Hui-Min Chen1,2, Zhi-Qiang Sha3,4,5, Hui-Zi Ma1,2, Yong He3,4,5, Tao Feng1,2,6. 1. Center for Neurodegenerative Disease, Department of Neurology, Beijing Tiantan Hospital, Capital Medical University, Beijing, China. 2. China National Clinical Research Center for Neurological Diseases, Beijing, China. 3. National Key Laboratory of Cognitive Neuroscience and Learning, Beijing Normal University, Beijing, China. 4. IDG/McGovern Institute for Brain Research, Beijing Normal University, Beijing, China. 5. Beijing Key Laboratory of Brain Imaging and Connectomics, Beijing Normal University, Beijing, China. 6. Parkinson's Disease Center, Beijing Institute for Brain Disorders, Capital Medical University, Beijing, China.
Abstract
AIMS: Deep brain stimulation of the subthalamic nucleus (STN-DBS) has become an effective treatment strategy for patients with Parkinson's disease. However, the biological mechanism underlying DBS treatment remains poorly understood. METHOD: In this study, we investigated how STN-DBS modulated the brain network using a bimodal positron emission tomography (PET)/functional magnetic resonance imaging (fMRI) dataset. We first performed an activation likelihood estimation meta-analysis of 13 PET/SPECT studies concerning STN-DBS effects on resting-state brain activity in Parkinson's disease. Additionally, using a functional connectivity analysis in resting-state fMRI, we investigated whether these STN-DBS-affected regions were functionally connected to constitute an effective network. RESULTS: The results revealed that STN-DBS reduced brain activity in the right thalamus, bilateral caudal supplementary area, and the left primary motor cortex, and it increased brain activity in the left thalamus during rest. Second, these STN-DBS-affected areas were functionally connected within an STN-DBS effective network. CONCLUSION: Deep brain stimulation of the subthalamic nucleus (STN-DBS) may deactivate the motor cortex as a remote and network effect, affecting the target and the neighboring subcortical areas. These areas may constitute an effective network of STN-DBS modulation. Our results shed light on the mechanisms of STN-DBS treatment from a network perspective and highlight the potential therapeutic benefits of targeted network modulation.
AIMS: Deep brain stimulation of the subthalamic nucleus (STN-DBS) has become an effective treatment strategy for patients with Parkinson's disease. However, the biological mechanism underlying DBS treatment remains poorly understood. METHOD: In this study, we investigated how STN-DBS modulated the brain network using a bimodal positron emission tomography (PET)/functional magnetic resonance imaging (fMRI) dataset. We first performed an activation likelihood estimation meta-analysis of 13 PET/SPECT studies concerning STN-DBS effects on resting-state brain activity in Parkinson's disease. Additionally, using a functional connectivity analysis in resting-state fMRI, we investigated whether these STN-DBS-affected regions were functionally connected to constitute an effective network. RESULTS: The results revealed that STN-DBS reduced brain activity in the right thalamus, bilateral caudal supplementary area, and the left primary motor cortex, and it increased brain activity in the left thalamus during rest. Second, these STN-DBS-affected areas were functionally connected within an STN-DBS effective network. CONCLUSION: Deep brain stimulation of the subthalamic nucleus (STN-DBS) may deactivate the motor cortex as a remote and network effect, affecting the target and the neighboring subcortical areas. These areas may constitute an effective network of STN-DBS modulation. Our results shed light on the mechanisms of STN-DBS treatment from a network perspective and highlight the potential therapeutic benefits of targeted network modulation.
Authors: A O Ceballos-Baumann; H Boecker; P Bartenstein; I von Falkenhayn; H Riescher; B Conrad; J R Moringlane; F Alesch Journal: Arch Neurol Date: 1999-08
Authors: U Sabatini; K Boulanouar; N Fabre; F Martin; C Carel; C Colonnese; L Bozzao; I Berry; J L Montastruc; F Chollet; O Rascol Journal: Brain Date: 2000-02 Impact factor: 13.501
Authors: B Haslinger; P Erhard; N Kämpfe; H Boecker; E Rummeny; M Schwaiger; B Conrad; A O Ceballos-Baumann Journal: Brain Date: 2001-03 Impact factor: 13.501
Authors: Takao Hashimoto; Christopher M Elder; Michael S Okun; Susan K Patrick; Jerrold L Vitek Journal: J Neurosci Date: 2003-03-01 Impact factor: 6.167
Authors: T Hershey; F J Revilla; A R Wernle; L McGee-Minnich; J V Antenor; T O Videen; J L Dowling; J W Mink; J S Perlmutter Journal: Neurology Date: 2003-09-23 Impact factor: 9.910
Authors: Stelvio Sestini; Anita Scotto di Luzio; Franco Ammannati; Maria Teresa R De Cristofaro; Alessandro Passeri; Sara Martini; Alberto Pupi Journal: J Nucl Med Date: 2002-06 Impact factor: 10.057
Authors: Rafael Rodriguez-Rojas; Jose A Pineda-Pardo; Raul Martinez-Fernandez; Rosalie V Kogan; Carlos A Sanchez-Catasus; Marta Del Alamo; Frida Hernández; Lina García-Cañamaque; Klaus L Leenders; Jose A Obeso Journal: Eur J Nucl Med Mol Imaging Date: 2019-11-08 Impact factor: 9.236
Authors: Julius Kricheldorff; Katharina Göke; Maximilian Kiebs; Florian H Kasten; Christoph S Herrmann; Karsten Witt; Rene Hurlemann Journal: Brain Sci Date: 2022-07-15