The pandemic of von Economo's disease which began in January 1917 preceded that of influenza of 1918-1919 by more than a year. Though it has been customary to link the two it seems unlikely that the latter was responsible for the former as has been proposed. It has been assumed that von Economo's disease (ED) was caused by a virus; but in fact the etiology is in question as no virus has yet been transmitted to experimental animals or cells in culture.
View Article and Find Full Text PDFA marked generalized astrogliosis was observed in the frontal and temporal white matter from a case of von Economo's disease and another of postencephalitic Parkinson's disease, which areas were otherwise devoid of any other demonstrable microscopic lesions. No similar astrocytic reaction of any severity was observed in the same areas in a number of other brain diseases or controls, except when other kinds of lesions were present in the same section, with reactive astrocytes being present within the primary or defining lesion or immediately close by. The marked astrogliosis in von Economo's and postencephalitic Parkinson's diseases in areas "distant" from the primary lesions seeming to indicate extensive pathological involvement, added to the strong qualitative and quantitative similarity of this reaction to that observed in concurrently studied cases of encephalitides caused by the human immunodeficiency virus, lend further factual support to the hypothesis of a viral etiology, albeit unspecified, in both von Economo's and postencephalitic Parkinson's diseases.
View Article and Find Full Text PDFThirty-eight patients newly diagnosed as having Parkinson's disease (mean age, 57.3 years; mean Parkinson's disease duration, 2.7 years) in the earlier phase of the disease (mean Hoehn/Yahr stage, 2; mean motor scores, 11.
View Article and Find Full Text PDFTwo hundred patients at a median age of 63 years, receiving conventional levodopa therapy for 8 years, who had had Parkinson's disease for 10 years, tried a regimen of selegiline (L-deprenyl), a type B monoamine oxidase inhibitor, at a daily dose of 10 mg, for varying periods from less than 6 months to more than 24 months (28% over 24 months). Selegiline does improve parkinsonism during the initial 6 months to 12 to 24 months of combined therapy in one third to almost half of patients with an end-of-dose type of response to long-term levodopa therapy. However, even this particular class of patients is unable to maintain such an improvement by 36 months, much less by 48 months, from the start of the selegiline trial.
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