Motor cortex excitability in chronic low back pain

Chronic pain is associated with dysfunctional cortical excitability. Research has identified altered intracortical motor cortex excitability in Chronic Lower Back Pain (CLBP). However, research identifying the specific intracortical changes underlying CLBP has been met with inconsistent findings. In...

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Bibliographic Details
Published inExperimental brain research Vol. 240; no. 12; pp. 3249 - 3257
Main Authors Corti, E. J., Marinovic, W., Nguyen, A. T., Gasson, N., Loftus, A. M.
Format Journal Article
LanguageEnglish
Published Berlin/Heidelberg Springer Berlin Heidelberg 01.12.2022
Springer
Springer Nature B.V
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Summary:Chronic pain is associated with dysfunctional cortical excitability. Research has identified altered intracortical motor cortex excitability in Chronic Lower Back Pain (CLBP). However, research identifying the specific intracortical changes underlying CLBP has been met with inconsistent findings. In the present case–control study, we examined intracortical excitability of the primary motor cortex using transcranial magnetic stimulation (TMS) in individuals with CLBP. Twenty participants with CLBP ( M age  = 54.45 years, SD age  = 15.89 years) and 18 age- and gender-matched, pain-free controls ( M  = 53.83, SD  = 16.72) were included in this study. TMS was applied to the hand motor area of the right hemisphere and motor evoked potentials (MEPs) were recorded from the first dorsal interosseous muscle of the contralateral hand. Resting motor threshold (rMT) and MEP amplitude were measured using single-pulse stimulation. Short interval intracortical inhibition (SICI) and intracortical facilitation (ICF) were assessed using paired-pulse stimulation. Individuals with CLBP had significantly higher rMT (decreased corticospinal excitability) and lower ICF compared to controls. No significant differences were found in MEP amplitude and SICI. These findings add to the growing body of evidence that CLBP is associated with deficits in intracortical modulation involving glutamatergic mechanisms.
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Communicated by Winston D Byblow.
ISSN:0014-4819
1432-1106
DOI:10.1007/s00221-022-06492-7