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Motor cortex excitability in chronic low back pain.

E J Corti1,2, W Marinovic3,4, A T Nguyen3,4

  • 1School of Population Health, Curtin University, GPO Box U1987, Perth, WA, 6845, Australia. Emily.corti@curtin.edu.au.

Experimental Brain Research
|October 26, 2022
PubMed
Summary
This summary is machine-generated.

Chronic lower back pain (CLBP) is linked to reduced motor cortex excitability and impaired intracortical facilitation. These findings suggest deficits in glutamatergic mechanisms contribute to CLBP.

Keywords:
Chronic lower back painExcitabilityIntracortical facilitationMotor cortexTranscranial magnetic stimulation

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Area of Science:

  • Neuroscience
  • Pain Research
  • Motor Control

Background:

  • Chronic pain, particularly Chronic Lower Back Pain (CLBP), is associated with altered cortical excitability.
  • Previous research on intracortical motor cortex changes in CLBP has yielded inconsistent results.
  • Understanding specific intracortical alterations is crucial for developing targeted therapies.

Purpose of the Study:

  • To investigate intracortical excitability of the primary motor cortex in individuals with CLBP.
  • To identify specific changes in motor cortex function associated with CLBP using transcranial magnetic stimulation (TMS).

Main Methods:

  • A case-control study involving 20 participants with CLBP and 18 pain-free controls.
  • Transcranial magnetic stimulation (TMS) applied to the hand motor area of the right hemisphere.
  • Measurement of resting motor threshold (rMT), motor evoked potential (MEP) amplitude, short interval intracortical inhibition (SICI), and intracortical facilitation (ICF).

Main Results:

  • Individuals with CLBP exhibited significantly higher rMT, indicating decreased corticospinal excitability.
  • Lower intracortical facilitation (ICF) was observed in the CLBP group compared to controls.
  • No significant differences were found in MEP amplitude or SICI between groups.

Conclusions:

  • CLBP is associated with reduced corticospinal excitability and impaired intracortical facilitation.
  • Findings suggest deficits in intracortical modulation, potentially involving glutamatergic mechanisms, are linked to CLBP.
  • Further research is warranted to explore the role of glutamatergic pathways in CLBP pathophysiology.