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High frequency electrical stimulation concurrently induces central sensitization and ipsilateral inhibitory pain modulation
Author(s) -
Vo L.,
Drummond P.D.
Publication year - 2013
Publication title -
european journal of pain
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.305
H-Index - 109
eISSN - 1532-2149
pISSN - 1090-3801
DOI - 10.1002/j.1532-2149.2012.00208.x
Subject(s) - sensitization , medicine , diffuse noxious inhibitory control , anesthesia , inhibitory postsynaptic potential , stimulation , forearm , conditioning , forehead , peripheral , threshold of pain , nociception , surgery , noxious stimulus , immunology , statistics , receptor , mathematics
Background In healthy humans, analgesia to blunt pressure develops in the ipsilateral forehead during various forms of limb pain. The aim of the current study was to determine whether this analgesic response is induced by ultraviolet B radiation ( UVB ), which evokes signs of peripheral sensitization, or by high‐frequency electrical stimulation ( HFS ), which triggers signs of central sensitization. Methods Before and after HFS and UVB conditioning, sensitivity to heat and to blunt and sharp stimuli was assessed at and adjacent to the treated site in the forearm. In addition, sensitivity to blunt pressure was measured bilaterally in the forehead. The effect of ipsilateral versus contralateral temple cooling on electrically evoked pain in the forearm was then examined, to determine whether HFS or UVB conditioning altered inhibitory pain modulation. Results UVB conditioning triggered signs of peripheral sensitization, whereas HFS conditioning triggered signs of central sensitization. Importantly, ipsilateral forehead analgesia developed after HFS but not UVB conditioning. In addition, decreases in electrically evoked pain at the HFS ‐treated site were greater during ipsilateral than contralateral temple cooling, whereas decreases at the UVB ‐treated site were similar during both procedures. Conclusions HFS conditioning induced signs of central sensitization in the forearm and analgesia both in the ipsilateral forehead and the HFS ‐treated site. This ipsilateral analgesia was not due to peripheral sensitization or other non‐specific effects, as it failed to develop after UVB conditioning. Thus, the supra‐spinal mechanisms that evoke central sensitization might also trigger a hemilateral inhibitory pain modulation process. This inhibitory process could sharpen the boundaries of central sensitization or limit its spread.