Neurophysiological Bases of Human Movement 2025

Modelling human movement neuromechanics for generalisable human-robot interfaces

Movement is critical for human wellbeing. Therefore, developing robotic technologies that can preserve our ability of moving as we age or restore it following an injury is a key necessity. Wearable robots, such as exoskeletons and exosuits, are rapidly evolving from assistive tools into intelligent platforms that can influence human musculoskeltal health.

Recent advancements in wearable exoskeletons have demonstrated the ability to reduce metabolic cost and neuromechanical effort during locomotion. Emerging improvements in actuation, sensing, and form factor now enable lighter, softer systems—bringing us closer to devices that can be worn continuously and unobtrusively, much like a “second skin.” As these systems become integrated into daily life across rehabilitation, industrial, and occupational domains, a critical paradigm shift is needed. Rather than only assisting movement in the short term, next-generation wearable robots must interface with the human body over extended periods to influence long-term musculoskeletal adaptation.

This raises fundamental new questions: How do neuromuscular tissues respond to robot-induced mechanical stimuli? Can we harness these responses to restore neuromuscular function for movement ? Answering these questions requires bridging knowledge gaps at the intersection of biomechanics, neuromechanics, and robotics.

This talk will outline ongoing work aimed at addressing these questions. Specifically, the talk will outline how we can use bioelectrical recording and numerical modelling to decode the activity of spinal motor neurons and concurrently derive the resulting force and stiffness-generating musculoskeletal function in the intact moving human in vivo. The second part of the talk will outline how the proposed approach can be extended to develop robotic technologies that could assist and potentially reshape the human neuromuscular system via targeted electro-mechanical stimuli deliverered at extreme ends of the spatio-temporal scale, e.g., cell-to-organ growth over weeks.

Over the next decade, this framework may transform wearable robots into proactive, adaptive tools for preventing chronic musculoskeletal conditions, promoting recovery, and maintaining physical independence—ultimately improving healthspan and quality of life.

Investigating the role of intrinsic plasticity in the human motor cortex during motor skill learning

Background

The brain’s ability to change in response to experience, known as plasticity, is crucial for learning, memory, and recovery from injury. Most research focuses on synaptic plasticity: changes at the connections between neurons. However, the brain also adapts through intrinsic plasticity, in which changes occur to the excitability of axons thereby regulating action potential firing^1,2. Intrinsic plasticity is poorly understood in humans due to a lack of specific, non-invasive measurement tools. Controllable pulse transcranial magnetic stimulation (cTMS) allows for the systematic variation of pulse shape to directly measure changes in axonal excitability³ thereby dissociating synaptic and intrinsic effects. We sought to determine if motor skill learning in humans is accompanied by changes to the strength-duration time constant (SDTC), a biophysical property reflecting voltage-gated sodium channel activity in the axonal membrane⁴, supporting a role for intrinsic plasticity in the human motor cortex.

Methods

11 healthy adults completed a ballistic thumb abduction task known to drive plasticity⁵. Task performance kinematics were recorded by accelerometery. Motor-evoked potentials (MEPs) were recorded by electromyography (EMG) in response to cTMS stimulation across a range of pulse widths (30, 60, 90, 120 µs) and intensities (90–120%RMT) to derive input-output curves and SDTC before and after practice (5-min, 30-min, 60-min) from the trained APB and a control muscle (ADM). Procedures adhered to the Declaration of Helsinki and were approved by the King’s College London Research Ethics Committee (HR-24/25-39903). All participants were free from neurological or psychiatric disorders and not taking neuroactive medications.

