Background & Aims

Low back pain (LBP) is a disabling condition with an estimated 80% lifetime prevalence and increasing global rate [1, 2]. While most acute cases improve, roughly one out of four LBP cases develop into chronicity with no identifiable cause [3]. Recent studies have employed transcranial magnetic stimulation (TMS) methods to investigate changes in corticomotor excitability in the context of chronic pain. By measuring corticomotor activity in the periphery through electromyography (EMG), researchers have identified abnormal corticomotor excitability in experimental acute and chronic pain [4, 5]. However, it is unknown whether sustained alterations in cortical excitability are associated with pain maintenance and/or severity. We aimed to examine whether abnormal corticomotor excitability was associated with pain chronicity and severity.

Methods

We hypothesized that corticomotor excitability would be reduced in those whose pain persisted for more than three months (chronic LBP; cLBP) compared to those that recovered (acute LBP; aLBP) over a six-month period. Using longitudinal data obtained from the UPWaRD (Understanding persistent Pain Where it ResiDes) study, we visually identified and statistically analyzed motor-evoked potentials (MEPs), cortical silent periods (CSPs), post-CSP bursts, and burst silent periods across three sessions (baseline, three-months, six-months). Pain and disability questionnaires were scored and correlated with cortical excitability.

Results

The results showed high intra-individual consistency, meaning no significant difference between sessions was detected between subjects. Compared to the aLBP cohort (n = 5), participants with cLBP (n = 5) displayed reduced MEP amplitudes (t =2.820, 95% CI [.005, .036]) and later MEP onsets (t = -.428, 95% CI [-.009, .006]) across all sessions. For cLBP patients, reduced MEPs correlated with worsened pain severity (r = -.3808, 95% CI [-.7473, 0.1634]) and disability (r=.6189, 95% CI [-.0768, .9093]). Similar associations were observed with late MEP onsets (disability: r=.2399; 95% CI [-.3105, .6698]) and attenuated MEP durations (severity: r = .5358, 95% CI [-.0395, .8714]); disability: r = .6848, 95% CI [.0380, .9272]).

Conclusions

The preliminary findings suggest an association between reduced corticomotor excitability and the progression from aLBP to cLBP. Further studies with larger samples are needed to confirm these findings.

References

1.Andersson, G. B. (1998). Acta Orthopaedica Scandinavica, 69(sup281).
2.Ferreira, M. L. et al., (2023). The Lancet Rheumatology, 5(6).
3.Meucci, R. D. et al., (2015). Revista de saude publica, 49.
4.Dubé, J. A., & Mercier, C. (2011). Clinical neurophysiology, 122(11).
5.Cavaleri, R. et al., (2021). Pain Medicine, 22(6).

Presenting Author

Thu Pham

Poster Authors

Thu Pham

University of Western Ontario

Lead Author

E-mail

Nafisa Diya

University of Western Ontario

Lead Author

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Negar Narskhani

University of Western Ontario

Lead Author

E-mail

Nahian Chowdhury

PhD

University of Sydney

Lead Author

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Siobhan Schabrun

University of Western Ontario

Lead Author

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Wei-Ju Chang

PhD

University of Newcastle

Lead Author

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Topics

  • Models: Transition to Chronic Pain