Original Article

Aetiological Causes Of Reversible Sensorineural Hearing Loss

A Aftab, S Quraishi

Keywords

aetiology, reversible, sensorineural hearing loss

Citation

A Aftab, S Quraishi. Aetiological Causes Of Reversible Sensorineural Hearing Loss. The Internet Journal of Otorhinolaryngology. 2005 Volume 4 Number 2.

Abstract

The vast majority of sensorineural hearing loss cases are irreversible. However there is a significant proportion of cases in which the hearing loss recovers. A knowledge of the aetiological causes of reversible sensorineural deafness cases can allow early diagnosis and correct treatment to be implemented. The purpose of this article is to review the documented literature on the aetiological causes of reversible sensorineural hearing loss.

 

Introduction

Reversible sensorineural hearing loss occurs in a significant proportion of cases. Although the precise pathophysiology in many of these causative factors remains unclear it is nevertheless important to be aware of numerous aetiologies to enable a prompt diagnosis and correct treatment to be implemented. This article reviews the documented aetiological causes of sensorineural hearing loss.

Aetiologies

(i) Ototoxicity

There are numerous drugs which are known to cause damage to the inner ear which can result in reversible or irreversible hearing loss, tinnitus and dysequilibrium. Drugs which have been associated with reversible sensorineural hearing loss (SNHL) include:

a) Salicylate-induced ototoxicity was first reported in 1877 by Muller.1 Aspirin is probably the most common cause of drug- induced ototoxicity although the majority of it is reversible.2 Tinnitus tends to precede the deafness which is bilateral and affects all the frequencies. Both the tinnitus and SNHL develop within a few days of treatment and tend to reverse within a few days of withdrawing aspirin.2,3,4,5 Although the required dose of aspirin to produce these symptoms is variable, most individuals exhibit some degree of symptoms at serum levels of 35mg/dl.2,5

The exact mechanism of action by the salicylates is not clearly understood. A change in the membrane permeability of the outer hair cells appears to play a significant role.2,3,4,5 A change in the cochlear blood supply as a result of the salicylate-induced imbalance of vasodilatory prostaglandins and vasoconstricting leukotrienes may also have an integral role.2,3,4

b) Quinine like aspirin can cause reversible SNHL associated with tinnitus and can occur in both healthy and malaria patients.2,6,7 The effects are rapid and resolve completely following withdrawal of the drug. It appears to alter the membrane function of the outer hair cells especially in the region of the lateral cisternae.2

Five months of treatment of rheumatoid arthritis with hydroxychloroquine which resulted in reversible SNHL has been reported in a patient.8 The mechanism of this ototoxicity is not known.

c) In 1965 Maher and Schreiner 9 first described the reversible SNHL and vertigo following intravenous administration of the loop diuretic ethacrynic acid. Loop diuretics e.g ethacrynic acid and frusemide may cause SNHL when administered parenterally in high doses, or if given rapidly even in low doses.10,11 Patients with existing hearing deficits, severe hypoalbinaemia, heart failure or severe renal failure are particularly susceptible to the ototoxic effects of these drugs.10,11 Experimental studies suggest that loop diuretics damage the stria vascularis and/or the outer hair cells of the cochlea 10It has been demonstrated that loop diuretics inhibit Na-K ATPase and adenyl cyclase in the stria.12Concurrent administration of loop diuretics with aminoglycosides can exacerbate or cause aminoglycoside ototoxicity.13

d) The macrolide antibiotic erythromycin is associated on rare occasions with SNHL which is reversible on discontinuation of the antibiotic.14,15,16,17,18,19 This bilateral and reversible loss is most likely to occur at doses of at least 4g/day.14,15,18Patients at increased risk of developing erythromycin-induced deafness include the elderly 15, patients with pre-existing hepatic or renal failure 15, and patients undergoing liver 19or renal transplantation.14

The precise mechanism of the loss of hearing is not known but it is thought that erythromycin exerts its effects on the central auditory pathway level, as there are associated reported features such as hallucinations and diplopia.14,15

e) Reversible bilateral SNHL has been reported following the administration of oral metronidazole. 20 Withdrawal of the antibiotic and oral steroid therapy resulted in return of normal hearing thresholds. The exact mechanism of action is unknown.

f) The chemotherapeutic agent cisplatin is known to cause permanent or transient SNHL.11,21,22,23,24 The deafness can also be associated with tinnitus 21 Clinical studies have shown that this type of hearing loss is directly related to the total dose of cisplatin administered and to the peak serum concentrations.11

The precise mechanism of action is unknown but there is associated hair cell damage, inhibition of Na+-K(ATPase) in the outer hair cells of the cochlea 23 and atrophy of the stria vascularis.2

g) With the increasing use of interferon, several new adverse effects including audiovestibular symptoms have been recognised. Sudden SNHL associated frequently with tinnitus has been reported to have developed several days after the commencement of interferon (both alpha and beta interferon).25,26,27 Complete resolution of the hearing loss in all the cases occurred within a month after discontinuation of interferon. The exact mechanism of action is unknown.

h) OKT3 (muromonab-CD3) is a murine monoclonal antibody used as an immunosuppressant following cadaveric renal transplants. Sudden SNHL (high frequency) within 48-72 hours of commencing OKT3 has been reported followed by complete resolution within 2 weeks after discontinuation of the drug.28,29 Transient tinnitus was also a frequent associated symptom. The mechanism of how OKT3 produces ototoxicity remains unclear.

i) Carbamazepine has been shown to be capable of delaying conduction of the auditory system both centrally and peripherally.30 Temporary bilateral SNHL has been reported following an overdose of carbamazepine (36g) in a patient.31 Two weeks later there was complete resolution of the deafness and the associated tinnitus and dizziness.

j) Treatment of partial seizures with sodium valproate has resulted in SNHL which resolved following discontinuation of the drug.32 The mechanism of this rare adverse effect of sodium valproate is unclear.

k) The anti-epileptic drug vigabatrin has recently been reported to cause reversible SNHL.33 Discontinuation of the drug led to complete recovery of the hearing loss. Vigabatrin is a GABA-based drug and animal studies have shown that GABA is an important inhibitory neurotransmitter for cochlear inner and outer hair cells.33

l) Chronic use of amphetamines has been reported to cause SNHL which has reversed within 4 to 10 days of cessation of amphetamine use.34 Prolonged and heavy use of amphetamines can lead to neuronal damage and neurotransmitter depletion but the precise mechanism of the ototoxic effect is unknown.

