## 4 Discussion
One reason could be the limitations of analysis techniques or because alterations in brain activity linked to illnesses are not always supported by large-scale evidence. Rather, they are visible across a small time-scale of seconds, necessitating short time-scale investigations to capture those deficit patterns. In our study, SZ patients exhibited decreased cuneus mean strength connectivity (dFC-Str) in several brain areas, such as the left cuneus and right calcarine, the right cuneus and right calcarine, the right cuneus and right calarine, the right cuneus and right lingual gyrus, and between the right cuneus and right-middle temporal gyrus. These changes were all observed in dFC and not in sFC, this may be because some brain disorders need short-time-scale analyses in order to capture subtle deficits., Previous and current rsfMRI researches on SZ have increasingly focused on dFC [1; 22; 23], especially in specific time intervals (windows) [15; 23; 103; 104; 105; 106; 107]. Our results are in accordance with [PERSON] et al. in SZ and [PERSON] et al. in Bipolar Disorder studies, who demonstrated how dynamic FC has more predictive accuracy than static FC [15; 108]. We also observed similar connections in different time. The evidence in Table 3 shows how the connections were lost in bigger window sizes (Table 3 at 75 TR) and at full-length (145 TR). Together, these findings point to the conclusion that information that is likely to be lost in static FC (bigger window sizes approaching to full-length) can be trapped in the dynamic FC. Although we only found a decrease in cuneus connectivity in this study, previous research has found that SZ can also cause an increase in cuneus connectivity. Notably, increased dynamic ReHo was also discovered in the super temporal gyrus, postcentral gyrus, thalamus, middle cingulum cortex, and cuneus in SZ patients [106]. Other regions have also been linked to an increased functional connectivity in SZ illnesses, such as an increased global-brain functional connectivity in the left superior frontal gyrus [109]. Even though the majority of SZ studies have emphasized the decreased FC patterns, the lack of increased connection patterns in these studies and our study could be linked to the type of SZ patients regarding the stage of illness and medication [110]. The brain compensatory mechanism's inability to recruit more resources to retain, maintain, or restore cognitive functioning, or in response to cognitive demands, can be viewed as the main indication of decreased connectivity in SZ. Since it has long been assumed that SZ is a spectrum of diseases caused by several pathophysiological processes rather than a single disease [111], other factors such as diverse samples and different preprocessing approaches could also lead to this inconsistency. Even though the cuneus is believed to be associated with cognitive functions such as behavior engagement [112], working memory [113], and cognitive control [43]. It is thought to be largely engaged in visual processing. The cuneus, in particular, appears to be involved in detecting changes in ocular position as a result of spontaneous eye movements [114]. Impairments in smooth-pursuit eye movements have been repeatedly recorded, especially in SZ patients [115]. These studies reveal that SZ patients, or those who are at risk of developing the condition, may have problems monitoring their own eye movements and this could be because of reduced connectivity in the cuneus. Evidenced by previous works, the SZ decreased connectivity in visual areas could also be because those affected typically perform worse in visual motion [116] and visual contrast [117]. Whether the cuneus anatomical abnormalities seen in the SZ subjects in this study are also related to abnormal eye tracking is a topic worthy of future discussion.