Reversible Hearing Loss Research Articles

Effects of aspirin on distortion product fine structure: Interpreted by the two-source model for distortion product otoacoustic emissions generation

Distortion product otoacoustic emission (DPOAE) fine structure is due to the interaction of two major components coming from different places in the cochlea. One component is generated from the region of maximal overlap of the traveling waves generated by the two primaries and is attributed to nonlinear distortion (nonlinear component). The other component arises predominantly from the tonotopic region of the distortion product and is attributed to linear coherent reflection (reflection component). Aspirin (salicylate) ototoxicity can cause reversible hearing loss and reduces otoacoustic emission generation in the cochlea. The two components are expected to be affected differentially by cochlear health. Changes in DPOAE fine structure were recorded longitudinally in three subjects before, during, and after aspirin consumption. Full data sets were analyzed for two subjects, but only partial data could be analyzed from the third subject. Resulting changes in the two components of DPOAE fine structure revealed variability among subjects and differential effects on the two components. For low-intensity primaries, both components were reduced with the reflection component being more vulnerable. For high-intensity primaries, the nonlinear component showed little or no change, but the reflection component was always reduced.

Reversible severe sensorineural hearing loss in a 7‐year‐old child (Case Presentation)

Reversible severe sensorineural hearing loss in a 7‐year‐old child (Case Presentation)

Reversible severe sensorineural hearing loss in a 7‐year‐old child (Discussion and Diagnosis)

Reversible severe sensorineural hearing loss in a 7‐year‐old child (Discussion and Diagnosis)

Azithromycin induced hepatocellular toxicity and hepatic encephalopathy in asymptomatic dilated cardiomyopathy

Azithromycin is a widely used macrolide derivative and has generally been considered to be a very safe medication. Though gastrointestinal symptoms and reversible hearing loss are common, potentially serious side effects including angioedema and cholestatic jaundice occurred in less than one percent of patients. We report a case of asymptomatic dilated cardiomyopathy with Azithromycin induced severe hepatocellular toxicity and hepatic encephalopathy.

Reversible Sensorineural Hearing Loss due to Pachymeningitis Associated with Elevated Serum MPO-ANCA

Hypertrophic pachymeningitis is a progressive disease resulting in a diffuse thickening of dura mater due to inflammation, tumor or autoimmune diseases, but most cases are idiopathic. It is seldom reported to be related to sensorineural hearing loss, but it can cause sensorineural hearing loss which can be potentially reversed through treatment. Here, we report the case of a 54-year-old woman who had progressive, bilateral, worse in the left, sensorineural hearing loss and visual disturbance with an accompanying headache over several months. Brain MRI showed diffusely thickened dura mater, highly enhanced after gadolinium administration, which was consistent with pachymeningitis. It was assumed to be related to autoimmune pathogenesis on the basis of elevated serum myeloperoxidase-antineutrophil cytoplasmic antibody (MPO-ANCA) titers. After empirical steroid and cyclophosphamide therapy, auditory impairment improved, especially in the high frequency region of the pure tone audiogram, and significant improvement in the word recognition test. Moreover, a follow-up MRI revealed much decreased enhancement of the dura mater, and the MPO-ANCA titer decreased to within the normal range. In the case of rapidly progressive sensorineural hearing loss or hearing impairment accompanying other cranial neuropathy, pachymeningitis should be taken into consideration, and brain MRI with gadolinium enhancement is the best method of detecting it. Also, to ensure proper treatment, a cautious evaluation including an ANCA work-up should be performed.

Reversible sensorineural hearing loss with normal brainstem auditory evoked potentials in pontine hemorrhage due to capillary telangiectasia

Capillary telangiectasias are vascular malformations most commonly found in the pons that are rarely associated with hemorrhage. We describe a unique case of pontine capillary telangiectasia causing central brainstem hemorrhage leading to reversible sensorineural deafness associated with a normal brainstem auditory evoked response.

Different Manifestations of Auditory Neuropathy

Auditory neuropathy (AN) is characterized by a range of auditory deficits including elevated pure tone thresholds, reduced speech recognition scores, absence of auditory brainstem responses (ABR), and preservation of evoked otoacoustic emissions and the cochlear microphonic (CM) response. With increased advocacy for early implantation, patients with auditory neuropathy may be considered for implantation at or before one year of age. The decision for early implantation of very young patients with clinical test results that suggest AN should be made cautiously as a subset of patients presenting with the clinical constellation of AN may demonstrate reversible hearing loss over time.

