The binaural interaction component (BIC) of the auditory brainstem response (ABR) reveals brainstem origin of listening difficulties in children

Children experiencing conductive hearing loss (CHL) often display binaural hearing impairments that persist after CHL resolution. The neurophysiological correlates of the deficits and where problems begin to emerge are unknown. The long-time dogma was that maladaptive changes occur in cortex because while cortex remains plastic the brainstem circuits were not thought amenable to plasticity. Figures 5 and 6 of Gunnarson A. D. and Finitzo T. (1991, “Conductive hearing loss during infancy: Effects on later auditory brain stem electrophysiology,” J Speech, Lang. Hear. Res. 34, 1207–1215) demonstrated that the brainstem could be a plausible site by revealing that the amplitude of the BIC was eliminated in children with CHL histories. The BIC is computed by subtracting the sum of left and right ear monaural ABRs from binaural-evoked ABRs. The amplitude of the most prominent BIC peak, DN1, scales with interaural time differences and correlates with performance on binaural tasks. The latency of DN1 corresponds to the binaural nuclei of the auditory brainstem that initially extract the binaural cues to sound location, the lateral and medial superior olive. The study established that listening difficulties due to CHL emerge in the brainstem, a result with implications for how to diagnose and develop treatments for listening difficulties.