Advances in understanding the pathogenesis of post-traumatic epilepsy: a literature review

Abstract

Severe head trauma can lead to seizures. Persistent epileptic seizures and their progression are associated with the severity of trauma. Although case reports have revealed that early use of anti-seizure drugs after trauma can prevent epilepsy, clinical case–control studies have failed to confirm this phenomenon. To date, many brain trauma models have been used to study the correlation between post-traumatic seizures and related changes in neural circuit function. According to these studies, neuronal and glial responses are activated immediately after brain trauma, usually leading to significant cell loss in injured brain regions. Over time, long-term changes in neural circuit tissues, especially in the neocortex and hippocampus, lead to an imbalance between excitatory and inhibitory neurotransmission and an increased risk of spontaneous seizures. These changes include alterations in inhibitory interneurons and the formation of new, over-recurrent excitatory synaptic connections. In this study, we review the progress of research related to post-traumatic epilepsy to better understand the mechanisms underlying the initiation and development of post-traumatic seizures and to provide theoretical references for the clinical treatment of post-traumatic seizures.

Inflammasomes at the crossroads of traumatic brain injury and post-traumatic epilepsy

“…The location and severity of TBIs are physical characteristics that have a significant impact on PTE incidence. Increased risk of PTE is linked to lesions in the temporal lobe and penetrating injuries in the temporal and parietal lobes [ 5 ]. For PTE, epileptogenesis often occurs months to years after the precipitating injury, and this delay period is referred to as the silent, or latent period [ 6 , 7 ].…”

Mechanisms of 3-Hydroxyl 3-Methylglutaryl CoA Reductase in Alzheimer’s Disease

“…On the one hand, glial cell proliferation can be mediated by increased levels of inflammatory-related factors, such as proinflammatory cytokines, iNOS, and COXs [ 77 ]. Systemic inflammation promotes the activation of microglia to generate neurotoxic substances, such as ROS and reactive nitrogen species (RNS), which damage healthy neurons [ 78 , 79 ].…”