Progression Of Sensorineural Hearing Loss Research Articles

Advances in the Study of Etiology and Molecular Mechanisms of Sensorineural Hearing Loss.

Sensorineural hearing loss (SNHL), a multifactorial progressive disorder, results from a complex interplay of genetic and environmental factors, with its underlying mechanisms remaining unclear. Several pathological factors are believed to contribute to SNHL, including genetic factors, ion homeostasis, cell apoptosis, immune inflammatory responses, oxidative stress, hormones, metabolic syndrome, human cytomegalovirus infection, mitochondrial damage, and impaired autophagy. These factors collectively interact and play significant roles in the onset and progression of SNHL. The present review offers a comprehensive overview of the various factors that contribute to SNHL, emphasizes recent developments in understanding its etiology, and explores relevant preventive and intervention measures.

Assessment of the effect of a health-improving program to preserve the professional suitability of employees at a gas transportation enterprise in territories equated to the Far North

Introduction. At the Russian gas transportation enterprises, we traditionally consider a noise as the main harmful production factor. Long-term work activity under its influence is associated with the risk of developing sensorineural hearing loss, which, with progression, entails loss of professional suitability. Risk factors for the development of sensorineural hearing loss at an enterprise of this profile operating in territories equated to the Far North are also arterial hypertension and an increase in total cholesterol. In such a situation, the prevention of hearing loss, adapted to the specifics of the work of the leading professional groups of the gas transportation enterprise, is of particular importance. In connection with these circumstances, the researchers developed and tested a comprehensive program for the prevention of the development and progression of sensorineural hearing loss, which contributed to the correction of risk factors.
 The study aims to evaluate the effectiveness of the long-term implementation of a comprehensive medical program for the prevention of the development and progression of chronic sensorineural hearing loss, correction of arterial hypertension and total cholesterol levels in employees of the main production of a gas transportation enterprise operating in conditions equated to the Far North.
 Materials and methods. Over a 10-year period, we have tracked the dynamics of the health status of 120 employees of the main production, whose work activities took place under the influence of industrial noise with an intensity from 50 to 94 dBA during a comprehensive program of medical prevention of the development and progression of sensorineural hearing loss. Preventive measures consisted of: a course of drug therapy, physiotherapy procedures with the use of transcranial electrical stimulation, rational nutrition, phytotherapy, physical therapy, classes in the format of a "Healthy lifestyle School" in order to form the patient's motivation to lead a healthy lifestyle.
 Results. Out of 96 workers with normal hearing, six people (6.25%) had hearing loss up to the first degree, which does not yet entail loss of professional suitability. Among 24 specialists with initially reduced hearing (from signs of noise exposure to hearing loss by second degree), the audiogram did not change in 3 people, in 15 people specialists observed improvement within one degree, in 6 people — progression in the same dimension. The proportion of patients with arterial hypertension and hypercholesterolemia did not change significantly, but we observed a significant decrease in the proportion of obese patients.
 Conclusion. Thus, we have shown the possibility of preventing the persistent loss of professional of workers caused by the development of sensorineural hearing loss in the degree from moderate to higher.
 Limitations. At enterprises operating in other climatic zones and using less noise-hazardous equipment, other results may be obtained.

Pediatric internal auditory canal cavernous hemangioma with rapid progression of sensorineural hearing loss: illustrative case.

Cavernous hemangioma of the internal auditory canal is extremely rare and is characterized by symptoms such as vertigo, sensorineural hearing loss, and facial nerve dysfunction. A health examination on an 11-year-old female in the fifth grade revealed hearing loss in the left ear. She also had dizziness that had persisted for approximately 1 year. Pure-tone audiometry revealed sensorineural hearing loss in her left ear. Rightward horizontal and rotatory nystagmus was detected. Facial paralysis was not present. Magnetic resonance imaging showed a lesion that was suspected to be hemangioma. The authors selected a left suboccipital retrosigmoid approach. The tumor showed a berry-tufted appearance throughout the cerebellopontine angle. The seventh cranial nerve penetrated the tumor and partly circulated outside the tumor with marked adhesion. The authors partially resected the tumor to avoid damaging the facial nerve. A histological examination identified cavernous hemangioma. The fundamental treatment for cavernous hemangioma of the internal auditory canal is complete surgical removal; however, any surgical intervention may result in hearing loss and facial paralysis. The extent of surgery needs to be decided intraoperatively based on the balance between preoperative symptoms and postoperative complications.

