Volume 4 Supplement 1

European Society for Neurochemistry Biannual Conference: Molecular Mechanisms of Regulation in the Nervous System

Open Access

Gliomas and epilepsy: Insights from neuropathological studies in humans

  • Eleonora Aronica1
SpringerPlus20154(Suppl 1):L9

https://doi.org/10.1186/2193-1801-4-S1-L9

Published: 12 June 2015

Keywords

Gliomaglioneuronal tumorepilepsy

Brain tumors represent a recognized cause of epilepsy in both children and adults. In principle, any tumor (extra-axial, intra-axial, benign or malignant, common or uncommon) can cause seizures. However, patients with supratentorial low-grade glial tumors are more likely to develop epilepsy. Several clinical studies emphasize that pharmacologically intractable epilepsy critically affects the daily life of patients with brain tumors, even if the tumor is under control. Recently, the term of long-term epilepsy associated tumour (LEAT) has been introduced. LEATs are low grade, slowly growing, cortically-based tumours which predominantly occur in young patients with long histories (often 2 years or more) of drug-resistant epilepsy. Glioneuronal tumors (GNT), including gangliogliomas (GG) and dysembryoplastic neuroepithelial tumors (DNTs), represent the most common tumor within the spectrum of LEAT. The advent of the neurosurgical treatment of epilepsy-associated brain lesions confirmed the strong epileptogenicity of these tumor entities. Understanding the mechanisms that underlie epileptogenesis in LEATs is essential to identify new treatment targets and to develop an effective therapy. Mechanisms such as alterations of the balance between excitation and inhibition and alterations in neuron-glia interactions might be involved. Astroglial cells express functional receptors for a variety of neurotransmitters and may critically modulate synaptic transmission. In addition, an increasing number of observations indicate that pro-epileptogenic inflammatory pathways are activated in GNT and may contribute to the onset and progression of seizures. The recent advances and likely candidate mechanisms and molecules involved in tumor-associated epileptogenesis will be discussed.

Declarations

Acknowledgements

EA is supported by the National Epilepsy Fund - “Power of the Small”, the Hersenstichting Nederland (NEF 013-1) and KIKA (Stichting Kinderen Kankervrij).

Authors’ Affiliations

(1)
Department of (Neuro)Pathology, Academic Medical Center and Swammerdam Institute for Life Sciences, Center for Neuroscience University of Amsterdam, The Netherlands, SEIN – Stichting Epilepsie Instellingen Nederland

Copyright

© Aronica. 2015

This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.