Presbycusis (also known as presbyacusis) is the progressive loss of hearing that occurs with age. Presbycusis is a form of sensorineural deafness (degeneration of the hair cells and nerve fibres in the inner ear), which makes sounds less clear and tones less audible.
Symptoms and causes
The symptoms of presbyacusis develop gradually. People with the condition often find it difficult to understand speech and cannot hear well when there is background noise. The severity and progression of the disorder vary considerably from person to person. Presbycusis may be exacerbated by exposure to high noise levels, diminished blood supply to the inner ear due to atherosclerosis (the buildup of fatty deposits on artery walls), and damage to the inner ear from drugs such as aminoglycoside drugs.
Diagnosis and treatment
Diagnosis is by physical examination using an otoscope, and by various hearing tests to determine the type and degree of hearing loss. Hearing-aids help most affected people.
Presbycusis in detail - technical
Synonyms for presbycusis include age-related hearing loss and presbyacusis
Presbycusis is the multifactorial progression to irreversible age-related sensorineural hearing loss. First labeled in 1885 by New York otologist St. John Roosa (1885), it was described as “a physiological . . . rather than a pathological, change in the ear . . . analogous to presbyopia, and . . . termed presbykousis,” derived from the Greek πρEσbυς (presbus), meaning “elder,” and akoύστe (acouste), “to hear.” The worsening auditory function of presbycusis is characterized by increasing hearing thresholds, particularly at high frequencies, as well as decreasing sound localization, speech comprehension, and central auditory processing that lead to difficulty hearing in noisy environments.
Presbycusis is likely caused by the accumulation of various auditory insults over years, including noise exposures (Agrawal et al. 2008), otologic diseases, age-related hair cell loss, strial dysfunction, or ototoxic exposure, with general progressive physiological deterioration. Many factors may contribute to its development or severity, including systemic insults like cardiovascular disease (Torre et al. 2005) or diabetes mellitus (Ren et al. 2009), genetic susceptibility and nutrition, with multifactorial processes overlapping the effects of aging.
Presbycusis – a general term used to describe hearing loss from a lifetime of insults to the auditory system.
Sensorineural hearing loss – hearing loss associated with disruption of both sensory (e.g., hair cells) and neural (i.e., spiral ganglion cells) elements of the cochlea.
Dementia – a class of disorders characterized by disruption of cognitive function beyond that expected from the normal aging process
Tinnitus – subjective sensation of sound in the absence of an external source
Speech perception – the cumulative process of hearing and cognitive processing leading to understanding of spoken language
Binaural interference – the process through which sounds arriving in one ear interfere with perception of those in the opposite ear
Central presbycusis – hearing disability beyond that expected from peripheral hearing loss, reflecting dysfunction in central pathways involved in speech perception
The global impact of presbycusis is steadily climbing as the world-wide population ages with increases in birth rate and longevity. The 2008 National Center for Health Statistics data (Agrawal et al. 2008) showed that US population has doubled over the past 50 years, with threefold increases in the number of adults over 65 years old, and five- and tenfold increases in those above 75 and 85 years old, respectively. The World Health Organization (WHO) estimates approximately 1.2 billion people over the age of 60 by 2025 (Parham et al. 2011), and population trends predict people 65 and older will comprise approximately 20% of the population in 20 years. Considering the prevalence of hearing loss in aging populations (77% in 60–69 years old (Agrawal et al. 2008)) compared to younger groups (under 10% in 20–29-year-olds (Agrawal et al. 2008)), the percentage of the population affected by hearing loss is increasing dramatically.
Another investigation estimates that among those 70 years or older, prevalence of hearing loss is 63% (Lin et al. 2011). The healthcare expenditures involved in the diagnosis and treatment of presbycusis are also rising, with common management options like hearing amplification through hearing aids beyond the financial reach of many patients. Only 20% of patients with the potential for improvement through amplification actually obtain hearing aids, and in the USA, the majority of Medicare patients do not have hearing aids as a covered benefit (Parham et al. 2011). Beyond the population-wide impact, hearing loss can significantly affect an individual’s social interactions and independence as it limits communication and functioning, worsening the risk of depression, anxiety, and cognitive decline (Heine and Browning 2002).
