Authors :
Presenting Author: Vasanth Raja, BS – Touro University California College of Osteopathic Medicine
Adam Fogarty, BS – Stanford Comprehensive Epilepsy Center; Scheherazade Le, MD – Stanford Comprehensive Epilepsy Center; Kimford Meador, MD – Stanford Comprehensive Epilepsy Center; Babak Razavi, MD, PhD – Stanford Comprehensive Epilepsy Center; Jordan Seliger, BA, MA – Stanford Neuroscience Clinical Research Group
Rationale:
The Wada test is used as part of pre-surgical evaluation of language dominance and risk of post-operative memory deficits in patients with drug-resistant temporal lobe epilepsy. The test involves intracarotid administration of an anesthetic agent such as amobarbital to simulate resection while the patient performs language and memory tasks. During the Wada test, electrical brain activity is typically measured using EEG to physiologically confirm anesthetic administration. The purpose of this study is to characterize the dynamics of quantitative intracranial EEG (iEEG) changes in response to anesthesia for identifying a potential biomarker for localizing the seizure-onset zone (SOZ).
Methods:
Four patients undergoing Wada testing with iEEG recordings as part of their standard pre-surgical evaluation were included in the study. Intracranial electrodes were implanted across a wide range of brain regions including the mesial temporal lobe structures (i.e., amygdala, hippocampus). Sampling rate was 500 Hz, thus facilitating analysis of brain activity up 250 Hz. Power spectral density was computed for each iEEG channel in a bipolar montage over time using 2-second, non-overlapping, sliding windows. The trends for changes in iEEG power were analyzed for different brain regions. Further, electrode contact locations were grouped as ipsi- versus contralateral to injection, and SOZ versus non-SOZ. SOZ was defined as electrode contacts with earliest involvement in the seizure based on visual clinical review of the iEEG by fellow and board-certified attending epileptologist.
Results:
Overall, iEEG power increased post-injection across different frequency bands and brain regions bilaterally. However, regions ipsilateral to injection exhibited markedly pronounced increases in iEEG power with an earlier time to reach peak power. Further, higher frequencies (alpha, beta, gamma, ripple) had delayed time to peak power compared to the lower frequencies (delta, theta). In contrast, brain regions contralateral to injection exhibited minimal or delayed increases in power (presumably due to diaschisis or potential anesthetic cross-filling to the contralateral hemisphere). SOZs exhibited greater mean baseline (pre-injection) power compared to non-SOZs for depth electrodes. Incidentally, the SOZs also occupied deeper structures, such as the mesial temporal lobe. In contrast, for strip and grid electrodes, non-SOZs exhibited greater mean baseline power compared to SOZs.
Conclusions:
Our data demonstrate diverse dynamics in quantitative iEEG in response to intracarotid anesthetic injection that are frequency- and location-dependent during Wada testing. The rise in iEEG power across frequency bands indicates a diffuse positive, or amplification, effect of anesthesia. The difference in pre-injection baseline mean power between SOZs and non-SOZs is potentially confounded by their varied anatomical locations. Further studies in a larger cohort may help further clarify these dynamics and propose a potential biomarker for identifying the SOZ.
Funding: There was no funding received in support of this abstract.