Post-Traumatic Seizures: A Deep-Dive Into Pathogenesis

Abstract

Post-traumatic seizures (PTS) have become an emerging challenge for neurologists worldwide with the rise of brain injuries. Trauma can lead to various outcomes, ranging from naive spasms to debilitating post-traumatic epilepsy (PTE). In this article, we will explore the pathogenesis of convulsions following a concussion. We will look at multiple studies to explain the various structural, metabolic, and inflammatory changes leading to seizures. Additionally, we will explore the association between severity and location of injury and PTE. PTE's pathophysiology is not entirely implicit, and we are still in the dark as to which anti-epileptic drugs will be useful in circumventing these attacks. The purpose of this narrative review is to explain the post-traumatic brain changes in detail so that such attacks can be either thwarted or treated more resourcefully in the future.

Keywords: brain injury and seizure; head injury and epilepsy; motor vehicle accident and epilepsy; post-traumatic epilepsy; post-traumatic seizure; trauma and epilepsy.

Figure 1. Classification of post-traumatic seizures.

Figure 2. Inflammatory changes after trauma: role of TLR, HMBP1 protein, and IL- β.

TLR: toll-like receptor, HMBP1 protein: high-mobility group box 1 protein, IL- β: interleukin-β, MAPK/ERK 1 pathway: mitogen-activated protein kinase/extracellular signal-related kinase 1, RAGE: receptor for advanced glycation end-products, mTOR/AKT: mechanistic target of rapamycin/protein kinase B, GOS: guluronate oligosaccharide