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These terms refer to a distinctive cerebral disease in which a rapidly progressive and profound dementia is associated with diffuse myoclonic jerks, and a variety of other neurologic abnormalities, mainly visual or cerebellar The major neuropathologic changes are in the cerebral and cerebellar cortices; the outstanding features are widespread neuronal loss and gliosis accompanied by a striking vacuolation or spongy state of the affected regions hence the designation subacute spongiform encephalopathy (SSE) Less severe changes in a patchy distribution are found in cases with a briefer clinical course These changes, both clinical and pathologic, occur with such uniformity from case to case that they doubtless form a nosologic entity It is generally referred to as Creutzfeldt-Jakob disease, an inappropriate eponym, since it is most unlikely that the patient described by Creutzfeldt and at least 3 of the 5 patients described by Jakob had the same disease that we now recognize as subacute

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spongiform encephalopathy (SSE) It would be desirable to keep them distinct from one another, or at least, whenever one speaks of Creutzfeldt-Jakob disease, to specify what is meant either SSE or the slower progressive dementia with signs of pyramidal and extrapyramidal affection originally described by Creutzfeldt and Jakob (the latter condition is discussed on page 913) However, decades of use makes the term Creutzfeld-Jakob disease and its acronym, CJD, virtually impossible to displace Precision in de nition of these states is of greater importance than before, since it was shown by Gibbs and Gajdusek that brain tissue from patients with SSE, injected into chimpanzees, can transmit the disease after an incubation period of a year or longer Epidemiology and Pathogenesis The disease appears in all parts of the world and in all seasons, with an annual incidence of 1 to 2 cases per million of population The incidence is higher in Israelis of Libyan origin, in immigrants to France from North Africa, and in Slovakia Although the reported incidence of SSE is somewhat higher in urban than in rural areas, temporospatial clustering of cases has not been observed, at least in the United States A small proportion of all series of cases is familial varying from 5 percent reported by Cathala and associates to 15 percent of 1435 cases analyzed by Masters and coworkers The occurrence of familial cases, not in the same household, suggests a genetic susceptibility to infection, although the possibility of common early exposure to the transmissible agent cannot be dismissed A small number of conjugal cases have also been reported The only clearly demonstrated mechanism of spread of SSE is iatrogenic, having occurred in a few cases after transplantation of corneas or dural grafts from infected individuals, after implantation of infected electroencephalographic depth electrodes, and after the injection of human growth hormone or gonadotropins that had been prepared from pooled cadaveric sources of these hormones At least one neurosurgeon is known to have acquired the disease Individuals exposed to scrapie-infected sheep and to patients with SSE are not disproportionately affected Recently, a great deal of attention has been drawn to an epidemic of prion disease among cows in the British Isles ( mad cow disease ) The epidemic began in 1985, with putative transmission of the disease to some two dozen humans These patients have been younger (average age of onset, 27 years) than those with typical SSE (65 years) and manifested curious psychiatric and sensory symptoms as the rst sign of illness; they did not exhibit the usual EEG ndings even as the illness advanced to its later stages (Will et al) This has been called new variant Creutzfeldt-Jakob disease It has recently been shown that the prion strain in these patients is identical to the one from affected cattle The mode of transmission, presumed to be the ingestion of infected meat, is reminiscent of the propagation of kuru in New Guinea by ceremonial ingestion of brain tissue from infected individuals Spongiform encephalopathy has now been fairly rmly associated with the conversion of a normal cellular protein, PrPc to an abnormal isoform, PrPSc The transformation involves a change in the physical conformation of the protein in which its helical proportion diminishes and the proportion of the pleated sheet increases (see reviews by Prusiner) Current theory holds that the infectivity of prions and their propagation in brain tissue may result from the susceptibility of the native prion protein to alter shape as a result of physical exposure to the abnormal protein, a so-called conformational disease Conformationally altered prions have a tendency to aggregate, and this may be the mode of cellular.

03-20-2005

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