Analysis of etiopathogenetic factors in the development and progression of perceptual hearing loss

Relevance: Sensorineural deafness is a polyetiological disease. The most studied etiopathogenesis factors are vascular, acoustic and age. Despite numerous studies, the factors of the development and progression of chronic sensorineural hearing loss, as well as tinnitus, remains unclear in 25-30% of cases. Purpose: to determine the most influential factors in the development and progression of sensorineural hearing loss in patients who work in conditions of increased sound load. Methods and materials: The study was conducted on the basis of the Kyiv Clinical Hospital on Railway Transport No. 2, as a division of the Department of Otolaryngology of the O.O. Bogomolets National Medical University. We conducted an examination of 678 patients who work under conditions of increased acoustic load (drivers, drivers' assistants, fitters, railway track fitters) with the aim of identifying perceptual disorders and analyzing the etiopathogenesis factors of chronic sensorineural hearing loss. Further examinations were carried out in 89 patients who had perceptual disorders. Results: The first degree of deafness was detected in 75.3% of patients, the second and third - in 12.35% each. The largest number was made up of patients aged 56 to 65 years, but even among those examined up to 45 years of age, there were 2 cases of third-degree hearing loss. The correlation between age and the degree of deafness in patients with perceptual disorders, as well as age and decreased whisper perception was weakly positive: 0.167 and 0.261, respectively; The relationship between indicators of work experience and the degree of hearing loss, as well as work experience and a decrease in the perception of whispered speech – the average degree of severity is 0.382 and 0.476, respectively. These data were confirmed with the help of two-factor analysis. Conclusions: Among patients with perceptual disorders who work in conditions of increased sound load, the largest number was aged 56-65 with more than 30 years of experience and had the first degree of hearing loss. The relationship between hearing impairment and age and work experience was found to be weak and medium, respectively. 11.1% of cases of third-degree hearing loss were found among patients under 45 years of age and with a work experience of up to 30 years. This may indicate the presence of other factors in them, for example, genetic disorders, which significantly affect the development and progression of sensorineural hearing loss and require further research.

Approaches to MitigateMitochondrialDysfunctionin Sensorineural Hearing Loss.

Mitochondria are highly dynamic multifaceted organelles with various functions including cellular energy metabolism, reactive oxygen species (ROS) generation, calcium homeostasis, and apoptosis. Because of these diverse functions, mitochondria are key regulators of cell survival and death, and their dysfunction is implicated in numerous diseases, particularly neurodegenerative disorders such as Alzheimer's Disease, Parkinson's Disease, and Huntington's Disease. One of the most common neurodegenerative disorders is sensorineural hearing loss (SNHL). SNHL primarily originates from the degenerative changes in the cochlea, which is the auditory portion of the inner ear. Many cochlear cells contain an abundance of mitochondria and are metabolically highly active, rendering them susceptible to mitochondrial dysfunction. Indeed, the causal role of mitochondrial dysfunction in SNHL progression is well established, and therefore, targeted for treatment. In this review, we aim to compile the emerging findings in the literature indicating the role of mitochondrial dysfunction in the progression of sensorineural hearing loss and highlight potential therapeutics targeting mitochondrial dysfunction for hearing loss treatment.

