Speech Perception and Hearing Aids

This paper summarizes twenty studies, published since 1989, that have measured experimentally the relationship between speech recognition in noise and some aspect of cognition, using statistical techniques such as correlation or factor analysis. The results demonstrate that there is a link, but it is secondary to the predictive effects of hearing loss, and it is somewhat mixed across study. No one cognitive test always gave a significant result, but measures of working memory (especially reading span) were mostly effective, whereas measures of general ability, such as IQ, were mostly ineffective. Some of the studies included aided listening, and two reported the benefits from aided listening: again mixed results were found, and in some circumstances cognition was a useful predictor of hearing-aid benefit.

Speech recognition was measured as a function of spectral resolution (number of spectral channels) and speech-to-noise ratio in normal-hearing (NH) and cochlear-implant (CI) listeners. Vowel, consonant, word, and sentence recognition were measured in five normal-hearing listeners, ten listeners with the Nucleus-22 cochlear implant, and nine listeners with the Advanced Bionics Clarion cochlear implant. Recognition was measured as a function of the number of spectral channels (noise bands or electrodes) at signal-to-noise ratios of + 15, + 10, +5, 0 dB, and in quiet. Performance with three different speech processing strategies (SPEAK, CIS, and SAS) was similar across all conditions, and improved as the number of electrodes increased (up to seven or eight) for all conditions. For all noise levels, vowel and consonant recognition with the SPEAK speech processor did not improve with more than seven electrodes, while for normal-hearing listeners, performance continued to increase up to at least 20 channels. Speech recognition on more difficult speech materials (word and sentence recognition) showed a marginally significant increase in Nucleus-22 listeners from seven to ten electrodes. The average implant score on all processing strategies was poorer than scores of NH listeners with similar processing. However, the best CI scores were similar to the normal-hearing scores for that condition (up to seven channels). CI listeners with the highest performance level increased in performance as the number of electrodes increased up to seven, while CI listeners with low levels of speech recognition did not increase in performance as the number of electrodes was increased beyond four. These results quantify the effect of number of spectral channels on speech recognition in noise and demonstrate that most CI subjects are not able to fully utilize the spectral information provided by the number of electrodes used in their implant.

Age-related and noise-induced hearing losses in humans are multifactorial, with contributions from, and potential interactions among, numerous variables that can shape final outcome. A recent retrospective clinical study suggests an age-noise interaction that exacerbates age-related hearing loss in previously noise-damaged ears (Gates et al., 2000). Here, we address the issue in an animal model by comparing noise-induced and age-related hearing loss (NIHL; AHL) in groups of CBA/CaJ mice exposed identically (8-16 kHz noise band at 100 dB sound pressure level for 2 h) but at different ages (4-124 weeks) and held with unexposed cohorts for different postexposure times (2-96 weeks). When evaluated 2 weeks after exposure, maximum threshold shifts in young-exposed animals (4-8 weeks) were 40-50 dB; older-exposed animals (> or =16 weeks) showed essentially no shift at the same postexposure time. However, when held for long postexposure times, animals with previous exposure demonstrated AHL and histopathology fundamentally unlike unexposed, aging animals or old-exposed animals held for 2 weeks only. Specifically, they showed substantial, ongoing deterioration of cochlear neural responses, without additional change in preneural responses, and corresponding histologic evidence of primary neural degeneration throughout the cochlea. This was true particularly for young-exposed animals; however, delayed neuropathy was observed in all noise-exposed animals held 96 weeks after exposure, even those that showed no NIHL 2 weeks after exposure. Data suggest that pathologic but sublethal changes initiated by early noise exposure render the inner ears significantly more vulnerable to aging.