Dr Peter Grant
Aboriginal Health
ENT
Sensorineural Hearing Loss
Synonyms: Sensorineural deafness, perceptive hearing loss, perceptive deafness.
This paper examines the literature on the aetiology of sensorineural hearing loss which is defined as "a permanent hearing threshold shift of 25 decibels (dB) or more, at 500, 1000, 2000 or 4000 hertz (Hz) due to a defect in the cochlea or the auditory nerve whereby nervous impulses from the cochlea to the brain are attenuated".1 1 Whilst the term "deafness" has been used to refer to both partial and complete auditory acuity impairment in the past, the protocol adopted here is to refer to a partial loss as a "hearing loss" and complete loss as "deafness".
2. Sensorineural hearing loss (SNHL) is to be distinguished from:-
a) conductive hearing loss, which is defined as "hearing loss due to a disorder of the pinna, external ear canal, the tympanic membrane, the ossicles or their attachments, including the oval and round windows."2 and3. Deterioration of hearing, especially for the higher frequencies, is described by Burns4 as a characteristic of growing older, but the reasons why this occurs are unknown. This form of SNHL is referred to as "presbyacusis". Although there is a degree of individual variation, the median hearing level increases with age in most people, even in the absence of significant noise exposure.5b) central hearing loss, which is defined as "hearing loss in the presence of normal function of the external ear, middle ear, cochlea and auditory nerve attributable to a disorder affecting the nerve pathways from the auditory nerve to the temporal lobe of the brain, where auditory sensations are represented."3
Definitions.
4. Many studies use the term "acoustic trauma" when referring to exposure to all types of increased noise. As an alternative, Burns6 classifies the types of noise which may affect hearing into three broad categories:
- temporary threshold shift,
- permanent threshold shift, and
- acoustic trauma.
7. "Acoustic trauma" is defined as sudden aural damage resulting from short term intense exposure or even a single exposure.9 Acoustic trauma produces a audiogram curve generally indistinguishable from that seen in presbyacusis10 with the greatest loss centred at 4000 Hz. The types of loud noise considered in this category include: fireworks, small arms fire, gunfire, grenade fire, exploding mines, and major explosions. Most literature does not specify the range of noise levels likely to occur with any of these types of explosions. Noise levels are probably well in excess of 120 dB. Extremely loud noises can rupture the ear drum and damage the ossicles. Less intense acoustic trauma may produce ear pain or a sensation of burning, temporary threshold shift or permanent threshold shift, and tinnitus. The severity of the loss varies with the magnitude of the explosion and proximity to the blast.
Temporary threshold shift.
8. Since these variables can only be estimated for individuals, it is not possible to provide general guidelines as to the prospects of complete recovery. Snow11 states that "recovery to a certain extent may occur over the next few days but a complete loss of hearing can result". The presence of ear pain, tinnitus or a sensation of burning does not necessarily mean that damage has occurred. Ward12 reports that gunners with normal hearing often report symptoms such as tinnitus and temporary hearing loss after previous episodes of blast trauma.9. Whilst TTS is of secondary importance to the issue at hand, a discussion of the concept of recovery is of some relevance. Ward13 found that the course of recovery is affected by the way in which TTS was produced. Exposure at noise at 105 dB sound pressure level (SPL)14 is shown to be associated with a markedly delayed recovery (in excessive of 1000 minutes). Delayed recovery of this order is found to occur with both continuous and intermittent noise exposure at 105 dB SPL.15 Studies of prolonged exposure (48 hours at 81.5 dB SPL and 29.5 hours at 92.5 dB SPL) found a recovery delay of 3 days and 6 days, respectively.16 10. The index for permanent hearing impairment was defined by Burns in 1973 as the attainment of a mean hearing level of 25 dB, from the individual hearing levels at the 500, 1000 and 2000 Hz audiometric frequencies.17 Davis18 states that reduced perception of faint speech commences when the arithmetical average of the hearing levels at 500, 1000 and 2000 Hz exceeds 26 dB. Snow19 prefers the definition of the American Guides to the Evaluation of Permanent Impairment20 which holds that a permanent impairment exists if the sum of the pure tone thresholds at 500, 1000, 2000 and 3000 Hz exceeds 91.7 dB in the ear concerned.
