Can permanent sensorineural hearing loss be caused by sleeping with an ear against a train window?

A patient presented to the authors with unilateral sensorineural hearing loss after falling asleep with his ear tightly pressed against a window of a moving train. This study set out to determine whether a train could generate sound levels of sufficient intensity to cause such a hearing loss. A sound level meter was used to measure the sound levels produced at the window of a moving train. Further measurements were made with a rubber attachment on the microphone, that simulated the effect of the ear stuck to the window. The sound levels were found to be amplified by the attachment but not to levels that could cause a hearing loss over a short period. In a second experiment eight healthy volunteers all perceived an increase in sound levels when their ears were pressed against a train window. It seems unlikely that sleeping with an ear against a train window can cause hearing loss, but it cannot be ruled out.     

Can Rh antigens be a risk factor in noise-induced hearing loss?

Noise-induced hearing loss (NIHL) is one of the most common occupational problems and is one of the main causes of deafness. Many factors cause NIHL. Individual susceptibility is one of them. Rhesus (Rh) antigens and ABO blood groups can be factors in determining individual susceptibility. We aim to investigate the relationship between the Rh antigens and NIHL. The study was conducted in 438 factory workers who had been exposed to a noise level more than 85 dB for 8 h a day for a period of ≥15 years. The audiologic results and blood groups were obtained from the individual health records of the factory workers. We determined NIHL in 236 (53.9%) workers. Two hundred and nineteen (55.4%) of Rh-positive workers and seventeen (39.5%) of Rh-negative workers have NIHL, and the difference between the two groups was statistically significant (P < 0.05), whereas no statistically significant difference was determined between the NIHL and ABO blood groups. In conclusion, we suggest that the people with Rh-positive blood group are more prone to develop NIHL.     

Low serum folate levels: a risk factor for sudden sensorineural hearing loss?

Objective Ischemic vascular damage of the inner ear is one of the known causes of sensorineural sudden hearing loss (SSHL). Folate is an emerging risk factor associated with an increased risk of vascular damage. The aim of this study was to investigate whether low serum folate levels are associated with SSHL.

Material and Methods Serum folate levels were determined in 43 patients with SSHL and in 24 controls.

Results Folate levels were found to be significantly lower in SSHL patients than in controls (mean difference ?1.96 ng/ml; 95% CI ?3.31, ?0.59 ng/ml; p=0.006). No significant relationship between folate levels and either sex, age, cigarette smoking, alcohol consumption or hypertension was observed, while a significant relationship was found between low folate levels and high homocysteine (HCY) levels in all 43 patients (p<0.01). The potential influence of low folate levels on hearing impairment in SSHL patients can be explained by the effects on HCY metabolism and the diminution of folate antioxidant capacity.

Conclusion Further studies are needed to elucidate whether low folate levels can be considered a risk factor for SSHL.     

Low serum folate levels: a risk factor for sudden sensorineural hearing loss?

OBJECTIVE: Ischemic vascular damage of the inner ear is one of the known causes of sensorineural sudden hearing loss (SSHL). Folate is an emerging risk factor associated with an increased risk of vascular damage. The aim of this study was to investigate whether low serum folate levels are associated with SSHL. MATERIAL AND METHODS: Serum folate levels were determined in 43 patients with SSHL and in 24 controls. RESULTS: Folate levels were found to be significantly lower in SSHL patients than in controls (mean difference -1.96 ng/ml; 95% CI -3.31, -0.59 ng/ml; p = 0.006). No significant relationship between folate levels and either sex, age, cigarette smoking, alcohol consumption or hypertension was observed, while a significant relationship was found between low folate levels and high homocysteine (HCY) levels in all 43 patients (p < 0.01). The potential influence of low folate levels on hearing impairment in SSHL patients can be explained by the effects on HCY metabolism and the diminution of folate antioxidant capacity. CONCLUSION: Further studies are needed to elucidate whether low folate levels can be considered a risk factor for SSHL.     

Autoimmune sensorineural hearing loss: is it still a clinical diagnosis?

Inner ear involvement with sensorineural hearing loss (SNHL) has been reported in many autoimmune disorders including ulcerative colitis. The pathogenetic mechanism of hearing loss in ulcerative colitis is thought to be immune mediated. Diagnostic tests are being developed to identify inner ear autoantibodies, that may be the cause of such hearing loss. The only test that is currently available for clinical use is the Otoblot test. This, however, tests only for antibodies against bovine heat shock protein 70 which is only one of the many cross-reacting proteins against the inner ear in suspected immune-mediated hearing loss. The clinical response to steroid therapy is thus the mainstay in the diagnosis of immune-mediated hearing loss. This paper presents a series of patients with clinically suspected autoimmune hearing loss. Diagnostic assays for this condition are discussed along with a review of the recent advances in the pathogenesis and laboratory diagnosis of immune-mediated sensorineural hearing loss.     

