Iatrogenic Creutzfeldt-Jakob Disease from Commercial Cadaveric Human Growth Hormone
Brian S. Appleby , Mei Lu, Alberto Bizzi, Michael D. Phillips, Sally M. Berri, Madeleine D. Harbison, and Lawrence B. Schonberger
Author affiliations: Cleveland Clinic Foundation, Cleveland, Ohio, USA (B.S. Appleby, M. Lu, M.D. Phillips); Instituto Clinico Humanitas,Milan, Italy (A. Bizzi); Case Western Reserve University, Cleveland (S.M. Berri); Mount Sinai School of Medicine, New York, New York, USA (M.D. Harbison); Centers for Disease Control and Prevention, Atlanta, Georgia, USA (L.B. Schonberger)
Figure. . . Maps showing axial fluid attenuated inversion recovery (FLAIR), diffusion-weighted imaging (DWI), and apparent diffusion coefficient (ADC) at the level of the basal nuclei (top row) and dorsal frontoparietal cortex (bottom row) of the brain of a 33.8-year-old man with agenesis of the corpus callosum, schizencephaly, and heterotopia. Note the symmetrical DWI signal hyperintensities in the striatum and dorsomedial part of the thalami. In addition, DWI signal hyperintensities occurred in the cingulate, precuneus and in the dysplastic gray matter along the anterior lips of the schizencephalic clefts at the level of the precentral gyri. The signal abnormalities are associated with decreased diffusivity on ADC maps and are much less prominent on FLAIR images. These findings are highly suggestive of Creutzfeldt-Jakob disease.
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