Brain : a journal of neurology
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Under 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. ⋯ 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.