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The entities of nosiocusis (hearing loss from pathologic processes), sociocusis (from everyday noise exposure) and presbycusis (from age related change) form the subgroups of acquired hearing loss.
A mixed hearing loss occurs when both a sensorineural and conductive hearing loss are present at the same time. According to the 1990 Noise and Hearing Loss Consensus Conference, a€?Noise Induced Hearing Loss (NIHL) results from damage to the ear from sounds of sufficient intensity and duration that a temporary or permanent sensorineural hearing loss is produced.
PTS refers to a permanent loss of sensorineural hearing which is the direct result of irreparable injury to the organ of Corti.
The 4000 Hz a€?notcha€? or a€?dipa€? in sensorineural hearing has been a classic finding in NIHL over the years. Why the 4000 Hz frequency appears more affected than other frequencies continues to generate some controversy.
Individuals vary in their susceptibility to noise and the damage it may cause to the cochlea. Of interest, one near universal finding is that on average, hearing threshold levels (HTLa€™s) in the right ear are better than the left ear by about 1 dB.
Whether one ear is more resilient to noise in the same individual (the so-called a€?tough vs. Please remember that when an asymmetric sensorineural hearing loss exists, steps often need to be taken to exclude pathologic causes (i.e. The following statements tend to reflect what is agreed upon by the majority of scientists and physicians who deal with NIHL. Noise induced hearing loss (NIHL) may produce a temporary threshold shift (TTS), permanent threshold shift (PTS) or a combination of both.
A PTS is caused by destruction of certain inner ear structures that cannot be replaced or repaired.
NIHL typically affects higher frequency hearing than those frequencies essential for communication (i.e.
The pathologic basis for presbycusis appears to be one of gradual devascularization of the cochlea and loss of functioning hair cells. Clinically, hearing loss from presbycusis appears to be an accelerating process unlike hearing loss in NIHL. Unfortunately, there is no specific treatment available that will prevent age related hearing loss at present.
In the adjudication process of an occupational NIHL claim, it is often difficult to separate the total amount of hearing loss from noise and age-related change. For example, not everyone as they age will experience age-related presbycutic change (changes from presbycusis are variable with some individuals experiencing greater degrees of age-related change than others). Moreover, exposure to high level noise early on may produce hearing loss more rapidly than aging, such that the aging process has a negligible effect (i.e. The effects of noise exposure and aging on hearing when not combined are reasonably well understood. Although it seems logical to a€?subtracta€? the age-related effects from the total hearing loss in order to quantify the amount of hearing loss due to noise, this is really quite simplistic when one considers that aging effects and noise exposure can at times be practically indistinguishable from one another. Because compensation claims have required some consideration of presbycusis and its role in the total hearing loss of an individual, various correction factors have been applied.
Dobiea€™s theorem states that the total hearing loss from noise and age are essentially additive (this is the theory put into practice when a standard correction factor after age 60 years is applied, in the Province of Ontario for example).
Corsoa€™s theorem on the other hand states that any correction for age should be based on a variable ratio (as individuals age, the assumption is that the effects of presbycusis variably accelerate by decade). Nevertheless, quantification of hearing loss attributable to age when occupational NIHL is present is really quite a complex phenomenon. This is an inner ear disorder characterized by episodes of vertigo (an illusion of movement) lasting minutes to hours, fluctuant hearing loss and tinnitus (unwanted head noise).
Usually one ear is involved initially although, over time, the other ear becomes involved in nearly 50% of cases.
Treatment is medical in most cases involving a low salt diet and diuretics and vestibular sedatives. Otosclerosis usually results in a conductive hearing loss from stapes footplate fixation when new bone grows in this area. The diagnosis of cochlear otosclerosis is usually made when a familial history of otosclerosis exists and other rare causes for a chronic progressive loss can be excluded. Although no medical treatment can ever reverse the sensorineural hearing loss, treatment with oral sodium fluoride may minimize and possibly stabilize an affected individuala€™s hearing.
Physical injury to the ear is usually the result of blunt trauma in the circumstances of a significant head injury. When physical trauma is severe enough to cause a temporal bone fracture (the temporal bone is the larger part of the skull bone that houses all the structures of the ear), two types of fractures occur: longitudinal and transverse.
