Yue Chen1, Chen Gong1, Ye Tian1, Natasza Orlov2, Jianguo Zhang3, Yi Guo4, Shujun Xu5, Changqing Jiang1, Hongwei Hao1, Wolf-Julian Neumann6, Andrea A Kühn6, Hesheng Liu7, Luming Li8. 1. National Engineering Laboratory for Neuromodulation, School of Aerospace Engineering, Tsinghua University, Beijing, 10084, China. 2. Athinoula A. Martinos Center for Biomedical Imaging, Department of Radiology, Massachusetts General Hospital, Harvard Medical School, Charlestown, MA, 02129, USA. 3. Department of Neurosurgery, Beijing Tiantan Hospital, Capital Medical University, Beijing, 100070, China. 4. Department of Neurosurgery, Peking Union Medical College Hospital, Beijing, 100032, China. 5. Department of Neurosurgery, Qilu Hospital of Shandong University, Shandong, 250012, China. 6. Movement Disorder and Neuromodulation Unit, Department of Neurology, Charité-Universitätsmedizin Berlin, Berlin, 10117, Germany. 7. Athinoula A. Martinos Center for Biomedical Imaging, Department of Radiology, Massachusetts General Hospital, Harvard Medical School, Charlestown, MA, 02129, USA; Department of Neuroscience, Medical University of South Carolina, Charleston, 29425, SC, USA. Electronic address: hesheng@nmr.mgh.harvard.edu. 8. National Engineering Laboratory for Neuromodulation, School of Aerospace Engineering, Tsinghua University, Beijing, 10084, China; Precision Medicine & Healthcare Research Center, Tsinghua-Berkeley Shenzhen Institute, Tsinghua University, Shenzhen, 518071, China; IDG/McGovern Institute for Brain Research at Tsinghua University, Beijing, 100084, China; Institute of Epilepsy, Beijing Institute for Brain Disorders, Beijing, 100093, China. Electronic address: lilm@tsinghua.edu.cn.
Abstract
BACKGROUND: Deep brain stimulation (DBS) holds great promise in treating various brain diseases but its chronic therapeutic mechanisms are unclear. OBJECTIVE: To explore the immediate and chronic effects of DBS on brain oscillations, and understand how different sub-bands of oscillations may be related to symptom improvement in Parkinson's patients. METHODS: We carried out a longitudinal study to examine the effects of DBS on local field potentials recorded by sensing-enabled neurostimulators in the subthalamic nuclei of Parkinson's patients, using a novel block-design stimulation paradigm. RESULTS: DBS significantly suppressed beta activity (13-35Hz) but the suppression effect appeared to gradually attenuate during a 6-month follow-up period after surgery (p = 0.002). However, beta suppression did not attenuate after repeated stimulation over several minutes (p > 0.110), suggesting that the changes in beta suppression may reflect a slow reconfiguration of neural pathways instead of habituation. Suppression of beta was also associated with clinical symptom improvement across subjects. Importantly, symptom-relevant features fell within the high beta band at month 1 but shifted to the low beta band at month 6, indicating that the high beta and the low beta oscillations may play different functional roles and respond differently to stimulation over the long-term treatment. CONCLUSION: These data may advance understanding of chronic DBS effects on beta oscillations and their association with clinical improvement, offering novel insights to the therapeutic mechanisms of DBS.
BACKGROUND: Deep brain stimulation (DBS) holds great promise in treating various brain diseases but its chronic therapeutic mechanisms are unclear. OBJECTIVE: To explore the immediate and chronic effects of DBS on brain oscillations, and understand how different sub-bands of oscillations may be related to symptom improvement in Parkinson'spatients. METHODS: We carried out a longitudinal study to examine the effects of DBS on local field potentials recorded by sensing-enabled neurostimulators in the subthalamic nuclei of Parkinson'spatients, using a novel block-design stimulation paradigm. RESULTS: DBS significantly suppressed beta activity (13-35Hz) but the suppression effect appeared to gradually attenuate during a 6-month follow-up period after surgery (p = 0.002). However, beta suppression did not attenuate after repeated stimulation over several minutes (p > 0.110), suggesting that the changes in beta suppression may reflect a slow reconfiguration of neural pathways instead of habituation. Suppression of beta was also associated with clinical symptom improvement across subjects. Importantly, symptom-relevant features fell within the high beta band at month 1 but shifted to the low beta band at month 6, indicating that the high beta and the low beta oscillations may play different functional roles and respond differently to stimulation over the long-term treatment. CONCLUSION: These data may advance understanding of chronic DBS effects on beta oscillations and their association with clinical improvement, offering novel insights to the therapeutic mechanisms of DBS.
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