Normal ipsilateral/contralateral asymmetries in infant multiple auditory steady-state responses to air- and...

Two-channel recordings of infants' air- and bone-conduction auditory brainstem responses to brief tones show ipsilateral and contralateral (to the stimulated ear) asymmetries which may be used to isolate which cochlea is the primary contributor to the response. The objective of this study was to determine whether similar ipsilateral/contralateral asymmetries are also present in the air- and bone-conduction "brainstem" (77 to 101 Hz) auditory steady-state responses (ASSRs) of infants.

Two-channel ASSRs were recorded in infants (2 to 11 mo) and adults (18 to 40 yr) with normal hearing. Multiple stimuli (carrier frequencies: 500 to 4000 Hz; amplitude/frequency modulated) were presented using a B-71 oscillator on the temporal bone or an ER3-A insert earphone. Bone-conduction ASSR amplitudes, phase delays, and thresholds were obtained for the electroencephalographic (EEG) channels ipsilateral and contralateral to the oscillator temporal-bone placement. Bone-conduction ASSRs were also obtained to the stimulus presented to the opposite temporal bone (at 40 dB HL only). Air-conduction ASSR amplitudes and phase delays were obtained at 60 dB HL in each ear for the EEG channels ipsilateral and contralateral to the transducer.

Infants showed more ipsilateral/contralateral asymmetries in both air- and bone-conduction ASSRs compared with adults. Mean bone-conduction ASSR thresholds in infants were 13 to 15 dB higher (i.e., poorer) in the contralateral EEG channel compared with the ipsilateral EEG channel for 500 to 4000 Hz. In adults, there were no large differences (i.e., within 1 dB) between ipsilateral and contralateral ASSR thresholds. Based on ipsilateral/ contralateral threshold differences in infants, interaural attenuation for bone-conducted stimuli was estimated to be at least 10 to 30 dB for most infants. In contrast, most adults showed little interaural attenuation for bone-conducted stimuli. ASSR amplitudes are larger and phase delays are shorter in the ipsilateral EEG channel. For infants, the difference in air-conduction ASSR amplitude between EEG channels was twice that observed for adults. Infants also had greater ASSR amplitude differences between EEG channels for bone-conduction stimuli compared with adults, but the difference was less than that seen for air-conduction stimuli. For air-conduction stimuli, infants had significantly longer phase delays in the contralateral EEG channel compared with the ipsilateral EEG channel. Adults showed no significant differences in air-conduction ASSR phase delay between EEG channels. For bone-conduction stimuli, both infants and adults had significantly longer phase delays in the contralateral EEG channel compared with the ipsilateral EEG channel; the differences in ASSR phase delays between EEG channels were much smaller in infants compared with adults and fewer adults had absent responses in the contralateral EEG channels compared with infants (12% versus 34%). When the transducers were switched to the opposite ear/mastoid, the infant and adult ipsilateral/contralateral asymmetries also switched.

Ipsilateral/contralateral asymmetries in air- and bone-conduction ASSRs are clearly present more often and are larger in infants compared with adults. Our findings also suggest that most infants have at least 10 to 30 dB of interaural attenuation to bone-conducted stimuli. These asymmetries in the bone-conduction ASSR have potential as a clinical tool for isolating the cochlea that is contributing to the response in infants.