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An ERP Investigation of the Acoustic Change Complex in High-Functioning ASD

Friday, 3 May 2013: 09:00-13:00
Banquet Hall (Kursaal Centre)
A. Bhatara1,2, T. Babikian3, E. Laugeson4, R. Tachdjian5, E. Ballat2 and Y. S. Sininger2, (1)Laboratoire Psychologie de la Perception, Université Paris Descartes, Paris, France, (2)Department of Head and Neck Surgery, UCLA, Los Angeles, CA, (3)Psychiatry and Biobehavioral Sciences, UCLA, Los Angeles, CA, (4)UCLA Semel Institute for Neuroscience & Human Behavior, Los Angeles, CA, (5)Departments of Medicine and Pediatrics, UCLA, Los Angeles, CA
Background: There is a growing body of evidence showing abnormalities in the auditory system of individuals with autism spectrum disorders (ASD). ERP studies examining auditory evoked responses in individuals with ASD have shown evidence of atypical lateralization and maturational patterns as well as increased sensitivity to changes in sound (Bomba & Pang, 2004). Auditory change detection has been investigated using paradigms that elicit a mismatch negativity (Gomot et al., 2011), but to our knowledge, no study on ASD has examined the acoustic change complex, which is elicited by changes in frequency or a silent gap (Martin & Boothroyd, 1999).

Objectives: To investigate the acoustic change complex in adolescents with high-functioning ASD.  

Methods: Fifteen adolescents aged 10-14 with high-functioning ASD and 16 age-matched typically developing (TD) controls listened passively to auditory stimuli with changes while cortical responses were measured using a 21-channel EEG cap. Stimuli were 1500 ms tones or noise presented monaurally, consisting of an onset stimulus lasting 700 ms followed by either a 50% frequency change (Task 1) or a 20-ms gap of silence (Task 2). Stimuli in Task 1 were tones of 500 or 4000 Hz and in Task 2 were tones of 1000 Hz or broadband noise. Frequency and ear of presentation were randomized within tasks, and tasks were counterbalanced. Each task continued until 150 trials for each frequency/ear combination were accepted. Peak measurements (amplitude and latency) were performed for the N1b wave at the vertex (Cz and Fz) and the T-complex at the temporal electrodes (T7 and T8), described here as N1a and N1c with a postitive Ta between them.

Results:  In Task 1 (Frequency), there was a group by ear interaction (p = .047): Whereas the ASD group showed a shorter latency N1a at the change in response to sounds presented to the left ear (LE) than to the right ear (RE), the TD group showed the reverse pattern. Relative to the TD group, the ASD group also showed higher amplitude N1a peaks (p = .005) and shorter latency of the Ta component (p = .047) implying increased sensitivity to the change. In Task 2 (Gap), at the onset of the stimuli, the TD group showed higher amplitude N1a peaks recorded at the left (T7) than at the right (T8) temporal electrode (p = .001), but the ASD group showed no difference between electrodes (p = .96). Also, the ASD group showed shorter latencies than the TD group for the Ta peak (p =.02) and higher amplitudes for N1b (p = .04). After the gap, the N1b peak had shorter LE latencies for the ASD group (p = .01), whereas the TD group showed no ear difference (p = .6).

Conclusions:  The ASD group showed evidence of atypical laterality, evidenced by both ear and electrode differences. In addition, increased amplitude and shortened latencies suggest increased sensitivity to change in the ASD group. Along with previous work, this supports the hypothesis that difficulties with language and nonverbal communication may have bases in atypical low-level auditory processing.

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