## 3 Results
While inflammation plays a significant role in the pathophysiology of IS, correlating the serum IL-6 levels with C-reactive protein (CRP) and other inflammatory markers is essential for evaluating the infarct volume and predicting clinical outcomes. Figure 5: Serum CNTF level in the study group compared to the control group (pg/mL) [15]. In this study, high serum IL-6 levels were detected in the study group, with a mean value of 22.02 \(\pm\) 2.143 pg/mL, ranging from 4.58 pg/mL to 65.71 pg/mL. In contrast, the control group exhibited IL-6 levels that were approximately ten times lower, with a mean value of 2.38 \(\pm\) 0.302 pg/mL, ranging from 0.01 pg/mL to 5.38 pg/mL. This difference was statistically significant (\(p<0.001\)) (Figure 7). The results of this study reveal that elevated serum IL-6 levels during the acute phase of IS, compared with those of healthy controls (\(p<0.001\)), were strongly associated with the infarct volume (\(p<0.004\)) and a less favorable prognosis during the six months post-stroke, as indicated by the severity of neurological sequelae (\(p<0.01\)). The assessment of serum IL-6 levels in children during the acute phase of ischemic stroke (IS) provides valuable insights into the severity of brain injury by reflecting the extent of neuroinflammation. It also serves as a predictor of the long-term neurological outcomes and overall prognosis in IS. A positive correlation was also observed between the CNTF and IL-6 levels in the main group (r = 0.580), highlighting their combined role in promoting and sustaining neuroinflammation, as well as in assessing the extent of brain injury resulting in serious sequelae in pediatric IS. In this study, there were no significant correlations found between other pro-inflammatory cytokines and immune mediators. Additionally, the S100B protein levels, measured six months after the onset of IS, were significantly higher in the main group, with a mean value of \"0.30 \(\pm\) 0.022 ng/mL\" and a  
Figure 6: Serum APA levels in the main and control groups (U/mL). Figure 7: Serum IL-6 level in the study group (pg/mL). range from *0.16 ng/mL to 0.81 ng/mL. In contrast, the control group exhibited relatively stable S100B levels (0.17 \(\pm\) 0.001 ng/mL) with minimal variability (0.16-0.18 ng/mL). This difference between the groups was statistically significant (\(p\) < 0.001) (Figure 8). An analysis of the S100B protein levels six months after in terms of disease-adjusted life years (DALYs) revealed a significant decrease in their mean values, confirmed by a statistically significant difference (*t = 2.702, \(p\) < 0.01) (Figure 9). Over this period, the S100B levels declined from *0.524 \(\pm\) 0.0850 ng/mL* to *0.30 \(\pm\) 0.022 ng/mL*, normalizing in most patients. This trend suggests the involvement of the S100B protein in recovery mechanisms following ischemic stroke. However, persistently elevated S100B levels in some patients, particularly those with severe brain injury, were noted six months post-stroke (e.g., from *4.390 ng/mL* at disease onset to *0.81 ng/mL* after six months). This persistence highlights the risk of recurrent  
Figure 8: Serum level of the S100B protein in the main group (6 months after IS) and in the control group (pg/mL) [15]. Figure 9: Mean serum level of the S100B protein in the acute period of acute IS in children and the values showing its dynamics (more than six months after disease), ng/mL. stroke and underscores S100B's potential as a biomarker for both the brain injury severity and the extent of ongoing neurological impairment. Similarly to that of the S100B protein, the mean VEGF level, when assessed six months after ischemic stroke (Figure 10), had decreased by nearly half in the main group, from 613.41 \(\pm\) 39.299 pg/mL to 374.96 \(\pm\) 19.506 pg/mL; the evident dynamics were also confirmed statistically (\(p\) < 0.01). To visualize the change in the VEGF values over time, it is represented in a flow-chart diagram.