• G Wasner, R Baron, and W Jänig.
• Klinik für Neurologie der Christian-Albrechts-Universität Kiel, Germany.
• Pain. 1999 Feb 1;79(2-3):113-9.

AbstractRecently, Cervero and Laird (NeuroReport, 7 (1996) 526-528; Pain, 68 (1996) 13-23) proposed a new pathophysiological mechanism of dynamic mechanical allodynia in skin. Using the capsaicin pain model in humans, they showed that light mechanical stimulation within an area of secondary mechanical allodynia induces vasodilatation measured by laser-Doppler flowmetry. They suggested that the low-threshold A beta-mechanoreceptive fibres depolarize the central terminals of nociceptive primary afferent neurons via interneurons. Consequently, the vasodilatation is produced by impulses conducted antidromically in nociceptive C-axons. The allodynia was proposed to result from depolarization of central terminals of primary afferent neurons with C-fibres with activation of nociceptive dorsal horn neurons. In order to extend these findings, we used the same experimental approach but additionally stimulated the A beta-fibres electrically to evoke secondary allodynia during simultaneous monitoring skin blood flow. Twenty microlitres of a 0.5% capsaicin solution was injected intradermally into the dorsal forearm. Skin sites that demonstrated dynamic mechanical allodynia but were not located within the area of primary hyperalgesia and flare were investigated. Ten mm away from a laser-Doppler probe, dynamic mechanical allodynia was induced for 1 min (1) by moving a cotton swab and (2) by electrically stimulating the afferent nerve endings transdermally. Increasing stimulus intensities were applied (0.3-4 mA, 40 Hz, pulse duration 0.2 ms). After intracutaneous injection of capsaicin, light mechanical stimulation elicited a burning painful sensation (numeric analogue scale (NAS) 1.5-3) and concomitant movement artefacts at the laser signal. Antidromic vasodilatation was never observed. In this area of dynamic allodynia, electrical stimulation at stimulus intensities that were not painful before capsaicin injection (A beta-stimulation) was now able to elicit a burning painful sensation (NAS 1.5-3). No change in blood flow was detected. When the stimulus intensities were increased reaching levels that were also painful before capsaicin treatment (C-fibre stimulation), an increase in blood flow could be induced showing the time course of an axon reflex vasodilatation. In conclusion, electrical stimulation of A beta-fibres in allodynic skin does not induce antidromic vasodilatation. Consequently, interaction of A beta-mechanoreceptive fibres and nociceptive C-fibres at a presynaptic level is unlikely to produce antidromically conducted impulses and therefore cannot explain the pathophysiology of mechanical allodynia. Alternatively, it is much more likely that under pathophysiological conditions, activity in A beta-fibres may activate nociceptive second-order neurons, i.e. in the spinal cord.

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