Permanent threshold shift.
11. The risk of permanent threshold shift is related to both the intensity and duration of sound exposure. The American National Standards Institute (ANSI), in an analysis of 200 audiograms evaluated in relation to intensity, found no apparent threshold shift at 80 dB SPL at 2000 Hz after periods of exposure in excess of 20 years, whilst after 10 years of exposure, 88 dB SPL produced 9 dB of threshold shift, and 95 dB produced 15 dB of threshold shift. A similar relation was found between SPL in the octave 1200-2400 Hz and threshold shifts at 4000 Hz.21 A simple analysis of the results of a study by Burns and Robinson22 (presented as a graph) suggests that a 25 dB permanent threshold shift at 4000 Hz occurred at one year with 115 dB SPL exposure, 3 years with 105 dB SPL exposure, 10 years with 100 dB SPL exposure, and 20 years with 95 dB SPL exposure. Other studies report that PTS occurs with lower levels of noise exposure (see paragraph 16).12. In a study of women employed continuously in weaving factories (with noise levels in the range 80 to 95 dB), Burns23 found that hearing impairment commenced after 5 to 9 years of exposure, with progression of hearing impairment with increasing duration of employment. The pattern of onset was typical for that described for occupational hearing loss, with the first sign being a small depression in the audiogram between 3000 and 6000 Hz (usually at 4000 Hz). For this particular occupational group however, the pattern of impairment exceeded that predicted. In a study by Ward24, a 25 dB increase in hearing impairment (or increase in hearing level) occurred after 5 years of continuous exposure at 92 dB SPL. As a corollary, the OSHA and the NIOSH recommend that the maximum permissible noise levels over a working lifetime should not exceed 90 dB and 85 dB, respectively, with the NIOSH setting an absolute ceiling of 115 dB for any short-term or intermittent unprotected noise exposure.25
Acoustic trauma.
13. Burns26 writes that there is a clear tendency for the ear to be more tolerant of noise at the low rather than the middle and higher frequencies. The ear appears to be particularly vulnerable to frequencies in the range 2000 to 4000 Hz, or even 6000 Hz. These frequencies are likely to be generated in industrial settings by various hammering, stamping, pressing, shipping and riveting operations27, and in military settings by gunfire and explosions. For the latter, Terkildsen28 has shown that a single intense, sudden sound can damage the ear before the aural reflex can act (that is, where sound is generated in a shorter time than 44 11 milliseconds). For repetitive sounds, the contraction of the stapedial muscles is maintained when repetition occurs less than once a second. In 1946, Murray and Reid29 showed that 28 single rounds fired several seconds apart produced substantial temporary threshold shifts whilst the same number of shots from an automatic (Bren) gun gave insignificant temporary changes.14. A pertinent issue is whether or not there is acceleration of the resulting PTS after exposure to acoustic trauma in the absence of further significant noise exposure. Taylor et al.30 found that the initial rapid increase in hearing level at 3000 and 4000 Hz is usually succeeded by a slowing down that is marked at 10 to 15 years, and deteriorates at a much slower rate for the next 30 years. At 2000 Hz, this saturation effect is not conspicuous, with appreciable deterioration continuing for a longer period. The conclusion drawn is that onset of PTS may be followed by a progressive increase in hearing levels in excess of that expected for age. As well, there is evidence to support the notion that a single exposure to acoustic trauma may possibly be sufficient to induce a state of permanent threshold shift, although in the absence of objective evidence of aural damage at the time of exposure, the relative risk with a single bout of acoustic trauma would increase minimally, if at all.
Industrial-type exposure.
