Abnormal Pre-Attentive Arousal in Young Children with Autism Spectrum Disorder Contributes to Their Atypical Auditory Behavior: An ERP Study

Abstract

Auditory sensory modulation difficulties and problems with automatic re-orienting to sound are well documented in autism spectrum disorders (ASD). Abnormal preattentive arousal processes may contribute to these deficits. In this study, we investigated components of the cortical auditory evoked potential (CAEP) reflecting preattentive arousal in children with ASD and typically developing (TD) children aged 3-8 years. Pairs of clicks (‘S1’ and ‘S2’) separated by a 1 sec S1-S2 interstimulus interval (ISI) and much longer (8-10 sec) S1-S1 ISIs were presented monaurally to either the left or right ear. In TD children, the P50, P100 and N1c CAEP components were strongly influenced by temporal novelty of clicks and were much greater in response to the S1 than the S2 click. Irrespective of the stimulation side, the ‘tangential’ P100 component was rightward lateralized in TD children, whereas the ‘radial’ N1c component had higher amplitude contralaterally to the stimulated ear. Compared to the TD children, children with ASD demonstrated 1) reduced amplitude of the P100 component under the condition of temporal novelty (S1) and 2) an attenuated P100 repetition suppression effect. The abnormalities were lateralized and depended on the presentation side. They were evident in the case of the left but not the right ear stimulation. The P100 abnormalities in ASD correlated with the degree of developmental delay and with the severity of auditory sensory modulation difficulties observed in early life. The results suggest that some rightward-lateralized brain networks that are crucially important for arousal and attention re-orienting are compromised in children with ASD and that this deficit contributes to sensory modulation difficulties and possibly even other behavioral deficits in ASD.

Sensory processing in autism spectrum disorders and Fragile X syndrome—From the clinic to animal models

“…Decreased amplitude of the P1 peak at fronto-central electrodes has been described using both a classical P1 suppression paradigm in children aged 7–12 years with Asperger’s syndrome (Madsen et al, 2015) and in children aged 7–12 years with ASD by presenting speech and non-speech sounds (Lepisto et al, 2005). This latter finding was replicated in a more recent study which reported decreased amplitude of a later component of the P1 in the central region in children aged 3–8 years with ASD (Stroganova et al, 2013). Increased variability of P1 amplitude and latency between trials may also occur in individuals with ASD (Milne, 2011).…”

Magnetoencephalography in the study of children with autism spectrum disorder

“…With regard to EEG, few studies have reported abnormal P1 components in children with ASD. 71,72 One previous study demonstrated shorter latencies of the P1 evoked by binaural tone stimuli (1 kHz) in children with ASD (eight boys, mean age 8.5 years old) than in typically developing (TD) children (nine boys, mean age 8.5 years old). 72 However, previous MEG studies have not reported a shorter latency of the P1m in children with ASD in either the right or left hemispheres, 7,26 and one recent MEG study demonstrated a longer latency in 6-10-year-old children with ASD in both the right and left hemispheres.…”

“…Further stimulus‐specific and age‐specific studies on children with a wider age range will be crucial for gaining insight into the underlying neurophysiology of these developing and complex phenomena. With regard to EEG, few studies have reported abnormal P1 components in children with ASD . One previous study demonstrated shorter latencies of the P1 evoked by binaural tone stimuli (1 kHz) in children with ASD (eight boys, mean age 8.5 years old) than in typically developing (TD) children (nine boys, mean age 8.5 years old) .…”

“…The majority of previous studies using auditory stimuli have focused on the AEF. In Figure 3, we show representative AEF waveforms of three children (36,71 and 121 months old). The AEF is a brain response recorded by MEG that is equivalent to the auditory-evoked potential (AEP) recorded by EEG.…”

Early auditory processing evoked potentials (N100) show a continuum of blunting from clinical high risk to psychosis in a pediatric sample

“…In animals, the N100 originates from activation of superficial supragranular layers of the cortex (Moore, 2002; Stroganova et al, 2013), the primary origin and termination of intracortical connections (Swenson, 2006). Thus, pathology affecting these layers and projections may reduce N100 responses.…”