m) Animal model studies have demonstrated SNHL induced by lithium 35 and also interleukin-2 36 which has reversed following discontinuation of the drugs.

n) Chronic carbon monoxide (CO) exposure usually results in permanent, symmetrical and high frequency hearing loss and was first documented in 1948.37 Reversible SNHL following chronic CO exposure has been reported with improvement occurring over a period ranging from several weeks to 21 months. 37,38,39

Acute CO exposure is less common and typically produces a U shaped audiogram which is usually bilateral and may be asymmetrical with recovery usually taking several months.39,40,41,42

Carbon monoxide poisoning is often associated with headaches, nausea, lethargy, pulmonary oedema and arrythmias.38 The symptoms are presumed to be due to tissue hypoxia due to the formation of carboxyhaemoglobin. Animal model studies suggest that free radicals may have an integral role 43 and there may be an excitotoxic component as MK-801 which blocks the glutamate NMDA receptor has been shown to protect against CO ototoxicity.44

ii) Anaesthesia

a) General anaesthesia

Sudden reversible and irreversible SNHL has been reported following general anaesthesia involving both otolaryngological and non-otolaryngological procedures. The reversible hearing loss is unilateral or bilateral and the degree of recovery is variable.45,46,47,48,49,50

It is thought that the anaesthetic agent has a causative role in the deafness. The most common anaesthetic agent in these cases is nitrous oxide. Two theories have been suggested-‘implosive' and ‘explosive' routes. In the first route, rapid penetration of the highly soluble nitrous oxide results in an acute increase in middle ear pressure and subsequent rupture of the round window membrane.51 In the second, the nitrous oxide-induced increases in the venous and CSF pressure are transmitted to the perilymphatic space via the cochlear duct causing displacement or rupture of the membrane.52 The other anaesthetic agents e.g isoflurane and fentanyl may act indirectly on the auditory pathway by altering the general haemodynamics e.g hypotension.53

b) Spinal anaesthesia and lumbar puncture

The first reported case of hearing impairment after spinal anaesthesia was reported in 1914.54 Since then, it has been well documented that reversible SNHL can occur after spinal anaesthesia and following procedures involving lumbar puncture.55,56,57,58,59,60,61 The hearing loss is either unilateral or bilateral, low frequency and usually reverses spontaneously although there are a few documented cases where the SNHL has not reversed.58

The precise mechanism of this transient hearing loss has not yet been completely established. It has been suggested that following dural puncture the decrease in the CSF volume and pressure that occurs leads to a decrease of perilymph as there is a direct communication between the CSF and perilymph via the cochlear aqueduct. The reduction in perilymphatic pressure would then induce a transient endolymphatic expansion for equilibration.55,62,63 This endolymphatic hydrops is associated with the hearing loss and restoration of the CSF and inner ear volumes would then lead to a return of normal hearing thresholds.

The contrast medium, metrizamide which is used in lumbar myelography is associated with transient deafness. The mechanism of action is probably due to a hydrostatic imbalance between the perilymph and CSF resulting from a decreased CSF osmolality.61

iii) Infective

a) Bacterial

Bacterial meningitis can leave up to 10% of patients particularly children with permanent SNHL.64, 65 Transient SNHL has also been reported following bacterial meningitis.66,67,68,69,70 Both types of hearing loss tend to develop in the early part of the illness.66,68 In the majority of the reports the deafness tends to reverse after weeks or months 68,69,70 but in a large multicentre trial involving children the improvement in most of the affected cases occurred within 48 hours.66

The cochlea appears to be auditory lesion site due to the loss of otoacoustic emissions.66 Animal studies also support the integral role played by the cochlea.71,72 The mechanism is unclear but it may result from the effect of bacterial toxins or inflammatory mediators on the hair cells of the organ of Corti.71,73

Syphilis (congenital or acquired) can produce otological manifestations including SNHL, tinnitus and imbalance.74,75,76,77,78,79 The SNHL may be sudden, fluctuant, progressive, unilateral or bilateral. Treponema pallidum has an ability to persist in several sites including the temporal bone.77 Treatment with antibiotics and steroids shows a variation in response.79

Lyme disease is caused by infection with the spirochaete Borrelia burgdorferi and like syphilis may result in neurological manifestations e.g facial nerve palsy and SNHL. The SNHL which is sudden in onset, can affect low or high frequencies and may respond to treatment with antibiotics. Both partial 80 and complete recovery 81 (usually after a few months) of the hearing loss following treatment has been reported. Indeed a case has been reported in which the hearing loss completely reversed more than two years following treatment.82 SNHL has been reported to occur in 15% of cases of late Lyme disease without recovery of hearing.83 The precise pathogenesis of hearing loss in Lyme disease is presently not known.82

Animal studies involving instillation of pseudomonas aeruginosa exotoxin A and pneumococcal toxins into middle ear have demonstrated the onset of SNHL which has reversed in a few weeks.84,85

b) Fungal

Reports in the literature have shown an association between hearing loss and cryptococcal meningitis. 86,87 A case of a patient with cryptococcal meningoencephalitis in whom the SNHL hearing loss reversed following antifungal treatment has been reported.87

c) Mycoplasmas

Infection with Mycoplasma pneumoniae has been reported in a case which resulted in unilateral SNHL (associated with tinnitus and vertigo) which reversed completely following treatment with doxycycline.88

Mycoplasma, bacteria and viruses have all been implicated in the aetiology of bullous myringitis. Prospective studies of bullous myringitis by Hoffman 89 and Hariri 90 have demonstrated a significant incidence of SNHL (65% and 66% respectively) with complete resolution of the hearing loss in 57% and 60% in the 2 series respectively The mechanism of the hearing loss remains unclear.

d) Viral

Infection with varicella zoster virus typically results in SNHL and facial palsy. There is great variation in the degree of hearing loss and the amount of recovery of the loss. Acute SNHL which is usually unilateral is a well reported reversible complication of mumps.91

