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Sensorineural hearing loss

sensorineural hearing loss, sensorineural hearing loss treatment
Sensorineural hearing loss SNHL is a type of hearing loss, or deafness, in which the root cause lies in the inner ear or sensory organ cochlea and associated structures or the vestibulocochlear nerve cranial nerve VIII or neural part SNHL accounts for about 90% of hearing loss reported SNHL is generally permanent and can be mild, moderate, severe, profound, or total Various other descriptors can be used such as high frequency, low frequency, U-shaped, notched, peaked or flat depending on the shape of the audiogram, the measure of hearing

Sensory hearing loss often occurs as a consequence of damaged or deficient cochlear hair cellsdisputed – discuss Hair cells may be abnormal at birth, or damaged during the lifetime of an individual There are both external causes of damage, including noise trauma, infection and ototoxic drugs, as well as intrinsic causes, including genetic mutations A common cause or exacerbating factor in sensory hearing loss is prolonged exposure to environmental noise, for example, being in a loud workplace without wearing protection, or having headphones set to high volumes for a long period Exposure to a very loud noise such as a bomb blast can cause noise-induced hearing loss

Neural, or 'retrocochlear', hearing loss occurs because of damage to the cochlear nerve CVIII This damage may affect the initiation of the nerve impulse in the cochlear nerve or the transmission of the nerve impulse along the nerve into the brainstem

Most cases of SNHL present with a gradual deterioration of hearing thresholds occurring over years to decades In some the loss may eventually affect large portions of the frequency range It may be accompanied by other symptoms such as ringing in the ears tinnitus, dizziness or lightheadedness vertigo SNHL can be genetically inherited or acquired as a result from external causes like noise or disease It may be congenital present at birth or develop later in life The most common kind of sensorineural hearing loss is age-related presbycusis, followed by noise-induced hearing loss NIHL

Frequent symptoms of SNHL are loss of acuity in distinguishing foreground voices against noisy backgrounds, difficulty understanding on the telephone, some kinds of sounds seeming excessively loud or shrill recruitment, difficulty understanding some parts of speech fricatives and sibilants, loss of directionality of sound, esp high frequency sounds, perception that people mumble when speaking, and difficulty understanding speech Similar symptoms are also associated with other kinds of hearing loss; audiometry or other diagnostic tests are necessary to distinguish sensorineural 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 Tympanometry and speech audiometry may be helpful Testing is performed by an audiologist

There is no proven or recommended treatment or cure for SNHL; management of hearing loss is usually by hearing strategies and hearing aid In cases of profound or total deafness, a cochlear implant is a specialised hearing aid which 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


  • 1 Signs and symptoms
  • 2 Causes
    • 21 Genetic
    • 22 Congenital
    • 23 Presbycusis
    • 24 Acquired
      • 241 Noise
      • 242 Disease or disorder
      • 243 Ototoxic and neurotoxic drugs and chemicals
      • 244 Head trauma
      • 245 Perinatal conditions
      • 246 Iodine deficiency / Hypothyroidism
      • 247 Brain stroke
  • 3 Diagnosis
    • 31 Case history
    • 32 Otoscopy
    • 33 Differential testing
    • 34 Tympanometry
    • 35 Audiometry
    • 36 Magnetic resonance imaging
  • 4 Pathophysiology
    • 41 Cochlear dead regions in sensory hearing loss
      • 411 Cochlear hair cells
        • 4111 Hair cell damage
    • 42 Neural tuning curves
      • 421 Frequency selectivity
      • 422 IHC vs OHC hearing loss
    • 43 Dead region audiometry
      • 431 Pure tone audiometry PTA
      • 432 Psychoacoustic tuning curves PTC and threshold equalizing noise TEN tests
      • 433 Perceptual consequences of a dead region
    • 44 Vestibulocochlear nerve pathology
  • 5 Prevention
  • 6 Treatment
  • 7 Research
    • 71 Pharmaceuticals
    • 72 Stem cell and gene therapy
  • 8 Sudden sensorineural hearing loss
    • 81 Presentation
    • 82 Diagnosis of SSHL
    • 83 Causes of SSHL
    • 84 Treatment for SSHL
  • 9 See also
  • 10 External links
  • 11 References

Signs and symptomsedit

Since the inner ear is not directly accessible to instruments, identification is by patient report and audiometric testing Of those who present to their doctor with sensorineural hearing loss, 90% report having diminished hearing, 57% report having plugged feeling in ear, and 49% report having ringing in ear tinnitus About half report vestibular vertigo problems

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 It is a 25-question survey of subjective symptoms1


Sensorineural hearing loss may be genetic or acquired ie as a consequence of disease, noise, trauma, etc People may have a hearing loss from birth congenital or the hearing loss may come on later Many cases are related to old age age-related


Hearing loss can be inherited More than 40 genes have been identified to cause deafness2 There are 300 syndromes with related hearing loss, and each syndrome may have causative genes

Recessive, dominant, X-linked or mitochondrial genetic mutations can affect the structure or metabolism of the inner ear Some may be single point mutations whereas others are due to chromosomal abnormalities Some genetic causes give rise to a late onset hearing loss Mitochondrial mutations can cause SNHL ie m1555A>G which makes the individual sensitive to the ototoxic effects of aminoglycoside antibiotics

Both dominant and recessive genes exist which can cause mild to profound impairment Rarely X-linked recessive genes for hearing loss occur and these are passed from unaffected mothers onto sons who then have hearing loss Daughters are unaffected carriers because the second X chromosome will provide the second normal copy of the gene, whereas the shorter Y chromosome does not Dominant and recessive hearing impairment can be syndromic or nonsyndromic Recent gene mapping has identified dozens of nonsyndromic dominant DFNA# and recessive DFNB# forms of deafness