15. The situation is less clear when noise exposure occurred only in an industrial or industrial like setting. Interpretation of Burns and Robinson's31 findings suggests minimum continuous exposure times of one year at 115 dB SPL, and three years at 105 dB SPL. More recent works suggest that PTS commences after a minimum of five years exposure at 90 dB SPL and around 3 years at 95 dB SPL. The latter figures approximate the safety levels recommended by major occupational health and safety authorities (supra vide). The application of these concepts to an individual case requires knowledge of the likely levels of noise in the service environment at the time, as well as the intensity and duration of noise exposure during civilian life.16. Whilst there is evidence that exposure to a single bout of acoustic trauma may produce a permanent threshold shift, this is considered an unlikely event unless there is objective evidence of concomitant middle ear damage such as a ruptured ear drum or bleeding from the ear canal. The likelihood of sensorineural damage is further reduced when adequate hearing protection is worn. The literature does not support a probable link between single or multiple exposures to acoustic trauma for a minimum of several months and a permanent threshold shift, even without adequate ear protection.
Ototoxic drugs
17. The aminoglycosides are among the most common cause of iatrogenic ototoxics. Members of this family include: gentamicin, streptomycin, kanamycin, neomycin, amikacin, tobramycin, netilmicin, vancomycin and viomycin.32 Ototoxicity is common, particularly when parenteral aminoglycosides are used for more than 7 days. Potentiation of this side-effect occurs when given in combination with diuretics such as furosemide or ethacrynic acid33, and in the presence of renal failure or hepatic failure.34 Hearing loss rarely begins within 5 days of commencing treatment and may be delayed for weeks or months after its cessation.35 In contrast, the absorption of aminoglycosides (eg. neomycin) from the gut and skin are poor, and ototoxicity is a rarely reported association when aminoglycosides are administered by these means, especially topically. For example, whilst studies in guinea pigs demonstrate a potential for cochlear damage, there is no clinical evidence that topical aminoglycosides applied to the external ear can lead to hearing loss, certainly in the presence of an intact ear drum.36 18. Ototoxic diuretics or loop diuretics (furosemide and ethacrynic acid) are known to be ototoxic under certain circumstances. Ethacrynic acid can cause both reversible and permanent hearing loss, especially when given intravenously, although SNHL was recorded in only 2 out of 184 patients taking ethacrynic acid in one study.37 Furosemide has been shown to be ototoxic at high doses in guinea pigs but has not been shown to cause hearing loss in humans at pharmacological doses, unless given in conjunction with aminoglycosides.38 19. Ototoxicity has been reported following the use of cytotoxic agents such as nitrogen mustard, bleomycin, cisplatinum,39 -difluoromethyl ornithine, vincristine, vinblastine40 and carboplatin. Specific dosage guidelines for the range of drugs involved is unlikely to assist in determining the degree of involvement but only oral or systemic forms of treatment to pose a risk for SNHL. Topical medicants do not seem to be involved.20. Both tinnitus and sensorineural hearing loss are known complications of treatment with salicylates, such as aspirin. The symptoms appear at serum levels of 300 mg/litre or higher, and are almost always reversible once therapy is ceased and serum levels fall below this level.41 Whereas permanent tinnitus may be an occasional sequelae of toxicity, there is marginal evidence that it leads to permanent sensorineural hearing loss.
21. Quinine and chloroquine amongst the antimalarials. are believed to implicated in ototoxicity. Sensorineural hearing loss usually follows long periods of therapy at pharmacological doses, and may be reversible. Martindale42 states that chloroquine is said to cause "nerve deafness". There are some reports of quinine causing SNHL, being mainly in overdose (toxicity) cases and the changes were often reversible.43 22. A number of miscellaneous drugs that are no longer available for general use are known to cause sensorineural hearing loss. These include practolol, hexamethadrine, and thalidomide (once widely used for treatment of nausea). For drugs still in common usage, hearing loss is reported as an occasional complication for ampicillin (perhaps due to a hypersensitivity reaction)44, erythromycin after high intravenous dosage45, polymixin E, chloramphenicol, propanolol, nortriptyline, propylthiouracil, bromocriptine, indomethacin, phenylbutazone, and ibruprofen.46 Vaccination with tetanus antitoxin may produce sensorineural hearing loss, but only in conjunction with serum sickness.
