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Advanced Neurology Epilepsy after traumatic brain injuries

Table 2. Recent neurological techniques to control epileptic attacks during TBI
Technique Description Current limitations
Neurostimulation VNS: Electrically stimulates the vagus nerve; RNS: Detects Invasive, potential surgical risks, variable efficacy, and
therapies abnormal activity and delivers targeted stimulation; long-term effects under research 51
DBS: Targets specific brain areas
Transcranial Non-invasive magnetic stimulation modulates cortical Optimal parameters for TBI-related epilepsy are not
magnetic stimulation excitability and suppresses hyperexcitable circuits well-established; limited evidence 52
Optogenetics Experimental light-based control of genetically modified Limited to preclinical studies; ethical and technical
neurons for precise seizure activity modulation. challenges 53
Advanced High-resolution imaging (e.g., fMRI, DTI) for epileptogenic Surgical risks are not suitable for all patients; limited
neuroimaging and focus localization; used in resective surgery or laser therapy accessibility 54
surgery
Pharmacogenomics Identification of genetic markers for personalizing drug Requires genetic screening; limited understanding of genetic
regimens, optimizing efficacy, and minimizing side effects influences on TBI-related epilepsy 55
Cannabinoid-based Cannabidiol has anticonvulsant effects, holding potential for Legal challenges, limited dosing guidelines, and safety profiles
therapies minimizing side effects arising from traditional AEDs usage under research 56
Closed-loop Systems combining real-time monitoring with automated Advanced infrastructure is required; validation is needed for
neuromodulation stimulation delivery for seizure control diverse TBI populations 57
Biomarker Predictive use of biomarkers like microRNAs and cytokines for Reliable TBI-specific biomarkers are still under identification;
monitoring seizure onset and tailored treatment strategies clinical implementation is in development 58
Abbreviations: AED: Antiepileptic drug; DBS: Deep brain stimulation; DTI: Diffusion tensor imaging; fMRI: Functional magnetic resonance imaging;
RNS: Responsive neurostimulation; TBI: Traumatic brain injury; VNS: Vagus nerve stimulation.

mechanical forces that cause the shearing and tearing of cell death). Free radical production initiates an influx of
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brain tissue, including blood vessels, neurons, and glial calcium and cellular dysfunction leads to the production
cells. This injury leads to the deformation of tissues and of free radicals, which cause oxidative damage to brain
necrotic cell death, resulting in immediate damage. In cells. Ultimately, the progression from primary to
hemorrhage and microhemorrhage, disruption of blood secondary injury results in widespread brain damage,
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vessels leads to bleeding within the brain, contributing which significantly impacts neurological function.
to further complications. Swelling of brain tissue due Understanding these processes is crucial for developing
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to fluid accumulation exacerbates the injury. A decrease therapeutic strategies aimed at mitigating the effects of
in cerebral blood flow and reduction in blood flow to the TBI. 66
brain results in ischemia, worsening brain cell function
and survival. Increased intracranial pressure, swelling, and 8. Advanced treatment of epilepsy
blood accumulation lead to increased pressure within the following TBI
skull, further impeding brain function. 61 TBI is a significant risk factor for the development of
epilepsy, with many individuals experiencing post-
7.2. Secondary injury: Progressive damage
traumatic seizures that can evolve into chronic epilepsy.
Secondary injury mechanisms further damage the brain The pathophysiology of TBI-induced epilepsy involves
over time. Secondary injury is driven by biochemical complex mechanisms such as neuronal excitability, synaptic
and cellular processes that amplify the initial insult. plasticity, and glial cell activation. These processes are
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Mechanical tissue damage occurs due to continued tissue exacerbated by neuroinflammation, oxidative stress, and
deformation and shearing exacerbates the neuronal BBB disruption, which all contribute to the development
damage, contributing to cellular death. Neuronal cell of epileptic activity following trauma. 67
damage to the neurons themselves leads to dysfunction
and cell death. Excitatory amino acid release-associated 8.1. Recent therapeutic approaches
injury causes the release of excitatory neurotransmitters, The current treatment paradigm for epilepsy post-TBI
such as glutamate, which further contributes to neuronal includes antiepileptic drugs (AEDs) such as phenytoin,
injury. Calcium influx also affects the release of excitatory valproic acid, levetiracetam, and carbamazepine, which are
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neurotransmitters that trigger the opening of ion channels, typically used to control acute seizures and prevent their
allowing excessive calcium ions to enter cells, disrupting recurrence. Branched-chain amino acids are commonly
cellular function, and triggering apoptosis (programmed used now in TBI. However, these treatments are not

Volume 4 Issue 4 (2025) 7 doi: 10.36922/an.8356