A1 Refereed original research article in a scientific journal
Brain metabolic response to repetitive transcranial magnetic stimulation to lesion network in cervical dystonia
Authors: Kokkonen, Aleksi; Corp, Daniel T.; Aaltonen, Juho; Hirvonen, Jussi; Kirjavainen, Anna K.; Rajander, Johan; Joutsa, Juho
Publisher: Elsevier
Publication year: 2024
Journal: Brain Stimulation
Journal name in source: Brain stimulation
Journal acronym: Brain Stimul
Volume: 17
Issue: 6
First page : 1171
Last page: 1177
ISSN: 1935-861X
eISSN: 1876-4754
DOI: https://doi.org/10.1016/j.brs.2024.10.004
Web address : https://doi.org/10.1016/j.brs.2024.10.004
Self-archived copy’s web address: https://research.utu.fi/converis/portal/detail/Publication/458630544
Background: A previous study identified a brain network underlying cervical dystonia (CD) based on causal brain lesions. This network was shown to be abnormal in idiopathic CD and aligned with connections mediating treatment response to deep brain stimulation, suggesting generalizability across etiologies and relevance for treatment. The main nodes of this network were located in the deep cerebellar structures and somatosensory cortex (S1), of which the latter can be easily reached via non-invasive brain stimulation. To date, there are no studies testing brain stimulation targeted to networks identified using lesion network mapping.
Objectives: To assess target engagement by stimulating the S1 and testing the brain's acute metabolic response to repetitive transcranial magnetic stimulation in CD patients and healthy controls.
Methods: Thirteen CD patients and 14 controls received a single session of continuous theta burst (cTBS) and sham to the right S1. Changes in regional brain glucose metabolism were measured using [18F]FDG-PET.
Results: cTBS increased metabolism at the stimulation site in CD (P=0.03) but not in controls (P=0.15; group difference P=0.01). In subcortical regions, cTBS increased metabolism in the brainstem in CD only (PFDR=0.04). The remote activation was positively associated with dystonia severity and efficacy of sensory trick phenomenon in CD patients.
Conclusions: Our results provide further evidence of abnormal sensory system function in CD and show that a single session of S1 cTBS is sufficient to induce measurable changes in brain glucose metabolism. These findings support target engagement, motivating therapeutic trials of cTBS to the S1 in CD.
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Funding information in the publication:
The study was financially supported by a private donation to the University of Turku. Additional funding, in form of personal grants, was received from The Finnish Parkinson Foundation, Finnish Brain Foundation and Maire Taponen Foundation (A.K.), and from Instrumentarium Research Foundation, Finnish Medical Foundation, and Sigrid Juselius Foundation (J.J). Research reported in this manuscript was also supported by the Dystonia Medical Research Foundation under award number DMRF-BCAD-2023-1 (D.C.). The authors would like to thank the personnel of the Turku PET Centre, as well as Leena Lauos and Mikael Eklund for their efforts in support of this study.