The diagnosis of presbycusis is based on patient history, physical examination, and a battery of audiologic testing. Definitive diagnosis is often delayed due to numerous challenges after the onset of symptoms. Presbycusis is by nature of its pathophysiology a progressive and sometimes insidious process, with affected individuals frequently less aware of their communication difficulties than the people around them. In addition, the inherent reduction in communication can result in compounding psychosocial effects including depression, anxiety, and isolation that further reduce the likelihood of patients seeking medical attention. As a result, clinicians should have a low threshold for suspecting hearing loss in older patients, particularly presenting with comorbidities like anxiety, depression, or apparent cognitive decline (Huang and Tang 2010).
The most common type of presbycusis affects highfrequency hearing first and as it progresses to the 2–4 kHz region of the cochlea, it impacts speech discrimination of voiceless consonants such as ch, k, p, s, t that help distinguish between different syllables and words. Other important high-frequency warning sounds (alarms, ringing tones, turn signals, etc.) also become more difficult to hear, which may compromise safety. As the hearing loss progresses, sound localization and identification are impacted as well. The isolation of hearing loss, along with its associated psychosocial implications, can delay presentation and diagnosis. Patients may present as a result of concerns from family members or acquaintances over communication difficulties, with poor self-perception of their hearing loss.
Patients presenting with hearing loss often disclose difficulties with tinnitus, specific communication issues like telephone use or conversations in loud environments, or family and friend reports of communication difficulties. Risk factors for presbycusis include noise exposure, hypertension, medication, tobacco use, and positive family history (Gates and Mills 2005), along with separate risks for noise-induced hearing loss like exposure to occupational or recreational noise. Differentiating a family history of hearing loss to broad categories of congenital, sudden, or progressive hearing losses can help distinguish the likelihood of related genetic risk factors.
Additionally, exposure to specific medications, including loop diuretics, salicylates, aminoglycosides, or platins, along with timing of their use in relation to hearing decline, may offer further potential etiologies. Physical examination is often normal, although possible curable causes of hearing loss – cerumen impaction, middle ear effusion – may be identified and addressed.
Hearing loss in older patients can be caused by dysfunction of any part of the ear, from the external auditory canal to the central auditory pathway. Outer and middle ear structures do undergo some age-related changes – e.g., collapse of the external auditory canal cartilage and stiffening of the tympanic membrane and ossicular chain (see “▶Middle Ear Physiology”). But as passive mechanical structures, these changes typically have minimal impact on their function. The cochlea, however, is a complex device with multiple interdependent passive and active mechanisms (see “▶Physiology of Cochlea”), and alterations in any component of the cochlea can result in dramatic changes in hearing thresholds. Physical changes in the basilar membrane, loss of hair cells, neural atrophy, and strial deterioration are several potential areas of pathology contributing to presbycusis.
Based on correlation between postmortem cochlear histopathology and pure-tone threshold audiogram findings by Schuknecht (1964), four main types of presbycusis were initially proposed: neural – associated with spiral ganglion loss; metabolic – associated with stria vascularis changes; sensory – associated primarily with hair cell loss; and conductive – without a clear pathologic correlate (Schuknecht and Gacek 1993).
Sensory presbycusis stems from outer hair cell loss, with lesions most frequently found in the first millimeters of the basal turn. Histologically, flattening and atrophy of the Organ of Corti is seen as hair cells and surrounding supportive cells collapse. An aging pigment, lipofuscin, may be seen in these cochlear lesions as well. The audiogram associated with sensory presbycusis is thought to show a sharply sloping high-frequency loss extending beyond the speech frequency range, and clinical evaluation reveals a slow, symmetric, and bilateral progression of hearing loss.