Reversible hearing impairment: delayed complication of murine typhus or adverse reaction to azithromycin?

Delayed and reversible hearing loss occurred in a 55-year-old male patient with murine typhus infection. The patient had the initial symptoms of headache, fever and chills, followed by the occurrence of bilateral hearing loss on day 9 from fever onset. Murine typhus was diagnosed with a high IgM titre by indirect immunofluorescence assay. After treatment with azithromycin and prednisolone, the fever and other symptoms subsided gradually and bilateral hearing loss improved 3 weeks later. Though an adverse reaction to azithromycin could not be ruled out, delayed onset of hearing loss was more likely a complication of murine typhus, mainly because the hearing loss did not occur during the azithromycin usage period. Although hearing loss due to murine typhus is rare, clinicians should be alert to the existence of such a delayed complication.

A Case of Bilateral Sensorineural Hearing Loss after Salicylate Intoxication

Salicylates, such as aspirin, are considered the most commonly used medicine in Korea for its anti-inflammatory, anti-pyretic, and analgesic properties. In spite of its wide range of benefits, aspirin produces unwanted adverse effects such as mucosal bleeding in the gastrointestinal tract, renal and hepatic dysfunction, Reye's syndrome in children, and hypersensitivity reactions, etc. Aspirin can also induce ototoxicity, such as reversible hearing loss and tinnitus. The pattern of hearing loss is typically mild to moderate and bilaterally flat in the absence of pre-existing hearing loss. Hearing usually recovers in 72 hours after medication. However, it's rare that salicylate-induced ototoxicity are encountered. So we present this case of bilateral hearing loss that occurred after salicylate intoxication with a review of relevant literature.

Expression of Insulin-like Growth Factors in a Mouse Model of Salicylate Ototoxicity

ObjectivesInsulin-like growth factors (IGFs) are known to be neurotrophic factors, and they efficiently signal to cells to grow, differentiate and survive. The purpose of study was to identify the expressions of IGFs in mice with salicylate ototoxicity, which is a typical reversible hearing loss model.MethodsThe mice were given intraperitoneal injections of salicylate (400 mg/kg) and about a 30 dB threshold shift was achieved at 3 hours. The expressions of IGF-1 and 2 were confirmed by semi-quantitative reverse transcription polymerase chain reaction (RT-PCR) and Western blotting. Localization of IGFs was confirmed using confocal immunofluorescence imaging. For in-vitro study on the HEI-OC1 auditory cells, the cell viability was calculated and the apoptotic features of the nuclei were observed with Hoechst staining.ResultsThe expressions of the IGFs mRNA and protein were significantly increased in the salicylate ototoxicity groups compared with that of the normal control group. Salicylate induced apoptosis and decreased viability of the HEI-OC1 auditory cells in a time- and dose-dependent manner. The expressions of IGFs were localized in the stria vascularis, and these IGFs play a protective role in the in-vivo condition of salicylate ototoxicity.ConclusionIGFs were highly expressed in the mice with salicylate ototoxicity, and this expression was mainly focused in the stria vascularis in the salicylate intoxicated mice. The systemic action of IGFs, which were expressed in the vascular-rich stria vascularis, can act as a major protective mechanism in a mouse model of salicylate ototoxicity.

