Sensorineural hearing loss ( SNHL ) is a type of hearing loss, or deafness, where the root cause lies in the inner ear or sensory organs (cochlea and related structures) or the vestibulocochlear nerve ( cranial nerve VIII). SNHL accounts for about 90% of reported hearing loss. SNHL is generally permanent and may be mild, moderate, severe, deep, or total. Various other descriptors may be used depending on the shape of the audiogram, such as high frequency, low frequency, U shape, notched, peaked, or flat.
Sensory Hearing loss often occurs as a result of damaged or deficient cochlear hair cells. Hair cells may be abnormal at birth, or be damaged during an individual's lifetime. There are external causes of damage, including voice trauma, infection, and ototoxic drugs, as well as intrinsic causes, including genetic mutations. A common cause or an exacerbation factor in sensory hearing loss is prolonged exposure to environmental noise, for example, being in a tough workplace without the use of a shield or using headphones at high volume for long periods of time. Exposure to very loud sounds like a bomb blast can cause hearing loss caused by sound.
Neural , or "retrocochlear", hearing loss occurs due to damage to the cochlear nerves (CVIII). This damage can affect the initiation of nerve impulses in the cochlear nerve or the transmission of nerve impulses along the nerve to the brain stem.
Most cases of SNHL present with a gradual decrease in threshold hearing over the years to decades. In some cases, loss can ultimately affect most frequency ranges. It may be accompanied by other symptoms such as ringing in the ears (tinnitus) and dizziness or dizziness (vertigo). The most common type of sensorineural hearing loss is age-related (presbycusis), followed by noise-induced hearing loss (NIHL).
The common SNHL symptoms are the loss of sharpness in distinguishing the foreground from a noisy background, the difficulty of understanding the phone, some sounds that sound too loud or shrill, difficulty understanding fricatives and sibilants, losing direction (especially with high-frequency voice), the perception that people mumble while talking, and have trouble understanding the conversation. Similar symptoms are also associated with other types of hearing loss; audiometry or other diagnostic tests are required to differentiate sensorineural hearing loss.
Identification of sensorineural hearing loss is usually done by performing a pure tone audiometry (audiogram) in which the bone conduction threshold is measured. Tympanometry and speech audiometry can be helpful. Testing is done by audiologist.
There is no proven or recommended treatment or cure for SNHL; management of hearing loss usually with hearing strategies and hearing aids. In the case of deep or total deafness, a cochlear implant is a special hearing aid that can restore the functional level of hearing. SNHL is at least partially preventable by avoiding environmental noise, chemicals and ototoxic drugs, and head trauma, and treating or injecting against certain disease and trigger conditions such as meningitis.
Video Sensorineural hearing loss
Signs and symptoms
Because the inner ear is not directly accessible to the instrument, identification is done with patient reports and audiometric testing. Among those who came to their doctors with sensorineural hearing loss, 90% reported experiencing hearing loss, 57% reported having feelings stuck in the ear, and 49% reported having ringing in the ears (tinnitus). About half the problem of vestibular reports (vertigo).
For a detailed description of useful symptoms for screening, a self-assessment questionnaire was developed by the American Academy of Otolaryngology, called Hearing Inventory for Hearing for Adults (HHIA). This is a 25-question survey about subjective symptoms.
Maps Sensorineural hearing loss
Cause
Sensoryineural hearing loss may be genetic or acquired (ie as a consequence of illness, noise, trauma, etc.). People may experience congenital hearing or hearing loss may occur later. Many cases are related to old age (age-related).
Genetic
Hearing loss can be inherited. More than 40 genes have been identified causing deafness. There are 300 syndromes with associated hearing loss, and each syndrome may have a causative gene.
Recessive, dominant, X-linked or mitochondrial gene mutations may affect the structure or metabolism of the inner ear. Some may be single point mutations, while others are due to chromosomal abnormalities. Some genetic causes cause late hearing loss. Mitochondrial mutations may cause SNHL ie m.1555A & gt; which makes individuals sensitive to the ototoxic effects of aminoglycoside antibiotics.