Neural presbycusis is associated with a loss of spiral ganglion cells, axons, or the nerves within the spiral osseous lamina, primarily in the basal turn of the cochlea, without structural changes in the Organ of Corti itself. The negative impact on cochlear nerve (CN VIII) transmission of the electrochemical signal from the cochlea into the auditory pathway is reflected in increased thresholds of compound action potentials (CAPs) and dysynchronous neural activity, which may be related to neural synapse abnormalities (Gates and Mills 2005). Classically, audiograms in neural presbycusis show a moderate downward slope into higher frequencies with a gradual worsening over time. A severe loss in speech discrimination is often described, out of proportion to the threshold loss, making amplification difficult due to poor comprehension.
Strial presbycusis, or metabolic presbycusis, occurs with stria vascularis deterioration or atrophy. It is slowly progressive and often genetic within families. The stria functions as the “battery” of the cochlea, maintaining endolymphatic potential. Audiograms classically associated with strial presbycusis show a flat loss with slow progression and good speech discrimination with no recruitment.
The Organ of Corti and the spiral ganglion cells are not affected structurally, but the loss of endolymphatic potential stunts their functionality. Significant improvement is possible with hearing aid amplification, since speech discrimination is not usually affected. Strial loss usually occurs in small, focal lesions in the extreme ends of the apex and lower basal turns of the cochlea, but can spread to involve larger segments or diffuse strial loss. Localized areas with only 20–30% loss may not result in much functional change, but greater than 50% loss leads to decreased endolymphatic potential and poor cochlear amplification with a variable loss of gain (20 dB in the cochlear apex up to 60 dB in the base).
Mechanical (or conductive) presbycusis is a category of age-related hearing impairment that was interpreted as arising from stiffening of the basilar membrane and atrophy of the spiral ligament. Spiral ligament atrophy is histologically identified most commonly in the apical turn and least in the basal turn. Occasionally, severe deterioration and cystic degeneration lead to full detachment of the Organ of Corti from the lateral cochlear wall, causing clear structural deformities. Audiograms in mechanical presbycusis have been described as an upward slope toward the high frequencies, with preserved speech discrimination.
Other proposed categories of presbycusis include vascular or noise-induced presbycusis, with threshold losses in vascular presbycusis correlated to hypertension, cardiac disease, stroke, and noise-induced losses related to the intensity, duration, and frequency of noise exposure. However, most cases of presbycusis do not separate into a specific type but have mixtures of these pathologies (mixed presbycusis) and about 25% of all cases of presbycusis show none of the above characteristics and were classified by Schuknecht as indeterminate presbycusis (Schuknecht and Gacek 1993).
Several recent studies looking specifically at these classic categories have failed to establish a correlation between type of pure-tone threshold audiogram and structural abnormalities in the cochlea, including a paper in 2003 (Nelson and Hinojosa 2003), that questioned the classic correlations between audiogram patterns and specific cochlear histopathology. For example, flat audiograms were associated with strial atrophy in Schucknecht’s scheme; however, Nelson and Hinojosa reported that this audiogram pattern was infrequently associated with strial atrophy, rather with outer hair cell loss alone or in combination with inner hair cell and spiral ganglion loss (Nelson and Hinojosa 2003). In contrast, the classic downwardsloping audiogram has been associated with the extent of degeneration of the stria vascularis, inner and outer hair cells, and spiral ganglion cells (Nelson and Hinojosa 2006).
Ultrastructural features, such as deformation of cuticular plate in surviving hair cells (Scholtz et al. 2001) or peripheral neurite loss pattern (Chen et al. 2006), may need to be taken into account to fully characterize cochlear changes in presbycusis. Although there is little agreement on cochlear pathology- audiogram correlation, the collective literature suggests that presbycusis can come about through disruption in any one or any combination of the key cochlear elements (inner and outer hair cells, spiral ganglion cells, and stria vascularis).
When elderly patients complain of hearing loss, they frequently report reasonable understanding in quiet environments and with slow speech but complain of significant difficulty in noisy environments, with rapid or heavily accented speech, or when few contextual cues are evident. These symptoms are interpreted as degeneration of central auditory pathways, known as central presbycusis (see Parham et al. 2011).
