## 4 Discussion  
This preliminary study, even if conducted in a very low number of subjects, provides novel information regarding a possible effect of tDCS on decreasing muscle stiffness in children with CP. The results of clinical studies demonstrate the potential of tDCS in treating neurological disorders and investigating modulation of cerebral cortex excitability [18; 19]. [PERSON] et al. [20] reported that even a single session of this type of treatment can significantly improve static balance and gait velocity in children with CP. [PERSON] et al. [21] conducted a similar research. As they stated, tDCS can prolong and enhance positive effects achieved in physical therapy. [PERSON] et al. [22] studied effects of tDCS combined with other physiotherapy modalities for adults with neurological disorders, such as stroke. By changing the membrane potential, a weak electrical current used in tDCS causes an increase in local synaptic efficiency. This can open a pathway to modulate cortex activity and preserve effects of rehabilitation [23]. The presented findings are in agreement with our research, providing evidence on the considerable effectiveness of this treatment. Although the precise mechanism that underlies tDCS is not yet completely understood, its effects on cortical activity are consistent and reliable [19]. A study conducted by [PERSON] et al. [24] showed that tDCS could induce specific changes in motor activity, as a function of targeted brain areas. The primary mechanism of tDCS stimulation of the cerebral cortex is a subthreshold modulation of neuronal resting membrane potential [25]. It is worth emphasizing that tDCS has the unique ability to induce antagonistic effects in cortical excitability according to the parameters of stimulation. Therefore, cathodal stimulation decreases cortical excitability, leading to hypo-polarization of axonal membrane potentials [26], whereas anodal stimulation increases it and leads to neuronal hyper-polarization [27]. Furthermore, stimulation duration over 7 min causes synaptic strengthening under the anode and synaptic weakening under the cathode [19]. We took these variables into consideration when designing our research. It is generally accepted that the possible cause of spasticity in CP patients lies within a decrease of cortical input in the corticospinal tract. In that case, the effects of anodal tDCS on increasing cortical activity might be an explanation for motor improvements in our study. Those were assessed as a decrease in muscle stiffness and Ashworth Scale score. The presented hypothesis is also supported by studies done by [PERSON] and colleagues. After evaluating pre- and post-anodal tDCS, they demonstrated a significant decrease in spasticity for the whole upper limb [28]. [PERSON] and [PERSON] [29] used tDCS to treat patients with stroke, showing promising results, i.e., a significant reduction of motor impairment in all individuals, and an increased resting state connectivity between ipsilesional motor cortex with contralesional premotor cortex and bilateral precuneus. This gives fresh insight into the treatment and possibilities for individuals with chronic neurological impairments where the time for spontaneous brain recovery is complete. Our research \begin{table}
\begin{tabular}{c c c} \hline \hline
**Sessions** & **m. Flexor Carpi Radialis** & **m. Biceps Brachi** \\ \hline
1 st day of the experiment & \(289.2\pm 50.8\) & \(187.4\pm 33.8\) \\
10 th day of the experiment & \(293.4\pm 47.3\) & \(183.2\pm 31.3\) \\ \hline \hline \end{tabular}
\end{table} 
Table 2: Mean \(\pm\) SD muscle stiffness (N/m) on the first and 10 th days of the experiment. did not focus on spasticity itself, but on general motor function improvements. However, it can be a valuable source of knowledge, as spasticity limits the ability to perform everyday activities. Our study showed a decrease in muscle stiffness, which is in line with a general improvement in motor function. Moreover, [PERSON] et al.