A 38-year-old woman with Chiari I malformation presented with spinal cord edema preceding syringomyelia manifesting as a 5-month history of nuchal pain and numbness of the upper extremities. Magnetic resonance imaging showed spinal cord edema, a poorly defined syrinx at the C-2 to T-2 levels, and distorted cerebellar tonsils. Computed tomography revealed cerebrospinal fluid (CSF) density in the center of spinal cord edema, and positron emission tomography revealed no uptake of L-[methyl-11 C]methionine, indicating a non-neoplastic lesion. Craniocervical decompression achieved excellent clinical and neuroradiological outcomes. The success of surgical treatment supports the theory that patients with Chiari I malformation have increased transmural flow of CSF, causing spinal cord edema that progresses to syringomyelia. Early treatment of patients with spinal cord edema is indicated to prevent permanent spinal cord injury due to progressive syringomyelia.
Autoradiographic study of (14C-methyl)-L-methionine with brain tumor bearing rats aimed at an elucidation of the mechanism of tracer accumulation in the protein synthesis of tumor. Twice as much tracer accumulated in the tumors compared as in the contralateral gray matter (nontumor region) at 90 min post intravenous injection. The protein-bound fraction of the tumors, expressed as acid-insoluble fraction (AIF), was 1.7 +/- 0.6 (mean +/- standard deviation, n = 6), significantly higher than that (0.8 +/- 0.2) of the nontumor region (p < 0.05 by the Mann-Whitney test). The tumor AIF comprised 82.3 +/- 9.2% of the total amount of the tracers accumulated in the tumors. The protein synthesis inhibitor cycloheximide reduced the tracer uptake and the AIF of the tumors to an almost same level as the nontumor region. These findings indicate that metabolic acceleration of protein synthesis may be a main reason for the high accumulation of (14C-methyl)-L-methionine in tumor.
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