Tumor factors Histology Seizures are common in patients with low-grade tumors such as dysembryoblastic<unk> epithelial tumors, gangligliomas, and oligodendrogliomas. The rapid growth of fast-growing high-grade brain tumors may damage the subcortical network essential for electrical transmission, whereas slow-growing tumors have been suggested to induce partial deafferentation of cortical regions, causing denervation hypersensitivity and producing an epileptogenic milieu. Studies strongly suggest that genetic factors may play a role in tumor development and tumor-related epilepsy. Tumor location The location of tumors is closely related to their histology. The majority of glioneuronal tumors occur in the temporal lobe. Some data have shown that oligodendroglial tumors were more likely to be located in frontal lobe, whereas astrocytomas were more commonly found in temporal locations. It may be postulated that tumor-related seizures have unique characteristics, which may share some common genetic pathways with tumorigenesis. Blood-brain barrier disruption (BBB) Human and animal studies have suggested that perturbations in<unk> vascular integrity and breakdown of the BBB lead to<unk> nal hypersynchronization and epileptiform activity. Relevant molecular changes in brain tumors that affect BBB structure and function include decreased expression of transmembrane junctional proteins and heightened release of vascular endothelial growth factor. Results suggest that pathological disruption of the BBB in brain tumor patients may contribute to seizure activity. Peri-tumoral factors Contemporary imaging techniques provide testimony to the remarkable differences between the peri-tumoral brain and normal tissue. Morphological changes Certain morphological changes in the peri-tumoral brain tissue, such as persistent<unk> ns in the white matter, inefficient<unk> nal migration, and changes in synaptic vesicles, are also believed to contribute to seizure generation. Hypoxia, acidosis and metabolic changes Tumors with insufficient blood supply often cause interstitial hypoxia, which subsequently contributes to acidosis. The intratumoral hypoxia and acidosis may extend to the surrounding tissue. Furthermore, hypoxia causes acidosis as a consequence of both heightened metabolic requirements of the proliferating tissue and impaired oxidative energy metabolism. Ionic changes Ionic changes in the peri-tumoral zone may influence<unk> nal activity. An interesting hypothesis was proposed by Sontheimer, who suggested that glioma invasion into the peri-tumoral zone is in part mediated by chloride channel overexpression, allowing cells to traverse the extracellular space through rapid changes in cell shape. Glutamate<unk> transmission Recent work has demonstrated a close link between seizure activity and high extracellular glutamate in tumor-related epilepsy. Glutamate activation of ionotropic receptors leads to a rapid excitatory signal based on cation influx that can cause release of calcium from intracellular stores.
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