Showing papers by "Herbert Budka published in 1994"

Patterns of oligodendroglia pathology in multiple sclerosis

Abstract: Patterns of inflammation, demyelination and oligodendrocyte pathology were studied in acute multiple sclerosis and during early and late exacerbations of chronic multiple sclerosis. Cells within lesions were identified by immunocytochemistry with markers for T lymphocytes, macrophages, oligodendro-cytes and astrocytes. In addition, in situ hybridization for proteolipid protein mRNA was used to identify myelinating and myelin supporting oligodendrocytes. Degenerating cells in the lesions were detected by DNA fragmentation in cell nuclei. The inflammatory reaction in all three types of multiple sclerosis lesions was shown to be dominated by T lymphocytes and macrophages. In late chronic multiple sclerosis lesions, a significant increase in the number of immunoglobulin producing plasma cells was found in infiltrates as compared with acute and early multiple sclerosis lesions. In all three types of multiple sclerosis, confluent plaques of demyelination were found to be present. In acute multiple sclerosis, demyelination was found to be associated with extensive destruction of other tissue elements, including oligodendrocytes, astro-Acytes and axons, but even in these destructive lesions a considerable number of oligodendrocytes was preserved and at disposal therefore, for rapid remyelination. During early exacerbations of chronic multiple sclerosis, selective demyelination was associated with almost complete preservation of oligodendrocytes in the majority of cases. Correspondingly, a high number of remyelinating lesions was present at that stage of disease. In lesions developing late after onset of multiple sclerosis, demyelination generally accompanied extensive destruction and loss of oligodendrocytes. In these lesions, remyelination was sparse and restricted to lesional borders. The observed patterns of cell death suggest that in some cases oligodendrocytes, in others myelin sheaths are the primary target of the destructive process. Our data indicate that the type and amount of inflammation, de- and remyelination, and of tissue damage vary between different forms of multiple sclerosis and between different stages of the disease, possibly reflecting different pathogenic mechanisms in a disease spectrum.

Neocortical changes in Parkinson's disease, revisited.

Abstract: In a series of 37 Parkinson's disease (PD) brains, cortical changes were reexamined by means of Bielschowsky silver impregnation and anti-ubiquitin immunocytochemistry Compared to routine HE staining, anti-ubiquitin immunostaining revealed neocortical Lewy bodies (LBs) in a significantly higher percentage (76% vs 32%) Neocortical senile plaques (SPs) occurred more frequently in brains with neocortical LBs than in cases without LBs (50% vs 11%; p < 005) Semiquantitative assessment of neocortical LB density correlated with the frequency of occurrence and density of neocortical SPs Dementia was confined to patients with abundant neocortical LBs, thus fulfilling histological criteria of diffuse Lewy body disease We conclude that neocortical LBs are a very frequent feature of PD, although abundance of cortical LBs is confined only to a small subgroup with prominent dementia: diffuse Lewy body disease