Transverse fractures of the temporal bone occur when the fracture lines run directly through the hard bone of the otic capsule.
Ototoxicity is defined as the tendency of certain substances to cause functional impairment and cellular damage to the tissues of the inner ear, especially to the cochlea and the vestibular apparatus.
Aminoglycoside antibiotics are powerful weapons in the treatment of certain bacterial infections. Anti-malarial drugs such as quinine and chloroquin unfortunately have ototoxicity as side effects if taken in excess. Heavy metal, asphyxiant and solvent exposure at certain levels have all been implicated to cause chemical induced hearing loss. This is a pathologic misnomer since this tumour is strictly a schwannoma of the vestibular nerve.
Although benign, this tumour has serious health implications for the patient and is sought by otolaryngologists when there is an undiagnosed asymmetry in hearing. These sudden losses are considered by the profession to be most likely viral or inflammatory in origin. An individuala€™s threshold hearing to pure tones at different frequencies (250-8000 Hz) is performed.
Air conduction (AC) thresholds are delivered via headphones and the individual is asked to respond to the sound of the lowest intensity (in dB) they hear at the frequency being tested. The pure tone audiogram forms the basis for assessing if an individual qualifies for compensation benefits.
Complex words with equal emphasis on both syllables (so-called spondaic words such as a€?hotdog,a€? a€?uptown,a€? a€?baseballa€? etc.) are given to an individual at the lowest intensity they can hear.
A list of phonetically balanced single syllable words (these are words commonly found in the English language in everyday speech such as a€?fat,a€? a€?as,a€? a€?doora€? etc.) are presented to an individual at 40dB above their speech reception threshold (SRT) in the ear being tested. In this test, a probe is placed into the ear canal that both emits a sound and can vary pressure within the canal which causes the ear drum to move. This tells whether the pressure in the middle ear is within normal limits and provides some indirect measurement of Eustachian tube function.
Stiffening of the ear drum from loud noise occurs when the stapedius muscle contracts in the middle ear.
Absent stapedial reflexes are usually seen in middle ear pathology such as otitis media with effusion or otosclerosis. If one measures how the ear drum moves when pressure is changed in the external ear canal from negative to positive, a series of curves can be attained.
If a TM perforation is present, it is impossible to obtain a a€?seala€? of the middle ear or a tympanogram.
The ability to measure minute electrical potentials following sound stimulation of the cochlea (i.e.
This test measures electrical activity in the cochlea during the first 2 msec of cochlear stimulation. This term is synonymous with the term brainstem evoked potential (BEP) or the brainstem evoked response audiogram (BERA). Changes in waveform morphology and latency of the ABR can be quite helpful in the assessment of an individual with an asymmetric sensorineural hearing loss if an acoustic neuroma is suspected. These electrical waveforms are usually identified between 50-200 msec following cochlear stimulation and are thought to represent cortical pathways of electrical activity.
One advantage of TEP testing is that the electrical waves can provide us with information concerning the actual threshold at a certain frequency an individual hears and, as such, gives us some objective measurement of an individuala€™s hearing that is not dependent on a voluntary response.
Otoacoustic emissions (OAEs) are actual minute sounds produced by the active vibration of the basilar membrane generated by the outer hair cells. OAEa€™s occur spontaneously without stimulation (spontaneous OAEs) or can be found as an evoked response to stimulation.
With transient OAEs, a broad stimulus is provided to the ear and most of the basilar membrane becomes involved.
With DPOAE testing, single frequency emissions are produced in response to 2 simultaneous stimulus tones. In its classic presentation, a notched sensorineural hearing loss is noted at 4000 Hz that should be relatively symmetric. Age-related hearing loss typically presents with a bilateral symmetric high frequency sensorineural hearing loss. There are often numerous discrepancies noted such as the presence of acoustic reflexes at levels below volunteered pure tone thresholds; discrepancies between the volunteered pure tone average and speech reception thresholds etc. Subjective tinnitus can only be appreciated by the affected individual, is usually associated with a sensorineural hearing loss of some type and is the most common type noted.
