This result is consistent with analogous findings in non-invasive brain stimulation studies in animals and humans that suggest that the response to transcranial stimulation is highly variable. In one recent lesion study using a feline model (Afifi et al., 2013), half the subjects positively responded to transcranial magnetic stimulation and half the subjects responded negatively,

and the dichotomy of the response was not reflected in the extent or the size of lesion. In humans, the response of the motor evoked potential amplitude to 1-Hz rTMS was similarly split: 75% of the participants displayed a decrease in the signal while 25% showed no change or an increase (Gangitano et al., 2002). Similar findings have been seen in studies of tDCS and depression (Loo et al., 2012). The biological basis of responsivity to transcranial stimulation Akt inhibitor Omipalisib research buy is an open question in need of resolution to achieve maximum efficacy. It is interesting to note

that the recovery of contralesional targets occurred in two phases. The basis of this recovery and whether each phase represents a different mechanism is unclear, although the time period between the two phases of recovery in the standard task is accompanied by a decrease in performance to targets in the ipsilesional hemifield in the more demanding laser and runway tasks. This finding suggests that tDCS may have done more than simply reduce aberrant hyperexcitability in the contralesional cerebral hemisphere. The posterior parietal cortex is critical for performance in the runway and laser tasks (Hardy & Stein, 1988; Afifi et al., 2013), and these data are consistent with the notion that tDCS is deactivating this cortex. This effect may best be considered a cost of this ultra-long

stimulation paradigm, and in this system the cost ultimately dissipated. However, this effect should be carefully considered during similar applications in the human, both as a potential side effect and also as an early signature of treatment response and a mechanism these which the lesioned hemisphere might require in order to adopt function. This is the first study to demonstrate that a 70-session tDCS regime to the contralesional (intact) brain hemisphere partially reverses lesion-induced deficits. The recovery was limited to moving stimuli located in the periphery of the contralateral visual hemifield, and occurred in two phases. A potential cost of the stimulation to intact targets was noted, but was minor and disappeared during the later phases of the stimulation regimen. These data indicate that increasing the number of tDCS sessions may improve the efficacy of non-invasive brain stimulation. This study was supported by NIH NS062317 (AV-C and RJR) and the FP68 ANR eraNET-NEURON “Beyondvis” and DRCD & AP-HP-PHRC Regional “Neglect” grants (AV-C). We thank Dr Linda Afifi for assisting with surgeries and behavioral training.