Table 11

Neuroimaging patterns in encephalopathy caused by Creutzfeldt-Jakob disease

Creutzfeldt-Jakob disease-related encephalopathy
 CTNon-specific generalised cortical and subcortical atrophy in the later phases of disease
  • ▸ T2 and FLAIR hyperintensities in the cerebral cortex and lesions in the putamen and caudate head isointense to cortex lesions in the putamen and caudate head isointense to cortical grey

  • ▸ Less frequently, hyperintensity can be detected in the globus pallidus, thalamus, the deep white matter, and the cerebral and cerebellar cortex. Laminar lesions may be observed in the cerebral cortex and cerebellum

  • ▸ DWI is most sensitive in early stages uncovering the altered diffusion in the regions aforementioned

  • ▸ In vCJD symmetrical hyperintensities of the pulvinar thalami (relative to the cortex and especially the anterior part of the putamen) are characteristic and known as the ‘pulvinar sign’

  • ▸ Decreased N-acetyl-aspartate and slightly increased levels of myoinositol in the striatum and the insular cortex on MRS

 SPECTHypoperfusion in the cerebral cortex
 PETHypometabolism in the cerebral cortex and the basal ganglia
  • DWI, diffusion-weighted imaging; FLAIR, fluid-attenuated inversion recovery; MRS, MR spectroscopy; PET, positron emission tomography; SPECT, single-photon emission CT; vCJD, variant Creutzfeldt-Jakob disease.