ReviewBrain sciences2019
Neuroinflammation in Post-Traumatic Epilepsy: Pathophysiology and Tractable Therapeutic Targets.
Review in Brain sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
46 citing papers in PubMed, 93 citations in OpenAlex.
- Article
- Neuronal toll-like receptor-4 regulation of matrix metalloproteinase-9 activity mediates dentate circuit dysfunction after traumatic brain injury.Journal of neuroinflammation · 2026Article
- Platelet-to-lymphocyte ratio as an indicator of idiopathic epilepsy in dogs.Journal of veterinary internal medicine · 2026Article
- WONOEP XVII appraisal: The immunopathogenesis of epilepsy.Epilepsia · 2026Review
- Glucocorticoid-Induced Tumor Necrosis Factor Receptor Ligand: Correlation and Therapeutic Potential for Cognitive Impairment in Temporal Lobe Epilepsy.Clinical and translational science · 2026Article
- Neuronal Toll-like Receptor-4 regulation of Matrix Metalloproteinase-9 Activity Mediates Dentate Circuit Dysfunction after Traumatic Brain Injury.bioRxiv : the preprint server for biology · 2026Article
- Cytokines and related signaling pathways in traumatic brain injury.Frontiers in immunology · 2026Review
- Effects of acute biperiden treatment following traumatic brain injury in male rats.Scientific reports · 2025Article
- Adenosine ANeuropharmacology · 2025Article
- Perceiving traumatic brain injury from glymphatic system.Molecular psychiatry · 2025Review
- IL-1β and HMGB1 in Epileptogenesis: Recent Advances and Clinical Translation.Pharmaceuticals (Basel, Switzerland) · 2025Review
- The Role of Neuroinflammation and Network Anomalies in Drug-Resistant Epilepsy.Neuroscience bulletin · 2025Review
- Post-traumatic epilepsy: bridging pathogenesis, diagnosis, and pharmacotherapeutic strategies.Frontiers in pharmacology · 2025Review
- P2X7R antagonism suppresses long-lasting brain hyperexcitability following traumatic brain injury in mice.Theranostics · 2025Article
- Pharmacokinetics and brain uptake of sodium selenate and selenium in naïve rats and a lateral fluid percussion injury rat model.Pharmacology research & perspectives · 2024Article
- WONOEP appraisal: The role of glial cells in focal malformations associated with early onset epilepsies.Epilepsia · 2024Review
- Neuroprotective effects of naltrexone in a mouse model of post-traumatic seizures.Scientific reports · 2024Article
- Insights into epileptogenesis from post-traumatic epilepsy.Nature reviews. Neurology · 2024Review
- mTOR and neuroinflammation in epilepsy: implications for disease progression and treatment.Nature reviews. Neuroscience · 2024Review
- Virus-Induced Epilepsy vs. Epilepsy Patients Acquiring Viral Infection: Unravelling the Complex Relationship for Precision Treatment.International journal of molecular sciences · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Epilepsy is a common chronic consequence of traumatic brain injury (TBI), contributing to increased morbidity and mortality for survivors. As post-traumatic epilepsy (PTE) is drug-resistant in at least one-third of patients, there is a clear need for novel therapeutic strategies to prevent epilepsy from developing after TBI, or to mitigate its severity. It has long been recognized that seizure activity is associated with a local immune response, characterized by the activation of microglia and astrocytes and the release of a plethora of pro-inflammatory cytokines and chemokines. More recently, increasing evidence also supports a causal role for neuroinflammation in seizure induction and propagation, acting both directly and indirectly on neurons to promote regional hyperexcitability. In this narrative review, we focus on key aspects of the neuroinflammatory response that have been implicated in epilepsy, with a particular focus on PTE. The contributions of glial cells, blood-derived leukocytes, and the blood-brain barrier will be explored, as well as pro- and anti-inflammatory mediators. While the neuroinflammatory response to TBI appears to be largely pro-epileptogenic, further research is needed to clearly demonstrate causal relationships. This research has the potential to unveil new drug targets for PTE, and identify immune-based biomarkers for improved epilepsy prediction.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.