Reflex sympathetic dystrophy syndrome (RSDS), complex regional pain syndrome-type 1 (CRPS 1), neuropathic pain: An equine perspective

Summary A review of the human medical literature in reference to reflex sympathetic dystrophy and alike syndromes was presented. This terminology was often applied where pain was either disproportionate with or anatomically displaced from a known condition or lesion. Symptoms of hyperaesthesia, mechano allodynia and bone deminer-alization as well as vasomotor and sudomotor anomalies were commonly reported. The syndrome had also been diagnosed post operatively, and had been associated with a number of medical and metabolic abnormalities. Initially, reduced sympathetic tone produced vasodilation, inflammation and bone demineralization. An apparent compensatory shift to humoral control of adrenergic effectors in the region then occurred. This was regarded as a logical ‘backup' system where sympathetic control of vasomotor tone was compromised. Normal levels of circulating norepinephrine were then able to maintain vascular tone; however, any increase in levels triggered more profound vasoconstriction, resulting in impairment of the nutritive skin blood flow. Initially, pain resulted from inflammation. Hyperaesthesia and mechano allodynia developed with upgraded adrenergic receptor sensitivity. Further sensitization led to persistent adrenergic receptor activity with the development of permanent cold sensations and unrelenting pain. It was postulated that this sympathetically mediated pain developed as an indirect form of self regulatory immobilization, to reduce physical activity which may have exacerbated the primary tissue trauma. Equine clinical presentations with elements that suggested states of altered sympathetic tone were discussed.