REVIEW

Neuroimaging findings in human prion disease

R G Macfarlane¹, S J Wroe¹, J Collinge¹, T A Yousry², H R Jäger²

¹ MRC Prion Unit, Department of Neurodegenerative Disease, Institute of Neurology, London, UK
² Lysholm Department of Neuroradiology, National Hospital of Neurology and Neurosurgery, Institute of Neurology, London, UK

Correspondence to:
MrsRebecca Macfarlane
National Prion Clinic, Institute of Neurology, Queen Square, London WC1N 3BG, UK; r.macfarlane{at}prion.ucl.ac.uk

Imaging occupies an important role in the investigation of dementia and neurodegenerative disease. The role of imaging in prion disease used to be one of exclusion of other conditions. Over the past decade, the non-invasive nature of MRI, the improved range of magnetic resonance sequences and the availability of clinical and neuropathological correlation have led to a more prominent position of MRI and its inclusion in the diagnostic criteria for variant Creutzfeldt–Jakob disease. As experience of imaging in human prion disease increases, patterns of change related to strain and genotype may improve the diagnostic potential of imaging in the future, may reduce the need for more invasive testing and prove useful in future therapeutic trials. This paper reviews the current knowledge of imaging appearances in human prion disease.

Abbreviations: ADC, apparent diffusion coefficient; DWI, diffusion weighted imaging; FDG, 2-(18F)fluorodeoxyglucose; FLAIR, fluid attenuated inversion recovery imaging; MRS, magnetic resonance spectroscopy; NAA, N-acetylaspartate; PET, positron emission tomography; sCJD, sporadic Creutzfeldt–Jakob disease; SPECT, single photon emission computed tomography; T2WI, T2 weighted imaging; vCJD, variant Creutzfeldt–Jakob disease

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