This Article  • Full text  • PDF  • Reply to article  • Send to a friend  • Save in My Folder  • Save to citation manager  • Permissions  Citing Articles  • Citation map  • Citing articles on HighWire  • Citing articles on ISI (56)  • Contact me when this article is cited  Related Content  • Related articles  • Similar articles in this journal  Topic Collections  • Pain  • Alert me on articles by topic

Complete Inhibition of Sympathetic Nerve Activity With Recovery

Gunnar Wasner, MD; Klaus Heckmann; Christoph Maier, MD; Ralf Baron, MD

Arch Neurol. 1999;56:613-620.

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.

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).

RELATED ARTICLES

Explaining Reflex Sympathetic Dystrophy
Robert J. Schwartzman
Arch Neurol. 1999;56(5):521-522.
EXTRACT | FULL TEXT  

Archives of Neurology Reader's Choice: Continuing Medical Education
Arch Neurol. 1999;56(5):634-636.
FULL TEXT  

THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES

Complex? Regional? Pain? Syndrome?
Schott
PN 2007;7:145-157.
FULL TEXT  

The Effect of Short-Term Dependency and Immobility on Skin Temperature and Colour in the Hand
SINGH and DAVIS
J Hand Surg Eur Vol 2006;31:611-615.
ABSTRACT | FULL TEXT  

Laser Doppler imaging: a developing technique for application in the rheumatic diseases
Murray et al.
Rheumatology (Oxford) 2004;43:1210-1218.
FULL TEXT  

Cortical reorganization during recovery from complex regional pain syndrome
Maihofner et al.
Neurology 2004;63:693-701.
ABSTRACT | FULL TEXT  

Involvement of the Sympathetic Nervous System in Complex Regional Pain Syndrome
Drummond
INT J LOW EXTREM WOUNDS 2004;3:35-42.
ABSTRACT  

Patterns of cortical reorganization in complex regional pain syndrome
Maihofner et al.
Neurology 2003;61:1707-1715.
ABSTRACT | FULL TEXT  

National Institutes of Health Workshop: Reflex Sympathetic Dystrophy/Complex Regional Pain Syndromes-- State-of-the-Science
Baron et al.
Anesth. Analg. 2002;95:1812-1816.
FULL TEXT  

Diagnostic criteria used in studies of reflex sympathetic dystrophy
van de Beek et al.
Neurology 2002;58:522-526.
ABSTRACT | FULL TEXT  

The important role of neuropeptides in complex regional pain syndrome
Birklein et al.
Neurology 2001;57:2179-2184.
ABSTRACT | FULL TEXT  

Pain increases during sympathetic arousal in patients with complex regional pain syndrome
Drummond et al.
Neurology 2001;57:1296-1303.
ABSTRACT | FULL TEXT  

A study of bone densitometry in patients with complex regional pain syndrome after stroke
Kumar et al.
Postgrad. Med. J. 2001;77:519-522.
ABSTRACT | FULL TEXT  

Vascular abnormalities in reflex sympathetic dystrophy (CRPS I): mechanisms and diagnostic value
Wasner et al.
Brain 2001;124:587-599.
ABSTRACT | FULL TEXT  

Reflex Sympathetic Dystrophy
Claeys et al.
NEJM 2000;343:1811-1813.
FULL TEXT  

New Treatments for Reflex Sympathetic Dystrophy
Schwartzman
NEJM 2000;343:654-656.
FULL TEXT  

Explaining Reflex Sympathetic Dystrophy
Schwartzman
Arch Neurol 1999;56:521-522.
FULL TEXT