Lyme disease--a reason for sudden sensorineural hearing loss and vestibular neuronitis?

BACKGROUND: Lyme disease has been described as one possible cause of sudden sensorineural hearing loss and vestibular neuronitis. The necessity of serological diagnosis and its therapeutic consequences have been discussed controversially. PATIENTS AND METHODS: 344 patients with acute sensorineural hearing loss and 66 patients with vestibular neuronitis were examined in retrospect. By means of ELISA (Enzygnost Borreliosis, Dade Behring Marburg) the specific prevalences of IgG- and IgM-antibodies against borrelia in serum were evaluated. The frequency of seroprevalences for both diseases were compared to those given in the literature. Neurootological findings of the seropositive patients were compared with those of seronegative and analysed statistically. RESULTS: 15.7 % of the patients with sudden sensorineural hearing loss had positive levels of IgG-antibodies. IgM-titers were elevated in 4.7 % of the patients. The seroprevalences for IgM and IgG were above those described by other investigators for the healthy population. Patients with positive IgM-antibodies showed more often low frequency hearing loss than IgG-positive patients. 18.2 % of the patients with neuronitis vestibularis had IgG- and 1.5 % IgM-antibodies against Borrelia. Whereas IgG occurred more often than known for the healthy population, IgM was within the limit for the healthy population. The seropositive group did not show any remarkable neurootological signs compared with the seronegative group. CONCLUSIONS: Because of the elevated seroprevalences Borrelia infections may be one possible but very rare cause of sudden sensorineural hearing loss and vestibular neuronitis. Low frequency hearing loss may be a sign for an infection with Borrelia as an etiological factor especially in combination with seropositive titers. In case of the presence of IgM-antibodies, patients may be treated with oral antibiotics (Doxycyclin, Cefuroxim). In patients with neuronitis vestibularis a neuroborreliosis should be excluded by means of lumbar puncture.     

Should hyperbaric oxygen be added to treatment in idiopathic sudden sensorineural hearing loss?

At present, there is still no agreement about the therapy of idiopathic sudden sensorineural hearing loss (ISSHL). Hyperbaric oxygen (HBO) is used in the therapy of ISSHL to increase the partial oxygen pressure and the oxygen concentration in the inner ear and also to improve the blood profile and the microcirculation. In our prospective randomized study, we aimed to investigate the therapeutic effects of HBO therapy in the 1st 2 weeks of the onset of ISSHL. Fifty-one hospitalized patients with confirmed ISSHL who had received therapy were grouped randomly into two groups. Twenty-one patients (group I) received steroids, plasma expander dextrans (rheomacrodex), diazepam, pentoxiphylline and salt restriction, and 30 patients (group II) received the same basic treatment with the addition of HBO therapy. Audiological assessments of the patients were performed before and after the treatment. The hearing gains at frequencies of 250, 500, 1,000, 2,000 and 4,000 Hz were calculated separately. The level of hearing loss at the five frequencies was assessed in three groups at the first visit: equal or below 60 dB, between 61–80 dB and equal or above 81 dB. The average of the mean hearing gains at the five frequencies of the patients according to the age groups in group II was compared. The mean hearing gains at the five frequencies were compared between the two groups, and statistically significant improvement was detected in all the frequencies except at 2,000 Hz in group II. The mean hearing gains in group II were found to be significantly high in patients with initial hearing levels up to 60 dB in comparison to patients with initial hearing levels below 60 dB. When age groups and mean hearing gains were compared, there was no statistically significant difference in group I. In group II, the mean hearing gains were 39.1±18.3 dB in patients younger than 50 years and 22.7±11.3 dB in patients older than 50 years (P=0.044). In conclusion, the addition of HBO therapy to conventional treatment modalities significantly improves the outcome of ISSHL, especially at the frequencies of 250, 500, 1,000 and 4,000 Hz and in hearing loss of above 61 dB. Furthermore, HBO therapy was found to be more effective in patients younger than 50 years.     

Is corticosteroid therapy effective for sudden-onset sensorineural hearing loss at lower frequencies?