Results

Our interim results (n=11) confirm that motor practice leads to performance gains measured as increased acceleration during thumb abduction (main effect of time: F_(4,40)=16.4, p<0.0001, η²=0.62; baseline vs 1-hr retention: 14.2±2.8 vs 35.5±5.5 m/s²; t₁₀=5.3, p_holm=0.002). We find MEP amplitudes for the APB are increased following motor practice with a clear trend towards a sustained elevation up to 60 min (5-min: t₁₀=2.4, p_holm=0.07, d=0.73; 30-min: t₁₀=2.7, p_holm=0.06, d=0.83; 60-min: t₁₀=1.8, p_holm=0.10, d=0.53). Crucially, we observe a pattern of transient increase in SDTC for the APB (5-min: 9±2%; 30-min: 7±2%) that appears to return to baseline levels over the same period (60-min: -3±1%) and is not apparent in the ADM (5-min: -2±2%). Whilst these trends do not reach statistical significance (muscle x time interaction effect: F_(4,40)=1.47, p=0.22) a power analysis indicates that n=26 will be sufficient to detect a significant muscle x time interaction (α=0.05, 1−β=0.8) which we will target with ongoing data collection.

Conclusions

Whilst preliminary, these findings hint towards a dissociation between synaptic and intrinsic effects: MEPs increase after training and remain elevated, whereas SDTC rises immediately but returns to baseline within 60 min. This pattern raises the possibility for interactions between the two mechanisms, where transient intrinsic changes facilitate (metaplasticity) or maintain balance (homeostasis) after synaptic facilitation; interactions not previously demonstrated in humans. Irrespective of the outcome, these findings will establish a role for intrinsic plasticity in the human motor cortex during motor skill learning, with clinical relevance to the development of neurorehabilitation strategies for patients recovering from stroke, brain injury, or other neurological conditions.

Does a global suppression mechanism for suppressing voluntary movements extend to involuntary movements?

Introduction: Humans are able to voluntarily suppress unnecessary or unwanted actions. The neural mechanism of such suppression is thought to rely on a prefrontal–basal ganglia network. A key neurophysiological marker of this network is a global motor system suppression, characterized by a widespread, transient downregulation of corticospinal excitability during reactive stopping of voluntary actions. However, it remains unclear whether this mechanism extends to the voluntary suppression of involuntary movements.

Aims: The present study aimed to determine whether global suppression is recruited when individuals suppress a sustained involuntary movement and to further characterize the temporal dynamics of this process.

Methods: Healthy adults were recruited in two experiments: Experiment 1 (N=20) and Experiment 2 (N=18). The Kohnstamm phenomenon, defined as involuntary arm elevation following sustained deltoid contraction, was used as a model of involuntary movement. In a within-subject design, participants either allowed the involuntary drift to occur naturally (Allow condition) or voluntarily suppressed it following a stopping cue (Suppress condition). To probe global suppression, motor-evoked potentials (MEPs) were recorded from a contralateral, task-unrelated muscle (first dorsal interosseous, FDI) using single-pulse transcranial magnetic stimulation (TMS). Two stimulation timings were employed: early TMS, delivered shortly after the arm crossed a threshold angle (ACT) (500 ms in Experiment 1; 150 ms in Experiment 2, the latter consistent with the latency of global suppression in reactive-stopping paradigms)^1,2, and late TMS, delivered 4.5 s after ACT. Arm kinematics were continuously tracked and extracted at ACT, early TMS, and late TMS. Electromyography (EMG) was recorded from the deltoid and latissimus dorsi; root mean square (RMS) amplitudes were calculated and compared across the induction phase and three critical epochs (500 ms before ACT, ACT–early TMS, 500 ms before late TMS). ANOVA was conducted to analyse condition by time interactions for arm position, EMG and MEP amplitudes.

Results: Behavioural and EMG analyses confirmed that participants successfully suppressed involuntary arm elevation (Condition × Time interaction: Exp.1, F(2,38)=31.87, p<.001; Exp.2, F(2,34)=38.80, p<.001), primarily through control of the agonist deltoid – preventing the rise in agonist activity (Condition × Time interaction: Exp.1, F(2,38)=4.03, p=.028; Exp.2, F(2,34)=25.10, p<.001), Condition × Time interaction: Exp.1, F(2,38)=1.67, p=.202; Exp.2, F(2,34)=3.87, p=.058). However, MEP analyses revealed no evidence of global suppression: at no timepoint were MEP amplitudes lower in Suppress than in Allow. A significant main effect of Condition was observed in both experiments (Exp.1: F(1,19)=13.73, p=.002; Exp.2: F(1,17)=21.21, p<.001), whereas the Condition × Time interaction reached significance only in Exp.1 (F(1,19)=7.30, p=.014). At early timepoints, no significant differences appeared (Exp.1: t(19)=-1.47, p=.158; Exp.2: t(17)=-1.94, p=.068). Indeed, at the late timepoint, MEPs in Suppress were consistently greater than in Allow (Exp.1: t(19)=-4.04, p<.001; Exp.2: t(17)=-2.52, p=.022), indicating that sustained suppression was not accompanied by widespread cortical downregulation.

