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Complex Regional Pain Syndromes: Causalgia and Reflex Sympathetic Dystrophy


Introduction

A myriad of terms has been used to describe post-noxious or traumatic pain accompanied by autonomic dysfunction and impaired extremity capacity. The most commonly used descriptors of this condition are reflex sympathetic dystrophy (RSD) in the United States and algodystrophy in Europe. However, the use of the term complex regional pain syndrome, as proposed by the International Association for the Study of Pain in 1993, provides categorization of the condition based upon clinical features, location, and specifics of the injury without implying mechanisms, etiology, or sympathetic maintenance (Stanton-Hicks IASP 1995). CRPS Type 1 is traditional RSD or algodystrophy without an identifiable peripheral nerve injury; CRPS Type 2 is "causalgia" which includes the clinical features of RSD and a peripheral nerve abnormality. Either form may be sympathetically maintained (SMP) or sympathetically independent (SMI). SMP is defined as the designation that can be identified by the improvement of signs and symptoms following sympatholytic blockade. CRPS as defined in the International Association of Society for Pain, is not synonymous with sympathetically maintained pain. This definition is in contradistinction to the consensus statement of the American Association of Hand Surgery in 1991 which defined RSD as synonymous with SMP (Amadio 1991). Sympathetically maintained pain or sympathetically independent pain may be used as a descriptor of either CRPS Type 1 or CRPS Type 2. Although this nomenclature appears confusing, CRPS represents an abnormally prolonged and exaggerated physiologic response to an initial noxious insult. CRPS persists in the absence of ongoing or impending cellular damage. Furthermore, CRPS initiates a complex series of peripheral and central events that affect peripheral autonomic control and central nervous system activity. A persistent "nociceptive" focus (i.e., mechanical irritation of the wrist secondary to an unstable distal radio ulnar joint or injury to a peripheral nerve) exaggerates physiologic responses mediated by alpha adrenergic activity (Raja 1991, 1996). Wide dynamic range neurons within the dorsal horn of the spinal cord (Campbell 1988, 1994; Dotson 1993; Ochoa 1993) amplify nociceptive input increasing the conscious appreciation of pain. Sympathetically maintained pain, a "receptor-disease", (Raja 1991) predominates and sympatholytic interventions such as intravenous phentolamine or stellate ganglion block, decreases alpha-adrenergic tone with subsequent improvement in pain, autonomic function and physical capability. Over time, anatomic adaptations, alteration of receptor/transmitter function makes permanent structural damage, in this case sympathetic blockade is ineffective, and pain becomes sympathetically independent.

The diagnosis of CRPS is based upon clinical findings. In CRPS, pain is initiated in the periphery by a noxious insult, is influenced by post-traumatic events, is attenuated by physiologic and/or anatomic variables, and is affected by congenital or genetic factors (Detakats 1965, 1943; Koman Peimer Ref 1995; Koman Green Ref 1999).

The diagnosis of CRPS requires the documentation of regional pain, autonomic dysfunction, atrophy, and functional impairment. In CRPS Type 1, no nerve injury is discernible; while in CRPS Type 2 there is an injury or abnormality of a peripheral nerve. In either case, pain maybe sympathetically maintained or sympathetically independent (Boas 1996; Campbell 1988; Campbell 1992). Sympathetically maintained pain may become sympathetically independent over time or vice-versa.