A1 Vertaisarvioitu alkuperäisartikkeli tieteellisessä lehdessä
Convergent mapping of a tremor treatment network
Tekijät: Goede, Lukas L.; Al-Fatly, Bassam; Li, Ningfei; Sobesky, Leon K.; Bahners, Bahne H.; Zvarova, Patricia; Neudorfer, Clemens; Reich, Martin; Volkmann, Jens; Zhang, Chencheng; Odekerken, Vincent J. J.; de Bie, Rob M. A.; Younger, Ellen F. P.; Corp, Daniel T.; Middlebrooks, Erik H.; Joutsa, Juho; Dirkx, Michiel; Deuschl, Günther; Helmich, Rick C.; Kühn, Andrea A.; Fox, Michael D.; Horn, Andreas
Kustantaja: Springer Science and Business Media LLC
Julkaisuvuosi: 2025
Journal: Nature Communications
Tietokannassa oleva lehden nimi: Nature Communications
Artikkelin numero: 4772
Vuosikerta: 16
Numero: 1
eISSN: 2041-1723
DOI: https://doi.org/10.1038/s41467-025-60089-6
Verkko-osoite: https://doi.org/10.1038/s41467-025-60089-6
Rinnakkaistallenteen osoite: https://research.utu.fi/converis/portal/detail/Publication/492322339
Tremor occurs in various forms across diverse neurological disorders, including Parkinson’s disease and essential tremor. While clinically heterogeneous, converging evidence suggests a shared brain network may underlie tremor across conditions. Here, we empirically define such a network using four modalities: lesion locations, atrophy patterns, EMG-fMRI, and deep brain stimulation outcomes. We show that network connectivity robustly explains clinical outcomes in independent cohorts undergoing deep brain stimulation of the subthalamic nucleus for Parkinson’s disease and the ventral intermediate nucleus for essential tremor. Maps from each cohort accounted for outcomes in the respective other, supporting a disorder-independent tremor network. A multimodal agreement map revealed consistent substrates in the primary motor cortex and motor cerebellum. To validate the network, we test its predictive power in a third, independent cohort treated with pallidal stimulation for Parkinson’s disease. Our findings define a robust, cross-condition tremor network that may guide both invasive and noninvasive neuromodulation strategies.
Ladattava julkaisu This is an electronic reprint of the original article. |  |
Julkaisussa olevat rahoitustiedot:
Data were provided in part by the Human Connectome Project, WU-Minn Consortium (Principal Investigators: David Van Essen and Kamil Ugurbil; 1U54MH091657) funded by the 16 NIH Institutes and Centers that support the NIH Blueprint for Neuroscience Research; and by the McDonnell Center for Systems Neuroscience at Washington University. The study was funded by Deutsche Forschungsgemeinschaft (DFG, German Research Foundation)—Emmy Noether Stipend 410169619, Project-ID 424778381—TRR 295). L.L.G. was participant in the BIH Charité Junior Clinician Scientist Program funded by the Charité - Universitätsmedizin Berlin and the Berlin Institute of Health at Charité (BIH). L.L.G. and B.H.B. were supported by the Thiemann foundation. P.Z. received support from a scholarship from the Einstein Center for Neurosciences Berlin. J.J. received grants from the Research Council of Finland, Sigrid Juselius Foundation, Finnish Medical Foundation, Sakari Sohlberg’s Foundation, Finnish Foundation for Alcohol Studies, Ane and Signe Gyllenberg Foundation, Finnish Parkinson Foundation, University of Turku (Sigrid Juselius Foundation, Private Donation) and Turku University Hospital (VTR funds); M.D.F. was supported by grants from the NIH (R01MH113929, R21MH126271, R56AG069086, R21NS123813, R01NS127892, R01MH130666, UM1NS132358), Neuronetics, the Kaye Family Research Endowment, the Ellison/Baszucki Family Foundation, and the Manley Family. A.H. was supported by the Schilling Foundation, the German Research Foundation (Deutsche Forschungsgemeinschaft, 424778381—TRR 295), Deutsches Zentrum für Luft- und Raumfahrt (DynaSti grant within the EU Joint Programme Neurodegenerative Disease Research, JPND), the National Institutes of Health (R01MH130666, 1R01NS127892-01, 2R01 MH113929 & UM1NS132358) as well as the New Venture Fund (FFOR Seed Grant).
