Neuronal hyperexcitability following mTBI: Cellular molecular mechanisms and therapeutical implications

Nicola Maggio, Vardit Rubovitch, Barry J. Hoffer, Bruce A. Citron, Nigel H. Greig, Chaim G. Pick

Research output: Chapter in Book/Report/Conference proceedingChapterpeer-review


Traumatic brain injury (TBI) remains the major cause of brain damage for children and young adults. While preventative measures may act to reduce the incidence of initial blunt trauma, well-tolerated drugs are needed to target the neurologically damaging internal cascade of molecular mechanisms that follow. Such processes, known collectively as the secondary injury phase, include inflammation, excitotoxicity, and apoptosis among other changes still subject to research. In this chapter, we aim to review the current trends in the molecular and cellular mechanisms in charge of neurological damage following mild TBI (mTBI) with a particular focus on neural hyperexcitability as well as discussing positive treatment findings that aim to mitigate the neuronal damage following mTBI.

Original languageEnglish
Title of host publicationNeurosensory Disorders in Mild Traumatic Brain Injury
Number of pages15
ISBN (Electronic)9780128123447
ISBN (Print)9780128125489
StatePublished - 1 Jan 2019


  • Chronic traumatic encephalopathy
  • Injury
  • Molecular mechanisms
  • Neuronal hyperexcitability
  • Novel therapeutical implications
  • mTBI


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