The exact mechanism has not yet been definitively proven but host immune mediated response in the cochlea appears significant.92

iv) Autoimmune

Autoimmune SNHL was first described as a clinical entity in 1979 by McCabe.93 Clinical presentation and prompt diagnostic confirmation can lead to successful management of the deafness by medical therapy. However recognition of the disease is not straight forward in particular due to lack of simple and reliable diagnostic tests and the paucity of temporal bone tissue from untreated patients.94,95

The precise mechanisms involved in the hearing loss are unclear. Animal model studies have led to several immunological mechanisms being postulated. These include humoral mechanisms involving specific autoantigens in the inner ear (Type II); circulating immune complexes involving bacterial and viral antibodies (Type III); cell mediated immunity involving cytotoxic T cells (Type IV); and autoantibodies directed against type II collagen.94 There are no randomised trials of therapy for autoimmune SNHL and the treatment approach is based upon anecdotal experience, case series and inference from treatment of related conditions. Steroid and cyclophosphamide immunosuppression has been the main form of treatment.93,95

Reversible SNHL has been reported in the following specific autoimmune disorders:

a) Cogan's syndrome

This syndrome is characterised by ocular inflammation classically interstitial keratitis and audio-vestibular symptoms including SNHL, vertigo and tinnitus.95 Hearing fluctuation coincides with exacerbations and remissions of the disease. Temporal bone histopathological findings include endolymphatic hydrops, lymphocyte infiltration and organ of Corti degeneration.96,97 Steroid and cyclophosphamide therapy are the mainstay of treatment.

b) Wegener's granulomatosis

The 3 main components of this disease are focal necrotising glomerulonephritis, necrotising granulomatous lesions in the upper and/or lower respiratory tracts and systemic vasculitis. In contrast to Cogan's syndrome the most common otologic deficit is conductive loss (otitis media with effusion).94,95 However SNHL usually in combination with conductive deafness has been reported.98,99,100,101 The SNHL has improved following treatment with steroids and cyclophosphamide.99,101

c) Polyarteritis nodosa

This vasculitic disease affects small and medium-sized arteries. Although uncommon SNHL which is sudden and bilateral has been reported.102,103,104 Temporal bone histopathological findings include arteritis of the internal auditory artery.105 Treatment with steroids and cyclophosphamide 102,103 or azathioprine 104 has resulted in improvement of the hearing loss.

d) Kawasaki disease

Kawasaki disease is an acute self-limited vasculitis that affects primarily medium sized arteries of infants and children. Prospective studies have demonstrated transient SNHL over a period ranging from 1 week to 4 months.106,107 The mechanism of the hearing loss remains unclear.

v) Metabolic

Haemodialysis

SNHL is frequently reported in patients with chronic renal failure.108 The aetiology of this hearing impairment remains unclear, however factors such as uraemic toxins, electrolyte imbalance and hypotension have been suggested to play a role.109 However opinion remains divided on the effect haemodialysis has on the hearing impairment. Studies involving long term haemodialysed patients who had been receiving dialysis ranging from 5 years 110 to 10 years 109 have shown no significant alteration in the hearing. These are supported by studies assessing hearing after a single haemodialysis session and hearing assessed by distortion product otoacoustic emissions both in children and adults.111,112 In contrast other studies have reported that following a single session of haemodialysis, the hearing impairment has either deteriorated 113,114 or improved.115,116,117

vi) Haematolgical

Hyperviscosity syndrome

The features of hyperviscosity syndrome include headache, visual disturbances, vertigo, tinnitus and SNHL. These clinical features are due to the elevated blood viscosity and resulting slowly circulating oxygen-deficient blood. It is postulated that the elevated viscosity causes partial occlusion of the cochlear vessels resulting in ischaemia of the cochlea and subsequent hearing loss.118

Haematological disorders that have exhibited reversible SNHL which is attributable to hyperviscosity syndrome include:

Leukaemia: recent studies have implicated both acute and chronic leukaemia in the development of sudden SNHL which can be the presenting clinical feature.118, 119, 120. Temporal bone histopathological studies of affected patients include leukocyte infiltration and inner ear haemorrhage.119,120 Lowering of the leukocyte count by leukapheresis or steroid and chemotherapy treatment can lead to reversal of the hearing loss.118,119,120

Essential thrombocytosis: a case of sudden SNHL in a patient with thrombocytosis which reversed following plateletpheresis is reported in the literature.121

Waldenstrom's macroglobulinaemia is an uncommon disorder in which there is excess production of monoclonal macroglobulin IgM. A case has been reported in a patient with Waldenstrom's macroglobulinaemia in whom the SNHL improved along with the other hyperviscosity-related symptoms following treatment with fludarabine.122

vii) Neoplasms

a) Vestibular schwannomas

Hearing loss associated with vestibular schwannomas (VS) has been reported to resolve spontaneously or to improve following corticosteroid treatment.123,124

Reports of hearing improvement after surgical removal of VS in particular small tumours exist but not extensively.125,126,127,128,129,130 Although the exact mechanism for the deafness is unclear, one theory that has been put forward is that it is due to a vascular compression phenomenon which is relieved following removal of the tumour129,130 and the reduction of tumour mass in the case of corticosteroids.129Others postulate a mechanical conduction block of the cochlear nerve action potential theory.131

b) Cerebello-pontine angle tumours

Recovery of severe SNHL following total surgical removal of cerebellopontine angle tumours –meningioma and jugular foramen neurinoma has been reported.132It is thought relief of tumour compression maintaining the arachnoidal sheaths of the cochlear nerve would make the recovery of its function possible.132

c) Carotid body tumour

Removal of a carotid body tumour in a patient with dysphagia, tinnitus and ipsilateral SNHL led to recovery of the hearing loss.133

viii) Vestibular

Meniere's disease

Meniere's disease is characterised by recurrent attacks of deafness, tinnitus and vertigo. The SNHL improves between attacks even to normal levels. The pattern of hearing loss is typically low frequency but eventually affects all frequencies and is progressive.134

Distension of the endolymphatic space is the main feature and another frequent histopathological finding is membraneous labyrinth rupture. The exact mechanism involved remains unclear. One theory involves rupture of the membranes leading to mixing of the endolymph and perilymph leading to electrochemical imbalance.135 Another theory postulates alteration in the blood supply leading to alteration in the constituents of the endolymph.134