Sensorineural hearing loss as a predictor of endothelial dysfunction in some non-communicable diseases in the working population (a review of interdisciplinary studies)

Interdisciplinary publications suggesting an etiopathogenetic relationship between sensorineural hearing loss and some chronic non-communicable diseases were reviewed. A substantial amount of data on atherogenesis, thrombosis and immunological processes affecting the blood circulation of inner ear receptor cells has so far been accumulated. Various reasons for sensorineural hearing loss have been studied, such as changes in the rheological properties of blood; arteriole hypertonicity; precapillar sphincter dysfunction; impaired lipid metabolism leading to the lack of tissue oxygenation and dystrophy and necrosis of the organ of Corti. The definition of endothelial dysfunction has been given. The role of vasomotor, thrombophilic, adhesive and angiogenic forms of endothelial dysfunction in the development and progression of sensorineural hearing loss under the influence of harmful work-related factors, with arterial hypertension, coronary heart disease, diabetes mellitus with the most common and aggressive disorders of the microvasculature has been determined. A clear relationship between the development of sensorineural hearing loss in diabetic microangiopathy has been established. Historical data on the study of the mechanisms of sensorineural hearing loss were analyzed. The aim of this article was to conduct a literature review of interdisciplinary publications with a particular focus on the role of sensorineural hearing loss in the working population in predicting endothelial dysfunction in some chronic non-communicable diseases. The novelty of this article consists in the consideration of occupational and population risk factors for chronic non-communicable diseases in the form of their cascade, which also leads to sensorineural hearing loss.

Two Cases of Localized Myeloperoxidase-Antineutrophil Cytoplasmic Antibody-Associated Vasculitis Manifested with Intractable Otitis Media

Localized form of myeloperoxidase-antineutrophil cytoplasmic antibody-associated vasculitis (MPO-AAV) in the ear is a rare disease. It manifests as a sudden otalgia with hearing loss accompanied by dizziness and facial nerve palsy. Early diagnosis and treatment with immunosuppressive agents are important to prevent the irreversible progression of sensorineural hearing loss. However, it is hard to diagnose AAV because it can be confused with other common otologic disease, such as acute otitis media or middle ear effusion with labyrinthitis.Here, we report two cases of localized form of MPO-AAV manifesting otologic symptoms that have been properly diagnosed and treated with steroid and immunosuppressant. Key words: Antibodies ㆍ Antineutrophil cytoplasmic ㆍ Otitis media ㆍ Myeloperoxidases

Prebiotic effect of fructo-oligosaccharides on the inner ear of DBA/2 J mice with early-onset progressive hearing loss

Nutrition and dietary habits contribute to the onset and progression of sensorineural hearing loss (SNHL). Fructo-oligosaccharides (FOS) are non-digestible oligosaccharides and are known as prebiotics, which enhance short-chain fatty acid (SCFA) production and antioxidant activity. Although a substantial number of studies have shown that FOS play a role in the prevention of lifestyle-related diseases as prebiotics, little is known about the effects on the inner ear. The purpose of this study is to investigate the effect of FOS on gene expression and spiral ganglion neuron (SGN) protection in the inner ear of DBA/2 J mice, which is a model for early-onset progressive hearing loss. DBA/2 J mice were fed either control diet or FOS diet contained 10% (w/w) of FOS for 8 weeks. Analysis of mice fed the FOS diet revealed a change in intestinal flora including an inversion of the ratio of Bacteroidetes and Firmicutes, which was followed by a significant increase in SCFAs in the cecum and a decrease in an oxidative stress marker in the serum. In the inner ear, gene expression of neurotrophin, brain-derived neurotrophic factor (BDNF), its receptor, tyrosine kinase receptor b (Trkb), and the SCFA receptor, free fatty acid receptor 3 (FFAR3), were increased by FOS. In addition, the survival rate of SGNs in the inner ear was maintained in FOS-fed mice. Altogether, these results suggest that a compositional variation of the intestinal flora due to a prebiotic effect may be involved in the progression of SNHL.

Should You Follow the Better-Hearing Ear for Congenital Cytomegalovirus Infection and Isolated Sensorineural Hearing Loss?