Cochlear manifestations of middle ear disease
23. Otosclerosis primarily causes progressive conductive deafness (usually bilateral), most often between the ages of 11 to 30 years. A small proportion occurs before 10 years of age, and an even smaller proportion after the age of 50. In 70 per cent of cases, the disease is familial and in 30 per cent it is of sporadic onset. Progress is inexorable but may be uneven. When sensorineural hearing loss develops it almost invariably follows the onset of the conductive component. It is unknown if sensorineural disease can occur in the absence of a conductive component. There is some support for the notion that otosclerosis may be the cause of otherwise unexplained sensorineural hearing loss in young to middle-aged adults.47 24. Whilst the cause of otosclerosis is unknown, early detection and treatment often serves to ameliorate the effects of the disease, and few cases, if treated late, are remediable. Acceleration of the hearing loss is known to occur with pregnancy, menopause, and with chronic stress reactions associated with major trauma.48 Aggravation by exposure to one of the ototoxic drugs is possible. Where SNHL is thought to be due to otosclerosis the contribution is only likely to be through the aggravation of the primary disease.25. Adults are more likely to develop acute suppurative otitis media (ASOM) than chronic suppuration (CSOM), which is predominantly found in children. In both cases, the associated hearing loss is invariably conductive49, tends to be insidious, and rarely exceeds 40 dB. Nadol50 states that whilst both acute and chronic suppurative otitis media normally cause a conductive hearing loss, a sensorineural component may supervene when CSOM is complicated by suppurative labyrinthitis. A diagnosis of suppurative labyrinthitis is needed for any probable link to be made. For acute otitis media, the presence of a sensorineural component is highly suggestive of herpes zoster otiticus as the cause.51
Meniere's disease
26. This is a condition of unknown aetiology with a prevalence of about 200 per 100,000. It can occur at any age but usually begins between 30 and 60 years of age. It usually present as a unilateral condition, with progression to bilaterality in 40 per cent at 20 years.52 The three cardinal symptoms are paroxysmal vertigo, tinnitus and sensorineural hearing loss, with the hearing loss usually presenting at the time of the first attack of vertigo. A single bout of Meniere's may be followed by along period of remission, or may occur in "cluster attacks". The loss of auditory acuity (involving the low tones at the start) tends to be episodic initially, and may even disappear between attacks. If Meniere's disease recurs, the hearing level inexorably increases and lesser degrees of recovery are seen between attacks.53 27. Whilst it is possible that trauma or infections may contribute to otic capsule damage54 (the supposed underlying cause of Meniere's disease), there is no evidence that either trauma or infection causes or aggravates Meniere's. The onset of one or more of the above triad of symptoms following certain types of infections, should be properly classified as the appropriate type of labyrinthine vertigo as distinct from Meniere's. The possibility that Meniere's disease is implicated in SNHL exists but is generally considered unlikely.
Acoustic neuroma.
(Synonyms: Vestibular Schwannoma, neurilemmoma, neurinoma).28. Acoustic neuromas are classified as benign tumours of the nerve root sheath of the superior vestibular or, rarely, the cochlear nerve. The classical symptoms are unilateral sensorineural hearing loss and tinnitus.55, sometimes followed by ataxia, nystagmus, facial weakness, hoarseness, dysphagia, failing vision and headache. Whereas the pattern of initial presentation may not necessarily include a sensorineural loss component, subsequent onset of hearing loss is to be expected. In some cases, worsening of the auditory impairment is an unavoidable outcome of surgery.
Vascular lesions.
29. Acute onset of sensorineural hearing loss has been described in relation to haemorrhage, thrombosis and vasospasm of the terminal branch of the anterior-inferior cerebellar artery or cochlear vessels. These events may be caused by diabetes mellitus, degenerative (mainly atherosclerotic) cardiovascular disease, and diseases associated with hyperviscosity, such as polycythaemia, macroglobulinaemia, the leukaemias, and sickle cell trait. Spontaneous haemorrhage into the inner ear has been described as a complication of leukaemia, Wegener's granulomatosis, subarachnoid haemorrhage and temporal bone trauma.56 30. The minimum duration of diabetes mellitus before vascular complications appear in other organ systems is in the order of 15 to 20 years.57 For atherosclerosis, evidence of atheroma in other organs is probably necessary for it to be considered as a possible cause of sudden hearing loss. Cochlear ischaemia can occur at any stage once a condition affecting blood viscosity, coagulation or clotting is present. The prospects of recovery vary greatly, but are usually in the order of 25 to 50 per cent. This may be partial or complete. Poor prognostic factors here include an elevated ESR, the presence of vertigo, and older age.58Viral infections
31. Known viral causes of sensorineural hearing loss are mumps, measles, pertussis, rubella, and varicella-zoster.59 These mainly cause sensorineural hearing loss in early childhood. Less certain associations exist for poliovirus, influenza B, cytomegalovirus, coxsackie virus, Epstein-Barr virus (infectious mononucleosis), and herpes simplex virus.60 In view of the uncertainties referred to above, all of the above viruses are considered to be possible risk factors for sensorineural hearing loss but only mumps, measles, pertussis, rubella, and varicella-zoster are likely and then only when a close temporal relationship exists.