Symptomatic relief of symptoms which is primarily aimed at vertigo includes dietary advice, medical e.g vestibular sedatives, and surgical interventions e.g saccus decompression.134

ix) Neurological

a) Multiple sclerosis

Sudden SNHL is a rare manifestation of multiple sclerosis (MS) and it tends to occur within the first years of the disease although later onset is also described.136 It is due to the demyelination of the auditory pathway and usually occurs when other areas of the brainstem are affected. Recovery of the hearing loss has been reported in the literature.136,137,138

b) Sarcoidosis

This multisystem granulomatous disease can involve the VIIIth cranial nerve leading to SNHL and vertigo. It is presumed that the symptoms are due to direct infiltration or compression of the cranial nerve.139 Reversal of the SNHL has been reported following steroid treatment but this is very rare.140

x) Traumatic

a) Blast injury

SNHL following blast injuries is most severe immediately after the explosion and usually recovers within 24 hours.141 This temporary threshold shift is often accompanied by vertigo and tinnitus which are also usually transient. The mechanism of the hearing loss involves damage to the outer hair cells.

b) Perilymph fistula

Leakage of perilymph into the middle ear following rupture of inner ear membranes can occur following head injury, diving barotraumas and stapedial surgery. Dizziness may be accompanied by tinnitus and SNHL which may fluctuate.134 Spontaneous resolution may occur following a period of bed rest with elevation of the head. Surgical attempt at closure of the leak may result in improvement of the dizziness and prevent further deterioration in the deafness.134

xi) Miscellaneous

a) Hypotension

A retrospective study demonstrated that a group of patients with sudden SNHL which improved had lower mean arterial pressures and in whom the deafness recovered more easily following treatment.142 This has led to the suggestion that at least in some cases cochlear damage may be caused by a perfusion deficit as a result of the combined effect hypotension and impaired vasomotor regulation.142

b) Biotinidase deficiency

A case of a child with total biotinidase deficiency who developed bilateral SNHL is reported.143 Treatment with biotin led to improvement of the hearing thresholds.

c) Menstrual cycle

Bilateral transient SNHL associated with the onset of menstruation has been reported in a patient.144 Treatment with diuretics perimenstrually led to improvement in the transient loss. The precise mechanism of action in this case remains unclear.

d) Psychogenic

A case of a patient with acute SNHL who demonstrated further deterioration in the hearing levels following a panic anxiety attack has been reported.145 Treatment with corticosteroids and psychiatric counselling resulted in a return to normal thresholds except in the high-frequency range immediately after the treatment.

e) Intra-operative deafness during posterior fossa surgery

Two patients undergoing microvascular decompression for trigeminal neuralgia developed intra-operative hearing loss diagnosed by complete loss of brainstem evoked potentials during the surgery. The resulting prominent vascular compression around the cochlear nerve in both patients was immediately decompressed resulting in restoration of the hearing loss.146

Conclusions

It must be emphasised that the above is not a complete list of all the aetiological causes of reversible SNHL but it is nevertheless hopefully a comprehensive report of the documented causes.

An accurate history taking with a background knowledge of the possible causes of SNHL can lead to appropriate investigations being undertaken. Although the vast majority of SNHL cases are irreversible, there are however as highlighted above certain aetiologies which can be reversed if recognised early and appropriate management implemented. A prompt and correct diagnosis and treatment may prevent further deterioration of the hearing loss and even result in recovery.

Correspondence to

Mr Aftab Ahmed Department of ENT Doncaster Royal Infrmary Armthorpe Road Doncaster. South Yorkshire DN2 5LT England. Email: ahmed.aftab@virgin.net

