Dynamic causal modelling highlights the importance of decreased self-inhibition of the sensorimotor cortex in motor fatigability.

Dynamic causal modelling Fatigue Functional MRI Motor areas Motor slowing Premotor areas

Journal

Brain structure & function
ISSN: 1863-2661
Titre abrégé: Brain Struct Funct
Pays: Germany
ID NLM: 101282001

Informations de publication

Date de publication:
28 Aug 2024
Historique:
received: 16 01 2024
accepted: 12 07 2024
medline: 28 8 2024
pubmed: 28 8 2024
entrez: 28 8 2024
Statut: aheadofprint

Résumé

Motor fatigability emerges when challenging motor tasks must be maintained over an extended period of time. It is frequently observed in everyday life and affects patients as well as healthy individuals. Motor fatigability can be measured using simple tasks like finger tapping at maximum speed for 30 s. This typically results in a rapid decrease of tapping frequency, a phenomenon called motor slowing. In a previous study (Bächinger et al, eLife, 8 (September), https://doi.org/10.7554/eLife.46750 , 2019), we showed that motor slowing goes hand in hand with a gradual increase in blood oxygen level dependent signal in the primary sensorimotor cortex (SM1), supplementary motor area (SMA), and dorsal premotor cortex (PMd). It is unclear what drives the activity increase in SM1 caused by motor slowing and whether motor fatigability affects the dynamic interactions between SM1, SMA, and PMd. Here, we performed dynamic causal modelling (DCM) on data of 24 healthy young participants collected during functional magnetic resonance imaging to answer this question. The regions of interest (ROI) were defined based on the peak activation within SM1, SMA, and PMd. The model space consisted of bilateral connections between all ROI, with intrinsic self-modulation as inhibitory, and driving inputs set to premotor areas. Our findings revealed that motor slowing was associated with a significant reduction in SM1 self-inhibition, as uncovered by testing the maximum à posteriori against 0 (t(23)=-4.51, p < 0.001). Additionally, the model revealed a significant decrease in the driving input to premotor areas (t(23) > 2.71, p < 0.05) suggesting that structures other than cortical motor areas may contribute to motor fatigability.

Identifiants

pubmed: 39196311
doi: 10.1007/s00429-024-02840-1
pii: 10.1007/s00429-024-02840-1
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Informations de copyright

© 2024. The Author(s).

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Auteurs

Caroline Heimhofer (C)

Neural Control of Movement Lab, Department of Health Sciences and Technology, ETH Zurich, Gloriastrasse 37/39, Zurich, 8092, Switzerland. caroline.heimhofer@hest.ethz.ch.
Neuroscience Center Zurich (ZNZ), University of Zurich, ETH Zurich, University and Balgrist Hospital Zurich, Zurich, Switzerland. caroline.heimhofer@hest.ethz.ch.

Marc Bächinger (M)

Neural Control of Movement Lab, Department of Health Sciences and Technology, ETH Zurich, Gloriastrasse 37/39, Zurich, 8092, Switzerland.

Rea Lehner (R)

Neural Control of Movement Lab, Department of Health Sciences and Technology, ETH Zurich, Gloriastrasse 37/39, Zurich, 8092, Switzerland.

Stefan Frässle (S)

Translational Neuromodeling Unit, University of Zurich, ETH Zurich, Zurich, Switzerland.

Joshua Henk Balsters (J)

Department of Psychology, Royal Holloway University of London, Egham, Surrey, UK.

Nicole Wenderoth (N)

Neural Control of Movement Lab, Department of Health Sciences and Technology, ETH Zurich, Gloriastrasse 37/39, Zurich, 8092, Switzerland.
Neuroscience Center Zurich (ZNZ), University of Zurich, ETH Zurich, University and Balgrist Hospital Zurich, Zurich, Switzerland.
Future Health Technologies, Singapore-ETH Centre, Campus for Research Excellence and Technological Enterprise (CREATE), Singapore, Singapore.

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