This is not a comprehensive list, simply some articles I have found along the way.
“The window of post-traumatic epileptogenesis, as well as the post-TBI window of vulnerability to a second injury, extends beyond the acute period. The pathophysiology that follows in the days, weeks and months after injury involve compensatory processes of receptor up and down regulation, alterations in subunit composition and a growing imbalance of glutamate driven excitation and GABA mediated inhibition. A recent study by Cantu and colleagues highlights the early phases of this imbalance in glutamate and GABA and points to mechanisms that may lead to post-traumatic epilepsy. In slice preparations, using a glutamate biosensor 2–4 weeks following controlled cortical impact they demonstrated extracellular glutamate signaling was increased in cortical networks. The highest glutamate signal occurs in perilesional tissue adjacent to the direct injury. Additionally, at the onset of a seizure the glutamate biosensor signal spreads from medial to lateral and proximal to distal away from the site of direct injury . The mechanism of these changes may be related to changes in cell populations, particularly loss of parvalbumin positive GABA interneurons [45,60,73,74] and/or differences in receptor populations for glutamate and GABA.” “Following experimental TBI, there are dynamic changes in excitatory-inhibitory balance that result in neuronal dysfunction and may result in long-term sequelae. This imbalance is a result of increased glutamate release, faulty reuptake, and changes in the population of receptors and inhibitory interneurons. Given the complexity of the pathophysiology and the heterogeneity of injuries it is crucial to continue building our understanding of this imbalance with the goal of finding therapeutic and neuroprotective targets.” Glutamate and GABA imbalance following traumatic brain injury. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4640931/
“High-speed glutamate biosensor imaging showed that glutamate signaling was significantly increased in the injured cortex. Elevated glutamate responses correlated with epileptiform activity, were highest directly adjacent to the injury, and spread via deep cortical layers. Immunoreactivity for markers of GABAergic interneurons were significantly decreased throughout CCI cortex. Lastly, spontaneous inhibitory postsynaptic current frequency decreased and spontaneous excitatory postsynaptic current increased after CCI injury. Our results suggest that specific cortical neuronal microcircuits may initiate and facilitate the spread of epileptiform activity following TBI. Increased glutamatergic signaling due to loss of GABAergic control may provide a mechanism by which TBI can give rise to post-traumatic epilepsy.” Traumatic Brain Injury Increases Cortical Glutamate Network Activity by Compromising GABAergic Control. https://www.ncbi.nlm.nih.gov/pubmed/24610117
“Animal models of mild traumatic brain injury (mTBI) suggest that metabolic changes in the brain occur immediately after a mechanical injury to the head. ” “These results suggest that changes in glutamate and GABA concentrations in the brain may be region-specific and may depend on the amount of time that has elapsed post-injury.” “Glutamate and GABA concentrations following mild traumatic brain injury: A pilot study” https://www.physiology.org/doi/abs/10.1152/jn.00896.2017
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