An Elephant Among Us: The Role of Dopamine in the Pathophysiology of Fibromyalgia

Abstract

Exploration of the pathophysiology underlying fibromyalgia (FM) has become an exciting field of inquiry as we strive to improve our understanding of this enigmatic disorder. While evidence of a neuro-dysregulatory state mounts and insights are gained as to potential contribution of specific neurotransmitters, a review of recent literature demonstrates that not all relevant neurotransmitters are being considered equally or with disinterest. Specifically, the potential contribution of serotonin and norepinephrine has been emphasized, ostensibly due in part to the qualified success of trials of serotonin-norepinephrine reuptake inhibitors, while a general awareness of the potential contribution of dopamine-related dysfunction lags. Indeed, the text of recent reviews, and even peer-reviewed continuing medical education test articles, have contained either scant reference or, in a majority of cases, conspicuous neglect regarding the question of dopamine’s role in FM. Despite the recent European League Against Rheumatism consensus recommendation to consider a dopamine agonist for treatment of FM1, most clinicians and even medical authorities in the field routinely fail to acknowledge the mounting evidence for a role for dopamine in the pathogenesis of FM. The proposition that a disruption of normal dopaminergic neurotransmission may make a substantial contribution to the pathophysiology of FM was initially based on 3 key observations: (1) FM has been characterized as a “stress-related” disorder due to its frequent onset and apparent exacerbation of symptoms in the context of stressful events2; (2) the experience of chronic stress results in disruption of dopaminergic activity in otherwise healthy organisms3; and (3) dopamine plays a dominant role in natural analgesia within multiple brain centers4. The first hint in the medical literature of a connection between FM and dopamine was provided by Russell, et al , who in 1992 reported lower concentrations of metabolites of dopamine, norepinephrine, and serotonin … Address reprint requests to Dr. Wood ; E-mail: pwood{at}anglerbiomedical.com