Titlebook: Symposium on Neuroglia / Symposium Concernant La Neuroglie / Symposium über die Neuroglia; Papers Presented on F. Erbslöh,A. Oksche,F. Sei

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Allgemeine Histopathologie der Glia,mparative neuropathology are stressed. The pathological changes of astrocytes, ependymal cells, Oligodendroglia and microglia are discussed. The modern trend in general pathology goes in direction of a molecular pathology. Though there is a considerable number of new methods, there is no principle c

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Gliazellen als Manifestationsorte von Stoffwechselkrankheiten,ectodermal, especially glial cells. We conclude, that it is no more justified, to suggest a general glial insufficiency in these diseases. The involved cell types are able to react upon other agents in a normal matter. On the other hand enzymatically normal cells give similar reactions to installed

FIR

Pathologie der Makro- und Mikroglia im elektronenmikroskopischen Bild,s an increase in bound glycogen is demonstrable. In reactive astrocytes glia filaments are formed in the cytoplasm. An emancipation of filament bundles from cytoplasmic processes was not observed even in old glial scars. In glial scars astrocytes often form multilayers of flat processes..Reactive mi

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Zur Ultrastruktur der Astroglia und des Status spongiosus, Held’s glia chambers or Obersteiner’s spaces is due to an hydrops of the pericapillary or perineuronal astrocyte processes, the . of the edema of the grey matter to a generalised astroglia hydrops. The ordinary edema of the white matter is produced by the dissociation of the fiber structure followi

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,Gliabefunde bei den diffusen und fokal-disseminierten Formen der spongiösen Neurodystrophien des fr the brain (infantile form of Wernicke’s encephalopathy and subacute necrotizing encephalopathy with predilection for the brain-stem)..In contrary to myelinisation, in the diffuse cases the development of glia was not disturbed, in the younger cases the so-called “myelinisation-glia” as described by

CORD

,Präsenile gliale Dystrophie,glia with increased fiber production and locally occuring spongy degeneration. There were no changes corresponding to Pick’s cortical atrophy, senile plaques and Alzheimer’s fibrillar degeneration. The pattern of lesions present is interpreted as a glial syndrome comparable with the already known ty

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Provenance

Autoradiographische Untersuchungen zum Verhalten der Glia- und Mesenchymzellen bei der Hirnwunde,s been investigated. Whilst with the light microscope cell proliferation has been observed as soon as after 72 hours and a vascular proliferation after 4 days, this method allows to detect the beginning of a cell proliferation in the brain lesion after 12 hours. In the following hours the number of

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