Converging metabolic and functional networks for tremor expression and deep brain stimulation-mediated control;
: Weigl, Benedikt; Pistorius, Regina; Brumberg, Joachim; Pozzi, Nicoló G.; Buck, Andreas; Muthuraman, Muthuraman; Isaias, Ioannis U.; Volkmann, Jens; Joutsa, Juho; Reich, Martin M.
Publisher: Springer Nature
: 2026
NPJ Parkinson's disease
: 119
: 12
: 1
: 2373-8057
DOI: https://doi.org/10.1038/s41531-026-01388-7
: https://www.nature.com/articles/s41531-026-01388-7
: https://research.utu.fi/converis/portal/detail/Publication/526593767
Emerging evidence indicates that movement disorders arise from symptom-specific rather than disease-specific brain network dysfunctions that can be influenced through targeted neuromodulation. Such networks are widely mapped using normative connectome analyses from lesion and stimulation sites. Here, we used [18F]-fluorodeoxyglucose (FDG)-PET in 14 essential tremor patients undergoing thalamic deep brain stimulation (DBS) to identify stimulation-induced and tremor related regional metabolic changes in a within-subject design and combined this with normative connectome results. Stimulation increased metabolism in motor cortical and cerebellar regions - key hubs of the previously proposed tremor treatment network as derived from normative functional connectivity. Importantly, individual alignment with this network predicted clinical tremor improvement (R2 = 0.593, p = 0.007). These same regions showed higher metabolism during tremor expression in the untreated condition, suggesting overlap between the circuits involved in symptom generation and therapeutic response. These findings support indirect connectome-based models by linking them to brain glucose metabolism changes and suggest that DBS relieves tremor by modulating the same circuit that underlies symptom expression.
Neurosciences & Neurology
:
This study was supported by the Deutsche Forschungsgemeinschaft (DFG, German Research Foundation; Project-ID 424778381, TRR 295). M.R. was supported by the Interdisziplinäres Zentrum für Klinische Forschung (IZKF) of the University Hospital Würzburg. B.W. and R.P. were supported by a grant of the German Excellence Initiative to the Graduate School of Life Sciences, University of Würzburg (Germany). J.B. was supported by the Berta-Ottenstein program for Advanced Clinician Scientist, Faculty of Medicine, University of Freiburg. J.J. was supported by the Research Council of Finland, Finnish Medical Foundation, Sigrid Juselius Foundation, Finnish Parkinson Foundation, Signe & Ane Gyllenberg Foundation, Sakari Sohlberg Foundation, Turku University Hospital (VTR funds), a private donation to University of Turku, Dystonia Medical Research Foundation and Dysphonia International. We thank Lukas L. Goede and Andreas Horn for sharing the tremor treatment network used in this study.
Open Access funding enabled and organized by Projekt DEAL.