Central abnormalities often coincide with age-related defects in peripheral hearing organs, following a model of maladaptive neural plasticity in which degeneration of spiral ganglion afferents (Nelson and Hinojosa 2006) induce a slow secondary neural loss further down the auditory pathway. Welldescribed peripheral auditory declines in the cochlea have been shown in mouse models of presbycusis to have direct and indirect consequences on the loss of neurons in the central auditory nuclei and potential reorganization of tonotopic mapping in the auditory cortex (Hwang et al. 2007).
Despite the predominance of peripheral causes of presbycusis early in the disease, dysfunction of central auditory processing contributes significantly to the pathology of late presbycusis (Gates et al. 2010) and is a large component of presbycusis in people over 70 years of age (Gates et al. 2008). These central changes are thought to play a major role in the manifestations of presbycusis and have implications for the management of older patients with hearing loss, including reorganization of A1 frequency maps with elevated acoustic reflex thresholds, and discomfort with higher volume in monaural hearing aid users.
These changes are expected to extend to association cortices, thus affecting higher order cognitive functions by altering representation of sound in primary and association cortices (Hwang et al. 2007). A 2007 study isolated specific differences in activation of the auditory pathways through functional magnetic resonance imaging (fMRI) testing of speech listening in young and geriatric subjects (Hwang et al. 2007).
Elderly subjects showed decreased activation of the auditory cortex compared to younger listeners, with even greater differences during geriatric speech listening in white noise compared to quiet listening. Specific sites of decreased activation included the anterior and posterior regions of the bilateral superior temporal gyrus (STG) with particularly distinct differences within the posterior left STG. Corpus callosum degeneration and resulting decreased interhemispheric neural transfer has also been implicated in asymmetric interaural responses during dichotic listening, with right-ear dominance frequently resulting (Hwang et al. 2007).
Further support for a neuroanatomical basis for central presbycusis comes from a recent study correlating hearing in quiet and noise with cortical structures evaluated with MRI (Wong et al. 2010). In older adults, a decline in the relative volume and cortical thickness of the prefrontal cortex was associated with a declining ability to perceive speech in a naturalistic environment. These findings were interpreted as being consistent with the decline-compensation hypothesis, which states that a decline in sensory processing caused by cognitive aging can be accompanied by an increase in the recruitment of more general cognitive areas as a means of compensation (Wong et al. 2010).
Defective central auditory processing is often associated with and further compounded by overall cognitive decline and generalized executive processing dysfunction, with studies demonstrating a consistent correlation between central presbycusis and dementia (Gates et al. 2010). These declines are known to compound and complicate the manifestations and management of patients with presbycusis.
Gates suggests that a decline in executive functioning may be a common etiology in both neurodegenerative processes, and that decline in understanding speech-innoise may be an early manifestation of the processes leading to dementia. Furthermore, he advocates that geriatric patients with substantial central auditory processing dysfunction should be referred for neurologic and neuropsychiatric evaluation for more complete workup and/or treatment (Gates et al. 2010), as poor performance in tests of central auditory processing may be a precursor to dementia (Gates et al. 2011).
Comparisons of single-frequency tuning fork examinations can provide a very rudimentary isolation of affected frequencies, but finger rubs and whisper assessments are non-standardized and unreliable in determining hearing loss. In patients at higher risk for presbycusis or over 60 years of age, simple screening measures including asking directly whether the individual has a hearing problem, or more detailed ten-question hearing handicap inventory for the elderly (HHIE-S), may be used along with screening audiograms at select frequencies and intensities (e.g., 1 kHz, 2 kHz, and 3 kHz from 25 to 60 dB). Abnormalities on a screening questions or screening audiogram require a formal audiologic assessment with pure-tone audiogram, speech recognition thresholds, and speech discrimination (Gates and Mills 2005).
Central presbycusis is typically diagnosed by tests of auditory processing, while the traditional peripheral changes of presbycusis are demonstrated on pure-tone audiometry. Central auditory testing is often utilized in patients showing a functional hearing loss that is inconsistent with audiologic testing. Also indicative of central degenerative processes is the phenomenon of auditory rollover, which demonstrates a 20% or greater decrease in speech recognition at high signal intensities (Gates and Mills 2005). Defects of central temporal processing may be identified by tests of rapid speech perception and temporal gap detection.
