Chronic Pain

Session Goals

The session's goal was to determine how the NIAMS can more effectively study and contribute toward personalized treatment options for patients who suffer from chronic musculoskeletal pain. The session was expected to position the NIAMS to capitalize on and contribute to what is known about how to prevent, identify, and manage chronic pain.

Background/Relevance to NIAMS Mission

Chronic pain can be an important aspect of many of the diseases that are part of the NIAMS' portfolio. The contribution of chronic musculoskeletal pain to patient suffering and burden, particularly when worsened by acute exacerbations, is likely to increase substantially as the U.S. population ages. The existence of chronic pain at a public health level suggests that clinically important aspects of pain are not adequately understood. While there have been many developments in our understanding of pain and how it is treated, these have not been easily translated into interventions for chronic pain.

The chronic pain session explored certain emerging aspects of this patient-focused topic, as noted Figure 1. Current thinking on the mechanisms of peripheral pain perception, transmission and central (brain) sensitization and how these processes might impact molecular and behavioral interventions was discussed. Information that supports the commonly accepted notion of central nervous system plasticity, which suggests that chronic pain, at least in some patients, is no longer a symptom, but a disease itself offering potentially different targets for further study and treatment intervention was reviewed. The role of genetic and environmental influences on chronic pain, along with efforts to obtain objective evidence of chronic pain (such as brain mapping and imaging techniques) also was presented.

In aggregate, this knowledge will help NIAMS identify gaps and opportunities toward achieving its mission of understanding the causes, treatment and prevention needs of chronic pain in both adults and children. This session also discussed ongoing efforts by the NIH Pain Consortium to develop NIH Roadmap initiatives on biomarkers and risk factors of chronic pain.

The recognition that pain and itch are linked by common mechanisms was discussed throughout the session, as appropriate. This link offers even more reason for NIAMS to focus on new thinking and approaches on how to treat, cure, and even prevent these all too common problems that substantially impact patient function and quality of life.

Key Questions

  • What aspects of pain research are appropriate for NIAMS to support? Which are of particular interest to the Institute? What elements are beyond the scope of its mission?
  • Which diseases or conditions within the NIAMS mission can serve as models for studies of chronic pain prevention, diagnosis, and management of chronic pain?
  • How can the NIAMS incorporate into existing efforts the latest knowledge about
    • Pain plasticity?
    • The genetic and environmental factors influencing chronic pain?
    • The behavioral and psychosocial aspects of chronic pain?
  • What other programs could facilitate the translation of biological information about chronic pain into diagnostic and therapeutic applications?
    • Is there a place for chronic pain research in tomorrow's discussion about ancillary studies to large clinical projects?
    • How can NIAMS-supported investigators participate in trans-NIH efforts, such as the CTSAs or the Pain Consortium's potential Roadmap initiatives?
  • What specific steps can the NIAMS take to advance the investigation of chronic pain in skin, rheumatic, and musculoskeletal diseases?


  • Diatchenko L, Nackley AG, Slade GD, Fillingim RB, Maixner W. Idiopathic pain disorders--pathways of vulnerability. Pain. 2006 Aug;123(3):226-30. PMID: 16777329.
  • Woolf CJ. Central sensitization: uncovering the relation between pain and plasticity. Anesthesiology. 2007 Apr;106(4):864-7. PMID: 17413924.
  • Harris RE, Clauw DJ. How do we know that the pain in fibromyalgia is "real"? Curr Pain Headache Rep. 2006 Dec;10(6):403-7. PMID: 17087863.
  • Woodcock J, Witter J, Dionne RA. Stimulating the development of mechanism-based, individualized pain therapies. Nat Rev Drug Discov. 2007 Sep;6(9):703-10. PMID: 17762885.

Additional Resources:

  • Diatchenko L, Nackley AG, Tchivileva IE, Shabalina SA, Maixner W. Genetic architecture of human pain perception. Trends Genet. 2007 Dec;23(12):605-13. PMID: 18023497.
  • Binshtok AM, Bean BP, Woolf CJ. Inhibition of nociceptors by TRPV1-mediated entry of impermeant sodium channel blockers. Nature. 2007 Oct 4;449(7162): 607-10. PMID: 17914397.
  • Kulkarni B, Bentley DE, Elliott R, Julyan PJ, Boger E, Watson A, Boyle Y, El-Deredy W, Jones AK. Arthritic pain is processed in brain areas concerned with emotions and fear. Arthritis Rheum. 2007 Apr;56(4):1345-54. PMID: 17393440.
  • Gwilym SE, Pollard TC, Carr AJ. Understanding pain in osteoarthritis. J Bone Joint Surg Br. 2008 Mar;90(3):280-7. PMID: 18310746.
  • Kim SH, Kim DH, Oh DH, Clauw DJ. Characteristic electron microscopic findings in the skin of patients with fibromyalgia--preliminary study. Clin Rheumatol. 2008 Mar;27(3):407-11. PMID: 18323007.

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