What does autonomic arousal tell us about locomotor learning?

Walking onto a stationary sled previously experienced as moving induces locomotor aftereffects (LAE, or “broken escalator phenomenon”). This particular form of aftereffect can develop after a single adaptation trial and occurs despite subjects being fully aware that the sled will not move. Here, we investigate whether such strong LAE expression may relate to arousal or fear related to instability during the gait adaptation process. Forty healthy subjects were allocated to three sled velocity groups; SLOW (0.6 m/s), MEDIUM (1.3 m/s), or FAST (2.0 m/s). Subjects walked onto the stationary sled for five trials (BEFORE), then onto the moving sled for 15 trials (adaptation or MOVING trials) and, finally, again onto the stationary sled for five trials (AFTER). Explicit warning regarding sled status was given. Trunk position, foot-sled contact timing, autonomic markers (electrodermal activity [EDA], ECG, respiratory movements) in addition to self-reported task-related confidence and state/trait anxiety were recorded. Trunk sway, EDA, and R-R interval shortening were greatest during the first MOVING trial (MOVING_1), progressively attenuating during subsequent MOVING trials. A LAE, recorded as increased gait velocity and trunk sway during AFTER_1, occurred in both MEDIUM and FAST sled velocity groups. The amplitude of forward trunk sway in AFTER_1 (an indicator of aftereffect magnitude) was related to EDA during the final adaptation trial (MOVING_15). AFTER_1 gait velocity (also an indicator of aftereffect magnitude) was related to MOVING_1 trunk sway. Hence, gait velocity and trunk sway components of the LAE are differentially related to kinematic and autonomic parameters during the early and late adaptation phase. The finding that EDA is a predictor of LAE expression indicates that autonomic arousal or fear-based mechanisms can promote locomotor learning. This could in turn explain some unusual characteristics of this LAE, namely its resistance to explicit knowledge and its generation with just a single adaptation trial.     

Attention modulates adaptive motor learning in the ‘broken escalator’ paradigm

The physical stumble caused by stepping onto a stationary (broken) escalator represents a locomotor aftereffect (LAE) that attests to a process of adaptive motor learning. Whether such learning is primarily explicit (requiring attention resources) or implicit (independent of attention) is unknown. To address this question, we diverted attention in the adaptation (MOVING) and aftereffect (AFTER) phases of the LAE by loading these phases with a secondary cognitive task (sequential naming of a vegetable, fruit and a colour). Thirty-six healthy adults were randomly assigned to 3 equally sized groups. They performed 5 trials stepping onto a stationary sled (BEFORE), 5 with the sled moving (MOVING) and 5 with the sled stationary again (AFTER). A ‘Dual-Task-MOVING (DTM)’ group performed the dual-task in the MOVING phase and the ‘Dual-Task-AFTEREFFECT (DTAE)’ group in the AFTER phase. The ‘control’ group performed no dual task. We recorded trunk displacement, gait velocity and gastrocnemius muscle EMG of the left (leading) leg. The DTM, but not the DTAE group, had larger trunk displacement during the MOVING phase, and a smaller trunk displacement aftereffect compared with controls. Gait velocity was unaffected by the secondary cognitive task in either group. Thus, adaptive locomotor learning involves explicit learning, whereas the expression of the aftereffect is automatic (implicit). During rehabilitation, patients should be actively encouraged to maintain maximal attention when learning new or challenging locomotor tasks.     

