Tumour associated epilepsy and glutamate excitotoxicity in patients with gliomas

J Clin Neurosci. 2014 Jun;21(6):899-908. doi: 10.1016/j.jocn.2014.02.012. Epub 2014 Apr 17.

Abstract

Tumour associated epilepsy (TAE) is common, debilitating and often not successfully controlled by surgical resection of the tumour and administration of multiple anti-epileptic drugs. It represents a cause of significant lost quality of life in an incurable disease and is therefore an important subject for ongoing research. The pathogenesis of TAE is likely to be multifactorial and involve, on the microscopic level, the interaction of genetic factors, changes in the peritumoural microenvironment, alterations in synaptic neurotransmitter release and re-uptake, and the excitotoxic effects of glutamate. On a macroscopic level, the occurrence of TAE is likely to be influenced by tumour size, location and interaction with environmental factors. The optimal treatment of TAE requires a multi-disciplinary approach with input from neurosurgeons, neurologists, radiologists, pathologists and basic scientists. This article reviews the current literature regarding the incidence, treatment, and aetiology of TAE.

Keywords: Epilepsy; Excitotoxicity; Glioma; Glutamate; Seizure.

Publication types

  • Review

MeSH terms

  • Animals
  • Brain Neoplasms / diagnosis
  • Brain Neoplasms / epidemiology
  • Brain Neoplasms / metabolism*
  • Epilepsy / diagnosis
  • Epilepsy / epidemiology
  • Epilepsy / metabolism*
  • Glioma / diagnosis
  • Glioma / epidemiology
  • Glioma / metabolism*
  • Glutamic Acid / metabolism*
  • Humans
  • Quality of Life
  • Synaptic Transmission / physiology

Substances

  • Glutamic Acid