- The most common cause of congenital hearing loss is recessive genetic in developed countries is DFNB1, also known as Connexin deafness or deafness related GJB2.
- The most common forms of syndromic hearing loss include Stickler syndrome (dominant) and Waardenburg syndrome, and (recessive) Pendred syndrome and Usher syndrome.
- Mitochondrial mutations cause rare deafness: MT-TL1 mutations cause MIDD (Maternally lowered guard and diabetes) and other conditions that may include deafness as part of the picture.
- The TMPRSS3 gene is identified by its association with congenital autosomal recessive oncell and childhood. This gene is expressed in the 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 perilymph and endolymph. It was also identified as tumor-associated tumors overexpressed in ovarian tumors.
- Charcot-Marie-Tooth disease is a delayed onset of neurologic disorder that affects the ear and other organs. Hearing loss in these conditions is often an ANSD (auditory neuropathy spectrum disorder) is the cause of neurological hearing loss.
- Muckle-Wells syndrome, a rare congenital autoinflammatory disorder, can cause hearing loss.
- Autoimmune disease: although it may be rare, it is possible for an autoimmune process to target specific cochlea, with no symptoms affecting other organs. Granulomatosis with polyangiitis, an autoimmune condition, can trigger hearing loss.
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- Infection:
- Congenital rubella syndrome, CRS, results from transplacental transmission of the rubella virus during pregnancy. CRS has been controlled by universal vaccinations (MMR or MMRV).
- Toxoplasmosis, a parasitic disease that affects 23% of the US population, can cause sensorineural deafness to the fetus in the womb.
- Hypoplastic hearing nerve or cochlear abnormalities
Presbycusis
Loss of age-related normal hearing deafness or sensitivity begins at age 18, especially affecting high frequency, and men more than women. Such losses may not be visible until much later. Presbycusis is by far the dominant cause of sensorineural hearing loss. Hearing loss accumulates with age but is caused by factors other than normal aging, such as hearing loss caused by noise, rather than presbycusis, although distinguishing the individual effects of many causes of hearing loss can be difficult. One in three had significant hearing loss at age 65; at age 75, one out of two. Age-related hearing loss can not be prevented or corrected.
Acquired
Noise
Most people living in modern societies suffer from progressive sensorineural disorders (ie permanent) hearing-impaired hearing loss and impair sensory or hearing nerves in the inner ear. NIHL is usually drop-out or notch centered on 4000 Hz. Both the intensity (SPL) and the duration of exposure, and repeated exposure to unsafe noise levels contribute to cochlear damage that causes hearing loss. The louder the sound, the shorter the amount of safe exposure. NIHL can be permanent or temporary, called threshold shift. Unsafe noise levels can be as small as 70 dB (about twice as hard as normal conversations) if there is prolonged extension (24 hours) or continuously. 125 dB (hard rock concert is ~ 120 dB) is the level of pain; sound above this level causes instant and permanent ear damage.
Noise and aging are the main causes of presbycus, or age-related hearing loss, the most common type of hearing loss in industrialized societies.
The cause of noise-related hearing loss is divided into extrinsic (nosocusis) and intrinsic (sosiocusis) causes. In the auditory system, extrinsic components include hearing loss due to otologic disease, dangerous sound exposure, acoustic trauma, and muscle-tic agents. The intrinsic component shows the wear and tear effects of normal everyday sound exposure. People living in non-industrial areas avoid both nosocusis and sociocusis and show excellent hearing to old age.
The hazards of exposure to environmental noise and occupation are widely recognized. Many national and international organizations have set standards for safe noise levels in industry, environment, military, transportation, agriculture, mining and other fields. Sound intensity or sound pressure level (SPL) is measured in decibels (dB). As reference:
A 6 dB increase represents a doubling of SPL, or sound wave energy, and therefore a tendency to cause ear damage. Since the human ear hears logarithmically, not linearly, it needs an increase of 10 dB to produce a sound that is considered twice as hard. The ear damage due to noise is proportional to the sound intensity, not the perceived loudness, so it is misleading to rely on subjective perceptions of loudness as an indication of the risk of hearing, that is, it can significantly underestimate the danger.
