Downbeat Nystagmus and Bilateral Sudden Hearing Loss by Suicidal Aspirin Intoxication.

Ototoxic side effects such as sensorineural hearing loss and tinnitus can be caused by acute salicylate intoxication. Bilateral symmetric sensori- neural hearing loss involving all tested frequencies is a typical pattern of hearing loss in acute salicylate intoxication, which usually resolves within 2 or 3 days without any specific treatment for ototoxicity. Herein, we report a case of suicidal aspirin intoxication resulting in sudden bilateral hearing loss and vertigo. The patient exhibited spontaneous downbeat nystagmus, and the mechanism underlying this characteristic nystagmus is discussed.

Intravenous methadone causes acute toxic and delayed inflammatory encephalopathy with persistent neurocognitive impairments.

BACKGROUND: The mu-opioid agonist methadone is administered orally and used in opioid detoxification and in the treatment of moderate-to-severe pain. Acute oral methadone-use and -abuse have been associated with inflammatory and toxic central nervous system (CNS) damage in some cases and cognitive deficits can develop in long-term methadone users. In contrast, reports of intravenous methadone adverse effects are rare. CASE PRESENTATION: Here, we report a patient who developed acute bilateral hearing loss, ataxia and paraparesis subsequently to intravenous methadone-abuse. While the patient gradually recovered from these deficits, widespread magnetic resonance imaging changes progressed and delayed-onset encephalopathy with signs of cortical dysfunction persisted. This was associated with changes in the composition of monocyte and natural killer cell subsets in the cerebrospinal fluid. CONCLUSION: This case suggests a potential bi-phasic primary toxic and secondary inflammatory CNS damage induced by intravenous methadone.

Bilateral Sensorineural Hearing Loss Associated With Nivolumab Therapy for Stage IV Malignant Melanoma.

OBJECTIVES: Present the case of a 67-year-old male with stage IV malignant melanoma who presented with uveitis and sensorineural hearing loss (SNHL) while on nivolumab and review the literature for likely etiologies. METHODS: A retrospective case review was conducted. The current literature was accessed to inquire about possible pathologic mechanisms and treatment options. RESULTS: A 67-year-old male with stage IV malignant melanoma was treated with nivolumab. During therapy, the patient presented with bilateral uveitis, vertigo, and bilateral moderate sloping to moderate-severe SNHL. After 4 cycles of nivolumab, restaging scans showed no evidence of disease. Nivolumab was discontinued. The patient was placed on a 3-week course of systemic high dose steroids and topical steroid eye drops. Both his uveitis and SNHL resolved after treatment. Nivolumab enhances the antitumor activity of T cells by inhibiting the programed death-1 receptor. While nivolumab has shown great promise in the treatment of many types of cancers, it has also been associated with many autoimmune side effects. We propose the etiology of this 67-year-old male's SNHL and uveitis are the result of an autoimmune process secondary to an augmented T cell response induced by nivolumab. CONCLUSION: While immunotherapeutic agents such as nivolumab have shown great promise in the treatment of cancer, one should maintain an awareness and caution of autoimmune side effects such as uveitis and SNHL.

Etiology of Childhood Bilateral Sensorineural Hearing Loss in Shandong Province, China.

Objectives The purpose of this study is to ascertain the etiology of bilateral sensorineural hearing loss (SNHL) in children aged ≤ 18 years living in Shandong province. Method Data were taken from a cross-sectional study, which was conducted between 2015 and 2017. The study included children aged ≤ 18 years, recruited from special schools for children with hearing loss and from hearing rehabilitation centers in Shandong province of China. Children were screened for bilateral SNHL through audiological testing. Clinical examination, genetic testing, and structured interviews were conducted for those children who were identified as having hearing loss to identify the potential cause. Results The etiology of bilateral SNHL in our sample was genetic in 874 (39.3%), acquired in 650 (29.3%), and unknown in 697 (31.4%) children. Among children with acquired SNHL, the cause was maternal viral infection in 75 (11.5%); perinatal factors in 238 (36.6%); meningitis, measles, and mumps in 146 (22.5%); and ototoxic exposure in 117 (18%) children. Among the children with genetic SNHL, only 44 (4.9%) were identified as having syndromic hearing loss, and the remainder (95.1%) were classified as nonsyndromic hearing loss. Conclusion The findings indicated that nearly 30% of bilateral SNHL in Shandong province could be preventable through immunization, early prenatal diagnosis, proper treatment of infections, and avoidance of prescription of ototoxic drugs. This finding emphasizes the need for programs aimed at improving the health services at primary and secondary levels of health care, which will in turn prevent childhood hearing loss.