To describe the progression of sensorineural hearing loss (SNHL) in the better- and poorer-hearing ears in children with asymptomatic congenital cytomegalovirus (CMV) infection with isolated SNHL. Longitudinal prospective cohort study. Tertiary medical center. We analyzed hearing thresholds of the better- and poorer-hearing ears of 16 CMV-infected patients with isolated congenital/early-onset or delayed-onset SNHL identified through hospital-based CMV screening of >30,000 newborns from 1982 to 1992. By 12 months of age, 4 of 7 patients with congenital/early-onset SNHL developed worsening thresholds in the poorer-hearing ear, and 1 had an improvement in the better-hearing ear. By 18 years of age, all 7 patients had worsening thresholds in the poorer-hearing ear and 3 patients had worsening thresholds in the better-hearing ear. Hearing loss first worsened at a mean age of 2 and 6 years in the poorer- and better-hearing ears, respectively. Nine patients were diagnosed with delayed-onset SNHL (mean age of 9 years vs 12 years for the poorer- and better-hearing ears), 6 of whom had worsening thresholds in the poorer-hearing ear and 1 in both ears. In most children with congenital CMV infection and isolated SNHL, the poorer-hearing ear worsened earlier and more precipitously than the better-hearing ear. This study suggests that monitoring individual hearing thresholds in both ears is important for appropriate interventions and future evaluation of efficacy of antiviral treatment.

Bilateral Tuberculous Otitis Media: A Rare Presentation

Abstract Introduction Tuberculosis is one of the most common infectious diseases in India. Tuberculosis of the middle ear is rare, usually seen in association with pulmonary tuberculosis or in patients with history of pulmonary tuberculosis. It is an uncommon and frequently misdiagnosed form of tuberculosis. In our experience, we have seen 50% of cases of tuberculous otitis media without pulmonary tuberculosis. These cases presented with rapid deterioration of hearing with more sensorineural component in hearing loss. Case Report This is a case report of 34-year-old woman presented to us with worsening of hearing over short duration of 3 months. She developed right profound hearing loss and left moderately severe mixed hearing loss, which deteriorated within duration of 2 weeks. Very few cases have been reported in literature affecting both the ears. In our experience, we have seen seven such cases with bilateral ear involvement. Conclusion Tuberculosis of the middle ear is a rare condition. For complete cure, medical therapy should be given at least for 9 months including 2 months 4 tablets (AKT4) and 7 months 3 tablets (AKT3) regimes, according to the INDEX-TB guidelines provided by government of India for extrapulmonary tuberculosis. Surgical treatment should be always added as emergency to prevent progression of sensorineural hearing loss and in cases of complications such as facial palsy.

Cochlear Homocysteine Metabolism at the Crossroad of Nutrition and Sensorineural Hearing Loss.

Hearing loss (HL) is one of the most common causes of disability, affecting 360 million people according to the World Health Organization (WHO). HL is most frequently of sensorineural origin, being caused by the irreversible loss of hair cells and/or spiral ganglion neurons. The etiology of sensorineural HL (SNHL) is multifactorial, with genetic and environmental factors such as noise, ototoxic substances and aging playing a role. The nutritional status is central in aging disability, but the interplay between nutrition and SNHL has only recently gained attention. Dietary supplementation could therefore constitute the first step for the prevention and potential repair of hearing damage before it reaches irreversibility. In this context, different epidemiological studies have shown correlations among the nutritional condition, increased total plasma homocysteine (tHcy) and SNHL. Several human genetic rare diseases are also associated with homocysteine (Hcy) metabolism and SNHL confirming this potential link. Accordingly, rodent experimental models have provided the molecular basis to understand the observed effects. Thus, increased tHcy levels and vitamin deficiencies, such as folic acid (FA), have been linked with SNHL, whereas long-term dietary supplementation with omega-3 fatty acids improved Hcy metabolism, cell survival and hearing acuity. Furthermore, pharmacological supplementations with the anti-oxidant fumaric acid that targets Hcy metabolism also improved SNHL. Overall these results strongly suggest that cochlear Hcy metabolism is a key player in the onset and progression of SNHL, opening the way for the design of prospective nutritional therapies.