The effect of gait approach velocity on the broken escalator phenomenon

Walking onto a stationary surface previously experienced as moving generates an after-effect commonly known as the “broken escalator” after-effect (AE). This AE represents an inappropriate expression of the locomotor adaptation necessary to step onto the moving platform (or escalator). It is characterised by two main biomechanical components, an increased gait approach velocity (GAV) and a forward trunk overshoot on gait termination. We investigated whether the trunk overshoot and other biomechanical measures are the direct inertial consequence of the increased GAV or whether these are the result of an independent adaptive mechanism. Forty-eight healthy young adults walked onto a movable sled. They performed 5 trials with the sled stationary at their preferred walking velocity (BEFORE trials), 5 with the sled moving (MOVING or adaptation trials), and 5 with the sled stationary again (AFTER trials). For the AFTER trials, subjects were divided into four groups. One group was instructed to walk slowly (“slower”), another with cueing at the BEFORE pace (“metronome”). The third group walked without cueing at the BEFORE pace (“normal”), and the fourth, fast (“faster”). We measured trunk pitch angle, trunk linear horizontal displacement, left shank pitch angular velocity and surface EMG from lower leg and trunk muscles. In the AFTER trials, an AE was observed in these biomechanical measures for all gait speeds, but these were not strongly dependent on GAV. An AE was present even when GAV was not different from that of BEFORE trials. Therefore, we conclude that, although contributary, the trunk overshoot is not the direct consequence of the increased GAV. Instead, it appears to be generated by anticipatory motor activity “just in case” the sled moves, herewith termed a “pre-emptive” postural adjustment.     

The broken escalator phenomenon. Aftereffect of walking onto a moving platform

We investigated the physiological basis of the 'broken escalator phenomenon', namely the sensation that when walking onto an escalator which is stationary one experiences an odd sensation of imbalance, despite full awareness that the escalator is not going to move. The experimental moving surface was provided by a linear motor-powered sled, moving at 1.2 m/s. Sled velocity, trunk position, trunk angular velocity, EMG of the ankle flexors-extensors and foot-contact signals were recorded in 14 normal subjects. The experiments involved, initially, walking onto the stationary sled (condition Before). Then, subjects walked 20 times onto the moving sled (condition Moving), and it was noted that they increased their walking velocity from a baseline of 0.60 m/s to 0.90 m/s. After the moving trials, subjects were unequivocally warned that the platform would no longer move and asked to walk onto the stationary sled again (condition After). It was found that, despite this warning, subjects walked onto the stationary platform inappropriately fast (0.71 m/s), experienced a large overshoot of the trunk and displayed increased leg electromyographic (EMG) activity. Subjects were surprised by their own behaviour and subjectively reported that the 'broken escalator phenomenon', as experienced in urban life, felt similar to the experiment. By the second trial, most movement parameters had returned to baseline values. The findings represent a motor aftereffect of walking onto a moving platform that occurs despite full knowledge of the changing context. As such, it demonstrates dissociation between the declarative and procedural systems in the CNS. Since gait velocity was raised before foot-sled contact, the findings are at least partly explained by open-loop, predictive behaviour. A cautious strategy of limb stiffness was not responsible for the aftereffect, as revealed by no increase in muscle cocontraction. The observed aftereffect is unlike others previously reported in the literature, which occur only after prolonged continuous exposure to a sensory mismatch, large numbers of learning trials or unpredictable catch trials. The relative ease with which the aftereffect was induced suggests that locomotor adaptation may be more impervious to cognitive control than other types of motor learning.     

The moving platform aftereffect: limited generalization of a locomotor adaptation

We have recently described a postural after-effect of walking onto a stationary platform previously experienced as moving, which occurs despite full knowledge that the platform will no longer move. This experiment involves an initial baseline period when the platform is kept stationary (BEFORE condition), followed by a brief adaptation period when subjects learn to walk onto the platform moving at 1.2 m/s (MOVING condition). Subjects are clearly warned that the platform will no longer move and asked to walk onto it again (AFTER condition). Despite the warning, they walk toward the platform with a velocity greater than that observed during the BEFORE condition, and a large forward sway of the trunk is observed once they have landed on the platform. This aftereffect, which disappears within three trials, represents dissociation of knowledge and action. In the current set of experiments, to gain further insight into this phenomenon, we have manipulated three variables, the context, location, and method of the walking task, between the MOVING and AFTER conditions, to determine how far the adaptation will generalize. It was found that when the gait initiation cue was changed from beeps to a flashing light, or vice versa, there was no difference in the magnitude of the aftereffect, either in terms of walking velocity or forward sway of the trunk. Changing the leg with which gait was initiated, however, reduced sway magnitude by approximately 50%. When subjects changed from forward walking to backward walking, the aftereffect was abolished. Similarly, walking in a location other than the mobile platform did not produce any aftereffect. However, in these latter two experiments, the aftereffect reappeared when subjects reverted to the walking pattern used during the MOVING condition. Hence, these results show that a change in abstract context had no influence, whereas any deviation from the way and location in which the moving platform task was originally performed profoundly reduced the size of the aftereffect. Although the moving platform aftereffect is an example of inappropriate generalization by the motor system across time, these results show that this generalization is highly limited to the method and location in which the original adaptation took place.     