Bacterial and other infections
32. Apart from suppurative labyrinthitis complicating chronic suppurative otitis media, SNHL is reported to occur in 5 to 30 per cent of survivors of bacterial meningitis (probably as a result of suppurative labyrinthitis or neuritis or both). Syphilis, both congenital and acquired, can produce unilateral or bilateral sensorineural hearing loss. Tuberculosis of the temporal bone is also a known cause of SNHL, as well as conductive hearing loss.61 The maximum latency period between onset of infection and development of SNHL is not clear. Since all of the above conditions are by nature chronic, and since SNHL may go undetected for a number of years, it is possible that a past infection could be implicated. Since all of these conditions are treatable, a close temporal connection is needed to even consider a likelihood of a causal nexus.
Head trauma.
33. Sensorineural hearing loss is known to follow closed or penetrating injuries to the skull. This is particular so for fractures of the temporal bone. The association is particularly strong for transverse temporal fractures, but is also reported for longitudinal fractures. The minimum degree of trauma necessary to produce sensorineural hearing loss is not defined but Nadol62 reports SNHL as having followed concussive injuries of the skull in the absence of fracture. Nadol63 also states that a fistula may occur (in the absence of barotrauma) after head injury, or heavy lifting or straining. This serves to complicate the issue somewhat. In the absence of a documented SNHL due to fistula formation a concussive head injury is a minimum for any chance to exist. No maximum time period is required for the possibility to continue; it is considered more probable than not that any resultant hearing loss would manifest within five years of the injury.
Barotrauma
34. Otitic barotrauma is defined as "damage to the middle ear from inequalities in pressure on each side of the tympanic membrane."64 The situations in which this is likely to occur are:
a) very sudden descent associated with sudden repressurisation when flying;35. Medial displacement or rupture of the tympanum results in a conductive hearing loss, which may recover completely or partially, depending on the degree of damage inflicted. Sensorineural hearing loss is a rare complication following otic barotrauma, and is attributed to rupture of either the stapediovestibular ligament or the round window, with the creation of a perilymph fistula.66 The literature does not state whether surgical correction of the fistula results in complete recovery of the hearing loss. Sensorineural hearing loss is more commonly seen following rapid ascent during diving whereupon gaseous nitrogen forms in the cochlea. This form of SNHL is generally irreversible.67 For divers and other underwater service personnel it is possible that where there is evidence of barotrauma (either aerial or marine) or when the person has undergone rapid ascent to the surface on at least one occasion a connection exists for an unspecified time. It is likely however that the onset of SNHL would be within 10 years.b) rapid underwater descent;
c) ascent to the surface when diving without adequate decompression; and
d) in a compression chamber during therapy with hyperbaric oxygen.65
Central nervous system conditions
36. Disorders of the central nervous system known to be associated with sensorineural hearing loss include: multiple sclerosis (MS), a variety of intracranial tumours mainly involving the temporal bone or the posterior intracranial fossa, viral labyrinthitis and basilar migraine.68 The onset of auditory involvement may be subtle and not detected until after a definitive diagnosis of MS is made. With brain tumours, sensorineural hearing loss usually occurs with invasion or encroachment of the inner ear or auditory nerve. The most common primary tumours arising in the temporal bone are acoustic neuroma, chemodectoma, squamous cell carcinoma adenocarcinoma and basal cell carcinoma. Hearing loss may be due to meningeal carcinomatosis involving the auditory nerve. The most common form of secondary tumours are adenocarcinoma of the breast in women, and prostatic and renal-cell carcinoma in men.69 Meningiomas may also arise in the region of the posterior cranial fossa and impinge on the auditory nerve.
