Evidence map›Paper›PMID 39196311›Full record

ArticleBrain structure & function2024

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

Caroline Heimhofer, Marc Bächinger, Rea Lehner, Stefan Frässle, Joshua Henk Balsters, Nicole Wenderoth

Abstract read
In one paragraph

Article in Brain structure & function, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

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3 · Its place in the literature

Who cites it

4 citing papers in PubMed.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors.

Caroline Heimhofer *Neural Control of Movement Lab, Department of Health Sciences and Technology, ETH Zurich, Gloriastrasse 37/39, Zurich, 8092, Switzerland. caroline.heimhofer@hest.ethz.ch.ORCID http://orcid.org/0009-0006-9591-8202
Marc Bächinger *Neural Control of Movement Lab, Department of Health Sciences and Technology, ETH Zurich, Gloriastrasse 37/39, Zurich, 8092, Switzerland.ORCID http://orcid.org/0000-0002-3726-542X
Rea LehnerNeural Control of Movement Lab, Department of Health Sciences and Technology, ETH Zurich, Gloriastrasse 37/39, Zurich, 8092, Switzerland.ORCID http://orcid.org/0000-0002-6497-2875
Stefan FrässleTranslational Neuromodeling Unit, University of Zurich, ETH Zurich, Zurich, Switzerland.ORCID http://orcid.org/0000-0002-8011-2226
Joshua Henk BalstersDepartment of Psychology, Royal Holloway University of London, Egham, Surrey, UK.ORCID http://orcid.org/0000-0001-9856-6990
Nicole WenderothNeural Control of Movement Lab, Department of Health Sciences and Technology, ETH Zurich, Gloriastrasse 37/39, Zurich, 8092, Switzerland.ORCID http://orcid.org/0000-0002-3246-9386

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

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.

Indexed as

Magnetic Resonance ImagingSensorimotor CortexAdultBrain MappingFatigueFemaleHumansMaleMotor CortexPsychomotor PerformanceYoung AdultDynamic causal modellingFatigueFunctional MRIMotor areasMotor slowingPremotor areas

Identifiers

PMID39196311
PMCPMC11611979

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.