Voluntary movement reverses the effect of cathodal transcranial direct current stimulation (tDCS) on corticomotor excitability

Voluntary movement reverses the effect of cathodal transcranial direct current stimulation (tDCS)... Motor cortex activity level is a critical part of the effect of transcranial direct current stimulation (tDCS) on corticomotor excitability. Based on homeostatic plasticity, the state of the stimulated cortical area influences the direction of neuroplastic changes induced by stimuli. Owing to homeostatic plasticity, cathodal tDCS (c-tDCS) would likely have a pronounced inhibitory effect on corticomotor excitability during a motor task, compared with the resting state. To test this hypothesis, we detected motor evoked potential (MEP) amplitude changes before and during c-tDCS with voluntary movement. Twelve healthy right-handed volunteers (9 males, 27–48 years) were enrolled in the study. Subjects performed little finger abduction motor task. Passive (APB) and active (ADM) muscles were studied. MEP amplitudes were measured during resting (baseline) and movement stages, and subsequently with the contralateral M1 modulated by c-tDCS. c-tDCS caused reduced baseline MEP amplitude in the ADM (p < 0.05) and APB (p < 0.001) muscles. Sham stimulation had no effect on the baseline MEP amplitudes. MEP amplitude ratio (MEP amplitude triggered by movement/baseline MEP amplitude) was higher during c-tDCS than before c-tDCS (p < 0.01). Our results suggested that during voluntary contraction, c-tDCS has an opposite effect on corticospinal excitability compared with resting state modulation effect. This contrast effect could be related to modulation of movement preparation and execution. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Experimental Brain Research Springer Journals

Voluntary movement reverses the effect of cathodal transcranial direct current stimulation (tDCS) on corticomotor excitability

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Publisher
Springer Berlin Heidelberg
Copyright
Copyright © 2017 by Springer-Verlag Berlin Heidelberg
Subject
Biomedicine; Neurosciences; Neurology
ISSN
0014-4819
eISSN
1432-1106
D.O.I.
10.1007/s00221-017-5001-9
Publisher site
See Article on Publisher Site

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