Complex Regional Pain Syndrome: What's in a Name?

Abstract

Within a two year period in the 1940's, two Boston physicians published dramatically opposing views on the underlying nature of a syndrome now known as complex regional pain syndrome (CRPS). Evans suggested, in several papers in [1946][1947], that sympathetic reflexes maintain pain and dystrophy in affected limbs. Foisie, in 1947, suggested arterial vasospasms were key in the etiology of this pain syndrome. Evans' hypothesis established the nomenclature for this syndrome for 60 years, and his term "reflex sympathetic dystrophy" guided clinical treatment and research activities over the same period. Foisie's proposed nomenclature was unrecognized, and had virtually no impact on the field. Recent evidence suggests that Evans' contribution to the field may have in fact lead clinicians and researchers astray all those years. This focus article on CRPS compares recent observations with these 2 earlier theories and asks the question --what if we had adopted Foisie's nomenclature from the beginning?

Capillary dysfunction and impaired tissue oxygenation in complex regional pain syndrome: A hypothesis

“…have proposed that CRPS is initiated by a compartment-like syndrome, during which injury-related edema compresses tissue microvessels and causes severe ischemia [7] and that subsequent reperfusion causes microvascular injury and a permanent state of vasospasm, slow flow, and deep tissue ischemia [6,7]. We have extended this notion by proposing that capillary flow disturbances, rather than arteriolar compressions or vasospasms, and tissue hypoxia rather than ischemia, may be central disease entities in CRPS.…”

“…Based on a chronic postischemic pain model [8] and earlier observations of vascular abnormalities in CRPS [6], Coderre et al…”

“…We further speculate that that the high oxygen extraction fraction [43] found in chronic 'cold' CRPS represents suppression of resting blood flow and blood flow responses by endothelial dysfunction [40] to maintain tissue oxygenation. Vasospasms, rather than being the source of ischemia CRPS and CRPS models [6,7], are thus predicted to compensate for downstream capillary dysfunction by attenuating the 'oxygen loss' that occur as blood is shunted through the capillaries at high flow rates. We believe that the intrinsic ROS production throughout these phases causes permanent capillary wall damage, propagating the condition [43,47].…”

Physiotherapy for pain and disability in adults with complex regional pain syndrome (CRPS) types I and II

“…The International Association for the Study of Pain (IASP) introduced the diagnostic label 'CRPS' in the 1990s in order to standardise inconsistencies in terminology and diagnostic criteria (Merskey 1994). Two sub-categories of CRPS have been described: CRPS type I (CRPS I) (formerly and variously referred to as reflex sympathetic dystrophy (RSD), algodystrophy, Sudek's atrophy) in which no nerve lesion is present and CRPS type II (CRPS II) (formerly referred to as causalgia, algoneurodystrophy), in which a co-existing nerve lesion (as determined by nerve conduction studies or surgical inspection for example) is present (Coderre 2011;Todorova 2013). …”

Algodystrophy: recent insight into the pathogenic framework

“…Secondly, some animal models allow to obtain a disease showing features similar to those observed in patient suffering from CRPS-I, despite the obvious limitations existing in comparing animal behaviors to the characteristic and entity of human pain. On the basis of these results, the most convincing pathogenic hypotheses have shifted to a local process of neuroinflammation, probably associated with the clinical features occurring in the first stage of the disease (edema, eritrosis, increased local temperature and sweating); later, in the following phases, the microcirculation impairment and the microvascular damage appear to be the pathophysiologic mechanism responsible for the clinical evolution that can be observed in most patients ("dystrophic" or "cold" phase), characterized by the reduction of edema, the presence of subcianosis and a decrease of the local temperature (4). The role of the hypothesized pathological coupling between the nociceptive afferents and sympathetic fibers as well as the functional changes at the level of the central nervous system still remain only hypotheses that need more strong demonstrations.…”