# Comparative Analysis of Pain Perception, Corticomotor Excitability, Disability, and Cognitive Function in Chronic Low Back Pain Patients and Age-Matched Healthy Controls

## TL;DR

This study compares chronic low back pain patients and healthy controls, finding significant differences in pain perception, motor system function, and cognitive abilities.

## Contribution

The study provides empirical evidence of central nervous system alterations in chronic low back pain patients through corticomotor excitability and cognitive function assessments.

## Key findings

- CLBP patients had higher RMT% and lower MEP amplitude compared to controls.
- CLBP patients showed significantly worse cognitive performance and prolonged ERP P300 latency.
- VAS and MODI scores were markedly elevated in CLBP patients compared to controls.

## Abstract

Background and introduction

Chronic low back pain (CLBP) is a common, disabling condition with a multifactorial aetiology that extends beyond nociceptive dysfunction. Among the Indian population, low backache is a significant contributor to years lived with disability (YLD). Recent evidence suggests that CLBP can cause significant alterations in central nervous system functioning and neuroplasticity, via deficits in intracortical modulation involving glutamatergic and gamma-aminobutyric acid (GABA)-mediated mechanisms. Understanding the broader impact of CLBP and its effects on the nervous system - particularly the motor system and cognition - is essential for developing comprehensive treatment strategies and evolving appropriate diagnostic and prognostic tools that extend beyond pain management.

Objective

The main objective of this study is to compare pain perception, disability, corticomotor excitability, and cognitive functions between patients with CLBP and age-matched healthy controls, to explore central nervous system alterations associated with CLBP.

Methodology

A total of 116 participants were enrolled, including 58 CLBP patients and 58 age- and gender-matched healthy controls. Pain intensity and disability were assessed using the Visual Analogue Scale (VAS) and the Modified Oswestry Disability Index (MODI), respectively. Corticomotor excitability was assessed using transcranial magnetic stimulation (TMS), which measured the resting motor threshold (RMT%) as a percentage of maximum stimulator output, and the motor evoked potential (MEP) amplitude in microvolts (µV). Cognitive function was assessed using the Self-Administered Gero-cognitive Examination (SAGE) score and event-related potential (ERP) P300. The P300 was measured for its latency (in milliseconds) and amplitude (in microvolts). The Mann-Whitney U test was used for statistical comparison between groups.

Results

CLBP patients showed significantly higher RMT% (median = 55%, interquartile range (IQR) = 15) and lower MEP amplitude (median = 144 µV, IQR = 218.75) compared to controls (median = 50%, IQR = 5, and median = 294.5 µV, IQR = 287) (p < 0.001). VAS and MODI scores were markedly elevated in the CLBP group (median = 6, IQR = 2, and median = 11.5, IQR = 9) versus 0 in controls (p < 0.001). Cognitive performance, as measured by SAGE, was significantly lower in patients with CLBP (median = 17, IQR = 4) than in controls (median = 19.5, IQR = 3) (p < 0.001). ERP results revealed prolonged P300 latency (median = 341 ms, IQR = 33.75) versus (median = 290 ms, IQR = 35.75) and reduced amplitude (median = 7.3 µV, IQR = 5.67) versus (median = 12.45 µV, IQR = 6.77) in the CLBP group (p < 0.001), as compared to healthy controls.

Conclusion

CLBP is associated with alterations in central nervous system functioning, with significant changes observed in corticomotor excitability, increased disability, and decreased cognitive function, along with delayed and diminished neurophysiological responses. A comprehensive, multidisciplinary treatment approach targeting both peripheral and central mechanisms - including neurocognitive rehabilitation - is required for chronic pain management.