References

1. MULLER G. (1877) Beitrag zur wirking der salicylasuren natrons beim dibetes melleus. Berlin klinik Wochenshrift. 14, 29-31
2. WRIGHT T. (1998) Ototoxicity. In:Diseases of the Ear Ludman H. & Wright T. (Eds) London, Arnold.p 503-515
3. JUNG T., RHEE C., LEE C. et al. (1993) Ototoxicity of salicylate, non-steroidal anti-inflammatory drugs and quinine. Otolaryngol Clin North Am. 26, 791-810
4. CAZALS Y. (2000) Auditory sensori-neural alterations induced by salicylate. Prog Neurobiol. 62, 583-631
5. MYERS E., BERNSTEIN J. & FOSTIROPOLOUS G. (1965) Salicylate ototoxicity: A clinical study. N Engl J Med. 273, 587-590
6. TANGE R.A., DRESCHLER W.A., CLAESSEN F.A. et al. (1997) Ototoxic reactions of quinine in healthy persons and patients with Plasmodium falciparum infection. Auris Nasus Larynx
24 (2), 131-136
7. ROCHE R.J., SILAMUT K., PUKRITTAYAKAMEE S. et al. (1990) Quinine induces reversible high tone hearing loss. Br J Clin Pharmacol. 29 (6), 780-782
8. SECKIN U., OZORAN K., IKINCIOGULLARI A. et al. (2000) Hydroxychloroquine ototoxicity in a patient with rheumatoid arthritis. Rheumotol Int. 19(5) 203-204
9. MAHER J.F. & SCHREINER G.E. (1965) Studies on ethacyrnic acid in patients with refractory oedema. Ann Intern Med. 62, 15-19
10. RYBAK L. (1993) Ototoxicity of loop diuretics. Otolaryngol Clin North Am. 26, 829-844
11. SELIGMANN H., PODOSHIN L., BEN-DAVID J. et al. (1996) Drug-induced tinnitus and other hearing disorders. Drug Saf. 14, 198-212
12. THALMANN R., ISE I., BOHNE B.A. et al. (1977) Actions of loop diuretics and mercurials upon the cochlea. Acta Otolaryngologica
83, 221-232
13. LERNER S. & MATZ G. (1980) Aminoglycoside ototoxicity. Am J Otolaryngol. 1, 169-179
14. VASQUEZ E.M., MADDUX S.M., SANCHEZ J. et al. (1993) clinically Significant hearing loss in renal allograft recipients treated with intravenous erythromycin. Arch Intern Med. 153, 879-882
15. SACRISTAN J.A., SOTO J. & de COS M.A. (1993) Erythromycin-induced hypoacusis: 11 new cases and literature review. Ann Pharmacother. 27, 950-955
16. MINTZ U., AMIR J. & de VRIES A. (1973) Transient perceptive deafness due to erythromycin lactobionate. JAMA
225, 1122-1123
17. KARMODY C.S. & WEINSTEIN L. (1977) Sensorineural hearing loss with intravenous erythromycin lactobionate. Ann Otol. 86, 9-11
18. BRUMMET R. & FOX K. (1989) Vancomycin and erythromycin-induced hearing loss in humans. Antimicrob Agents Chemother. 33, 791-796
19. MORAL A., NAVASA M., RIMOLA A. et al. (1994) Erythromycin ototoxicity in liver transplant patients. Transplant
7,
62-64
20. IQBAL S.M., MURTHY J.G., BANNERJEE P.K. et al. (1999) Metronidazole ototoxicity - report of two cases. J Laryngo Otol.
113, 355-357
21. HAYES D.M., CVITKOVIC E. & GOLBEY R.B. (1977) High dose cisplatinum diammine dichloride. Cancer
39, 1372-1381
22. MONTAGUTI M., BRANDOLINI C., FERRI G.G. et al. (2002) Cisplatin and carboplatin-induced ototoxicity in children: clinical aspects and perspectives for prevention. Acta Otorhinolatyngol Ital. 22(1), 14-18
23. REED E. (1993) Anticancer drugs: Platinum analogs. In:Cancer Principles and Practice of Oncology. Devita V, Hellman S, Rosenberg S (Eds) Philadelphia, J.B. Lippincott. 390-397
24. RIGGS L., BRUMMETT R., GUITJENS S.et al. (1996) Ototoxicity resulting from combined administration of cisplatin and gentamicin. Laryngoscope
106, 401-406
25. KANDA Y., SHIGENO K., KINOSHITA N. et al. (1994) Sudden hearing loss associated with interferon. Lancet
343, 1134-1135
26. KANDA Y., SHIGENO K., MATSUO H. et al. (1995) Interferon-induced sudden hearing loss. Audiology
34(2), 98-102
27. GORUR K., KANDEMIR O., UNAL M. et al. (2003) The effect of recombinant interferon alpha treatment on hearing thresholds in patients with chronic viral hepatitis B. Auris Nasus Larynx
30, 41-44
28. HARTNICK C.J, COHEN A.F. & SMITH R.V. (1997) Reversible sensorineural hearing loss after renal transplant immunosuppression with OKT3 (muromonab-CD3). Ann Otol Rhinol Laryngol. 106(8), 640-642
29. HARTNICK C.J., SNITH R.V., TELLIS V. et al. (2000) Reversible sensorineural hearing loss following administration of muromonab-CD3 (OKT3) for cadaveric renal transplant immunosuppression. Ann Otol Rhinol Laryngol. 109, 45-47
30. JAPARIDZE G., KVEMADZE D., GELADZE T. et al (1993) Effects of carbamazepine on auditory brainstem response and slow cortical potential in epileptic patients. Epilepsia
34, 1105-1109
31. de la CRUZ M. & BANCE M. (1999) Carbamazepine-induced sensorineural hearing loss. Arch Otolaryngol Head Neck Surg. 125, 225-227
32. ARMON C., BROWN E., CARWILE S. et al. (1990) Sensorineural hearing loss: a reversible effect of valproic acid. Neurology
40, 1896-1898
33. PAPADEAS E., POLYCHRONOPOULOS P., PAPATHANASOPOULOS P. et al. (2003) Sensorineural hearing loss: a reversible effect of vigabatrin. Neurology
61(7), 1021-1022
34. IQBAL N. (2002) Hearing loss in amphetamine users. J Psychoactive Drugs
34(4), 401-407
35. HORNER K.C., HUANG Z.W., HIGUERIE D. et al. (1997) Reversible hearing impairment induced by lithium in the guinea pig. Neuroreport
14;8(6), 1341-1345
36. KUBO T., ANNIKO M., STENQVIST M. et al. (1998) Interleukin-2 affects cochlear function gradually but reversibly. ORL J Otorhinolaryngol Relat Spec. 60(5), 272-277
37. LUMIO J. (1948) Clinical findings following chronic carbon monoxide exposure. Acta Otolaryngol 1-112
