The pathogenesis of tumour associated epilepsy

Abstract

Tumour associated epilepsy (TAE) is a poorly understood manifestation of many gliomas, meningiomas and metastatic brain tumours that has important clinical and social implications. Etiological mechanisms underlying tumour associated epilepsy include theories invoking peritumoural amino acid disturbances, local metabolic imbalances, cerebral oedema, pH abnormalities, morphological changes in the neuropil, changes in neuronal and glial enzyme and protein expression and altered immunological activity. It has also been suggested that the pathology involves perturbations in distribution and function of the NMDA subclass of glutamate receptors. The often capricious response of the seizure disorder following removal of the causative neoplasms suggests multiple factors are involved. Further understanding about the pathogenesis of TAE will await the development and characterisation of suitable animal models that demonstrate the clinical manifestations and physiological changes comparable to those seen in human cerebral tumours. With such a model it is hoped that progress may one day be made in understanding and subsequently treating this debilitating clinical problem.