  • The most common cause of recessive genetic congenital hearing impairment in developed countries is DFNB1, also known as Connexin 26 deafness or GJB2-related deafness
  • The most common syndromic forms of hearing impairment include dominant Stickler syndrome and Waardenburg syndrome, and recessive Pendred syndrome and Usher syndrome
  • MT-TL1 mutations cause hearing loss, along with diabetes and other symptoms
  • TMPRSS3 gene was identified by its association with both congenital and childhood onset autosomal recessive deafness This gene is expressed in fetal cochlea and many other tissues, and is thought to be involved in the development and maintenance of the inner ear or the contents of the perilymph and endolymph It was also identified as a tumor associated gene that is overexpressed in ovarian tumors
  • Charcot–Marie–Tooth disease3 an inherited neurological disorder with delayed onset that can affect the ears as well as other organs
  • Muckle–Wells syndrome, a rare inherited autoinflammatory disorder, can lead to hearing loss
  • Autoimmune disease: although probably rare, it is possible for autoimmune processes to target the cochlea specifically, without symptoms affecting other organs Granulomatosis with polyangiitis, an autoimmune condition, may precipitate hearing loss


  • Infections:
    • Congenital rubella syndrome, CRS, results from transplacental transmission of rubella German measles virus during pregnancy CRS has been controlled by universal vaccination MMR or MMRV vaccine
    • Human Cytomegalovirus HCMV transmission to a developing fetus during pregnancy congenital infection is currently the most common infectious cause of congenital hearing loss HCMV congenital infection can lead to sensorineural hearing loss that may be identified shortly after birth although many affected children have no hearing loss until later Classically the hearing loss is progressive over the first decade and possibly later Worldwide, HCMV congenital infection impacts between 05 and 2% of all live births, with sensorineural hearing loss estimated to occur in 10 to 20% of infected newborns Thus, an estimated 7,000,000 people alive today have suffered hearing loss attributed to HCMV congenital disease The majority of cases do not have recognisable hearing loss at birth but develop it in the first decade of life
    • toxoplasmosis, a parasitic disease affecting 23% of the population in the US that can cause sensorineural deafness to the fetus in utero
  • hypoplastic auditory nerves or abnormalities of the cochlea


Main article: Presbycusis

Normal progressive age-related loss of hearing acuity or sensitivity starting as early as age 18, primarily affecting the high frequencies, and men more than women Such losses may not become apparent until much later in life Presbycusis is by far the dominant cause of sensorineural hearing loss Hearing loss that accumulates with age but is caused by factors other than normal aging, such as noise-induced hearing loss, is not presbycusis, although differentiating the individual effects of multiple causes of hearing loss can be difficult One in three persons have significant hearing loss by age 65; by age 75, one in two Age-related hearing loss is neither preventable nor reversible



Main article: Noise-induced hearing loss

Most people living in modern society suffer from some degree of progressive sensorineural ie permanent noise-induced hearing loss NIHL resulting from overloading and damaging the sensory or neural apparatus of hearing in the inner ear NIHL is typically a drop-out or notch centered at 4000 Hz Both intensity SPL and duration of exposure, and repetitive exposure to unsafe levels of noise contribute to cochlear damage that results in hearing loss The louder the noise is, the shorter the safe amount of exposure is NIHL can be either permanent or temporary, called a threshold shift Unsafe levels of noise can be as little as 70 dB about twice as loud as normal conversation if there is prolonged 24-hour or continuous exposure 125 dB loud rock concert ~120 dB is the pain level; sounds above this level cause instant and permanent ear damage

Noise and ageing are the primary causes of presbycusis, or age-related hearing loss, the most common kind of hearing loss in industrial society4

Noise-related causes of hearing loss are divided into extrinsic nosocusis and intrinsic sociocusis causes: In the auditory system, the extrinsic component nosocusis includes hearing loss due to otologic disease, hazardous noise exposure, acoustic trauma, and ototoxic agents The intrinsic component sociocusis indicates the wear-and-tear effects of exposure to the everyday sounds of normal living People who live in nonindustrialized regions avoid both nosocusis and sociocusis and demonstrate excellent hearing into old agecitation needed

The dangers of environmental and occupational noise exposure are widely recognized 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 areas5 Sound intensity or sound pressure level SPL is measured in decibels dB For reference,

dB levels
  • 45dB ambient noise level around the home
  • 60dB quiet office,
  • 60-65dB normal conversation
  • 70dB city street noise at 25' or average TV audio,
  • 80dB a noisy office
  • 95-104dB nightclub dance floor,
  • 120dB close in thunder, loud rock concert
  • 150-160dB gunshot handheld sidearm

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 our ears hear logarithmically, not linearly, it takes an increase of 10 dB to produce a sound that is perceived to be twice as loud Ear damage due to noise is proportional to sound intensity SPL, not perceived loudness, so it's misleading to rely on our subjective perception of loudness as an indication of the risk to hearing, ie, it can significantly underestimate the danger

While the standards differ moderately in levels of intensity and duration of exposure considered safe, some guidelines can be derived6

The safe amount of exposure is reduced by a factor of 2 for every exchange rate 3 dB for NIOSH standard or 5 dB for OSHA standard increase in SPL For example, the safe daily exposure amount at 85 dB 90 dB for OSHA is 8 hours, while the safe exposure at 94 dBA nightclub level is only 1 hours Noise trauma can also cause a reversible hearing loss, called a temporary threshold shift This typically occurs in individuals who are exposed to gunfire or firecrackers, and hear ringing in their ears after the event tinnitus

  • ambient environmental noise — Populations living near airports, railyards and train stations, freeways and industrial areas are exposed to levels of noise typically in the 65 to 75 dBA range If lifestyles include significant outdoor or open window conditions, these exposures over time can degrade hearing US Dept of Housing and Urban Development sets standards for noise impact in residential and commercial construction zones HUD’s noise standards may be found in 24 CFR Part 51, Subpart B Environmental noise above 65 dB defines a noise-impacted area
  • Personal audio electronics, such as iPods iPods often reaching 115 decibels or higher, can produce powerful enough sound to cause significant NIHL7
  • Repeated exposure to loud noise 90-95 dB or more can cause progressive hearing loss Sound levels at places where live or dance music is performed typically range from 95 dB to 104 dB
  • acoustic trauma — Exposure to a single event of extremely loud noise such as explosions can also cause temporary or permanent hearing loss A typical source of acoustic trauma is a too-loud music concert
  • workplace noise — OSHA standards 191095 General Industry Occupational Noise Exposure, and 192652 Construction Industry Occupational Noise Exposure identify the level of 90 dBA for 8 hour exposure as the level necessary to protect workers from hearing loss