Conclusions: Across two independent experiments, we consistently found that voluntary behavioural suppression of sustained involuntary movement does not depend on neural global suppression mechanism. Instead, behavioural suppression may be achieved through selective neural suppression of the primary agonist muscle representation.

Does passive blood flow restriction affect central neuromodulation and motoneuron excitability?

Introduction and Aim: Blood flow restriction (BFR) is a method that is used in training and rehabilitation settings to improve functional outcomes. Although widely and successfully applied, the underlying neuromuscular mechanisms are not yet fully understood. By tracking the same motor units (MU) active before and after BFR (trapezoid ramp contractions), we showed an increased MU discharge rate after BFR. Persistent inward currents (PICs) are known to impact synaptic inputs to motoneurons by providing additional excitatory current. Thus, this study aimed at investigating the acute passive BFR effects on the central neuromodulation of PICs (Gorassini et al. 2002).

Methods: Thirteen uninjured male handball players (age: 24 [SD 3] years, body mass index: 24 [2] kg/m²) participated in the study after providing written informed consent (IRB approval number: 2024-167). High-Density surface EMG (HDsEMG) grids (HD08MM1305) were placed on participants’ dominant lower limbs over the vastus medialis (VM) and lateralis (VL) muscles. Signals were recorded before and after a 5-minute passive BFR intervention at 80% of maximal arterial occlusion pressure (AOP: 157 [14] mmHg). Maximal AOP was defined using a mobile Doppler ultrasound in the popliteal fossa. Isometric force-matching triangular contractions (duration 20 s) at 20% maximal voluntary contraction (4.06 [0.84] Nm/kg) were performed before and immediately after BFR. HDsEMG signals recorded before BFR were decomposed (Negro et al. 2016) into firing instances of MU action potentials. To compare the properties of the same MU, the MU identified before BFR were tracked after BFR using their MU filters (Francic & Holobar 2021). Analyses were performed in Python with the openhdemg V0.1.1 library (Valli et al. 2024) by applying the paired MU analysis technique (Gorassini et al. 2002). Thereby, low recruitment threshold MU (control units) were paired with higher recruitment threshold MU (test units). Delta frequency (F) values of each test-control unit pair were estimated and served as the outcome. Effects were assessed utilizing the linear mixed effects model.

Results: In total, 97 (96%) out of 101 identified MUs were successfully tracked after BFR for VL and 56 (71%) out of 79 for VM. The linear mixed effects model revealed a significant main effect of Time (p < 0.001) on the estimated Delta F values. Specifically, the Delta F values increased by 20.3% after BFR (from 2.63 [0.24] to 3.17 [0.24] pps). No relevant effects for the main effect of Muscle (p = 0.65) or the Time*Muscle interaction (p = 0.49) were observed.

Conclusions: This study analyzed the effects of a passive BFR intervention on central neuromodulation indirectly by estimating the PICs of thigh muscles. The absence of an effect of Muscle underscores the underlying central mechanisms caused by local ischaemic interventions at the extremities (McNulty et al. 2002). Since individuals with knee joint injuries suffer from altered motor system excitability and reduced volitional muscle activation BFR, particularly the passive mode, may be used to counteract these neuromuscular alterations by enhancing excitatory plasticity.

