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Tumor Necrosis Factor-α, the Pathological Key to Post-Traumatic Epilepsy: A Comprehensive Systematic Review
- Source :
- ACS chemical neuroscience. 11(13)
- Publication Year :
- 2020
-
Abstract
- Post-traumatic epilepsy (PTE) is one of the detrimental outcomes of traumatic brain injury (TBI), resulting in recurrent seizures that impact daily life. However, the pathological relationship between PTE and TBI remains unclear, and commonly prescribed antiepileptic drugs (AED) are ineffective against PTE. Fortunately, emerging research implicates neuroinflammation, particularly, tumor necrosis factor-α (TNF-α), as the key mediator for PTE development. Thus, this review aims to examine the available literature regarding the role of TNF-α in PTE pathology and, subsequently, evaluate TNF-α as a possible target for its treatment. A comprehensive literature search was conducted on four databases including PubMed, CINAHL, Embase, and Scopus. Articles with relevance in investigating TNF-α expression in PTE were considered in this review. Critical evaluation of four articles that met the inclusion criteria suggests a proportional relationship between TNF-α expression and seizure susceptibilit and that neutralization or suppression of TNF-α release results in reduced susceptibility to seizures. In conclusion, this review elucidates the importance of TNF-α expression in epileptogenesis postinjury and urges future research to focus more on clinical studies involving TNF-α, which may provide clearer insight into PTE prevention, therefore improving the lives of PTE patients.
- Subjects :
- Oncology
medicine.medical_specialty
Physiology
Traumatic brain injury
Cognitive Neuroscience
CINAHL
Biochemistry
Epileptogenesis
Epilepsy
Seizures
Internal medicine
Brain Injuries, Traumatic
medicine
Humans
Post-traumatic epilepsy
Pathological
Tumor necrosis factor α
Neuroinflammation
business.industry
Tumor Necrosis Factor-alpha
Cell Biology
General Medicine
medicine.disease
Epilepsy, Post-Traumatic
Anticonvulsants
business
Subjects
Details
- ISSN :
- 19487193
- Volume :
- 11
- Issue :
- 13
- Database :
- OpenAIRE
- Journal :
- ACS chemical neuroscience
- Accession number :
- edsair.doi.dedup.....aa3ed74c5f4146c26cf221c9b4f9936a