## 4 Conclusions
\begin{table}
\begin{tabular}{c c c c c} \hline \hline
**Position** & **Study** & **Population** & **Key Findings** & **Interpretation** \\ \hline Supporting Evidence & [61] & ASD & Reduced _mn_ suppression during action observation & Suggests deficient sensorimotor mirroring contributing to social deficits \\ \hline  & [73] & Schizophrenia & Attenuated _mn_ rhythm suppression during motor tasks & Indicates impaired MNS functioning in schizophrenia \\ \hline  & [76] & \begin{tabular}{c} Early psychosis \\ and ASD \\ \end{tabular} & \begin{tabular}{c} Reduced biological motion-induced _mn_ suppression \\ linked to negative symptoms \\ \end{tabular} & \
\begin{tabular}{c} Supports MNS impairment as a shared mechanism in both conditions \\ \end{tabular} \\ \hline Opposing Evidence & [60] & ASD & Typical _mn_ suppression and preserved imitation abilities & Challenges the universality of MNS deficits in ASD \\ \hline  & [72] & Schizophrenia & Normal _mn_ suppression in response to biological motion &
\begin{tabular}{c} Implies intact mirroring mechanisms in at least some schizophrenia subgroups \\ \end{tabular} \\ \hline  & [62] & ASD & _mn_ suppression modulated by visual attention & Suggests attentional factors may account for prior findings of MNS dysfunction \\ \hline \hline \end{tabular}
\end{table} 
Table 3: Comparative evidence supporting and opposing the broken mirror theory in ASD and schizophrenia. The studies selected for this paper have investigated \(mu\) rhythm suppression in schizophrenia and ASD as a proxy for discrepancies in the function and activation of the MNS, implementing EEG paradigms. In the case of ASD, numerous research studies have presented evidence for reduced \(mu\) rhythm suppression during tasks that require observation of biological actions. The theory of broken MNs has been approached through a critical lens in this review, including studies that report no links between \(mu\) rhythm suppression and task performance, whereas others present findings that support this hypothesis and attribute the core deficits in social navigation and communication in ASD to a dysfunctional MNS. A thematic comparison of MNS abnormalities in ASD and schizophrenia on the basis of the studies that have been reviewed, reveals both overlapping features and condition-specific differences. In ASD, [PERSON] and [PERSON] [61] proposed widespread MNS dysfunction as a core mechanism behind social and communicative impairments. However, more recent investigations offer a more nuanced picture. [PERSON] et al. [60] and [PERSON] et al. [63] found intact MNS activity under certain task conditions, suggesting that task effects, such as task demands and cognitive engagement, may influence MNS responses. Furthermore, [PERSON] et al. [62] demonstrated that visual attention plays a key modulatory role in \(mu\) rhythm suppression in autistic individuals, indicating that attentional deficits may underlie MNS anomalies. [PERSON] et al. [59] and [PERSON] et al. [63] also emphasized that while automatic motor resonance may be atypical in ASD, higher-order inferential processes remain relatively preserved. In schizophrenia, the picture is similarly complex. [PERSON] et al. [72] observed preserved \(mu\) suppression in individuals with schizophrenia, challenging the assumption of a pervasive MNS dysfunction. Yet, [PERSON] et al. [73] and [PERSON] et al. [81] reported deficits in \(mu\) rhythm modulation and empathy-related activation, suggesting that MNS anomalies may emerge more prominently in relation to negative symptoms or reduced social functioning in schizophrenia. [PERSON] et al. [76] further demonstrated that biological motion-induced \(mu\) rhythm suppression was diminished in early psychosis patients with concurrent ASD traits, thus highlighting potential transdiagnostic features of MNS dysfunction. [PERSON] et al. [82], while not directly measuring \(mu\) rhythm suppression, contributed to the debate by showing that oxytocin modulates social brain activity, which may interact with MNS-related pathways.