One widely available and standardized central auditory test is the Synthetic Sentence Identification with either an Ipsilateral Competing Message (SSI-ICM) or a Contralateral Competing Message (SSI-CCM) (Holmes 2003). The SSI-ICM presents one of a series of ten nonsense sentences to the listener over a competing auditory message of an interesting narrative at 50 dB above the pure-tone average at 0 dB signal-to-noise ratio. The listener then selects the correct nonsense phrase from a written list, with 80% or better correct identification of 10–30 sentences indicating a normal response.
The SSI-ICM appears to be more sensitive to dementia than the contralateral form. The Dichotic Sentence Identification test (DSI) (Gates et al. 2010) uses six of the same sentences from the SSI-ICMwith one of two different sentences being presented to each ear simultaneously. The listener then identifies the two sentences from a written list, with scores above 80% indicating normal performance. Performance is generally better when the subject is asked to focus on one ear at a time.
The dichotic digits test (DDT) utilizes five single-digit pairs (excluding seven) with different numbers presented to each ear simultaneously, with correct identification of above 90% of presented numbers indicating a normal score.
Recent studies prompt speculation about the relations of central auditory testing, executive functioning, and dementia (Gates and Mills 2005). First, it is clear that in people with dementia, there is a notable loss of the ability to extract speech out of a background of competing speech and that loss is greatest for those persons with the poorest dementia status.
Second, because central auditory tests may be abnormal years before the dementia becomes clinically evident, it may be the case that the performance burden of central auditory tests upon diminishing executive functioning and cortical association structures is greater than the burden upon usual and customary tasks of daily living, such that one might theorize that abnormal central auditory tests in the geriatric patient are a sign of preclinical dementia. Third, the strong associations between executive function and central auditory function suggest a common mechanism.
Whether central auditory testing abnormalities are indicators of decline of executive function or whether a third factor is responsible for the association cannot be determined on the basis of available data. Nonetheless, the high prevalence of both central auditory dysfunction and mild cognitive deficits in the geriatric patient argues for continued research into the mechanism(s) involved. It appears prudent to include central auditory testing in the evaluation of older people with hearing problems and consider referral of those cases with substantial loss of auditory processing ability for neuropsychiatric evaluation. With the possibility of treatment to forestall the progression of dementia on the horizon, early identification assumes great importance, and these data suggest that auditory processing deficits may be a risk factor for the subsequent onset of clinical dementia.
Other causes of hearing loss include abnormalities of the middle ear (effusion), acute otitis media, chronic suppurative otitis media, other inflammatory diseases, granulomatous diseases, cholesteatoma, benign or malignant tumors, tympanosclerosis, otosclerosis, sudden sensorineural hearing loss, syndromic and genetic sensorineural hearing loss, autoimmune disorders, ototoxicity, perilymphatic fistula, temporal bone fracture, or pathology of the central auditory pathway (cerebellospinal angle tumors, petrous apex tumors).
Presbycusis is not reversible or curable but the hearing loss and associated communication difficulties can be improved with a spectrum of available interventions. Treatment options vary depending on the severity and type of hearing loss. Early interventions include communication adaptations that improve both the focus of the listener and clarity of the speaker, optimize environmental factors to decrease competing sounds, or provide speech (lip) reading or auditory training to augment listening.
Amplification of available sound is one of the most commonly utilized treatments of presbycusis, ranging from hearing-assistive devices to hearing aids, bone-anchored hearing aids, and cochlear implants. Hearing-assistive devices can provide amplification directly from the source to improve the signal-to-noise ratio (FM system) or signal the user through visual or auditory alerts, and can be particularly useful in environments with poor acoustics or large areas with additional background noise.
Amplification with hearing aids is the workhorse of presbycusis treatment, often pursued after average hearing thresholds on audiogram testing surpass 40 dB. A broad range of models are available that use analog or digital systems to collect, process, and amplify environmental sounds. Behind-the-ear, in-canal, completely-in-canal, and vented/open-fit/skeleton models are available, with varying benefits to individual users depending on frequencies of hearing loss, manual dexterity, device fit, and other factors.Programmable modes, directional microphones, noise suppression, and different model types are available that can augment the utility of the device as well as affecting the cost of the device.