OBJECTIVE: To assess the efficacy of corticosteroid therapy for sudden-onset sensorineural hearing loss at lower frequencies. DESIGN: Retrospective, nonrandomized, controlled study. PATIENTS AND METHODS: The recovery rate, recovery/improvement rate, and period between the start of therapy and improvement of symptoms were studied in 2 groups: the control group, consisting of 36 patients treated with adenosine triphosphate disodium, kallidinogenase, and cyanocobalamin between March 1, 2000, and January 31, 2001; and the corticosteroid-treated group, consisting of 42 patients treated with corticosteroids in addition to the previously mentioned drugs between April 1, 1997, and February 29, 2000. RESULTS: No significant difference (P =.83) was noted in the recovery rate between the control group (81%) and the corticosteroid-treated group (79%), and the recovery/improvement rate was the same for the 2 groups (83%). In addition, there was no significant difference (P =.84) for the mean +/- SD period between the start of therapy and improvement of symptoms between the control group (3.9 +/- 2.7 days) and the corticosteroid-treated group (3.7 +/- 2.1 days). CONCLUSION: Corticosteroids were not effective for sudden-onset sensorineural hearing loss at lower frequencies.     

Dose passive smoking induce sensorineural hearing loss in children?

Objectives

Smoking plays major role in development of vascular and respiratory serious diseases. It has been reported that negative smoker children are prone for conductive hearing impairment due to repeated attacks of Eustachian tube dysfunction and middle ear effusion. This study aims to identify negative smoking as potential risk factor for development of sensorineural hearing loss.

Study

This study was done between January 2010 and November 2012. 411 children aged 5-11 years (8.2 ± 1.5) participated in this study; they were children attending the Ear, Nose, and Throat clinic of a tertiary care hospital and their siblings. The inclusion criteria were: (i) normal speech and language, (ii) absence of any disease or condition that may cause sensorineural hearing loss, and (iii) normal middle ear function on the day of hearing assessment. They were divided into three groups according to the exposure to second-hand smoke at home; group of “no exposure” whereas no smoker in the family (131 children), group of ‘mild exposure” whereas the father was the only smoking parent and smoking was prohibited at home (155 children), and group of “heavy exposure”, whereas the mother was smoking, or the father was freely smoking at home and in the presence of his children (125 children). Audiological evaluation in the form of pure tone and speech audiometry and immitancemetry was done for the study group.

Results

Audiological evaluation revealed that the prevalence of hearing loss was 3.8%, 4.5% and 12% in the “no exposure”, “mild exposure”, and “heavy exposure” groups, respectively. Significant difference was only detected between the high exposure group and the other two groups. All children had minimal sensorineural hearing loss, i.e. threshold of frequencies showing hearing loss was 20 or 25 dB HL. The risk ratios (95% confidence interval) for hearing loss in the study subgroups were 1.18 (0.38, 3.64) for mild exposure group (p > 0.05), 3.14 (1.18, 8.3) for heavy exposure group (p < 0.05).

Conclusions

Passive smoking in childhood correlates with sensorineural hearing loss, and it is an important risk factor for development of minimal hearing loss. Strict prevention of children exposure to second-hand smoke should be encouraged by every mean.     

A new disease: pregnancy-induced sudden sensorineural hearing loss?

Sudden sensorineural hearing loss (SSNHL) may occur during pregnancy, but its prevalence is very low. It is conjectured that SSNHL is closely related to the changes in the cardiovascular system, hematological system, endocrine system, and/or some other systems due to pregnancy. These changes possibly evoke disorders of cochlear circulation or cochlear fluid homeostasis leading to SSNHL. Two SSNHL cases were observed in our clinic, and their clinical features were analyzed. In one patient the SSNHL was likely to be related to the disturbance of cochlear fluid homestasis and in the other it might be induced by some disorders in cochlear circulation. Based on their distinct clinic profiles, we defined a new disease, called "pregnancy-induced sudden sensorineural hearing loss," similar to the definition of "pregnancy-induced hypertension." This study also deepened our understanding of the etiology of SSNHL.     

Is familial adenomatous polyposis associated with sensorineural hearing loss?

Abstract

The mutation causing familial adenomatous polyposis (FAP) affects the adenomatous polyposis coli (Apc) gene, which has a role in the cytoskeleton and has been shown to be important in the structure of supporting cells in the cochlea. One previous study suggested that FAP sufferers may have sensorineural hearing loss. In order to demonstrate whether this is the case we invited patients known to suffer from familial adenomatous polyposis to take part in our study. Audiograms were performed and compared to normal values for that patient's age and gender calculated using ISO standard data. Thirteen patients were included in the study analysis. No conductive hearing losses were identified. A statistically significant greater hearing loss was identified at 500 Hz (2.8 dBHL, P = 0.03) and 1000 Hz (2.5 dBHL, P = 0.05). No audiometric difference could be identified between the patients with FAP and attenuated FAP. A power calculation demonstrated that the study was of adequate size. This study did not demonstrate a clinically significant difference in hearing loss between the FAP group and the calculated normal values.