While standards differ moderately in intensity levels and the duration of exposure is considered safe, some guidelines may be lowered.
Some of the over-the-counter medicines as well as prescription drugs and certain industrial chemicals are ototoxic. This exposure may cause temporary or permanent hearing loss.
Some drugs cause permanent damage to the ear, and are limited in their use for this reason. The most important group is the aminoglycoside (the main member of gentamicin). Rare mitochondrial mutations, m.1555A & gt; may increase the susceptibility of individuals to the effects of ototoxic aminoglycosides. Abuse of long-term hydrocodon (Vicodin) is known to cause progressive sensorineural hearing loss, usually without vestibular symptoms. Methotrexate, a chemotherapy agent, is also known to cause hearing loss. In many cases, hearing loss does not recover when the drug is stopped. Paradoxically, methotrexate is also used in the treatment of hearing impairment caused by autoimmune inflammation.
Various other drugs can decrease hearing in a reversible way. These include loop diuretics, sildenafil (Viagra), high doses or sustained NSAIDs (aspirin, ibuprofen, naproxen, and various prescription medications: celecoxib, etc.), quinine, and macrolide antibiotics (erythromycin, etc.).
Prolonged or repeated exposure of the environment or work to the chemicochemicals may also cause sensorineural hearing loss. Some of these chemicals are:
- butyl nitrite - a chemical used recreationally known as "poppers"
- carbon disulfide - a solvent used as a building block in many organic reactions
- styrene, chemical precursors of the polystyrene industry, plastics
- carbon monoxide, a toxic gas produced from incomplete combustion
- heavy metals: lead, tin, manganese, mercury
- hexane, industrial solvents and one of the important constituents of gasoline
- ethylbenzene, industrial solvents used in styrene production
- toluene and xylene, highly toxic petrochemical solvents. Toluene is a high-octane gasoline component; xylene is used in the production of fibers and polyester resins.
- trichloroethylene, industrial degreasing solvents
- Organophosphoric pesticides
Head trauma
There can be damage either to the ear itself or to the central auditory track that processes the information conveyed by the ear. People suffering from head injuries are prone to hearing loss or tinnitus, whether temporary or permanent. Contact sports like football (U.S. NFL), hockey, and cricket have a head injury incident (concussion). In one survey of retired NFL players, all of whom reported one or more concussions during their playing career, 25% had hearing loss and 50% had tinnitus.
Perinatal condition
This is much more common in premature infants, especially those under 1500 at birth. Premature birth may be associated with problems causing sensorineural hearing loss such as anoxia or hypoxia (poor oxygen levels), jaundice, intracranial hemorrhage, meningitis. Fetal alcohol syndrome is reported to cause hearing loss in up to 64% of babies born to alcoholic mothers, from the autotoxic effects on developing fetuses, plus malnutrition during pregnancy due to excessive alcohol intake.
Lack of iodine/Hypothyroidism
Iodine deficiency and endemic hypothyroidism are associated with hearing loss. If a pregnant woman is not getting enough iodine intake during pregnancy it affects the development of the inner ear on the fetus leading to sensorineural deafness. It occurs in certain areas of the world, such as the Himalayas, where iodine lacks soil and thus diet. In these areas there is a high incidence of endemic endemism. The cause of this deaf is prevented by adding iodine to salt.
Brain stroke
Brain strokes in an area affecting hearing function such as posterior circulatory infarction have been associated with deafness.
Diagnosis
Case history
Prior to the examination, case histories provide guidance on the context of hearing loss.
- main concern
- pregnancy and delivery information
- medical history
- development history
- family history
Otoscopy
Direct examination of external channels and tympanic membrane (eardrum) with otoscope, medical device inserted into ear canal using light to check the condition of external ears and tympanic membrane, and middle ear through semi-translucent membrane.
Differential testing
Differential tests are most useful when there is unilateral hearing loss, and differentiate the conductive from sensorineural loss. This is done with a low frequency tuning fork, usually 512 Hz, and air and bone contrast measurements are transmitted.
- Weber test, where tuning fork is touched to the midline of the forehead, localized normal ears in people with unilateral sensorineural hearing loss.