Case of neuromyelitis optica: bilateral sensorineural hearing loss and transverse myelopathy following intrathecal chemotherapy.

Neurotoxicity from intrathecally administered chemotherapeutic drugs is frequent, particularly with some agents like methotrexate, which are more prone to developing adverse effects. Myelopathy ranks among the most frequently reported neurological entities; with the diagnosis being straightforward, after ruling out infectious, metabolic, autoimmune or paraneoplastic causes. Scarcity of cases precludes evidence-based recommendations for the management of these complications. The most common therapeutic approach consists of the suspension of chemotherapy, exclusion of infectious and neoplastic causes, with prompt administration of high-dose steroids. We report a 21-year-old patient with acute lymphoblastic leukaemia, who developed acute transverse myelitis and bilateral sensorineural hearing loss, after five rounds of intrathecal methotrexate and cytarabine. Although neurotoxicity from both agents has been documented, this combination has not been previously reported.

Cochlear Implantation after Bromate Intoxication-Induced Bilateral Deafness: A Case Report.

Hearing loss is a common consequence of the strong acidosis induced by bromate poisoning. Partial hearing recovery has been achieved through medical or rehabilitative therapy but reports of surgical otology treatment for this condition are rare. We report the case of a 48-year-old female patient who underwent cochlear implantation after bromate intoxication had induced bilateral deafness. In cases with life-threatening renal damage, the diagnosis of hearing loss is sometimes delayed, but in our case, hearing impairment was unavoidable despite early detection of symptoms and early disruption of the use of diuretics that could cause hearing damage. Hearing loss 12 hours after bromate ingestion was successfully reversed through cochlear implantation (CI) six months after completing acute phase treatment, including dialysis for acute kidney injury. The benefit of CI for deafness by bromate intoxication is highlighted by this case.

Bilateral sensorineural hearing loss induced by regorafenib.

WHAT IS KNOWN AND OBJECTIVE: Regorafenib is a novel multi-targeted tyrosine kinase inhibitor approved for use in refractory metastatic colorectal cancer, advanced gastrointestinal stromal tumours and hepatocellular carcinoma. We report a case of bilateral sensorineural hearing loss caused by regorafenib. CASE SUMMARY: A 48-year-old woman was diagnosed with colon cancer that had metastasized to the liver, ureter and left ovary. She was initially treated with oral regorafenib at the lowest recommended dosage of 80 mg/d for 2 weeks, at which point the dose was increased to 120 mg/d. On the second day after the regorafenib dosage increase (ie, 15 days after starting regorafenib), she suddenly developed a bilateral hearing loss. Regorafenib was discontinued immediately, and the patient was treated with a course of intravenous steroids. Five weeks later, her bilateral hearing had subjective partial improvement. WHAT IS NEW AND CONCLUSION: This is the first report of bilateral sensorineural hearing loss induced by regorafenib.

An audiological profile of patients infected with multi-drug resistant tuberculosis at a district hospital in KwaZulu-Natal.

BACKGROUND: The increased incidence of multi-drug-resistant tuberculosis (MDR-TB) and the consequent use of aminoglycosides with their ototoxic potential necessitate a better understanding of the audiological pattern of infected patients. OBJECTIVE: To describe the occurrence and nature of hearing loss in patients with MDR-TB receiving aminoglycosides over a period of 6 months. METHODS: Baseline and five consecutive monthly audiological assessments were conducted on 52 adults at a hospital in KwaZulu-Natal. A longitudinal descriptive study was implemented. A conventional audiological test battery, extended high frequency audiometry and otoacoustic emission testing were conducted. Data were analysed using SPSS version 19 statistical software package. RESULTS: Decreased hearing was the most common audiological symptom experienced. Bilateral sensorineural hearing loss was predominant. Ototoxic hearing loss was noted in 27 participants (52%) in 1 month post-treatment. Hearing loss progressed from mild to moderate at post-treatment one, to moderate to severe at post-treatment three and severe to profound at post-treatment five. Changes in hearing function were noted in 52 participants (100%) by post-treatment five. High and ultra-high frequencies were most affected. Speech discrimination scores deteriorated over time. The number of patients with absent distortion product otoacoustic emissions increased over treatment duration. CONCLUSION: The greatest effects were observed in the high frequencies before manifesting in the lower frequencies. This highlights the importance of inclusion of high frequency audiometry in the early detection of ototoxicity which can go undiagnosed with traditional audiometry. The high prevalence of hearing loss has implications for the provision of audiological service to this patient population.

