Presbycusis (also spelled presbyacusis, from Greek πρέσβυς presbys "old" + ἄκουσις akousis "hearing"), or age-related hearing loss, is the cumulative effect of aging on hearing. It is a progressive and irreversible bilateral symmetrical age-related sensorineural hearing loss resulting from degeneration of the cochlea or associated structures of the inner ear or auditory nerves. The hearing loss is most marked at higher frequencies. Hearing loss that accumulates with age but is caused by factors other than normal aging (nosocusis and sociocusis) is not presbycusis, although differentiating the individual effects of distinct causes of hearing loss can be difficult. The cause of presbycusis is a combination of genetics, cumulative environmental exposures and pathophysiological changes related to aging. At present there are no preventive measures known; treatment is by hearing aid or surgical implant. Presbycusis is the most common cause of hearing loss, affecting one out of three persons by age 65, and one out of two by age 75. Presbycusis is the second most common illness next to arthritis in aged people. Many vertebrates such as fish, birds and amphibians do not experience presbycusis in old age as they are able to regenerate their cochlear sensory cells, whereas mammals including humans have genetically lost this regenerative ability.
Presentation
Primary symptoms:
sounds or speech becoming dull, muffled or attenuated need for increased volume on television, radio, music and other audio sources difficulty using the telephone loss of directionality of sound difficulty understanding speech, especially women and children difficulty in speech discrimination against background noise (cocktail party effect) Secondary symptoms:
hyperacusis, heightened sensitivity to certain volumes and frequencies of sound, resulting from "recruitment" tinnitus, ringing, buzzing, hissing or other sounds in the ear when no external sound is present Usually occurs after age 50, but deterioration in hearing has been found to start very early, from about the age of 18 years. The ISO standard 7029 shows expected threshold changes due purely to age for carefully screened populations (i.e. excluding those with ear disease, noise exposure etc.), based on a meta-analysis of published data. Age affects high frequencies more than low, and men more than women. One early consequence is that even young adults may lose the ability to hear very high frequency tones above 15 or 16 kHz. Despite this, age-related hearing loss may only become noticeable later in life. The effects of age can be exacerbated by exposure to environmental noise, whether at work or in leisure time (shooting, music, etc.). This is noise-induced hearing loss (NIHL) and is distinct from presbycusis. A second exacerbating factor is exposure to ototoxic drugs and chemicals. Over time, the detection of high-pitched sounds becomes more difficult, and speech perception is affected, particularly of sibilants and fricatives. Patients typically express a decreased ability to understand speech. Once the loss has progressed to the 2–4 kHz range, there is increased difficulty understanding consonants. Both ears tend to be affected. The impact of presbycusis on communication depends on both the severity of the condition and the communication partner. Older adults with presbycusis often exhibit associated symptoms of social isolation, depression, anxiety, frailty and cognitive decline. The risk of having cognitive impairment increased 7 percent for every 10 dB of hearing loss at baseline. No effect of hearing aids was seen in the Lin Baltimore study.
Causes
Hearing is lost gradually as the hair cells in the Corti stiffen and die. Changes in the inner ear, middle ear, and complex changes along the nerve pathways from the ear to the brain can also affect hearing. Long-term exposure to noise and some medical conditions can also play a role. In addition, new research suggests that certain genes make some people more susceptible to hearing loss as they age. Other risk factors include preexisting noise-induced hearing loss and exposure to ototoxic medications.
Pathophysiology There are four pathological phenotypes of presbycusis:
Sensory: characterised by degeneration of the organ of Corti, the sensory organ for hearing. Located within the scala media, it contains inner and outer hair cells with stereocilia. The outer hair cells play a significant role in the amplification of sound. Age-related hair cell degeneration is characterized by loss of stereocilia, shrinkage of hair cell soma, and reduction in outer hair cell mechanical properties, suggesting that functional decline in mechanotransduction and cochlear amplification precedes hair cell loss and contributes to age-related hearing loss. At the molecular level, hair cell aging is associated with key molecular processes, including transcriptional regulation, DNA damage/repair, autophagy, and inflammatory response, as well as those related to hair cell unique morphology and function. A 2020 study suggests that the main cause of presbycusis is the loss of inner ear sensory cells and that the main cause of this loss is noise exposure. Neural: characterised by degeneration of cells of the spiral ganglion. Strial/metabolic: characterised by atrophy of stria vascularis in all turns of cochlea. Located in the lateral wall of the cochlea, the stria vascularis contains sodium-potassium-ATPase pumps that are responsible for producing the endolymph resting potential. As individuals age, a loss of capillaries leads to the endolymphatic potential becoming harder to maintain, which brings a decrease in cochlear potential. Cochlear conductive: due to stiffening of the basilar membrane thus affecting its movement. This type of pathology has not been verified as contributing to presbycusis. In addition there are two other types:
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