## 4 Discussion  
We applied the contralesional cathodal tDCS in addition to the ipsilesional high-frequency rTMS, which also showed a clear increase in behavioral changes for motor assessment. In ITS, we show that mu wPLI was higher than for the healthy controls in the contralesional M1 before stimulation, but mu GC increased in the ipsilesional M1 after stimulation. There was no difference in STS from the healthy controls before stimulation, but mu GC increased in the ipsilesional M1 after stimulation. In addition, beta GC-based LI also showed a clear change before and after stimulation only in ITS. Finally, even in the link with cognition, ITS showed a significant relationship with motor function but not in STS. As such, we found that the effect of dual-mode NBS varies depending on the lesion location. Before stimulation, we found that the ITS had a higher mu wPLI over the contralesional M1 and had a lower LI of beta GC compared to the healthy controls. This difference was not found in STS with ITS or healthy controls before stimulation. When stroke occurs, neuronal excitability in the lesion side decreases, whereas the contralesional side increases. As a result, facilitatory or inhibitory effects are induced by contralesional hemisphere changes, resulting in abnormalities in the interhemispheric interaction [3]. The changes in neuronal excitability are shown as an increase in the wPLI in terms of functional connectivity, which is evident in the difference in the contralesional M1 before NBS. In particular, differences according to the lesion location are related to their recovery process. In ITS, interhemispheric balance recovers, while in STS, global network reorganization leads to recovery [22]. This aspect seems to be related to the difference in the LI only in ITS before stimulation. Ultimately, the difference in the LI between healthy controls and ITS is recovered in patients with ITS due to dual-mode NBS. After dual-mode NBS, in the ipsilesional M1, mu GC was significantly increased over both ITS and STS compared to the healthy controls. As mentioned earlier, when stroke occurs, the neuroexcitability of the lesion area decreases. We applied 10 Hz TMS to induce brain activity in this respect, so this change seems plausible. However, regarding interhemispheric connectivity, LI increased after stimulation only in ITS. This is believed to be related to the interhemispheric disruption and balance in ITS [22]. In this regard, it is important to discuss the relationship between brain connectivity changes and motor recovery. In fact, brain connectivity changes were observed alongside motor recovery, as shown by the decreased beta wPLI between the left DLPFC and the ipsilesional M1, and as shown by the increased mu GC from the left DLPFC to the ipsilesional M1 after stimulation in ITS. These findings highlight the therapeutic significance of neuromodulatory approaches. Notably, there was a difference in the mu band related to intrahemispheric connectivity and the beta band related to interhemispheric connectivity. Damage to the sensorimotor pathways caused by stroke leads to motor deficits [22]. In the end, even if the same motor function has eventually deteriorated, damage and recovery to certain sensorimotor pathways cause this difference according to lesion location. In the motor network, the mu band is associated with motor planning, allocating computational resources by focusing on oscillatory activity, whereas the beta band is associated with kinetic motor execution [23]. This is believed to be due to the characteristics of the beta band being related to the level of motor engagement [21]. ITS is the occurrence of lesions in deeper areas, eventually affecting the interaction between the two hemispheres more strongly than STS, indicating