Visuo-vestibular influences on the moving platform locomotor aftereffect

After walking onto a moving platform subjects experience a locomotor aftereffect (LAE), including a self-generated stumble, when walking again onto a stationary platform. Thus this LAE affords examination of the role of vestibular input during an internally generated postural challenge. The experiments involved walking onto the stationary sled (BEFORE trials), walking onto the moving sled (MOVING), and a second set of stationary trials (AFTER). We investigated 9 bilateral labyrinthine defective subjects (LDS) and 13 age-matched normal controls (NC) with eyes open. We repeated the experiment in 5 NC and 5 LDS but this time the AFTER trials were performed twice, first eyes closed and then on eye reopening. During MOVING trials, LDS were considerably unstable, thus confirming the established role of the vestibular system during externally imposed postural perturbations. During AFTER trials, both groups experienced an aftereffect with eyes open and closed, shown as higher approach gait velocity, a forward trunk overshoot, and increased leg EMG. However, there were no significant group differences due to the fact that stopping the forward trunk overshoot was accomplished by anticipatory EMG bursts. On eye reopening the aftereffect re-emerged, significantly larger in LDS than that in NC. The lack of group differences in AFTER trials suggests that when facing internally generated postural perturbations, as in this adaptation process, the CNS relies less on vestibular feedback and more on anticipatory mechanisms. Reemergence of the aftereffect on eye reopening indicates the existence of a feedforward visuo-contextual mechanism for locomotor learning, which is adaptively enhanced in the absence of vestibular function.     

Transcranial direct-current stimulation reduced the excitability of diaphragmatic corticospinal pathways whatever the polarity used

We investigated effects of transcranial direct-current stimulation (tDCS) on the diaphragmatic corticospinal pathways in healthy human. Anodal, cathodal, and sham tDCS were randomly applied upon the left diaphragmatic motor cortex in twelve healthy right-handed men. Corticospinal pathways excitability was assessed by means of transcranial magnetic stimulation (TMS) elicited motor-evoked-potential (MEP). For each tDCS condition, MEPs were recorded before (Pre) tDCS then after 10 min (Post1, at tDCS discontinuation in the anodal and cathodal sessions) and 20 min (Post2). As result, both anodal and cathodal tDCS significantly decreased MEP amplitude of the right hemidiaphragm at both Post1 and Post2, versus Pre. MEP amplitude was unchanged versus Pre during the sham condition. The effects of cathodal and anodal tDCS applied to the diaphragm motor cortex differ from those observed during tDCS of the limb motor cortex. These differences may be related to specific characteristics of the diaphragmatic corticospinal pathways as well as to the diaphragm's functional peculiarities compared with the limb muscles.     

The effect of trial number on the emergence of the ‘broken escalator’ locomotor aftereffect

