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May 1999

Vascular Abnormalities in Acute Reflex Sympathetic Dystrophy (CRPS I): Complete Inhibition of Sympathetic Nerve Activity With Recovery

Author Affiliations

From the Neurology Clinic (Drs Wasner and Baron and Mr Heckmann) and Anesthesiology Clinic (Dr Maier), Christian-Albrechts-Universität Kiel, Kiel, Germany; and the Department of Neurology, University of California, San Francisco (Dr Baron).

Arch Neurol. 1999;56(5):613-620. doi:10.1001/archneur.56.5.613

Background  Reflex sympathetic dystrophy/complex regional pain syndrome type I (RSD/CRPS I) is a painful neuropathic disorder that may develop as a disproportionate consequence of a trauma affecting the limbs without overt nerve injury. Clinical features are spontaneous pain, hyperalgesia, impairment of motor function, swelling, changes in sweating, and vascular abnormalities.

Objective  To investigate pathophysiological mechanisms of vascular abnormalities in RSD/CRPS I.

Design  Case study.

Setting  Autonomic test laboratory at a university hospital.

Participants  A patient with an early stage of RSD/CRPS I of the upper limb and 2 healthy control subjects.

Interventions  Cutaneous sympathetic vasoconstrictor innervation was assessed by measuring cutaneous blood flow (laser Doppler flowmetry) and skin temperature (infrared thermometry). To quantify sympathetic vasoconstrictor function, phasic (induced by deep inspiration) and tonic (induced by controlled thermoregulation) sympathetic reflexes were analyzed. Venous norepinephrine levels were determined bilaterally. The same tests were performed in the controls after induction of cutaneous antidromic vasodilation produced by histamine dihydrochloride application.

Main Outcome Measure  Sympathetic cutaneous vasoconstrictor function in RSD/CRPS I.

Results  Two weeks after the onset of RSD/CRPS I, skin temperature on the affected side was higher (close to core body temperature) than on the contralateral side at room temperature and during controlled thermoregulation, indicating maximal vasodilation. Phasic and tonic stimulation of cutaneous vasoconstrictor neurons did not induce a decrease of skin blood flow or temperature on the affected side but were normal on the contralateral side. Venous norepinephrine levels were lower on the affected side. Parallel to clinical improvement, loss of vasoconstrictor function completely recovered within weeks. Results of investigations in healthy subjects ruled out the possibility that antidromic vasodilation caused by activation of nociceptive afferents is responsible for the complete depression of sympathetic vasoconstrictor reflexes.

Conclusions  Demonstrated for the first time is a complete functional loss of cutaneous sympathetic vasoconstrictor activity in an early stage of RSD/CRPS I with recovery. The origin of this autonomic dysfunction is in the central nervous system.