New Dimensions in Fibromyalgia
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).
