Presbycusis

Sociocusis is the condition of those who have hearing loss attributed to continuous noise exposures, unrelated to their job or occupation. This exposure to these stimuli is frequent, and are often considered common "background noises" that affect the hearing abilities of individuals. Examples of sociocusis-related stimuli are the continuous noises from traffic, home appliances, music, television, and radio. The accumulated exposure to these noises over many years can lead to a condition similar to pure presbycusis.

Nosocusis factors are those that can cause hearing loss, which are not noise-based and separate from pure presbycusis. They may include:[9]

• Ototoxic drugs: Ingestion of ototoxic drugs like aspirin may hasten the process of presbycusis.
• vascular degeneration
  • Atherosclerosis: May diminish vascularity of the cochlea, thereby reducing its oxygen supply.
    • Dietary habits: Increased intake of saturated fat may accelerate atherosclerotic changes in old age.
    • Smoking: Is postulated to accentuate atherosclerotic changes in blood vessels aggravating presbycusis.
  • Diabetes: May cause vasculitis and endothelial proliferation in the blood vessels of the cochlea, thereby reducing its blood supply.
  • Hypertension: causes potent vascular changes, like reduction in blood supply to the cochlea, thereby aggravating presbycusis.

However, a recent study found that diabetes, atherosclerosis and hypertension had no correlation to presbycusis, suggesting that these are nosocusis (acquired hearing loss) factors, not intrinsic factors.[10]

An examination of the external ear canal and tympanic membrane performed by a medical doctor, otolaryngologist, or audiologist using an otoscope, a visual instrument inserted into the ear. This also allows some inspection of the middle ear through the translucent tympanic membrane.

A test administered by a medical doctor, otolaryngologist or audiologist of the tympanic membrane and middle ear function using a tympanometer, an air-pressure/sound wave instrument inserted into the ear canal. The result is a tympanogram showing ear canal volume, middle ear pressure and eardrum compliance. Normal middle ear function (Type A tympanogram) with a hearing loss may suggest presbycusis. Type B and Type C tympanograms indicate an abnormality inside the ear and therefore may have an additional effect on the hearing.

This may include a blood or other sera test for inflammatory markers such as those for autoinflammatory diseases.

A hearing test administered by a medical doctor, otolaryngologist (ENT) or audiologist including pure tone audiometry and speech recognition may be used to determine the extent and nature of hearing loss, and distinguish presbycusis from other kinds of hearing loss. Otoacoustic emissions and evoked response testing may be used to test for audio neuropathy. The diagnosis of a sensorineural pattern hearing loss is made through audiometry, which shows a significant hearing loss without the "air-bone gap" that is characteristic of conductive hearing disturbances. In other words, air conduction is equal to bone conduction. Persons with cochlear deficits fail otoacoustic emissions testing, while persons with 8th cranial nerve (vestibulocochlear nerve) deficits fail auditory brainstem response testing.

As part of differential diagnosis, an MRI scan may be done to check for vascular anomalies, tumors, and structural problems like enlarged mastoids. MRI and other types of scan cannot directly detect or measure age-related hearing loss.

In cases of severe or profound hearing loss, a surgical cochlear implant is possible. This is an electronic device that replaces the cochlea of the inner ear. Electrodes are typically inserted through the round window of the cochlea, into the fluid-filled scala tympani. They stimulate the peripheral axons of the primary auditory neurons, which then send information to the brain via the auditory nerve. The cochlea is tonotopically mapped in a spiral fashion, with lower frequencies localizing at the apex of the cochlea, and high frequencies at the base of the cochlea, near the oval and round windows. With age, comes a loss in distinction of frequencies, especially higher ones. The electrodes of the implant are designed to stimulate the array of nerve fibers that previously responded to different frequencies accurately. It is important to note that due to spatial constraints, the cochlear implant may not be inserted all the way into the cochlear apex. It provides a different kind of sound spectrum than natural hearing, but may enable the recipient to recognize speech and environmental sounds.

These are surgically implanted hearing aids inserted onto the middle ear. These aids work by directly vibrating the ossicles, and are cosmetically favorable due to their hidden nature.

