The everyday experience of stepping onto a stationary escalator causes a stumble, despite our full awareness that the escalator is broken. In the laboratory, this "broken escalator" phenomenon is reproduced when subjects step onto an obviously stationary platform (AFTER trials) that was previously experienced as moving (MOVING trials) and attests to a process of motor adaptation. Given the critical role of M1 in upper limb motor adaptation and the potential for transcranial direct current stimulation (tDCS) to increase cortical excitability, we hypothesized that anodal tDCS over leg M1 and premotor cortices would increase the size and duration of the locomotor aftereffect. Thirty healthy volunteers received either sham or real tDCS (anodal bihemispheric tDCS; 2 mA for 15 min at rest) to induce excitatory effects over the primary motor and premotor cortex before walking onto the moving platform. The real tDCS group, compared with sham, displayed larger trunk sway and increased gait velocity in the first AFTER trial and a persistence of the trunk sway aftereffect into the second AFTER trial. We also used transcranial magnetic stimulation to probe changes in cortical leg excitability using different electrode montages and eyeblink conditioning, before and after tDCS, as well as simulating the current flow of tDCS on the human brain using a computational model of these different tDCS montages. Our data show that anodal tDCS induces excitability changes in lower limb motor cortex with resultant enhancement of locomotor adaptation aftereffects. These findings might encourage the use of tDCS over leg motor and premotor regions to improve locomotor control in patients with neurological gait disorders.
The cardinal features of vestibular dysfunction are illusory self-motion (vertigo) and spatial disorientation. Testing 18 acute focal cortical lesion patients, Kaski et al. show that temporoparietal junction lesions impair vestibular-guided spatial orientation but not self-motion perception. Distinct cortical substrates thus mediate the vestibular percepts of spatial orientation and self-motion.
The response to stimulating the visual cortex with transcranial magnetic stimulation (TMS) depends on its initial activation state, for example, visual motion adaptation biases perceived TMS-induced phosphene characteristics (e.g., color). We quantified this state dependence by assessing the probability of reporting a phosphene (P(λ) ) with "threshold" TMS (i.e., the TMS intensity producing P(λ) = 0.5 at baseline) following visual motion adaptation to a random dot motion display. Postadaptation, P(λ) was increased, and this effect was confined to the adapted neuronal population. We then adapted subjects using a population of moving dots of fixed average motion direction with standard deviations (SD) ranging from 1° to 128° (SD fixed for a given trial). P(λ) was significantly increased at all dot motion SDs except SD = 1°. Neuronal adaptation increases the susceptibility of the neuronal population to activation by threshold intensity TMS. Thus the process of neuronal adaption is not necessarily synonymous with a downmodulation of neuronal excitability.
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