Objectives Tourette syndrome is a neurodevelopmental disorder commonly associated with involuntary movements, or tics. We currently lack an ideal animal model for Tourette syndrome. In humans, clinical manifestation of tics cannot be captured via functional imaging due to motion artefacts and limited temporal resolution, and electrophysiological studies have been limited to the intraoperative environment. The goal of this study was to identify electrophysiological signals in the centromedian (CM) thalamic nucleus and primary motor (M1) cortex that differentiate tics from voluntary movements.
Methods The data were collected as part of a larger National Institutes of Health-sponsored clinical trial. Four participants (two males, two females) underwent monthly clinical visits for collection of physiology for a total of 6 months. Participants were implanted with bilateral CM thalamic macroelectrodes and M1 subdural electrodes that were connected to two neurostimulators, both with sensing capabilities. MRI scans were performed preoperatively and CT scans postoperatively for localisation of electrodes. Electrophysiological recordings were collected at each visit from both the cortical and subcortical implants.
Results Recordings collected from the CM thalamic nucleus revealed a low-frequency power (3–10 Hz) increase that was time-locked to the onset of involuntary tics but was not present during voluntary movements. Cortical recordings revealed beta power decrease in M1 that was present during tics and voluntary movements.
Conclusion We conclude that a human physiological signal was detected from the CM thalamus that differentiated tic from voluntary movement, and this physiological feature could potentially guide the development of neuromodulation therapies for Tourette syndrome that could use a closed-loop-based approach.
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JNC and MSO are joint first authors.
Contributors JNC: Collected data, performed data analysis, wrote first draft. MSO: Designed and clinically supervised study, and edited manuscript. KF: Performed surgical implantation and edited manuscript. AG: Designed and supervised study, and edited manuscript.
Funding This work was supported by grants from the National Institutes of Health R01NS096008 (MSO and AG) and National Science Foundation PECASE Award (Presidential Early Career Award for Scientists and Engineers) 1553482 (AG). Devices used in this study were donated by Medtronic for investigational purposes only.
Competing interests None declared.
Patient consent for publication Obtained.
Ethics approval This study was approved by both the Institutional Review Board of the UF and the US Food and Drug Administration through an Investigational Device Exemption.
Provenance and peer review Not commissioned; externally peer reviewed.
Data availability statement Data are available on reasonable request.
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