Immune-mediated sensorineural hearing loss
37. Several systemic immune-mediated disabilities are associated with sensorineural hearing loss. These include systemic lupus erythematosis, rheumatoid disease, periarteritis nodosa, scleroderma, dermatomyositis, Wegener's granulomatosis, Cogan's syndrome, relapsing polychondritis, giant-cell arteritis, and Behet's syndrome.70 More recently, a form of immune-mediated sensorineural hearing loss without any other systemic manifestations has been recognised. The hearing loss is usually bilateral, and is rapidly progressive (measured in weeks to months). Its cause is unknown and no tests exist currently to confirm the diagnosis.
Iatrogenic sensorineural hearing loss
38. Apart from ototoxic drugs, SNHL may also occur as a complication of surgery to the middle ear, inner ear or posterior cranial fossa in the region of the auditory nerve71, following lumbar puncture, and with therapeutic irradiation of the head and neck directed at lesions within the temporal bone or adjacent areas.72 The presumed cause is radiation labyrinthitis.References
1 Occupational Safety and Health. (1991). Scientific American Medicine. CTM. Chapter VII. p. 18.2 Burns, W. (1973). Noise and Man. Second edition. John Murray: London. p. 110.
3 Ibid. p. 113.
4 Ibid.. p. 112.
5 Ibid. p. 102.
6 Ibid. p. 190.
7 Scott-Brown's Diseases of the Ear, Nose and Throat. (1979). Fourth edition. Eds. J. Ballantyne and J. Groves. Butterworths: London. Volume 2. p. 568.
8 Burns, W. (1973). op. cit. p. 190.
9 Ward, W. D. (1980). Noise Induced Hearing Damage.; in, Otolaryngology. Second Edition. Eds. M. M. Paparella and D. A. Shumrick. Volume 2. p. 1789.
10 Snow, J. B. (1988). Management and therapy of trauma to the external ear and auditory and vestibular systems.; in, Alberti, P. W., and Ruben, R. J. Otologic Medicine and Surgery. Churchill Livingstone: New York. (Chapter 61). Volume 2. p. 1568.
11 Ibid. p. 1569.
12 Ward, W. D. (1970). Temporary threshold shift and damage-risk criteria for intermittent noise exposure. J. Acoustic Soc. Am. 48, p. 561.; cited in, Burns, W. (1973). op. cit. p.198.
13 Ibid. p. 198.
14 SPL or "sound pressure level" =3D 20 log10 p/pref dB re pref where p =3D sound pressure (RMS), pref =3D reference sound pressure., in; Burns. W. (1973). op. cit. p. 43 and pp. 375-6.
15 Ward, W. D. (1970). op. cit.; in Burns, W. (1973). p. 207.
16 Mills, J. H., et al. (1970). Temporary changes of the auditory system due to exposure to noise for one to two days. J Acoust. Soc. Am. 48, p. 524.; in Burns, W. (1973). op, cit. p. 212.
17 Burns, W. (1973). op. cit. p. 242.
18 Davis, H. (1962). Opening address, Report of the Royal National Institute of the Deaf 1962 Conference. RNID: London, p. 4.; cited in, Burns, W. (1973). op. cit. p. 290.
19 Snow, J. B. (1988). op. cit. p. 1575.
20 Guides to the Evaluation of Permanent Impairment. (1993). Fourth edition. American Medical Society: Chicago. p. 224.
21 ANSI. (1954). The relations of hearing loss to noise exposure. Report Z24-X-2. New York, ANSI.; cited in, Burns, W. (1973). op. cit. p. 221.
22 Burns, W. and, Robinson, D. W. (1970). An investigation of the effects of occupational noise on hearing, in, Sensorineural hearing loss. Ed. Wolstenholms, G. E. W. and Knight, J. Churchill: London; cited in, Burns, W. (1973). op. cit. p. 222.
