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The Auditory Brain and Age-Related Hearing Impairment
The increasingly older human population suffers from many age-related disorders. There is currently a surge in publications on aspects of aging on hearing loss, on the benefits of hearing aids and cochlear implants in the elderly, and on the strong correlation between hearing loss, cognitive decline, and early onset of dementia. A separate large body of literature on the human brain connectome elucidates the brain network changes associated with aging. More and more data appear on the detrimental effects of hearing loss on the auditory and more general prefrontal cortex. These largely concern structural brain changes, and likely are predictive of functional brain changes affecting cognitive functions such as memory, attention, and executive functions.
Given the changing demographics, treatment of age-related hearing impairment need not just be bottom-up (i.e., by amplification and/or cochlear implantation), but also top-down by addressing the impact of the changing brain on communication. The role of age-related capacity for audiovisual integration and its role in assisting treatment have only recently been investigated, and need more attention. This book aims to provide this. It is divided into four sections: Manifestations of age-related hearing impairment; Causes for Degradation of Sound Processing; Compensatory Changes in the Aging Brain; and Rehabilitation and Intervention.
These topics are covered over ten chapters, major aspects thereof are:
Age-related hearing impairment (ARHI) is, by number of people affected, the dominant age-related disorder but this appears largely undervalued. ARHI combines the effects of hearing loss (in the ear) and hearing problems (in the brain). Hearing problems may occur even in the absence of audiometric hearing loss (Chapter 1). In hearing-impaired elderly patients, the age-related decline of peripheral and central auditory processing interacts with the diminished cognitive functions and leads to reduced auditory perception of speech. An important aspect is that sound, especially speech, besides the central auditory system also activates neurons in the prefrontal cortex and other non-classical auditory areas. Changes in these areas often correlate with declining speech discrimination. Thus, the auditory brain extends well beyond the classical auditory areas in the cortical temporal lobe.
Age-related hearing loss—presbycusis—comes in various forms as reflected in the different shape of the audiogram. We distinguish purely sensory, typically high-frequency hearing loss, and purely metabolic forms, related to dysfunction of the inner energy supply, that are reflected in flat hearing losses. Mixed sensory-metabolic forms do occur as well and are dominant (Chapter 2). However, a sizeable proportion of elderly have clinically normal audiograms. Hearing loss, when it is present, results in degraded speech representation in the auditory system. Understanding degraded speech requires extra cognitive efforts such as increased attention. Because attention span is limited, increased attentional load makes it harder to integrate degraded speech perception into the communication process. The lack of understanding speech may lead to reduce or abolish interacting with other people, which could result in social withdrawal and this in turn might advance the onset of mild cognitive impairment.
Good speech perception (Chapter 3) depends first of all on adequately processing the speech sound. Hearing loss, especially in the high frequencies, reduces the distinction of the consonants, whereas the vowels are not or less affected. Therefor only part of the speech is understood and confusion abounds. This type of problem is often incorrectly attributed to mumbled speech or bad articulation of the speaker. However, decreased speech-in-background noise understanding by hearing-impaired persons cannot be fully explained by the amount of hearing loss, suggesting it is due to less effective involvement of the central nervous system. Underlying this are changes of gray matter (comprising nerve cells) in the brain that among others shows up as age-related local volume reduction (read extensive loss of nerve cells) in primary auditory cortex.
Auditory processing by elderly hearing-impaired listeners is more related to individual differences in cognitive function rather than auditory function. Working memory span is the most important variable accounting for speech recognition performance. Consistent with a framework, in which the additional cognitive demands caused by a degraded acoustic signal uses resources, that would otherwise be available for memory encoding for both young and older adults, this affects speech understanding and language comprehension (Chapter 4).
The elderly brain is slower (Chapter 5). This lead to a reduction in processing speed and leads to impaired cognitive functioning. Two mechanisms involved are the ‘limited-time mechanism’ and the ‘simultaneity mechanism’. Cognitive performance is degraded when processing is slow because relevant operations cannot be successfully executed (limited time) and because the products of early processing may no longer be available when later processing is complete (lack of simultaneity). Older adults’ receptive speech difficulties may also emerge as a result of deficient and distorted auditory encoding at pre-attentive, subcortical stages of speech processing.