Walking onto a stationary platform, which had been previously experienced as moving generates a locomotor aftereffect (LAE), which resembles the ‘broken escalator’ phenomenon. Experimentally, this is achieved by having subjects walk initially onto a stationary sled (BEFORE condition), then onto a moving sled (MOVING condition, or adaptation trials) and then again onto the stationary sled (AFTER condition). Subjects are always appropriately warned of the change in conditions. In this paper, we ask how many adaptation trials are needed to produce such a LAE. Thus, in two experiments, the number of MOVING trials was varied between 20 and 5 (Experiment 1) and between 8 and 1 (Experiment 2). Gait velocity, trunk position, foot contact timing and EMG of the ankle flexor-extensors muscles were measured. In comparison with BEFORE trials all groups in the AFTER trials walked inappropriately fast, experienced a large overshoot of the trunk and showed increased leg EMG, indicating that all groups showed a LAE. In each experiment, and for all variables, no significant difference between the groups (i.e. 20 down to one MOVING trials) was found. The study shows that this LAE, in contrast to other motor aftereffects reported in the literature, can be generated with only one or two adaptation trials and without requiring unexpected ‘catch’ trials. The fast aftereffect generation observed is likely to depend on two types of mechanisms: (1) the nature of the sensorimotor adaptation process, involving multiple sensory feedbacks (visual, vestibular and proprioceptive), anticipatory control and large initial task errors and (2) the involvement of two phylogenetically old neural mechanisms, namely locomotion and fear. Fear-relevant mechanisms, which are notably resistant to cognitive control, may be recruited during the adaptation trials and contribute to the release of this LAE.     

Modulating locomotor adaptation with cerebellar stimulation

Human locomotor adaptation is necessary to maintain flexibility of walking. Several lines of research suggest that the cerebellum plays a critical role in motor adaptation. In this study we investigated the effects of noninvasive stimulation of the cerebellum to enhance locomotor adaptation. We found that anodal cerebellar transcranial direct current stimulation (tDCS) applied during adaptation expedited the adaptive process while cathodal cerebellar tDCS slowed it down, without affecting the rate of de-adaptation of the new locomotor pattern. Interestingly, cerebellar tDCS affected the adaptation rate of spatial but not temporal elements of walking. It may be that spatial and temporal control mechanisms are accessible through different neural circuits. Our results suggest that tDCS could be used as a tool to modulate locomotor training in neurological patients with gait impairments.     

Enhancement of pinch force in the lower leg by anodal transcranial direct current stimulation

Transcranial direct current stimulation (tDCS) is a procedure to polarize human brain. It has been reported that tDCS over the hand motor cortex transiently improves the performance of hand motor tasks. Here, we investigated whether tDCS could also improve leg motor functions. Ten healthy subjects performed pinch force (PF) and reaction time (RT) tasks using the left leg before, during and after anodal, cathodal or sham tDCS over the leg motor cortex. The anodal tDCS transiently enhanced the maximal leg PF but not RT during its application. Neither cathodal nor sham stimulation changed the performance. None of the interventions affected hand PF or RT, showing the spatial specificity of the effect of tDCS. These results indicate that motor performance of not only the hands but also the legs can be enhanced by anodal tDCS. tDCS may be applicable to the neuro-rehabilitation of patients with leg motor disability.     

After-effects of transcranial direct current stimulation (tDCS) on cortical spreading depression

Abnormal cortical excitability influences susceptibility to cortical spreading depression (CSD) in migraine. Because transcranial direct current stimulation (tDCS) is capable of inducing lasting changes of cortical excitability, we investigated the after-effects of tDCS on the propagation velocity of CSD in the rat. Twenty-five anesthetised rats received either anodal, cathodal or sham tDCS. The stimulation was applied for 20 min at a current strength of 200 microA after the recording of three baseline CSD measurements. Starting 5 min after tDCS, a further three CSDs were elicited and CSD velocity recorded at intervals of 20 min. tDCS and CSD recording was performed under anaesthesia with chloralose and urethane. As compared to the baseline velocity of 3.14 mm/min, anodal tDCS induced a significant increase of propagation velocity during the first post-tDCS recording (3.49 mm/min). In contrast to anodal tDCS, neither cathodal tDCS nor sham tDCS, which consisted of an initial ramped DC stimulation lasting only 20 s, showed a significant effect on CSD propagation velocity. As anodal tDCS is known to induce a lasting increase of cortical excitability in the clinical setting, our results support the notion that CSD propagation velocity reflects cortical excitability. Since cortical excitability and susceptibility to CSD is elevated in migraine patients, anodal tDCS - by increasing cortical excitability - might increase the probability of migraine attack in these patients, even beyond the end of its application.     