- The Rinne test, which tests air conduction vs. bone conduction is positive, since bone and air conduction is reduced equally.
- Bing and Schwabach variants are less common than Rinne tests.
- Bone conduction absolute test (ABC).
Table 1 . The table compares the sensorineural with conductive hearing loss
Other auditory function tests, more complex, are needed to differentiate different types of hearing loss. Bone conduction thresholds can differentiate sensorineural hearing loss from conductive hearing loss. Other tests, such as auto-acoustic emissions, acoustic stapedial reflexes, sound audiometry and audiometric response are required to distinguish sensory, nerve and hearing loss.
Tympanometry
Tympanogram is a test result with a tympanometer. It tests the function of the middle ear and mobility of the eardrum. It may help identify conductive hearing loss due to middle ear disease or eardrums from other types of hearing impairment including SNHL.
Audiometry
Audiogram is the result of a hearing test. The most common type of hearing test is pure pure Audiometry (PTA). It maps the hearing sensitivity threshold on a standard frequency selection between 250 and 8000 Hz. There is also a high frequency pure tone audiometry that tests frequencies from 8,000-20,000 Hz. PTA can be used to distinguish between conductive hearing loss, sensorineural hearing loss and mixed hearing loss. Hearing loss can be depicted on the degree of mild, moderate, severe or deep, or the shape of high or low frequency, low frequency or rising, curved, U-shaped or 'bite', peaked or flat.
There are also other types of audiometry designed to test the sharpness of hearing rather than sensitivity (speech audiometry), or to test the transmission of auditory nerve pathways (generating an audiometric response).
Magnetic resonance imaging
MRI scans can be used to identify the causes of structural hearing loss. They are used for congenital hearing loss when deformation of the inner ear or hearing nerve can help diagnose the cause of hearing loss. They are also useful in cases where the tumor is suspected or to determine the extent of damage to hearing loss caused by a bacterial infection or auto-immune disease. Scanning has no value in deaf due to age.
Pathophysiology
Sensory hearing loss is caused by the abnormal structure or function of the organs of the organs in the cochlea. Impaired nerve hearing due to damage to the eighth cranial nerve (vestibulocochlear nerve) or brainstem hearing tract. If a higher level of auditory channels is affected this is known as deafness. Central deafness may be present as sensorineural deafness but must be distinguished from historical and audiological testing.
Cochlear dead area in sensory hearing loss
Hearing loss may be associated with damage to the hair cells in the cochlea. Sometimes there may be a complete loss of function of deep hair cells (IHCs) over a particular area of ​​the cochlea; this is called "dead area". This region may be defined in terms of the characteristic frequency range (CF) of the IHC and/or neurons adjacent to the dead region.
koklear hair cells
Outer hair cells (OHCs) contribute to the Organ structure of the Corti, which lies between the basilar membrane and the tectorial membrane in the cochlea (See Figure 3). The corti tunnel, which flows through the Corti Organs, divides the OHC and the inner hair cells (IHCs). OHC is connected to the reticular laminar and Deiters cells. There are about twelve thousand OHCs in every human ear, and these are arranged in up to five lines. Each OHC has small bundles of 'hair', or cilia, on their upper surface known as stereocilia, and these are also arranged into highly rated rows. There are about 140 stereocilia on each OHC.
The fundamental role of OHC and IHCs serves as sensory receptors. The main function of IHCs is to transmit voice information through afferent neurons. They do this by transmitting mechanical motions or signals into neural activity. When stimulated, the stereocilia on the IHCs move, causing the flow of electric current to pass through the hair cells. This electric current creates an action potential in connected afferent neurons.
OHC is different because they actually contribute to the active mechanism of the cochlea. They do this by receiving mechanical signals or vibrations along the basilar membrane, and transmitting them into electrochemical signals. Stereosilia found in OHCs come into contact with the tectorial membrane. Therefore, when the basilar membrane moves due to vibration, stereocilia bend. The direction in which they are bent, determines the degree of burning of auditory neurons connected to the OHC.