Generally, analog hearing aids are less expensive, but lack the flexibility of modifying programs found in digital hearing aids that can reduce acoustic feedback or background noise, or augment specific frequency ranges, among other features. With this large variety of choices and multiple patient factors influencing the potential benefits of hearing aids, audiologists are critical to the process of hearing aid selection in order to tailor a device to the needs of the individual patient. But despite significant recent advances in hearing aid technology, even the highest fidelity amplification does not restore hearing input to preloss “normal,” and augmentation of hearing aid use with communication adaptations and auditory rehabilitation have been shown to increase quality of life and functional communication outcomes (Chen et al. 2006).
In addition, the impact of central presbycusis is an important factor in determining the utility of amplification. Hearing aids increase the volume of auditory input, but do not address cognitive central deficits, and may worsen auditory processing (Gates et al. 2010). The question of whether to fit a geriatric person with one versus two hearing aids is controversial, since binaural amplification provides improved sound localization, tinnitus suppression and prevents auditory deprivation (Holmes 2003). Furthermore, monaural amplification may create or exacerbate interaural asymmetry due to auditory deprivation where a unilateral reduction of acoustic input to the auditory pathways results in maladaptive neural plasticity (Holmes 2003).
Nevertheless, in patients with superimposed central auditory processing disorders, binaural amplification exposes or introduces more amplification challenges. In these instances, the auditory information presented to each ear is processed differently resulting in a limitation of binaural amplification, i.e., binaural interference. In these cases of binaural interference in which the auditory input from each ear is processed differently, binaural amplification might further compound speech intelligibility and worsen communication outcomes (Martin and Jerger 2005).
Walden &Walden demonstrated these potential limitations of binaural amplification in 2005 (Walden and Walden 2005) comparing bilateral amplification to unilateral amplification using tests of speech recognition in background noise. Eighty two percent of listeners demonstrated better speech recognition with unilateral amplification and generally better aided speech recognition in the right ear than in the left ear.
The implications of these findings are clinically significant because it suggests that speech recognition in background noise – one of the main complaints in central presbycusis – may be better addressed with unilateral amplification instead of bilateral amplification.
For elderly patients who express significant limitation of their ability to understand speech in background noise, the simple suggestion of removing one hearing aid in noisy environments may minimize any underlying binaural interference and improve communication. Aural rehabilitation to improve central processing has also been shown to improve outcomes in central presbycusis as well, utilizing the same flexibility of neural plasticity to reverse pathologic changes in the pathway and improve auditory functioning.
Practically, use of hearing aids for presbycusis can be restricted due to decreased access to audiologic services, technologic or financial limitations, or delay of presentation. Once a patient is fitted with an appropriate hearing aid, 25–40% of users will stop using the device or use it rarely (Walden and Walden 2005) due to concern of perceived social stigma of visible hearing aids, reasons of discomfort or device disrepair, or frustration over sound results.
Recognition of these issues by the clinician and appropriate interventions are important to maximize the utility of hearing aids and improve hearing and communication in the face of mild to moderate presbycusis. Appropriate use of hearing aids has been shown to improve quality of life and decrease depression (Huang and Tang 2010), while the addition of aural rehabilitation promoting faster adaptation to hearing aid neural input will even further improve functional results.
In cases of severe or profound presbycusis, standard hearing aid amplification no longer improves functional speech recognition and cochlear implants may be indicated for these individuals with bilateral severe loss. Cochlear implants do not amplify sound like hearing aids, instead translating environmental sound into electrical stimulation delivered directly to the auditory nerve. These have been shown to be effective in older patients (Sprinzl and Riechelmann 2010) despite previous concerns that higher surgical risk or decreased central processing would negate the potential benefits from cochlear implantation.
While central processing deficits generally increase with age, success after implantation appears to be related directly to the duration of deafness (Sprinzl and Riechelmann 2010). As in patients of all ages, screening patients for cochlear implants is important and involves preimplantation evaluation including radiologic evidence of cochlea and cochlear nerve, medical clearance for surgery, adequate support, and appropriate expectation of outcomes.
