Article Figures & Data
Figures
- Figure 1.
The overview of phase and frequency targeting, and TMS evoked potentials (TEPs). A, An example of phase targeting during the training phase of the educated temporal prediction (ETP) algorithm. ETP algorithm accurately targets rising, peak, trough, and falling phases of both mu and beta frequency bands. The rendering of the brain shows the Laplacian montage of the electrodes (FC5, FC3, FC1, C5, C1, CP5, CP3, and CP1) used to extract the C3 signal. The coil was placed on the motor hotspot corresponding to first dorsal interosseus (FDI) muscle. B, Example of motor evoked potentials (MEPs) acquired from FDI muscle for a single participant with bold trace representing the mean MEP. Bottom panel shows the montage used for EMG acquisition from FDI muscle. C, The global average TEP signal for each target frequency band. The bold trace indicates the C3 signal. The topography of the three components, N15, P50, and N100 used to characterize cortical responses are shown below each trace. The global average spectrum of pre-TMS power (−550 to −50 ms window prior to TMS stimulation) is shown in Extended Data Figure 1-1. The phase consistency of mu and beta oscillations following TMS stimulation is shown in Extended Data Figure 1-2. Since the evidence for TEP generation by phase reset or adding on the ongoing oscillation is ambiguous, we quantify cortical responses through peak-to-peak TEP components.
- Figure 2.
Phase dependency of TEP components for mu and beta rhythms. Left, Phase dependency of the early component, P50-N15. Mu target rhythm showed significant increased modulation of TEP amplitude for trough and falling phases compared with peak and rising (p < 0.02). For beta target rhythm, rising phase showed significantly higher TEP amplitude modulation compared with peak phase (p = 0.02). Right, Phase dependency of the late component, P50-N100. The late component showed opposite amplitude modulation for mu and beta phases where mu showed significant increase of amplitude for trough phase compared with peak phase (p = 0.001) and vice versa for mu phase (p = 0.04). The shaded area represents the 95% confidence interval.
- Figure 3.
Relationship between corticospinal excitability and cortical responses. A, The comparison of relative changes of MEP and TEP amplitudes for the early component for mu and beta oscillations. B, The same comparison for the late component.
- Figure 4.
Individual phase preferences of MEP and TEP components. Top, MEPs generated during mu target rhythm have a phase preference of rising and trough phases while the early TEP component is preferentially modulated by falling and trough phases. The late component shows a phase preference similar to that of MEPs where the preferred orientation is toward trough and rising phases. Bottom, MEPs generated when phases of beta rhythm were targeted are preferentially modulated by falling and peak phases (opposite to mu). Neither the early component nor the late component showed a preferential modulation of TEP amplitude to a specific phase. The phase preferences of early and late TEP components relative to MEP could be attributed to the cortical origins of TEP components as shown in Extended Data Figure 4-1.
- Figure 5.
The effects of pre-TMS power on TEP components. A, The group level correlation between pre-TMS power and TEP components. Pre-TMS mu (8–13 Hz) band power showed a strong correlation with both early (r = 0.57; p = 0.008) and late (r = 0.76; p < 0.001) TEP components (left). Pre-TMS beta (14–30 Hz) bad power showed a moderate correlation with the early TEP component (r = 0.45; p = 0.048); however, the correlation was not significant for the late component (r = 0.42, p = 0.067). Each dot in the scatterplot represents the average power and average TEP amplitude across the four phases per participant. B, The combined effect of pre-TMS mu and beta power on the TEP components. The early component showed highest modulation when both mu and beta power were high and lowest modulation when both mu and beta power were low. High mu-low beta and low mu-high beta resulted in higher than average and lower than average modulation, respectively. Wilcoxon rank sum tests showed that the relative changes of TEP amplitudes in these groups were significantly different (left). The modulation of late component was not affected by beta power. Regardless of beta power, high mu power resulted in higher TEP modulation and low mu power resulted in lower TEP modulation. Significant differences were not observed within groups with high mu power or low mu power. However, differences were significant across groups with high mu power and low mu power (right). C, The power of other bands of interest, delta and theta, did not contribute to modulation of both early and late components. Outliers are marked in black circles. *p < 0.05, n.s., not significant.
Extended Data
Figure 1-1
Global pre-TMS power spectrum. The original power spectrum and the periodic power spectrum calculated by irregular resampling auto-spectral analysis (IRASA) in the 500 ms window prior to TMS delivery. There is dominant mu activity and low beta activity. Download Figure 1-1, TIF file.
Figure 1-2
Phase Preservation Index (PPI) for phase specific targeting. PPI values are calculated with reference to mu phase at 100 ms prior to TMS pulse, at 100 ms intervals. Blue trace indicates the PPI values for real TMS, and green trace indicates PPI for TMS trigger without actual pulse. Shaded region depicts the standard error of mean (SEM) of PPI. Plots for all electrodes in the Laplacian montage (FC5, FC3, FC1, C5, C3, C1, CP5, CP3 and CP1) are shown here. Black vertical line indicates the TMS trigger, and the red horizontal line (PPI = 0.1) indicates the threshold for phase preservation calculated according to Fischer, 1993. Phase preservation for mu (left) and beta (right) are shown here. For real TMS condition, there is no substantial evidence for mu or beta phase preservation after TMS delivery. Download Figure 1-2, TIF file.
Figure 4-1
EEG sources computed at latencies of TEP components. EEG source reconstruction by minimum norm estimate show distributed activity in motor, somatosensory association and auditory cortices the ipsilateral hemisphere at = 15 ms. At t = 50 ms, the activity is localized to the ipsilateral motor cortex at t = 50 ms. At t = 100 ms the source activity is distributed bilaterally in the motor and somatosensory areas. The spatial distribution of the sources that generate the TEP responses could partially explain the discrepancy between TEP-MEP phase relationship. Download Figure 4-1, TIF file.
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