Neurohormonal aspects of fibromyalgia syndrome

The overriding theme of this article is that a central abnormality in the function of a neurotransmitter such as serotonin could be involved in many, if not all, of the clinical manifestations of FS. Under the single umbrella of serotonin deficiency can be gathered the musculoskeletal pain, the anxiety, the insomnia, the pseudodepression, the bowel-related complaints, the dysesthesias, the hypothyroidism, the weather-related exacerbations, and even the dysfunction of immune cells. Such an integration of the disparate manifestations seen in FS would be very appealing, but it's not likely to be that easy. On the other hand, many clinical disorders seemed mysterious until their pathogenesis was understood. The advantage derivable from developing hypothetical models is that they provide a basis on which further study can be mobilized to confirm, modify, or totally disprove the proposed hypotheses. There is no recognized animal model for FS, and there never will be one as long as the most objective finding is tenderness to palpation at a few somatic structures. Finding ways to test the proposed hypotheses in patients with FS will not be an easy task. On the other hand, FS is a common disorder and patients are generally eager to participate in research that may lead to a better understanding of their symptoms.