Nociplastic Pain

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Musculoskeletal conditions can cause not only localised pain as a direct result from the condition, but also chronic widespread pain. This phenomenon has many terms with subtle differences in meaning, including central sensitisation, and nociplastic pain.[1]

Central sensitisation is found in 10 to 40 percent of those with osteoarthritis, rheumatoid arthritis, spondyloarthritis, psoriatic arthritis, and systemic lupus erythematosus. It is also common in chronic trauma-induced low back and neck pain, complex regional pain syndrome, joint hypermobility syndrome, lateral elbow tendinopathy, and carpal tunnel syndrome. It is also thought to be a pain mechanism in fibromyalgia and other related chronic pain conditions, such as irritable bowel syndrome, bladder pain syndrome, and temporomandibular dysfunction.[1]

Epidemiology

The prevalence of chronic pain in New Zealand, when defined as lasting for 6 months or longer, was measured at 16.9% in 2011. Prevalence increased with age and economic deprivation. Pacific and Asian peoples had lower rates of chronic pain than European/other.[2] Around one fifth of people with chronic pain have predominantly neuropathic pain.[citation needed] Neuropathic pain is more disabling than other forms of pain and is associated with a lower quality of life.[citation needed]

Definitions

The IASP definitions of pain can be found on their website.

IASP Definition of Pain

The IASP definition of pain was recently updated in 2020.[3]

An unpleasant sensory and emotional experience associated with, or resembling that associated with, actual or potential tissue damage

—IASP Definition of Pain 2020
Sensitisation

Increased responsiveness of nociceptive neurons to their normal input, and/or recruitment of a response to normally subthreshold inputs...a neurophysiological term, may only be inferred indirectly from phenomena such as hyperalgesia or allodynia

Central Sensitisation

Woolf discussed the differences between pain versus pathology versus "pain syndromes."[4] The central component of post-injury pain hypersensitivity was first termed sensitisation in 1987.[5]

Any sensory experience greater in amplitude, duration and spatial extent than that would be expected from a defined peripheral input under normal circumstances qualifies as potentially reflecting a central amplification due to increased excitation or reduced inhibition. These changes could include a reduction in threshold, exaggerated response to a noxious stimulus, pain after the end of a stimulus, and a spread of sensitivity to normal tissue

—Woolf 2011

The IASP define central sensitisation as follows:

Increased responsiveness of nociceptive neurons in the central nervous system to their normal or subthreshold afferent input.

—IASP
Peripheral sensitisation

Increase Responsiveness and reduced threshold of nociceptive neurons in the periphery to the stimulation of their receptive fields

Nociceptive Pain

actual or threatened damage , non-neural tissue, activation of nociceptors.

Neuropathic pain

Primary lesion or disease of the somatosensory nervous system.

Pain Mechanisms

Some patients with fibromyalgia actually have unrecognised small-fibre polyneuropathy (SFPN). Oaklander et al found SFPN in 41% of skin biopsies of patients diagnosed with fibromyalgia, compared to 3% of controls. This is a disease that causes dysfunction and degeneration of peripheral small-fibre neurons.[6]

Anatomical and Functional Changes

Clinical Features

Diagnosis

Management

Prognosis

  • Osteoarthritis: In patients with osteoarthritis of the knee or hip who undergo joint replacement, chronic widespread pain (CWP) correlates with poorer pain outcomes, and increased analgesic use.[1]
  • Autoimmune and inflammatory rheumatological conditions: CWP is correlated with increased pain and worse outcomes when measured by self-report questionnaires.[1]
  • Chronic low back pain: CWP is present in 25% of patients, and correlated with greater disability.[1]
  • Chronic neck pain: CWP at one month post neck injury is correlated with poor outcomes at 6 months.[1]
  • Carpal tunnel syndrome: worse outcomes with CWP[1]
  • Shoulder pain: worse outcomes with CWP[1]
  • Lateral elbow tendinopathy: Worse outcomes with CWP[1]

Key Articles

  • {{#l:Cohen2016 - nociplastic pain third mechanistic descriptor.pdf}}
  • {{#l:Woolf2011 - Central sensitisation.pdf}}
  • {{#l:Woolf2014 - Nociceptive amplification naming.pdf}}
  • {{#l:Yunus2008 - Central sensitivity syndrome.pdf}}

References

  1. โ†‘ 1.0 1.1 1.2 1.3 1.4 1.5 1.6 1.7 1.8 Goldenberg, D et al. Overview of chronic widespread (centralized) pain in the rheumatic diseases. In: UpToDate, Post, TW (Ed), UpToDate, Waltham, MA, Jan 23 2020.
  2. โ†‘ Dominick et al.. Patterns of chronic pain in the New Zealand population. The New Zealand medical journal 2011. 124:63-76. PMID: 21946879.
  3. โ†‘ International Association for the Study of Pain (2020) IASPโ€™s New Definition of Pain. Available at: https://www.iasp-pain.org/PublicationsNews/NewsDetail.aspx?ItemNumber=10475 (accessed 27 July 2020).
  4. โ†‘ Woolf. Central sensitization: implications for the diagnosis and treatment of pain. Pain 2011. 152:S2-15. PMID: 20961685. DOI. Full Text.
  5. โ†‘ Woolf et al.. Prolonged primary afferent induced alterations in dorsal horn neurones, an intracellular analysis in vivo and in vitro. Journal de physiologie 1988. 83:255-66. PMID: 3272296.
  6. โ†‘ Oaklander et al.. Objective evidence that small-fiber polyneuropathy underlies some illnesses currently labeled as fibromyalgia. Pain 2013. 154:2310-6. PMID: 23748113. DOI. Full Text.