degeneration of Purkinje cells was detected while the general layering was normal and granule cells and Golgi cells appeared preserved.

Animals↗