[논문]Neural activation and connectivity during cued eye blinks in Chronic Tic Disorders

Loo, Sandra K.; Miyakoshi, Makoto; Tung, Kelly; Lloyd, Evan; Salgari, Giulia; Dillon, Andrea; Chang, Susanna; Piacentini, John; Makeig, Scott

doi:10.1016/j.nicl.2019.101956

Neural activation and connectivity during cued eye blinks in Chronic Tic Disorders 원문보기

NeuroImage : Clinical, v.24, 2019년, pp.101956 -

Loo, Sandra K. (Semel Institute for Neuroscience and Human Behavior, University of California, Los Angeles) , Miyakoshi, Makoto (Swartz Center for Neural Computation, University of California, San Diego) , Tung, Kelly (Semel Institute for Neuroscience and Human Behavior, University of California, Los Angeles) , Lloyd, Evan (Semel Institute for Neuroscience and Human Behavior, University of California, Los Angeles) , Salgari, Giulia (Semel Institute for Neuroscience and Human Behavior, University of California, Los Angeles) , Dillon, Andrea (Semel Institute for Neuroscience and Human Behavior, University of California, Los Angeles) , Chang, Susanna (Semel Institute for Neuroscience and Human Behavior, University of California, Los Angeles) , Piacentini, John (Semel Institute for Neuroscience and Human Behavior, Unive) , Makeig, Scott

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Abstract Objective The pathophysiology of Chronic Tic Disorders (CTDs), including Tourette Syndrome, remains poorly understood. The goal of this study was to compare neural activity and connectivity during a voluntary movement (VM) paradigm that involved cued eye blinks among children with and without CTDs. Using the precise temporal resolution of electroencephalography (EEG), we used the timing and location of cortical source resolved spectral power activation and connectivity to map component processes such as visual attention, cue detection, blink regulation and response monitoring. We hypothesized that neural activation and connectivity during the cued eye blink paradigm would be significantly different in regions typically associated with effortful control of eye blinks, such as frontal, premotor, parietal, and occipital cortices between children with and without CTD. Method Participants were 40 children (23 with CTD, 17 age-matched Healthy Control [HC]), between the ages of 8–12 (mean age = 9.5) years old. All participants underwent phenotypic assessment including diagnostic interviews, behavior rating scales and 128-channel EEG recording. Upon presentation of a cue every 3 s, children were instructed to make an exaggerated blink. Results Behaviorally, the groups did not differ in blink number, latency, or ERP amplitude. Within source resolved clusters located in left dorsolateral prefrontal cortex, posterior cingulate, and supplemental motor area, children with CTD exhibited higher gamma band spectral power relative to controls. In addition, significant diagnostic group differences in theta, alpha, and beta band power in inferior parietal cortex emerged. Spectral power differences were significantly associated with clinical characteristics such as tic severity and premonitory urge strength. After calculating dipole density for 76 anatomical regions, the CTD and HC groups had 70% overlap of top regions with the highest dipole density, suggesting that similar cortical networks were used across groups to carry out the VM. The CTD group exhibited significant information flow increase and dysregulation relative to the HC group, particularly from occipital to frontal regions. Conclusion Children with CTD exhibit abnormally high levels of neural activation and dysregulated connectivity among networks used for regulation and effortful control of voluntary eye blinks. Highlights First cortical source level EEG study on brain activity and connectivity in CTD. Children with CTD exhibit aberrant levels of neural activation and connectivity. Neural activation was significantly associated with tic severity and premonitory urge.

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Neural activation and connectivity during cued eye blinks in Chronic Tic Disorders 원문보기

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