Hearing Loss in Children With Asymptomatic Congenital Cytomegalovirus Infection.

To assess the prevalence, characteristics, and risk of sensorineural hearing loss (SNHL) in children with congenital cytomegalovirus infection identified through hospital-based newborn screening who were asymptomatic at birth compared with uninfected children. We included 92 case-patients and 51 controls assessed by using auditory brainstem response and behavioral audiometry. We used Kaplan-Meier survival analysis to estimate the prevalence of SNHL, defined as ≥25 dB hearing level at any frequency and Cox proportional hazards regression analyses to compare SNHL risk between groups. At age 18 years, SNHL prevalence was 25% (95% confidence interval [CI]: 17%-36%) among case-patients and 8% (95% CI: 3%-22%) in controls (hazard ratio [HR]: 4.0; 95% CI: 1.2-14.5; P = .02). Among children without SNHL by age 5 years, the risk of delayed-onset SNHL was not significantly greater for case-patients than for controls (HR: 1.6; 95% CI: 0.4-6.1; P = .5). Among case-patients, the risk of delayed-onset SNHL was significantly greater among those with unilateral congenital/early-onset hearing loss than those without (HR: 6.9; 95% CI: 2.5-19.1; P < .01). The prevalence of severe to profound bilateral SNHL among case-patients was 2% (95% CI: 1%-9%). Delayed-onset and progression of SNHL among children with asymptomatic congenital cytomegalovirus infection continued to occur throughout adolescence. However, the risk of developing SNHL after age 5 years among case-patients was not different than in uninfected children. Overall, 2% of case-patients developed SNHL that was severe enough for them to be candidates for cochlear implantation.

Novel TECTA Mutations Identified in Stable Sensorineural Hearing Loss and Their Clinical Implications

TECTA is a causative gene of autosomal dominant (DFNA8/A12) and autosomal recessive (DFNB 21) nonsyndromic sensorineural hearing loss (NSHL). Mutations in TECTA account for 4% of all autosomal dominant NSHL cases in some populations and are thus thought to be one of the major causes of autosomal dominant NSHL. A genotype-phenotype correlation for autosomal dominant mutations in the TECTA gene has been proposed. Two families (SB146 and SB149), which segregated moderate NSHL in an autosomal dominant fashion, were included in this study. We performed targeted resequencing of 134 known deafness genes (TRS-134) and bioinformatics analyses to find causative mutations for NSHL in these 2 families. Through TRS-134, we detected 2 novel mutations, i.e. c.3995G>T (p.C1332F) and c.5618C>T (p.T1873I), in the TECTA gene. These mutations cosegregated with NSHL in the studied families and were not detected in normal controls. The mutations c.3995G>T and c.5618C>T reside in the von Willebrand factor type D3-D4 (vWFD3-D4) interdomain of the zonadhesin (ZA) domain and the zona pellucida (ZP) domain, respectively. p.C1332F is the first mutation detected in the vWFD3-D4 interdomain of the ZA domain. The mutations p.C1332F and p.T1873I were associated with stable high-frequency and mid-frequency hearing loss, respectively. Notably, the cysteine residue mutated to phenylalanine in SB146 was not related to progression of sensorineural hearing loss, which argues against the previous hypothesis. Here we confirm a known genotype-phenotype correlation for the ZP domain and propose a hypothetical genotype-phenotype correlation which relates mutations in vWFD3-D4 to stable high-frequency NSHL in Koreans. This clinical feature makes subjects with the missense mutation in the vWFD3-D4 interdomain of TECTA potentially good candidates for middle ear implantation. i 2014 S. Karger AG, Basel

Mesenchymal stem cell transplantation to the mouse cochlea as a treatment for childhood sensorineural hearing loss

