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Fibromyalgia: Non-nociceptive Aspects of Persistent Musculoskeletal Pain
R. C. Kramis, Ph.D.
Central sensitization, defective central inhibitory mechanisms, and/or central deafferentation can produce hyperexcitability of pain-related nociceptive spinal neurons. This hyperexcitability can provide a neuronal basis for pathologically persistent pain. It is often not recognized, however, that sensitized, disinhibited or deafferented central neurons can be drive to “painful” levels of activity by input from non-nociceptive afferents…i.e., from afferents which normally mediate only non-painful sensations associated with light touch, normally innocuous deep pressure, normal movements, and normally innocuous warmth or coolness. This type of pain, i.e., “non-nociceptive pain,” can be as severe as nociceptive pain and often may be more distressing due to its apparently inexplicable origin. Unfortunately, because it is mediated at least partly by physiological mechanisms which differ from those that mediate nociceptive pain, non-nociceptive pain is often unresponsive to interventions effective in relation to nociceptive pain. Considerable evidence suggests that fibromyalgia may be one form of persistent “non-nociceptive” pain.
The absence of identifiable, ongoing somatic pathology in a painful region of the body combined with a poor response of the painful condition to normally effective pain interventions frequently distresses both physician and patient and may lead to concerns that the pain is of psychogenic or “functional” origin. We have recently reviewed evidence which suggests that basic neurophysiological mechanisms, even at the spinal level and perhaps including proprioceptive afferent excitation of sensitized spinal neurons, may underlie the major painful and fatigue-related symptoms of fibromyalgia (Kramis, et al, JOSPT, 1996).
National Fibromyalgia
Research Association
PO Box 500, Salem, OR 97302
