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Causal Underpinnings of Sensory Hypersensitivities in Autism
Sensory hypersensitivities are diagnostic of autism spectrum disorder (ASD). Estimates are that 88% of individuals with ASD experience sensory hypersensitivities, the most common being auditory. We posit that impaired neural habituation may be a causal factor. Habituation to repeated sensory stimuli frees cognitive resources to process new information. Impairments in habituation would make for a confusing situation in which all sensory elements would be treated as equally salient. If one’s ability to discount even highly repetitive sensory streams were impaired, the overwhelming sensory bombardment may manifest as a need to avoid further stimulation.
We studied habituation to auditory stimuli in children and young adults with ASD using two distinct measures of sensory sensitivity, one peripheral, galvanic skin response (GSR) and one central, magnetoencephalography (MEG).
Objectives:
To determine whether auditory habituation is impaired in ASD using GSR and MEG.
Methods:
GSR
Participants were 18 ASD and 20 age-matched NT controls. Electrodermal responses were recorded using Flexcomp Infinity™ encoder with a sampling rate of 2048 Hz. Two Ag-AgCl electrodes approximately 3 cms apart were attached to the palm of the non-dominant hand. Participants sat in a quiet room for baseline measurement and then listened to discrete beeps (1KHz, 73dB, beep duration=0.116s), with 1 second ISI for 5 minutes.
MEG
Participants were 14 ASD, 4 ASD siblings, and 5 age-matched NT controls. A metronomic sequence of 300 auditory beeps was presented. MEG signals were recorded from 306 channels (Elektra Neuromag TRIUX) at a sampling rate of 1000Hz, band-pass filtered between 0.03 and 330Hz. Auditory responses were obtained from MEG sensors near auditory cortices. Two auditory evoked response fields (ERFs) were computed by averaging 600ms signal fragments corresponding to the first and last 50 trials.
Results:
GSR
NT participants showed a decline in GSR prior to the onset of the tones as well as during the tone sequence; the onset of the tones elicited a transient response followed by a sustained decline. ASD participants, however, showed an increase in GSR during the tone sequence. The slopes of GSR traces were calculated and group differences were significant. These analyses revealed negative slopes for NTs but positive ones for ASD. The difference between the average GSR amplitude during the first and last 60 seconds of the auditory presentations were also significant. ASD participants showed a significant increase in GSR amplitude over time, further evidence of reduced habituation.
MEG
NT participants showed marked habituation over the course of the auditory sequence; ERFs evoked by the impulses in the initial section of the auditory train were stronger than those evoked by the later ones. By contrast, the amplitude of auditory evoked responses in ASD participants consistently increased over time, resulting in stronger magnetic deflections during the final 50 trials relative to the first 50 trials, indicating a lack of habituation.
Conclusions:
ASD symptomology involves impaired habituation. Two distinct measures of sensitivity to auditory stimuli, GSR and MEG, revealed that while NT individuals habituated to tones, ASD did not. The findings have widespread implications for ASD clinical symptomology.