Disease or disorderedit

  • Inflammatory
    • Suppurative labyrinthitis or otitis interna inflammation of the inner ear
  • diabetes mellitus Main article: Diabetes mellitus and deafness A recent study found that hearing loss is twice as common in people with diabetes as it is in those who don't have the disease Also, of the 86 million adults in the US who have prediabetes, the rate of hearing loss is 30 percent higher than in those with normal blood glucose It has not been established how diabetes is related to hearing loss It is possible that the high blood glucose levels associated with diabetes cause damage to the small blood vessels in the inner ear, similar to the way in which diabetes can damage the eyes and the kidneys Similar studies have shown a possible link between that hearing loss and neuropathy nerve damage
  • tumor
    • Cerebellopontine angle tumour junction of the pons and cerebellum - The cerebellopontine angle is the exit site of both the facial nerveCN7 and the vestibulocochlear nerveCN8 Patients with these tumors often have signs and symptoms corresponding to compression of both nerves
    • Acoustic neuroma vestibular schwannoma - benign neoplasm of Schwann cells affecting the vestibulocochlear nerve
    • Meningioma - benign tumour of the pia and arachnoid mater
  • Ménière's disease - causes sensorineural hearing loss in the low frequency range 125 Hz to 1000 Hz Ménière's disease is characterized by sudden attacks of vertigo, lasting minutes to hours preceded by tinnitus, aural fullness, and fluctuating hearing loss
  • pneumococcal Meningitis may damage the cochlea - Hearing loss is one of the most common after-effects of meningitis It has been estimated that 30% of meningitis cases result in mild to severe hearing loss Children are most at risk: seventy percent of all bacterial meningitis occurs in young children under the age of five
  • viral
    • AIDS and ARC patients frequently experience auditory system anomalies
    • Mumpsepidemic parotitis may result in profound sensorineural hearing loss 90 dB or more, unilaterally one ear or bilaterally both ears
    • Measles may result in auditory nerve damage but more commonly gives a conductive hearing loss or very rarely, bilaterally
    • Ramsay Hunt syndrome type II herpes zoster oticus
  • bacterial
    • Syphilis is commonly transmitted from pregnant women to their fetuses, and about a third of the infected children will eventually become deaf

Ototoxic and neurotoxic drugs and chemicalsedit

Main article: ototoxicity

Some over-the-counter as well as prescription drugs and certain industrial chemicals are ototoxic Exposure to these can result in temporary or permanent hearing loss

Some medications cause irreversible damage to the ear, and are limited in their use for this reason The most important group is the aminoglycosides main member gentamicin A rare mitochondrial mutation, m1555A>G, can increase an individual's susceptibility to the ototoxic effect of aminoglycosides Long term hydrocodone Vicodin abuse is known to cause rapidly progressing sensorineural hearing loss, usually without vestibular symptoms Methotrexate, a chemotherapy agent, is also known to cause hearing loss In most cases hearing loss does not recover when the drug is stopped Paradoxically, methotrexate is also used in the treatment of autoimmune-induced inflammatory hearing loss

Various other medications may reversibly degrade hearing This includes loop diuretics, sildenafil Viagra, high or sustained dosing of NSAIDs aspirin, ibuprofen, naproxen, and various prescription drugs: celecoxib, etc, quinine, and macrolide antibiotics erythromycin, etc

Prolonged or repeated environmental or work-related exposure to ototoxic chemicals can also result in sensorineural hearing loss Some of these chemicals are:

  • butyl nitrite - chemical used recreationally known as 'poppers'
  • carbon disulfide - a solvent used as a building block in many organic reactions
  • styrene, an industrial chemical precursor of polystyrene, a plastic
  • carbon monoxide, a poisonous gas resulting from incomplete combustion
  • heavy metals: tin, lead, manganese, mercury
  • hexane, an industrial solvent and one of the significant constituents of gasoline
  • ethylbenzene, an industrial solvent used in the production of styrene
  • toluene and xylene, highly poisonous petrochemical solvents Toluene is a component of high-octane gasolne; xylene is used in the production of polyester fibers and resins
  • trichloroethylene, an industrial degreasing solvent
  • Organophosphate pesticides

Head traumaedit

There can be damage either to the ear itself or to the central auditory pathways that process the information conveyed by the ears People who sustain head injury are susceptible to hearing loss or tinnitus, either temporary or permanent Contact sports like football US NFL, hockey and cricket have a notable incidence of head injuries concussions In one survey of retired NFL players, all of whom reported one or more concussions during their playing careers, 25% had hearing loss and 50% had tinnituscitation needed

Perinatal conditionsedit

These are much more common in premature babies, particularly those under 1500 g at birth Premature birth can be associated with problems that result in sensorineural hearing loss such as anoxia or hypoxiapoor oxygen levels, jaundice, intracranial haemorrhages, meningitis Fetal alcohol syndrome is reported to cause hearing loss in up to 64% of infants born to alcoholic mothers, from the ototoxic effect on the developing fetus, plus malnutrition during pregnancy from the excess alcohol intake

Iodine deficiency / Hypothyroidismedit

Iodine deficiency and hypothyroidism are associated with hearing loss8 Depending on age of onset, may be correctable by iodine or thyroid medication

Brain strokeedit

Brain stroke in a region affecting auditory function such as a posterior circulation infarct has been associated with deafness


Case historyedit

Before examination, a case history provides guidance about the context of the hearing loss

  • major concern
  • pregnancy and childbirth information
  • medical history
  • development history
  • family history


Direct examination of the external canal and tympanic membrane ear drum with an otoscope, a medical device inserted into the ear canal that uses light to examine the condition of the external ear and tympanic membrane, and middle ear through the semi-translucent membrane

Differential testingedit

Differential testing is most useful when there is unilateral hearing loss, and distinguishes conductive from sensorineural loss These are conducted with a low frequency tuning fork, usually 512 Hz, and contrast measures of air and bone conducted sound transmission

  • Weber test, in which a tuning fork is touched to the midline of the forehead, localizes to the normal ear in people with unilateral sensorineural hearing loss
  • Rinne test, which tests air conduction vs bone conduction is positive, because both bone and air conduction are reduced equally
  • less common Bing and Schwabach variants of the Rinne test
  • absolute bone conduction ABC test

