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Two Types of C Nociceptors in Human Skin and Their Behavior in Areas of Capsaicin-Induced Secondary Hyperalgesia

²Neuropathic Pain Unit, Hospital General de Catalunya, 08190 Barcelona, Spain; ³Departamento de Ciencias Neurológicas, Universidad de Chile, Santiago 10D, Chile; and ⁴Sobell Department, Institute of Neurology, University College London, Queen Square, London WC1N 3BG, United Kingdom; and ¹Oregon Nerve Center, Good Samaritan Hospital and Medical Center, Oregon Health Sciences University, Portland, Oregon 97210.

Submitted 12 June 2003; accepted in final form 12 January 2004

Peripheral nociceptor sensitization is accepted as an important mechanism of cutaneous primary hyperalgesia, but secondary hyperalgesia has been attributed to central mechanisms since evidence for sensitization of primary afferents has been lacking. In this study, microneurography was used to test for changes in sensitivity of C nociceptors in the area of secondary hyperalgesia caused by intradermal injection of capsaicin in humans. Multiple C units were recruited by electrical stimulation of the skin at 0.25 Hz and were identified as discrete series of dots in raster plots of spike latencies. Nociceptors slowed progressively during repetitive stimulation at 2 Hz for 3 min. According to their response to mechanical stimulation, nociceptors could be classified as either mechano-sensitive (CM) or mechano-insensitive (CM_i). These two nociceptor subtypes had different axonal properties: CM_i units slowed by 2% or more when stimulated at 0.25 Hz after a 3-min pause, whereas CM units slowed by <1%. This stimulation protocol was used before capsaicin injection to identify nociceptor subtype without repeated probing, thus avoiding possible mechanical sensitization. Capsaicin, injected 10–50 mm away from the site of electrical stimulation, had no effect on any of 29 CM units, but induced bursts of activity in 11 of 15 CM_i units, after delays ranging from 0.5 to 18 min. The capsaicin injections also sensitized a majority of the CM_i units, so that 11 of 17 developed immediate or delayed responsiveness to mechanical stimuli. This sensitization may contribute a peripheral C fiber component to secondary hyperalgesia.

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