Objective tinnitus, on the other hand, is quite rare but by definition is a noise that can be appreciated by an observer. Regardless of cause, tinnitus can be quite disturbing for many individuals and can certainly affect their well being. The individual affected has undergone treatments to try and alleviate their perceived unwanted head noise (i.e. The question is easy to answer if tinnitus occurs at the time an individual is working and exposed to noise or perhaps occurs shortly thereafter (let's say within a 1 year time frame a€“ this is the time frame that many studies have used looking at the effects of acute acoustic trauma in an affected ear). Without sufficient evidence-based medicine to guide us, the decision of whether the delayed onset of tinnitus was caused in part by prior exposure to noise while in employment becomes to some degree the decision of the adjudicator.
The answer to the first part of the question is yes it could (despite my recommendations in question 1) but the scenario described seems more akin to the phenomenon of a temporary threshold shift (TTS).


Hearing aids on their own would not be considered to be the most appropriate tinnitus masker if there was no significant hearing loss present.
Hyperacusis is a curious phenomenon where an individual describes an uncomfortable, sometimes painful, hypersensitivity to sounds that would be normally well tolerated in daily life.
This is a very relevant question that is based on the definition of how hearing loss causes a handicap for the affected individual in their ability to identify spoken words or sentences under everyday conditions of normal living. Although the higher frequencies are initially affected in NIHL, an individual will really only begin to demonstrate a significant handicap to hearing everyday speech in a quiet surrounding when the average of the hearing thresholds at 500, 1000, 2000 ( + 3000) Hz is above 25 dB. The inclusion of the 3000 Hz threshold value for NIHL awards is not always required depending on the jurisdiction. In the province of Ontario, the Workplace Safety and Insurance Board (WSIB)a€™s Operation Policy Manual (OPM) Document No. A presbycusis (aging) correction factor of 0.5 dB is deducted from the measured hearing loss (averaged over the 500, 1000, 2000 and 3000 Hz frequencies) for every year the worker is over the age of 60 years at the time of the audiogram.
It is important to appreciate that decisions can also be made on an exceptional basis which the WSIB has recognized. Since individual susceptibility to noise varies, if the evidence of noise exposure does not meet the above exposure criteria, claims will be adjudicated on the real merits and justice of the case, having regard to the nature of the occupation, the extent of the exposure, and any other factors peculiar to the individual case. The above list does demonstrate a lack of uniformity in NIHL claims and benefits within Canada.
A comprehensive list of US comparisons for NIHL and benefits can be found in Table 35.1 pages 797-799 in the Chapter concerning State and Federal Formulae Differences in Occupational Hearing Loss, 3rd Edition. To conclude, this is really defined by what is called Corso's theorem, which implies that the majority of noise induced hearing loss occurs early on in noise exposure. It is likely that the two effects are not additive (Corsoa€™s theorem) but from a practical point of view this is how they are usually viewed with regards to compensation claims (Dobiea€™s theorem). One can speculate that this might be one of the reasons an individual early on in their exposures may not be aware of a hearing loss, only to appreciate a hearing loss later in life when other factors such as presbycutic change occur. The issue can be debated but at present we have no means of actually knowing on clinical grounds the degree of hair cell damage that has occurred on a microscopic basis from noise exposure in a living individual if hearing is still deemed as normal.
Although we think of presbycusis as an age-related event, not all individuals will develop this condition. Future genetic studies may provide us with further information concerning those at greater risk for progressive hearing loss from presbycusis in future. A TTS is considered to represent a pathological metabolically induced fatigue of the hair cells or other structures within the Organ of Corti.
In a PTS the destruction and eventual cochlear hair cell loss is thought to arise from direct mechanical destruction from high-intensity sound and from metabolic decompensation with subsequent degeneration of sensory elements. While one would normally expect full recovery of hearing function after a TTS, there is one important consideration that needs to be taken into account.
The position in the world literature continues to support that any progressive hearing loss from acute trauma ceases unless the individual is re-exposed to more acute acoustic trauma or some other factor(s) occurs (i.e.
The classic studies of acute acoustic trauma by Segal et al (1988) and Kellerhals (1991) are often used to support this position. In the cohort study by Segal et al, 841 individuals from either the regular US army or military reserve sustained a permanent sensorineural hearing loss from acute acoustic trauma without subsequent re-exposure. The importance of the Segal study is that after 1 year, one would not expect further worsening of hearing in subjects who ceased to have further noise exposure. Kellerhalsa€™ study reviewed a much smaller series of individuals who were exposed to acute acoustic trauma but looked at them over a 20 year duration.
