**2. Prevalence**

Presbycusis is a rather common disorder. According to the World Health Organization (WHO), more than 5% of global population (about 328 millions of adults) suffers from any degree of hearing loss, while among people older than 65 years of age, the prevalence of hearing loss exceeds 30% [10].

Its prevalence increases every year that may be due to the general trend of increased life duration—much more adults reach aged (from 60 to 74 years old according to the WHO classification) and senile (75 years old and more) periods. The world population is rapidly aging. At the period between 2000 and 2050, the proportion of the world's population over 60 years will double from about 11 to 22%. The absolute number of people aged 60 years and over is expected to increase from 605 million to 2 billion over the same period. The number of people aged 80 years or older will have almost quadrupled between 2000 and 2050 to 395 million [11]. Approximately one in three people in the United States between the age of 65 and 74 has hearing loss, and nearly half of those older than 75 have difficulties in hearing. Having trouble hearing can make it hard to understand and follow a doctor's advice, respond to warnings, and hear phones, doorbells, and smoke alarms. Hearing loss can also make it hard to enjoy talking with family and friends, leading to feelings of isolation.

#### **3. Etiology**

There are many causes of age-related hearing loss. Most commonly, it not only arises from changes in the inner ear as we age but can also result from changes in the middle ear, or from multiple changes that occur along the nerve pathways directed toward the brain from the inner ear. Associated medical conditions and some medications may also exert an influence. Many factors can contribute to hearing loss as you get older. It can be difficult to distinguish age-related hearing loss and hearing impairment caused by other reasons, for example, noiseinduced hearing loss. Noise-induced hearing loss is caused by long-term exposure to sounds that are either too loud or last too long. This kind of noise exposure can damage the sensory hair cells of the inner ear and is responsible for hearing loss. Once these hair cells are damaged, they do not grow back, and the ability to hear is diminished.

Conditions that are more common in older people, such as high blood pressure or diabetes, can contribute to hearing loss. Medications that are toxic to the sensory cells in our ears (e.g., some chemotherapy drugs) can also cause hearing loss. Aged and senile persons have a lot of biological and social risk factors of hearing disorder development. According to some authors [3], age-related hearing loss results from biological aging process of tissue elements in the auditory system and prolonged noise exposure. SNHL is considered to be a polyetiological process with partly unidentified factors of pathogenesis. There are more than 100 causes of SNHL: infections, intoxications, acoustic trauma, genetic factors, unfounded use of aminoglycoside antibiotics, irrational treatment of acute and chronic middle ear disorders, autoimmune diseases, and so on.

Different authors sometimes interpret this term differently. Some researchers meant (imply under this term) age-related hearing disorders caused by involutional changes only in the cochlea, and others meant that changes involve all parts of the auditory system [1, 2]. Presbycusis is considered to be one of the forms of progressive SNHL, which is associated with age-related involutional changes of different parts of the hearing system and is presented by symmetric pure tone audiogram with flat loss toward high-frequency range (less steep than 20 dB/oct) [3]. Numerous studies are dedicated to anatomical and functional risk factors of the presbycusis [4–9]. The significance of the presbycusis problem is determined by its social importance, lack of data about its etiology, and need for clinical practice to accurately determine an impaired area of auditory system and to identify the presbycusis genesis.

Presbycusis is a rather common disorder. According to the World Health Organization (WHO), more than 5% of global population (about 328 millions of adults) suffers from any degree of hearing loss, while among people older than 65 years of age, the prevalence of hear-

Its prevalence increases every year that may be due to the general trend of increased life duration—much more adults reach aged (from 60 to 74 years old according to the WHO classification) and senile (75 years old and more) periods. The world population is rapidly aging. At the period between 2000 and 2050, the proportion of the world's population over 60 years will double from about 11 to 22%. The absolute number of people aged 60 years and over is expected to increase from 605 million to 2 billion over the same period. The number of people aged 80 years or older will have almost quadrupled between 2000 and 2050 to 395 million [11]. Approximately one in three people in the United States between the age of 65 and 74 has hearing loss, and nearly half of those older than 75 have difficulties in hearing. Having trouble hearing can make it hard to understand and follow a doctor's advice, respond to warnings, and hear phones, doorbells, and smoke alarms. Hearing loss can also make it hard to enjoy

There are many causes of age-related hearing loss. Most commonly, it not only arises from changes in the inner ear as we age but can also result from changes in the middle ear, or from multiple changes that occur along the nerve pathways directed toward the brain from the inner ear. Associated medical conditions and some medications may also exert an influence. Many factors can contribute to hearing loss as you get older. It can be difficult to distinguish age-related hearing loss and hearing impairment caused by other reasons, for example, noiseinduced hearing loss. Noise-induced hearing loss is caused by long-term exposure to sounds that are either too loud or last too long. This kind of noise exposure can damage the sensory hair cells of the inner ear and is responsible for hearing loss. Once these hair cells are dam-

talking with family and friends, leading to feelings of isolation.

aged, they do not grow back, and the ability to hear is diminished.

