Persisting Pain States & Fibromyalgia

Chronic Pain

Overview

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.

Anatomy & Pathophysiology

Pain has three recognised mechanisms:

  • Nociceptive pain - activation of peripheral nociceptors by actual or threatened tissue damage (e.g. trauma, OA).
  • Neuropathic pain - lesion or disease of the somatosensory system (e.g. radiculopathy, diabetic neuropathy, post-herpetic).
  • Nociplastic pain - altered nociception in the absence of clear tissue or nerve damage, attributed to changes in central pain processing. Fibromyalgia is the prototype.

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.

Biopsychosocial model (biological, psychological, social domains) and pain-fear avoidance cycle. Cornerstones of modern persisting pain management.

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:

  • Biological: central sensitisation, neurochemical changes, non-restorative sleep, deconditioning, comorbidities (IBS, chronic fatigue, TMJ dysfunction).
  • Psychological: beliefs about pain, fear-avoidance, catastrophising, depression, anxiety, low self-efficacy.
  • Social: work stress, relationships, isolation, financial concerns, adverse childhood experiences, cultural context.

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.

Clinical Pearl
  • Three pain mechanisms: nociceptive (tissue damage), neuropathic (nerve lesion), nociplastic (altered central processing). Fibromyalgia is the prototype nociplastic syndrome.
  • Central sensitisation is the physiological underpinning - allodynia, hyperalgesia, widespread pain reflect amplified CNS processing, not ongoing tissue damage.
  • Biopsychosocial model: biological + psychological + social - all three must be addressed. Analgesic-only approaches fail.
  • Pain-fear avoidance cycle (pain to catastrophising to fear to avoidance to deconditioning to more pain) is broken by graded exercise and pain neuroscience education.
  • Descending serotonergic and noradrenergic inhibition is dysfunctional in fibromyalgia - the rationale for amitriptyline and duloxetine.

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