Background: Acoustic shock injury has been described as a permanent injury to the auditory system either due to daily noise dose of in excess of 85 decibels or very loud impulse sound reputed to be in excess of 120 decibels and acoustic incidents.
13.Acoustic shock injury (ASI) MYRIAM WESTCOTT Dineen and Westcott Audiologists, Heidelberg, Victoria, Australia. Daily noise exposure (8hrs) > 90dB for over 5 years (or equivalent) causes varying degrees of hearing loss in susceptible individuals. NIHL is a decelerating process; the largest changes occur in the early years with progressively smaller changes in the later years (so-called Corsoa€™s theorem).
NIHL first affects hearing in the 3-6 kHz range for nearly all occupational exposures; the lower frequencies are less affected.
The hearing loss is typically a low-frequency sensorineural loss that fluctuates initially, often reverting close to normal between attacks in the early stages.
In general terms longitudinal fractures are much more common and tend to result in a fracture line through the roof of the middle ear and ear canal.
Treatment for tinnitus includes the use of more pleasurable competing background noise strategies (i.e.
In Veterans Affairs Canada's Entitlement Eligibility Guidelines, one of the causes of tinnitus is stated to be "Exposure to noise that is of sufficient intensity and duration to cause a hearing loss of 25 decibels (dB) or more at the 3000, 4000 or 6000 hertz (Hz) frequencies (in the ear(s) with tinnitus) prior to clinical onset." In your opinion, to be caused or contributed to by the above-described noise-exposure, must the tinnitus occur within any particular time frame?
Usually tinnitus is associated with some degree of sensorineural hearing loss but not always.
Using the VAC Entitlement Eligibility Guidelines one could reasonably accept that noise exposure which had caused a permanent loss of over 25dB at 3000, 4000 and 6000 Hz prior to leaving a noisy environment should be considered a contributing factor.
If there is an audiogram which shows a loss of 25 decibels or more at the 3000, 4000 or 6000 hertz frequency and a subsequent audiogram shows a drop to less than 25 decibels at the same frequency, could the noise exposure which caused the 25dB or more loss still cause or contribute to tinnitus? They however work best in combination with a patient who has both a hearing loss and related tinnitus that can receive benefit from amplification and for tinnitus management. Once the hearing loss has occurred one would not anticipate further injury to what has already been lost. Age-related hearing loss affects all frequencies, although the higher frequencies are usually more affected. Age-related hearing loss is an accelerating process where the rate of change increases with age. As previously mentioned there is a certain redundancy of cochlear hair cells for tonal awareness and one can probably have significant loss of hair cells yet maintain normal hearing.
Some of this is based on the redundancy principle within the inner ear: not all hair cells possibly recover following a TTS but enough do so as to prevent hearing loss.
This study was performed to compare the results of audiogram and the newer diagnostic method distortion product otoacoustic emissions (DPOAEs) parameters due to acoustic shock injury in call center professionals working in a noisy environment and prone to acoustic injury. Evaluation of acoustic shock induced early hearing loss with audiometer and distortion product otoacoustic emissions. There is a concern regarding issues of health and safety that are unique to this new and developing industry.
Effects of industrial noise exposure on distortion product otoacoustic emissions (DPOAEs) and hair cell loss of the cochlea - long term experiments in awake guinea pigs.
The relation among hearing loss, sensory cell loss and tuning characteristics in the chinchilla.
Sensitivity of transient evoked and distortion product otoacoustic emissions to the direct effectsof noise on the human cochlea. Monitoring noise susceptibility: Sensitivity of otoacoustic emissions and subjective audiometry. Autoimmunity and inner ear disorders: An immune-complex mediated sensorineural hearing loss. Etanercept therapy for immune-mediated cochleovestibular disorders: Preliminary results in a pilot study. Corticosteroid pharmacokinetics in the inner ear fluids: An animal study followed by clinical application. The problem with tinnitus, however, is that it is difficult to quantify objectively and to fully appreciate how it affects an individuala€™s well being. Unprotected exposure to injurious noise levels does affect the higher frequencies of hearing initially and in the classic clinical description has been associated with a notched 4000 Hz hearing loss (but not always).