Table 1 A table comparing sensorineural to conductive hearing loss

Criteria Sensorineural hearing loss Conductive hearing loss
Anatomical site Inner ear, cranial nerve VIII, or central processing centers Middle ear ossicular chain, tympanic membrane, or external ear
Weber test Sound localizes to normal ear in unilateral SNHL Sound localizes to affected ear ear with conductive loss in unilateral cases
Rinne test Positive Rinne; air conduction > bone conduction both air and bone conduction are decreased equally, but the difference between them is unchanged Negative Rinne; bone conduction > air conduction bone/air gap

Other, more complex, tests of auditory function are required to distinguish the different types of hearing loss Bone conduction thresholds can differentiate sensorineural hearing loss from conductive hearing loss Other tests, such as oto-acoustic emissions, acoustic stapedial reflexes, speech audiometry and evoked response audiometry are needed to distinguish sensory, neural and auditory processing hearing impairments


A tympanogram is the result of a test with a tympanometer It tests the function of the middle ear and mobility of the eardrum It can help identify conductive hearing loss due to disease of the middle ear or eardrum from other kinds of hearing loss including SNHL


An audiogram is the result of a hearing test The most common type of hearing test is pure tone audiometry PTA It charts the thresholds of hearing sensitivity at a selection of standard frequencies between 250 and 8000 Hz There is also high frequency pure tone audiometry which tests frequencies from 8000-20,000 Hz PTA can be used to differentiate between conductive hearing loss, sensorineural hearing loss and mixed hearing loss A hearing loss can be described by its degree ie mild, moderate, severe or profound, or by its shape ie high frequency or sloping,low frequency or rising, notched, U-shaped or 'cookie-bite', peaked or flat

There are also other kinds of audiometry designed to test hearing acuity rather than sensitivity speech audiometry, or to test auditory neural pathway transmission evoked response audiometry

Magnetic resonance imagingedit

MRI scans can be used to identify gross structural causes of hearing loss They are used for congenital hearing loss when changes to the shape of the inner ear or nerve of hearing may help diagnosis of the cause of the hearing loss 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 Scanning is of no value in age-related deafness


Sensory hearing loss is caused by abnormal structure or function of the hair cells of the organ of Corti in the cochleadisputed – discuss Neural hearing impairments are consequent upon damage to the eighth cranial nerve the vestibulocochlear nerve or the auditory tracts of the brainstem If higher levels of the auditory tract are affected this is known as central deafness Central deafness may present as sensorineural deafness but should be distinguishable from the history and audiological testing

Cochlear dead regions in sensory hearing lossedit

Hearing impairment may be associated with damage to the hair cells in the cochlea Sometimes there may be complete loss of function of inner hair cells IHCs over a certain region of the cochlea; this is called a "dead region" The region can be defined in terms of the range of characteristic frequencies CFs of the IHCs and/or neurons immediately adjacent to the dead region

Cochlear hair cellsedit

Figure 3: Cross-section of the cochlea

Outer hair cells OHCs contribute to the structure of the Organ of Corti, which is situated between the basilar membrane and the tectorial membrane within the cochlea See Figure 3 The tunnel of corti, which runs through the Organ of Corti, divides the OHCs and the inner hair cells IHCs OHCs are connected to the reticular laminar and the Deiters’ cells There are roughly twelve thousand OHCs in each human ear, and these are arranged in up to five rows Each OHC has small tufts of 'hairs', or cilia, on their upper surface known as stereocilia, and these are also arranged into rows which are graded in height There are approximately 140 stereocilia on each OHC9

The fundamental role of the OHCs and the IHCs is to function as sensory receptors The main function of the IHCs is to transmit sound information via afferent neurons They do this by transducing mechanical movements or signals into neural activity When stimulated, the stereocilia on the IHCs move, causing a flow of electric current to pass through the hair cells This electric current creates action potentials within the connected afferent neurons

OHCs are different in that they actually contribute to the active mechanism of the cochlea They do this by receiving mechanical signals or vibrations along the basilar membrane, and transducing them into electrochemical signals The stereocilia found on OHCs are in contact with the tectorial membrane Therefore, when the basilar membrane moves due to vibrations, the stereocilia bend The direction in which they bend, dictates the firing rate of the auditory neurons connected to the OHCs10

The bending of the stereocilia towards the basal body of the OHC causes excitation of the hair cell Thus, an increase in firing rate of the auditory neurons connected to the hair cell occurs On the other hand, the bending of the stereocilia away from the basal body of the OHC causes inhibition of the hair cell Thus, a decrease in firing rate of the auditory neurons connected to the hair cell occurs OHCs are unique in that they are able to contract and expand electromotility Therefore, in response to the electrical stimulations provided by the efferent nerve supply, they can alter in length, shape and stiffness These changes influence the response of the basilar membrane to sound910 It is therefore clear that the OHCs play a major role in the active processes of the cochlea9 The main function of the active mechanism is to finely tune the basilar membrane, and provide it with a high sensitivity to quiet sounds The active mechanism is dependent on the cochlea being in good physiological condition However, the cochlea is very susceptible to damage10

Hair cell damageedit

SNHL is most commonly caused by damage to the OHCs and the IHCsdisputed – discuss There are two methods by which they might become damaged Firstly, the entire hair cell might die Secondly, the stereocilia might become distorted or destroyed Damage to the cochlea can occur in several ways, for example by viral infection, exposure to ototoxic chemicals, and intense noise exposure Damage to the OHCs results in either a less effective active mechanism, or it may not function at all OHCs contribute to providing a high sensitivity to quiet sounds at a specific range of frequencies approximately 2–4 kHz Thus, damage to the OHCs results in the reduction of sensitivity of the basilar membrane to weak sounds Amplification to these sounds is therefore required, in order for the basilar membrane to respond efficiently IHCs are less susceptible to damage in comparison to the OHCs However, if they become damaged, this will result in an overall loss of sensitivity10

