FACILITATION OF THE HUMAN NOCICEPTIVE REFLEX BY STIMULATION OF ALPHA-BETA-FIBERS IN A SECONDARY HYPERALGESIC AREA SUSTAINED BY NOCICEPTIVE INPUT FROM THE PRIMARY HYPERALGESIC AREA

Citation
Ok. Andersen et al., FACILITATION OF THE HUMAN NOCICEPTIVE REFLEX BY STIMULATION OF ALPHA-BETA-FIBERS IN A SECONDARY HYPERALGESIC AREA SUSTAINED BY NOCICEPTIVE INPUT FROM THE PRIMARY HYPERALGESIC AREA, Acta Physiologica Scandinavica, 155(1), 1995, pp. 87-97
Citations number
31
Categorie Soggetti
Physiology
ISSN journal
00016772
Volume
155
Issue
1
Year of publication
1995
Pages
87 - 97
Database
ISI
SICI code
0001-6772(1995)155:1<87:FOTHNR>2.0.ZU;2-0
Abstract
Hyperalgesia was induced in healthy volunteers by topical capsaicin ap plied on the dorsum of the foot within the receptive field of the sura l nerve. Under presence of hyperalgesia different normally non-noxious conditioning stimuli were applied to the hyperalgesic area and the po lysynaptic nociceptive spinal reflex and pain ratings were used to ass ess central excitability. The nociceptive reflex was measured in the k nee extensor and flexor muscles evoked by electrical stimulation of th e sural nerve trunk at an intensity of 1.5 times the initial reflex th reshold (an intensity above the pain threshold). Thermal stimulation o f the primary hyperalgesic area (re)established both on-going spontane ous pain and secondary hyperalgesia. Thus, increased nociceptive refle xes were recorded and increased pain intensity reported when A beta-fi bres in the secondary hyperalgesic area were activated concurrently wi th the reflex testing after a non-noxious thermal stimulation of the p rimary hyperalgesic area. The A beta-fibre activation was achieved by continuous low-intensity electrical stimulation (40 Hz) that was initi ated after on-going pain produced by the thermal stimulation had waned . The same measurement without prior thermal conditioning stimulation of the primary area resulted in no reflex facilitation, indicating rap id changes in the central excitability with existence of on-going noci ceptive activity. This indicates that the development and maintenance of secondary hyperalgesia are dependent on sustained peripheral nocice ptive activity. The study also shows that a central summation of nocic eptive and non-nociceptive afferent activity can occur once secondary hyperalgesia is present.