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Updated: Feb 9, 2026

Controlled Cortical Impact Model for Traumatic Brain Injury
Published on: August 5, 2014
Electrophysiological biomarkers of epileptogenicity after traumatic brain injury
Piero Perucca1, Gregory Smith2, Cesar Santana-Gomez3
1Department of Neuroscience, Central Clinical School, Monash University, Melbourne, VIC, Australia; Department of Neurology, The Royal Melbourne Hospital, Melbourne, VIC, Australia; Department of Neurology, Alfred Health, Melbourne, VIC, Australia; Melbourne Medical School, The University of Melbourne, Melbourne, VIC, Australia.
Abstract:
Post-traumatic epilepsy is the architype of acquired epilepsies, wherein a brain insult initiates an epileptogenic process culminating in an unprovoked seizure after weeks, months or years. Identifying biomarkers of such process is a prerequisite for developing and implementing targeted therapies aimed at preventing the development of epilepsy. Currently, there are no validated electrophysiological biomarkers of post-traumatic epileptogenesis. Experimental EEG studies using the lateral fluid percussion injury model have identified three candidate biomarkers of post-traumatic epileptogenesis: pathological high-frequency oscillations (HFOs, 80-300 Hz); repetitive HFOs and spikes (rHFOSs); and reduction in sleep spindle duration and dominant frequency at the transition from stage III to rapid eye movement sleep. EEG studies in humans have yielded conflicting data; recent evidence suggests that epileptiform abnormalities detected acutely after traumatic brain injury carry a significantly increased risk of subsequent epilepsy. Well-designed studies are required to validate these promising findings, and ultimately establish whether there are post-traumatic electrophysiological features which can guide the development of 'antiepileptogenic' therapies.
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