Neuromagnetic Oscillations Predict Evoked-Response Latency Delays and Core Language Deficits in Autism Spectrum Disorders

Abstract

Previous studies have observed evoked response latency as well as gamma band superior temporal gyrus (STG) auditory abnormalities in individuals with autism spectrum disorders (ASD). A limitation of these studies is that associations between these two abnormalities, as well as the full extent of oscillatory phenomena in ASD in terms of frequency and time, have not been examined. Subjects were presented pure tones at 200, 300, 500, and 1,000 Hz while magnetoencephalography assessed activity in STG auditory areas in a sample of 105 children with ASD and 36 typically developing controls (TD). Findings revealed a profile such that auditory STG processes in ASD were characterized by pre-stimulus abnormalities across multiple frequencies, then early high-frequency abnormalities followed by low-frequency abnormalities. Increased pre-stimulus activity was a ‘core’ abnormality, with pre-stimulus activity predicting post-stimulus neural abnormalities, group membership, and clinical symptoms (CELF-4 Core Language Index). Deficits in synaptic integration in the auditory cortex are associated with oscillatory abnormalities in ASD as well as patient symptoms. Increased pre-stimulus activity in ASD likely demonstrates a fundamental signal-to-noise deficit in individuals with ASD, with elevations in oscillatory activity suggesting an inability to maintain an appropriate ‘neural tone’ and an inability to rapidly return to a resting state prior to the next stimulus.

Resting-State Alpha in Autism Spectrum Disorder and Alpha Associations with Thalamic Volume

“…Cortical oscillatory abnormalities (oscillopathies) in ASD have been reported in several studies (Edgar et al 2013; Rojas et al 2008; Wilson et al 2007). It is frequently argued that cortical oscillopathies are due to an imbalance of excitatory (e.g., glutamatergic) and inhibitory (e.g., GABAergic) activity in inhibitory interneuron and pyramidal cell cortical networks (e.g., see Gandal et al 2010).…”

Brain oscillations and connectivity in autism spectrum disorders (ASD): new approaches to methodology, measurement and modelling

“…Consequent on the emerging synergies between the neurocognitive and neurophysiological models of ASD, a focus of attention in neurocognitive ASD research over the last decade or so has been on "oscillopathies" (Edgar et al, 2015) and atypical connectivity patterns (Gepner & Féron, 2009). These are summarised below.…”

Inhibition-Based Biomarkers for Autism Spectrum Disorder

“…In one such model [54], MEG functions as a scaled-up version of intracellular recordings, with gamma oscillations (high-frequency activity that is locally phase-locked) measured instead of spikes in response to a stimulus, and intertrial coherence (the fraction of MEG signals that are in-phase across multiple trials of a time-locked activity) used as a marker of fidelity of information transmission. In human and mouse models of ASD [55,56], intertrial coherence is lower than in controls, suggesting that a smaller number of signals are in phase across trials [54]. Evoked gamma power is also lower than in controls [55][56][57], suggesting a lower amplitude (and thus lower number of involved neurons) of high-frequency activity in response to trials, on average [54].…”

“…In human and mouse models of ASD [55,56], intertrial coherence is lower than in controls, suggesting that a smaller number of signals are in phase across trials [54]. Evoked gamma power is also lower than in controls [55][56][57], suggesting a lower amplitude (and thus lower number of involved neurons) of high-frequency activity in response to trials, on average [54].…”