**2. Prevalence**

64 Gerontology

**3. Etiology**

ing loss exceeds 30% [10].

Genetic determinacy of the presbycusis cannot be excluded, and diseases acquired throughout the lifetime, hemorheological changes, and other factors can trigger or exacerbate age-related hearing loss. It is difficult to define that whether or not presbycusis depends on genetic factors because other factors potentially contributing to a hearing loss development are closely associated with an aging process. Nevertheless, some epidemiological studies argue in favor of genetic influence on age-related hearing loss development, especially in the case of metabolic type of the presbycusis, according to Schuknecht [12], which is caused by the atrophy of the stria vascularis [13, 5]. Genetic factor in the presbycusis origin is acknowledged by many authors [3, 14, 15]. This fact is confirmed in our study as well. Hearing heredity is revealed to be presented more often in patients with presbycusis. Identification of genes, underlying this pathology, could be extremely helpful for many people in our aging society.

Numerous genes are responsible for functioning of the auditory system, and some of them can contribute to the presbycusis development and determine a degree and time of onset of age-related hearing loss. However, neither of them is known to be the gene responsible for the presbycusis [4, 5]. The gene of age-related hearing loss was identified in mice. This gene encodes cadherin 23 (Cdh23) and is supposed to predispose an early onset of age-related hearing loss in mice [16]. A mutation of a similar gene in human Cdh23 can incline a susceptibility to the presbycusis [17]. However, genes of monogenic deafness detected in mice are doubtfully to be the same in human.

The last gene that was considered to be a cause of the presbycusis development in human was revealed in wide genome study of age-related hearing loss, which was conducted in the House Ear Institute, Gonda Research Center for Cell and Molecular Biology, USA. Specialists from Los Angeles collaborated with Translational Genomics Research Institute and University of Antwerp (Belgium). Friedman et al. [18] studied 3434 twins aged between 53 and 67 years old—patients of eight medical centers from six European countries. After hearing assessment using routine methods, 846 pairs with one normal hearing and one hearing impaired brother or sister have been selected. Family genomes were marked by numerous genetic markers, and the comparative analysis was performed. Scientists looked for spots with different nucleotides in the same genes. And a number of such genes were revealed. After applying an excluding method, only one potential gene was left in result. It was the gene GRM7 (metabotropic glutamate receptor type 7), which takes a part in a glutamate metabolism—it encodes one of the receptors of this amino acid. Glutamate (or glutamic acid) is one of the most important excitatory neurotransmitters of the mammal's neural system. It is involved in the functioning of different brain areas and provides neurotransmission. Studies performed on mice and humans showed that gene GRM7 is highly active in the hair cells and the spiral ganglion cells of the inner ear. The glutamate is very toxic in high concentration. Its overexciting results in neuron disruption. The excess amount of the glutamate is suspected to cause a hearing loss in twins as the study authors considered. Genetic analysis showed that after getting "protein casts" with certain variations in a gene GRM7 improperly operating glutamate receptor was obtained. It can result in the amino acid storage in the synaptic fissure and damage of the outer and the inner hair cells in the cochlea [18].

clinical and audiological examination of women of different ages: 28 elderly women with presbycusis (the main group) and 28 elderly women with normal hearing (the control group). The mean age of menopause onset was less in patients of the main group than in the control one by 3.2 ± 1.0 years, which argues in favor of the earlier aging of a whole organism including the auditory system in patients with presbycusis. The comparison of biochemical and clinical blood profiles of the main and control groups did not reveal any significant differences. The essential role of hyperlipidemia in the hearing loss progression was revealed by analysis of correlation between the lipid profile and hearing thresholds in the patients of the main group:

Characteristics of Hearing in Elderly People http://dx.doi.org/10.5772/intechopen.75435 67

the worse the lipid profile, the worse the hearing thresholds have been revealed [27].

hearing than people of the same age with diminished intellectual activity [3].

**4. Diagnostics and clinical presentation of the presbycusis**

hearing loss pathogenesis [29].

**4.1. Asking about complaints and anamnesis**

60 minutes to avoid the fatigue of a patient and loss of his attention.

