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Updated: May 25, 2026

Evaluating Postural Control and Lower-extremity Muscle Activation in Individuals with Chronic Ankle Instability
Published on: September 18, 2020
Corticomotor control of deep abdominal muscles in chronic low back pain and anticipatory postural adjustments
Hugo Massé-Alarie1, Véronique H Flamand, Hélène Moffet
1Laboratory of clinical neuroscience and neurostimulation, Neuroscience Unit, CHUQ Research Center, Université Laval (Rehabilitation Dept), RC-9800, 2705 boul. Laurier, Québec, QC G1V 4G2, Canada.
Abstract:
Contralateral transversus abdominis muscle (cTrA) is known to be anticipatory to rapid focal movement. The activation of ipsilateral TrA (iTrA) follows cTrA, but their anticipatory interaction in healthy subjects seems to be delayed in low back pain (LBP) patients. TrA delay in LBP is linked with reorganization of the primary motor cortex (M1), thus supporting that cortical changes underlie the altered postural control. Our study tested whether differences in postural adjustments were present in LBP for TrA onsets and co-activation, and whether these differences were paralleled by cortical motor changes. Thirteen chronic LBP patients and 9 healthy Controls were enrolled. Surface recordings of cTrA/internal oblique (IO) and iTrA/IO were collected during a rapid shoulder flexion task while standing. Transcranial magnetic stimulation of M1 tested TrA/IO corticospinal excitability, active motor threshold and short-interval intracortical inhibition (SICI). In LBP compared to Controls, iTrA/IO activation was delayed, co-activation was absent, timing between TrA/IO onsets was impaired, and SICI was missing. Between-outcomes correlations observed in one group were not significant in the other. Delay of iTrA/IO and the lacking co-activation were not explained by between-group differences of transcranial magnetic stimulation outcomes. TrA/IO co-activation is present during rapid focal movement in healthy subjects only. LBP patients displayed an important alteration of the control of spine stability that can be explained by altered mechanisms of M1 motor programming.
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