Neural tuning curvesedit

Frequency selectivityedit

Figure 4: Neural tuning curve for normal hearing

The traveling wave along the basilar membrane peaks at different places along it, depending on whether the sound is low or high frequency Due to the mass and stiffness of the basilar membrane, low frequency waves peak in the apex, while high frequency sounds peak in the basal end of the cochlea9 Therefore, each position along the basilar membrane is finely tuned to a particular frequency These specifically tuned frequencies are referred to as characteristic frequencies CF10

If a sound entering the ear is displaced from the characteristic frequency, then the strength of response from the basilar membrane will progressively lessen The fine tuning of the basilar membrane is created by the input of two separate mechanisms The first mechanism being a linear passive mechanism, which is dependent on the mechanical structure of the basilar membrane and its surrounding structures The second mechanism is a non-linear active mechanism, which is primarily dependent on the functioning of the OHCs, and also the general physiological condition of the cochlea itself The base and apex of the basilar membrane differ in stiffness and width, which cause the basilar membrane to respond to varying frequencies differently along its length The base of the basilar membrane is narrow and stiff, resulting in it responding best to high frequency sounds The apex of the basilar membrane is wider and much less stiff in comparison to the base, causing it to respond best to low frequencies10

This selectivity to certain frequencies can be illustrated by neural tuning curves These demonstrate the frequencies a fiber responds to, by showing threshold levels dB SPL of auditory nerve fibers as a function of different frequencies This demonstrates that auditory nerve fibers respond best, and hence have better thresholds at the fiber's characteristic frequency and frequencies immediately surrounding it The basilar membrane is said to be ‘sharply tuned’ due to the sharp ‘V’ shaped curve, with its ‘tip’ centered at the auditory fibers characteristic frequency This shape shows how few frequencies a fiber responds to If it were a broader ‘V’ shape, it would be responding to more frequencies See Figure 49

IHC vs OHC hearing lossedit

Figure 5: Neural tuning curve for OHC loss Adapted from10 Figure 6: Neural tuning curve for OHC front row loss and IHC loss Adapted from10

A normal neural tuning curve is characterised by a broadly tuned low frequency ‘tail’, with a finely tuned middle frequency ‘tip’ 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 Ie where the neural tuning curve would normally be most sensitive at the ‘tip’ See Figure 510

Where both the OHCs and the IHCs are damaged, the resulting neural tuning curve would show the elimination of sensitivity at the ‘tip' However, due to IHC damage, the whole tuning curve becomes raised, giving a loss of sensitivity across all frequencies See Figure 6 It is only necessary for the first row of OHCs to be damaged for the elimination of the finely tuned ‘tip’ to occur This supports the idea that the incidence of OHC damage and thus a loss of sensitivity to quiet sounds, occurs more than IHC loss10

When the IHCs or part of the basilar membrane are damaged or destroyed, so that they no longer function as transducers, the result is a ‘dead region’ Dead regions can be defined in terms of the characteristic frequencies of the IHC, related to the specific place along the basilar membrane where the dead region occurs Assuming that there has been no shift in the characteristic frequencies relating to certain regions of the basilar membrane, due to the damage of OHCs This often occurs with IHC damage Dead regions can also be defined by the anatomical place of the non-functioning IHC such as an “apical dead region”, or by the characteristic frequencies of the IHC adjacent to the dead region11

Dead region audiometryedit

Pure tone audiometry PTAedit

Dead regions affect audiometric results, but perhaps not in the way expected For example, it may be expected that thresholds would not be obtained at the frequencies within the dead region, but would be obtained at frequencies adjacent to the dead region Therefore, assuming normal hearing exists around the dead region, it would produce an audiogram that has a dramatically steep slope between the frequency where a threshold is obtained, and the frequency where a threshold cannot be obtained due to the dead region11

Figure 7: Response of the basilar membrane to a pure tone Figure 8: Response of the basilar membrane to a pure tone, when there is a dead region

However, it appears that this is not the case Dead regions cannot be clearly found via PTA audiograms This may be because although the neurons innervating the dead region, cannot react to vibration at their characteristic frequency 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 Therefore, a response from the patient at the test frequency will be obtained This is referred to as “off-place listening”, and is also known as ‘off-frequency listening’ This will lead to a false threshold being found Thus, it appears a person has better hearing than they actually do, resulting in a dead region being missed Therefore, using PTA alone, it is impossible to identify the extent of a dead region See Figure 7 and 811

Consequently, how much is an audiometric threshold affected by a tone with its frequency within a dead region This depends on the location of the dead region Thresholds at low frequency dead regions, are more inaccurate than those at higher frequency dead regions This has been attributed to the fact that excitation due to vibration of the basilar membrane spreads upwards from the apical regions of the basilar membrane, more than excitation spreads downwards from higher frequency basal regions of the cochlea This pattern of the spread of excitation is similar to the ‘upward spread of masking’ phenomenon If the tone is sufficiently loud to produce enough excitation at the normally functioning area of the cochlea, so that it is above that areas threshold The tone will be detected, due to off-frequency listening which results in a misleading threshold11

To help to overcome the issue of PTA producing inaccurate thresholds within dead regions, masking of the area beyond the dead region that is being stimulated can be used This means that the threshold of the responding area is sufficiently raised, so that it cannot detect the spread of excitation from the tone This technique has led to the suggestion that a low frequency dead region may be related to a loss of 40-50 dB1213 However, as one of the aims of PTA is to determine whether or not there is a dead region, it may be difficult to assess which frequencies to mask without the use of other tests11

Based on research it has been suggested that a low frequency dead region may produce a relatively flat loss, or a very gradually sloping loss towards the higher frequencies As the dead region will be less detectable due to the upward spread of excitation Whereas, there may be a more obvious steeply sloping loss at high frequencies for a high frequency dead region 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 thresholds11 Although it is clear that PTA is not the best test to identify a dead region14

Psychoacoustic tuning curves PTC and threshold equalizing noise TEN testsedit

Figure 9: Psychoacoustical tuning curve

Although some debate continues regarding the reliability of such tests,15 it has been suggested weasel wordsthat psychoacoustic tuning curves PTCs and threshold-equalising noise TEN results may be useful in detecting dead regions, rather than PTA PTCs are similar to neural tuning curves They illustrate the level of a masker dB SPL tone at threshold, as a function of deviation from center frequency Hz9 They are measured by presenting a fixed low intensity pure tone while also presenting a narrow-band masker, with a varying center frequency The masker level is varied, so that the level of masker needed to just mask the test signal is found for the masker at each center frequency The tip of the PTC is where the masker level needed to just mask the test signal is the lowest For normal hearing people this is when the masker center frequency is closest to the frequency of the test signal See Figure 914

