Geoffery S. Young, Presenter: Nothing to Disclose

Yi-ru Lin BS, Abstract Co-Author: Nothing to Disclose

Nan-Kuei Chen PhD, Abstract Co-Author: Nothing to Disclose

William P. Dillon MD, Abstract Co-Author: Nothing to Disclose

Stephen Wong PhD, Abstract Co-Author: Nothing to Disclose

Abnormal diffusion and T2 prolongation involving cerebral gray matter have been reported in Jakob-Creutzfeldt disease (CJD) since the advent of diffusion weighted imaging (DWI). A recent study performed by members of our group examined the patterns of abnormality typical of CJD found that while involvement of striatum, thalamus and neocortex was typical, the Rolandic cortex was spared. The purpose of this study was to quantitatively evaluate the ADC values in somatosensory cortex, to see if Rolandic cortex is affected by the disease.

We reanalyzed the subgroup of the previously published cases, including 8 control and 6 CJD patients. ADC maps were created on a pixel-by-pixel basis by using the formula ADC=-ln(S1/S0)/b1, where S0 and S1 signifies the DWI signal intensity (SI) at b0=0 and b1=1000 s/mm². The ADC values for the 3 orthogonal directions were then averaged to derive the mean ADC. ADC measurements were made in regions of interest (ROIs) manual selected to exclude the cerebrospinal fluid and white matter, and include gray matter areas in superior frontal gyrus, precentral gyrus, postcentral gyrus, supramarginal gyrus, thalamus, putamen, and head of caudate nucleus.

The ADC values in CJD patients were statistically lower than controls in all areas, including Rolandic cortex. The ADC values in different areas ranged from 793±82 to 933±80 (10-6mm2/s) in controls, and 650±77 to 833±86 in CJD patients. The trend to decreased ADC in caudate nucleus, putamen, and thalamus correlates with previously published results. The overall magnitude of ADC decrease in Rolandic cortex was similar to that in adjacent frontal and parietal neocortex.

Quantitative ADC measurements demonstrate diffusion abnormality in Rolandic cortex in CJD patients similar in magnitude to the ADC abnormality elsewhere in neocortex. This is consistent with the protean nature of prion disease, and suggests that the previously reported 'sparing' of these areas found on visual inspection of DWI more likely represents an artifact of baseline low SI on DWI in these areas - related to undefined distinctive cytoarchitectural features – than to true sparing by prion disease.

Young, G, Lin, Y, Chen, N, Dillon, W, Wong, S, Abnormality of Apparent Diffusion Coefficient (ADC) in Somatosensory Cortex in Jakob-Creutzfeld disease (CJD): Is Rolandic Cortex Really Spared?.  Radiological Society of North America 2005 Scientific Assembly and Annual Meeting, November 27 - December 2, 2005 ,Chicago IL. http://archive.rsna.org/2005/4407979.html