Sudden hearing loss after a methadone overdose

Sir, We read with interest the case report by Schrock et al. “Sudden sensorineural hearing loss after heroin injection” published in the March 2008 issue of this journal [1]. Over the years, several cases of bilateral sudden sensorineural hearing loss (SHL) after a heroin overdose have been described, including the recent case in this journal. Although these cases all suggest that a large dose of opiates may cause acute hearing loss, the fact that the heroin used in these cases was illegal makes it impossible to rule out an eVect of a heroin contaminant. We now report a patient who, after taking an accidental overdose of prescribed methadone, developed acute, reversible bilateral hearing loss. After taking 15 tablets of 5 mg of methadone a 37-yearold man was admitted to our hospital with nausea, deafness, confusion, and a low respiratory rate. His condition responded well to a single dose of naloxone and a urine sample tested positive for methadone. After regaining full consciousness the patient complained of profound hearing loss with a mild tinnitus. He had no vestibular symptoms or aural fullness. Neurological examination was normal and examination of the tympanic membranes showed no abnormalities. The patient had no history of hearing problems, had never used opiates before and admitted that he had taken the methadone from his brother who was enrolled in a heroin withdrawal program. An ototoxic medication eVect was suspected but the patient consistently denied the use of other drugs or medications including over-the-counter analgesics in the previous weeks. Pure tone audiometry performed a day later revealed bilateral SHL of on average i57 db in the right ear and i40 dB in the left ear (Fig. 1). Within a day, the patient reported marked improvement in hearing and a repeated audiometry 10 days later was completely normal. In our case of sudden, bilateral SHL after an overdose of prescribed methadone an eVect of a contaminant is very unlikely. As our case shows that a methadone overdose can precede bilateral SHL, this supports the claim that in the previous cases of heroin induced hearing loss, heroin itself was indeed the cause. A possible explanation for the fact that this is only the Wrst reported case of bilateral SHL after a methadone overdose is that methadone overdoses are much rarer than heroin overdoses [2]. In theory, it is possible that in our case (and the other cases) the hearing loss was purely coincidental and not because of the overdose itself. Nevertheless, it should be kept in mind that SHL and in particular when it is bilateral is rare and that there was a clear time relation between the overdose and the onset of the hearing loss. In conclusion our case shows that, as with heroin, a methadone overdose may herald sudden bilateral SHL.

Long-term administration of salicylate enhances prestin expression in rat cochlea

Salicylate, a common drug frequently used long term in the clinic, is well known for causing reversible hearing loss and tinnitus. Our previous study, however, demonstrated that chronic administration of salicylate progressively raised the amplitude of distortion product of otoacoustic emissions (DPOAEs), which are mainly caused by (outer hair cell) OHC electromotility. How salicylate affects OHC electromotility to cause this paradoxical increase remains unclear. One possibility is that it could affect prestin, which is a motor protein that contributes to the mechano-electrical properties of OHCs. In this experiment, we assessed the effect of acute and chronic salicylate treatment on prestin expression. Interestingly, after long-term salicylate injection (200 mg/kg, twice daily for 14 days), prestin gene and protein levels were up-regulated about twofold. These levels returned to baseline 14 days after treatment stopped. Acute injection of salicylate (single injection, 400 mg/kg) did not affect prestin levels. These data reveal that chronic salicylate administration markedly, but reversibly, increased prestin levels which may contribute to the enhanced DPOAE amplitudes we observed previously with similar salicylate treatment, which may be responsible for salicylate-induced tinnitus generation.

Reversible Conductive Hearing Loss: Restored Activity in the Central Auditory System

The effect of a reversible, unilateral hearing loss on 2-deoxyglucose (2-DG) uptake in the central auditory system was studied using young gerbils. All animals had a unilateral conductive hearing loss (CHL), induced by atresia, on postnatal day 21 (P21). One week later, on P28, animals had their atresia repaired (CHL/R), or not repaired (CHL/NR), and CHL/NR animals entered the 2-DG experiments. CHL/R animals were allowed a 1-week period of restored binaural hearing experience prior to entering 2-DG experiments on P35. Animals in each group were injected with 2-DG and exposed to ambient sounds for 45 min prior to sacrifice. Uptake of 2-DG was measured in the anteroventral cochlear nucleus (AVCN), the medial superior olive (MSO), and the inferior colliculus (IC) on both sides of the brain. In CHL/NR animals, there were significant differences in uptake between the AVCN, MSO, and IC ipsilateral versus contralateral to the manipulated ear, indicating an imbalance in ascending afferent activity. In CHL/R animals, there were no significant differences, suggesting that 1 week after CHL repair, the appearance of balanced afferent activity had been restored.

A probable case of gabapentin-related reversible hearing loss in a patient with acute renal failure

