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Shiro Yamamoto, MD; Makoto Kinoshita, MD; Satoshi Furukawa, MD; Koji Kajiyama, MD, PhD

Arch Neurol. 2007;64(3):450-451.

	Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

A 72-year-old man presented with a 1-year history of progressive bilateral limb weakness, aphasia, and apathy. Diffusion-weighted magnetic resonance imaging demonstrated hyperintense signal change in the frontal, temporal, occipital, and parietal cortical gyri of the bilateral hemisphere (Figure A) although computed tomographic scan showed no abnormalities (Figure B). The results from cerebrospinal fluid examination were normal except for the elevation of neuron-specific enolase levels (47ng/mL); analysis for 14-3-3 protein was also positive. Prion protein gene analysis revealed a mutation of proline to leucine at codon 102.

Figure appears in full text version. Figure. Diffusion-weighted magnetic imaging (A) revealed hyperintensity in the cortical gyri of the bilateral hemisphere although computed tomographic scan (B) showed no abnormality. Computed tomographic scans performed 2 (C) and 8 months later (D) indicated remarkable progression of cortical atrophy and subcortical hypodense lesions.

His condition gradually deteriorated over . . . [Full Text of this Article]

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