If the noise exposure had not caused a loss of over 25dB then one perhaps should not consider the exposure as being considered a significant factor to the individual's tinnitus. Or, to put it another way, must the 25dB or more hearing loss continue at the same frequency if the tinnitus is to be attributed to the noise exposure which first lead to the 25dB loss? It would certainly require documentation of the individual that their noise had occurred when the threshold hearing was > 25 dB and that it persisted despite an improvement in their hearing.
For tinnitus alone one might reasonably consider masking devices (which generally produce a white band noise) or even the wearing of commercially available products such as MP3 players, iPods etc. Continued exposure, however, would be expected to continue to worsen hearing (albeit at a slower rate) and for that reason the use of hearing protection would still be recommended. Once noise exposure has stopped other factor(s) would need to be involved to therefore worsen hearing. It is only when a quantum number of hair cells are injured irreparably that we then begin to clinically notice a permanent threshold shift (PTS) in hearing. Materials and Methods: Hearing functions of 340 subjects were first assessed with pure tone audiometry and then DPOAEs results were compared among acoustic shock exposed subjects with normal audiogram and those with abnormal audiogram. A triad of vascular, viral and membrane rupture are the known theories for the causation of sudden SNHL. When vertigo is incapacitating, the balance function of the inner ear may be destroyed by transtympanic instillation of gentamicin with varying hearing preservation. Results: Out of 340 acoustic shock exposed subjects 304 were normal on audiometric testing and 34 had abnormal audiograms. It has been defined as the temporary or permanent disturbance of the functioning of the ear or of the nervous system which may be caused to the user of a telephone ear phone by a sudden sound in the acoustic pressure produced by it.
The DPOAE test consisted of presenting two primary tones at frequencies f1 and f2 at levels L1 and L2. Now various autoimmune disorders have also been suggested to play a role in the pathogenesis.Autoimmune inner ear disease (AIED) is a relatively new etiological mechanism of sudden or rapidly progressive hearing loss, which has been added to the previously accepted triad of viral, vascular and membrane rupture.
In complex situations (mixed hearing losses), it may be necessary to a€?maska€? the ear not being tested (to prevent crossover of sound to the other ear). I unfortunately do not have the source information to know how this decision came to be made and what criteria were used specifically for a loss > 25dB at 3000,4000 and 6000 Hz.
That usually is the reason why we state that following noise exposure other factor(s) would be likely to cause further hearing loss in an individual.
Subsequently on DPOAE testing out of 304 acoustic shock exposed subjects with normal audiogram 125 failed and 181 passed.


Conclusions: This study showed that DPOAEs are more sensitive than audiometry to detect pre-symptomatic inner ear damage. These are the results of regular and repeated acoustic shock, which has damaged the outer hair cells of the inner ear that interpret sound vibrations as words, music, or other sounds.Acoustic shock-induced hearing loss is permanent and not correctable by medical or surgical treatment, but is the most preventable type of hearing impairment. The stimuli levels were held constant at L1=65 dB sound pressure level (SPL) and L2=55 dB SPL.
He reported 18 patients with bilateral rapidly progressive SNHL for which no cause could be identified.Scleroderma, an autoimmune disease, also known as systemic sclerosis, is characterized by sclerotic skin changes that are often accompanied by multi-system disease.
Acoustic shock-induced hearing loss is currently detected and monitored with pure-tone audiometry. If a person experiences repeated TTS with a shift in excess of 40 dB, the recovery time is longer and can result, over time, in a PTS.
This method is subjective, time consuming, and not quite sensitive to small changes in pure tone thresholds.
Cutaneous manifestations usually include sclerodactyly, mat like telengectasias and Raynaud's phenomenon. Since recently, a modern diagnostic method, otoacoustic emissions (OAEs), may be used as an accurate, objective, fast, and noninvasive tool for assessing the function of outer hair cells in clinical practice.
Also, acoustic shock differs from noise-induced hearing loss as it is believed to occur at sound pressure levels below those which present an immediate risk to hearing damage.OAEs are low-level sounds originating within the cochlea.
The pure tone audiometry thresholds for 4000 Hz were significant in group with abnormal audiogram. Progressive fibrosis, resulting from increased deposition of collagen in the interstitium and intima of small arteries and connective tissue of involved organs is the pathologic hallmark of the disease. Through reverse propagation, some of this acoustic energy leaks from the cochlea and travels through the middle ear to the external auditory meatus, where it can be recorded using a sensitive microphone.
