Why the study?
Does increased sympathetic muscle vasoconstrictor activity influence capsaicin-induced muscle pain in healthy volunteers?
Does increased sympathetic muscle vasoconstrictor activity influence capsaicin-induced muscle pain in healthy volunteers?
Increased sympathetic muscle vasoconstrictor activity does not influence experimentally induced deep somatic pain from intramuscular capsaicin.
No support for sympathetic modulation of experimental muscle pain; leaves open relevance in clinical pain states.
Neuropathic pain syndromes with sympathetically maintained pain are often associated with a deep somatic pain component. An adrenergic interaction between sympathetic vasoconstrictor neurons and cutaneous afferents has been demonstrated. To determine whether a sympathetic-afferent interaction exists in deep somatic tissues, we investigated the effect of sympathetic muscle vasoconstrictor activity on experimentally induced pain. In 12 healthy volunteers, capsaicin was infused into the anterior tibial muscle. Intensity and quality of muscle and referred pain were assessed. The analyses were performed during the presence of low sympathetic muscle vasoconstrictor activity induced by breathing 100% O(2) gas (normocapnia), and during high activity induced by inspiration of 95% O(2) and 5% CO(2) (hypercapnia). The degree of sympathetic muscle vasoconstrictor discharge was monitored indirectly by measuring systemic blood pressure and end-expiratory CO(2) and by performing duplex sonography of muscle resistance vessels. The intensity, quality, and spatial distribution of muscle and referred pain were not significantly different during resting and increased sympathetic muscle vasoconstrictor discharge, indicating that such activity does not influence pain after intramuscular infusion of capsaicin.
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Wasner et al. (2002) studied this question.
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