Evidence map›Paper›PMID 40505828›Full record

ArticleExperimental neurology2025

Interactions between descending and spinal circuits on motor output.

G Taccola, A G Steele, R Apicella, J Oh, V Dietz, S Rajendran, S M Barber, A H Faraji, P J Horner, D G Sayenko

Abstract read
In one paragraph

Article in Experimental neurology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. 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

10 authors.

G TaccolaCenter for Neuroregeneration, Houston Methodist Research Institute, 6670 Bertner Ave, Houston, TX 77030, United States of America; Department of Neurosurgery, Center for Neural Systems Restoration, Houston Methodist Hospital, 6550 Fannin Street, Houston, Texas 77030, United States of America; Neuroscience Department, International School for Advanced Studies (SISSA), via Bonomea, 265 - 34136 Trieste, Italy.
A G SteeleCenter for Neuroregeneration, Houston Methodist Research Institute, 6670 Bertner Ave, Houston, TX 77030, United States of America; Department of Neurosurgery, Center for Neural Systems Restoration, Houston Methodist Hospital, 6550 Fannin Street, Houston, Texas 77030, United States of America.
R ApicellaCenter for Neuroregeneration, Houston Methodist Research Institute, 6670 Bertner Ave, Houston, TX 77030, United States of America; Neuroscience Department, International School for Advanced Studies (SISSA), via Bonomea, 265 - 34136 Trieste, Italy.
J OhCenter for Neuroregeneration, Houston Methodist Research Institute, 6670 Bertner Ave, Houston, TX 77030, United States of America; Department of Neurosurgery, Center for Neural Systems Restoration, Houston Methodist Hospital, 6550 Fannin Street, Houston, Texas 77030, United States of America.
V DietzCenter for Neuroregeneration, Houston Methodist Research Institute, 6670 Bertner Ave, Houston, TX 77030, United States of America; Department of Neurosurgery, Center for Neural Systems Restoration, Houston Methodist Hospital, 6550 Fannin Street, Houston, Texas 77030, United States of America.
S RajendranCenter for Neuroregeneration, Houston Methodist Research Institute, 6670 Bertner Ave, Houston, TX 77030, United States of America; Department of Neurosurgery, Center for Neural Systems Restoration, Houston Methodist Hospital, 6550 Fannin Street, Houston, Texas 77030, United States of America.
S M BarberCenter for Neuroregeneration, Houston Methodist Research Institute, 6670 Bertner Ave, Houston, TX 77030, United States of America; Department of Neurosurgery, Center for Neural Systems Restoration, Houston Methodist Hospital, 6550 Fannin Street, Houston, Texas 77030, United States of America.
A H FarajiCenter for Neuroregeneration, Houston Methodist Research Institute, 6670 Bertner Ave, Houston, TX 77030, United States of America; Department of Neurosurgery, Center for Neural Systems Restoration, Houston Methodist Hospital, 6550 Fannin Street, Houston, Texas 77030, United States of America.
P J HornerCenter for Neuroregeneration, Houston Methodist Research Institute, 6670 Bertner Ave, Houston, TX 77030, United States of America; Department of Neurosurgery, Center for Neural Systems Restoration, Houston Methodist Hospital, 6550 Fannin Street, Houston, Texas 77030, United States of America.
D G SayenkoCenter for Neuroregeneration, Houston Methodist Research Institute, 6670 Bertner Ave, Houston, TX 77030, United States of America; Department of Neurosurgery, Center for Neural Systems Restoration, Houston Methodist Hospital, 6550 Fannin Street, Houston, Texas 77030, United States of America. Electronic address: dgsayenko@houstonmethodist.org.

Funding

Harnessing Neuroplasticity of Postural Sensorimotor Networks Using Non-Invasive Spinal Neuromodulation to Maximize Functional Recovery After Spinal Cord InjuryR01NS119587 · NINDS · METHODIST HOSPITAL RESEARCH INSTITUTE · PI Dimitry Sayenko · 2022 to 2026
$3.2M
NINDS NIH HHS R01 NS119587
6 · The paper itself

Abstract

introductionSupraspinal influence on spinal networks remains incompletely understood yet is crucial for restoring motor function after neurological insults, including spinal cord injury or stroke. Neuromodulation interventions have been employed with varying success to aid recovery and can be utilized to investigate the relationship between supraspinal and spinal networks. MATERIAL AND

methodsWe elicited hindlimb muscle responses by motor cortex stimulation paired with either epidural or transcutaneous spinal stimulation in neurologically intact Long-Evans rats and Yucatan miniature pigs.

resultsOur findings indicate that modulation of sensorimotor networks using the two stimulation modalities varies with the intensity of spinal stimulation. Specifically, spinal stimulation at near-motor-threshold levels modulates the magnitude of the weak descending volleys, with pronounced increases in compound motor evoked potential magnitude of up to 400-500 %. As spinal stimulation intensity increased, we observed a transition from modulated cortically evoked motor responses toward modulated spinally evoked motor responses. However, when the intensity of spinal stimulation exceeded the supra-motor-threshold, the conditioned responses were abolished. We also examined the effects of timing between paired cortical and spinal stimulation and found that the highest modulation occurred when delivering spinal stimulation using a latency approximately equal to the central conduction time of cortical stimulation.

conclusionThe capacity of cortical stimulation to modulate the effects of spinal modulation can be described as a convergence of supraspinal and spinal networks on the motor pathway. Overall, our results suggest potential stimulation strategies that capitalize on supraspinal-spinal interactions without the need for targeting individual motor pools with focal spinal stimulation.

Indexed as

Evoked Potentials, MotorMotor CortexSpinal CordAnimalsElectric StimulationElectromyographyFemaleHindlimbMaleMuscle, SkeletalRatsRats, Long-EvansSpinal Cord StimulationSwineSwine, MiniatureMotor controlNeuromodulationSpinal cord stimulationTranscranial magnetic stimulation

Identifiers

PMID40505828
PMCPMC12225539

What OpenQuestion holds

Textmetadata
LicenceTDM
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.