2026 ECNP Congress
PS03-3179Electrophysiological markers of facial emotion processing: an umbrella review integrating magnetoencephalographic and event-related potential evidence in schizophrenia and depression
Introduction
Social cognitive deficits characterize major psychiatric disorders, including schizophrenia and major depressive disorder (MDD) [1]. These impairments are associated with social withdrawal as well as deficits in implicit facial emotion processing (iFEP) and explicit facial emotion recognition (FER) [2]. In psychiatric disorders, iFEP and FER were linked to alterations in electrophysiological markers, including event-related potentials (ERPs) such as P100, N170, and N250.Notably, the P300 component, reflecting attentional allocation and context updating, represents a core neurocognitive process supporting social functioning [3]. However, whether P300 abnormalities vary according to emotional valence remains unclear. Complementarily, magnetoencephalography (MEG) enables the characterization of fast oscillatory dynamics and functional connectivity underlying iFEP and FER [4].
Aims
To integrate evidence from ERP and MEG studies in order to characterize neural alterations during emotional processing in psychiatric disorders. Specifically, we assess P300 amplitude differences between patients with schizophrenia and healthy controls (HCs) across implicit (i.e., passive viewing of facial expressions) and explicit tasks (i.e., emotion identification requiring behavioral responses), examining potential valence-specific effects. In parallel, we identify magnetoencephalographic spatiotemporal patterns of neural activity and connectivity across schizophrenia and MDD under the same implicit and explicit conditions.
Methods
Two systematic reviews were conducted following PRISMA guidelines. For the ERP analysis, PubMed, Web of Science, and SCOPUS were searched until May 2025 for studies reporting P300 responses to positive and negative facial expressions in adults with schizophrenia compared to HCs. For the MEG analysis, PubMed, Web of Science, and CINAHL were searched until February 2025 for studies examining facial processing and recognition in schizophrenia and MDD.
Results
Ten ERP studies met inclusion criteria, with six included in the meta-analysis. In response to positive facial expressions (k=5; n=237), P300 amplitude was significantly reduced in individuals with schizophrenia (Hedges’ g=−0.40, 95% CI [−0.59, −0.21], p<0.001). For negative expressions (k=6; n=281), a smaller, marginally significant reduction was observed (Hedges’ g=−0.31, 95% CI [−0.62, 0.00], p=0.05). One study investigating implicit FER reported no significant differences. Eighteen MEG studies met inclusion criteria (4 schizophrenia, 14 MDD). Across disorders, transdiagnostic patterns emerged, including early temporal cortical hyperactivation (50–150 ms) during iFEP and early amygdala hyper-reactivity (within 100 ms), followed by reduced prefrontal recruitment (100–500 ms) during FER, alongside disrupted cortico-limbic connectivity. Disorder-specific findings included increased theta–gamma coupling and unidirectional visual–limbic–prefrontal connectivity in schizophrenia, and a shift from early gamma hyper-synchrony (50–150 ms) to later beta/gamma hypo-synchrony (250–500 ms), with reduced fronto-limbic and fusiform–amygdala connectivity in MDD.
Conclusions
Converging evidence from ERP and MEG studies supports temporally and functionally distinct alterations in facial processing across psychiatric disorders. In schizophrenia, P300 attenuation appears more pronounced for positive emotional stimuli, potentially reflecting altered salience attribution and reduced reward sensitivity. MEG findings suggest a shared pattern across schizophrenia and MDD of early hyper-reactivity and later prefrontal hypo-recruitment within cortico-limbic circuits, alongside disorder-specific oscillatory signatures. Deficits in iFEP and FER may represent a viable mechanism underlying social withdrawal [5], with electrophysiological markers providing potential transdiagnostic targets for neuromodulatory interventions.
References
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