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NEUROLOGY 1989;39:90
© 1989 American Academy of Neurology

Experimental meningeal carcinomatosis selectively depresses local cerebral glucose utilization in rat brain

E. M. Hiesiger, MD, A. Picco-Del Bo, MD, L. E. Lipschutz, BA, G. A. Basler, MA, H. T. Thaler, PhD, J. B. Posner, MD and W. R. Shapiro, MD

George C. Cotzias Laboratory of Neuro-Oncology, Department of Neurology, and the Division of Biostatistics, Memorial Sloan-Kettering Cancer Center, and the Department of Neurology, Cornell University Medical College, New York, NY.

Using quantitative autoradiography, we investigated the effect of meningeal carcinomatosis on local cerebral glucose utilization (LCGU). A rat model of meningeal carcinomatosis using Walker 256 tumor was used. LCGU was evaluated using 14C-2-deoxy-D-glucose according to the Sokoloff method. Thirty-one neuroanatomic structures were evaluated, both separately and as part of five functional or neuroanatomic groups: olfactory, auditory, visual, limbic, and white matter. The relationship between tumor and LCGU of underlying brain was examined. Compared with controls, there was no global change of LCGU in the experimental group that applied to all structures. However, mean LCGU was significantly depressed in olfactory cortex, temporal cortex, olfactory tubercle, amygdala, caudate/putaman, inferior colliculus, medial geniculate, anterior commissure, and corpus callosum, and the functional groups that make up the olfactory and auditory systems. There was no correlation between extent of regional tumor burden and degree of depression of LCGU in underlying structures. In meningeal carcinomatosis, tumor results in selective regional depression of LCGU. This occurs both in structures underlying tumor and those anatomically remote, but in certain cases, functionally related to structures subadjacent to tumor. These data may help to explain the diversity of neurologic dysfunction seen in patients with meningeal cancer.

Address correspondence and reprint requests to Dr. Shapiro, 1275 York Avenue, New York, NY 10021.

Supported by grants CA 18856, CA 39208, and CA 08748 from the National Institutes of Health and by a grant to Dr. Hiesiger from the Norman and Rosita Winston Foundation.

Presented in part at the thirty-fourth annual meeting of the American Academy of Neurology, Washington, DC, April 1982.

Received January 26, 1988. Accepted for publication in final form June 28, 1988.






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