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Otoacoustic Emissions and Efferent Feedback in ASD

Friday, 3 May 2013: 09:00-13:00
Banquet Hall (Kursaal Centre)
A. E. Luebke1, P. D. Allen2,3, J. DeSanctis4, R. M. Nelson4, A. Lord4 and L. Bennetto4, (1)Biomedical Engineering and Neurobiology & Anatomy, University of Rochester Medical Center, Rochester, NY, (2)University of Rochester Medical Center, Rochester, NY, (3)Neurobiology & Anatomy, University of Rochester Medical Center, Rochester, NY, (4)Clinical and Social Sciences in Psychology, University of Rochester, Rochester, NY
Background: Filtering auditory information in background noise is required for a person’s social communication abilities, and impairment of such filtering abilities is one of the key features of autism spectrum disorders (ASD).  A potential physiological basis for filtering relevant auditory information is caused by descending regulation by the brain onto cochlear activity—the olivocochlear efferent feedback systems. The olivocochlear efferent systems consist of two components whose cell bodies are found in the superior olivary complex: a medial olivocochlear (MOC) system projecting primarily to cochlear outer hair cells (OHCs); and a lateral olivocochlear (LOC) system projecting primarily to the dendrites of cochlear afferent neurons in the region beneath inner hair cells. The contractile activity of the OHCs can be evaluated in human subjects, because contractions of the OHCs generate acoustic signals (otoacoustic emissions; OAEs), which can be recorded in the external ear canal, making it possible to directly measure auditory filtering processes at the cochlear periphery. It has previously been shown that adolescents and children with ASD have reduced MOC efferent feedback strength using transient OAEs (TrOAEs) and greater asymmetries in their responses (right vs. left ear) when compared with typical controls. Additionally, when brains have been examined from adults with ASD (using autopsy or MRI), the superior olivary complex was found to be either absent, greatly reduced, or disorganized when compared with age-matched control brains, again suggesting that the olivocochlear region is affected in individuals with ASD.

Objectives:   Our objective was to specifically measure efferent feedback strength and baseline otoacoustic emissions in children with ASD when compared with matched, typically developing controls.

Methods: Children with ASD (n=25) and typically developing controls (n=26), ages 6 through 17, participated in this study. Groups were rigorously characterized via ADI-R and ADOS, and matched on age, gender, and verbal ability.  Exclusion criteria included diagnoses of neurological or genetic disorders, and other conditions or illnesses that could affect hearing. Hearing was evaluated via audiometry; all subjects had thresholds below 20 dB SPL for 500, 100, 2000, and 4000 Hz, and <25 dB SPL for 8000 Hz. To perform the measurement of cochlear efferent feedback strength and baseline otoacoustic measures, we tested right and left ears of all subjects in in a sound attenuated room, with i) baseline DPOAE (distortion-product) and TrOAE (transient) conditions (without binaural broadband noise stimulation); then ii) TrOAEs with broadband suppression (400-750 ms).

Results: High-functioning children and adolescents with ASD have greatly reduced DPOAE responses in the 1-2 kHz speech frequency range (~8dB SPL, f2=1 kHz, p<0.001), yet have comparable DPOAE responses at 0.5 and 4-8 kHz regions.  The analysis of the spectral features of the TrOAE baseline and efferent measures are underway, but expect these measures to be similarly reduced in ASD.

Conclusions: Non-invasive measures of cochlear function and efferent feedback strength may serve as an early physiological biomarker for ASD.

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