Loudness in the Normal-Hearing Ear of Single- Sided Deaf Patients

Abstract

Background: Single-sided deafness (SSD) has been shown to lead to a reduction in inhibition and an increase in excitatory responses in inferior colliculus and auditory cortex in the ipsilateral hemisphere when sounds are presented to the normal ear. These increased excitatory responses may lead to an increase in loudness. Therefore, we examined SSD patients hypothesizing an increase in loudness compared to normal-hearing (NH) controls. Additionally, we examined the effect of cochlear implantation (CI) in the deaf ear on loudness in the normal ear of the SSD patients.

Methods: We applied the Oldenburg Adaptive Categorical Loudness Scaling (ACALOS) procedure monaurally on 16 adult NH subjects (age range 22-55 years) and 18 SSD subjects (age range 19-73 years). The NH subjects were tested at each ear and the SSD subjects were tested twice: 1 to 4 months before and 4 to 8 months after CI. Accordingly, data were fitted yielding 3 outcome measures: slope of the lower segment of the loudness function (mlow), slope of the higher segment (mhigh), and the level at the intersection of the two slopes (Lcut). Additionally, the effect of age and PTA thresholds on loudness was measured.

Results: Firstly, the level at the intersection of the two slopes, Lcut, was lower for SSD subjects than for NH subjects by 2 to 8 dB (p = 0.060), most prominently at 0.5 and 1 kHz, which reflects an increase in loudness in the SSD group. Secondly, Lcut increased with older age and PTA thresholds. Thus, the older age and hearing loss resulted in a decrease of loudness, while SSD seemed to result in an increase of loudness. Lastly, CI of the deaf ear had no significant effect on loudness in the normal ear of the SSD patients.

Conclusion: Our data confirmed the hypothesis of an increase in loudness, although age and hearing loss counteracted this effect slightly. Nevertheless, we assume that the increase in loudness is caused by an increase in excitatory neural responses in the ipsilateral hemisphere, which in its turn is caused by a reduction in inhibition from the contralateral ear.