Neurotrophic and antioxidant effects of silymarin comparable to 4-methylcatechol in protection against gentamicin-induced ototoxicity in guinea pigs.

BACKGROUND: Despite that gentamicin is a very effective aminoglycoside, its potential ototoxicity which is of irreversible nature makes a challenge and limitation for its use. This study was designed to investigate possible neurotrophic and antioxidant effects of silymarin comparable to 4-methylcatechol in protection against gentamicin-induced ototoxicity. METHODS AND RESULTS: Twenty pigmented guinea pigs were divided into four equal groups, where group I served as normal control group. The other groups received gentamicin (120 mg/kg/day, ip) for 19 days where group II given vehicle of 1% CMC, group III and group IV were pre-treated 2h before gentamicin by 4-methylcatechol (10 µg/kg, ip) and silymarin (100mg/kg, oral gavage), respectively. The main findings indicated that silymarin exhibited restoration of nerve growth factor (NGF) levels and increased tropomyosin-related kinase receptors-A (Trk-A) m-RNA expression in cochlear tissue and preservation of hair cells of organ of Corti by scanning electron microscopy (SEM) with significant decrease in auditory brainstem response (ABR) threshold compared to 4-methylcatechol. Only silymarin caused significant amelioration in oxidative stress state by reducing malondialdehyde (MDA) levels and increasing catalase activity. CONCLUSIONS: Silymarin exerts superiority over 4-methylcatechol when recommended as protective agent against gentamicin ototoxicity based on its efficient neurotrophic and antioxidant activities.

High prevalence of cisplatin-induced ototoxicity in Cape Town, South Africa.

BACKGROUND: Cisplatin is administered as the first-line treatment of soft-tissue cancers. It has a reported cure rate of up to 85%, but is associated with a high incidence of ototoxicity, characterised by irreversible bilateral hearing loss and affecting 23 - 50% of adults who receive the drug. OBJECTIVES: To determine the incidence of cisplatin-induced ototoxicity at Groote Schuur Hospital (GSH), Cape Town, South Africa. METHODS: retrospective cross-sectional study of cisplatin-receiving cancer patients attending GSH between January 2006 and August 2011. RESULTS: A total of 377 patients were recorded as receiving cisplatin therapy during the study period. A 300% increase in new cisplatin-receiving patients receiving audiological monitoring was observed between 2006 and 2010. However, only patients with all clinical data as well as baseline and follow-up audiometric analyses were investigated. One hundred and seven such patients were identified, 55.1% of whom developed cisplatin-induced ototoxicity while receiving high-dose (> or = 60 mg/m2) cisplatin treatment. Higher cumulative cisplatin dosages were associated with development of significant hearing loss (p = 0.027). The odds of developing cisplatin-induced hearing loss were elevated for patients with head and neck tumours and lymphoma (p = 0.0465 and p = 0.0563, respectively) and were significantly lower for those with reproductive cancers (p = 0.0371). CONCLUSION: Comprehensive audiological monitoring should be available for every patient during cisplatin treatment to minimise the development of disabling hearing loss.

A child with severe hearing loss associated with maternal cisplatin treatment during pregnancy.

BACKGROUND: Cisplatin is considered safe to use during the second and third trimesters of pregnancy in patients with cancer. CASE: A 34-year-old pregnant woman was diagnosed with cervical cancer. She received five weekly dosages of cisplatin and paclitaxel, starting at 26 5/7 weeks of gestation. An elective cesarean delivery was performed at 34 4/7 weeks of gestation. After birth, the neonate was diagnosed with severe bilateral perceptive hearing loss. CONCLUSION: Cisplatin during the second and third trimesters of pregnancy may lead to fetal ototoxicity.

[Plasmodium falciparum and Salmonella Typhi co-infection: a case report]. / Plasmodium falciparum ve Salmonella Typhi koenfeksiyonu: Bir olgu sunumu.