Entrainment of motor unit firing by deep brain stimulation for Parkinson’s disease

Motivation: Deep brain stimulation (DBS) is a well-established therapy for reducing the motor symptoms of Parkison’s disease. The mechanisms by which it affects motor function and more specifically motor unit activity and recruitment patterns, however, are not well understood. It has been established that DBS antidromically stimulates pyramidal tract neurons projecting from the cortex to the subthalamic nucleus (STN) (Li et al., 2012). Motor evoked potentials may also be observed during low frequency, high amplitude stimulation. The effect of DBS at the motor unit level at clinically relevant frequencies and amplitudes, however, has not yet been investigated. To investigate this, high-density EMG was used to examine the effect of DBS on motor unit firing patterns during isometric contraction of the first dorsal interosseous (FDI) muscle.

Methods: Following institutional ethical approval, 17 (4 females, aged 60.8 ± 7.4 years, Time since Diagnosis: 11.3 ± 3.7 years) participants volunteered for the study. Isometric index finger abduction was performed at 10%-30% of maximum voluntary contraction (MVC) in 4 conditions: DBS ON and OFF, with and without medication. High-density EMG was recorded from the FDI using a 126-electrode array and the data were decomposed into the constituent motor unit firing trains. Power spectra of the EMG signals, individual motor unit spike trains and cumulative spike trains were computed using Welsh’s method. Synchronization was estimated from the cross-correlogram between pairs of motor unit discharges, with short- and long-term synchrony defined as an increased probability of motor units firing within 10ms or greater than 10 ms of each other, respectively.

Results: DBS led to entrainment of a subset of motor unit firing times at the stimulation. This was observed as a significant increase in power in the EMG power spectra at the DBS frequency and higher harmonics during DBS ON (p< 0.001). A significant increase was also observed in the power spectra of the cumulative spike trains of the decomposed EMG data during DBS ON (p < 0.001). Eight participants exhibited a peak in the power spectra of both EMG and cumulative spike trains. In four participants, peaks in the power spectrum of the spike trains of individual motor units were observed, with secondary peaks consistent with pulse frequency modulation of the motor unit mean firing rate at the DBS frequency. In these participants, motor unit synchronization of units was increased (p = 0.038) during DBS ON with cross-correlogram peaks at multiples of the DBS interpulse interval.

Conclusion: The presence of peaks in the EMG and motor unit power spectra, and increased motor unit synchronization, are consistent with entrainment of motor unit firing during high frequency DBS (79-130 Hz). The results provide evidence of orthodromic activation of pyramidal tract neurons during STNS DBS at clinically relevant amplitudes and frequencies. In addition to providing insight into changes in motor unit firing during DBS, the findings suggest potential new biomarkers for optimization of DBS parameters based on motor unit activity.

Exploring the role of vestibular input in muscle reflex function

Introduction

Balance control is a complex, multisensory process that depends on the integration of visual, proprioceptive, and vestibular inputs to generate appropriate reflexive responses and adaptive motor behaviours that maintain postural stability. Balance impairments are common in older adults and various clinical populations, leading to increased risk for falls. Emerging research has highlighted the potential clinical utility of noisy subthreshold vestibular stimulation (termed, ‘noisy galvanic vestibular stimulation’) applied to the mastoids to reduce imbalance. However, our understanding of the mechanisms underpinning these effects remains poor. This study tested the hypothesis that noisy galvanic vestibular stimulation enhances balance by modulating spinal reflexes.

Methods

19 healthy young adults took part in our study. Participants received noisy galvanic vestibular stimulation (± 0.35 mA) during standing whilst H-reflexes were measured. H-reflex was elicited through stimulation in the popliteal fossa and the EMG was measured across the right soleus. Standing H-reflex amplitude was measured during standing balance (eyes closed), whilst receiving either active or sham vestibular stimulation. The protocol was conducted on both a foam and a solid surface to compare across different levels of vestibular dependence: standing on foam with eyes closed results in the CNS relying predominately on vestibular input to regular balance. Average normalised H-reflex amplitudes were calculated for each condition. All participants provided informed consent and the study was approved by the local ethics committee.