Background: As described in the literature, gabapentin toxicity in patients with impaired renal function can manifest as coma, myoclonus, tremulousness, or altered mental status. Gabapentin is an antiepileptic agent indicated for use as an adjunct therapy in partial seizures and postherpetic neuralgia but is also prescribed for the treatment of diabetic peripheral neuropathy. Case summary: A 46-year-old white woman (height, 167 cm; weight, 177 kg; body mass index, 62.8 kg/m 2) with a 6-year history of diabetes mellitus and previously normal renal function, presented to the emergency department of Wake Forest University Baptist Medical Center with anuria (a serum creatinine level of 7.4 mg/dL), hearing loss, myoclonus, and confusion with hallucinations lasting for 3 days. Her blood pressure was 110/74 mm Hg. The patient's preadmit medication list included: lisinopril (40 mg QD), hydrochlorothiazide (25 mg QD), and furosemide (80 mg QD) for hypertension; atorvastatin (10 mg QD) for hyperlipidemia; omeprazole (20 mg QD) for gastroesophageal reflux disease; salmeterol/fluticasone inhaler (100/50 μg; 1 puff BID) and albuterol metered-dose inhaler (90 μg as needed) for asthma; metformin (500 mg BID) and insulin lispro per sliding scale for type 2 diabetes mellitus; oxycodone controlled release (60 mg TID) for chronic osteoarthritis and low back pain; alprazolam (0.5 mg every 8 hours as needed) for generalized anxiety disorder; venlafaxine (150 mg BID) for depression; and gabapentin (300 mg TID) for diabetic peripheral neuropathy. The patient's symptoms (hearing loss, myoclonus, and confusion) improved after 1 session of hemodialysis (~10 hours following admission) and had resolved at the time of discharge (4 days later). On admission, the gabapentin concentration was 17.6 μg/mL, and following hemodialysis, the gabapentin concentration was undetectable (by discharge/day 4). The timing of the patient's last dose of gabapentin is unknown. Normal doses for the treatment of diabetic peripheral neuropathy range from 900 to 3600 mg/d divided 3 times daily. Conclusions: We report a patient with acute renal failure who developed hearing loss, myoclonus, and confusion with hallucinations in the presence of elevated gabapentin concentrations. Due to rapid improvement after hemodialysis and discontinuation of gabapentin, we believe that these symptoms were probably due to gabapentin toxicity.

Sensorineural Hearing Loss After Dental Extraction Under General Anesthesia: Report of a Case

Sudden sensorineural hearing loss (SNHL) is an uncommon event, with an estimated incidence of 5 to 20 cases per year per 100,000 population. It is often idiopathic or secondary to infection. 1 Byl Jr, F.M. Sudden hearing loss: Eight years' experience and suggested prognostic table. Laryngoscope. 1984; 94: 647 Crossref PubMed Google Scholar It is a well-recognized event after a cardiopulmonary bypass, with a reported incidence of 1 in 1,000. This is attributed to microemboli from the cardiopulmonary tree. 2 Plasse H.M. Mittleman M. Frost J. Unilateral sudden hearing loss after open heart surgery A detailed study of seven cases. Laryngoscope. 1981; 91: 101 Crossref PubMed Google Scholar Other causes include lesions of the external, middle, and inner ear, internal auditory meatus, cerebellopontine angle, and central nervous system. 3 Goodhill V. Harris I. Brockman S.J. Sudden deafness and labyrinthine window rupture. Ann Otol Rhinol Laryngol. 1973; 82: 2 PubMed Google Scholar It is considered an otologic emergency, and early diagnosis and treatment may result in a favorable outcome. 4 Pau H. Selvadurai D. Murty G.E. Reversible sensorineural hearing loss after non-otological surgery under general anaesthetic. Postgrad Med J. 2000; 76: 304 Crossref PubMed Scopus (9) Google Scholar It is, however, extremely uncommon after general anesthesia (GA) for noncardiac and nonotologic procedures. Only 44 such cases were reported in the literature, mainly after spinal, abdominal, gynecologic, and ophthalmic procedures. 3 Goodhill V. Harris I. Brockman S.J. Sudden deafness and labyrinthine window rupture. Ann Otol Rhinol Laryngol. 1973; 82: 2 PubMed Google Scholar , 4 Pau H. Selvadurai D. Murty G.E. Reversible sensorineural hearing loss after non-otological surgery under general anaesthetic. Postgrad Med J. 2000; 76: 304 Crossref PubMed Scopus (9) Google Scholar , 5 Park P. Toung J.S. Smythe P. et al. Unilateral sensorineural hearing loss after spine surgery: Case report and review of literature. Surg Neurol. 2006; 66: 415 Abstract Full Text Full Text PDF PubMed Scopus (17) Google Scholar , 6 Farrel R.W. Pemberton M.N. Parker A.J. et al. Sudden deafness after dental surgery. Br Med J [Clin Res]. 1991; 303: 1270 Google Scholar , 7 Evan K.E. Tavill M.A. Goldberg A.N. et al. Sudden sensorineural hearing loss after general anaesthesia for nonotological surgery. Laryngoscope. 1997; 107: 747 Crossref PubMed Scopus (26) Google Scholar , 8 Goodhill V. Labyrinthine membrane ruptures in sudden sensorineural hearing loss. Proc R Soc Med. 1976; 69: 565 PubMed Google Scholar We are aware of only 1 previous report of SNHL after dental extraction under GA. We report on a case of sudden SNHL after a dental extraction under GA, and we review the relevant literature.