Transcranial direct current stimulation effects on I-wave activity in humans

Transcranial direct current stimulation (tDCS) of the human cerebral cortex modulates cortical excitability noninvasively in a polarity-specific manner: anodal tDCS leads to lasting facilitation and cathodal tDCS to inhibition of motor cortex excitability. To further elucidate the underlying physiological mechanisms, we recorded corticospinal volleys evoked by single-pulse transcranial magnetic stimulation of the primary motor cortex before and after a 5-min period of anodal or cathodal tDCS in eight conscious patients who had electrodes implanted in the cervical epidural space for the control of pain. The effects of anodal tDCS were evaluated in six subjects and the effects of cathodal tDCS in five subjects. Three subjects were studied with both polarities. Anodal tDCS increased the excitability of cortical circuits generating I waves in the corticospinal system, including the earliest wave (I1 wave), whereas cathodal tDCS suppressed later I waves. The motor evoked potential (MEP) amplitude changes immediately following tDCS periods were in agreement with the effects produced on intracortical circuitry. The results deliver additional evidence that tDCS changes the excitability of cortical neurons.     

Modulation of internal model formation during force field-induced motor learning by anodal transcranial direct current stimulation of primary motor cortex

Human subjects can quickly adapt and maintain performance of arm reaching when experiencing novel physical environments such as robot-induced velocity-dependent force fields. Using anodal transcranial direct current stimulation (tDCS) this study showed that the primary motor cortex may play a role in motor adaptation of this sort. Subjects performed arm reaching movement trials in three phases: in a null force field (baseline), in a velocity-dependent force field (adaptation; 25 N s m⁻¹) and once again in a null force field (de-adaptation). Active or sham tDCS was directed to the motor cortex representation of biceps brachii muscle during the adaptation phase of the motor learning protocol. During the adaptation phase, the global error in arm reaching (summed error from an ideal trajectory) was similar in both tDCS conditions. However, active tDCS induced a significantly greater global reaching (overshoot) error during the early stage of de-adaptation compared to the sham tDCS condition. The overshoot error may be representative of the development of a greater predictive movement to overcome the expected imposed force. An estimate of the predictive, initial movement trajectory (signed error in the first 150 ms of movement) was significantly augmented during the adaptation phase with active tDCS compared to sham tDCS. Furthermore, this increase was linearly related to the change of the overshoot summed error in the de-adaptation process. Together the results suggest that anodal tDCS augments the development of an internal model of the novel adapted movement and suggests that the primary motor cortex is involved in adaptation of reaching movements of healthy human subjects.     

Anodal transcranial direct current stimulation of prefrontal cortex enhances working memory

Previous studies have claimed that weak transcranial direct current stimulation (tDCS) induces persisting excitability changes in the human motor cortex that can be more pronounced than cortical modulation induced by transcranial magnetic stimulation, but there are no studies that have evaluated the effects of tDCS on working memory. Our aim was to determine whether anodal transcranial direct current stimulation, which enhances brain cortical excitability and activity, would modify performance in a sequential-letter working memory task when administered to the dorsolateral prefrontal cortex (DLPFC). Fifteen subjects underwent a three-back working memory task based on letters. This task was performed during sham and anodal stimulation applied over the left DLPFC. Moreover seven of these subjects performed the same task, but with inverse polarity (cathodal stimulation of the left DLPFC) and anodal stimulation of the primary motor cortex (M1). Our results indicate that only anodal stimulation of the left prefrontal cortex, but not cathodal stimulation of left DLPFC or anodal stimulation of M1, increases the accuracy of the task performance when compared to sham stimulation of the same area. This accuracy enhancement during active stimulation cannot be accounted for by slowed responses, as response times were not changed by stimulation. Our results indicate that left prefrontal anodal stimulation leads to an enhancement of working memory performance. Furthermore, this effect depends on the stimulation polarity and is specific to the site of stimulation. This result may be helpful to develop future interventions aiming at clinical benefits.Felipe Fregni and Paulo S. Boggio contributed equally to this work.     