Results

In total we analysed 1520 H-reflexes (n=80 per participant). There was no significant change in normalised H-reflex amplitude between sham and active stimulation on the solid surface (t(18)=-0.481, p=0.636). However, on the foam surface we found a significant increase in H-reflex amplitude during active stimulation (t(18)=2.149, p=0.046).

Discussion

Our results indicate that noisy galvanic vestibular stimulation modulates spinal reflexes during challenging, vestibular-dominant balance conditions (standing on a foam surface). Our findings support spinal reflex modulation as a possible mechanism for the improvements in balance seen with noisy galvanic vestibular stimulation. The contrasting results on the foam and solid surfaces are a likely result of sensory reweighting, whereby the body up-regulates vestibular contributions to balance and down regulates the visual and somatosensory inputs which are inherently less reliable under these conditions (eyes closed and foam). This increased reliance on vestibular inputs likely potentiates the effect of vestibular stimulation. Our results provide new evidence for the possible mechanism/s behind noisy galvanic vestibular stimulation’s effect on balance, which may help further enhance future clinical use.

High-density electrospinography reveals altered high-frequency oscillations at cervical spinal levels in Multiple Sclerosis: Towards a marker of spinal dysfunction

Background:

Electrophysiological techniques have been widely used to study the functional mechanisms of the brain’s sensory-motor networks in both health and neurodegeneration. However, such assessments of spinal cord activity remain highly challenging and underexplored. This gap is concerning, considering that cervical spinal degeneration[1] is a key clinical indicator of disease severity and future disability in neurological conditions such as Multiple Sclerosis (MS)[2].

To address this gap, our team recently developed a standardised high-density electrospinography (HD-ESG) system (SC10X/U)[3], an up to 76-channel platform designed to reliably record spinal cord electrical activity and enable assessment of spinal function. This is especially relevant in conditions like MS, which features a clinico-radiological paradox, i.e., changes in structural spinal MRI measures, such as atrophy, fail to predict or correlate with disability progression despite strong clinical evidence of spinal involvement.

Objective:

Here, we used HD-ESG to quantify signatures of spinal High-frequency oscillations (HFOs) in response to the median nerve stimulation (MNS), in MS. HFOs are a measure of localised synchronous presynaptic neural activity[4], [5], reflective of functional integrity. To our knowledge, this is the first study to investigate spinal-HFO responses in people with MS (pwMS).

Methodology:

64-channel ESG[3] was recorded in response to the stimulation (right wrist, 1.5 X Motor Threshold, 2Hz) from 14 pwMS and 18 controls. A total of 1400 evoked responses were recorded per participant. Signals were pre-processed and bandpass filtered between 350- 1400 Hz. The evoked HFO (phase-locked) responses were obtained by averaging the resulting signals across all responses.

Temporal HFO characteristics were compared between groups using the Mann-Whitney U test with adaptive false discovery rate (q = 0.05). Characteristics include: onset latency, peak latency, and normalised peak amplitude (Peak_amp).

Results:

A highly lateralised (p < 0.05) evoked HFOs were observed at lower cervical levels, with the maximum response observed at the LL8 electrode (C6 vertebral level (Cv6): right-lateral channel) for both groups [pwMS: 0.26 ± 0.11, controls: 0.4 ± 0.2]. The observed Peak_amp at the LL8 electrode was significantly lower in pwMS (p = 0.021). No significant differences were observed for onset or peak latency.

During the 8-15 ms post-stimulation period, both groups demonstrated broadband activity between 400-600 Hz at lower cervical levels. However, this activity was significantly reduced in the pwMS.

Discussion:

This first-of-its-kind study reveals specific disease-relevant alterations in pwMS, highlighting the potential of HD-ESG-based investigations towards a viable marker of spinal dysfunction. The reduction in peak HFO amplitude likely reflects temporal dispersion due to demyelination in MS[6], indicative of impaired cervical spinal integrity. A similar decrease in HFO amplitude has previously been reported at the somatosensory cortex in pwMS[6]. Our findings indicate that these alterations are detectable even at the cervical spinal level, suggesting that HFO-alterations may represent a signature of network-level dysfunction.

