Molecular biomarkers in drug-resistant epilepsy: Facts & possibilities

Int J Surg. 2016 Dec;36(Pt B):483-491. doi: 10.1016/j.ijsu.2015.08.029. Epub 2015 Aug 22.

Abstract

Despite great advances in our understanding of the process of epileptogenesis we are yet to develop reliable biomarkers that have the potential to accurately localize the epileptogenic zone (EZ), and to resolve the issue of heterogeneity in epilepsy surgery outcome. Inability to precisely localize the epileptogenic foci is one of the reason why more than 30% of these DRE patients are not benefited. Molecular and cellular biomarkers in combination with imaging and electrical investigations will provide a more specific platform for defining epileptogenic zone. Potential molecular biomarkers of epileptogenesis including markers of inflammation, synaptic alterations and neurodegeneration may also have the potential for localizing EZ. At molecular level components derived from epileptogenic tissues, such as metabolites, proteins, mRNAs and miRNAs that are significantly altered can serve as biomarkers and can be clubbed with existing techniques to preoperatively localize the EZ. Neurosurgeons across the world face problems while defining the margins of the epileptogenic tissues to be resected during surgery. In this review we discuss molecular biomarkers reported so far in the context of epileptogenesis and some of the unexplored markers which may have the potential to localize EZ during surgery. We also discuss "Intelligent knife" technique that couples electrosurgery and mass spectrometry allowing near-real-time characterization of human tissue and may prove to be instrumental in defining the margins of the epileptogenic zone during surgery.

Keywords: Biomarkers; Drug resistant epilepsy; Epigenetics; Epileptogenesis; Epileptogenic zone; Mass spectrometry.

Publication types

  • Review

MeSH terms

  • Blood-Brain Barrier
  • Drug Resistance
  • Electrosurgery
  • Epigenesis, Genetic
  • Epilepsy / diagnosis
  • Epilepsy / drug therapy
  • Epilepsy / surgery*
  • Humans
  • Inflammation / etiology
  • Signal Transduction
  • TOR Serine-Threonine Kinases / physiology

Substances

  • TOR Serine-Threonine Kinases