The research team, led by M. C. Hall of Monash University together with colleagues including S. Jaberzadeh, recruited nineteen healthy adults, ten men and nine women, with a mean age of 41.8 years. None had neurological, psychological or physical impairments, and none were taking medications. Each volunteer completed a safety screening questionnaire, gave informed consent under the Declaration of Helsinki, and was tested at roughly the same time of day, around ten in the morning, after abstaining from caffeine and alcohol for twenty-four hours. The entire experiment, in which every participant experienced both stimulus directions, fit into a single session of approximately forty minutes, with the order of conditions randomized to guard against fatigue or order effects.

The target muscle was the tibialis anterior, the shin muscle that lifts the foot, recorded through surface electromyography electrodes placed over its belly with a ground electrode on the patella. Participants sat upright in a chair with legs extended and head supported while a figure-of-eight butterfly coil, driven by a MagPro R30 stimulator, delivered pulses over the left motor cortex. The researchers first identified the hotspot, the scalp location roughly one centimetre lateral and posterior to the vertex that produced the largest and most consistent motor evoked potentials across at least five consecutive stimuli. That hotspot was then marked and monitored throughout the session to guarantee that both stimulus directions probed the same patch of cortex.

The two orientations compared were the classic oblique directions used in most motor cortex work: posterior-to-anterior, in which the induced current sweeps from the back of the head toward the front at forty-five degrees to the midline, and anterior-to-posterior, the reverse sweep at one hundred thirty-five degrees. Contemporary biophysical models suggest that stimulus direction does not simply alter the gross flow of current in the brain. Instead, it biases the recruitment of distinct neuronal populations and intracortical networks depending on cortical geometry and the orientation of axons within the motor cortex. Posterior-to-anterior stimulation tends to engage earlier-recruited interneuronal circuits, whereas anterior-to-posterior stimulation more strongly engages later-recruited networks. Because these partially overlapping circuits underpin different excitability measures, the direction of the pulse can, in principle, tilt the balance of what the coil reveals.

Resting motor threshold, the stimulator intensity needed to evoke a reliable response in a resting muscle, was measured with a maximum-likelihood estimation program, the TMS Motor Threshold Assessment Tool, using a criterion of a motor evoked potential above fifty microvolts. The result was strikingly dull: thresholds were almost identical between directions, at 61.16 plus or minus 13.28 percent of maximum stimulator output for anterior-to-posterior and 60.58 plus or minus 11.26 percent for posterior-to-anterior, a difference that was nowhere near statistical significance. The test intensity needed to evoke a standardized baseline response of roughly half a millivolt also did not differ between orientations. In other words, the raw corticospinal output of the leg motor cortex, the direct highway from cortex to spinal cord, appeared indifferent to which way the current was flowing.

The paired-pulse experiments told a more interesting story. In these paradigms, a subthreshold conditioning pulse precedes a suprathreshold test pulse at a defined interval, probing the intracortical circuits that the conditioning pulse activates. Short-interval intracortical inhibition, measured at a three-millisecond interval, is thought to reflect fast-acting inhibition mediated by GABA-A receptors. Intracortical facilitation, measured at ten milliseconds, is believed to involve facilitatory glutamatergic mechanisms, particularly NMDA receptor activity. Long-interval intracortical inhibition, probed here with two suprathreshold pulses separated by one hundred fifty milliseconds, indexes slower inhibition carried by GABA-B receptors. For each measure, thirty paired-pulse trials were recorded per direction, and conditioned responses were expressed as a percentage of the unconditioned test response for the same orientation.

When the team analyzed these trial-level data with a linear mixed-effects model, treating participants as random intercepts to account for the nesting of repeated observations, a weak but statistically significant interaction emerged between stimulus direction and paired-pulse condition. Post hoc analyses traced this interaction to a single measure: intracortical facilitation. Anterior-to-posterior stimulation produced significantly greater facilitation than posterior-to-anterior stimulation, with conditioned responses averaging about 154.85 percent of the test response in the anterior-to-posterior direction against about 144.33 percent in the posterior-to-anterior direction. Short-interval and long-interval inhibition, by contrast, showed no significant differences between directions at all. The GABA-A and GABA-B mediated inhibitory processes of the leg motor cortex appeared essentially blind to pulse direction, while the excitatory facilitatory networks responded differently depending on which way the current swept.

This pattern is the mirror image of several upper-limb findings. In the hand area, studies comparing the same oblique orientations have often reported stronger inhibitory responses, including greater short-interval and long-interval inhibition, with anterior-to-posterior stimulation. The authors suggest that the deeper cortical representation of the leg, its distinct geometry near the interhemispheric fissure, and the greater scalp-to-cortex distance may reduce directional sensitivity in the leg motor cortex, or may bias recruitment toward different intracortical networks than those engaged in the hand area. They are careful to note that paired-pulse TMS cannot isolate specific I-wave components or descending volleys; the findings reflect net intracortical excitability, and interpretations about preferential recruitment of particular interneuronal populations remain indirect, resting on prior literature rather than direct physiological confirmation.

