Brain, Vol. 115, No. 2, 607-621, 1992
© 1992 Oxford University Press
research-article |
THE PLASTICITY OF CUTANEOUS HYPERALGESIA DURING SYMPATHETIC GANGLION BLOCKADE IN PATIENTS WITH NEUROPATHIC PAIN
1Department of Neurosurgery Baltimore, USA 2Department of Anesthesiology and Critical Care Medicine, The Johns Hopkins University Baltimore, USA
Correspondence to:
Correspondence to: Srinivasa N Raja, MD, Department of Anesthesiology and Critical Care Medicine, Osler 304, The Johns Hopkins Hospital, Baltimore, MD 21205, USA.
In order to investigate the plasticity of cutaneous sensory abnormalities in neuropathic pain, we monitored sensory and vasomotor effects of diagnostic sympathetic ganglion blocks in 24 patients, who suffered from chronic pain and cutaneous hyperalgesia following peripheral nerve or tissue injury. Ongoing pain was rated on a visual analogue scale, and pain evoked by innocuous tactile and cooling stimuli (hyperalgesia) on a verbal rating scale Skin temperatures were determined at symmetric sites. In two patients, cutaneous blood flow was measured with a laser Doppler device
The sympathetic blocks led to a significant reduction of the group mean ongoing pain (40%) and cutaneous hyperalgesia (50%). Between patients, however, there was a large variability that could not be related merely to adequacy of sympathetic blockade. Neither the magnitude of change in skin temperature nor the final skin temperature after the block correlated with the amount of pain relief The relief of hyperagesia, however, correlated with the relief of ongoing pain.
Nine patients experienced pain relief of greater than 50%. In these patients, the time course of hyperalgesia relief was similar to the time course of relief of ongoing pain Pain relief occurred simultaneously with or a few minutes before cutaneous vasodilatation. During the block, even vigorous mechanical or cold stimuli did not rekindle hyperalgesia. In all patients, pain and hyperalgesia returned within a day after the block In three patients tested, passive warming of the limb to the temperature achieved by the sympathetic block had negligible effects on pain and hyperalgesia.
The hyperalgesia of sympathetically maintained pain is thought to be due to sensitization of central pain-signalling neurons to mechanoreceptor input. The present data indicate that this sensitization is highly plastic even when the disease has persisted for months or years. It could be reversed within minutes by a sympathetic blockade, but returned when sympathetic block subsided. Mechanoreceptor input by itself was not sufficient to maintain or rekindle the central sensitization This supports the hypothesis that low-grade activity of nociceptors, possibly due to development of
-adrenergic sensitivity after injury, is involved in the maintenance of central sensitization
.
Received March 19, 1991. Revised November 7, 1991. Accepted December 12, 1991.
*Present address Institute of Physiology, University Hospital Eppendorf, D-2000 Hamburg 20, Germany
**Present address Department of Physiology, University of Toronto, Toronto, Canada M5S-1A8
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