Central mechanisms of offset analgesia
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Reduction from a more to a less noxious stimulus intensity produces a disproportionate but transient decrease in perceived pain. Although the relationship between the central nervous system and this offset analgesia has come under investigation using brain imaging, whether offset analgesia is primarily mediated by central rather than peripheral mechanisms has not been established. Here we investigate this question in healthy volunteers using thermal stimuli while recording continuous pain ratings. We constructed a composite stimulus using one Peltier thermode to deliver a constant painful test stimulus while a separate thermode coincidentally delivered a shorter but more intense conditioning stimulus at a distinct location. Three spatial configurations were investigated all delivering stimulation to the ventral forearm either proximally or distally from one another on the same forearm or with thermodes on opposing forearms. We demonstrate a decrease in test stimulus pain levels following offset of an ipsilateral but not contralateral conditioning stimulus. This decrease is comparable in magnitude to that observed during a single thermode classic offset analgesia stimulation. The manifestation of analgesia in one sensory field following cessation of stimulation in a distinct sensory field shows antinociceptive adaptation of primary afferent neurons is unnecessary to produce offset analgesia, and demonstrates central mechanisms are sufficient to achieve temporal filtering of nociceptive information during stimulus offset.