Reflex sympathetic dystrophy: facts and hypotheses

Abstract

Reflex sympathetic dystrophy (RSD) syndrome has been recognized clinically for many years. It is most often initiated by trauma to a nerve, neural plexus, or soft tissue. Diagnostic criteria are the presence of regional pain and other sensory changes following a noxious event. The pain is associated with changes in skin colour, skin temperature, abnormal sweating, oedema, and sometimes motor abnormalities. The clinical course is commonly divided into three stages: first (acute or hyperaemic), second (dystrophic or ischaemic), and third (atrophic) stage. The diagnosis is primarily clinical, but roentgenography, scintigraphy, thermography, electromyography and assessment of nerve conduction velocity can help to confirm the diagnosis. Although a wide variety of treatments have been recommended, the only therapies found to be effective in large studies aim at interfering with the activity of the sympathetic nervous system. To this end, efferent sympathetic nerve activity can be interrupted surgically or chemically. Alternatively, adrenoceptor blockers may be used to relieve pain. Numerous theories have been proposed to explain the pathophysiology. Sympathetic dysfunction, which often has been purported to play a pivotal role in RSD, has been suggested to consist of an increased rate of efferent sympathetic nerve impulses towards the involved extremity induced by increased afferent activity. However, the results of several experimental studies suggest that sympathetic dysfunction consists of supersensitivity to catecholamines induced by (partial) autonomic denervation. Besides, it has been suggested that excitation of sensory nerve fibres at axonal level causes release of neuropeptides at the peripheral endings of these fibres. These neuropeptides may induce vasodilation, increase vascular permeability, and excite surrounding sensory nerve fibres -- a phenomenon referred to as neurogenic inflammation. At the level of the central nervous system, it has been suggested that the increased input from peripheral nociceptors alters the central processing mechanisms.

Heart Rate Variability in Complex Regional Pain Syndrome during Rest and Mental and Orthostatic Stress

“…Edema is a wellknown phenomenon in CRPS that can arise from such venous pooling and may increase after dependency of the affected extremity. 42 Moreover, the sympathetically mediated vasoconstrictor response during dependency is attenuated in patients with CRPS in the clinically affected and unaffected extremity, 43 and there are reports of increased capillary permeability in CRPS. 44 If the tilt-induced abnormal decrease in cardiac output in the patients was due to regional pooling in the affected extremity, the reduction should be highest in the patients with an affected lower extremity due to the greater venous system in the legs.…”

The Application of Implant Technology for Cybernetic Systems

“…It is theorized that sympathetic nerve fibers form connections with the injured peripheral nerve, which can then cause aberrant sensory stimulation. 6 For this reason, the subject performed the Southampton Hand Assessment Procedure 7 before, during, and after the implantation, and the subject's ability to perform 2-point discrimination was regularly assessed for signs of neuropathy. No perceivable loss of hand sensation or motion control was experienced by the subject, and regular testing after extraction has not indicated any measurable long-term defects other than minor scarring.…”

Diagnostic Performance of Three-Phase Bone Scan for Complex Regional Pain Syndrome Type 1 with Optimally Modified Image Criteria

“…It was suggested that CRPS-1 has clinical stages [25] and TPBS findings change according to clinical stages [15][16][17]. It was reported that F/P normalizes or even decreases, and afterward, DU normalizes as the disease progresses [15].…”