Abstract

While impaired facial emotion recognition and magnocellular deficits in visual perception are core features of schizophrenia, their relationship is still unclear. Our aim was to analyze the oscillatory background of these processes and to investigate the connection between the magnocellular pathway deficit and the abnormal facial affect processing. Thirty-nine subjects with schizophrenia and forty socially matched healthy controls subjects were enrolled. A 128 channel EEG was recorded in three experimental tasks: first, participants viewed magnocellular biased low-spatial frequency (LSF) and parvocellular biased high-spatial frequency (HSF) Gabor-patches, then faces and houses were presented and in the third task a facial affect recognition task was presented with happy, sad and neutral faces. Event-related theta (4–7 Hz) synchronization (ERS) (i.e. an increase in theta power) by magnocellular biased stimuli was decreased in patients relative to controls, while no similar differences were found between groups in the parvocellular biased condition. ERS was significantly lower in patients compared to healthy controls both in the face and in the emotion recognition task. Theta ERS to magnocellular biased stimuli, but not to parvocellular biased stimuli, were correlated with emotion recognition performance. These findings indicate a bottom up disruption of face perception and emotion recognition in schizophrenia.

Highlights

  • Schizophrenia is a severe mental disorder characterized by positive, negative and cognitive symptoms

  • The magnocellular pathway is more sensitive to low-spatial frequency (LSF) and the parvocellular system is more sensitive to high-spatial frequency (HSF) stimuli[8]

  • Stage of perception can be linked to P100, the structural decoding of the face indicated by the N170 and the higher level processing of facial emotions indexed by N250 component

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Summary

Introduction

Schizophrenia is a severe mental disorder characterized by positive, negative and cognitive symptoms. The bottom-up model of schizophrenia states that the early sensory impairments lead to higher level process deficits such as facial emotion processing, which further contribute to the psychosocial functioning impairments[33]. Recent behavioral studies examined the interaction between early visual processing deficit and impaired emotion recognition via spatial frequency biased pictures of faces[35,36,37]. In a recent study Martinez et al analyzed the correlation between visual sensory function and face emotion recognition They showed that reduced motion sensitivity correlated with impaired face-emotion recognition in patients with schizophrenia and attenuated psychosis[40]. Previous investigations indicate that altered magnocellular pathway function contribute to impaired facial affect recognition, the exact neurobiological background is still unclear

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