Persisting (chronic) pain is defined as pain that continues or recurs for longer than 3 months. NICE NG193 (2021) distinguishes chronic primary pain (pain itself is the condition - no underlying disease adequately explains it) from chronic secondary pain (pain as a symptom of an identifiable condition such as OA, RA, or neuropathy). The two can coexist. Fibromyalgia is the archetypal chronic primary pain syndrome: widespread musculoskeletal pain, fatigue, sleep disturbance, and cognitive dysfunction, more common in women. For the MSK clinician, these patients form a large proportion of workload and are frequently mismanaged with long-term opioids. NICE NG193 mandates a biopsychosocial approach: exercise, psychological therapies, acupuncture, and antidepressants - paracetamol, NSAIDs, opioids, gabapentinoids, and benzodiazepines should NOT be initiated for chronic primary pain.
Pain has three recognised mechanisms:
Central sensitisation is the physiological underpinning of nociplastic and persisting pain. The CNS enters a heightened reactive state through wind-up of dorsal horn neurones, expanded receptive fields, impaired descending inhibition (serotonin and noradrenaline from PAG/RVM), enhanced descending facilitation, and neuroplastic changes in pain-processing cortical regions. Clinical manifestations: allodynia (pain from a non-painful stimulus), hyperalgesia (exaggerated response), widespread pain extending beyond the original site, temporal summation, and after-sensations. Persisting pain therefore does NOT equal ongoing tissue damage.
Fibromyalgia is understood as a disorder of central pain processing with impaired descending inhibition. Other observations include elevated CSF substance P, reduced serotonin and noradrenaline (the rationale for amitriptyline and duloxetine), non-restorative sleep with alpha-wave intrusion, altered HPA axis function, and reduced intraepidermal nerve fibre density in a subgroup.
The biopsychosocial model is essential, and all three domains must be addressed:
The pain-fear avoidance cycle perpetuates disability: pain leads to catastrophising, then fear of movement, then avoidance of activity, then deconditioning and increased sensitivity, then more pain. Breaking the cycle requires graded exercise and pain neuroscience education.
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