Cerebellar direct current stimulation enhances motor learning in older adults

Developing novel approaches to combat age related declines in motor function is key to maintaining health and function in older adults, a subgroup of the population that is rapidly growing. Motor adaptation, a form of motor learning, has been shown to be impaired in healthy older subjects compared with their younger counterparts. Here, we tested whether excitatory anodal transcranial direct current stimulation (tDCS) over the cerebellum could enhance adaptation in older subjects. Participants performed a “center-out” reaching task, adapting to the sudden introduction of a visual cursor rotation. Older participants receiving sham tDCS (mean age 56.3 ± 6.8 years) were slower to adapt than younger participants (mean age 20.7 ± 2.1 years). In contrast, older participants who received anodal tDCS (mean age 59.6 ± 8.1 years) adapted faster, with a rate that was similar to younger subjects. We conclude that cerebellar anodal tDCS enhances motor adaptation in older individuals. Our results highlight the efficacy of the novel approach of using cerebellar tDCS to combat age related deficits in motor learning.     

Time course of the induction of homeostatic plasticity generated by repeated transcranial direct current stimulation of the human motor cortex

Several mechanisms have been proposed that control the amount of plasticity in neuronal circuits and guarantee dynamic stability of neuronal networks. Homeostatic plasticity suggests that the ease with which a synaptic connection is facilitated/suppressed depends on the previous amount of network activity. We describe how such homeostatic-like interactions depend on the time interval between two conditioning protocols and on the duration of the preconditioning protocol. We used transcranial direct current stimulation (tDCS) to produce short-lasting plasticity in the motor cortex of healthy humans. In the main experiment, we compared the aftereffect of a single 5-min session of anodal or cathodal tDCS with the effect of a 5-min tDCS session preceded by an identical 5-min conditioning session administered 30, 3, or 0 min beforehand. Five-minute anodal tDCS increases excitability for about 5 min. The same duration of cathodal tDCS reduces excitability. Increasing the duration of tDCS to 10 min prolongs the duration of the effects. If two 5-min periods of tDCS are applied with a 30-min break between them, the effect of the second period of tDCS is identical to that of 5-min stimulation alone. If the break is only 3 min, then the second session has the opposite effect to 5-min tDCS given alone. Control experiments show that these shifts in the direction of plasticity evolve during the 10 min after the first tDCS session and depend on the duration of the first tDCS but not on intracortical inhibition and facilitation. The results are compatible with a time-dependent "homeostatic-like" rule governing the response of the human motor cortex to plasticity probing protocols.     

Modulating parameters of excitability during and after transcranial direct current stimulation of the human motor cortex

Weak transcranial direct current stimulation (tDCS) of the human motor cortex results in excitability shifts which occur during and after stimulation. These excitability shifts are polarity-specific with anodal tDCS enhancing excitability, and cathodal reducing it. To explore the origin of this excitability modulation in more detail, we measured the input–output curve and motor thresholds as global parameters of cortico-spinal excitability, and determined intracortical inhibition and facilitation, as well as facilitatory indirect wave (I-wave) interactions. Measurements were performed during short-term tDCS, which elicits no after-effects, and during other tDCS protocols which do elicit short- and long-lasting after-effects. Resting and active motor thresholds remained stable during and after tDCS. The slope of the input–output curve was increased by anodal tDCS and decreased by cathodal tDCS. Anodal tDCS of the primary motor cortex reduced intracortical inhibition and enhanced facilitation after tDCS but not during tDCS. Cathodal tDCS reduced facilitation during, and additionally increased inhibition after its administration. During tDCS, I-wave facilitation was not influenced but, for the after-effects, anodal tDCS increased I-wave facilitation, while cathodal tDCS had only minor effects. These results suggest that the effect of tDCS on cortico-spinal excitability during a short period of stimulation (which does not induce after-effects) primarily depends on subthreshold resting membrane potential changes, which are able to modulate the input-output curve, but not motor thresholds. In contrast, the after-effects of tDCS are due to shifts in intracortical inhibition and facilitation, and at least partly also to facilitatory I-wave interaction, which is controlled by synaptic activity.     