The study has clear limits that the authors acknowledge. Medio-lateral and latero-medial orientations, which some prior lower-limb work has suggested may be optimal for leg stimulation, were not tested, so the conclusions apply only to the two oblique directions compared. Neuronavigation was not used, although consistent hotspot localization procedures were maintained across conditions. Motor evoked potential onset latencies and descending volleys were not directly assessed, and the sample size estimate relied on paired t-test approximations rather than formal mixed-model power calculations, meaning smaller directional effects may have gone undetected. Considerable inter-individual variability in TMS measures, shaped by cortical anatomy, coil-to-cortex distance and corticospinal organization, was not specifically probed.

Even so, the selective directional sensitivity of facilitatory circuits in the leg motor cortex carries practical weight. For researchers using paired-pulse TMS to study the neural control of gait, balance and mobility, or to track plasticity in neurological conditions affecting the lower limbs, the direction of the coil may matter more for excitatory measures than for inhibitory ones, and standardizing orientation across studies could be critical for comparability. The authors point toward future work incorporating MRI-guided neuronavigation, individualized electric field modeling with tools such as SimNIBS, and within-subject comparisons of all four major stimulus directions to clarify how cortical anatomy and field orientation shape recruitment of corticospinal and intracortical networks during lower-limb stimulation. For now, the message is that when it comes to the brain’s control of the legs, which way the current flows may quietly decide what the magnet reveals.

Subject of Research: The effects of transcranial magnetic stimulation coil direction on corticospinal and intracortical excitability of the lower limb motor cortex in healthy adults

Article Title: The effects of TMS stimulus direction on corticospinal and cortico‐cortical excitability of the lower limb in healthy adults

Article References: Hall, M. C., Zoghi, M., Perraton, L., & Jaberzadeh, S. (2026). The effects of TMS stimulus direction on corticospinal and cortico‐cortical excitability of the lower limb in healthy adults. Physiological Reports, 14(20), Article e71144. https://doi.org/10.14814/phy2.71144

Image Credits: AI Generated

DOI: 10.14814/phy2.71144

Keywords: transcranial magnetic stimulation, motor cortex, tibialis anterior, intracortical facilitation, short-interval intracortical inhibition, long-interval intracortical inhibition, resting motor threshold, lower limb, GABA, corticospinal excitability, paired-pulse TMS, Physiological Reports

The study, led by Yuehua Geng and colleagues at Hebei University of Technology together with a collaborator at Tianjin Huanhu Hospital, rests on a growing body of evidence that the vestibular organs of the inner ear are exquisitely sensitive to magnetic fields. The dominant theory holds that the tiny crystals of calcium carbonate embedded in the vestibular system’s otoconia, which normally act as gravity sensors, behave faintly like magnets when exposed to strong, static or low-frequency magnetic fields. When a magnetic field is applied asymmetrically, these crystals experience forces that trick the brain into perceiving head movement that never happened. This is why patients emerging from high-field MRI scanners often report vertigo and involuntary eye movements called nystagmus. Rather than treating this effect as a nuisance, the researchers asked whether it could be harnessed deliberately, and in a controlled dose, to counteract the sensory conflict that gives rise to VIMS.

That conflict is thought to sit at the heart of motion sickness itself. When the eyes report swift, sweeping motion through a virtual landscape while the vestibular system reports a body sitting perfectly still, the brain receives mismatched signals about self-motion. The prevailing explanation, often framed through sensory conflict or postural instability theory, suggests that this discrepancy triggers the classic symptoms of nausea, dizziness, sweating, fatigue and headache. If magnetic vestibular stimulation can add a calibrated vestibular signal to the mix, the researchers reasoned, it might partially reconcile the conflicting streams of information, or at least shift the balance system’s set point in a way that reduces the perceived conflict. Conversely, an improperly tuned stimulation could add yet another discordant signal and make the sickness worse. The study was designed to test precisely this dose-dependence.

Twenty healthy young adults took part in a repeated-measures experiment in which each participant completed five separate sessions. One session served as a baseline control with no virtual reality exposure. In the remaining four, participants viewed VR videos known to provoke VIMS. During those VR sessions, magnetic vestibular stimulation was delivered at three different intensities, set at 90 percent, 100 percent and 110 percent of each individual’s resting motor threshold, a standard reference measure in brain stimulation research that personalizes the stimulation strength to the participant’s own nervous system. Anchoring the intensities to the resting motor threshold, typically measured by observing responses in hand muscles to transcranial magnetic stimulation, ensured that every participant received comparable relative doses despite natural variation in neural excitability between individuals.