Agrawal Y, Platz EA, Niparko JK (2008) Prevalence of hearing loss and differences by demographic characteristics among US adults: data from the national health and nutrition examination survey, 1999–2004. Arch Intern Med 168:1522–1530
Chen MA, Webster P, Yang E, Linthicum FH Jr (2006) Presbycusic neuritic degeneration within the osseous spiral lamina. Otol Neurotol 27:316–322
Gates GA, Mills JH (2005) Presbycusis. Lancet 366:1111–1120
Gates GA, Feeney MP, Mills D (2008) Cross-sectional age-changes of hearing in the elderly. Ear Hear 29:865–874
Gates GA, Gibbons LE, McCusrry SM et al (2010) Executive dysfunction and presbycusis in older persons with and without memory loss and dementia. Cogn Behav Neurol 23:218–223
Gates GA, Anderson ML, McCurry SM, Feeney MP, Larson EM (2011) Central auditory dysfunction as a harbinger of Alzheimer dementia. Arch Otolaryngol Head Neck Surg 137:390–395
Heine C, Browning CJ (2002) Communication and psychosocial consequences of sensory loss in older adults: overview and rehabilitation directions. Disabil Rehabil 24:763–773
Holmes AE (2003) Bilateral amplification for the elderly: are two aids better than one? Int J Audiol 42(Suppl 2):2S63–2S67
Huang Q, Tang J (2010) Age-related hearing loss or presbycusis. Eur Arch Otorhinolaryngol 267:1179–1191
Hwang JH, Li CW, Wu CW, Chen JH, Liu TC (2007) Aging effects on the activation of the auditory cortex during binaural speech listening in white noise: an fMRI study. Audiol Neurootol 12:285–294
Lin FR, Thorpe R, Gordon-Salant S, Ferucci L (2011) Hearing loss prevalence and risk factors among older adults in the United States. J Gerontol A Biol Sci Med Sci 66A:582–590
Martin JS, Jerger JF (2005) Some effects of aging on central auditory processing. J Rehabil Res Dev 42(4 Suppl 2):25–44
Nelson EG, Hinojosa R (2003) Presbycusis: a human temporal bone study of individuals with flat audiometric patterns of hearing loss using a new method to quantify stria vascularis volume. Laryngoscope 113:1672–1686
Nelson EG, Hinojosa R (2006) Presbycusis: a human temporal bone study of individuals with downward sloping audiometric patterns of hearing loss and review of the literature. Laryngoscope 116(9 Pt 3 Suppl 112):1–12
Parham K, McKinnon BJ, Eibling D, Gates GA (2011) Challenges and opportunities in presbycusis. Otolaryngol Head Neck Surg 144(4):491–495
Ren J, Zhao P, Chen L, Xu A et al (2009) Hearing loss in middleaged subjects with type 2 diabetes mellitus. Arch Med Res 40:18–23
Scholtz AW, Kammen-Jolly K, Felder E et al (2001) Selective aspects of human pathology in high-tone hearing loss of the aging inner ear. Hear Res 157:77–86
Schuknecht HF (1964) Further observations on the pathology of presbycusis. Arch Otolaryngol 80:369–382
Schuknecht HF, Gacek MR (1993) Cochlear pathology in presbycusis. Ann Otol Rhinol Laryngol 102:1–16
Sprinzl GM, Riechelmann H (2010) Current trends in treating hearing loss in elderly people: a review of the technology and treatment options – a mini-review. Gerontology 56:351–358
St John Roosa DB (1885) Presbykousis. Trans Am Otol Soc 3:449–460
Torre P 3rd, Cruickshanks KJ, Klein BE et al (2005) The association between cardiovascular disease and cochlear function in older adults. J Speech Lang Hear Res 48:473–481
Walden TC, Walden BE (2005) Unilateral versus bilateral amplification for adults with impaired hearing. J Am Acad Audiol 16(8):574–584
Wong PC, Ettlinger M, Sheppard JP, Gunasekera GM, Dhar S (2010) Neuroanatomical characteristics and speech perception in noise in older adults. Ear Hear 31(4):471–479.