Effects of transcranial direct current stimulation over the human motor cortex on corticospinal and transcallosal excitability

Weak transcranial direct current stimulation (tDCS) can induce long lasting changes in cortical excitability. In the present study we asked whether tDCS applied to the left primary motor cortex (M1) also produces aftereffects distant from the site of the stimulating electrodes. We therefore tested corticospinal excitability in the left and the right M1 and transcallosal excitability between the two cortices using transcranial magnetic stimulation (TMS) before and after applying tDCS. Eight healthy subjects received 10 min of anodal or cathodal tDCS (1 mA) to the left M1. We examined the amplitude of contralateral motor evoked potentials (MEPs) and the onset latency and duration of transcallosal inhibition with single pulse TMS. MEPs evoked from the tDCS stimulated (left) M1 were increased by 32% after anodal and decreased by 27% after cathodal tDCS, while transcallosal inhibition evoked from the left M1 remained unchanged. The effect on MEPs evoked from the left M1 lasted longer for cathodal than for anodal tDCS. MEPs evoked from the right M1 were unchanged whilst the duration of transcallosal inhibition evoked from the right M1 was shortened after cathodal tDCS and prolonged after anodal tDCS. The duration of transcallosal inhibition returned to control values before the effect on the MEPs from the left M1 had recovered. These findings are compatible with the idea that tDCS-induced aftereffects in the cortical motor system are limited to the stimulated hemisphere, and that tDCS not only affects corticospinal circuits involved in producing MEPs but also inhibitory interneurons mediating transcallosal inhibition from the contralateral hemisphere.     

Transcranial direct current stimulation of the primary motor cortex affects cortical drive to human musculature as assessed by intermuscular coherence

Intermuscular coherence analysis can be used to assess the common drive to muscles. Coherence in the β-frequency band (15–35 Hz) is thought to arise from common cortical sources. Intermuscular coherence analysis is a potentially attractive tool for the investigation of motor cortical excitability changes because it is non-invasive and can be done relatively quickly. We carried out this study to test the hypothesis that intermuscular coherence analysis was able to detect cortical excitability changes in healthy subjects following transcranial direct current stimulation (tDCS). tDCS has been shown to increase (anodal stimulation) or decrease (cathodal stimulation) the size of the muscle potential evoked by TMS. We found that anodal tDCS caused an increase in motor evoked potential (MEP) size that was paralleled by an increase in β-band intermuscular coherence. Similarly, the reduction in MEP size produced by cathodal tDCS was paralleled by a reduction in β-band intermuscular coherence, while sham stimulation did not result in any change in either MEP amplitude or β-band intermuscular coherence. The similar pattern of change observed for MEP and intermuscular coherence may indicate similar mechanisms of action, although this cannot be assumed without further investigation. These changes do suggest that at least some of the action of tDCS is on cortical networks, and that combined tDCS and intermuscular coherence analysis may be useful in the diagnosis of pathologies affecting motor cortical excitability.     

Transcranial direct current stimulation modulates motor responses evoked by repetitive transcranial magnetic stimulation

Introduction

Repetitive transcranial magnetic stimulation (rTMS) and transcranial direct current stimulation (tDCS) are non-invasive techniques able to induce changes in corticospinal excitability. In this study, we combined rTMS and tDCS to understand possible interactions between the two techniques, and investigate whether they are polarity dependent.

Materials and methods

Eleven healthy subjects participated in the study. Each patient underwent both anodal and cathodal conditioning tDCS in two separate sessions; brief 5 Hz-rTMS trains were delivered over the primary motor cortex at an intensity of 120% the resting motor threshold (RMT) before tDCS (T0), immediately after (T1) and 10 min after current offset (T2). We then analysed changes induced by cathodal and anodal tDCS on TMS variables.

Results

Our results showed that in both anodal and cathodal sessions, the motor evoked potential (MEP) amplitude increased significantly in size before stimulation (T0). Conversely, after anodal tDCS, the MEP facilitation measured at T1 and T2 was absent, whereas after cathodal tDCS it was preserved.

Conclusions

Our findings provide new direct neurophysiological evidence that tDCS influences primary motor cortex excitability.