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Neurobiology of Craniofacial/Deep Tissue Persistent Pain


Symposium Funded by the National Institute of Neurological Disorders and Stroke
And
Office of Rare Diseases
NIH
Sponsored by the American Pain Society

March 13-14, 2002

Symposium Summary

A symposium was held March 13-14, 2002 to assess the current status of neuroscience research on deep tissue persistent pain in order to identify new research avenues for craniofacial disorders, such as temporal mandibular disorders (TMD), migraine headache, and trigeminal neuralgia (TN). These are highly prevalent, disabling, and/or chronic conditions, especially among women. Because their pathophysiology is poorly understood, research on management and treatment has lagged behind that for other pain conditions. The symposium was held in conjunction with the Annual Meeting of the American Pain Society.

A constellation of cutting-edge research at the molecular, cellular, and systems level was described in experimental models and in humans of deep tissue persistent pain. Speakers relayed their findings on muscle and joint pain, visceral and cardiovascular pain, inflammation and cytokines, molecular and cell biology, gender, and neuroimaging. A major theme of the symposium was that models of visceral and deep tissue pain are more relevant for understanding craniofacial pain than are models of cutaneous pain.

Among the highlights of the symposium were new findings about experimental models of musculoskeletal pain in the absence of tissue damage; the role of NGF and pro-inflammatory cytokines in persistent pain states; the great degree of variability in response to nociceptive stimulation depending on sex, initiating stimuli (e.g., location, nature, intensity), time during development, and co-morbid pain syndromes; and, lastly, the contributions of multiple cortical areas in human pain processing and regulation through neuroimaging.

These new avenues of research for craniofacial/deep tissue persistent pain were suggested at the symposium:

  • New model systems that better mimic the clinical features of craniofacial disorders, including those in which deep tissues are affected.
  • The development of more clinically relevant assays of nociception in human studies.
  • The role of glial cell activation and cytokine release in central and peripheral pathophysiology of craniofacial/deep tissue persistent pain.
  • The role of growth factors in pathophysiology and treatment.
  • The role of estrogen (both genomic and non-genomic effects) in pathophysiology, including potential interactions between estrogen and growth factors.
  • The relative roles of central (including descending modulation) and peripheral plasticity (including effector functions of afferent fibers) in mediating the onset of chronic pain in craniofacial regions.
  • The changes in gene expression in the trigeminal ganglion, spinal cord, and brain in response to nociceptive stimuli using gene chip technology.
  • The central processing and integration of afferent input from craniofacial region with that from non-craniofacial regions, which directly or indirectly innervate the same CNS regions. This information is key to unraveling the high degree of co-morbidity of craniofacial disorders with musculoskeletal, and gastrointestinal and pelvic pain disorders.
  • The presence and role of acid- sensitive ion channels in jaw muscles and other deep tissues of the craniofacial region.
  • The role of exercise (nature and timing) in inhibition of hyperalgesia.
  • Greater attention in human studies to sensory, cognitive, affective, and other aspects of nociceptive stimulation on central processing. Greater attention to sex and individual differences in response to nociceptive stimulation.

Last updated April 8, 2011