• Brain Stimul · Jan 2016

    Randomized Controlled Trial

    Not an Aspirin: No Evidence for Acute Anti-Nociception to Laser-Evoked Pain After Motor Cortex rTMS in Healthy Humans.

    • Claire Bradley, Caroline Perchet, Taïssia Lelekov-Boissard, Michel Magnin, and Luis Garcia-Larrea.
    • NEUROPAIN Team, Centre de Recherche en Neurosciences de Lyon, Inserm U1028 - CNRS UMR5292, Université Claude Bernard Lyon 1, Lyon, France. Electronic address: clairebradleyhartmann@gmail.com.
    • Brain Stimul. 2016 Jan 1; 9 (1): 48-57.

    BackgroundHigh-frequency repetitive transcranial magnetic stimulation (HF-rTMS) has shown efficacy in relieving neuropathic pain. Whether its analgesic effect also applies to acute physiological nociception remains unclear due to previous contradictory findings.ObjectiveTo provide an in-depth investigation of the effects of motor cortex HF-rTMS on acute laser-evoked pain and excitability of nociceptive networks in healthy subjects.MethodsRandomized, placebo-controlled, double-blind, cross-over study in 20 healthy participants. Laser heat stimuli at nociceptive threshold were delivered to the right hand, allowing assessment of: (a) subjective pain intensity and unpleasantness; (b) laser-evoked potentials (LEPs, 128 electrodes) and their source model; (c) sympathetic skin responses, and (d) spino-thalamic pathway excitability. Data were collected before and 20 minutes after a session of neuro-navigated 20 Hz rTMS to the contralateral motor cortex.ResultsSubjective pain reports to thermal laser pulses, amplitude of late cortical potentials and sympathetic skin responses were decreased after cortical stimulation, to a similar extent whether it was active or placebo. Early cortical potentials and nociceptive network excitability remained identical before and after rTMS, as did anatomical sources of LEPs.ConclusionsOur results do not provide evidence for a genuine anti-nociceptive effect of rTMS on acute physiological pain. We suggest that motor cortex rTMS may act upon high-order networks linked to the emotional and cognitive appraisal of chronic pain, and/or modulate pathologically sensitized networks, rather than change the physiological transmission within an intact nervous system. Such dichotomy is reminiscent of that observed with most drugs used for neuropathic pain.Copyright © 2015 Elsevier Inc. All rights reserved.

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