ArticlePloS one2018
Effect of pain on deafferentation-induced modulation of somatosensory evoked potentials.
Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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0 citing papers in PubMed, 7 citations in OpenAlex.
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4 authors at 1 institution in 1 country.
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Abstract
There is a large body of evidence showing substantial sensorimotor reorganizations after an amputation. These reorganizations are believed to contribute to the development of phantom limb pain, but alternatively, pain might influence the plasticity triggered by the deafferentation. The aim of this study was to test whether pain impacts on deafferentation-induced plasticity in the somatosensory pathways. Fifteen healthy subjects participated in 2 experimental sessions (Pain, No Pain) in which somatosensory evoked potentials (SSEPs) associated with electrical stimulation of the ulnar nerve were assessed before and after temporary ischemic deafferentation induced by inflation of a cuff around the wrist. In the Pain session capsaicin cream was applied on the dorsum of the hand 30 minutes prior to cuff inflation. Results show that pain decreased the amplitude of the N20 (main effect of condition, p = 0.033), with a similar trend for the P25. Temporary ischemic deafferentation had a significant effect on SSEPs (main effect of time), with an increase in the P25 (p = 0.013) and the P45 amplitude (p = 0.005), together with a reduction of the P90 amplitude (p = 0.002). Finally, a significant time x condition interaction, reflecting state-dependent plasticity, was found for the P90 only, the presence of pain decreasing the reduction of amplitude observed in response to deafferentation. In conclusion, these results show that nociceptive input can influence the plasticity induced by a deafferentation, which could be a contributing factor in the cortical somatosensory reorganization observed in chronic pain populations.
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