Note first that presbycusis is also spelled presbyacusis by some.
Presbycusis is the high frequency hearing loss that typically accompanies aging. Presbycusis has an extremely high prevalence. Self-reported hearing impairment ranges from 5.4% in 18-44 year old persons to 29.6% in those 65 and older (Schoenborn and Marano, 1988). The prevalence of hearing impairment on hearing testing is is high as 83% in people between the age of 57 and 89 (Mosicki et al, 1985). More detailed data can be found from the government survey result reported here (pdf file).
The progressive decline in hearing sensitivity generally begins in the third decade of life. The hearing loss is generally sensorineural and begins at the higher frequencies. In many cases hearing loss is accompanied by tinnitus. While hearing can be often improved by hearing aids, many hearing aid recipients prefer not to use them because electrical amplification cannot replace natural hearing..
While individuals with presbycusis are generally considered as a monolithic group, it is possible to split them up. Schuknecht (1993) divided presbycusis into four pathological subgroups: 1). sensory characterized by hair cell loss in the basal turn where high-frequency hearing is served 2). Neural, characterized by spiral ganglion cell loss and disproportionate loss of speech understanding, 3). Stria vascularis loss (vascular), and 4). Conductive (middle ear disease). However the pattern and severity of cochlear degeneration often do not correlate well with the level of hearing loss.
Christov et al (2018) recently reported that there was also no relationship between cell counts in the medical superior olive and presbycusis, suggesting that presbycusis is not likely to be a brainstem disorder. This is hardly suprising given that the hair cells are the weak link in hearing.
Urban populations appear to have more presbycusis, suggesting that environmental noise and/or ototoxin exposure contributes to presbycusis. It also seems likely that genetic factors play a role in determining susceptibility. For example, certain strains of mice show a rapid deterioration of hearing function that resemble human hearing loss (Henry and Chole, 1980; Li, 1994). In humans, a recent study suggested that heritability of medium and low frequencies was .38 and .31 (DeStefano et al, 2003).
A variety of hypotheses have been advanced to explain this deterioration. A decline in mitochondrial function is currently a popular hypothesis as the mitochondria are the powerplants of the cell and there is a well known increase in mitochondrial DNA mutations with age, associated with a decline in mitochondrial respiratory function (Liannaine et al, 1989). A strong correlation between mitochondrial DNA mutations and cell atrophy has been shown in muscle and perhaps this also applies to the ear. Mitochondrial mutations may cause cell damage because of inadaquete energy or production of free radicals. The latter are highly reactive chemicals that are often the product of incomplete oxidative processes. Free radicals are produced after nearly any type of cellular injury, and are also produced in the ear.
A second train of evidence relates to programmed cell death or apoptosis. In general there is a delicate balance in the body between cell death and risk of damaged cells surviving and consequent neoplasia (cancer). Cell death is associated with depletion of energy stores and therefore it would be expected that cells with mutated mitochondrial DNA would be more likely to undergo apoptosis than normal cells.
The sensorineural component of presbycusis can be treated with hearing aids, when it is not severe. Conductive type presbycusis can also be treated with hearing aids but also can sometimes be treated with surgery. Avoidance of excessive noise and ototoxin exposure is certainly wise in any individual with hearing loss. There is currently a trend towards recommending of antioxidant foods and medications over long periods in an attempt to slow the progression of presbycusis.