There is a relatively long history of the use of the ??-adrenergic antagonist, phenoxybenzamine, for the treatment of complex\r\nregional pain syndrome (CRPS). One form of this syndrome, CRPS I, was originally termed reflex sympathetic dystrophy (RSD)\r\nbecause of an apparent dysregulation of the sympathetic nervous system in the region of an extremity that had been subjected\r\nto an injury or surgical procedure. The syndrome develops in the absence of any apparent continuation of the inciting trauma.\r\nHallmarks of the condition are allodynia (pain perceived froma nonpainful stimulus) and hyperalgesia (exaggerated pain response\r\nto a painful stimulus). In addition to severe, unremitting burning pain, the affected limb is typically warm and edematous in the\r\nearly weeks after trauma but then progresses to a primarily cold, dry limb in later weeks andmonths. The later stages are frequently\r\ncharacterized by changes to skin texture and nail deformities, hypertrichosis, muscle atrophy, and bone demineralization. Earlier\r\ntreatments of CRPS syndromes were primarily focused on blocking sympathetic outflow to an affected extremity. The use of an ??-\r\nadrenergic antagonist such as phenoxybenzamine followed from this perspective. However, the current consensus on the etiology\r\nof CRPS favors an interpretation of the symptomatology as an evidence of decreased sympathetic activity to the injured limb and\r\na resulting upregulation of adrenergic sensitivity. The clinical use of phenoxybenzamine for the treatment of CRPS is reviewed,\r\nand mechanisms of action that include potential immunomodulatory/anti-inflammatory effects are presented. Also, a recent study\r\nidentified phenoxybenzamine as a potential intervention for painmediation fromits effects on gene expression in human cell lines;\r\non this basis, it was tested and found to be capable of reducing pain behavior in a classical animal model of chronic pain.
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