Article Figures & Data
Figures
- Figure 1.
Stimulation protocol and task. A, Tactile stimulation was applied to participants' right index finger with a vibrotactile actuator. B, Three protocols were used: (1) WN stimulation was created by random amplitude modulation of the 150 Hz carrier sine-wave. The spectral content of WN sequences was flattened between 0 and 75 Hz. (2) SSSEP stimulation was created by rhythmic amplitude modulation of the 150 Hz carrier sine-wave at one specific frequency on each trial (12-39 Hz). Perceptual targets were embedded in both WN and SSSEP sequences by decreasing the frequency of the carrier sine-wave from 150 to 127.5 Hz. (3) Single-pulse stimulation consisted of 200 ms fixed amplitude increases of a carrier 150 Hz wave. C, Experimental procedure and stimulation protocols.
- Figure 2.
A, Cross correlation procedure. The cross-correlation between WN sequences and EEG data from corresponding (same) trials results in the impulse response function: the brain response to a single impulse (right, blue line). Cross-correlation of WN sequences with randomly shuffled (different) trials (surrogate IRF) serves as a null hypothesis (EEG and WN are uncorrelated) and produces an almost flat line (right, purple line). C, IRF duration was estimated by extracting beta band power envelope from TFR of IRF signal. B, IRF duration was defined as FWHM between beta power peak at fmax and intersects x1 and x2 between the envelope and 95% quantile of the surrogate IRF power distribution at the same frequency.
- Figure 3.
IRFs and their corresponding TFRs from 2 representative subjects. A, The observed IRFs (blue lines) were calculated by cross-correlating tactile WN sequences with the recorded EEG signal. Red lines indicate cross-correlation result after randomly shuffling trials (null hypothesis: EEG and WN are uncorrelated). B, TFR of the single subject IRF at the individual channel of interest (CP3). C, Topography of average IRF beta power (15-40 Hz, 0-200 ms). D-F, Same as in A-C, but for a different subject (channel CP5).
- Figure 4.
A, Grand average TFR of IRF (averaged over individual channels of interest). Black contours represent contiguous time-frequency points at which the observed IRF was significantly different from surrogate IRFs at p < 0.05 (corrected for multiple comparisons across time-frequency points using FDR). B, Grand-average power spectrum of the IRF calculated in the 0-200 ms time window. Individual subjects showed spectral peaks distributed around a mean of 25.1 Hz. C, Topography of IRF beta band power (15-40 Hz, 0-200 ms). Black dots indicate the distribution of electrodes that were identified as a subject-specific channel of interest. D, TFR (averaged over individual channels of interest) and β topography of the phase-locked EEG response (ERP). E, Grand-average power-spectra calculated in the 0-400 ms time window over individual channels of interest for the phase-locked EEG response. G, Grand average TFR of non–phase-locked EEG response. Black contours represent regions in which contiguous time-frequency points were significantly different from the prestimulus baseline at p < 0.05 (corrected for multiple comparisons using FDR). Purple contours represent a region, in which the real IRF was significant (the same as black contour in A). H, Same as in E, but for non–phase-locked EEG response. Individual subjects showed local minima at frequencies distributed around a mean of 23.1 Hz. F, I, Topography of beta band power (15-40 Hz, 0-400 ms) for the phase-locked and non–phase-locked part of the EEG response.
- Figure 5.
A, Within- and between-subject correlation of IRF and phase-locked EEG response (ERP) TFRs. Pixel values within the black outlined area were correlated using Pearson correlation. B, Resulting correlation matrix. C, Individual within-subject correlation values (light gray circles) and between-subject correlations (dark gray bars; error bars indicate 95% CIs). D, t test between within-subject and average between-subject correlation values (error bars indicate 95% CIs). E, Characterization or ERP in time and frequency domain (group average, channel CP5).
- Figure 6.
Steady-state somatosensory potential analysis. A, Electrode-level analysis results. Each topographical map represents single-subject power (expressed in SNR units) averaged across all stimulation frequencies (12-39 Hz, 18 frequencies). Note the individual variability in scalp projections of the SSSEP responses. B, Topographical representation of single-subject spatial filter corresponding to each subject's resonance SSSEP frequency. Note the high similarity across subjects and dipolar appearance of the components. C, Subject-average normalized spatial filter weights depicted in B (left) and the associated putative anatomic generators of SSSEPs. D, Subject-average SSSEP power expressed in SNR units plotted as a function of vibrotactile stimulation frequency (left): Input frequencies are depicted on the y axis and output frequencies on the x axis. Brighter colors represent stronger response, with maximal responses observed, as expected, at the stimulus frequency. Right, SSSEP power at stimulation frequencies (diagonal from the matrix of power spectra on the left), with the resonance peak at 26 Hz. Black line “H0 hypothesis” indicates SSSEP amplitude at each of the tested frequencies on trials when stimulation at that frequency was not delivered and can be expected as a result of overfitting. Black line on the x axis indicates that SSSEPs at all frequencies were statistically significant at p < 0.001 (corrected for multiple comparisons across frequencies using cluster-based permutation testing).
- Figure 7.
Peak frequency correlation analysis. Spearman correlations were calculated between individual peak frequencies of IRFs, non–phase-locked EEG response, and spontaneous bursts measured during baseline. Correction for multiple comparisons was performed using FDR.
