Hashizume K, Tanaka T
Department of Neurosurgery, Asahikawa Medical College, Japan.
Epilepsy Res. 1998 Nov;32(3):389-99. doi: 10.1016/s0920-1211(98)00065-5.
Experimental animal studies on multiple subpial transection (MST) to modify epilepsy have been limited, and its mechanism of therapeutic benefit remains unclear. We examined the effect of MST on the electroencephalogram and cerebral glucose metabolism using a focal cortical epilepsy model in rats. Focal cortical seizures were induced by injecting kainic acid into the left sensorimotor cortex (SMC). Epileptic activity propagated from the focus to neighboring cortex, then to the contralateral SMC. All animals developed right forelimb clonus and/or secondarily generalized convulsions. Sagittal cortical transections on both sides of the focus suppressed the propagation to the ipsilateral hemisphere. However, epileptic activity was not suppressed in the focus and contralateral SMC, and clinical seizures infrequently occurred even following MST. In [14C]2-deoxyglucose autoradiograms, MST did not affect glucose metabolism in naive animals. During focal seizures, MST reduced focal hypermetabolism in the left SMC, although the ipsilateral caudate nucleus, thalamus, and opposite SMC still demonstrated hypermetabolism. These results suggest that MST suppressed focal epileptic activity and its propagation to the neighboring cortical areas. However, clinical seizures were not completely inhibited because vertical interactions between the focus and subcortical areas were preserved. Glucose metabolic changes provided evidence of conserved cortical function following MST.