Malaria and salmonella infections are endemic especially in developing countries, however malaria and salmonella co-infection is a rare entity with high mortality. The basic mechanism in developing salmonella co-infection is the impaired mobilization of granulocytes through heme and heme oxygenase which are released from haemoglobin due to the breakdown of erythrocytes during malaria infection. Thus, a malaria infected person becomes more susceptible to develop infection with Salmonella spp. In this report a case with Plasmodium falciparum and Salmonella Typhi co-infection was presented. A 23-year-old male patient was admitted to hospital with the complaints of diarrhea, nausea, vomiting, abdominal pain, fatigue and fever. Laboratory findings yielded decreased number of platelets and increased ALT, AST and CRP levels. Since he had a history of working in Pakistan, malaria infection was considered in differential diagnosis, and the diagnosis was confirmed by the detection of P.falciparum trophozoites in the thick and thin blood smears. As he came from a region with chloroquine-resistant Plasmodium, quinine (3 x 650 mg) and doxycycline (2 x 100 mg/day) were started for the treatment. No erythrocytes, parasite eggs or fungal elements were seen at the stool microscopy of the patient who had diarrhoea during admission. No pathogenic microorganism growth was detected in his stool culture. The patient's blood cultures were also taken in febrile periods starting from the time of his hospitalization. A bacterial growth was observed in his blood cultures, and the isolate was identified as S. Typhi. Thus, the patient was diagnosed with P.falciparum and Salmonella Typhi coinfection. Ceftriaxone (1 x 2 g/day, 14 days) was added to the therapy according to the results of antibiotic susceptibility test. With the combined therapy (quinine, doxycycline, ceftriaxone) the fever was taken under control, his general condition improved and laboratory findings turned to normal values. However, on the fifth day of his anti-malaria therapy sudden bilateral hearing loss developed due to quinine use. Thus, the treatment was replaced with an artemisinin-based (arthemeter/lumefantrine) combination therapy. No adverse effects were detected due to artemisinin-based therapy, and the patient completely recovered. In conclusion, if a patient is diagnosed with malaria, he/she should be closely monitored in terms of having co-infections and appropriate diagnostic methods including blood cultures taken in febrile episodes should be performed.

Bilateral hearing loss after dichloromethane poisoning: a case report.

Dichloromethane is a widely used organic solvent. Occupational exposure to dichloromethane is frequent and can result in both acute and chronic toxicity, affecting mostly the central nervous system, directly or through its metabolite, carbon monoxide. The effects of dichloromethane on the peripheral nervous system are debated. Here we report the case of a 37-year-old woman who was accidentally exposed to dichloromethane. In the days following the incident she experienced bilateral hypoacusis. Hearing loss regressed after 25 days treatment with hyperbaric oxygen. This is the first report of sudden hearing loss after acute exposure to dichloromethane, suggesting a possible toxic effect of this solvent on the auditory system.

Methadone-induced bilateral severe sensorineural hearing loss.

Methadone, a long-acting opiate agonist, and naltrexone, an opiate receptor antagonist, are both commonly used to treat patients with morphine and heroin addiction. We present a rare case of methadone-induced persistent bilateral sensorineural hearing loss (SNHL) after chronic naltrexone use and review opioid-induced hearing loss in the literature. Methadone-induced hearing loss has been described previously described in the literature with all reported cases recovering functional hearing. This is the first description of persistent bilateral severe SNHL following methadone ingestion. We propose opiate receptor sensitization from prolonged naltrexone use as a predisposing factor for methadone-induced irreversible cochlear injury.

Hearing loss associated with xylene exposure in a laboratory worker.

BACKGROUND: Xylene is an organic solvent, widely used in histology laboratories and other occupational settings. Research in animals has demonstrated that xylene induces outer hair cell damage. Evidence regarding the effects of xylene in humans is only available from studies investigating workers exposed to mixtures of solvents containing xylene. These data indicate that mixtures of solvents containing xylene may induce hearing loss and central auditory dysfunction. PURPOSE: To comprehensively evaluate the peripheral and central auditory system of a histology laboratory worker exposed to xylene, who had presented with bilateral mild sensorineural hearing loss at an initial assessment. RESEARCH DESIGN: A case report of a male histology laboratory worker who has been exposed to xylene for over 20 yr. RESULTS: A diagnosis of bilateral mild sensorineural hearing loss of cochlear origin was made on the basis of otological, neuroimaging, and audiological examinations. Results indicating the absence of transient-evoked otoacoustic emissions, and auditory brainstem responses as expected for a mild cochlear hearing loss, were obtained. CONCLUSIONS: The observed bilateral mild sensorineural hearing loss was considered to have been induced by xylene exposure, due to the absence of any other etiological factors related to the onset of hearing loss. The results found in this patient are in agreement with animal data indicating xylene-induced ototoxicity. Xylene-exposed individuals should be audiologically monitored on a regular basis.

Bilateral cochlear implantation after ethylene glycol intoxication: a case report.