To quantify how sick participants felt, the researchers used the Simulator Sickness Questionnaire, a widely adopted instrument that yields a total score along with subscores for nausea, oculomotor strain and disorientation. Questionnaires were administered before and after each session, allowing the team to compute symptom changes attributable to each experimental condition. In parallel, the researchers recorded resting-state electroencephalography after every session and analyzed the data using brain functional network analysis across multiple EEG frequency bands. This approach goes beyond simple power measurements, treating the brain as a network of interacting regions and computing parameters that describe how strongly and how efficiently those regions communicate at rest, from the slow delta and theta rhythms through alpha and beta up into the faster gamma range.

The symptom data told a strikingly non-linear story. Compared with VR exposure alone, stimulation at 110 percent of resting motor threshold was associated with a more favorable symptom profile on the Simulator Sickness Questionnaire, with participants reporting reduced sickness overall. Stimulation at 90 percent, however, showed the opposite pattern: it was associated with aggravated symptoms, leaving participants feeling worse than they did after VR alone. The intermediate 100 percent condition fell between these extremes. In other words, magnetic vestibular stimulation was not simply good or bad for motion sickness; its effect hinged critically on dose, with stronger stimulation appearing protective and weaker stimulation apparently compounding the sensory conflict rather than resolving it.

The EEG network analysis added a neurophysiological dimension to these behavioral findings. Although the authors describe these network results as exploratory, they observed session-related differences in functional network characteristics across multiple frequency bands. Notably, the patterns recorded after the 110 percent stimulation sessions generally resembled the baseline condition more closely than the patterns seen after VR exposure alone or with lower-intensity stimulation. This suggests that high-intensity magnetic stimulation may have helped the brain’s resting network organization recover toward its normal configuration after the disruptive VR experience, hinting that the subjective symptom relief tracked measurable changes in large-scale brain dynamics. Differences appeared in networks spanning several frequency ranges, consistent with the idea that vestibular input propagates widely through cortical and subcortical circuits that govern spatial orientation, autonomic responses and arousal.

The authors are careful to frame these conclusions within the limits of the study. The sample was small, consisting of twenty healthy young adults, and the network-level EEG findings are exploratory rather than definitive. The researchers explicitly state that their findings should be confirmed in larger studies before any clinical or consumer applications are pursued. Individual differences in inner-ear anatomy, the orientation of the labyrinth relative to the applied field, and personal susceptibility to motion sickness are all known to modulate responses to magnetic vestibular stimulation, and these variables would need systematic attention in follow-up work. The protocol also involved repeated sessions, and the authors’ funding came from the CAS Superconducting Research Project and the Hebei Natural Science Foundation, reflecting the superconducting magnet technology underlying the stimulation approach.

Even with those caveats, the implications are considerable. If the dose-dependence holds up in larger trials, the study points toward a design principle rather than a single fix: vestibular stimulation for motion sickness must be calibrated individually, and getting the dose wrong could actively harm the user experience. A future VR headset or clinical device might one day pair with a magnetic stimulation module that tunes intensity to a user’s resting motor threshold, offering a drug-free, non-invasive way to extend comfortable session times for training simulators, rehabilitation programs, telemedicine and entertainment. Beyond VR, the same principle could benefit passengers prone to seasickness or simulator sickness in aviation and driving simulation. The work also strengthens the scientific case that the vestibular system is a legitimate and tractable target for magnetic neuromodulation, a field that has matured from the serendipitous observation of MRI-induced dizziness into a quantitative discipline with dosing frameworks, personalized thresholds and objective neuroimaging endpoints. For the millions of would-be VR users who currently abandon headsets within minutes, that progression carries real promise: the sensory conflict behind their discomfort may soon be something engineers can measure, model and magnetically quiet.

Subject of Research: The dose-dependent regulatory effect of magnetic vestibular stimulation on visually induced motion sickness and resting-state EEG networks in virtual reality users

Article Title: Study on the regulatory effect of magnetic vestibular stimulation on visually induced motion sickness

Article References: Geng, Y., Li, X., Li, Y., Zhai, X., & Xu, G. (2026). Study on the regulatory effect of magnetic vestibular stimulation on visually induced motion sickness. Medical & Biological Engineering & Computing. https://doi.org/10.1007/s11517-026-03666-1

Image Credits: AI Generated

DOI: 10.1007/s11517-026-03666-1

Keywords: magnetic vestibular stimulation, visually induced motion sickness, virtual reality, EEG functional networks, Simulator Sickness Questionnaire, resting motor threshold, vestibular system, brain stimulation, cybersickness, neuromodulation, regulatory, effect