The firing increase is due to sensitization brought on by molecular and cellular changes at the primary afferent nociceptor, such as increased expression of voltage-gated sodium channel RNA (particularly Na v1.3, an embryonic channel), increased expression of a cold/menthol-sensitive channel (TRPM8), and mutations in the encoding of sodium channels (an example is the SCN9A gene of the Na v1.7 channel). Spontaneous ectopic firing, however, increases abnormally after peripheral nerve injury. Ĭ fibers (unmyelinated) and Aδ fibers (thinly myelinated) are responsible for eliciting pain sensations in response to noxious stimuli. Nociceptive pain is proportional to the intensity of the stimulus neuropathic pain is not-a small stimulus may provoke increased sensations of pain. In neuropathic pain, signals are generated by the injured nerve, sent to the brain, and interpreted as pain. In nociceptive pain, tissue damage causes the generation of prostaglandins that cause vasodilation, increased blood flow, inflammatory exudates, and the sensitization of nociceptive nerve endings. In particular, pain signaling areas of the peripheral or central nervous system are injured, causing neuropathic pain. Neuropathic pain differs from nociceptive pain in that nociceptive pain is caused by tissue damage, whereas neuropathic pain is produced by nerve damage. Evoked pain includes mechanical allodynia (pain caused by normally nonpainful pressure), heat or cold allodynia (pain caused by normally nonpainful hot/cold stimuli), hyperalgesia (increased sensitivity to a normally painful stimulus), and temporal summation (increasing pain sensation from repetitive application of identical stimuli). Spontaneous sensations include paroxysmal pain (shooting pain that lasts several seconds) and superficial pain (an ongoing, burning sensation). Neuropathic pain presents itself in many different forms.
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