John C. Rothwell

This study shows that transcranial magnetic stimulation of the human leg motor area elicits iTEPs similar to those from the hand area, suggesting a general cortical response.

The paper examines how cortical and corticospinal excitability changes during different beta-band states of movement, finding opposing patterns in their modulation.

This study finds that children and adolescents with Tourette syndrome (TS) show delayed maturation of cortical motor excitability, reaching adult levels later than neurotypical controls.

The paper directly measures motor cortical inhibition using immediate TMS-evoked potentials (iTEPs) instead of motor-evoked potentials (MEPs), showing iTEPs provide a more accurate reflection of GABAergic inhibition.

This study examines how urgency affects corticospinal suppression during movement preparation, finding no suppression under high urgency and increased disruption from external events.

This study uses a BiLSTM machine learning model to distinguish TMS-evoked EEG responses from sham stimulations across multiple datasets, achieving high accuracy with few trials.

This study examines how sodium channel blockers affect the strength-duration properties of human motor cortex neurons using TMS, revealing distinct effects between carbamazepine and lacosamide.

This study attempts to replicate the effects of 5Hz-rTUS on corticospinal excitability but finds no significant effects, suggesting variability in the technique's outcomes.

This paper corrects a computational model of theta-burst TMS by fixing code inconsistencies and introducing a non-convex optimisation method, improving its accuracy in describing MEP amplitudes.

This study investigates whether TACS modulates corticospinal beta entrainment in humans using simulations and electromyography, finding no consistent effect.

This paper introduces a new method to detect motor-evoked potentials below the conventional noise floor, revealing that responses can be evoked at lower stimulation levels than previously thought.

The paper compares conventional electrodes and ultrasound monitoring for measuring TMS-evoked muscle contraction, finding a strong correlation between EMG and ultrasound measures in accessible and inaccessible muscles.

This study compares rise-to-threshold and dynamical systems models of proactive inhibition by analyzing motor cortex stimulation effects on interneuron circuits during movement tasks.

This paper demonstrates a method to suppress essential tremor by disrupting neural oscillation coherence through phase-locked electrical stimulation of the cerebellum.

The paper introduces improved methods to measure corticospinal transmission delays of beta rhythms and shows they align with fastest axon speeds, suggesting two possible mechanisms for fast transmission.

This study shows that ropinirole, a dopamine agonist, impairs proactive inhibition in healthy adults, suggesting a mechanism for impulse control disorders in Parkinson's patients.

The paper investigates corticospinal excitability changes during movement preparation and finds that preparatory inhibition is a necessary state for planned movements, with different triggering strategies for reaction time and self-paced tasks.

This study investigates whether TMS combined with EEG can measure short-interval intracortical inhibition (SICI) in healthy volunteers, aiming to develop an objective marker for upper motor neuron involvement in ALS.

This study shows that transcranial direct current stimulation of the right inferior frontal gyrus modulates brain networks differently based on brain state and polarity.

This study shows that tDCS modulates cortico-spinal excitability differently based on the orientation of current flow relative to cortical columns and TMS coil orientation.

This study shows reward and punishment enhance motor adaptation and retention in stroke patients, similar to healthy controls.

This study investigates how subthreshold TMS affects corticospinal volleys with different conduction times, revealing complex interactions beyond local inhibitory connections.