No Such Thing as Fibromyalgia
The October issue of The Rheumatologist featured an article on fibromyalgia by Daniel Clauw. Fibromyalgia does not exist. What is called fibromyalgia is part of the spectrum of chronic pain. The tender points are tender in everyone. Fibrous tissue and muscle are not involved. In other words, fibromyalgia is a misnomer. Like silicone breast implant syndrome and other now-forgotten diseases, it will disappear.
George E. Ehrlich, MD
Dr. Clauw Responds:
To Dr. Ehrlich, thank you for your comments. I am quite aware that some people refuse to change their minds even in the face of overwhelming data.
Daniel J. Clauw, MD
Professor of Anesthesiology and Medicine (Rheumatology)
University of Michigan in Ann Arbor
I read Dr. Clauw’s recent review of the pathogenesis and therapy of fibromyalgia (FM) with a good deal of interest.1,2 While his description of FM as an example of “central [nervous system] sensitization (CS)” resulting in pain amplification has appeal on a heuristic basis, I believe that it fails to identify a fundamental pathophysiologic explanation for the initiation and perpetuation of pain in the FM syndrome.
Dr. Clauw’s construct suggests the presence of certain “environmental stressors” that “trigger” FM in the susceptible individual, but then disappear (at least from that individual’s immediate environment), while leaving a mysteriously self-perpetuating CS/FM in its wake. This “non-nociceptive” form of CS (see Table 2 in Reference 1) is deemed to be self-evident since there are, Dr. Clauw says, no—or very few—peripheral indicators of tissue damage in FM. Supporting evidence for these assertions includes abnormal brain functional imaging studies (showing areas of hyperactive pain integration), and a clinical, pain-lessening effect for centrally acting pharmacological therapies, such as amitrptyline and pregabalin.
Dr. Clauw’s review is worthy of comment for a number of reasons. First, he has nicely sensitized rheumatologists, who are better known for their appreciation of the immune system and for being students of inflammation than for being neurophysiologists, to the role of CS in rheumatic disease pain production. I am afraid, however, that he has left the impression that FM is a disorder primarily of the central nervous system. He does not, for example, point out that many, and probably most, CS syndromes require constant peripheral nociceptive input in order to be maintained,3,4 though this maintenance may require only low levels of continuing nociceptive stimulation.5 The larger question for the rheumatologist may, therefore, revolve around determining from where and how that nociceptive input continues to arise in FM.