38. LEE C., ROBINSON P. & CHELLADURAI J. (2002) Reversible sensorineural hearing loss. Int J Pediatr Otorhinolaryngol. 66(3), 297-301
39. HASSAN M.S., RAY J. & WILSON F. (2003) Carbon monoxide poisoning and sensorineural hearing loss. J Laryngol Otol. 117, 134-137
40. MORRIS T.M. (1969) Deafness following acute carbon monoxide poisoning. J Laryngol Otol. 83, 1219-1225
41. BAKER S. & LILLEY D. (1977) Hearing loss from acute carbon monoxide intoxication. Ann Otol Rhinol Laryngol. 86, 323-328
42. MAKASHIMA K. (1988) Otoneurologic manifestations following carbon monoxide poisoning. J Acoust Soc Am. 84, 38
43. FLETCHER L., LIU T. & PEARCE T. (1997) Cochlear protection from carbon monoxide exposure by free radical blockers in the guinea pig. Toxicol Appl Pharmacol. 142, 47-55
44. LIU Y. & FLETCHER L. (1995) MK-801 protects against carbon monoxide induced hearing loss. Toxicol Appl Pharmacol. 132, 196-202
45. PAU H., SELVADURAI. & MURTY G.E. (2000) Reversible sensorineural hearing loss after non-otological surgery under general anaesthesia. Postgrad Med J. 76 (895), 304-306
46. PATTERSON M.E. & BARLETT P.C. (1979) Hearing impairment caused by intratympanic pressure changes during general anaesthesia. Laryngoscope
86, 399-404
47. MILLEN S.J., TOOHILL R.J. & LEHMEN R.H. (1982) Sudden sensorineural hearing loss: operative complication in non-otological surgery. Laryngoscope
92, 613-617
48. SEGAL S., MAN A. & WINERMAN I. (1984) Labyrinthine membrane rupture caused by elevated intratympanic pressure during general anaesthesia. Am J Otol. 5, 308-310
49. HOCHERMANN M. & REIMER A. (1989) Hearing loss after general anaesthesia. A case report and review of literature. J Laryngol Otol. 101, 1079-1082
50. BELAN A., RIDA A., HAMOUD N. et al. (1994) bilateral sensorineural hearing loss after general anaesthesia. Ann Fr Anesth Reanim. 13, 400-402
51. GOODHILL V. (1971) Sudden deafness and round window rupture. Laryngoscope
81, 1462-1474
52. GOODHILL V., HARRIS I., BROCKMAN S.J. et al. (1973) Sudden deafness and labyrinthine window rupture. Ann Otol Rhinol Laryngol. 82, 2-12
53. KAUFMAN L. & TABERNER P.V. (1996) Pharmacology in the practice of anaesthesia. London, Arnold, 71, 420-422
54. TERRIEN F. & PRELAT P. (1914) Paresis of the sixth cranial nerve and bilateral hearing decrease following spinal anaesthesia. Arch d'opthalmol. 34, 111-116
55. WALSTED A. (2000) Effects of cerebrospinal fluid loss on hearing. Acta Otolaryngol. 543, 95-98
56. LEE C. (1990) Hearing loss after spinal anaesthesia. Anesth Analg. 71, 561-569
57. FOG J., WANG L., SUNBERG A. et al. (1990) Hearing loss after spinal anaesthesia is related to needle size. Anesth Analg. 70, 517-522
58. MICHEL O. & BRUSIS T. (1992) Hearing loss as a sequel of lumbar puncture. Ann Otol Rhinol Laryngol.
101, 390-394
59. PANNING B., MEHLER D. & LEHNHARDT E. (1983) Transient low frequency hypoacusis after spinal anaesthesia. Lancet
2, 582
60. WANG L.P., FOG J. & BOVE M. (1987) Transient hearing loss following spinal anaesthesia. Anaesthesia
42, 1258-1263
61. HUSSAIN S.S.M., HEARD C.M.B. & BEMBRIDGE J.L. (1996) Hearing loss following spinal anaesthesia with bupivicaine. Clin Otolaryngol. 21, 449-454
62. WALSTED A. (1998) Effects of cerebrospinal fluid loss on the auditory system. Clinical and experimental investigations. Dan Med Bull. 45/3, 268-281
63. MARCHBANKS R.J. & REID A. (1990) Cochlear and cerebrospinal fluid pressure: their inter-relationship and control mechanisms. Br J Audiol. 24, 179-187
64. BARAFF L.J., LEE S.J. &SCHRINGER D.L. (1993) Outcomes of bacterial meningitis in children: a meta-analysis. Paediatr Infect Dis J. 12, 389-394
65. FORTNUM H.M. (1992) Hearing impairment after bacterial meningitis. Arch Dis Chil. 67, 1228-1233
66. RICHARDSON M.A., REID A., TARLOW M.J. et al. (1997) Hearing loss during bacterial meningitis. Arch Dis Child. 76, 134-138
67. GUISCAFRE H., BENITEZ-DIAZ L., MARTINEZ M.C. et al. (1984) Reversible hearing loss after meningitis: prospective assessment using auditory evoked responses. Ann Otol Rhinol Laryngol. 93, 229-232
68. KAPLAN S.L., CATLIN F.I., WEAVER T. et al. (1984) Onset of hearing loss in children with bacterial meningitis. Paediatrics
73, 575-578
69. NADOL J.B. (1978) Hearing loss as a sequela of meningitis. Laryngoscope
88, 739-755
70. OZDAMAR O., KRAUS N. & STEIN L. (1983) Auditory brainstem responses in infants recovering from bacterial meningitis. Arch Otolaryngol. 109, 13-18
71. TARLOW M.J., COMIS S.D. & OSBORNE M.P. (1991) Endotoxin induced damage to the cochlea in guinea pigs. Arch Dis Child. 66, 181-184
72. BHATT S.M., LAURETANO A., CABELLOS C. et al. (1993) Progression of hearing loss in experimental pneumococcal meningitis: correlation with cerebrospinal fluid cytochemistry. J Infect Dis. 167, 675-683
73. HUANG M.H., DULON D. & SCHACHT J.S. (1990) Outer hair cells as potential targets of inflammatory mediators. Ann Otol Rhinol Laryngol. 99, 35-38
74. KARMODY C.S. & SCHUKNECHT H.F. (1966) Deafness in congenital syphilis. Arch Otolaryngol. 83, 18-27
75. BECKER G.D. (1979) Late syphilitic hearing loss: A diagnostic and therapeutic dilemma. Laryngoscope
89, 1273-1288
76. McNULTY J.S. & FASSETT R.L. (1981) Syphilis; An otolaryngologic perspective. Laryngoscope
91, 889-905
