Hiroya Ono1, Masaki Sonoda2, Brian H Silverstein3, Kaori Sonoda4, Takafumi Kubota5, Aimee F Luat6, Robert Rothermel7, Sandeep Sood8, Eishi Asano9. 1. Department of Pediatrics, Children's Hospital of Michigan, Wayne State University, Detroit, MI 48201, USA; Department of Pediatric Neurology, National Center of Neurology and Psychiatry, Joint Graduate School of Tohoku University, Tokyo 1878551, Japan. 2. Department of Pediatrics, Children's Hospital of Michigan, Wayne State University, Detroit, MI 48201, USA; Department of Neurosurgery, Graduate School of Medicine, Yokohama City University, Yokohama 2360004, Japan. 3. Translational Neuroscience Program, Wayne State University, Detroit, MI 48201, USA. 4. Department of Pediatrics, Children's Hospital of Michigan, Wayne State University, Detroit, MI 48201, USA; Department of Pediatrics, Graduate School of Medicine, Yokohama City University, Yokohama 2360004, Japan. 5. Department of Pediatrics, Children's Hospital of Michigan, Wayne State University, Detroit, MI 48201, USA; Department of Neurology, University Hospitals of Cleveland Medical Center, Case Western Reserve University, Cleveland, OH 44106, USA. 6. Department of Pediatrics, Children's Hospital of Michigan, Wayne State University, Detroit, MI 48201, USA; Department of Neurology, Children's Hospital of Michigan, Wayne State University, Detroit, MI 48201, USA; Department of Pediatrics, Central Michigan University, Mt. Pleasant, MI 48858, USA. 7. Department of Psychiatry, Children's Hospital of Michigan, Wayne State University, Detroit, MI 48201, USA. 8. Department of Neurosurgery, Children's Hospital of Michigan, Wayne State University, Detroit, MI 48201, USA. 9. Department of Pediatrics, Children's Hospital of Michigan, Wayne State University, Detroit, MI 48201, USA; Department of Neurology, Children's Hospital of Michigan, Wayne State University, Detroit, MI 48201, USA; Translational Neuroscience Program, Wayne State University, Detroit, MI 48201, USA. Electronic address: easano@med.wayne.edu.
Abstract
OBJECTIVE: We clarified the clinical and mechanistic significance of physiological modulations of high-frequency broadband cortical activity associated with spontaneous saccadic eye movements during a resting state. METHODS: We studied 30 patients who underwent epilepsy surgery following extraoperative electrocorticography and electrooculography recordings. We determined whether high-gamma activity at 70-110 Hz preceding saccade onset would predict upcoming ocular behaviors. We assessed how accurately the model incorporating saccade-related high-gamma modulations would localize the primary visual cortex defined by electrical stimulation. RESULTS: The dynamic atlas demonstrated transient high-gamma suppression in the striatal cortex before saccade onset and high-gamma augmentation subsequently involving the widespread posterior brain regions. More intense striatal high-gamma suppression predicted the upcoming saccade directed to the ipsilateral side and lasting longer in duration. The bagged-tree-ensemble model demonstrated that intense saccade-related high-gamma modulations localized the visual cortex with an accuracy of 95%. CONCLUSIONS: We successfully animated the neural dynamics supporting saccadic suppression, a principal mechanism minimizing the perception of blurred vision during rapid eye movements. The primary visual cortex per se may prepare actively in advance for massive image motion expected during upcoming prolonged saccades. SIGNIFICANCE: Measuring saccade-related electrocorticographic signals may help localize the visual cortex and avoid misperceiving physiological high-frequency activity as epileptogenic.
OBJECTIVE: We clarified the clinical and mechanistic significance of physiological modulations of high-frequency broadband cortical activity associated with spontaneous saccadic eye movements during a resting state. METHODS: We studied 30 patients who underwent epilepsy surgery following extraoperative electrocorticography and electrooculography recordings. We determined whether high-gamma activity at 70-110 Hz preceding saccade onset would predict upcoming ocular behaviors. We assessed how accurately the model incorporating saccade-related high-gamma modulations would localize the primary visual cortex defined by electrical stimulation. RESULTS: The dynamic atlas demonstrated transient high-gamma suppression in the striatal cortex before saccade onset and high-gamma augmentation subsequently involving the widespread posterior brain regions. More intense striatal high-gamma suppression predicted the upcoming saccade directed to the ipsilateral side and lasting longer in duration. The bagged-tree-ensemble model demonstrated that intense saccade-related high-gamma modulations localized the visual cortex with an accuracy of 95%. CONCLUSIONS: We successfully animated the neural dynamics supporting saccadic suppression, a principal mechanism minimizing the perception of blurred vision during rapid eye movements. The primary visual cortex per se may prepare actively in advance for massive image motion expected during upcoming prolonged saccades. SIGNIFICANCE: Measuring saccade-related electrocorticographic signals may help localize the visual cortex and avoid misperceiving physiological high-frequency activity as epileptogenic.
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