The Precise Timing of Pathological High-Frequency Oscillations and Epileptic Spikes in the Hippocampus Determines Their Disruptive Impact on Verbal Memory Encoding and Retrieval
Abstract number :
1.279
Submission category :
3. Neurophysiology / 3G. Computational Analysis & Modeling of EEG
Year :
2025
Submission ID :
171
Source :
www.aesnet.org
Presentation date :
12/6/2025 12:00:00 AM
Published date :
Authors :
Presenting Author: Weichen Huang, PhD – Stanford University
Eugene Liang, N/A – Stanford University
Aidan Chan, N/A – Stanford University
Gayle Deutsch, MD – Stanford University School of Medicine
Vivek Buch, MD – Stanford University
Josef Parvizi, MD, PhD – Stanford University School of Medicine
Rationale: Patients with temporal lobe epilepsy (TLE) often experience progressive memory decline, leading to significant personal hardship and societal burden. However, the precise spatiotemporal mechanisms and the impact of the timing of hippocampal epileptic activity, including spikes and pathological high-frequency oscillations (pHFOs), on successful memory processing remain poorly understood.
Methods: In this study, we investigated the pathophysiology of memory impairment in TLE using intracranial hippocampal electroencephalography (iEEG) recordings from 26 patients performing an incidental encoding and recognition memory task. We identified iEEG signatures of successful memory processing, marked by dynamic changes in theta power, high-frequency activity (HFA), and ripple rates at specific time points during encoding and recognition. Additionally, we identified epileptic activity, including spikes and pHFOs, within task durations as well as across 24-hour wake and sleep baseline periods.
Results: Within individuals, we found that word stimuli presented in the presence of epileptic activity during critical time windows of encoding and recognition failed to evoke typical HFA and theta responses and were more likely to be remembered poorly. Moreover, the overall burden of epileptic activity during rest, as well as across 24-hour wake and sleep baseline periods, correlated with the severity of memory deficits observed in standard neuropsychological assessments.
Conclusions: By using pathological neural events (pHFOs and spikes) as a window into brain function, our study provides causal insight into the mechanisms supporting normal memory processes. These findings suggest a promising direction for future research that suppressing hippocampal epileptic activity could reduce memory impairment in patients with TLE, potentially alleviating both individual suffering and the broader societal costs associated with the condition.
Funding: The study was supported by research grants from the US National Institute of Neurological Disorders and Stroke (R01NS078396) to JP.
Neurophysiology