First paragraph (this article has no abstract)

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.