DOI: The Greek E-Journal of Perioperative Medicine 2004; 2:2-10

Although the experience of nociceptive pain ultimately depends on interpretation by the cerebral cortex, it occurs primarily as a result of a noxious stimulus (one which when prolonged produces damage resulting in the humoral and cellular responses of inflammation) activating myelinated A-δ and unmyelinated C noci-ceptors. A-δ nociceptors are only mechanically sensitive, have a multipunctate receptive field, conduct at 5-25m/sec, and transduce pricking or stabbing sensations (fast or first pain) which cause organisms to withdraw. C-polymodal nociceptors, usually cover a single receptive area, conduct at less than 2m/sec, and convey messages generated by tissue damage, (slow or second pain), which cause the organism to immobilize. They are polymodal because they respond to noxious thermal, mechanical, and chemical stimuli [1].

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