Age-related hearing loss has both a genetic and an environmental origin (Chapter 6). The genetic components that predispose for presbycusis may be similar to those that increase susceptibility to noise-induced hearing loss. Mitochondrial DNA common deletion levels in human inner ear tissue are related to the severity of hearing loss in individuals with presbycusis. In addition, reactive-oxygen species formation and apoptosis are key events in the pathology of presbycusis.
The most important environmental aspects that affect age-related hearing loss are noise exposure, use of ototoxic drugs, and smoking (Chapter 6). Lifelong exposure to high-level sounds may cause hearing loss. However, the role of environmental or occupational noise exposure on presbycusis is not clear. Epidemiological studies have found little evidence that prior occupational noise exposure plays an important role in the onset or progression of hearing impairment in older adults. Thus, even if occupational noise exposure is an important source of hearing damage in industrial workers, it is still possible that the effects have been overestimated, as few studies considered other factors. Long-term exposure to ‘safe’ environmental sound still may lead to central auditory processing deficits.
Animal studies (Chapter 7) have presented considerable support for the major involvement of microvasculature in age-related degeneration of the inner ear. Studies in several mouse strains have shown that the effects of noise-induced hearing loss and age-related hearing loss are non-additive—that is, the resulting hearing loss in the noise-exposed ear is greater than expected on the basis of combining the hearing thresholds in pure noise-induced hearing loss and pure age-related hearing loss groups. Noise exposure early in life of certain mouse strains has been shown to trigger late-onset progressive neuronal loss, the hallmark of age-related hearing impairment. Old rats show a central increase in synaptic gain, resulting from a steady down-regulation of inhibitory and up-regulation of excitatory transmitter efficacy in the central nervous system with age. Findings suggest that the resulting increased activation is potentially a compensatory response to loss of input to the brain from the damaged inner ear. Loss of the protective aspects of efferent feedback from the central auditory system to the inner ear accelerates the age-related amplitude reduction in cochlear neural responses and increased the loss of synapses between hair cells and the terminals of auditory nerve fibers.
Localizing the age-related hearing impairment problem areas in the human brain is based on neural imaging using both magnetic resonance imaging-based and electrophysiology-based approaches. Correlations between nerve tract degradation and poorer cognitive performance suggest that age-associated disruption of large-scale brain systems is an important contributor to cognitive decline (Chapter 8). Consistent alterations in three major functional networks, the default-mode network, the salience network, and the sensorimotor network, correspond strongly with the decline in cognitive functions. In contrast, primary auditory information processing in normal healthy aging is maintained. The connectivity within and between these networks depends on both hearing loss and aging. This could also include a compensation mechanism evolving with aging to support higher-level cognitive functioning.
Age-related decline in neural synchrony is reflected in the reduced amplitude of brain rhythms. In the human auditory system, these changes have been inferred from recordings of auditory evoked potentials in the brainstem and cortex (Chapter 9). Distinctive auditory evoked potential components, serve as measures of auditory event detection, auditory sensory memory processing, and attention switching. Aging typically causes a larger effect on late cognitive processes than on the perceptual and pre-attentive ones. There is, however, an apparent discrepancy between behavioral cognitive tests such as reaction times and evoked potential outcomes. This lack of a relationship suggests that these two measures reflect at least partially different sets of cognitive processes.
Hearing aids and cochlear implants are the most commonly used interventions to improve or restore hearing. These rehabilitative interventions could directly improve perceptual processing of speech and thereby free resources for other cognitive functions. However, do they work in the elderly? The added burden of cognitive decline in older persons also needs considerable attention in outcome measures of hearing aid use and benefit (Chapter 10). Hearing aid use is associated with better cognition, independently of social isolation and depression. The important role that training and therapy play in promoting compensatory brain reorganization as older adults acclimatize to new technologies is emphasized.
Cochlear implants are a last resort when the hearing loss is so severe that hearing aids cannot provide sufficient amplification. Cochlear implants provide frequency-specific information of sound via electrical activation of restricted regions of the cochlea. There is increasing evidence that cochlear implantation is a successful treatment for improving speech recognition and assist deafened elderly patients in everyday life.
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