The effects of anodal-tDCS on corticospinal excitability enhancement and its after-effects: Conventional vs. unihemispheric concurrent dual-site stimulation Academic Article uri icon


  • Previous researchers have approved the ability of anodal transcranial direct current stimulation (a-tDCS) of the primary motor cortex (M1) to enhance corticospinal excitability (CSE). The primary aim of the current study was to investigate the effect of concurrent stimulation of M1 and a functionally connected cortical site of M1 on CSE modulation. This new technique is called unihemispheric concurrent dual-site a-tDCS (a-tDCSUHCDS). The secondary aim was to investigate the mechanisms underlying the efficacy of this new approach in healthy individuals. In a randomized crossover study, 12 healthy right-handed volunteers received a-tDCS under five conditions: a-tDCS of M1, a-tDCSUHCDS of M1-dorsolateral prefrontal cortex (DLPFC), a-tDCSUHCDS of M1-primary sensory cortex (S1), a-tDCSUHCDS of M1-primary visual cortex (V1), and sham a-tDCSUHCDS. Peak-to-peak amplitude of transcranial magnetic stimulation (TMS) induced MEPs, short-interval intracortical inhibition (SICI) and intracortical facilitation (ICF) were assessed before and four times after each condition. A-tDCSUHCDS conditions induced larger MEPs than conventional a-tDCS. The level of M1 CSE was significantly higher following a-tDCSUHCDS of M1-DLPFC than other a-tDCSUHCDS conditions (p < 0.001), and lasted for over 24 h. The paired-pulse TMS results after a-tDCS of M1-DLPFC showed significant facilitatory increase and inhibitory change. A-tDCSUHCDS of M1-DLPFC increases M1 CSE twofold that of conventional a-tDCS. A-tDCSUHCDS of M1-DLPFC enhances the activity of glutamergic mechanisms for at least 24 h. Such long-lasting M1 CSE enhancement induced by a-tDCSUHCDS of M1-DLPFC could be a valuable finding in clinical scenarios such as learning, motor performance, or pain management. The present study has been registered on the Australian New Zealand Clinical Trial at with registry number of ACTRN12614000817640.

publication date

  • 2015