In the case of dead regions, when the test signal lies within the boundaries of a dead region, the tip of the PTC will be shifted to the edge of the dead region, to the area that is still functioning and detecting the spread of excitation from the signal In the case of a low frequency dead region, the tip is shifted upwards indicating a low frequency dead region starting at the tip of the curve For a high frequency dead region, the tip is shifted downwards from the signal frequency to the functioning area below the dead region14 However, the traditional method of obtaining PTCs is not practical for clinical use, and it has been arguedweasel words that TENs are not accurate enough1415 A fast method for finding PTCs has been developed and it may provide the solution However, more research to validate this method is required, before it can be accepted clinically

Perceptual consequences of a dead regionedit

Audiogram configurations are not good indicators of how a dead region will affect a person functionally, mainly due to individual differences10 For example, a sloping audiogram is often present with a dead region, due to the spread of excitation However, the individual may well be affected differently from someone with a corresponding sloped audiogram caused by partial damage to hair cells rather than a dead region They will perceive sounds differently, yet the audiogram suggests that they have the same degree of loss Huss and Moore investigated how hearing impaired patients perceive pure tones, and found that they perceive tones as noisy and distorted, more on average than a person without a hearing impairment However, they also found that the perception of tones as being like noise, was not directly related to frequencies within the dead regions, and was therefore not an indicator of a dead region This therefore suggests that audiograms, and their poor representation of dead regions, are inaccurate predictors of a patient’s perception of pure tone quality16

Research by Kluk and Moore has shown that dead regions may also affect the patient’s perception of frequencies beyond the dead regions There is an enhancement in the ability to distinguish between tones that differ very slightly in frequency, in regions just beyond the dead regions compared to tones further away An explanation for this may be that cortical re-mapping has occurred Whereby, neurons which would normally be stimulated by the dead region, have been reassigned to respond to functioning areas near it This leads to an over-representation of these areas, resulting in an increased perceptual sensitivity to small frequency differences in tones17

Vestibulocochlear nerve pathologyedit

  • congenital deformity of the internal auditory canal,
  • neoplastic and pseudo-neoplastic lesions, with special detailed emphasis on schwannoma of the eighth cranial nerve acoustic neuroma,
  • non-neoplastic Internal Auditory Canal/CerebelloPontine Angle pathology, including vascular loops,


Presbycucis is the leading cause of SNHL and is progressive and nonpreventable, and at this time, we do not have either somatic or gene therapy to counter heredity-related SNHL But other causes of acquired SNHL are largely preventable, especially nosocusis type causes This would involve avoiding environmental noise, and traumatic noise such as rock concerts and nightclubs with loud music Use of noise attenuation measures like acoustic ear plugs is an alternative


Treatment modalities fall into three categories: pharmacological, surgical, and management As SNHL is a physiologic degradation and considered permanent, there are as of this time, no approved or recommended treatments

There have been significant advances in identification of human deafness genes and elucidation of their cellular mechanisms as well as their physiological function in mice1819 Nevertheless, pharmacological treatment options are very limited and clinically unproven20 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

Profound or total hearing loss may be amenable to management by cochlear implants, which stimulate cochlear nerve endings directly A cochlear implant is surgical implantation of a battery powered electronic medical device in the inner ear Unlike hearing aids, which make sounds louder, cochlear implants do the work of damaged parts of the inner ear cochlea to provide sound signals to the brain These consist of both internal implanted electrodes and magnets and external components21 The quality of sound is different than natural hearing but may enable the recipient to better recognize speech and environmental sounds Because of risk and expense, such surgery is reserved for cases of severe and disabling hearing impairment

Management of sensorineural hearing loss involves employing strategies to support existing hearing such as lip-reading, enhanced communication etc and amplification using hearing aids Hearing aids are specifically tuned to the individual hearing loss to give maximum benefit



  • Antioxidant vitamins - Researchers at the University of Michigan report that a combination of high doses of vitamins A, C, and E, and Magnesium, taken one hour before noise exposure and continued as a once-daily treatment for five days, was very effective at preventing permanent noise-induced hearing loss in animals22
  • Tanakan - a brand name for an international prescription drug extract of Ginkgo biloba It is classified as a vasodilator Among its research uses is treatment of sensorineural deafness and tinnitus presumed to be of vascular origin
  • Coenzyme Q10 - a substance similar to a vitamin, with antioxidant properties It is made in the body, but levels fall with age23
  • ebselen, a synthetic drug molecule that mimics glutathione peroxidase GPx, a critical enzyme in the inner ear that protects it from damage caused by loud sounds or noise 24

Stem cell and gene therapyedit

Hair cell regeneration using stem cell and gene therapy is years or decades away from being clinically feasible25 However, studies are currently underway on the subject, with the first FDA-approved trial beginning in February 201226

Sudden sensorineural hearing lossedit

Sudden sensorineural hearing loss SSHL, commonly known as sudden deafness, occurs as an unexplained, rapid loss of hearing—usually in one ear—either at once or over several days Nine out of ten people with SSHL lose hearing in only one ear It should be considered a medical emergency Delaying diagnosis and treatment may render treatment less effective or ineffective

Experts estimate that SSHL strikes one person per 5,000 every year, typically adults in their 40s and 50s The actual number of new cases of SSHL each year could be much higher because the condition often goes undiagnosed


Many people notice that they have SSHL when they wake up in the morning Others first notice it when they try to use the deafened ear, such as when they use a phone Still others notice a loud, alarming "pop" just before their hearing disappears People with sudden deafness often become dizzy, have ringing in their ears tinnitus, or both

Diagnosis of SSHLedit

SSHL is diagnosed via pure tone audiometry If the test shows a loss of at least 30db in three adjacent frequencies, the hearing loss is diagnosed as SSHL For example, a hearing loss of 30db would make conversational speech sound more like a whisper

