Neural synchrony examined with magnetoencephalography (MEG) during eye gaze processing in autism spectrum disorders: preliminary findings.

Renée Lajiness-O’Neill,Kelly Vogt,Daniel Jacobson,Alfred Mansour,Annette E Richard,Laszlo A Erdodi,Susan M Bowyer,Aimee M Moore,John E Moran,Amy Olszewski,Lesley Pawluk

doi:10.1186/1866-1955-6-15

Abstract

BackgroundGaze processing deficits are a seminal, early, and enduring behavioral deficit in autism spectrum disorder (ASD); however, a comprehensive characterization of the neural processes mediating abnormal gaze processing in ASD has yet to be conducted.MethodsThis study investigated whole-brain patterns of neural synchrony during passive viewing of direct and averted eye gaze in ASD adolescents and young adults (M Age = 16.6) compared to neurotypicals (NT) (M Age = 17.5) while undergoing magnetoencephalography. Coherence between each pair of 54 brain regions within each of three frequency bands (low frequency (0 to 15 Hz), beta (15 to 30 Hz), and low gamma (30 to 45 Hz)) was calculated.ResultsSignificantly higher coherence and synchronization in posterior brain regions (temporo-parietal-occipital) across all frequencies was evident in ASD, particularly within the low 0 to 15 Hz frequency range. Higher coherence in fronto-temporo-parietal regions was noted in NT. A significantly higher number of low frequency cross-hemispheric synchronous connections and a near absence of right intra-hemispheric coherence in the beta frequency band were noted in ASD. Significantly higher low frequency coherent activity in bilateral temporo-parieto-occipital cortical regions and higher gamma band coherence in right temporo-parieto-occipital brain regions during averted gaze was related to more severe symptomology as reported on the Autism Diagnostic Interview-Revised (ADI-R).ConclusionsThe preliminary results suggest a pattern of aberrant connectivity that includes higher low frequency synchronization in posterior cortical regions, lack of long-range right hemispheric beta and gamma coherence, and decreased coherence in fronto-temporo-parietal regions necessary for orienting to shifts in eye gaze in ASD; a critical behavior essential for social communication.

Highlights

Gaze processing deficits are a seminal, early, and enduring behavioral deficit in autism spectrum disorder (ASD); a comprehensive characterization of the neural processes mediating abnormal gaze processing in ASD has yet to be conducted
[1] Failure to detect and/or respond in a typical manner to information conveyed by eye gaze is possibly the most important early hallmark of autism spectrum disorders (ASD) [2]
One of the hallmarks of ASD is a failure to detect and/ or respond in a typical manner to information conveyed by eye gaze

Summary

Introduction

Gaze processing deficits are a seminal, early, and enduring behavioral deficit in autism spectrum disorder (ASD); a comprehensive characterization of the neural processes mediating abnormal gaze processing in ASD has yet to be conducted. Orienting to eye gaze is a vital skill present from birth and underlies effective non-verbal communication and social interaction [1] Failure to detect and/or respond in a typical manner to information conveyed by eye gaze is possibly the most important early hallmark of autism spectrum disorders (ASD) [2]. Research suggests that reflexive responses to eye gaze cues may be intact in individuals with ASD [10,11], studies indicate that orienting voluntarily to eye gaze is impaired and those with ASD may not demonstrate preferential sensitivity to eye gaze as a social cue [12,13,14,15] Instead, it appears that for these individuals, others’ eyes may merely serve as a spatial cue, much like a directional arrow [16]

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Discussion

Conclusion