The bending of stereocilia against the basal body of OHC causes the excitation of hair cells. Thus, an increase in the rate of burning of auditory neurons connected to hair cells occurs. On the other hand, bending of stereocilia from the basal body of OHC causes inhibition of hair cells. Thus, a reduced burning rate of auditory neurons connected to hair cells occurs. OHCs are unique because they can contract and expand (electromotility). Therefore, in response to electrical stimuli provided by the efferent supply of nerve, they can alter length, shape and stiffness. These changes affect the basilar membrane response to sound. It is therefore clear that OHC plays a major role in the active process of the cochlea. The main function of the active mechanism is to enhance the basilar membrane, and provide it with a high sensitivity to quiet sound. The active mechanism depends on the presence of the cochlea in good physiological conditions. However, the cochlea is very susceptible to damage.
Hair cell damage
SNHL is most often caused by damage to OHC and IHCs. There are two methods that make them become corrupted. First, the entire hair cell can die. Second, stereocilia may become distorted or destroyed. Cochlear damage can occur in several ways, for example by viral infections, exposure to ototoxic chemicals, and intense sound exposure. Damage to the OHC results in an ineffective active mechanism, or it may not work at all. OHCs contribute to providing high sensitivity to quiet sound over a certain frequency range (about 2-4 kHz). Thus, damage to the OHC results in a reduction in the sensitivity of the basilar membrane to weak sounds. Amplification of these sounds is required, so the basilar membrane responds efficiently. IHCs are less susceptible to damage compared to OHC. However, if they become damaged, this will result in a total loss of sensitivity.
Neural tuning curves
Frequency selectivity
Waves travel along the top of the basilar membrane in different places along it, depending on whether the sound is low or high frequency. Due to the mass and stiffness of the basilar membrane, the peak of the low frequency wave is at the peak, while the high frequency sounds peak at the tip of the cochlear basal. Therefore, each position along the basilar membrane is set to a specific frequency. This adjusted special frequency is called the characteristic frequency (CF).
If the sound entering the ear moves from the characteristic frequency, then the response strength of the basilar membrane will decrease. The fine tuning of the basilar membrane is created by the input of two separate mechanisms. The first mechanism is a linear passive mechanism, which depends on the mechanical structure of the basilar membrane and surrounding structures. The second mechanism is a non-linear active mechanism, which depends mainly on the function of OHC, as well as the general physiological conditions of the cochlea itself. The base and peak of the basilar membrane differ in stiffness and width, causing the basilar membrane to respond to different frequencies along its length. The base of the basilar membrane is narrow and rigid, thus responding best to high-frequency sound. The peak of the basilar membrane is wider and much less than the base, causing it to respond best to low frequencies.
This selectivity for a particular frequency can be illustrated by a neural tuning curve. This shows the fiber frequency responding, by indicating the threshold level (dB SPL) of the auditory nerve fibers as a function of different frequencies. This shows that the auditory nerve fibers provide the best response, and therefore have a better threshold on the frequency characteristics and frequency of the fibers that surround it. The basilar membrane is said to be 'sharply tuned' because the sharp 'V' curve, with its 'end' centered on the characteristic frequency of auditory fibers. This form shows how some fiber frequencies respond. If it's a broader 'V' shape, it will respond to more frequencies (See Figure 4).
IHC vs OHC hearing loss
A normal neural tuning curve is characterized by a broadly tuned 'tail' of frequency, with a finely tuned center 'tip'. However, where there is partial or complete damage to the OHC, but with unharmed IHCs, the resulting tuning curve will show the deletion of sensitivity to a quiet sound. That is. in which the neural tuning curve is usually most sensitive (at 'tip') (See Figure 5).
Where both OHC and IHCs are damaged, the resulting neural tuning curve will show the deletion of sensitivity to the 'tip'. However, due to IHC damage, the entire adjustment curve becomes increased, giving a loss of sensitivity across all frequencies (See Figure 6). This is only necessary for the first row of damaged OHCs due to deletion of the 'tip' set to happen. This supports the idea that the incidence of OHC damage and thus the loss of sensitivity to quiet sounds, occurs more than IHC losses.
