Kristian Kjaer Petersen1,2, Ole Simonsen3,4, Anne Estrup Olesen3,5, Carsten Dahl Mørch1,2, Lars Arendt-Nielsen1. 1. SMI, Department of Health Science and Technology, School of Medicine, Aalborg University, Aalborg, Denmark. 2. Center for Neuroplasticity and Pain, Department of Health Science and Technology, School of Medicine, Aalborg University, Aalborg, Denmark. 3. Department of Clinical Medicine, Aalborg University, Aalborg, Denmark. 4. Department of Orthopedic Surgery, Aalborg University Hospital, Aalborg, Denmark. 5. Department of Clinical Pharmacology, Aalborg University Hospital, Aalborg, Denmark.
Abstract
BACKGROUND: Conditioned pain modulation (CPM) and offset analgesia are different features of descending pain inhibition. This study investigated CPM, offset analgesia and clinical pain measures in patients with knee osteoarthritis (KOA) before and after treatment with the combination of a non-steroidal anti-inflammatory drug (NSAIDs) plus acetaminophen. METHODS: Forty-two patients with KOA received Ibuprofen 1.2 g/daily and acetaminophen 3.0 g/daily for three weeks. Before administration, CPM magnitude was assessed as the difference between cuff pain detection (cPDT) with and without a conditioning stimulus (evoked by tourniquet pain). Offset analgesia was assessed as the pain intensities evoked by a constant 46°C for 30-s stimulus compared to an offset analgesia paradigm of 46°C for 5-s, 47°C for 5-s and 46°C for 20-s. The worst pain within the last 24-hr and pain during activity were assessed before and after treatment. RESULTS: Clinical pain significantly decreased after treatment (p < 0.001) and less efficient CPM before treatment was associated with weaker analgesic effect (R = 0.354, p = 0.043). No significant modulation of CPM or offset analgesia was found for the treatment. CONCLUSION: This study found that less efficient CPM is associated with reduced analgesic effect of NSAIDs plus acetaminophen in patients with KOA whereas the treatment did not modulate CPM nor offset analgesia magnitude. SIGNIFICANCE: This study demonstrated that conditioned pain modulation is correlated with the response to a standard pharmaceutical interventions treating osteoarthritis pain. Furthermore, we demonstrated that a decrease in clinical pain intensity is not associated with a normalization of conditioned pain modulation or offset analgesia, which questions if restoring these descending pain inhibitory mechanisms are pain intensity driven.
BACKGROUND: Conditioned pain modulation (CPM) and offset analgesia are different features of descending pain inhibition. This study investigated CPM, offset analgesia and clinical pain measures in patients with knee osteoarthritis (KOA) before and after treatment with the combination of a non-steroidal anti-inflammatory drug (NSAIDs) plus acetaminophen. METHODS: Forty-two patients with KOA received Ibuprofen 1.2 g/daily and acetaminophen 3.0 g/daily for three weeks. Before administration, CPM magnitude was assessed as the difference between cuff pain detection (cPDT) with and without a conditioning stimulus (evoked by tourniquet pain). Offset analgesia was assessed as the pain intensities evoked by a constant 46°C for 30-s stimulus compared to an offset analgesia paradigm of 46°C for 5-s, 47°C for 5-s and 46°C for 20-s. The worst pain within the last 24-hr and pain during activity were assessed before and after treatment. RESULTS: Clinical pain significantly decreased after treatment (p < 0.001) and less efficient CPM before treatment was associated with weaker analgesic effect (R = 0.354, p = 0.043). No significant modulation of CPM or offset analgesia was found for the treatment. CONCLUSION: This study found that less efficient CPM is associated with reduced analgesic effect of NSAIDs plus acetaminophen in patients with KOA whereas the treatment did not modulate CPM nor offset analgesia magnitude. SIGNIFICANCE: This study demonstrated that conditioned pain modulation is correlated with the response to a standard pharmaceutical interventions treating osteoarthritis pain. Furthermore, we demonstrated that a decrease in clinical pain intensity is not associated with a normalization of conditioned pain modulation or offset analgesia, which questions if restoring these descending pain inhibitory mechanisms are pain intensity driven.
Authors: Andrew C Heisler; Jing Song; Lutfiyya N Muhammad; Alyssa Wohlfahrt; Wendy Marder; Marcy B Bolster; Clifton O Bingham; Daniel J Clauw; Dorothy D Dunlop; Tuhina Neogi; Yvonne C Lee Journal: Arthritis Rheumatol Date: 2020-11-04 Impact factor: 10.995
Authors: Luis Matesanz-García; Ferran Cuenca-Martínez; Ana Isabel Simón; David Cecilia; Carlos Goicoechea-García; Josué Fernández-Carnero; Annina B Schmid Journal: J Clin Med Date: 2022-02-18 Impact factor: 4.964