Persisting Pain States & Fibromyalgia

Chronic Pain
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Overview

Persisting (chronic) pain is pain that persists or recurs for more than 3 months.

NICE distinguishes chronic primary pain, where no underlying condition adequately accounts for the pain or its impact, from chronic secondary pain, where an identifiable condition such as osteoarthritis, rheumatoid arthritis or neuropathy does. Both can be present together.

Fibromyalgia is a type of chronic primary pain: widespread pain with fatigue, unrefreshing sleep and cognitive symptoms, more common in women. Management is biopsychosocial, with a limited role for medicines.

Anatomy & Pathophysiology

Pain has 3 recognised mechanisms:

  • Nociceptive: activation of nociceptors by actual or threatened tissue damage, such as trauma or osteoarthritis
  • Neuropathic: a lesion or disease of the somatosensory nervous system, such as radiculopathy or diabetic neuropathy
  • Nociplastic: altered nociception without clear tissue or nerve damage, attributed to changes in central pain processing; fibromyalgia is the prototype

Central sensitisation underlies nociplastic and much persisting pain: dorsal horn wind-up, expanded receptive fields and impaired descending inhibition (serotonin and noradrenaline) amplify pain. It shows as allodynia, hyperalgesia and pain spreading beyond the original site. Persisting pain therefore does not mean ongoing tissue damage.

Biopsychosocial model (biological, psychological and social domains) and the pain-fear avoidance cycle, which graded exercise and pain neuroscience education aim to break.

In fibromyalgia, proposed mechanisms include impaired descending inhibition, raised cerebrospinal fluid substance P and non-restorative sleep.

The biopsychosocial model addresses all 3 domains:

  • Biological: central sensitisation, poor sleep, deconditioning
  • Psychological: pain beliefs, fear-avoidance, catastrophising, low mood
  • Social: work, relationships, isolation, adverse childhood experiences

The pain-fear avoidance cycle (pain, catastrophising, fear of movement, avoidance, deconditioning, more pain) is broken by graded exercise and pain neuroscience education.

Clinical Pearl
  • •Nociplastic pain reflects amplified central processing, not ongoing tissue damage
  • •Allodynia, hyperalgesia and spreading pain are the clinical signs of central sensitisation
  • •Address biological, psychological and social factors together; an analgesic-only approach fails

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