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Biomedical subjects

Charles M Poser

Publications and source records attributed to Charles M Poser.

6 recordsLinked to original sources
PubMed2003

Epilepsy and multiple sclerosis.

A review of 29 published clinical series of adult patients who had epileptic seizures and multiple sclerosis (MS) yielded a prevalence of 2.3%, about three to six times that in the general adult population. The probable anatomic basis for the seizures is areas of inflammation, edema, and/or demyelination in the cerebral cortex and the juxtacortical white matter generated by a mechanism that is not completely understood; the fact that these plaques are very common suggests that other factors must operate in view of the rarity of seizures in MS. Seizures have been observed before and presumably marking the clinical onset of the disease, and during acute bouts. In some instances convulsions appear to be the only manifestations of an attack of MS, but there is no general acceptance of seizures as the first and only symptoms of the disease. The coincidental occurrence of both diseases, the nonspecific triggering effect of MS on latent epilepsy, and actual causation by MS are all possible explanations, but the last named is, in our opinion, extremely unusual.

Brain↗
PubMed2002

Notes on the history of the prion diseases. Part I.

The astute observation by William Hadlow, an American veterinary neuropathologist of the similarity between the histopathology of kuru, an obscure disease of the primitive tribe in New Guinea, and scrapie of sheep, was the first clue to the etiology of the transmissible spongiform encephalopathies (TSE). The knowledge that scrapie was transmissible but only after an unusually long incubation period, that the causative agent was highly resistant to heat and formalin, and that it seemed to be able to replicate in the absence of nucleic acid, eventually led to the discovery of the prion by Stanley Pruisner and the still controversial protein-only hypothesis of etiology of the TSE.

Animals↗
PubMed2002

Notes on the history of the prion diseases. Part II.

The protein-only theory of transmission of the prion diseases remains controversial. Other mechanisms such as the virus, virino, and viroid hypotheses are still under consideration. All these fit in the concept of 'slow' infections that had been proposed in 1954 by Bjorn Sigurdsson, an Icelandic pathologist. Regardless of the exact mode of infection, the presence of prions in the brain has served to unite Creutzfeldt-Jakob disease (CJD), the Gerstmann-Sträussler-Scheinker syndrome and fatal familial insomnia, as well as scrapie and a number of other animal diseases, into a single pathological entity, the transmissible spongiform encephalopathies. The appearance of bovine spongiform encephalopathy in the United Kingdom and its putative relationship to new variant CJD, have put a new and unpredictable light on these unusual and uncommon diseases.

Disease Transmission, Infectious↗