ObjectiveThere is no treatment established for congenital sensorineural hearing loss because the majority of the cases are hereditary. Although congenital sensorineural hearing loss is thought to be hereditary, this hearing loss occur postnatally. We hypothesized that the transplantation of MSCs (mesenchymal stem cells) to the cochlea would be an effective therapy for stopping or delaying the progression of sensorineural hearing loss in childhood. MethodsCultured mouse MSCs were labeled with EGFP (enhanced green fluorescence protein) using retroviruses. EGFP-MSCs were transplanted into the posterior semicircular canal of mice at 2–3 weeks (young group) and 24–26 weeks (adult group) of age by a novel perilymphatic perfusion technique. Engraftment of MSCs was evaluated immunohistologically at 1 week and 2 weeks after transplantation. ResultsIn young mice, migrated MSCs were detected in the cochlea tissue by immunofluorescence for EGFP and by immunohistochemistry for fibronectin. The differentiation of migrated MSCs into fibrocyte-like cells was demonstrated by immunofluorescence for connexin 26. There were no adverse effects on auditory function by MSC transplantation, and the auditory brain stem responses threshold did not significantly shift after surgery. In contrast, neither MSC migration nor differentiation was detected in the adult mice canal after MSC transplantation. ConclusionThe bone marrow derived MSCs were successfully transplanted into the cochlea of young mice by the perilymphatic perfusion technique and were further differentiated into fibrocyte-like cells without any adverse effects on auditory function.

Hearing loss in Muckle‐Wells syndrome

Muckle-Wells syndrome (MWS) is an inherited autoinflammatory disease characterized by fevers, rashes, arthralgia, conjunctivitis, and sensorineural hearing loss. In MWS, NLRP3 gene mutations are associated with excessive interleukin-1 release. The aims of this study were to determine the otologic characteristics of MWS, define trajectories of hearing loss, and explore the association with distinct NLRP3 genotypes. A prospective observational cohort study of children and adults diagnosed as having MWS was conducted at a single center. NLRP3 gene mutations were determined. Patients underwent standardized clinical, laboratory, and otologic assessments, including pure tone audiometry, vestibular organ testing, and tinnitus evaluation. Trajectories of hearing loss were defined for each genotype. The genotype-specific risk of progression of hearing loss was determined. A total of 33 patients ages 3-75 years who were members of 5 families with 4 different NLRP3 gene mutations were included. The majority of patients (67%) experienced bilateral sensorineural hearing loss. Even in cases of profound hearing loss vestibular reactivity remained normal. Fourteen adult patients reported nondebilitating tinnitus. Overall, hearing impairment progressed with age. Patients with the T348M mutation were at highest risk of rapid progression of sensorineural hearing loss. Patients with MWS are at risk of developing progressive sensorineural hearing loss without vestibular involvement. Hearing impairment starts at high frequencies and can subsequently progress to profound hearing loss. Progression is age dependent. Patients with different NLRP3 mutations had distinctly different trajectories of hearing loss, suggesting a mutation-specific risk that should be considered when making treatment decisions.

Hearing Loss in Children With Congenital Cytomegalovirus Infection in Relation to the Maternal Trimester in Which the Maternal Primary Infection Occurred

The purpose of this work was to study the relation between maternal trimester of primary infection with cytomegalovirus and the occurrence of sensorineural hearing loss in the congenitally infected offspring. Thirty-four consecutive live-born children diagnosed with a congenital cytomegalovirus infection after maternal primary cytomegalovirus infections were included in the study. Five were lost for follow-up, and 1 died. Of the remaining 28 congenitally infected children, an estimation of the maternal trimester in which cytomegalovirus primary infection occurred was performed. All of the children were investigated for potential sensorineural hearing loss. Five of the maternal infections occurred in the first trimester, 12 in the second trimester, and 11 in the third trimester of pregnancy. Sensorineural hearing loss was detected in 4 (80%) of the 5 congenitally infected children who were infected after a primary maternal infection in the first trimester of pregnancy and in 1 (8%) of the 12 children when the maternal infection occurred in the second trimester of pregnancy. No sensorineural hearing loss was detected after primary maternal infection occurring in the third trimester. Fluctuation and improvement of sensorineural hearing loss were seen regardless the trimester of pregnancy during which maternal primary infection occurred. Progression of sensorineural hearing loss occurred in 2 children born after a maternal primary infection of the first trimester. Hearing loss seemed more common in infants with congenital cytomegalovirus infection who were born to women who experienced a primary cytomegalovirus infection in the first trimester of pregnancy than when infection took place later in pregnancy.

