Age-related hearing loss is one of the most prevalent health conditions among the elderly. Hearing loss may lead to social isolation, depression, and cognitive decline in older adults. The mechanistic basis for the association between hearing loss and decreased cognitive function remains unknown as does the potential for improving cognition through hearing rehabilitation. To that end, we asked whether the restoration of sensory input through the use of hearing aids would improve cognitive and auditory neural function. We compared a group of first-time hearing aid users with a hearing-matched control group after a period of six months. The use of hearing aids enhanced working memory performance and increased cortical response amplitudes. Neurophysiologic changes correlated with working memory changes, suggesting a mechanism for decreased cognitive function with hearing loss. These results suggest a neural mechanism for the sensory-cognitive connection and underscore the importance of providing auditory rehabilitation for individuals with age-related hearing loss to improve cognitive and neural function. Our findings of improved cognitive function with hearing aid use may lead to increased adoption of hearing loss remedies.

Increased phase locking and amplitude and decreased latency in midbrain suggest that amplification may improve neural representation of the speech signal in new hearing aid users. The improvement with amplification was also found in cortex, and, in particular, decreased P1 latencies and lower N1 amplitudes may indicate greater neural efficiency. Further investigations will evaluate changes in subcortical and cortical responses during the first 6 months of hearing aid use.

Objectives The authors investigated aging effects on the envelope of the frequency following response to dynamic and static components of speech. Older adults frequently experience problems understanding speech, despite having clinically normal hearing. Improving audibility with hearing aids provides variable benefit, as amplification cannot restore the temporal precision degraded by aging. Previous studies have demonstrated age-related delays in subcortical timing specific to the dynamic, transition region of the stimulus. However, it is unknown whether this delay is mainly due to a failure to encode rapid changes in the formant transition because of central temporal processing deficits or as a result of cochlear damage that reduces audibility for the high-frequency components of the speech syllable. To investigate the nature of this delay, the authors compared subcortical responses in younger and older adults with normal hearing to the speech syllables /da/ and /a/, hypothesizing that the delays in peak timing observed in older adults are mainly caused by temporal processing deficits in the central auditory system. Design The frequency following response was recorded to the speech syllables /da/ and /a/ from 15 younger and 15 older adults with normal hearing, normal IQ, and no history of neurological disorders. Both speech syllables were presented binaurally with alternating polarities at 80 dB SPL at a rate of 4.3 Hz through electromagnetically shielded insert earphones. A vertical montage of four Ag–AgCl electrodes (Cz, active, forehead ground, and earlobe references) was used. Results The responses of older adults were significantly delayed with respect to younger adults for the transition and onset regions of the /da/ syllable and for the onset of the /a/ syllable. However, in contrast with the younger adults who had earlier latencies for /da/ than for /a/ (as was expected given the high-frequency energy in the /da/ stop consonant burst), latencies in older adults were not significantly different between the responses to /da/ and /a/. An unexpected finding was noted in the amplitude and phase dissimilarities between the two groups in the later part of the steady-state region, rather than in the transition region. This amplitude reduction may indicate prolonged neural recovery or response decay associated with a loss of auditory nerve fibers. Conclusions These results suggest that older adults’ peak timing delays may arise from decreased synchronization to the onset of the stimulus due to reduced audibility, though the possible role of impaired central auditory processing cannot be ruled out. Conversely, a deterioration in temporal processing mechanisms in the auditory nerve, brainstem, or midbrain may be a factor in the sudden loss of synchronization in the later part of the steady-state response in older adults.

The findings of the current study provide evidence for clinicians that the use of HAs may prevent further loss of auditory function resulting from sensory deprivation.