77. BOOTH J.B. (1982) Medical management of sensorineural hearing loss. J Laryngol Otol.
96, 673-684
78. ADAMS D.A., KERR A.G., SMYTH G.D.L. et al. (1983) Congenital syphilitic deafness - a further review. J Laryngol Otol. 97, 399-404
79. STECKELBERG J.M., ROCHESTER M.N & McDONALD T.J. (1984) Otologic involvement in late syphilis. Laryngoscope
94, 753-757
80. HANNER P., ROSENHALL U., EDSTROM S. et al. (1989) Hearing impairment in patients with antibody production against Borrelia burgdoferi antigen. Lancet 13-15
81. MOSCATELLO A.L., WORDEN D.L., NADELMAN R.B. et al. (1991) Otolaryngologic aspects of Lyme disease. Laryngoscope
101, 592-595
82. QUINN S.J., BOUCHER B.J. & BOOTH J.B. (1997) Reversible sensorineural hearing loss in Lyme disease. J Laryngol Otol. 111, 562-564
83. LOGIGIAN E.L., KAPLAN R.F. & STEERE A.C. (1990) Chronic neurologic manifestations of Lyme disease. N Engl J Med. 323, 1438-1444
84. STENQVIST M., ANNIKO M. & PETTERSSON A. (1997) Effect of pseudomonas aeruginosa exotoxin A on inner ear function. Acta Otolaryngol. 117, 73-79
85. KUBO T., ANNIKO M., HSU W.J. et al. (1998) Pneumococcal toxins reversibly affect cochlear eletrophysiology. Oto Rhino Laryngologia-Nova. 8(2), 59-65
86. TJOIE L.T., YEW K.Y. & CHAI B.T. (1985) Cryptococcal meningitis. J Neurol Neurosurg Psychyiatry
48, 853-858
87. MAYER J.M., CHEVALIER X., ALBERT E. et al. (1990) Reversible hearing loss in a patient with cryptococcosis. Arch Otolaryngol Head Neck Surg. 116, 962-964
88. SHANON E., REDIANU C., ZIKK D. (1982) Sudden deafness due to infection by Mycoplasma pneumoniae. Ann Otol Rhinol Laryngol. 91, 163-165
89. HOFFMEN R.A. & SHEPSMAN D.A (1983) Bullous myringitis and sudden hearing loss. Laryngoscope
93, 1544-1545
90. HARIRI M.A. (1990) Sensorineural hearing loss in bullous myringitis. A prospective study of eighteen patients. Clin Otolaryngol. 15, 351-353
91. HYDEN D. (1996) Mumps labyrinthitis, endolymphatic hydrops and sudden deafness in succession in the same ear. ORL J Otorhinolaryngol Relat Spec. 58(6), 338-342
92. HARRIS J.P.& SHARP P. (1990) Inner ear autoantibodies in patients with rapidly progressive sensorineural hearing loss. Laryngoscope
100, 516-524
93. McCABE B.F. (1979) Autoimmune sensorineural hearing loss. Ann Otol. 88, 585-589
94. MATHEWS J. & KUMAR B.N. (2003) Autoimmune sensorineural hearing loss. Clin Otolaryngol. 28, 479-488
95. STONE J.H. & FRANCIS H.W. (2000) Immune-mediated inner ear disease. Curr Opin Rheumatol. 12, 32-40
96. WOLFF D., BERNHARD W.G., TSUTSUMI S. et al. (1965) The pathology of Cogan's Syndrome causing profound deafness. Ann Otol Rhinol Laryngol. 74, 507-520
97. SCHUKNECHT H. & NADOL J. (1994) Temporal bone pathology in a case of Cogan's syndrome. Laryngoscope
104, 1135-1142
98. ILLUM P.& THORBING K. (1982) Otological manifestations of Wegener's granulomatosis. Laryngoscope
92, 801-804
99. McCAFFREY T.V., McDONALD T.J. et al. (1980) Otologic manifestations of Wegener's granulomatosis. Otolaryngol Head NeckSurg. 88 (5),
100. KEMPF H.G. (1989) Ear involvement in Wegener's granulomatosis. Clin Otolaryngol. 14, 451-456
101. CLEMENTS P.R., MISTRY C.D. et al. (1989) Recovery from sensorineural deafness in Wegener's granulamotosis. J Laryngol Otol. 103, 1234
102. TSUNODA K., AKAOGI J., OHYA N. et al. (2001) Sensorineural hearing loss as the initial manifestation of polyarteritis nodosa. J Laryngol Otol. 115(4), 311-312
103. WOLF M., KRONENBERG J. et al. (1987) Rapidly progressive hearing loss as a symptom of polyarteritis nodosa. Am J Otolaryngol. 8(2), 105-108
104. ROWE-JONES J.M., MACALLAN D.C. & SOROOSHIAN M. (1990) Polyarteritis nodosa presenting as bilateral onset cochleo-vestibular failure in a young woman. J Laryngol Otol. 104, 562-564
105. GUSSEN P. (1977) Polyarteritis nodosa and deafness: a human temporal bone study. Arch Otorhinolaryngol. 217, 263-271
106. SUNDEL R.P., NEWBURGER J.W., McCILL T. et al. (1990) Sensorineural hearing loss associated with Kawasaki disease. J Paediatrics
117, 371-377
107. KNOTT P.D., ORLOFF L.A., HARRIS J.P. et al. (2001) Sensorineural hearing loss and Kawasaki disease: a prospective study. Am J Otolaryngol. 22(5), 343-348
108. BERGSTROM L., JENKINS P., SANDO I. et al. (1973) Hearing loss in renal disease: clinical and pathological studies. Ann Otol. 82, 555-576
109. BAZZI C., VENTURINI C.T., PAGANI C. et al. (1995) Hearing loss in short and long-term haemodialysed patients. Nephrol Dial Transplant. 10, 1865-1868
110. MIRAHMADI M.K. & VAZIRI N.D. (1980) Hearing loss in end-stage renal disease - effects of dialysis. J Dial. 4, 159-162
111. STAVROULAKI P., NIKOLOPOULOS T.P., PSAROMMATIS I. et al. (2001) Hearing evaluation with distortion-product otoacoustic emissions in young patients undergoing haemodialysis. Clin Otolaryngol. 26, 235-242
112. OZTURAN O. & LAM S. (1998) The effect of haemodialysis on hearing using pure tone audiometry and distortion-product otoacoustic emissions. ORL. 60, 306-313
113. RIZVI S.S. & HOLMES R.A. (1980) Hearing loss from haemodialysis. Arch Otolaryngol. 106, 751-754
114. YASSIN A., SAFWAT F. & FATT-HI A. (1966) Ear, nose and throat manifestations in cases of renal failure treated by dialysis. Ann Rhinol Laryngol. 75, 192-201
115. GATLAND D., TUCKER B., CHALSTREY S. et al. (1991) Hearing loss in chronic renal failure: hearing threshold changes following haemodialysis. J R Soc Med.
