A common cause or exacerbating factor in SNHL is prolonged exposure to environmental noise, or noise-induced hearing loss.

Exposure to a single very loud noise such as a gun shot or bomb blast can cause noise-induced hearing loss.

Identification of sensorineural hearing loss is usually made by performing a pure tone audiometry (an audiogram) in which bone conduction thresholds are measured.

In cases of profound or total deafness, a cochlear implant is a specialised device that may restore a functional level of hearing.

SNHL is at least partially preventable by avoiding environmental noise, ototoxic chemicals and drugs, and head trauma, and treating or inoculating against certain triggering diseases and conditions like meningitis.

[citation needed] For a detailed exposition of symptoms useful for screening, a self-assessment questionnaire was developed by the American Academy of Otolaryngology, called the Hearing Handicap Inventory for Adults (HHIA).

[citation needed] Recessive, dominant, X-linked, or mitochondrial genetic mutations can affect the structure or metabolism of the inner ear.

[citation needed] Progressive age-related loss of hearing acuity or sensitivity can start as early as age 18, primarily affecting the high frequencies, and men more than women.

Numerous national and international organizations have established standards for safe levels of exposure to noise in industry, the environment, military, transportation, agriculture, mining and other areas.

For reference: An increase of 6 dB represents a doubling of the SPL, or energy of the sound wave, and therefore its propensity to cause ear damage.

Because human ears hear logarithmically, not linearly, it takes an increase of 10 dB to produce a sound that is perceived to be twice as loud.

[citation needed] While the standards differ moderately in levels of intensity and duration of exposure considered safe, some guidelines can be derived.

Long term hydrocodone (Vicodin) abuse is known to cause rapidly progressing sensorineural hearing loss, usually without vestibular symptoms.

This includes loop diuretics, sildenafil (Viagra), high or sustained dosing of NSAIDs (aspirin, ibuprofen, naproxen, and various prescription drugs: celecoxib, etc.

[citation needed] Prolonged or repeated environmental or work-related exposure to ototoxic chemicals can also result in sensorineural hearing loss.

Premature birth can be associated with problems that result in sensorineural hearing loss such as anoxia or hypoxia (poor oxygen levels), jaundice, intracranial haemorrhages, meningitis.

[12] If a pregnant mother has insufficient iodine intake during pregnancy it affects the development of the inner ear in the foetus leading to sensorineural deafness.

Sensory hearing loss is caused by abnormal structure or function of the hair cells of the organ of Corti in the cochlea.

[13] The main function of the active mechanism is to finely tune the basilar membrane, and provide it with a high sensitivity to quiet sounds.

However, where there is partial or complete damage to the OHCs, but with unharmed IHCs, the resulting tuning curve would show the elimination of sensitivity at the quiet sounds.

If the basilar membrane vibration is large enough, neurons tuned to different characteristic frequencies such as those adjacent to the dead region, will be stimulated due to the spread of excitation.

Although it is likely that the slope represents the less pronounced downward spread of excitation, rather than accurate thresholds for those frequencies with non-functioning hair cells.

Mid-frequency dead regions, with a small range, appear to have less effect on the patient's ability to hear in everyday life, and may produce a notch in the PTA thresholds.

[18] Although some debate continues regarding the reliability of such tests,[19] it has been suggested [weasel words]that psychoacoustic tuning curves (PTCs) and threshold-equalising noise (TEN) results may be useful in detecting dead regions, rather than PTA.

Audiogram configurations are not good indicators of how a dead region will affect a person functionally, mainly due to individual differences.

This therefore suggests that audiograms, and their poor representation of dead regions, are inaccurate predictors of a patient's perception of pure tone quality.

They are also useful in cases where a tumour is suspected or to determine the degree of damage in a hearing loss caused by bacterial infection or auto-immune disease.

There have been significant advances in identification of human deafness genes and elucidation of their cellular mechanisms as well as their physiological function in mice.

[24] Such pharmaceutical treatments as are employed are palliative rather than curative, and addressed to the underlying cause if one can be identified, in order to avert progressive damage.

Osteoporosis, stapedectomy surgery, pneumococcal vaccinations, mobile phone users, and hyperbilirubinemia at birth are among some of the known risk factors.