Establishing safety limits for transcranial direct current stimulation.

The recent resurgence in the use of transcranial Direct Current Stimulation (tDCS) for electrotherapy and human cognition studies was motivated by studies demonstrating lasting change in cortico-spinal excitability following tDCS (Priori et al., 1998; Nitsche and Paulus, 2000, 2001) including at the University of Gottingen. Subsequent tDCS studies have largely adapted the Gottingen protocols including the use of relatively-large wet sponges with size nominally 25–35 cm 2 and currents of 1–2 mA applied for durations up to 20 min (resulting in charge densities of 343–960 C/m 2). Reproduction of these protocols across a wide range of applications and subjects (Nitsche et al. the need for continued vigilance in examining potential hazards, combined with the desire by clinicians to explore increasing intensity protocols and duration of after effects (Nitsche et al., 2004b; Fregni et al., 2006) warrants investigation of the thresholds and mechanisms of potential tDCS hazards. In developing safety guidelines for tDCS, several biophysical qualifications should be made. Firstly, if and what type of injury results from electrical stimulation is wholly dependent on the precise stimulation hardware and waveform applied; thus while one can draw general insights from a broad range of electrical safety studies (Agnew and McCreery, 1987; Merrill et al., 2005), it is neither accurate nor prudent to determine quantitative safety standards for tDCS from these reports. Moreover, tDCS itself represents a constellation of technologies and approaches (e.g. sponge salinity, electrode configurations, ramp waveform, intensity; Bikson et al., 2008) such that the safety standards may be tDCS protocol specific. Second, the injurious effects of tDCS on skin and brain are not necessarily linked, and should be considered independently from both the risk and mitigation standpoint. Acute pain and tissue damage of skin can further be distinguished, as should brain cognitive impairment versus brain tissue damage factors. The report in this edition by Liebetanz and colleagues in Gottin-gen is a valuable contribution towards this last factor. Brain tissue damage was accessed in a rat model following epicranial electrode stimulation (Liebetanz et al., 2009). By fixing the electrode directly on the cranium, and using a large counter electrode on the ventral thorax, the study design maximized the electrode current that crosses directly into the skull; thus in this model the peak current density in the rat brain may approach the current density at the electrode. Liebetanz and colleagues report that brain lesions were observed at a minimum cathodal electrode current …