However scleroderma as the cause of sudden bilateral SNHL has not been reported much in English literature.
Signal noise ratio >6 dB was regarded as an indication of a DP being present, and the subjects were assigned as a pass (normal) case. She had taken medicines outside and developed rashes and patchy bluish discoloration of skin on the arms and finger tips and distal half of feet and toes both sides.
DPOAEs may be an alternative to pure-tone audiometry in monitoring cochlear changes in subjects exposed to occupational noise. This method is subjective, time consuming, and not quite sensitive to subtle small changes in pure tone thresholds.
On examination, right tympanic membrane was congested and bulging and left side had central perforation. OAEs are a diagnostic method that is used as an accurate, objective, sensitive, fast, and noninvasive tool for assessing the function of outer hair cells. Subjects had no underlying disease (diabetes mellitus, hypertension, dyslipidemia) and were selected on the basis of the lack of exposure to ototoxic agents, ear trauma or surgery, chronic ear diseases, and a family history of hearing loss.
For these reasons, OAES have been proposed as an alternative method for monitoring cochlear function in cases with noise exposure.
Results from several studies have demonstrated that OAES parameters are depressed following noise exposure.
Pure tone audiogram [Figure 1] showed profound SNHL in the right ear and mixed hearing loss left side. They had no history of upper respiratory tract infection or ear problems and were not under the influence of alcohol, so any confounding effects were avoided.
After 4 days, gangrenous changes were noted in middle fingers of both hands and toes (Raynaud's Disease) [Figure 2]. Exclusion criteria were the presence of cardiovascular events, diabetes, hyperlipidemia, and immeasurable audiometric data because of poor collaboration by the participant.
Cochlear dysfunction in noise-induced hearing loss may extend beyond the frequency region suggested by the audiogram. The inclusion criterion was exposure to a mean (SD) noise level equivalent to 85 dB (A) for 2 years and use of the same noise-protection equipment.The research proposal was approved by the ethical committee, Vydehi Institute of Medical Sciences and Research Center, and informed consents were obtained in all subjects. Procedures The subjects completed a questionnaire regarding the history of noise exposure, ear diseases, and underlying diseases. Conventional pure-tone audiometry and DPOAEs were conducted after otoscopic examination, which included the removal of wax from the ear canal.
Results range from very slight dips at 4 and 6 kHz to a moderate degree of hearing impairment with flat pattern, similar to that noted by Beastall (1992) [11] and in those cases of cordless telephone handset injury reported by other researchers.
Rheumatoid arthritis (RA) factor-qualitative and quantitative (highly elevated) and C reactive proteins were positive.
Conventional pure-tone audiometry The conventional pure-tone audiometry was conducted in a sound-treated room. Myriamwescott [13] attributed the acoustic shock injury to the possible neurophysiological phenomenon, in particular the tonic tensor tympani syndrome.
Cytoplasmic antineutrophil cytoplasmic antibodies (C-ANCA) and anti-cyclic citrullinated peptide were positive, and anti-nuclear antibody was equivocal, whereas perinuclear-ANCA was negative. A cluster of symptom-attributed acoustic shock were complained by the subjects in our study too, but we could not correlate our study outcome with any middle ear pathology and neurophysiological syndrome. The examined ear was defined as "normal" if a threshold shift larger than 25 dB was not found over the whole frequency range. Antibiotics, high doses of steroids, peripheral vasodilators, oral glycerin, and and local applications of nitroglycerine were administered. 26 out of 34 subjects in the acoustic shock-exposed group with abnormal audiogram were found to have failed in the OAES test which was expected, whereas 125 out 304 subjects of the group with normal audiogram were found to have failed in the OAES test which forms significant proportion.Though overall pass percentage was more than fail percentage giving audiometry its existing due credibility what was more shocking to observe was that the majority in the acoustic shock-exposed group with normal audiogram failed in OAES leading to lower pass percentages.
Lower pass rates in the acoustic shock-exposed group with normal audiograms we found out with our study will clearly indicate the importance of DPOAE testing to detect early changes due to acoustic shock.
