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Creutzfeldt-Jakob disease MRI

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Overview

MRI findings in CJD include high signal abnormalities in caudate nucleus and/or putamen on diffusion-weighted imaging (DWI) or fluid attenuated inversion recovery (FLAIR).[1] Additional findings on diffusion weighted imaging include cortical, subcortical, and thalamic involvement. An abnormal signal in the poster thalami on T2 (pulvinar sign) and diffusion weighted images and fluid-attenuated inversion recovery sequences on brain MRI, in the appropriate clinical context, is highly specific for variant Creutzfeldt-Jakob disease.

MRI

  • Cortical hyperintensity (25%-70% of cases)
  • Subcortical abnormalities (5% of cases)
  • Thalamic involvement, usually in posterior thalamus (more strongly associated with variant Creutzfeldt-Jakob disease than with classic Creutzfeldt-Jakob disease)[3]
  • An abnormal signal in the poster thalami on T2 (pulvinar sign) and diffusion weighted images and fluid-attenuated inversion recovery sequences on brain MRI, in the appropriate clinical context, is highly specific for variant Creutzfeldt-Jakob disease.

References

  1. “http://www.cdc.gov/ncidod/dvrd/cjd/diagnostic_criteria.html”. Retrieved 17 February 2014. External link in |title= (help)
  2. Young, Geoffrey S. (June–July 2005). “Diffusion-Weighted and Fluid-Attenuated Inversion Recovery Imaging in Creutzfeldt-Jakob Disease: High Sensitivity and Specificity for Diagnosis”. American Journal of Neuroradiology. American Society of Neuroradiology. 26: 1551–1562. Retrieved 2007-10-30. Unknown parameter |coauthors= ignored (help)
  3. Tschampa, Henriette J. (May 2003). “Thalamic Involvement in Sporadic Creutzfeldt-Jakob Disease: A Diffusion-Weighted MR Imaging Study”. American Journal of Neuroradiology. American Society of Neuroradiology. 24: 908–915. Retrieved 2007-10-30. Unknown parameter |coauthors= ignored (help)


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