23 Burns, W. (1973). op. cit. pp. 223-226.
24 Ward, W. D. (1980). op. cit. p. 1796.
25 Occupational Safety and Health. (1991). op. cit. p. 18.
26 Burns, W. (1973). op. cit. p. 244.
27 Ibid. p. 209.
28 Terkildsen, K. (1960). The intra-aural muscle reflexes in normal persons and in workers exposed to industrial noise. Acta oto-laryng. (Stockh.) 52, p. 384.; cited in, Burns, W. (1973) op. cit. p. 209.
29 Murray, N. E., and Reid, G. (1946). Temporary deafness due to gunfire. J. Laryngology 61, p. 92.; cited in, Burns, W. (1973). op. cit. p. 210.
30 Taylor, W., et al. (1965). Study of noise and hearing in jute weaving. J, Acoust. Soc. Am. 38, p 113.
31 Burns, W. and, Robinson, D. W. (1970). op. cit. p. 222.
32 Matz, G. J. (1993). Aminoglycoside cochlear toxicity. Otolaryngology Clinics of North. America. 26(5), pp. 705-712.
33 Bochner, F., et al. (1978). Handbook of Clinical Pharmacology. Little, Brown : Boston. p. 99.
34 Mawson's Diseases of the Ear. (1988). Fifth edition. Ed. Harold Ludman. Edward Arnold: London. p. 615.
35 Ibid. pp. 615-616.
36 Ibid. p. 618.
37 Martindale: The Extra Pharmacopoiea. (1989). Twenty-nineth edition. Ed. James E. F. Reynolds. The Pharmaceutical Press: London. p. 985.
38 Mawson's Diseases of the Ear. op. cit. p. 616.
39 Ibid. p. 617.
40 Schweitzer, V. G. (1993). Ototoxicity of chemotherapeutic agents. Otolaryngology Clinics of North. America. 26(5), pp. 759-789.
41 Mawson's Diseases of the Ear. (1988). op. cit. p. 617.
42 Martindale. op. cit. p. 508.
43 Ibid. p. 518.
44 Mawson's Diseases of the Ear. (1988). op. cit. p. 617.
45 Brummett, R. E. (1993). Ototoxic liability of erythromycin and analogues. Otolaryngology Clinics of North. America. 26(5), pp. 811-819.
46 Mawson's Diseases of the Ear. (1988). op. cit. p. 617.
47 Ibid. p. 568.
48 Mawson's Diseases of the Ear. (1988). op. cit. p. 563.
49 Ibid. p. 468.
50 Nadol, J. B. (1993). Hearing loss (Review). The New England Journal of Medicine. 329(15), pp. 1092-1102.
51 Mawson's Diseases of the Ear. (1988). op. cit. p. 412.
52 Ibid. p. 620.
53 Ibid. p. 623.
54 Ibid. p. 622.
55 Ibid. p. 650.
56 Nadol, J. B. (1993). op. cit p. 1098.
57 Harrison's Principles of Internal Medicine. (1994) 13 ed. McGraw-Hill: New York. p. 1994.
58 Mawson's Diseases of the Ear. (1988). op. cit. p. 607.
59 Ballenger, J. J. B. (1991). Diseases of the Nose, Throat, Ear, Head, and Neck. Fourteenth edition. Lea & Febiger: London. p. 1209.
60 Mawson's Diseases of the Ear. (1988). op. cit. p. 606.
61 Nadol, J. B. (1993). op. cit. p. 1094.
62 Ibid. p. 1097.
63 Ibid. p. 1097
64 Mawson's Diseases of the Ear. (1988). op. cit. p. 397.
65 Encyclopaedia of Occupational Health and Safety. (1983). Third (revised) edition. Ed. Luigi Parmeggiani. International Labour Office: Geneva. pp. 593-596.
66 Mawson's Diseases of the Ear. (1988). op. cit. pp. 397-398
67 Encyclopaedia of Occupational Health and Safety. (1983). op. cit. p. 596.
68 Nadol, J. B. (1993). op. cit. p. 1098.
69 Ibid. p. 1098.
70 Mawson's Diseases of the Ear. (1988). op. cit. p. 613.
71 Ibid. p. 606.
72 Nadol, J. B. (1993). op. cit. p. 1097.
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