When IHC or part of the basilar membrane is damaged or destroyed, so they no longer function as transducers, the result is 'dead area'. The dead region can be defined in terms of the frequency of IHC characteristics, related to the specific place along the basilar membrane where the dead area occurs. Assuming that there is no shift in characteristic frequencies associated with a particular region of the basilar membrane, due to OHC damage. This often happens with IHC damage. The dead area may also be defined by anatomical sites of non-functioning IHCs (such as "apical dead regions"), or by the frequency of IHC characteristics adjacent to the dead area.
Audiometry of dead region
Pure tone audiometry (PTA)
The dead area affects the audiometry results, but may not be as expected. For example, it may be expected that the threshold will not be obtained at frequencies inside the dead area, but will be obtained at frequencies adjacent to the dead region. Therefore, assuming normal hearing is around the die region, it will produce a dramatically steeper audiogram between the frequency at which the threshold is obtained, and the frequency at which the threshold can not be obtained due to the dead region.
However, this does not seem to be the case. The dead area can not be found clearly through the PTA audiogram. This may be because although neurons that inoculate the dead region, can not react to vibrations at their characteristic frequencies. If the vibration of the basilar membrane is large enough, the neuron is tuned to a different characteristic frequency as adjacent to the dead region, will be stimulated due to the spread of excitation. Therefore, the patient's response to 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 found false threshold. Thus, it appears that a person has better hearing than the actual one, thereby causing the dead area to be missed. Therefore, using PTA alone, it is not possible to identify the level of dead region (See Figures 7 and 8).
Consequently, how many audiometric thresholds are affected by tones with their frequencies in the dead area? It depends on the location of the dead region. The threshold at low frequency die area, more inaccurate than the high frequency die area. This has been attributed to the fact that excitation due to vibration of the basilar membrane spreads upward from the apical region of the basilar membrane, more than the excitation spreads downward from the higher basal area of ​​the frequency of the cochlea. This pattern of excitation spread is similar to the 'upward spreading' phenomenon. If the tone is loud enough to produce sufficient excitation in a functioning normal cochlear area, it is above the threshold of the area. The tone will be detected, because it listens to low frequencies that produce a misleading threshold.
To help solve PTA problems that result in inaccurate thresholds in the dead area, covering the area outside the dead area that is being stimulated can be used. This means that the responding area threshold is raised enough, so it can not detect the spread of excitation from the tone. This technique has led to suggestions that low frequency die areas may be associated with a 40-50 dB loss. However, as one of the purposes of PTA is to determine whether there are dead areas or not, it may be difficult to assess which frequencies should be closed without using other tests.
Based on research it has been suggested that low frequency die areas can result in relatively flat losses, or losses that are highly skewed towards higher frequencies. Because the dead area will be less detectable due to the spread of excitation upward. In fact, there may be a sharper and steeper losses at high frequencies for high frequency die areas. Although it is likely that the slope represents a downward depth that is less clear, than the accurate threshold for those frequencies with non-functioning hair cells. The intermediate frequency dead area, with a small range, appears to have a less effect on the patient's ability to hear in everyday life, and can generate a notch on the PTA threshold. Although it is clear that PTA is not the best test to identify dead areas.
Psychoacoustic (Psychoacoustic) shoots and threshold equalization noise (TEN) test
Although some debate continues regarding the reliability of such tests, it has been suggested that the psychoacoustic tuning curve (PTC) and the sound threshold (TEN) results may be useful in detecting dead areas, rather than PTA. PTC is similar to the neural tuning curve. They describe the level of mask (dB SPL) tone on the threshold, as a function of deviation from the middle frequency (Hz). They are measured by presenting a pure, low-intensity tone fixed while also presenting a narrow-band mask, with variable center frequencies. The mask level varies, so the level of mask required to simply disguise the test signal is found for the mask in every center frequency. The tip of the PTC is where the mask level required to disguise the test signal is the lowest. For normal hearing, this is when the center frequency of the mask is closest to the signal test frequency (See Figure 9).
