Fibromyalgia seen as a neuropathic pain syndrome

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Fibromyalgia seen as a neuropathic pain syndrome



April 12, 2006



Janis

Mexico City, Mexico - Fibromyalgia (FM) is best described as a

" sympathetically maintained neuropathic pain syndrome, " says Dr

Manual ez-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.

ez-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, " ez-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

ez-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, " ez-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, " ez-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. "







Sources



ez-Lavin M. Fibromyalgia is a neuropathic pain syndrome. J

Rheumatol 2006; 33:827-829. 

Dworkin RH, Fields HL. Fibromyalgia from the perspective of

neuropathic pain. J Rheumatol 2005; 32 Suppl 75:1-5.