Large endolymphatic duct and sac syndrome

The aim of this study was to clarify the clinical course of large endolymphatic duct and sac syndrome (LEDS). Although LEDS is the most common form of radiologically detectable inner ear malformation associated with sensorineural hearing loss (SNHL), it is relatively unknown in the German-speaking countries. We hoped to derive useful pointers for clinical care. We evaluated the clinical audiometric records and imaging findings of 169 patients with clinically suspected inner ear malformation seen between 1994 and 2003. Following identification of all LEDS cases, we serially investigated the anamnestic and functional data with regard to severity and course. Among 169 patients, 17 (median age 12 years; 12 females) showed LEDS. A total of 28 ears were affected. Clinically, most cases were of prelingual or perilingual onset and displayed steady or fluctuatingly progressive severe SNHL with emphasis on the high frequencies or deafness. Episodes of sudden hearing loss were relatively frequent. No correlation could be demonstrated between the severity of morphological changes and the degree of SNHL. Progression of SNHL and episodes of sudden hearing loss were seen mainly in late childhood or adolescence. This should be taken into account when informing and advising patients and planning therapy.

Effect of Atorvastatin on Progression of Sensorineural Hearing Loss and Tinnitus in the Elderly

To test whether the 3-hydroxy-3-methylglutaryl- coenzyme A reductase inhibitor atorvastatin can slow down the progression of presbycusis. Fifty patients 60- to 75-years-old with presbycusis and moderately elevated serum cholesterol. In a double-blind design, patients were randomly assigned to treatment with either atorvastatin (40 mg/d orally) or placebo. Pure-tone audiometry and tinnitus evaluation at enrolment and after 7 and 13 months. Development of hearing thresholds after 7 and 13 months showed no significant differences between the groups. Tinnitus score continuously improved in the atorvastatin group (34.8 at 7 and 27.6 at 13 mo), whereas it slightly deteriorated in the placebo group (24.8 at 7 and 26.8 at 13 mo). The effect on tinnitus was a tendency without statistic significance (p = 0.0833). Atorvastatin had no effect on the development of hearing thresholds, but resulted in a trend toward a relief of tinnitus.

Effect of Atorvastatin on Progression of Sensorineural Hearing Loss and Tinnitus in the Elderly

Effect of Atorvastatin on Progression of Sensorineural Hearing Loss and Tinnitus in the Elderly

Fluoride Therapy for Cochlear Otosclerosis? An Audiometric and Computerized Tomography Evaluation

The progress of sensorineural hearing loss (SNHL) in patients with cochlear otosclerosis was compared for 19 patients treated with fluoride for 1-5 years and 22 untreated controls. CT scans of eight patients before and after fluoride treatment were evaluated visually. Fluoride therapy arrested the progression of SNHL in the low (250, 500 and 1,000 Hz) (p<0.001) and high (2 and 4 kHz) (p=0.008) frequencies. It seemed to be more effective for the higher frequencies in cases with an initial SNHL of <50 dB. Fluoride administration for 4 years did not seem to be superior to a shorter treatment period (1-2 years). For six patients followed up after discontinuing fluoride therapy there was minimal deterioration in SNHL. There was no clear relationship between the size and site of otospongiotic lesions on CT and the severity of SNHL. Follow-up with CT evaluation did not provide reliable information as to the efficacy of fluoride therapy.