Methods and mechanisms of transcranial direct current stimulation

Weak direct current stimulation induces neuroplastic changes of cortical excitability in animals and humans. The effects depend on polarity and duration of the direct current stimulation as well as on the applied current strength. Originally based on animal experiments of the 1950s and 1960s, the technique of transcranial direct current stimulation (tDCS) has recently been successfully transferred to the human motor cortex. Here, cathodal tDCS results in a decreased cortical excitability whereas the anodal form leads to an enhancement of TMS-assessed cortical excitability. Depending on the stimulation duration, after-effects can be achieved that last up to one hour. Pharmacological studies, which combined tDCS with a premedication of the Na channel-blocking carbamazepine and the NMDA receptor antagonist dextromethorphan, demonstrate that the after-effects of tDCS involve polarity-specific shifts of membrane potentials and a consecutive NMDA receptor-mediated transformation of synaptic strength. Therefore, the mechanisms of tDCS after-effects share similarities with those of the well-known neuroplastic effects of UP and LTD. With respect to the therapeutic potential of tDCS, pilot studies suggest positive effects of anodal tDCS in patients with chronic pain, chronic stroke and major depression. For cathodal tDCS, recent animal and clinical studies demonstrated antiepileptic properties, supporting the hypothesis that cathodal tDCS might serve as a therapeutic option in drug-refractory focal epilepsy, particular in cases with superficial foci as in patients with epilepsia partialis continua or cortical dysplasia. Before these piloting results of beneficial tDCS effects can be transformed into a broader therapeutic application of tDCS in patients with epilepsy, chronic stroke or major depression, further research should optimize the power and stability of the induced neuroplastic effects.