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<p>Traumatic brain injury (TBI) can have a multitude of effects on neural functioning. In extreme cases, TBI can lead to seizures both immediately following the injury as well as persistent epilepsy over years to a lifetime. However, mechanisms of neural dysfunctioning after TBI remain poorly understood. To address these questions, we analyzed human and animal data and we developed a biophysical network model implementing effects of ion concentration dynamics and homeostatic synaptic plasticity to test effects of TBI on the brain network dynamics. We focus on three primary phenomena that have been reported <i>in vivo</i> after TBI: an increase in infra slow oscillations (&lt;0.1 Hz), increase in Delta power (1 - 4 Hz), and the emergence of broadband Gamma bursts (30 - 100 Hz). Using computational network model, we show that the infra slow oscillations can be directly attributed to extracellular potassium dynamics, while the increase in Delta power and occurrence of Gamma bursts are related to the increase in strength of synaptic weights from homeostatic synaptic scaling triggered by trauma. We also show that the buildup of Gamma bursts in the injured region can lead to seizure-like events that propagate across the entire network; seizures can then be initiated in previously healthy regions. This study brings greater understanding of the network effects of TBI and how they can lead to epileptic activity. This lays the foundation to begin investigating how injured networks can be healed and seizures prevented.</p>

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Network effects of traumatic brain injury: from infra slow to high frequency oscillations and seizures

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2025年2月28日

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  • Brianna Marsh,
  • Sylvain Chauvette,
  • Mingxiong Huang,
  • Igor Timofeev,
  • Maxim Bazhenov

摘要

Traumatic brain injury (TBI) can have a multitude of effects on neural functioning. In extreme cases, TBI can lead to seizures both immediately following the injury as well as persistent epilepsy over years to a lifetime. However, mechanisms of neural dysfunctioning after TBI remain poorly understood. To address these questions, we analyzed human and animal data and we developed a biophysical network model implementing effects of ion concentration dynamics and homeostatic synaptic plasticity to test effects of TBI on the brain network dynamics. We focus on three primary phenomena that have been reported in vivo after TBI: an increase in infra slow oscillations (<0.1 Hz), increase in Delta power (1 - 4 Hz), and the emergence of broadband Gamma bursts (30 - 100 Hz). Using computational network model, we show that the infra slow oscillations can be directly attributed to extracellular potassium dynamics, while the increase in Delta power and occurrence of Gamma bursts are related to the increase in strength of synaptic weights from homeostatic synaptic scaling triggered by trauma. We also show that the buildup of Gamma bursts in the injured region can lead to seizure-like events that propagate across the entire network; seizures can then be initiated in previously healthy regions. This study brings greater understanding of the network effects of TBI and how they can lead to epileptic activity. This lays the foundation to begin investigating how injured networks can be healed and seizures prevented.