Causes of SSHLedit

Only 10 to 15 percent of the cases diagnosed as SSHL have an identifiable cause Most cases are classified as idiopathic, also called sudden idiopathic hearing loss SIHL and idiopathic sudden sensorineural hearing loss ISSHL or ISSNHL2728 The majority of evidence points to some type of inflammation in the inner ear as the most common cause of SSNHL

  • Viral - The swelling may be due to a virus A herpes type virus is believed to be the most common cause of sudden sensorineural hearing loss The herpes virus lays dormant in our bodies and reactivates for an unknown reason
  • Vascular ischemia of the inner ear or cranial nerve VIII CN8
  • Perilymph fistula, usually due to a rupture of the round or oval windows and the leakage of perilymph The patient will usually also experience vertigo or imbalance A history of trauma is usually present and changes to hearing or vertigo occur with alteration in intracranial pressure such as with straining; lifting, blowing etc
  • Autoimmune - can be due to an autoimmune illness such as systemic lupus erythematosus, granulomatosis with polyangiitis

Treatment for SSHLedit

About half of people with SSNHL will recover some or all of their hearing spontaneously, usually within one to two weeks from onset Eighty-five percent of those who receive treatment from an otolaryngologist sometimes called an ENT will recover some of their hearing

  • vitamins and antioxidants
  • vasodilators
  • betahistine Betaserc, an anti-vertigo drug
  • hyperbaric oxygen29
  • anti-inflammatory agents, primarily oral corticosteroids such as prednisone, methylprednisone
  • Intratympanic administration - Gel formulations are under investigation to provide more consistent drug delivery to the inner ear30 Local drug delivery can be accomplished through intratympanic administration, a minimally invasive procedure where the ear drum is anesthetized and a drug is administered into the middle ear From the middle ear, a drug can diffuse across the round window membrane into the inner ear30 Intratympanic administration of steroids may be effective for sudden sensorineural hearing loss for some patients, but high quality clinical data has not been generated31 Intratympanic administration of an anti-apoptotic peptide JNK inhibitor is currently being evaluated in late-stage clinical development32

See alsoedit

  • Otosclerosis, a sometimes associated or predecessor conductive hearing loss condition of the middle ear
  • Conductive hearing loss, hearing loss caused primarily by conditions in the middle ear
  • Hearing loss
  • Cortical deafness, another kind of nerve deafness
  • Tinnitus, ringing in the ears, a common accompaniment of SNHL
  • Inner ear, the innermost portion of the ear containing the sensorineural apparatus of hearing

