Paired Associative Stimulation with Interstimulus Intervals of Short-latency Afferent Inhibition on Motor Plasticity

Abstract

A BSTRACT Background: Short-latency afferent inhibition (SAI) is a method used to assess sensorimotor integration. Inhibition typically occurs at an interstimulus interval (ISI) of 20–22 ms or N20 + 2 ms. Paired associative stimulation (PAS) applied at certain ISIs consecutively can induce changes in corticospinal excitability. Usually, ISIs of 10 and 25 ms are applied in PAS. In this study, we aimed to investigate the relationship between ISIs of SAI and PAS, a neuromodulation paradigm. To achieve this, we first identified the optimal ISIs that produced maximum inhibition and facilitation during SAI by evaluating multiple ISIs. Subsequently, we applied the PAS paradigm with these ISIs. Materials and Methods: Twelve healthy participants were recruited for the study conducted over three sessions. During the first session, we examined the ISI of maximum inhibitory and ISI of facilitatory or minimum inhibitory (if facilitation was absent) in each participant at multiple ISIs. In the other two sessions, we applied PAS at the ISI of maximum inhibitory and the ISI of facilitatory or minimum inhibitory. We compared the motor-evoked potential (MEP) amplitudes before PAS, immediately after PAS, and 30 min after PAS. Results: The highest inhibition in SAI was observed at an ISI of 22 ms. In 60% of the participants, inhibition was most prominent at this ISI. Facilitation was not observed in 50% of the participants. During the PAS paradigm, which used the ISI of maximum inhibitory, significant facilitation was observed 30 min after the procedure compared with baseline ( P = 0.011) and immediately post-PAS ( P = 0.026). The mean MEP amplitude decreased significantly 30 min after the procedure compared with the baseline in ISI of only detected facilitation ( P = 0.041). Conclusion: Our findings suggest that the ISI of maximum inhibition can vary among individuals, and that facilitation may not be observed in everyone within the ISI range of 22 ms to 40 ms. The results indicate that paired stimuli at ISI of maximum inhibitory in SAI increase corticospinal excitability. In addition, PAS at ISI of only facilitation decreases excitability. These changes in excitability may be explained by spike-timing-dependent plasticity.