Abstract
BackgroundAutism spectrum disorder (ASD) is associated with hyper- and/or hypo-sensitivity to sensory input. Spontaneous alpha power, which plays an important role in shaping responsivity to sensory information, is reduced across the lifespan in individuals with ASD. Furthermore, an excitatory/inhibitory imbalance has also been linked to sensory dysfunction in ASD and has been hypothesized to underlie atypical patterns of spontaneous brain activity. The present study examined whether resting-state alpha power differed in children with ASD as compared to TD children, and investigated the relationships between alpha levels, concentrations of excitatory and inhibitory neurotransmitters, and atypical sensory processing in ASD.MethodsParticipants included thirty-one children and adolescents with ASD and thirty-one age- and IQ-matched typically developing (TD) participants. Resting-state electroencephalography (EEG) was used to obtain measures of alpha power. A subset of participants (ASD = 16; TD = 16) also completed a magnetic resonance spectroscopy (MRS) protocol in order to measure concentrations of excitatory (glutamate + glutamine; Glx) and inhibitory (GABA) neurotransmitters.ResultsChildren with ASD evidenced significantly decreased resting alpha power compared to their TD peers. MRS estimates of GABA and Glx did not differ between groups with the exception of Glx in the temporal-parietal junction. Inter-individual differences in alpha power within the ASD group were not associated with region-specific concentrations of GABA or Glx, nor were they associated with sensory processing differences. However, atypically decreased Glx was associated with increased sensory impairment in children with ASD.ConclusionsAlthough we replicated prior reports of decreased alpha power in ASD, atypically reduced alpha was not related to neurochemical differences or sensory symptoms in ASD. Instead, reduced Glx in the temporal-parietal cortex was associated with greater hyper-sensitivity in ASD. Together, these findings may provide insight into the neural underpinnings of sensory processing differences present in ASD.
Highlights
Autism spectrum disorder (ASD) is an etiologically complex, heterogeneous condition affecting 1 in 54 children, making it one of the most prevalent neurodevelopmental disorders [1]
The current study examines whether differences in alpha-band power are present in children and adolescents with ASD compared to their typically developing (TD) peers and investigates whether a relationship exists between alpha and measures of ASD symptomatology, sensory processing differences
There was a significant effect of regions of interest (ROI), F(2, 120) = 122.4, p < .001, ηp2 = 0.67, as power was greater at the posterior compared to both frontal, t(61) = − 9.6, p < .001, and central, t(61) = − 13.5, p < .001, ROI, and greater at the frontal compared to central ROI, t(61) = 3.8, p
Summary
Autism spectrum disorder (ASD) is an etiologically complex, heterogeneous condition affecting 1 in 54 children, making it one of the most prevalent neurodevelopmental disorders [1]. Pre-stimulus (i.e., spontaneous) alpha power is associated with the detection of briefly presented visual and tactile stimuli [10,11,12] In light of these and other findings, several theories have outlined how alpha activity may play an active role in modulating sensory input [9, 13, 14]. Jensen and Mazaheri [13] and Mathewson and colleagues [14] have proposed that alpha oscillations may function as a sensory gating mechanism through pulsed inhibition, which is mediated by activity of GABAergic inhibitory interneurons Together, these theories suggest that ongoing alpha oscillatory activity plays a critical role in shaping perception of and responses to incoming sensory information. The present study examined whether resting-state alpha power differed in children with ASD as compared to TD children, and investigated the relationships between alpha levels, concentrations of excitatory and inhibitory neurotransmitters, and atypical sensory processing in ASD
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