Association of nociceptive responsivity with clinical pain and the moderating effect of depression

The role of central sensitization (CS) in clinical pain reported by FMS patients is unclear. In this report, we sought to establish evidence of a prospective association between clinical pain and an objective measure of spinal nociception (nociceptive flexion reflex [NFR] threshold) and explore whether depression moderates this relationship. We collected measures that included the NFR threshold (in the range of 0-60 milliamperes (mA); a lower threshold represents greater nociceptive responsivity) and clinical variables (ie, Fibromyalgia Impact Questionnaire (FIQ)-total, FIQ-pain, depression and current pain intensity) at 3 time points (baseline, weeks 6 and 12). Using linear mixed effects models, clinical variables were treated as time-varying covariates. Across time, current pain intensity [estimate -1.79 mA (.8), P = .03] and the presence of depression [estimate -6.30 mA (3.2), P = .059] were significantly associated with NFR threshold. The interaction of current pain intensity and depression was also significantly associated with NFR threshold. Specifically, the relationship between current pain intensity and NFR threshold was present in the nondepressed group but not in the depressed group (estimate -3.9 versus .07, P = .01). Both FIQ-total and FIQ-pain were not associated with NFR threshold. In conclusion, higher level of clinical pain intensity correlated with greater nociceptive responsivity, and that depression moderated this association.

Given that clinical pain correlated with nociceptive responsiveness, our findings support the mechanistic role of CS in fibromyalgia. If replicated in larger studies, NFR threshold may serve as a biomarker of clinical pain in nondepressed fibromyalgia patients. Also, our results may have future implication for treatment of FMS with and without comorbid depression.