Brain, Vol. 112, No. 5, 1317-1331, 1989
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HEAT AND MECHANICAL HYPERALGESIA INDUCED BY CAPSAICIN
CROSS MODALITY THRESHOLD MODULATION IN HUMAN C NOCICEPTORS
1Department of Biochemistry, Dartmouth Medical School Hanover, New Hampshire 2Department of Neurology, Good Samaritan Hospital and Medical Center and Department of Neurology, Oregon Health Sciences University Portland, Oregon, USA
Correspondence to:
Correspondence to Dr J Ochoa, Peripheral Nerve Disease Unit, Good Samaritan Hospital and Medical Center, 1040 NW 22nd Avenue, Suite 460, Portland, OR 97210, USA.
Quantitative thermal and mechanical algometry was studied in 4 human subjects exposed to various concentrations of capsaicin administered topically to the skin of the palm or forearm Treated skin patches were assessed for changes in heat pain threshold and in mechanical pain threshold at various controlled temperatures The results showed that: (1) in addition to heat hyperalgesia, capsaicin consistently induces overt mechanical hyperalgesia; (2) thermal and mechanical hyperalgesias are linearly dependent on the log of capsaicin dose, (3) mechanical hyperalgesia is increased by increasing skin temperature; (4) mechanical hyperalgesia is abolished by cooling the skin to a point about 10° C below the threshold for heat pain, a temperature that does not impair touch or sharp pain sensation. These sensory effects of capsaicin are mediated by C fibres, since dissociated A fibre block established by compression-ischaemia does not abolish either spontaneous pain or mechanical hyperalgesia. In addition, abolition of mechanical hyperalgesia by cooling persists during A fibre block Cooling thus appears to act directly, presumably decreasing hyperexcitability of the C nociceptor. Hyperalgesia is also transiently depressed for at least 30 min during the postischaemic period, well beyond the duration of paraesthesiae or overt hyperaemia. Sensory changes identical to those induced experimentally by capsaicin have been observed in patients with a particular variety of neuropathic pain (ABC syndrome) and have been termed polymodal hyperalgesia and cross modality threshold modulation (Ochoa, 1986, Ochoa et al, 1987) Based on these overall observations, it is postulated here that the sensory abnormalities induced by capsaicin and those observed in this particular variety of patients relate to primary hyperalgesia and share a common mechanism in that the excitable receptor membrane of polymodal C nociceptors behaves as if it ‘misreads’ temperature.
Received July 8, 1988. Revised November 29, 1988. Accepted December 20, 1988.
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