84, 587-589
116. KOMSUOGLU S., MEHTA R., JONES L.A. et al. (1985) Brainstem auditory evoked potentials in chronic renal failure and maintenance haemodialysis. Neurology
35, 419-423
117. MAGLIULO G. GAGLIARDI M. & RALLI G. (1987) BSER audiometry in haemodialysis patients. Clin Otolaryngol. 12, 249-254
118. CHAE S.W., CHO J.H., LEE J.H. et al. (2002) Sudden hearing loss in chronic myelogenous leukaemia implicating the hyperviscosity syndrome. J Laryngol Otol. 116, 291-293
119. VELING M.C., WINDMILL I. & BUMPOUS J.M. (1999) Sudden hearing loss as a presenting manifestation of leukaemia. Otolaryngol Head Neck Surg. 120, 954-956
120. BAER M.R., STEIN R.S. & DESSYPRIS E.N. (1985) Chronic lymphocytic leukaemia with hyperleukocytosis: the hyperviscosity syndrome. Cancer
56, 2865-2869
121. GRISELL D.L. & MILLS G.M. (1986) Reversible acute sensorineural hearing loss associated with essential thrombocytosis. Arch Intern Med. 146, 1813
122. SYMS M.J., ARCILA M.E. & HOLTEL M.R. (2001) Waldenstrom's macroglobulinaemia and sensorineural hearing loss. Am J Otolaryngol. 22(5), 349-353
123. BERENHOLZ L.P., ERIKSEN C. & HIRSCH F.A. (1992) Recovery from repeated sudden hearing loss with corticosteroid use in the presence of an acoustic neuroma. Ann Otol Rhinol Laryngol. 101, 827-831
124. BERG H.M., COHEN N.L., HAMMERSCHLAG P.E. et al (1986) Acoustic neuroma presenting as sudden hearing loss with recovery. Otolaryngol Head Neck Surg. 94, 15-22
125. COHEN N.L., RANSOHOFF J. & JACOBS J. (1985) Restoration of speech discrimination following subocciptal, transmeatal excision of extracanalicular acoustic neuroma. Otolaryngol Head Neck surg. 93, 126-131
126. FISCHER G., CONSTANTINI J.L. & MERCIER P. (1980) Improvement of hearing after microsurgical removal of acoustic neurinoma. Neurosurgery
7, 154-159
127. SHELTON C. & HOUSE W.F. (1990) hearing improvement after acoustic tomour removal. Otolaryngol Head Neck Surg. 103, 963-965
128. TELIAN S.A., KEMINK J.L. & KILENY P.R. (1988) Hearing recovery following suboccipital excision of acoustic neuroma. Arch Otolaryngol Head Neck Surg
114, 85-87
129. YANAGIHARA N. & ASAI M. (1993) Sudden hearing loss induced by acoustic neuroma: significance of small tumours. Laryngoscope
103, 308-311
130. MEITELES L.Z., LIU J.K. & COULDWELL W.T. (2002) Hearing restoration after resection of an intracanalicular vestibular schwannoma: a role for emergency surgery? J Neurosurg. 96, 796-800
131. SAUNDERS J.E., LUXFORD W.M. ,DEVGAN K.K. et al. (1995) Sudden hearing loss in acoustic neuroma patients. Otolaryngol Head Neck Surg.
113, 23-31
132. VELLUTINI E.A.S., CRUZ O.L.M., VELASCO O.P. et al. (1991) Reversible hearing loss from cerebellopontine angle tumours. Neurosurgery
28(2), 310-312
133. TEMMEL A.F., KIERNER A.C., MUHM M. et al. (1999) Reversible sensorineural hearing impairment induced by a carotid body tumour. Eur Arch Otorhinolaryngol. 256(9), 466-469
134. LUDMAN H. (1998) Vestibular disorders. In: Diseases of the Ear. Ludman H & Wright T. (Eds) London, Arnold. 516-534
135. BROWN D.H. McCLURE J. & DOWNAR-ZAPOLSKI Z. (1988) The membrane rupture theory of Meniere's disease - is it valid? Laryngoscope
98, 599-601
136. MARANGOS N. (1996) Hearing loss in multiple sclerosis: localisation of the auditory pathway lesion according to electrocochleographic findings. J Laryngol Otol. 110, 252-257
137. DRULOVIC B., RIBARIC-JANKES K., KOSTIC V.S. et al. (1994) Multiple sclerosis as the cause of sudden pontine deafness. Audiology
33, 195-201
138. TABIRA T., TSUJI S., NAGASHIMA T. et al. (1981) Cortical deafness in multiple sclerosis. J Neurol Neurosurg Psych. 44, 433-436
139. JONES N. & LUDMAN H. (1998) Acquired sensorineural hearing loss. In: Diseases of the Ear. Ludman H & Wright T. (Eds) London, Arnold 495-502
140. JAHRSDOERFER R.A., THOMPSON E.G., JOHNS M.E. et al. (1981) Sarcoidosis and fluctuating hearing loss. Ann Otol Rhinol Laryngol. 90, 161-163
141. KERR A.G. & BYRNE J.E.T. (1975) Concussive effects of a bomb blast on the ear. J Laryngol Otol. 89, 131-143
142. PIRODDA A., SAGGESE D., FERRI G.G. et al. (1997) The role of hypotension in the pathogenesis of sudden hearing loss. Audiology
36, 98-108
143. STRAUSSBERG R., SAIAG E., HAREL L. et al. (2000) Reversible deafness caused by bitidinase deficiency. Paediatr Neurol. 23(3), 269-270
144. SOUAID JP. & RAPPAPORT J.M. (2000) Fluctuating hearing loss associated with the menstrual cycle. J Otolaryngol. 30(4), 246-250
145. MORI S., FUJIEDA S., YAMAMOTO T. et al. (2002) Psychogenic hearing loss with panic anxiety attack after the onset of acute inner ear disorder. J Otorhinolarygol Relat Spec. 64(1), 41-44
146. WAHLIG J.B., KAUFMANN A.M., BALZER J. et al. (1999) Intra-operative loss of auditory function relieved by microvascular decompression of the cochlear nerve. Can J Neurol Sci. 26(1), 44-47

Author Information

Ahmed Aftab, FRCS (ORL-HNS)
Specialist Registrar, Department of Otolaryngology, Doncaster Royal Infirmary

Shahed Quraishi, FRCS (ORL-HNS)
Consultant, Department of Otolaryngology, Doncaster Royal Infirmary

Your free access to ISPUB is funded by the following advertisements:

 

 

Close

Enter the site

Login

Password

Remember me

Forgot password?

Login

SIGN IN AS A USER

Use your account on the social network Facebook, to create a profile on BusinessPress