Repetitive Passive Movement Modulates Corticospinal Excitability: Effect of Movement and Rest Cycles and Subject Attention

Repetitive passive movement (PM) affects corticospinal excitability; however, it is unknown whether a duty cycle which repeats movement and rest, or subjects’ conscious attention to movements, affects corticospinal excitability. We aimed to clarify the effect of the presence or absence of a duty cycle and subjects’ attention on corticospinal excitability. Three experiments were conducted. In Experiment 1, PM of the right index finger was performed for 10 min. Three conditions were used: (1) continuous PM (cPM) at a rate of 40°/s; (2) intermittent PM (iPM) with a duty cycle at 40°/s; and (3) iPM at 100°/s. In conditions 1 and 3, motor evoked potential (MEP) amplitude was significantly reduced. In Experiment 2, PM was performed for 30 min: condition 1 comprised cPM at a rate of 40°/s and Condition 2 comprised iPM at 40°/s. MEP amplitude significantly decreased in both conditions. In Experiment 3, PM was performed for 10 min: condition 1 comprised paying attention to the moving finger during iPM and Condition 2 was similar to Condition 1 but while counting images on a monitor without looking at the movement finger, and Condition 3 comprised counting images on a monitor without performing PM. MEP amplitude significantly increased only under Condition 1. Thus, afferent input from movements above a certain threshold may affect corticospinal excitability reduction. Furthermore, corticospinal excitability increases when paying attention to passive finger movement

Repetitive Passive Finger Movement Modulates Primary Somatosensory Cortex Excitability

Somatosensory inputs induced by repetitive passive movement (RPM) modulate primary motor cortex (M1) excitability; however, it is unclear whether RPM affects primary somatosensory cortex (S1) excitability. In this study, we investigated whether RPM affects somatosensory evoked potentials (SEPs) and resting state brain oscillation, including alpha and beta bands, depend on RPM frequency. Nineteen healthy subjects participated in this study, and SEPs elicited by peripheral nerve electrical stimulation were recorded from the C3’ area in order to assess S1 excitability (Exp. 1: n = 15). We focused on prominent SEP components such as N20, P25 and P45-reflecting S1 activities. In addition, resting electroencephalograms (EEGs) were recorded from C3’ area to assess the internal state of the brain network at rest (Exp. 2: n = 15). Passive abduction/adduction of the right index finger was applied for 10 min at frequencies of 0.5, 1.0, 3.0, and 5.0 Hz in Exp. 1, and 1.0, 3.0, and 5.0 Hz in Exp. 2. No changes in N20 or P25 components were observed following RPM. The 3.0 Hz-RPM decreased the P45 component for 20 min (p < 0.05), but otherwise did not affect the P45 component. There was no difference in the alpha and beta bands before and after any RPM; however, a negative correlation was observed between the rate of change of beta power and P45 component at 3.0 Hz-RPM. Our findings indicated that the P45 component changes depending on the RPM frequency, suggesting that somatosensory inputs induced by RPM influences S1 excitability. Additionally, beta power enhancement appears to contribute to the P45 component depression in 3.0 Hz-RPM

Effects of Passive Finger Movement on Cortical Excitability

This study examined the effects of joint angle and passive movement direction on corticospinal excitability. The subjects were 14 healthy adults from whom consent could be obtained. We performed two experiments. In Experiment 1, we measured motor evoked potential (MEP) amplitude, F-wave and M-wave at 0° and 20° adduction during adduction or abduction movement, in the range of movement from 10° abduction to 30° adduction. In Experiment 2, MEPs were measured at static 0° and 20° adduction during passive adduction from 10° adduction to 30° adduction and static 20° adduction. MEP, F-waves and M-waves were recorded from the right first dorsal interosseous (FDI) muscle. Experiment 1 revealed significantly increased MEP amplitude at 0° during passive adduction compared to static 0° (p < 0.01). No other significant differences in MEP, M-wave and F-wave parameters were observed. In Experiment 2, MEP amplitude was significantly higher at 20° adduction during passive adduction compared with static 0° (p < 0.01). Based on these findings, it appears that fluctuations in MEP amplitude values during passive movement are not influenced by joint angle, but rather it is possible that it is due to intracortical afferent facilitation (AF) dependent on afferent input due to the start of movement and interstimulus interval (ISI) of transcranial magnetic stimulation (TMS)

The effect of combined transcranial direct current stimulation and peripheral nerve electrical stimulation on corticospinal excitability.

Transcranial direct current stimulation (tDCS) and peripheral nerve electrical stimulation (PES) can change corticospinal excitability. tDCS can be used to non-invasively modulate the cerebral cortex's excitability by applying weak current to an electrode attached to the head, and the effect varies with the electrode's polarity. Previous studies have reported the effect of combined tDCS and PES on corticospinal excitability; when compared to single stimulation, combined stimulation increases cortical excitability. In contrast, another study reported that the effect of tDCS is attenuated by PES; hence, there is no consensus opinion on the effect on combined stimulation. Therefore, this study aimed to clarify the effect of combined tDCS and PES on corticospinal excitability. In Experiment 1, the combined stimulation of anodal tDCS and PES (anodal tDCS + PES) was performed, and in Experiment 2, a combined stimulation with PES, after cathodal tDCS (PES after cathodal tDCS), was performed using a homeostatic metaplasticity theoretical model. In Experiment 1, anodal tDCS produced a significant increase from baseline in motor-evoked potential (MEP) amplitude 10 min after stimulation, but no significant changes in MEP amplitude were observed with PES or the anodal tDCS + PES condition. Experiment 2 showed a significant decrease in MEP amplitude immediately after cathodal tDCS, and a significant increase in MEP amplitude 15 min after PES, but no significant change in MEP amplitude was observed with sequential PES following cathodal tDCS. In conclusion, our data indicate that PES with anodal tDCS suppressed the effect of tDCS. Also, PES after cathodal tDCS did not induce homeostatic metaplasticity and increase corticospinal excitability