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Fibromyalgia: The Answer Is Blowin' in the Wind (continued)

© KEVIN P. WHITE, MD, PhD,

Our hateful disregard for FM also is not defendable by arguing that the FM label is a distinctly poor one, although it is true that the FM label may be flawed. The tautologic (round-about) method by which FM was defined in 1990(29) (collecting a group of individuals believed to have FM and then looking for characteristics that distinguish them from those believed not to have FM) is the same scientific method that has been used to develop classification criteria for every other disorder (including SLE and RA) for which they exist. What other method might be employed in the absence of a gold standard confirmatory test? And what possible justification could there be to develop classification criteria for a disorder in which a gold standard confirmatory test already exists? The answer to both of these questions: there is none.

The FM label, like those of SLE, RA, and many other disorders, may be tenuous. But that may just be the nature of the diagnostic labeling process itself. The myth in medicine that we have 999 diseases is a myth. The truth is that we have 999 labels. Some of these labels, such as pneumococcal pneumonia or gout, work very well. FM, SLE, RA, PMR, and many other disorders that fall under the rheumatic disease umbrella are not well labeled. Nonetheless these labels do serve many purposes. Certainly, there is very little discussion about discarding the SLE label, or the RA label, or the PMR label. Why must we discard the FM label?

Despite arguments to the contrary, there is no evidence that the FM label is any more or less useful than those of SLE and RA. The most oft-used argument has been that the FM label is harmful by creating illness behavior and disability, causing individuals to take on a "sick role" and behave as if they are ill(19,28,30,31). But this argument is flawed at both ends.

First, as has been shown repeatedly in controlled studies of FM patients versus controls, these people are ill. As stated earlier, the FM cohort differs physiologically from the normal population, in many instances in a physiologically predictable way. One would expect individuals reporting high levels of pain to have higher levels of neurotransmitter pain agonists in CSF, and FM patients do(15). One would expect individuals reporting nonrestorative sleep to have electrophysiologic alterations in deep sleep, and FM patients do(9). In fact, as stated earlier, the number of alpha wave intrusions in Stage IV sleep is highly correlated with daytime symptoms(10). Hence, this cohort of patients with symptoms of illness and pathophysiologic changes consistent with illness, irrespective of

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