Abstracts

Rationale: Since Hans Berger first recorded alpha activity on EEG in the early 20th century, investigators have documented the presence of posterior dominant alpha rhythm suppressed by eye opening and augmented by eye closure. Until now, such reactive alpha activity has been used clinically as a biomarker of brain function during resting state, but the cortical origin and propagation of alpha activity have not been fully clarified. In the present study, we quantified the amplitude of alpha activity responsive to eye opening and closure on ECoG, and determined where alpha activity was initially modulated, and also when and where alpha modulation was propagated. We likewise determined the spatiotemporal dynamics of high-gamma activity at 70-110 Hz modulated by eye opening and closure. Methods: We studied 10 patients (age: 6-20 years) who underwent extraoperative ECoG recording as part of the presurgical evaluation of drug-resistant focal epilepsy. Electrode channels excluded from the analysis included those classified as the seizure onset zone, epileptogenic lesions, or irritative zone. We employed time-frequency analysis to quantify the percent change of amplitude of alpha (8-12 Hz) and high-gamma activities following spontaneous eye closure and opening. We then animated the spatiotemporal dynamics of alpha and high-gamma modulations on a 3D standard surface image. Results: At 50-100 ms following the onset of eye closure, the posterior-striatal and lateral-occipital regions of both hemispheres began to show alpha augmentation and high-gamma attenuation. At 100 ms and afterward, both alpha augmentation and high-gamma attenuation intensely involved bilateral posterior-fusiform regions in a posterior-to-anterior direction. At 50-100 ms following the onset of eye opening, the entire striatal regions showed high-gamma augmentation, whereas alpha attenuation in the striatal regions became evident afterward. High-gamma augmentation and alpha attenuation subsequently involved bilateral lateral-occipital, posterior-parahippocampal, and posterior-fusiform regions in a sustained manner. Conclusions: This study delineated the origin and propagation of alpha and high-gamma modulations elicited by eye opening and closure. ECoG modulations after eye closure may not strictly mirror those after eye opening. Eye closure may augment alpha activity and suppress high-gamma activity preferentially in the visual cortices subserving central vision to which given patients attend before eye closure. Eye opening may augment high-gamma activity and suppress alpha activity in the larger visual cortices. Funding: NIH grant NS064033 (to E. Asano).