Assessment of exercise‐induced hypoalgesia in chronic low back pain and potential associations with psychological factors and central sensitization symptoms: A case–control study

Abstract

Introduction: Exercise is the most recommended treatment for chronic low back pain (CLBP) and is effective in reducing pain, but the mechanisms underlying its effects remain poorly understood. Exercise-induced hypoalgesia (EIH) may play a role and is thought to be driven by central pain modulation mechanisms. However, EIH appears to be disrupted in many chronic pain conditions and its presence in people with CLBP remains unclear. As people suffering from chronic pain often exhibit psychological factors and central sensitization symptoms influencing pain perception, EIH might be associated with these factors. Objective: The aim of this study is to compare the level of EIH between participants with and without CLBP following back and wrist exercises and to assess the associations between EIH, psychological factors, and symptoms of central sensitization (using the central sensitization inventory -CSI) in CLBP. Method: Twenty-eight participants with CLBP and 23 without pain were recruited. Pressure pain thresholds (PPT) were measured at 4 sites (2 bony sites = capitate, S1|2 muscle sites = wrist flexors, lumbar erector spinae) before and after each of two exercises (wrist flexion and lumbar extension). Exercise-induced hypoalgesia was defined as percent change in PPT from pre-to post-exercise. Participants with CLBP also completed questionnaires to measure psychological factors (e.g., kinesiophobia, catastrophizing, anxiety, and self-efficacy) and symptoms of central sensitization (CSI), and correlations with EIH were calculated. Results: After wrist exercise, EIH measured at the muscle sites was lower in the CLBP group compared with the pain-free group (p = 0.047) but no differences were found at bony sites (p = 0.49). No significant differences for EIH were observed following back exercise at muscle sites (p = 0.14) or at bony sites (p = 0.65). Exerciseinduced hypoalgesia was not correlated with any psychological factors or with the CSI score. Conclusion:The lower EIH following wrist exercises may represent an alteration in pain modulation control in CLBP. However, psychological factors and central sensitization symptoms may not explain the differences observed.

Alterations in functional connectivity in patients with non-specific chronic low back pain after motor control exercise: a randomized trial

“… 44 The decreased rsFC between the cerebellum and superior parietal gyrus might account for the lower over-responsiveness to sensory inputs in patients with CLBP after exercise. 45 Interestingly, the reduced rsFC of the right posterior cerebellum-left insula after MCE was significantly positively associated with the ODI scores. As mentioned previously, posterior lobules are activated during the anticipation of pain, 40 but Crus II is exceptional; it may also participate in pain and motor processing and motion control.…”

Low back pain self-management mobile applications: a systematic review on digital platforms

“…Furthermore, it results in absenteeism, decreased labor productivity and socioeconomic impacts ( 6 ) , and its prevalence continues to increase. CLBP, previously seen as a symptom of an underlying condition, is now recognized in the International Classification of Diseases as a primary disease with multiple interacting factors, including biological, psychological and social aspects ( 7 ) .…”

Within-Session Test-Retest Reliability of Pressure Pain Threshold and Mechanical Temporal Summation in Chronic Low Back Pain

“…6 Potential alteration in these brain areas could explain the lower efficacy of pain modulation in participants with CLBP measured through psychophysical paradigms, such as conditioned pain modulation (CPM) 7 or exercise-induced hypoalgesia (EIH). [8][9][10] Indeed, EIH and CPM involve pain modulation systems, such as the opioidergic system, which are known to produce antinociceptive effects. [11][12][13][14][15] CPM represents the decrease in pain sensitivity after a painful stimulus on a remote body part (eg, the cold pressor task-cold water immersion of a limb as conditioning stimulus).…”

“…For example, brain areas involved in pain processing and modulation, such as the thalamus, the primary somatosensory cortex, and the periaqueductal gray, differ in CLBP compared with pain-free controls 6. Potential alteration in these brain areas could explain the lower efficacy of pain modulation in participants with CLBP measured through psychophysical paradigms, such as conditioned pain modulation (CPM) 7 or exercise-induced hypoalgesia (EIH) 8–10. Indeed, EIH and CPM involve pain modulation systems, such as the opioidergic system, which are known to produce antinociceptive effects 11–15.…”