• R Baron and M Saguer.
• Klinik für Neurologie, Christian-Albrechts-Universität Kiel, Germany.
• Brain. 1993 Dec 1;116 ( Pt 6):1477-96.

AbstractUnder normal conditions acute stimulation and sensitization of polymodal nociceptive C-fibres cause pain and, due to afferent axon reflex activation, a local skin vasodilatation, flare reaction and skin temperature increase. Two questions arise: (i) Do sensitized C-nociceptors signal allodynia in chronic postherpetic neuralgia? (ii) If not, does ongoing peripheral nociceptive C-fibre input maintain a central process that accounts for allodynia? Ten patients with postherpetic neuralgia and tactile allodynia and 10 control subjects were studied using a laser Doppler perfusion monitor. Peripheral nociceptive C-fibre function was assessed by quantitative measurement of the axon reflex vasodilatation and flare reaction induced by histamine iontophoresis and compared with non-neural vasodilatation induced by local skin heating. Resting skin temperature, skin resistance and resting skin blood flow were the same in the allodynic area and the contralateral homologous skin area. The histamine responses (vasodilatation and flare) were significantly reduced or nearly abolished in the allodynic area compared with the contralateral side, whereas the temperature-dependent vasodilatation in patients and the histamine responses in healthy controls showed no side differences. C-fibre mediated pain and itch sensations were also decreased in the allodynic area. These findings indicate a considerable impairment of cutaneous nociceptive C-fibre function in the allodynic area. Allodynic stimuli of 20 s did not cause any local blood flow change. Impairment of C-fibre function was positively correlated with intensity of neuropathic pain. We conclude that sensitized nociceptive C-fibres are not involved in signalling allodynia. Changes in CNS processing may occur after zoster infection that strengthen the synaptic ties between central pain signalling pathways and low-threshold mechanoreceptors with A beta-fibres. This altered central processing is not maintained by ongoing cutaneous nociceptive C-fibre input, at least in some patients with postherpetic neuralgia. On the contrary, an anatomical synaptic reorganization depending on afferent C-fibre degeneration seems to be more likely, particularly in advanced stages of postherpetic neuralgia.

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