Complex regional pain syndrome (CRPS) is characterized by a triad of sensor
y, motor and autonomic dysfunctions, with long-standing pain and temperatur
e differences of the affected and contralateral limb as predominant symptom
s. The pathogenesis of the disorder still remains unclear. Among the main h
ypotheses of an underlying pathophysiology we find inflammatory processes a
nd dysfunction of the sympathetic nervous system. Whether the main site of
dysfunction is found centrally or peripherally is not known. With psychophy
sical methods we studied patterns of hyperalgesia to obtain a better unders
tanding of the neuropathic pain component in CRPS. Forty patients in an acu
te phase of CRPS and a median duration of the disease of 10 weeks, were inc
luded in the study. Hyperalgesia to heat was tested with a thermode providi
ng feedback-controlled temperature increases. Two forms of mechanical hyper
algesia were examined: phasic mechanical stimuli by using a custom-made imp
act stimulator for the determination of individual pain thresholds, tonic m
echanical stimuli were applied using a pinch-device. Additionally a 'wind-u
p' paradigm was used to study a pain phenomenon of presumed central origin:
a defined impact stimulus was given once and five times in repetition. A s
ubpopulation of patients was reevaluated for mechanical hyperalgesia after
i.v. injection of 500 mg acetyl-salicylic acid. Hyperalgesia to heat was in
significant. We found, however, a marked mechanical hyperalgesia to phasic
impact stimuli (P < 0.005), whereas, static stimulation (squeezing skin fol
ds) results were insignificant again. Wind-up related pain was also signifi
cantly enhanced in the affected limb (P < 0.02). The anti-inflammatory agen
t had no effect. These results indicate a non-inflammatory pathogenesis in
CRPS presumably central in origin. (C) 1999 International Association for t
he Study of Pain. Published by Elsevier Science B.V.