• Hearing aids help improve hearing of many elderly. Hearing aids can now be tuned to specific frequency ranges of hearing loss.
• Aural rehabilitation for the affected person and their communication partners may reduce the impact on communication. Techniques such as squarely facing the affected person, enunciating, ensuring adequate light, minimizing noise in the environment, and using contextual cues are used to improve comprehension.[6]

Pharmacological treatment options are limited, and remain clinically unproven. Among these are the water-soluble coenzyme Q10 formulation, the prescription drug Tanakan, and combination antioxidant therapy.

• In a study performed in 2010, it was found that the water-soluble formulation of coenzyme Q10 (CoQ10) caused a significant improvement in liminar tonal audiometry of the air and bone thresholds at 1000 Hz, 2000 Hz, 4000 Hz, and 8000 Hz.[11]
• Antioxidant therapy – age-related hearing loss was reduced in animal models with a combination agent comprising six antioxidant agents that target four sites within the oxidative pathway: L-cysteine-glutathione mixed disulfide, ribose-cysteine, NW-nitro-L-arginine methyl ester, vitamin B12, folate, and ascorbic acid.[12] It is thought that these supplements attenuate the decline of cochlear structure due to prolonged oxidative stress. However, more recent studies have had conflicting results. In 2012, a study was done with CBA/J female mice. They were placed on an antioxidant-rich diet for 24 months consisting of vitamins A, C, E, L-carnitine, and α-lipoic acid. While this increased the inner ear's antioxidant capacity, the actual hearing loss was unaffected. Therefore, in this study, antioxidants were shown not to improve presbycusis mechanisms.[13]
• The effects of the pharmaceutical drug Tanakan were observed when treating tympanophonia in elderly women.[14] Tanakan was found to decrease the intensity of tympanitis and improve speech and hearing in aged patients, giving rise to the idea of recommending treatment with it to elderly patients with presbycusis or normal tonal hearing.[14]
• AM-111, an otoprotective peptide, was shown in a chinchilla study to rescue and protect against hearing loss following impulse noise trauma. AM-111 acts as a cell-permeable inhibitor of JNK-mediated apoptosis. IP injections or local injections into membrane of the round window were given, and permanent threshold shifts (PTS) were measured three weeks after impulse noise exposure. AM-111 animals had significantly lower PTS, implicating AM-111 as a possible protective agent against JNK-mediated cochlear cell death and against permanent hearing deficits after noise trauma.[15]
• The anti-inflammatory, anti-oxidant substance Ebselen was observed to reduce hearing loss in a study done in 2007.[16] It has been previously shown that noise trauma correlates with decreases in glutathione peroxidase (GPx) activity, which has been linked to loss of the outer hair cells. GPx1, an isoform of GPx, is predominantly expressed in stria vascularis, cochlea, spiral ligament, organ of Corti, and spiral ganglion cells. The stria vascularis displayed significant decreases in GPx1 immunoreactivity and increased swelling following noise exposure in rats. There was also significant outer hair cell loss in the cochlea within five hours of noise exposure. Administration of Ebselen before and after the noise stimulus reduced stria vascularis swelling as well as cochlear outer hair cell loss. This implicates Ebselen as a supplement for GPx1 in the outer hair cell degradation mechanism of hearing loss. This treatment is currently in active clinical trials.
• A γ-secretase inhibitor of Notch signaling was shown to induce new hair cells and partially recover hearing loss.[17] Auditory hair cell loss is permanent damage due to the inability of these cells to regenerate. Therefore, deafness due to this pathology is viewed as irreversible. Hair cell development is mediated by Notch signaling, which exerts lateral inhibition onto hair cells. Notch signaling in supporting hair cells leads to prevention of differentiation in surrounding hair cells. After identifying a potent γ-secretase inhibitor selective for stimulating differentiation in inner ear stem cells, it was administered in acoustically injured mice. The animals who received the injury and treatment displayed an increased hair cell number and stimulated hearing recovery. This suggests that γ-secretase inhibition of Notch signaling can be a potential pharmacological therapy in approaching what was previously viewed as permeant deafness.

• A fetal thymus graft, or rejuvenation of the recipient immunity by inoculation of young CD4+ T cells, also prevents presbycusis as well as up-regulation of the interleukin 1 receptor type II gene (IL1R2) in CD4+ T cells and degeneration of the spiral ganglion in Samp1 mice, a murine model of human senescence.[18] This technology remains years or even decades away from human application.