In the case of the dead area, when the test signal lies within the borders of the dead region, the PTC tip will shift to the edge of the dead area, to a functioning area and detect the spread of excitation from the signal. In the case of a low frequency die area, the tip shifts upward indicating a low-frequency die area starting at the end of the curve. For high frequency off areas, the tip is shifted down from the signal frequency to the area that works below the dead area. However, the traditional method of obtaining PTC is not practical for clinical use, and it has been said that TEN is not accurate enough. A quick method to find PTC has been developed and can provide solutions. However, further research to validate this method is necessary, before it can be clinically accepted.
Consequences of perception of dead region
Audiogram configuration is not a good indicator of how a dead region will affect a person functionally, especially because of individual differences. For example, a slanted audiogram often comes with a dead area, due to the spread of excitation. However, the individual may be affected differently from a person with an appropriate skewed audiogram caused by partial damage to hair cells rather than dead areas. They will feel different sounds, but the audiogram shows that they have the same loss rate. Huss and Moore investigated how patients with hearing impairment felt a pure tone, and found that they felt the tone as noisy and distorted, more (average) than people without hearing impairment. However, they also found that the perception of the tone as sound-like, is not directly related to the frequency in the dead area, and therefore is not an indicator of the dead region. Therefore this shows that the audiogram, and their poor representation of the dead region, are an inaccurate predictor of the patient's perception of pure tone quality.
Research by Kluk and Moore has shown that dead areas can also affect the patient's perception of frequencies outside the dead area. There is an increased ability to distinguish between very few different tones of frequency, in areas outside the dead area compared to the more distant tones. An explanation for this may be cortical mapping has occurred. Where, a neuron normally stimulated by a dead region, it has been moved to respond to the functioning area around it. This leads to over-representation of these areas, resulting in increased perception sensitivity to small tone frequency differences.
Vestibulocochlear nerve pathology
- built-in deformity of the internal auditory channel, neoplastic and pseudo-neoplastic lesions, with special emphasis on schwannoma on the eighth cranial nerve (acoustic neuroma),
- The non-neoplastic Internal Auditory Line/CerebelloTopin Angle pathology, including the vascular loop,
Prevention
Presbycucis is a major cause of SNHL and is progressive and unavoidable, and currently, we have no somatic therapy or genes to combat the hereditary-related SNHL. But other causes of acquired SNHL are largely preventable, especially causes of nosocusis. This will involve avoiding environmental noise, and traumatic sounds such as rock concerts and nightclubs with loud music. The use of noise attenuation measures such as acoustic ear plugs is an alternative.
Treatment
Treatment modalities are divided into three categories: pharmacological, surgical, and management. Because SNHL is a physiological degradation and is considered permanent, there is currently no treatment approved or recommended.
There have been significant advances in the identification of human deafness genes and their explanation of cellular mechanisms as well as their physiological function in mice. However, pharmacological treatment options are very limited and not clinically proven. Pharmaceutical treatments such as those used are palliative rather than curative, and addressed to the underlying cause if a person can be identified, to prevent progressive damage.
Huge or total hearing loss may be managed by management with cochlear implants, which stimulate cochlear nerve endings directly. Cochlear implants are surgical implantation of battery-powered electronic medical devices in the inner ear. Unlike hearing aids, which make the sound louder, cochlear implants do the work of the damaged part of the inner ear (cochlea) to provide a sound signal to the brain. It consists of both internal and embedded internal electrodes and components. The sound quality is different from natural hearing but can allow the receiver to better recognize speech and sound environment. Due to risks and costs, such operations are provided for cases of severe hearing loss and disability
Management of sensorineural hearing loss involves using strategies to support existing hearing such as lip reading, improved communication etc. and amplification using hearing aids. Hearing aids are specifically tailored to individual hearing loss to provide maximum benefit.
Research
Pharmacy
- Vitamin antioxidants - Researchers at the University of Michigan report that a combination of high doses of vitamin D, C, and E, and Magnesium, is taken one hour before exposure to noise and continued as a one-day treatment for five days. day, is very effective to prevent hearing loss caused by noise in animals.
- Plant - brand name for Ginkgo biloba international prescription drug extract. These are classified as vasodilators. Among his studies using sensorineural and tinnitus deafness are thought to originate from blood vessels.