Reversible bilateral sensorineural hearing loss in a woman with cerebral venous thrombosis

Reversible bilateral sensorineural hearing loss in a woman with cerebral venous thrombosis

A case of delayed endolymphatic hydrops due to mumps viral infection treated with the Meniett device

Objective: We report a case of delayed endolymphatic hydrops due to complicating mumps virus infection that was treated with the Meniett device.Method: Case reports and a review of the world literature on delayed development of endolymphatic hydrops after mumps virus infection are presented.Results: The case of a woman who presented with unilateral, reversible sensorineural hearing loss following mumps infection and was successfully treated with the Meniett device is presented. This woman developed profound sensorineural hearing loss and intractable vertigo spells a few months after contracting mumps. In this case, the incubation period interval between the development of mumps infection and the diagnosis of DEH was only one year. DEH (Delayed endolymphatic hydrops) is a clinical entity characterized by profound sensorineural hearing loss in one ear during its early phase; after a prolonged period of time, DEH enters the late phase, which is characterized by different otologic symptoms. Although the most common causes of DEH are inflammation, trauma and other unidentified events during childhood, viral infections, including mumps, represent one of the known causes of DEH. Mumps infection sometimes represents a confirmed etiology of DEH Sometimes DEH can definitively be diagnosed as being caused by mumps infection.Conclusion: This is the first case report to demonstrate the efficacy of the Meniett device in the treatment of DEH due to complicating mumps infection.

Reversible hearing loss in temporal association with chemoprophylactic mefloquine use

A 67 year old Caucasian lady received pre-travel immunizations against tetanus, diphtheria, typhoid fever, hepatitis A, and mefloquine chemoprophylaxis. Left sided hearing loss consequent upon tympanic rupture was present since childhood; she was otherwise in good health and without history of recent upper respiratory tract infection. After 1 dose of mefloquine right sided tinnitus and hearing loss developed; audiometry revealed mixed left sided loss and right sided sensorineural loss (-90db at 1kHz; -70dB at 4kHz). Prednisone, aspirin and omeprazole were prescribed; mefloquine chemoprophylaxis was discontinued. On day 9 of her hearing loss the tinnitus suddenly disappeared, and right sided hearing improved. Audiometry on day 93 revealed normal right sided hearing (-10dB at 1kHz; -10dB at 4kHz). Causality remains undetermined, but it may be prudent to avoid mefloquine chemoprophylaxis in individuals with known hearing impairment.

Salicylate Ototoxicity and its Implications for Cochlear Microphonic Potential Generation

Salicylic acid causes a reversible sensori-neural hearing loss. Its ototoxicity is probably related to its effect on prestin, the motor protein of the outer hair cells. In order to gain further insight into the mechanism and implications of its ototoxicity, auditory nerve brainstem evoked responses, compound action potentials of the auditory nerve, distortion product otoacoustic emissions, and cochlear microphonic potentials (CM) and vestibular evoked potentials were recorded before and after systemic salicylate administration. These responses were depressed, except for the CM and the vestibular evoked potential. This result and additional considerations provide evidence that the extracellularly recorded CM does not represent the summation of intracellular outer hair cell receptor potentials. It is possible that the CM reflects an early stage of mechano-electrical transduction by the outer hair cells, before the activation of the cochlear amplifier and the later stages of transduction.

Myeloma cast nephropathy presenting as acute onset bilateral reversible hearing loss

A case of myeloma cast nephropathy masquerading as bilateral deafness of acute onset, probably due to hyperviscosity syndrome, is presented. Audiometry and kidney biopsy confirmed the diagnosis. Despite the presence of multiple poor prognostic features, the patient responded satisfactorily to plasmapharesis, dialysis and chemotherapy (VAD regimen) along with other supportive measures. The patient had excellent renal recovery, but hearing improvement was delayed for 1 month. Various causes of hearing loss in patients with multiple myeloma and available therapeutic options are discussed.