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Approximately 30&#x0025; of patients with epilepsy do not respond to anti-epileptogenic drugs. Surgical removal of the epileptogenic zone (EZ), the brain regions where the seizures originate and spread, can be a possible therapy for these patients, but localizing the EZ is challenging due to a variety of clinical factors. High-frequency oscillations (HFOs) in intracranial electroencephalography (EEG) are a promising biomarker of the EZ, but it is currently unknown whether HFO rates and HFO morphology modulate as pathological brain networks evolve in a way that gives rise to seizures. To address this question, we assessed the temporal evolution of the duration of HFO events, amplitude of HFO events, and rates of HFOs per minute. HFO events were quantified using the 4AP in vivo rodent model of epilepsy, inducing seizures in two different brain areas. We found that the duration and amplitude of HFO events were significantly increased for the cortex model when compared to the hippocampus model. Additionally, the duration and amplitude increased significantly between baseline and pre-ictal HFOs in both models. On the other hand, the two models did not display a consistent increasing or decreasing trend in amplitude, duration or rate when comparing ictal and postictal intervals. Clinical Relevance- We assessed the amplitude, duration, and rate of HFOs in two acute in vivo rodent models of epilepsy. The significant modulation of HFO morphology from baseline to pre-ictal periods suggests that these features may be a robust biomarker for pathological tissue involved in epileptogenesis. Moreover, the differences in HFO morphology observed between cortex and hippocampus animal models possibly indicate that different structural network characteristics of the EZ cause this modulation. In all, we found that HFO features modulate significantly with the onset of seizures, further highlighting the need to consider of HFO morphology in EZ-localizing studies.

Temporal and morphological characteristics of high-frequency oscillations in an acute in vivo model of epilepsy