Fibromyalgia: The Answer Is Blowin' in the Wind

For more than 10 years, we have known of various hormonal and other biochemical changes such as abnormal diurnal variations in corticosteroid secretion(11), low serum concentrations of somatomedin-C(12) and tryptophan(13), low cerebrospinal fluid (CSF) levels of 5-hydroxytryptophan(14), and high CSF levels of substance P(15). More recent research has provided a potential explanation for some of these findings, including reduced serum activity of prolylendopeptidase (a cytosolic endopeptidase responsible for the inactivation of a variety of algesic peptides, including substance P)(16).

Thermographically measured skin temperature appears to be lower in the back(17) and higher in the hands(18) in FM patients compared to healthy controls, implying some alteration in normal dermal sympathetic activity in FM. More recent research has shown further evidence of altered autonomic nerve function in response to orthostatic stress(19). Two small recent studies suggest an alteration in the pattern of cerebral blood flow(20,21), which may help to explain the debilitating fatigue and cognitive difficulties described by these patients. The list of scientifically demonstrated physiologic abnormalities in FM patients goes on and on. Detailing them all is far beyond the scope of this editorial. Nonetheless, this research exists and no critic should verbalize his or her opinions without performing an educated and unbiased review of it.

Through all this research, FM has become the prototype chronic, systemic pain disorder, much the way that SLE is the prototype chronic, systemic autoimmune disorder. Scientists who accept that we have much to learn about pain have learned much, much of this knowledge coming from studying FM. Such knowledge has been attained by reaching beyond the oversimplistic, grossly anatomic view of the world to which so many of us seem confined.

Some argue that these pathophysiologic irregularities are not specific for FM. But this, also, is not a valid argument against the acceptance of FM. If it were, we would be forced to question the validity of an almost endless number of otherwise well-accepted disorders for which all pathophysiologic changes are nonspecific.

Foremost among these would be SLE. The positive predictive value of the detection of antinuclear antibodies (ANA) is no greater than one percent, which makes the testing for ANA 50 times less predictive than the flip of a coin. In addition, not one of the many other pathophysiologic abnormalities of SLE is specific to SLE. Does SLE not exist? How about rheumatoid arthritis (RA)? Polymyalgia rheumatica (PMR)? The list goes on.

Claiming that FM is psychological is no defense either. When are we going to finally discard the outdated concept that psychological and physical illnesses are opposites? A huge body of

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