Superior neuromuscular recovery during high-intensity resistance exercise using five-minute versus two-minute rest intervals between sets.

Introduction: It is well established that manipulating rest intervals (RIs) between sets can affect acute performance of resistance exercise (RE) such as training volume and intensity (Grgic et al., 2017), which can modulate development of muscular characteristics such as hypertrophy, strength and power. Previous research has highlighted maintenance of greater torque, muscle activity, and volume over multiple sets with five-minute RIs compared to two-minutes (McMahon et al., 2024). However, it has never been shown how RIs modulate specific neuromuscular strategies during RE. This study aims to investigate how neuromuscular behaviour is impacted by a moderate and longer RI duration using high-density electromyography (HDEMG).

Methods: Ten (n=10) participants (male; 29 ± 5 years; 12 ± 6 years RE experience) completed two randomly assigned acute bouts of RE; four-sets of five-second isometric knee extensions to failure at 80% maximal voluntary isometric contractions (MVIC) with two-minute (REST-2) or five-minute (REST-5) RIs.Participants had ≥4-days’ rest between sessions. Neuromuscular characteristics were measured using HD-EMG (Quattrocentro EMG, Bio Elettronica) on the vastus lateralis. Muscle fibre conduction velocity (MFCV) was measured during MVICs pre-, 0-MINS-POST-, 5-MINS-POST-, and 10-MINS-POST-exercise. Recruitment threshold (relative to MVIC), firing rates (PPS Mean), coefficient of variation of inter spike interval (CVISI), and motor unit conduction velocity (MUCV) were measured during RAMP contractions at 20%MVIC (increasing 5%MVIC per second until 20% [RAMP-Up] and holding for 10-seconds [RAMP Plateau]) pre-exercise, at the end of RIs between sets, 0-MINS-POST-, 5-MINS-POST-, and 10-MINS-POST-exercise. A linear mixed model was used to examine the effects of rest interval and time on EMG variables.

Results:

MVICs

MFCV, there were no effects (p>0.05).

RAMPs

Recruitment threshold showed a main effect for time (p<0.05) but not rest, nor rest × time interaction

During RAMP-Up, mean firing rates showed a main effect for rest, time, and rest × time interaction (p<0.05) with REST-2 significantly higher than REST-5(Figure 2). For CVISI, there was a main effect for rest (p<0.05).

During RAMP-Plateau, mean firing rates showed a main effect for rest and rest × time interaction (p<0.05) REST-2 significantly higher than REST-5 (figure 3). There were no effects for CVISI. For MUCV, there was a main effect for time (p<0.05) (Figure 4), but not rest or rest × time interaction. For MUCV correlation coefficient, there were no effects (p>0.05).

Conclusion: The current findings suggest that five-minute RIs facilitate superior neuromuscular performance compared to two-minutes. The greater firing rates suggests the central nervous system compensating for greater residual fatigue to maintain force output for two-minute RIs. In contrast, lower firing rates shown for five-minute RIs indicate superior recovery going into subsequent sets, and throughout the recovery period.

The combined contraceptive pill facilitates spike-timing-dependent plasticity in long-term users

Introduction: Endogenous ovarian hormones have been shown to contribute to modulations in cortical excitability (1) inhibition (2), and neuroplasticity (3). However, little is known about the physiological effects of the synthetic versions of these hormones (e.g., ethinyl oestradiol), despite morphological changes in brain grey matter volume occurring with long-term use (4). The contraceptive pill is used by 151 million people world-wide and creates a daily micro cycle of synthetic hormones (~ 4-fold changes, 5), but the neurophysiological effects of these acute changes are yet to be investigated. Accordingly, the aim of this study was to determine the effect of the combined monophasic contraceptive pill on corticospinal excitability and plasticity.

