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Journal Article

Citation

Lucke-Wold BP, Nguyen L, Turner RC, Logsdon AF, Chen YW, Smith KE, Huber JD, Matsumoto R, Rosen CL, Tucker ES, Richter E. Seizure 2015; 33: 13-23.

Affiliation

Department of Neurosurgery, West Virginia University School of Medicine, Morgantown, WV 26506, USA; The Center for Neuroscience, West Virginia University School of Medicine, Morgantown, WV 26506, USA. Electronic address: eorichter@hsc.wvu.edu.

Copyright

(Copyright © 2015, Elsevier Publishing)

DOI

10.1016/j.seizure.2015.10.002

PMID

26519659

Abstract

Post-traumatic epilepsy continues to be a major concern for those experiencing traumatic brain injury. Post-traumatic epilepsy accounts for 10-20% of epilepsy cases in the general population. While seizure prophylaxis can prevent early onset seizures, no available treatments effectively prevent late-onset seizure. Little is known about the progression of neural injury over time and how this injury progression contributes to late onset seizure development. In this comprehensive review, we discuss the epidemiology and risk factors for post-traumatic epilepsy and the current pharmacologic agents used for treatment. We highlight limitations with the current approach and offer suggestions for remedying the knowledge gap. Critical to this pursuit is the design of pre-clinical models to investigate important mechanistic factors responsible for post-traumatic epilepsy development. We discuss what the current models have provided in terms of understanding acute injury and what is needed to advance understanding regarding late onset seizure. New model designs will be used to investigate novel pathways linking acute injury to chronic changes within the brain. Important components of this transition are likely mediated by toll-like receptors, neuroinflammation, and tauopathy. In the final section, we highlight current experimental therapies that may prove promising in preventing and treating post-traumatic epilepsy. By increasing understanding about post-traumatic epilepsy and injury expansion over time, it will be possible to design better treatments with specific molecular targets to prevent late-onset seizure occurrence following traumatic brain injury.


Language: en

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