Abstract

This chapter discusses various multimechanism by which tumors may cause epilepsy. Both developmental and acquired tumors may be associated with hippocampal sclerosis. It is found that hippocampal sclerosis is much less frequent in patients with extratemporal tumors. The likely role of the hippocampus in the generation of the seizure disorder may be enhanced if the tumor itself lies within or impinges on the hippocampus. Both animal and human tumor studies have demonstrated not only peritumoral changes in cerebral blood flow and metabolism, but sometimes more widespread-distant or mismatched abnormalities in these parameters. It is observed that in addition to ischemic changes, damage to blood vessels may lead to hemosiderin deposits associated with cerebral tumors. Tumors invading the cortex will likely cause massive damage to these local circuits, whereas the subcortical components of the lesion may further isolate areas of cortex. It is found that mechanical effects could cause direct tissue injury, changes in regional cerebral blood flow and perfusion, and interference with local neuronal circuits, as well as the electrophysiological properties of affected cortex. The animal models of epilepsy that have demonstrated the development of secondary epileptic foci in distant areas following chronic localized seizure activity are also elaborated.

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