ABS 006: The Role Of Neuroinflammation In The Pharmacodynamics Of Antiepileptic Drugs And How This Interaction Affects Seizure Control

Yatharth Manjunath¹

¹ Conestoga

The Van Wickle Journal (2026) Volume 2, ABS006

Introduction: Neuroinflammation is an immune response in the central nervous system that disrupts neuronal signaling and heightens seizure susceptibility. Activated microglia and astrocytes release cytokines, chemokines, and reactive oxygen species that alter ion channels, receptors, and neurotransmitter systems. These changes interfere with how antiepileptic drugs act on their targets and contribute to inconsistent seizure control, highlighting the need to understand inflammation role in treatment effectiveness. Understanding these interactions is essential for developing therapies that remain effective even when the brain is inflamed.

Methods: Science Core Collection (WOSCC). To identify studies focused on neuroinflammation-driven changes in antiepileptic drug pharmacodynamics, we applieda keyword-based screening protocol using established CNS inflammatory markers.
Keywords included “neuroinflammation”, “pharmacodynamics”, and “seizure control. The article title, Web of Science Categories, and Research Areas were combined into one text string for each paper. Using regular expression detection in R (str_detect()), studies containing at least one mechanistic keyword were classified as eligible, resulting in 49 eligible and 51 non-eligible papers. Eligible studies underwent a detailed review, and extracted variables were compiled into a shared dataset. We then performed a comparative
analysis across mechanistic categories to evaluate how neuroinflammatory pathways alter AED pharmacodynamics, including effects on drug target function, ion channels and receptors, neurotransmitter signaling, and blood-brain barrier integrity. These findings informed our assessment of how neuroinflammation may reduce AED effectiveness and contribute to inconsistent seizure control.

Results: We found that neuroinflammation significantly reduces the effectiveness of antiepileptic drugs by altering ion channels, disrupting neurotransmitter signaling, and weakening the blood–brain barrier. These inflammatory changes contribute to drug resistance within neural pathways, increasing the likelihood of recurrent seizures despite treatment. Our findings suggest that targeting inflammation alongside conventional antiepileptic therapy may improve drug response and seizure control in patients with epilepsy.

Discussion: The findings highlight the interference that occurs within the functioning of pharmacodynamics as a result of neuroinflammation. Given that neuroinflammation happens due to damage or trauma to the central nervous system, analyzing the effects of it in epileptic patients is integral to understanding how they are affected. While there is a lag in the studies currently being done in this field, there is important development seen within studies done on inflammatory markers as they relate to antiepileptic drugs, particularly NLRP3, toll-like receptor 4 (TLR4), tumor necrosis factor (TNF), and interleukin-1 beta (IL-1β). Looking forward, it is important for more studies to be done in this field, given how vulnerable epileptic patients are to the effects of neuroinflammation on antiepileptic drugs, as this is what allows for seizure control.