OBJECTIVE: To report a case of deafness and blindness caused by ethylene glycol poisoning and treated by bilateral simultaneous cochlear implantation. STUDY DESIGN: Case report. SETTING: University teaching hospital, tertiary referral center. PATIENT: 37 years old man poisoned with ethylene glycol. INTERVENTION: Bilateral simultaneous Medel Sonata cochlear implants. OUTCOME MEASURE: BKB sentences (Bamford-Kowal-Bench sentence tests); AB words (Arthur Boothroyd monosyllabic words). RESULTS: Successful rehabilitation of hearing in a case of deafness and blindness of acute onset. CONCLUSION: Bilateral CI is an effective method of hearing rehabilitation in presence of additional disability (blindness).

Outcomes with bilateral cochlear implantation following sudden dual sensory loss after ethylene glycol poisoning.

Acute loss of vision accompanied by profound loss of hearing is fortunately rare, but has a catastrophic effect on both the patient and their family. Re-establishing communication and spatial awareness are high priorities. We describe the case of a 45 year-old man who presented as a result of poisoning by ethylene glycol. Following assessment by clinicians who learned the deaf-blind alphabet in order to communicate, he had his hearing successfully rehabilitated with simultaneous bilateral cochlear implants. The patient recovered the ability to understand speech near perfectly in quiet, to attend to the ear giving the clearer signal in noise, and to localise sources of sound. The patient reported that the latter skill facilitated mobility. This is the first reported case of a patient with acute dual sensory loss due to ethylene glycol poisoning benefiting from bilateral cochlear implants.

Sudden bilateral sensorineural hearing loss following polysubstance narcotic overdose.

BACKGROUND: Auditory disorders associated with substance abuse are rare. Hearing loss secondary to heroin and hydrocodone abuse has been described variously as not always responsive to steroid management, as not always reversible, and in some cases, as nonresponsive profound sensorineural hearing loss requiring cochlear implantation. We present a case of a teenager with sudden-onset moderate to severe bilateral sensorineural hearing loss after documented polysubstance "binging." The hearing loss improved substantially after high-dose steroid and vasoactive therapy. PURPOSE: The purpose of this report is to describe the hearing disorder of a patient who had awakened with a bilateral severe hearing loss following a night of recreational drug abuse. RESEARCH DESIGN: Case report and review of the literature. DATA COLLECTION AND ANALYSIS: The subject of this report is an 18-yr-old patient with a history of substance abuse. Data collected were magnetic resonance /computed tomography brain imaging; metabolic, infectious disease, and autoimmune evaluation; and extensive audiologic evaluation, including pure-tone and speech audiometry, immittance measures, distortion-product otoacoustic emissions, and auditory brainstem response testing. Serial audiograms were collected for 10 mo following the onset of symptoms. RESULTS: Two days of polysubstance abuse (heroin, benzodiazepine, alcohol, and crack [smoked cocaine]) resulted in moderately severe sensorineural hearing loss bilaterally. The loss responded to a 1 mo course of high-dose prednisone and a 10 mo course of pentoxifylline. Hearing sensitivity subsequently improved, leaving only residual high-frequency sensorineural hearing loss. CONCLUSIONS: This case report highlights the importance of "recreational" drug abuse in the evaluation of sudden hearing loss. Potential etiologies include altered pharmacokinetics, vascular spasm/ischemia, encephalopathy, acute intralabyrinthine hemorrhage, and genetic polymorphisms of drug-metabolizing enzymes.

Sudden bilateral sensorineural hearing loss as an unusual consequence of accidental ingestion of potassium hydroxide.

OBJECTIVE: To discuss the possible etiopathogenetic mechanism of inner ear damage induced by the ingestion of potassium hydroxide (KOH). CLINICAL PRESENTATION AND INTERVENTION: We report the case of a 37-year-old patient with sudden bilateral sensorineural hearing loss after accidental ingestion of a KOH solution. The first ear, nose and throat examination disclosed only mild edema of the upper airways. He was treated in the intensive care unit and prescribed high-dose steroids, proton pump inhibitors and sucralfate for 2 weeks. Unfortunately, there was no recovery of the hearing loss, and no audiogram changes were noticed after 12 months of follow-up. CONCLUSION: After exploring the possible etiopathogenetic mechanism involved, the authors believe that in this case, a transient severe hemodynamic imbalance can actually be considered to be the most reliable explanation for the inner ear damage and subsequent onset of permanent bilateral sensorineural hearing loss.