A multi-modal evaluation of experimental pain and psychological function in women with carpometacarpal osteoarthritis.

Objective: Thumb carpometacarpal osteoarthritis (CMC1 OA) is a prevalent and debilitating condition that lacks effective treatments. Understanding the multidimensional pain experience across CMC1 OA disease stages is crucial to improving treatment outcomes. This study examined how radiographic CMC1 OA severity is associated with physical, psychological, and somatosensory function.

Method: Thirty-one women with early-stage (Eaton-Littler 1-2) or end-stage (Eaton-Littler 3-4) radiographic CMC1 OA completed validated questionnaires to assess pain, disability, and psychological function. Additionally, experimental pain was measured in each participant using quantitative sensory testing (QST) (mechanical, pressure, vibratory, thermal) at seven body sites (thenar, hypothenar, brachioradialis bi-laterally; quadriceps on affected side). Cohort differences (early-vs. end-stage) across all variables were analyzed using a multivariable modeling approach that included fixed effects and interactions; notably, age was controlled as a confounder.

Results: End-stage CMC1 OA participants had higher scores in the pain (p ​= ​0.01) and function (p ​= ​0.02) portions of the AUSCAN assessment, self-reported disability of the DASH questionnaire (p ​= ​0.04), and painDETECT scores (p ​= ​0.03), indicating greater pain and disability compared to early-stage participants. Additionally, end-stage CMC1 OA participants demonstrated reduced vibratory detection and heat pain thresholds at multiple body sites (p's ​< ​0.05), with significant interactions observed across the mechanical and cold stimuli.

Conclusion: Findings revealed women with end-stage CMC1 OA exhibited increased neuropathic pain characteristics and somatosensory loss compared to those with early-stage CMC1 OA. These results underscore the importance of addressing both peripheral and centralized pain mechanisms and the need for multimodal approaches in the treatment of CMC1 OA.