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Updated: Sep 8, 2025

A Contusive Model of Unilateral Cervical Spinal Cord Injury Using the Infinite Horizon Impactor
Published on: July 24, 2012
Trunk Neuromuscular Impairment Following Spinal Cord Injury: Insights into Bidirectional and Nonlinear
Abstract:
Spinal cord injury (SCI) leads to disruptions in trunk motion patterns due to alterations in trunk neuromuscular control, with these changes remaining incompletely understood. This study investigates how SCI alters bidirectional and nonlinear trunk corticomuscular coupling (CMC). Seventeen SCI individuals and eighteen healthy controls experienced unexpected sagittal seated perturbations at 70% of their maximal acceptable intensity. Surface electromyography recorded bilateral activity of the pectoralis major, latissimus dorsi, rectus abdominis (RA), and erector spinae (ES). Cortical hemodynamics were simultaneously measured using functional near-infrared spectroscopy over the bilateral prefrontal cortex, primary motor cortex, supplementary motor area (SMA), premotor cortex (PMC), and primary somatosensory cortex. Activation speed and magnitude for both muscles and cortical regions, along with CMC measured by the nonlinear time-delay maximal information coefficient (NTDMIC), were compared between groups. Individuals with SCI showed significantly reduced agonist activation speed and increased antagonist activation speed. During backward perturbations, the activation magnitude of left SMA and right PMC was lower in individuals with SCI than in healthy controls. Meanwhile, individuals with SCI exhibited decreased NTDMIC in agonists and increased NTDMIC in antagonists, both in cortex-to-muscle and muscle-to-cortex directions. In conclusion, SCI disrupts the coordinated neural control of trunk muscles. The results illustrate a complex neuromuscular adaptation involving diminished cortical drive combined with abnormal reliance on descending subcortical pathways and hyper-excitable activation of spinal reflex circuits during demanding perturbations. Targeting cortical neuromodulation shows promise, with the CMC ratio of RA to ES emerging as a potential biomarker of inefficient central compensation after SCI.
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