Abstract
A 76-year-old obese male presented for cognitive decline, mainly with deficits in the verbal domain (anomia and verbal perseverations), drowsiness, mild camptocormic posture with left arm bradykinesia, and recurrent falls. In the clinical suspect of a primary progressive aphasia with parkinsonism, the patient was referred to a [18F]FDG PET/MR that showed moderate cortical hypometabolism in the left temporal pole extending to the homolateral insular region. A co-acquired high-resolution diffusion-weighted imaging (DWI) sequence (Resolve, Siemens), however, showed (b value of 1000s/mm2) linear hyperintensity following the cortical rim corresponding to the [18F]FDG hypometabolism. A sporadic, atypical Creutzfeldt–Jacob disease (CJD) was supposed and subsequently confirmed by a real-time quaking-induced conversion (RT-QuIC) assay in the CSF.
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References
Tschampa HJ, Kallenberg K, Kretzschmar HA, et al. Pattern of cortical changes in sporadic Creutzfeldt-Jakob disease. AJNR Am J Neuroradiol. 2007;28:1114–8.
Eisenmenger L, Porter M-C, Carswell C, et al. Evolution of diffusion-weighted magnetic resonance imaging signal abnormality in sporadic Creutzfeldt-Jakob disease, with histopathological correlation. JAMA Neurol. 2016;73(1):76–84.
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Cecchin, D., Gabelli, C., Anglani, M. (2022). Case 36: Creutzfeldt–Jakob Disease. In: Varrone, A., Morbelli, S., Garibotto, V. (eds) Clinical Nuclear Medicine in Neurology. Springer, Cham. https://doi.org/10.1007/978-3-030-83598-9_36
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DOI: https://doi.org/10.1007/978-3-030-83598-9_36
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