Variability in conditioned pain modulation predicts response to NSAID treatment in patients with knee osteoarthritis

• Published in: BMC musculoskeletal disorders 2016-07, Vol.17 (1), p.284-284, Article 284
• Main Authors: Edwards, Robert R, Dolman, Andrew J, Martel, Marc O, Finan, Patrick H, Lazaridou, Asimina, Cornelius, Marise, Wasan, Ajay D
• Format: Article
• Language: English
• Subjects: Administration, Topical; Anti-Inflammatory Agents, Non-Steroidal - administration & dosage; Anti-Inflammatory Agents, Non-Steroidal - therapeutic use; Care and treatment; Case-Control Studies; Complications and side effects; Diclofenac - administration & dosage; Diclofenac - therapeutic use; Disability; Female; Gels; Humans; Hyperalgesia - drug therapy; Inflammation; Male; Middle Aged; Osteoarthritis; Osteoarthritis, Knee - complications; Osteoarthritis, Knee - drug therapy; Pain - etiology; Pain Management - methods; Pain Measurement; Pain Threshold - drug effects; Risk factors; Treatment Outcome
• ISSN: 1471-2474; 1471-2474
• DOI: 10.1186/s12891-016-1124-6

Patients with painful knee osteoarthritis (OA) demonstrate hyperalgesia and altered pain-modulatory responses. While some prior work has demonstrated cross-sectional associations between laboratory and clinical pain measures, it is unknown whether individual variability in quantitative sensory testing (QST) responses at baseline can prospectively predict analgesic treatment responses. Patients with knee OA (n = 35) were compared on QST responses to a demographically-matched pain-free control group (n = 39), after which patients completed a month-long treatment study of diclofenac sodium topical gel (1 %), applied up to 4 times daily. OA patients demonstrated reduced pain thresholds at multiple anatomic sites, as well as reduced conditioned pain modulation (CPM) and enhanced temporal summation of pain. The most pain-sensitive patients tended to report the most intense and neuropathic OA pain. Following diclofenac treatment, the knee OA cohort showed a roughly 30 % improvement in pain, regardless of the presence or absence of neuropathic symptoms. Baseline CPM scores, an index of endogenous pain-inhibitory capacity, were prospectively associated with treatment-related changes in clinical pain. Specifically, participants with higher CPM at baseline (i.e., better functioning endogenous pain-inhibitory systems) showed more reduction in pain at the end of treatment (p