- Coenzyme Q10 - a substance similar to vitamins, with antioxidant properties. It is made in the body, but its level decreases with age.
- ebselen, a synthetic drug molecule that mimics glutathione peroxidase (GPx), an important enzyme in the inner ear that protects it from damage caused by loud noises or sounds
Stem cells and gene therapy
Regeneration of hair cells using stem cells and gene therapy is many years or decades away from clinically feasible. However, research is currently being conducted on the subject, with the first FDA-approved trial begun in February 2012.
Sudden sensorineural hearing loss
Sudden sensorineural hearing loss (SSHL), commonly known as sudden deafness, occurs as a hearing, rapidly hearing loss, usually in one ear - either simultaneously or for several days. Nine out of ten people with SSHL lose their hearing in just one ear. This should be considered a medical emergency. Delaying diagnosis and treatment can make the treatment less effective or ineffective.
Experts estimate that SSHL attacks one person per 5,000 each year, usually adults in their 40s and 50s. The actual number of new SSHL cases each year can be much higher because these conditions are often undiagnosed.
Presentations
Many people notice that they have SSHL when they wake up in the morning. Other people first see it when they try to use deaf ears, like when they use the phone. Still others see a hard and worrisome "pop" just before their hearing disappears. People with sudden deafness often become dizzy, ear buzzing (tinnitus), or both.
Diagnosis
SSHL is diagnosed through pure tone audiometry. If the test indicates a loss of at least 30db in three adjacent frequencies, then the hearing loss is diagnosed as SSHL. For example, a 30dB hearing loss will make the conversation sound more like a whisper.
Cause
Only 10 to 15 percent of cases diagnosed as SSHL have an identifiable cause. Most cases are classified as idiopathic, also called idiopathic sudden hearing loss (SIHL) and idiopathic sudden hearing sensorineural (ISSHL or ISSNHL) The majority of evidence suggests some type of inflammation in the inner ear as the most common cause of SSNHL.
- Viral - Swelling may be caused by a virus. Herpes-type virus is believed to be the most common cause of sudden sensorineural hearing loss. The herpes virus falls asleep on our body and goes back on for an unknown reason.
- Ischemia inner inner vascular or cranial nerve VIII (CN8)
- Perilymph fistula, usually due to rupture of round or oval windows and perilymph leak. Patients will usually also experience vertigo or imbalance. History of trauma is usually present and changes in hearing or vertigo occur with changes in intracranial pressure such as straining; lift, blow etc.
- Autoimmune - can be caused by autoimmune diseases such as systemic lupus erythematosus, granulomatosis with polyangiitis
Treatment
About half of people with SSNHL will recover part or all of their hearing spontaneously, usually within one to two weeks of onset. Eighty-five percent of those receiving treatment from an otolaryngologist (sometimes called ENT) will recover some of their hearing.
- vitamins and antioxidants
- vasodilator
- betahistine (Betaserc), anti-vertigo drug
- hyperbaric oxygen
- anti-inflammatory agents, especially oral corticosteroids such as prednisone, methylprednisone
- Intratympanic Administration - Gel formulations are being investigated to provide a more consistent delivery of drugs to the inner ear. Local drug delivery can be achieved through intratympanic administration, a minimally invasive procedure in which the eardrum is anesthetized and medication is given to the middle ear. From the middle ear, the drug can diffuse across the round window membrane into the inner ear. Intratympanic steroids may be effective for impaired sensorineural hearing loss for some patients, but high quality clinical data have not been produced. Intratympanic administration of anti-apoptotic peptide (inhibitor JNK) is currently being evaluated in late stage clinical development.
See also
- The loss of conductive hearing, hearing loss is mainly due to conditions in the middle ear
- Cortical deafness, another type of nerve deaf
- Hearing loss
- The inner ear, the innermost part of the ear containing sensorineural hearing
- Otosclerosis, hearing-impaired auditory ear hearing or hearing loss
- Tinnitus, ringing in the ear, SNHL general accompaniment
Note
References
External links
- Hearing Loss Web,
Source of the article : Wikipedia
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