Wednesday, September 21st
Plenary Lecture | Virtual Program
Plenary Room (Exhibit Halls F/G)
Mechanisms and Manifestations in Musculoskeletal Pain – from Experimental to Clinical Pain Settings
Musculoskeletal pain is extremely frequent, a major socio-economic burden, and contemporary treatment is inadequate. Acute musculoskeletal pain presents with localised and referred pain as well as localised deep-tissue hyperalgesia, whereas chronic pain often presents with expanded pain areas and widespread hyperalgesia. The mechanistic interplay in the transition from acute to chronic musculoskeletal pain is unclear. Insights can be gained from human mechanistic pain biomarkers combined with experimental human musculoskeletal pain models prolonged for several days. Deep-tissue has the capacity to nociceptively provoke local and/or referred pain and localised hyperalgesia. Referred pain areas expand with prolonged pain. Temporal summation of deep-tissue pain (a pro-nociceptive spinal mechanism) is facilitated in persistent musculoskeletal pain and may partly predict pain sensitivity in asymptomatic subjects exposed to long-term pain models, and the treatment outcome in musculoskeletal pain patients. Anti-nociceptive mechanisms governed by descending inhibitory controls is intriguing as an impairment may explain widespread hyperalgesia. Nonetheless, conditioning pain modulation (an anti-nociceptive mechanism) in experimental pain models and chronic musculoskeletal pain have demonstrated impaired efficacy with inconsistency. Studies of the brain circuitry in musculoskeletal pain have generally demonstrated reorganisation and neuroplastic manifestations in chronic conditions, and experimental pain studies show that cortical adaptations happen immediately or within days. Overall, a trait of the musculoskeletal pain system being more vulnerable to persistent pain could be hypothesised as 1) spinal mechanisms which easily become sensitised, and 2) less flexible brain reactions when adaptive responses are normally requested (less neuroplastic capacity), thus affecting the control of e.g., the spinal excitability.