Methods: The study received institutional ethical approval. Seventeen female participants (age: 23 ± 5 years) volunteered to take part, all were long term (45 ± 46 months) combined contraceptive pill users. Participants visited the lab in two pill cycle phases: withdrawal and active. Visits comprised of baseline assessments of corticospinal excitability (motor evoked potential [MEP]/M_max), short-intracortical inhibition (SICI), and intracortical facilitation (ICF) measures, recorded in the resting first dorsal interosseous. Participants then took their pill and after 90 minutes rest assessments were repeated. This was followed by a paired associative stimulation (PAS) protocol, utilising ulnar nerve and transcranial magnetic stimulation (25 ms interstimulus interval) to induce spike-timing-dependent plasticity. To assess the time course of spike-timing-dependent plasticity, measurements were repeated at 15 and 30-minutes post PAS.

Results: Prior to taking the pill, corticospinal excitability (MEP/M_max) was 12 ± 9% lower in the active phase (p <0.001) compared to withdrawal, with no differences observed for SICI or ICF (p ≥ 0.203). 90 minutes after taking the pill, a further reduction in MEP/M_max was observed in the active phase (86 ± 3% pre-pill, p < 0.001), with no change in the withdrawal phase (98 ± 3% pre-pill, p = 0.526). ICF increased pre-to-post regardless of phase (p = 0.007), but there were no changes in SICI (p = 0.347). PAS elicited an increase in MEP/M_max in active only, whereby at 15-minutes (118 ± 5% pre-PAS, p < 0.001), and at 30-minutes responses were facilitated (119 ± 5% pre-PAS, p < 0.001). PAS failed to elicit any facilitation in the withdrawal phase at either 15 minutes (101 ± 5% pre-PAS) or 30 minutes (106 ± 5% pre-PAS, p ≥ 0.424).

Conclusion: The present data contains two novel findings. Firstly, the oral contraceptive has acute neuroactive effects, reducing corticospinal excitability. Secondly, that oral contraceptive users are only able to experience synaptic plasticity during the active pill consumption phase, with blunted responses when not taking the pill. This has potential implications for neurorehabilitation, with individuals potentially needing to consider timing their pill consumption around motor performance.

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Meeting dates	16 – 17 December 2025

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Tuesday 16 December - Wednesday 17 December 2025

Neurophysiological Bases of Human Movement 2025

Date

Location

10:00

10:30 SA01 Modelling human movement neuromechanics for generalisable human-robot interfaces

11:00 SA02 Early development of stepping and locomotor control

12:00 C01 Investigating the role of intrinsic plasticity in the human motor cortex during motor skill learning

12:15 C02 Does a global suppression mechanism for suppressing voluntary movements extend to involuntary movements?

12:30 C03 Does passive blood flow restriction affect central neuromodulation and motoneuron excitability?

12:45 C04 Entrainment of motor unit firing by deep brain stimulation for Parkinson’s disease

16:00 SA03 Combining imaging and deep brain recordings in humans to understand the role of the brainstem in Parkinson's disease

16:30 Between nothing and everything: Phenomenology in movement disorders

17:00 SA04 The borderlands of motor control and behaviour: Movement disorders in neuropsychiatric conditions

08:30 SA05 The common basis of movement decisions and movement adjustments.

09:00 SA06 The vestibular system: A fundamental reference for human behaviour

09:30 SA07 How action prediction shapes perception

10:30 SA08 Cortical activity signatures of perceptual-cognitive-motor interactions in health and disease

11:00 SA09 Neurophysiology based closed-loop deep brain stimulation for movement disorders

11:30 SA10 Sensing the self: Psychophysics and neuroimaging of somatosensory processing in voluntary movements

12:45 C05 Exploring the role of vestibular input in muscle reflex function

13:00 C06 High-density electrospinography reveals altered high-frequency oscillations at cervical spinal levels in multiple sclerosis: Towards a marker of spinal dysfunction

13:15 C07 Superior neuromuscular recovery during high-intensity resistance exercise using five-minute versus two-minute rest intervals between sets.

13:30 C08 The combined contraceptive pill facilitates spike-timing-dependent plasticity in long-term users

14:15 Does motor control need cognitive neuroscience?

14:45 The black box approach vs the mechanistic approach to studying human movement: Which is better?

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