The diagnosis of the inner ear autoimmune disorder depends mainly on relatively distinct clinical course, immunological investigations and treatment response. DPOAEs provided functional information about well-defined frequency-specific regions of the cochlea.It has been shown that there is little intra-subject variability in OAE measurements. The clinical picture usually consists of bilateral SNHL, bilateral reduced vestibular loss and symptoms of pressure with tinnitus and rarely tissue destruction of middle and external ear. There is vasculitis, ghosts of blood vessels and granulomatous substrate in the temporal bone pathology in confirmed AIED.It is characterized by proliferative vascular lesion and marked deposition of collagen in various tissues and organs. Workers with abnormal DP screening results, even if audiometric results are normal, should have follow-up counseling and evaluation of hearing-protective-device effectiveness to prevent irreversible noise-induced hearing loss.
Autoimmune disease that affects the inner ear may be either due to organ-specific disease or systemic disorder. However, there are no guidelines for the use of OAEs to detect and monitor noise-induced hearing loss now.
Clarifying advantages of DPOAEs in terms of sensitivity to early manifestations of noise insults, or their utility in predicting future loss in hearing, will require a longitudinal follow up in which the same people are watched over time to see how their hearing changed with their OAEs.In conclusion, the presenting results are in agreement with the findings of previous studies, in that DPOAE testing was shown to be more sensitive to pre-symptomatic inner ear damage than conventional audiometry but cannot estimate hearing thresholds. DPOAE testing should be implemented as a screening and monitoring test for noise-exposed workers rather than as a replacement of audiometry. Probable organ-specific AIED includes tympanosclerosis, otosclerosis, otitis media with effusion, chronic suppurative otitis media with cholesteatoma and menier's disease. The clinical picture of AIED differs from other causes of severe SNHL in that it is usually rapidly progressive (over weeks to month) rather than sudden (hours to days), bilateral, asymmetric SNHL.Scleroderma is an aggressive, multistage autoimmune disorder, also known as systemic sclerosis with high mortality.
It is characterized by sclerotic skin changes that are often accompanied by multi-system disease.
Cutaneous manifestations include sclerodactyly, mat like telengectasias and raynauds phenomenon.
The etiology and pathogenesis of scleroderma remains unknown and probably multifactorial, both cell and humoral mediated. Increased collagen production and vascular damage are potential explanations of hearing loss in scleroderma. Monteiro et al., [6] in a study of twenty six patients revealed that patients with diffuse cutaneous systemic sclerosis have a high prevalence of sensorineural hearing impairment and otological complaints.
The inner ear perilymph is capable of responding to antigen challenge and inner ear is an effective route for systemic immunization. Taleb and Linthicum [10] described the histopathological finding in the temporal bone in a case of scleroderma.No medication has been universally accepted and effective as the treatment of choice in all cases of sudden SNHL and scleroderma. High doses of steroids, vasodilators, anticoagulants, parenteral immunoglobin, methotrexate, and cyclophosphamide have been used individually or in combination. Intravenous immunoglobin has been reported successful in a single case of hearing loss with scleroderma.
Intratympanic injection of glucosteroids in the middle ear have been found to be better than oral or parenteral routes. Concentrations of steroids in perilymph through intratympanic route have been found to be higher when compared to oral or parenteral routes. Methylprednisolone is a better option since its level in endolymph have been found to be higher than hydrocortisone and dexamethasone.
Circulating antibodies, antigens, and immune complexes are removed, which may enhance the effects of immunosuppresive agents.
Stem cell has become a promising tool in the treatment of autoimmune disease by promoting tissue repair and protection from immune-attack associated damage. It can be devastating to patients and frustrating for the otolaryngologist to diagnose and treat. The diagnosis is based on the presence of bilateral progressive or sudden asymmetrical SNHL and the response to immunosuppresive therapy. Steroids in high doses with or without cytotoxic agents have been advocated by various authors. In all cases of bilateral sudden sensorineural loss, AIED must be kept in mind as one of the cause, investigated and treated accordingly.



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Comments Bilateral high tone sensorineural hearing loss

  1. EMRE
    Healthful nerves and ear due to fluid imbalance.
  2. snayper_lubvi
    Speech, Language for several operating on the 3 year project, which has been.
  3. axlama_ureyim
    Please note: Tinnitus, by itself, does how great I had it I am afraid ear and.