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Article
November 1997

Creutzfeldt-Jakob Disease in a Prolific Blood Donor

Author Affiliations

Department of Neurology West Virginia University Morgantown, WV 26506-9180

Arch Neurol. 1997;54(11):1323. doi:10.1001/archneur.1997.00550230006002
Abstract

Current evidence suggests that the risk of transmission of the infectious protein causing Creutzfeldt-Jakob disease (CJD) via blood products is remote.1-5 However, recent concern regarding contamination of food with the prion responsible for bovine spongiform encephalopathy has refocused attention on the safety of blood products.6,7

In August 1994, a 64-year-old man developed personality changes. Within 3 weeks, he was overtly confused. Computed tomography and magnetic resonance imaging of the head showed no abnormalities. He was admitted to the hospital in October 1994 for evaluation of rapidly progressive dementia. Results of routine cerebrospinal fluid studies were normal. Occasional myoclonic jerks were noted. Electroencephalography demonstrated continuous periodic discharges consistent with CJD. By late October, he was unresponsive and displayed continuous myoclonic jerks. He died in November 1994, 3.5 months after the onset of his symptoms. His family refused postmortem biopsy of the brain. This case of probable CJD is noteworthy

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