Recently, Martinez-Lavin 1 proposed a model of sympathetically maintained neuropathic pain syndrome that has the merit of scrutinizing possible mechanisms behind the central sensitization model 2. Eisinger 3, in an editorial comment, raises the issue of heterogeneity permeating Martinez-Lavin's proposition. Since it is difficult to establish a traumatic trigger event in all cases, Eisinger considers multicausality as more reasonable than a single post-traumatic etiology for all cases. Félix and Fontenele 4 further explored this venue, speculating that the orthostatic intolerance symptoms seen in the majority of fibromyalgia patients are a consequence of sympathetic hyperactivity. The idea that a COMT val-158-met polymorphism may cause higher cathecolamine levels has been explored 5. Loevinger and colleagues 6 have shown that the metabolic syndrome is more common in individuals with fibromyalgia who also have higher body mass index, blood pressure, and waist-to-hip ratio than controls.
Interestingly, elevated body mass index, blood pressure, and waist-to-hip ratio are associated with sleep-disordered breathing. We recently reported in a study that 50% of the women with obstructive sleep apnea syndrome or upper airway resistance syndrome had chronic pain and more than 11 tender points when pressed with 4 kgf/cm2 7. Guille-minault and colleagues 8 reported orthostatic intolerance in patients with upper airway resistance syndrome. We believe that the authors investigating this theme should discuss the possibility of sleep-disordered breathing being the missing link between fibromyalgia, pain, disturbed sleep, alpha-delta sleep, hypotension, sympathetic hyperactivity, and metabolic syndrome.
We are conducting investigations into whether exposition to the typical stress of sleep-disordered breathing – with repeated arousal episodes and hypoxemia – has fibromyalgia as a possible outcome. Our preliminary results underline the need to consider and further explore this hypothesis.