Bidirectional motor cortical excitability changes induced by decapulse transcranial ultrasound stimulation: A pilot study

Patterned transcranial ultrasound stimulation (TUS) over the human primary motor cortex (M1) has been shown to induce lasting excitability changes, though typically unidirectional. We developed a novel patterned TUS protocol capable of inducing bidirectional after-effects in M1. Thirteen healthy participants were studied. Two protocols were used, both employing decapulse stimulation (DPS)—10 ultrasound pulses per burst—with identical ultrasound intensity, frequency (0.5 MHz), total and net sonication durations (400 s and 8 s). The protocols differed in pulse repetition frequency (200 Hz vs. 10 Hz) and duty cycle (40% vs. 2%). These were named DPS5 and DPS100, expected to induce excitatory and inhibitory after-effects. We assessed motor-evoked potentials (MEPs) via transcranial magnetic stimulation of the corticospinal tract neurons at the cortical level and their axons at the cervicomedullary junction brainstem level, as well as resting motor threshold (RMT), short-interval intracortical inhibition (SICI), intracortical facilitation (ICF), and short-interval intracortical facilitation (SICF) before and after TUS. DPS5 enhanced cortical MEP amplitude, while DPS100 reduced it, with both effects lasting 60–90 minutes post-sonication. No significant changes were observed in brainstem MEP, RMT, SICI, ICF, or SICF. These results show that DPS protocols can induce long-lasting, bidirectional changes in motor cortical excitability without detectable changes in paired-pulse TMS measures of intracortical inhibition or facilitation, holding promise as a novel, clinically applicable mechanism for inducing motor cortex excitability changes. • We developed two protocols of 10-pulse transcranial ultrasound stimulation. • The two protocols induce bidirectional motor cortical plasticity for 60-90 minutes. • No changes were detected in paired-pulse TMS measures of intracortical inhibition/facilitation. • A novel non-synaptic mechanism is suggested for motor cortex plasticity induction.