Fibromyalgia seen as a neuropathic pain syndrome

Janis Kelly

April 12, 2006

April 12, 2006

Mexico City, Mexico - Fibromyalgia (FM) is best described as a "sympathetically maintained neuropathic pain syndrome," says Dr Manual Martinez-Lavin (National Institute of Cardiology, Mexico City, Mexico) [ 1 ]. The future of FM research is likely to be influenced by methods already developed by pain researchers, he believes, adding that one attractive therapeutic possibility is the use of sodium channel blockers.

Martinez-Lavin airs his views in a letter in the April 2006 issue of the Journal of Rheumatology, prompted by a recent special supplement to the journal [ 2 ] that explored the possibility that fibromyalgia pain is at least in part due to an underlying nervous-system dysfunction.

"I have little doubt that fibromyalgia pain is due to an intrinsic nerve-system dysfunction. Sympathetic hyperactivity (with its concurrent hyporeactivity to stress) explains all of the features of fibromyalgia," Martinez-Lavin told rheumawire , when asked to expand on his views. "It is interesting to notice that nonpharmacological therapies that have been proven useful in fibromyalgia (biofeedback, cognitive-behavioral approaches, graded aerobic exercises) also improve resting autonomic tone."

Pain maintained by sympathetic nervous system

Martinez-Lavin notes that neuropathic pain is stimuli-independent and is accompanied by allodynia and paresthesia, which are also common features of fibromyalgia. He also points out that the most important characteristic of neuropathic pain is not the nerve lesion, but the resulting nerve dysfunction.

Although fibromyalgia typically has no underlying structural damage and no signs of inflammation, there is an apparent dysfunction in central-nervous-system sensitization, including abnormal temporal summation of pain and abnormal spinal-cord reflexes. "Central sensitization is an expression of neuroplasticity and is the major cause of hypersensitivity to pain after injury," he writes.

The dysfunction in FM appears to be sympathetically maintained, as controlled studies have shown that FM patients "display signs of relentless sympathetic hyperactivity," and FM pain often responds to sympathetic blockade but can be rekindled by norepinephrine injections. Animal studies of sympathetically maintained pain have shown sympathetic sprouting at the dorsal-root ganglia, with formation of basketlike structures around large-diameter, axotomized sensory neurons. Animal studies have also shown abnormal posttraumatic connections in the dorsal horn of the spinal cord.

"We have no direct evidence yet that these changes also occur in humans with fibromyalgia," Martinez-Lavin comments, but he adds: "As far as I know, nobody has looked specifically for these structural abnormalities."

However, there are other indirect clues that suggest that this type of neuroplasticity may occur in fibromyalgia. In rats, intraventricular infusion of nerve-growth factor induces sympathetic sprouting in the dorsal-root ganglia. Patients with fibromyalgia have increased cerebrospinal fluid levels of nerve-growth factor, and in a "pilot study in patients with Alzheimer's disease, an intraventricular infusion of nerve-growth factor led to the patients developing diffuse back pain, and so the study was stopped."

This suggests that "we have to look at the 'state of the art' in neuropathic pain research and treatment and translate it to fibromyalgia," Martinez-Lavin urges. "There is much to be learned of the central sensitization and neuroplasticity that undeniably occur in neuropathic pain and may apply to fibromyalgia. Likewise, we must take advantage of the ongoing pharmacological research in neuropathic pain and consider the possibility that some of those discoveries may be also useful in fibromyalgia."


  1. Martinez-Lavin M. Fibromyalgia is a neuropathic pain syndrome. J Rheumatol 2006; 33:827-829.

  2. Dworkin RH, Fields HL. Fibromyalgia from the perspective of neuropathic pain. J Rheumatol 2005; 32 Suppl 75:1-5.


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