Klinische Neurophysiologie 2009; 40 - P348
DOI: 10.1055/s-0029-1216207

Transcranial direct current stimulation: functional lateralization in healthy subjects with a virtual lesion?

R Fleischmann 1, S Schmidt 1, J Roehmel 1, A Kraft 1, SA Brandt 1
  • 1Berlin

The excitability of the human primary motor cortex can be increased or decreased following anodal and cathodal transcranial direct current stimulation (tDCS), respectively (Nitsche, 2001 and 2003; Priori, 2003). Studies in animals and humans show that primary motor cortices are strongly connected by transcallosal fibers and inhibit each other. This suggests that modification of excitability of the one motor cortex should effect the excitability in the homologous contralateral cortex in an opposite manner. This can be quantified by the lateralization index, which compares the differential employment of bilateral motor cortices (Carey, 2006) and has led to application of inhibition to contralesional areas to facilitate resitutive processes e.g. in stroke patients (Hummel, 2005; Fregni, 2005 and 2006). Lateralization in healthy subjects remains to be investigated. Here, we hypothesize that the contralesional („virtual lesion“) effects induced by anodal and cathodal tDCS will reflect lateralization processes. Transcranial magnetic stimulation (TMS) was used to quantify changes of cortical excitability.

We applied 15 minutes of anodal, cathodal or sham tDCS to the primary motor cortex of the dominant hemipshere in 5 healthy subjects. Electromyographic signals (EMG) were recorded from the abductor pollicis brevis and first dorsal interosseus muscle. The muscle evoked potential (MEP) amplitude was defined by peak-to-peak measures from belly-tendon surface recordings. We performed single-pulse measurements of corticospinal output excitability and paired-pulse measurements to quantify intracortical facilitation and inhibiton.

Mean MEP changes of up to 50%, increase or decrease for anodal or cathodal stimulation condition, respectively, were found in the stimulated hemisphere. The same stimulation exerted opposing effects in the contralateral primary motor cortex as indicated by changes in mean MEP amplitudes of up to 20%. Paired-pulse stimulation protocols showed consistent results in either hemipshere.

We find that tDCS not only modifies cortical activity underneath the stimulation electrode but also induces lateralization in healthy subjects. This complements our knowledge about the effects of tDCS at distant sites of the brain in healthy subjects and highlights the capability of tDCS as a tool to induce a virtual lesion, which in at least two measures resembles maladaptive excitability changes in the cerebral cortex shown for the chronic phase of stroke.