Evidence map›Paper›PMID 41063967›Full record

ArticleBrain communications2025

Reduced beta bursting underpins loss of corticomuscular coherence in amyotrophic lateral sclerosis.

Katie Yoganathan, Michael Trubshaw, Oliver Kohl, Chetan Gohil, Irene Echeverria-Altuna, Thanuja Dharmadasa, Alicia Northall, Nahid Zokaei, David Lester, Gayle Garcia and 7 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Brain communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

3 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
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

17 authors.

Katie YoganathanNuffield Department of Clinical Neurosciences, University of Oxford, Oxford OX3 9DU, UK.
Michael TrubshawNuffield Department of Clinical Neurosciences, University of Oxford, Oxford OX3 9DU, UK.ORCID https://orcid.org/0000-0002-4848-6156
Oliver KohlOxford Centre for Human Brain Activity, Wellcome Centre for Integrative Neuroimaging, Department of Psychiatry, University of Oxford, Oxford OX3 7JX, UK.ORCID https://orcid.org/0000-0003-3166-8145
Chetan GohilOxford Centre for Human Brain Activity, Wellcome Centre for Integrative Neuroimaging, Department of Psychiatry, University of Oxford, Oxford OX3 7JX, UK.ORCID https://orcid.org/0000-0002-0888-1207
Irene Echeverria-AltunaOxford Centre for Human Brain Activity, Wellcome Centre for Integrative Neuroimaging, Department of Psychiatry, University of Oxford, Oxford OX3 7JX, UK.
Thanuja DharmadasaNuffield Department of Clinical Neurosciences, University of Oxford, Oxford OX3 9DU, UK.
Alicia NorthallOxford Centre for Human Brain Activity, Wellcome Centre for Integrative Neuroimaging, Department of Psychiatry, University of Oxford, Oxford OX3 7JX, UK.ORCID https://orcid.org/0000-0002-5435-7916
Nahid ZokaeiOxford Centre for Human Brain Activity, Wellcome Centre for Integrative Neuroimaging, Department of Psychiatry, University of Oxford, Oxford OX3 7JX, UK.ORCID https://orcid.org/0000-0003-1399-3809
David LesterNuffield Department of Clinical Neurosciences, University of Oxford, Oxford OX3 9DU, UK.
Gayle GarciaNuffield Department of Clinical Neurosciences, University of Oxford, Oxford OX3 9DU, UK.
Alexis CollinsNuffield Department of Clinical Neurosciences, University of Oxford, Oxford OX3 9DU, UK.
Benazir AmeinNuffield Department of Clinical Neurosciences, University of Oxford, Oxford OX3 9DU, UK.
Anna C NobreOxford Centre for Human Brain Activity, Wellcome Centre for Integrative Neuroimaging, Department of Psychiatry, University of Oxford, Oxford OX3 7JX, UK.
Kevin TalbotNuffield Department of Clinical Neurosciences, University of Oxford, Oxford OX3 9DU, UK.ORCID https://orcid.org/0000-0001-5490-1697
Alexander G ThompsonNuffield Department of Clinical Neurosciences, University of Oxford, Oxford OX3 9DU, UK.ORCID https://orcid.org/0000-0003-1063-3277
Mark WoolrichOxford Centre for Human Brain Activity, Wellcome Centre for Integrative Neuroimaging, Department of Psychiatry, University of Oxford, Oxford OX3 7JX, UK.
Martin R TurnerNuffield Department of Clinical Neurosciences, University of Oxford, Oxford OX3 9DU, UK.ORCID https://orcid.org/0000-0003-0267-3180

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Biomarkers of disease activity that holistically capture motor system dysfunction are needed to accelerate drug discovery in amyotrophic lateral sclerosis. Magnetoencephalography is a sensitive, non-invasive measure of cortical neurophysiology. Corticomuscular coherence reflects the functional coupling of cortical oscillations with downstream muscle activity recorded by electromyography. Cortical beta frequency bursting is known to represent a core feature of the neurophysiology underpinning movement. This study aimed to characterize disruption of beta frequency activity in both cortex and muscle to refine the understanding of corticomuscular coherence loss in amyotrophic lateral sclerosis. The study analysed 42 people living with amyotrophic lateral sclerosis and 33 healthy age-matched controls. Participants undertook an isometric hand gripping task during magnetoencephalography. Muscle contraction was measured using bipolar surface electromyography recordings at both forearms. All participants performed 120 trials of the gripper task bilaterally, and 60 trials unilaterally on each side. For each trial type, the mean corticomuscular coherence over trials was calculated for each participant and the groups were compared via cluster-based permutations tests. Beta burst metrics were calculated for the motor cortex (magnetoencephalography) and flexor forearm muscles (surface electromyography) including burst fractional occupancy, burst duration and amplitude. During muscular contraction, beta frequency corticomuscular coherence from the motor cortices contralateral to the gripper task was markedly reduced in amyotrophic lateral sclerosis patients, despite no significant difference in grip strength compared with controls. Source localization analysis showed globally reduced corticomuscular coherence in amyotrophic lateral sclerosis with significant differences in the motor regions contralateral to the engaged hand. There were no significant beta frequency activity changes in the engaged-hand electromyography signal in amyotrophic lateral sclerosis compared with controls. In contrast, analysis of the cortical motor regions revealed reduced rate of beta bursting and higher amplitude during the contraction phase of the task in amyotrophic lateral sclerosis. The corticomuscular coherence disruption in amyotrophic lateral sclerosis appears driven more by cerebral pathology than by muscle denervation. Equal grip strength during the task implies compensatory pathways in disease that are not captured by corticomuscular coherence. Interneuronal dysfunction may underlie the disruption to motor cortex beta bursting. Motor cortical beta frequency metrics have potential as secondary outcome measures in therapeutic trials and need exploration as prodromal markers in asymptomatic individuals genetically predisposed to amyotrophic lateral sclerosis.

Indexed as

beta burstsbeta oscillationscoherencemagnetoencephalographyMEG

Identifiers

PMID41063967
PMCPMC12501500

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.