Brain Magnetic Resonance Diffusion Abnormalities in Creutzfeldt-Jakob Disease

Abstract

The diffusion-weighted magnetic resonance brain images demonstrated bilaterally symmetrical marked increase in signal intensity in the caudate nuclei, putamina, thalami, cingulate gyri, and right inferior frontal cortex. The apparent diffusion coefficient map showed abnormally low diffusion in these regions (as low as 40% of normal in the caudate head). This suggests that there is restricted diffusion in these regions. The T2-weighted images demonstrated slightly increased signal bilaterally in the caudate nuclei and putamina. These findings indicate that diffusion magnetic resonance imaging might be a sensitive means of imaging the abnormalities seen in Creutzfeldt-Jakob disease.

Iatrogenic Creutzfeldt-Jakob disease following human growth hormone therapy: case report

“…MRI finding in this case -increased signal intensity bilaterally in the striatum, most evident in the diffusion-weighted sequences -is similar to that reported in sporadic 18,19 and in a few familial 20 cases of CJD. We did not find other report of abnormal diffusion-weighted MRI in iatrogenic CJD in the literature.…”

Stroke-Like Presentation in a Case of Creutzfeldt-Jakob Disease

“…Interestingly, the reduced ADC was observed for a longer period than in acute stroke, possibly indicating the continuous severe neurodegeneration in CJD. MRI-pathologic correlation studies have suggested astrogliosis, which is noted in T 2 -weighted and DWI hyperintense lesions [15,16], and the presence of vacuoles in spongiform encephalopathy as potential causes of the low ADC values [17].…”

MR Findings of Cerebral White Matter in Cockayne Syndrome

“…16 As another mechanism of diŠusion-weighted high intensity, Bahn and associates suggested in their paper,``Brain Magnetic Resonance DiŠusion Abnormalities in Creutzfeldt-Jakob disease,'' that restriction of diŠusion related to the presence of vacuoles seen histologically in spongiform encephalopathy. 17 Although we have no information about the spongiform encephalopathy in Cockayne syndrome, this mechanism cannot be denied.…”