Abstract
BackgroundDuring the chronic stage of Complex Regional Pain Syndrome (CRPS), impaired microcirculation is related to increased vasoconstriction, tissue hypoxia, and metabolic tissue acidosis in the affected limb. Several mechanisms may be responsible for the ischemia and pain in chronic cold CPRS.DiscussionThe diminished blood flow may be caused by either sympathetic dysfunction, hypersensitivity to circulating catecholamines, or endothelial dysfunction. The pain may be of neuropathic, inflammatory, nociceptive, or functional nature, or of mixed origin.SummaryThe origin of the pain should be the basis of the symptomatic therapy. Since the difference in temperature between both hands fluctuates over time in cold CRPS, when in doubt, the clinician should prioritize the patient's report of a persistent cold extremity over clinical tests that show no difference. Future research should focus on developing easily applied methods for clinical use to differentiate between central and peripheral blood flow regulation disorders in individual patients.
Highlights
During the chronic stage of Complex Regional Pain Syndrome (CRPS), impaired microcirculation is related to increased vasoconstriction, tissue hypoxia, and metabolic tissue acidosis in the affected limb
Since the difference in temperature between both hands fluctuates over time in cold CRPS, when in doubt, the clinician should prioritize the patient's report of a persistent cold extremity over clinical tests that show no difference
Complex Regional Pain Syndrome (CRPS) is a painful disorder that usually develops as a disproportionate consequence of trauma
Summary
Mediators of changes in blood flow The endothelium, the largest organ of the body, releases agents that regulate vasomotor function, trigger inflammatory processes and affect hemostasis in response to shear stress and hormonal stimuli, such as vasoactive substances [42]. Given the pathology of muscle tissue (including lipofuscin deposits, atrophic fibers, and severely thickened capillary basal membranes) observed in the amputated limbs of CRSP patients as described by van der Laan et al [7], as well as the role of muscle pathology (increased lipid peroxidation products, pro-inflammatory cytokines and lactate) in mechanical allodynia of rats with ischemia-reperfusion injury, alterations in deep tissue blood flow, as well as skin blood flow, may be important in CRPS. Intradermal injections of either norepinephrine or the endothelial NO synthase inhibitor N5(1-Iminoethyl)-L-ornithine dihydrochloride (L-NIO) (both of which should reduce blood flow) induce sustained nociceptive behaviours in rats with hind paw ischemia-reperfusion injuries; the nociceptive behaviours induced by NE are reduced by local or systemic administration of the NO donors sodium nitroprusside and SIN1, respectively [96] This observation raises the possibility that sympathetically maintained pain may depend more on NE-induced vasoconstriction than on sympatheticafferent coupling. Bolel et al described a non-invasive stellate ganglion blockade using diadynamic current [148] that could provide a simple and easy to perform method to differentiate between SMP and SIP
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