Autonomic disturbances
A partial nerve lesion is the important preceding event in CRPS II (Reflex Regional Pain Syndrome). Therefore, it has generally been assumed that abnormalities in skin blood flow within the territory of the lesioned nerve are due to peripheral impairment of sympathetic function and sympathetic denervation. During the first weeks after transection of vasoconstrictor fibers, vasodilatation is present within the denervated area. Later the vasculature may develop increased sensitivity to circulating catecholamines, probably due to upregulation of adrenoceptors.66 Similar observations were recently described in the chronic nerve constriction injury model in rats.67,68 The skin on the lesioned side was abnormally warm for about the first post-operative week and then evolved to a chronically cold status. The late-stage cold skin was present despite a complete absence of fluorescence for norepinephrine. Thus, in this animal model, the skin is cold due to denervation supersensitivity of adrenoceptors rather than excessive sympathetic vasoconstrictor activity.Further important signs of sympathetic dysfunction in CRPS are unilateral sweating abnormalities.78 Quantitative measurements of sudomotor activity show enhanced sweat production in the disturbed limb in the acute and chronic stage of the disease in many CRPS patients.23,26 This unilateral hyperhidrosis indicates enhanced sympathetic sudomotor activity.
In conclusion, the combination of increased sudomotor and decreased cutaneous sympathetic vasoconstrictor outflow is a well known centrally regulated thermoregulatory function to keep body core temperature constant in different environments. However, under physiological conditions all extremities are involved. Therefore, the unilateral activation of sudomotor and inhibition of cutaneous sympathetic vasoconstrictor neurons indicates a centrally located thermoregulatory dysfunction in CRPS.
Complex regional pain syndrome – diagnostic, mechanisms,
CNS involvement and therapy
G Wasner1 (#aff1) , J Schattschneider1 (#aff1) , A Binder1 (#aff1) and R Baron1 (#aff1)
Spinal Cord (2003) 41, 61–75. doi:10.1038/sj.sc.3101404