External linksedit

  • Hearing Loss Web ,


  1. ^ Newman CW, Weinstein BE, Jacobson GP, Hug GA 1991 "Test-retest reliability of the Hearing Handicap Inventory for Adults" Ear Hear 12 5: 355–357 PMID 1783240 doi:101097/00003446-199110000-00009 CS1 maint: Multiple names: authors list link
  2. ^ Matsunaga, T 2009 "Value of genetic testing in the otological approach for sensorineural hearing loss" The Keio journal of medicine 58 4: 216–222 PMID 20037285 doi:102302/kjm58216 
  3. ^ Papadakis CE, Hajiioannou JK, Kyrmizakis DE, Bizakis JG May 2003 "Bilateral sudden sensorineural hearing loss caused by Charcot-Marie-Tooth disease" J Laryngol Otol 117 5: 399–401 PMID 12803792 doi:101258/002221503321626465 
  4. ^ Gates, George A; Mills, John H September 2005 "Presbycusis" The Lancet 366 9491: 1111–1120 doi:101016/S0140-67360567423-5 Presbycusis or presbyacusis is a general term that refers to hearing loss in the elderly and, as such, represents the contributions of a lifetime of insults to the auditory system Of these, ageing and noise damage are the chief factors, plus genetic susceptibility, otological disorders, and exposures to ototoxic agents 
  5. ^ A few prominent ones are American National Standards Institute ANSI, International Organization for Standardization ISO, Deutsches Institut für Normung DIN, Swedish Standards Institute SSI, Canadian Standards Association CSA, British Standards Institute BSI, Austrian Standards Institute ÖNORM, and in the United States, Environmental Protection Agency EPA, Occupational Safety and Health Administration OSHA and numerous state agencies, and Department of Defense DOD among others
  6. ^ The various standards quantify nose exposure with a set of specified measures, usually with respect to a reference exposure time of 8 hours, a typical working day The measures include, a weighting scale usually A with a sample time, a threshold value in dB, a criterion sound pressure level in dB with an exposure time usually in hours, and an exchange rate in dB A weighted SPL is denoted dBX where X is a weighting scale, usually A, but sometimes C A refers to A-weighting of SPL, which is an adjustment to measured SPL to compensate for the frequency response of the human ear, which is less sensitive to low frequencies The criterion level is the average sound pressure level permitted over the exposure time The threshold sound pressure level is the level above which sound will be integrated into the average The sample time fast, slow or impulse is the rate of sampling — a slow sample time is 1 second; a fast sample time is 1/8 second, and impulse sample time is 35 milliseconds The effect of a slower sample time means that very short duration sounds may not be fully sampled or even sampled at all in rare cases, so the noise exposure may be underestimated The exchange rate is the amount by which the permitted sound level may increase if the exposure time is halved
  7. ^ "Sound Output Levels of the iPod and Other MP3 Players: Is There Potential Risk to Hearing" Archived from the original on October 30, 2007 Retrieved 2007-11-20 
  8. ^ Kochupillai, N; Pandav, CS; Godbole, MM; Mehta, M; Ahuja, MM 1986 "Iodine deficiency and neonatal hypothyroidism" Bulletin of the World Health Organization 64 4: 547–51 PMC 2490891  PMID 3490923 
  9. ^ a b c d e f Gelfand SA Hearing: An Introduction to Psychological and Physiological Acoustics 4th ed New York: Marcel Dekker; 2004
  10. ^ a b c d e f g h i j k Moore BCJ Cochlear Hearing Loss London: Whurr Publishers; 1998
  11. ^ a b c d e f Moore, BC April 2004 "Dead regions in the cochlea: conceptual foundations, diagnosis, and clinical applications" Ear and hearing 25 2: 98–116 PMID 15064655 doi:101097/01aud000012035949711d7 
  12. ^ Terkildsen K 1980 "Hearing impairment and audiograms" Scand Audiol 10: 27–31  Cited in: Moore BC 2001 "Dead Regions in the Cochlea: Diagnosis, Perceptual Consequences, and Implications for the Fitting of hearing aids" Trends Amplif 5 1: 1–34 PMC 4168936  PMID 25425895 doi:101177/108471380100500102 
  13. ^ Thornton AR, Abbas PJ 1980 "Low-frequency hearing loss: Perception of filtered speech, psychophysical tuning curves and masking" J Acoust Soc Am 67 2: 638–43 PMID 7358904 doi:101121/1383888  Cited in: Moore BC 2001 "Dead Regions in the Cochlea: Diagnosis, Perceptual Consequences, and Implications for the Fitting of hearing aids" Trends Amplif 5 1: 1–34 PMC 4168936  PMID 25425895 doi:101177/108471380100500102 
  14. ^ a b c d Sek, A; Alcántara, J; Moore, BC; Kluk, K; Wicher, A July 2005 "Development of a fast method for determining psychophysical tuning curves" International journal of audiology 44 7: 408–20 PMID 16136791 doi:101080/14992020500060800 
  15. ^ a b Summers, V; Molis, MR; Müsch, H; Walden, BE; Surr, RK; Cord, MT April 2003 "Identifying dead regions in the cochlea: psychophysical tuning curves and tone detection in threshold-equalizing noise" Ear and hearing 24 2: 133–42 PMID 12677110 doi:101097/01AUD000005814827540D9 
  16. ^ Huss M, Moore BCJ 2005 "Dead Regions and noisiness of pure tones" Int J Audiol 44 10: 599–611 PMID 16315451 doi:101080/02640410500243962 
  17. ^ Kluk K, Moore BC 2006 "Dead regions and enhancement of frequency discrimination: Effects of audiogram slope, unilateral versus bilateral loss, and hearing-aid use" Hear Res 222 1–2: 1–15 PMID 17071031 doi:101016/jheares200606020 
  18. ^ Safieddine, Saaid; El-Amraoui, Aziz; Petit, Christine 2012 "The Auditory Hair Cell Ribbon Synapse: From Assembly to Function" Annual Review of Neuroscience 35: 509–28 PMID 22715884 doi:101146/annurev-neuro-061010-113705 
  19. ^ Wichmann, C; Moser, T 2015 "Relating structure and function of inner hair cell ribbon synapses" Cell and Tissue Research 361 1: 95–114 PMC 4487357  PMID 25874597 doi:101007/s00441-014-2102-7 
  20. ^ Nakagawa, Takayuki 2014 "Strategies for developing novel therapeutics for sensorineural hearing loss" Frontiers in Pharmacology 5: 206 PMC 4165348  PMID 25278894 doi:103389/fphar201400206 
  21. ^ "Sensorineural Hearing Loss" HealthCentral Retrieved 8 June 2013 
  22. ^ "Nutrients Prevent Noise Induced Hearing Loss" Webarchiveorg 2013-05-08 Archived from the original on 8 May 2013 Retrieved 2016-02-25 
  23. ^ Coenzyme Q10CoQ10 supports mitochondrial function and has significant antioxidant properties Quinzii 2010 Animal studies have found that supplementation with CoQ10 reduced noise-induced hearing loss and the death of hair cells Hirose 2008; Fetoni 2009, 2012 Human studies have also yielded promising results, as 160-600 mg of CoQ10 daily was found to reduce hearing loss in people with sudden sensorineural hearing loss and presbycusis Ahn 2010; Salami 2010; Guastini 2011 Also, a small preliminary trial found that CoQ10 supplementation alleviated tinnitus in those whose CoQ10 blood levels were initially low Khan 2007 Another small trial found CoQ10 may slow progression of hearing loss associated with a mitochondrial genetic mutation Angeli 2005
  24. ^ "Sound Pharmaceuticals submits positive Phase 2 clinical trial data on SPI-1005 for the - SEATTLE, Feb 18, 2014 /PRNewswire/" Prnewswirecom Retrieved 2016-02-25 
  25. ^ Parker, M A 2011 "Biotechnology in the Treatment of Sensorineural Hearing Loss: Foundations and Future of Hair Cell Regeneration" Journal of Speech, Language, and Hearing Research 54 6: 1709–1731 PMC 3163053  PMID 21386039 doi:101044/1092-43882011/10-0149 
  26. ^ "Study Using Stem Cells to Treat Sensorineural Hearing Loss Underway" HealthyHearing 2 February 2012 Retrieved 8 June 2013 
  27. ^ "Sudden Deafness | Massachusetts Eye and Ear" Masseyeandearorg Retrieved 2016-02-25 
  28. ^ "H912" ICD-10 Version:2010 appswhoint 2010 
  29. ^ Bennett, M H; Kertesz, T; Perleth, M; Yeung, P; Lehm, J P 17 October 2012 "Hyperbaric oxygen for idiopathic sudden sensorineural hearing loss and tinnitus Review" Cochrane Database of Systematic Reviews 10: CD004739 PMID 23076907 doi:101002/14651858CD004739pub4 
  30. ^ a b McCall AA; et al 2010 "Drug delivery for treatment of inner ear disease: current state of knowledge" Ear Hear 31 2: 156–65 PMC 2836414  PMID 19952751 doi:101097/AUD0b013e3181c351f2 CS1 maint: Explicit use of et al link
  31. ^ Crane RA; et al 2015 "Steroids for treatment of sudden sensorineural hearing loss: a meta-analysis of randomized controlled trials" Laryngoscope 125 1: 209–17 PMID 25045896 doi:101002/lary24834 CS1 maint: Explicit use of et al link
  32. ^ Suckfuell M; et al 2014 "Efficacy and safety of AM-111 in the treatment of acute sensorineural hearing loss: a double-blind, randomized, placebo-controlled phase II study" Otol Neurotol 35 8: 1317–26 PMID 24979398 doi:101097/mao0000000000000466 CS1 maint: Explicit use of et al link

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