[Note: to read the free full text of this article by the originators of the Dopamine Theory of Fibromyalgia, click here.]
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 FM, 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 events;
2. The experience of chronic stress results in disruption of dopaminergic activity in otherwise healthy organisms; and
3. Dopamine plays a dominant role in natural analgesia within multiple brain centers.
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 …
Source: The Journal of Rheumatology, Feb 2009. 36(2). PMID: 19208556, by Wood, PB, Holman AJ. Angler Biomedical Technologies, LLC, Jonestown, Texas; Pacific Rheumatology Research, Inc., Renton, Washington, USA. [E-mail: email@example.com]
Note: See also Dr. Wood’s recent article “Hippocampal Metabolite Abnormalities in Fibromyalgia: Correlation with Clinical Features,” published online Sep 2008 in The Journal of Pain.