1/2. The distribution of Alzheimer's neurofibrillary tangles and gliosis in chronic subacute sclerosing panencephalitis.In two cases of clinically verified chronic subacute sclerosing panencephalitis (case 1, male, 15 years with a 9-year history; case 2, male, 20 years with a 9-year history) numerous Alzheimer's tangles (AT) were identified throughout the cerebral cortex (containing paired helical filament on electron microscopical examination). The brains were severely atrophic with hydrocephalus ex vacuo, occasional scattered microglial nodules, scant perivascular inflammatory infiltrates and demyelination. Only in case 1 were a few atypical intranuclear inclusion bodies noted. In the six-layered neocortex, a distinct distribution pattern of AT was observed; these lesions were mainly seen in laminae II, III and V (laminar distribution). The glial fibrillary acidic protein stain displayed extensive laminar gliosis mainly of the layers I, IIa, IV and VI; layers III and V, largely occupied by the AT, remained conspicuously spared from gliosis (especially the lamina III). gliosis was prevalent in the white matter which was atrophic and shrunk. In the hippocampus, the AT involved many pyramidal neurons and, in this layer gliosis was lighter than in the surrounding white matter. In case 2, AT were present in the nucleus of Meynert, hypothalamus and in raphe centralis of the upper brain stem. overall, the distribution of AT resembled that seen in Alzheimer's disease and aging; however, the senile plaques, vascular amyloidosis and granulovacuolar change were totally absent in both cases.- - - - - - - - - - ranking = 1keywords = nucleus (Clic here for more details about this article) |
2/2. Cerebral glucose metabolism in the course of subacute sclerosing panencephalitis.Regional cerebral glucose metabolism was studied in a 15-year-old boy with subacute sclerosing panencephalitis before and after therapy with human interferon beta, using positron emission tomography of fluorine 18-2-fluoro-2-deoxyglucose. At first examination, metabolism was symmetrically decreased in the thalamus, cerebellum, and all cortical areas except prerolandic motor cortex, but increased in lentiform nucleus. A computed tomographic scan was normal. Six months later, bilateral focal necrosis centered in the previously hypermetabolic putamen was demonstrated by computed tomography and magnetic resonance imaging. The caudate nucleus and the superoposterior part of the putamen were spared, still showing increased metabolism. Corresponding with some clinical improvement, cortical glucose consumption rates had returned to a normal level.- - - - - - - - - - ranking = 2keywords = nucleus (Clic here for more details about this article) |