Some authors mention that variable professions are not statistically associated with presbycusis [19]. However, Lopotko et al. noted that intellectuals in aged and senile periods have better

In the middle of the last century, Schuknecht described four forms of the presbycusis: (1) sensory (caused by gradual degeneration of sensorineural elements of the inner ear); (2) neural (determined by the cell reduction in the spiral ganglion, auditory nerve fibers, and central auditory pathways); (3) metabolic (associated with atrophic changes in the stria vascularis); and (4) cochlear conductive or mechanical (associated with the process of the basal membrane thickening and loss of its elasticity). According to the author, all these forms manifest in increased tonal thresholds, and the neural one also manifests in the impaired speech intelligibility [12]. CAPD is shown to join the peripheral disorders with the aging process, so they also contribute to the presbycusis [28]. One of the keys of solving presbycusis problem is to define the proportion of peripheral and central disorders. Currently, potential role of disorders at all levels of the auditory system is taken into account, and it is realized as an integrated functional system and taken into consideration while understanding the age-related involutional

To diagnose an age-related hearing loss and to determine all risk factors of rapid hearing loss progression complete examination is necessary to begin with history taking (anamnesis), complex audiologic examination using instrumental methods in order to identify a level of a disorder, and finally, biochemical blood tests and general practitioner and neurologist consultations. All these examinations should be performed in the morning in kindly calm and comfortable conditions. The total duration of the audiological examination should not exceed

While collecting a medical history, the absence of any reasons of hearing loss except of the age is noted. These patients do not have any serious somatic illnesses, middle ear pathology, professional noisy environment, or other determined reasons of the impaired hearing. Genetic factors and hearing loss duration should be taken into account while analyzing an

Of the genetic point of view, presbycusis is the complex pathology. In the case of monogenic disease, a simple mutation is enough to cause a clinical onset/presentation. This type of disease is easy to determine. Meanwhile, in the case of complex genetic disorder, the interaction between genetic and environmental factors is obligatory, and the only factor is not enough for disease manifestation. In the case of genetic predisposition, a degree of hearing loss and a duration of hearing impairment depend on the summary of ototoxic factors, environmental noise during lifetime, as well as acquired diseases, changes of the blood quilts, and other factors contributing to hearing loss progression [19]. These studies are considered to define various factors that influence on the presbycusis development and to determine a degree of hearing disorder in aged and senile periods. They are still significant and must result in developing standards for prognosticating and preventing this pathology.

Thus, all abovementioned endo- and exogenous factors that are presented throughout the lifetime are considered to contribute to hearing disorder development in aged and senile periods. Nevertheless, hearing impairment does not occur in everyone and is affected by harmful factors.

The role of the atherosclerosis in the age-related hearing loss development has been studied since the middle of the last century. Does the severity of the atherosclerosis and the cochlear dysfunction correlate? Some authors confirm the presence of this correlation between these pathologies [20, 21]. A close interrelation between hearing loss and high serum cholesterol levels is shown in several studies, and the dependence of hearing function on some other atherogenic lipid levels in the blood is found. Inverse correlation of high significance between high-density lipoproteins (HDL) level of the peripheral blood and hearing acuity at the frequency of 4 kHz was revealed [22]. Morphological and functional damages of the cochlea and their correlations with hyperlipidemia, atherosclerosis, and endothelial dysfunction in mice are described in studies of Guo et al. [23].

Increased blood viscosity is known to influence a SNHL development. Hildesheimer et al. examined a group of 33 patients with SNHL with unknown cause; a high-blood viscosity was revealed in many of them, which was interpreted by the authors as a possible etiologic factor of SNHL [24]. Other authors also suggest that rheological properties of the blood and characteristics of the red blood cells can be considered to be a SNHL development risk factor in all patients [25].

In the majority of countries, women are registered to have longer lifespan than men that is explained by the biological distinguishing features of the female organism and differences of the atherosclerosis development process in people of different sex [26]. This mismatch has to be taken into account in the study of presbycusis problem. Efimova performed a complex clinical and audiological examination of women of different ages: 28 elderly women with presbycusis (the main group) and 28 elderly women with normal hearing (the control group). The mean age of menopause onset was less in patients of the main group than in the control one by 3.2 ± 1.0 years, which argues in favor of the earlier aging of a whole organism including the auditory system in patients with presbycusis. The comparison of biochemical and clinical blood profiles of the main and control groups did not reveal any significant differences. The essential role of hyperlipidemia in the hearing loss progression was revealed by analysis of correlation between the lipid profile and hearing thresholds in the patients of the main group: the worse the lipid profile, the worse the hearing thresholds have been revealed [27].

Some authors mention that variable professions are not statistically associated with presbycusis [19]. However, Lopotko et al. noted that intellectuals in aged and senile periods have better hearing than people of the same age with diminished intellectual activity [3].
