Etiopathogenesis of livedoid vasculopathy remains elusive, and this condition is still frequently designated as idiopathic or secondary to various disorders. While several etiologies have been proposed, neither are they always associated with the disease, nor do they necessarily include livedoid vasculopathy in their course. Moreover, treatments described in the literature do not present reproducible results. We present the case of a 42-year-old man with livedoid vasculopathy who presented a good response to treatment with carbamazepine, a previously unattempted approach. In view of the very scarce evidence for vascular inflammation, discrepancies in the proposed etiologies of this pathological state and the intense pain that is the hallmark symptom; and considering recent reports on the neural participation in coagulation processes, the authors here address the question of a potential association between the vascular and nervous systems in the etiology of this vasculopathy.
Blood coagulation; Epinephrine; Sodium channels; Vasculitis
