30715
Early Visual Processing Indicates E/I Imbalance in Adults with Autism and Schizophrenia
Visual Evoked Potentials (VEP) are robust and well characterized EEG responses that index the integrity of the visual system with amplitudes that reflect the ratio of excitation and inhibition (E/I) in the brain. Past research has shown attenuated P1-N1 amplitude in disorders with sensory features, including autism (ASD) and schizophrenia (SZ); these disorders share a neural phenotype of attenuated VEP P1-N1 amplitudes and overlapping behavioral phenotypes of social and communicative difficulties, termed negative symptoms in schizophrenia. The use of VEPs as a transdiagnostic measure of cortical function and a neural correlate of behavior may lead to a better understanding of the neurobiological underpinnings of these disorders with implications for prognostic evaluation and treatment selection.
Objectives:
Determine shared features of low-level visual processing as a metric of E/I imbalance in adults with autism and schizophrenia and explore the relationship of these neural markers with social and communicative severity.
Methods:
Participants were 18-40 year old adults with ASD (n=23; mean IQ=105), SZ (n=15; mean IQ=99), and typical development (TD; n=29; mean IQ=114), matched for age (mean age=24.6 years). All participants were extensively behaviorally characterized, including the Autism Diagnostic Observation Schedule (ADOS) and Positive and Negative Symptom Scale (PANSS). EEG was recorded with a 128 sensor Hydrocel Geodesic Sensor Net while participants viewed a black and white checkerboard reversing at a rate of 1 Hz. EEG was filtered from 0.1-30 Hz, re-referenced, segmented from -150 to 300 ms, artifact detected, and averaged. Peak amplitudes and latencies were extracted for the N1 (60-100 ms) and P1 (80-180 ms) components at electrode 75 (Oz). The difference in N1 and P1 amplitudes was calculated for all participants. One-way ANOVAs tested for differences in P1 and N1 latency and P1-N1 amplitude. Pearson correlations were used to assess relationships of ERP components with social abilities as measured by the ADOS and the negative symptom scale of the PANSS.
Results:
No main effects of diagnosis were seen for N1 [F(2, 64)=2.57, p>.05] or P1 [F(2, 64)=.32, p>.05] latency. There was a significant main effect of diagnosis on P1-N1 amplitude [F(2, 64)=5.37, p=.007]. Post hoc tests revealed the difference was driven by greater P1-N1 amplitude in the ASD group as compared to the TD group [t(29)=2.9, p=.007]; no differences were seen between the SZ group and either group (ps>.1). Collapsing across clinical groups (ASD, SZ) revealed a significantly greater P1-N1 amplitude compared to the TD group [t(57)=-2.9, p=.004]. P1-N1 amplitude was positively correlated with ADOS calibrated severity scores (r=.291, p=.017) and PANSS negative symptom total score (r=.31, p=.012) across all participants.
Conclusions:
Differences in the P1-N1 amplitudes of the VEP in adults with ASD and SZ are consistent with intact visual processing circuitry but atypical E/I balance. P1-N1 amplitude is associated with clinician-reported social symptomatology in both ASD and SZ, demonstrating a link between objective neural responses and social function. These findings suggest a degree of shared pathophysiology between SZ and ASD and demonstrate the promise of transdiagnostic research for informing social-communicative biomarker development in neurodevelopmental disorders.