Demographic information of each group and clinical scores of the USN and non-USN patients matched by Mahalanobis distance

Experimental paradigm.

The strobe light flickered for 10 seconds in 3-Hz steps, from 3 Hz to 30 Hz, with 10-second inter-train intervals. Participants were lying down with their eyes closed during the EEG recording.

SSVEP power for different responses and flicker frequencies.

The power spectrum at the response frequency (y-axis) is shown for the O2 electrode (affected hemisphere in patients) as a function of flicker frequency (x-axis). Spectra are normalized to the baseline from the resting-state interval. The fundamental frequency and the first harmonic (gray dashed lines) are evident across groups.

Hemispheric differences in SSVEP power at different flicker frequencies.

Power in the intact hemisphere was stronger than that in the affected hemisphere with 9-Hz stimulation (***p < 0.001) in the USN group only (middle panel). Error bars represent 2 standard errors.

Hemispheric differences in SSVEP power at different flicker frequencies.

(A) No hemispheric difference between C3 and C4 electrodes. (B) No hemispheric difference between F3 and F4 electrodes. Error bars represent 2 standard errors.

SSVEP power during stimulation at 9 Hz and rest.

(A) Box plots indicate the power of SSVEP responses in the intact (O1 electrode) and affected (O2 electrode) hemispheres. A significantly higher response power was observed in the intact hemisphere of the USN group than in the left hemisphere of the healthy control group. The non-USN patients also displayed higher alpha power in both hemispheres than healthy controls without hemispheric bias (***p < 0.001). (B) During the resting state interval, no significant differences in alpha power were observed between groups. Box plots depict medians and 25th/75th percentiles, with whiskers showing the 10th/90th percentiles overlaid onto individual data points (circles). The + represents outliers. Outliers exceeding a power value of 50 were truncated and plotted at the 50 mark.

Hemispheric differences in PAC in response to 9-Hz flickering stimuli.

The MI measuring the coupling between the alpha phase (7–12 Hz) and gamma power (35–45 Hz) represents the hemispheric asymmetry in the USN group (indicated by the black outline). No such pattern was present in the non-USN or healthy control group.

Hemispheric differences in information flow between the visual and frontal areas in response to 9-Hz flickering stimuli.

(A) Box plots show left-right hemispheric asymmetry in transfer entropy (TE) from visual to frontal areas (feedforward direction). In the USN group, information flow from the right visual cortex (O2) to the left frontal area (left panel) was significantly stronger than from the left visual cortex (O1) to the left frontal area (*p < 0.05), and this asymmetry was significantly greater than in healthy controls (**p < 0.01). No significant hemispheric differences were observed in information flow to the right frontal area (right panel). (B) Box plots show left-right hemispheric asymmetry in TE from frontal to visual areas (feedback direction), with no significant asymmetry detected in any group for either left or right frontal areas. Arrows on topographical plots indicate the direction of information flow. Box plots show medians and 25th/75th percentiles, with whiskers at 10th/90th percentiles. The + represents outliers.

Correlation between SSVEP power and BIT score in USN patients.

(A) Scatter plots represent the relationship between SSVEP power at 9 Hz and BIT score for the left hemisphere (O1 electrode, left panel) and right hemisphere (O2 electrode, right panel). A significant positive correlation was found in the right hemisphere (r = 0.70, p < 0.007) but not in the left hemisphere (r = 0.38, p = 0.18). (B) Correlation coefficients between SSVEP power and BIT score across frequencies (3–30 Hz) for each hemisphere. Significant correlations were observed in the right hemisphere only at 9 and 12 Hz after FDR correction (**p < 0.01).

Hemispheric imbalance in model simulations.

Upper panels (A-C) show schematic illustrations of three different model configurations. Lower panels show corresponding order parameter differences between hemispheres across stimulus frequencies. (A) Model with asymmetric interhemispheric coupling (KR→L = 0.8, KL→R = 0.2) reproduced the experimental findings, showing significant hemispheric bias at 9 Hz. The red bar indicates the values without external stimulation (F(t) = 0). (B) Model with enhanced left intrahemispheric coupling (KL = 0.8, KR = 0.2) produced a persistent bias across frequencies. (C) Model with different natural frequencies between hemispheres (ωL = 9, ωR = 7) led to frequency-specific biases at both hemispheres’ natural frequencies. Asterisks indicate significant differences (*p < 0.05, FDR corrected). Error bars represent 2 standard errors

Lesion overlap maps in non-USN and USN patients.

Maps are shown for non-USN patients (top) and USN patients (bottom), with warmer colors indicating a greater number of overlapping lesions at each voxel. MRI was performed on a 1.5-T scanner, and T2-weighted and 3D T1-weighted whole-brain images were acquired. Stroke lesions were manually delineated on T2-weighted MRI and normalized to Montreal Neurological Institute (MNI) space using the Clinical Toolbox (Rorden et al. 2012) in SPM8 (Tierney et al. 2025). Acquisition details are reported elsewhere (Kawano et al. 2020). Both groups predominantly showed lesions involving the right MCA territory, but lesion volume was significantly larger in the USN group than in the non-USN group (USN: 72,419 ± 73,778 mm³; non-USN: 11,739 ± 23,907 mm³; Mann–Whitney U = 361.0, p = 1.41 × 10⁻⁵).

Scalp distribution of SSVEP power across groups.

Topographical maps show EEG power at the fundamental (stimulation) frequency in the non-USN, USN, and healthy control groups. Power at each frequency was log10-transformed, baseline-corrected by subtracting the pre-stimulus period (−9.5 to −0.5 s), and then averaged across stimulation frequencies and participants. In all groups, the strongest responses were observed over occipital electrodes (O1 and O2).

Correlations between BIT score and hemispheric imbalance measures during 9-Hz stimulation in USN patients.

(A) Correlation between BIT score and the hemispheric imbalance of 9-Hz SSVEP power shown in Figure 3. (B) Correlation between BIT score and the hemispheric imbalance of PAC. PAC was calculated as the modulation index between the 9-Hz phase and gamma-band amplitude (33–46 Hz), corresponding to the significant cluster shown in Figure 6, and averaged across this gamma-frequency range. (C) Correlation between BIT score and the hemispheric imbalance of TE shown in Figure 7, separately for feedforward and feedback interactions.