Sumario

La mutación que causa la poliposis adenomatosa familiar (FAP) afecta el gene polipomatosis adenomatosa coli (Apc), que tiene un papel cuya importancia en el citoesqueleto y en la estructura de las células de sostén de la cóclea se ha demostrado. Un estudio previo sugirió que quienes sufren la FAP pueden tener una pérdida auditiva sensorineural. Con objeto de demostrar si esto es así, invitamos a pacientes que (sabíamos) sufrían la enfermedad para tomar parte en este estudio. Los audiogramas que se practicaron fueron comparados con los valores normales de acuerdo con la edad y el género de los pacientes, usando los datos ISO estándar. Se incluyeron trece pacientes para el análisis del estudio. No se identificaron pérdidas auditivas conductivas. Si hubo una pérdida auditiva mayor, estadísticamente significativa en 500 Hz (2.8 dBHL, P = 0.03) y en 1000 Hz (2.5 dBHL, P = 0.05). No se pudo identificar una diferencia audiométrica entre los pacientes con FAP o con FAP atenuada. Un cálculo especial demostró que el estudio fue de un tamaño adecuado. Este estudio no mostró una diferencia clínicamente significativa de la pérdida auditiva entre el grupo con FAP y los valores calculados como normales.     

Lyme borreliosis, an etiological factor in sensorineural hearing loss?

The incidence of Lyme borreliosis was studied prospectively in 165 patients with acute idiopathic sensorineural hearing loss. The prevalence of positive levels of antibodies against Borrelia burgdorferi was sixfold higher in patients with sensorineural hearing loss than in the general population in Finland. Four patients fulfilled the criteria for Lyme borreliosis. No specific risk factors were found with which to predict the occurrence of Lyme borreliosis among patients with hearing loss. In logistic regression modeling the poor outcome of hearing loss was best explained by advanced age, high-frequency or flat-type hearing loss, and absence of positive levels of antibodies against B. burgdorferi. Although the causal relationship between Lyme borreliosis and sensorineural hearing loss is difficult to verify, we suggest that Lyme borreliosis is a rare but potentially treatable cause of sudden deafness. We propose that in endemic areas antibodies against Lyme borreliosis should be determined in patients with idiopathic sensorineural hearing loss. Received: 22 March 1999 / Accepted: 14 September 1999     

Can unilateral,progressive or sudden hearing loss be immune-mediated in origin?

Objective: The aim of the present study was to demonstrate that the positivity of nonspecific immunological tests could be found not only in bilateral hearing loss but also in unilateral cases, either sudden or progressive.

Method: An observational case series study included subjects suffering from unilateral or bilateral, sudden or progressive, symmetric or asymmetric sensorineural hearing loss (SNHL). All the patients underwent pure tone audiometry and the following battery of blood exams: anti-nuclear antibody (ANA), extractable nuclear antigen (ENA) antibody screening, anti-thyroperoxidase (anti-TPO), anti-thyroglobulin and anti-smooth muscle antibody (ASMA).

Results: The positivity to nonspecific immunological test was found in nearly 70% of the study groups. ASMA and ANA were found to be present in both bilateral and unilateral cases, without statistical difference. Considering the correlation between positivity/negativity and systemic autoimmune pathologies, in the bilateral forms of hearing loss, a high incidence of thyroid pathologies has been identified, with a higher percentage of systemic autoimmune diseases in respect to the normal population.

Conclusions: The nonspecific autoimmune tests are worth to be performed also when SNHL is not bilateral and progressive, since an immunological mechanism could also underlie unilateral and sudden SNHL cases.     

Is auditory brainstem response a prognostic factor in patients with sudden sensorineural hearing loss?

Abstract

Background: Serum thyroid hormone levels are closely related to the normal functioning of the cochlea. However, the relationship between initial auditory brainstem response (ABR) results and levels of thyroid hormone remained unclear until we adopted ABR as a prognostic factor in Idiopathic sudden sensorineural hearing loss (ISSNHL) patients.

Objective: This investigation aimed to elucidate the association between ABR and outcomes in patients with ISSNHL.

Material and methods: Thirty-three patients presenting with unilateral ISSNHL underwent blood sampling and ABR tests on the day of admission. The mean latencies of the ABR results were compared among the groups which were classified by ISSNHL outcome, based on Siegel’s criteria. The association between the ABR results and the thyroid hormone serum levels (TSH, T3, and free T4) were assessed.

Results: The overall successful recovery rate was 60.6% (n?=?20). The mean latencies of all the ABR parameters were not significantly different between the different treatment outcome groups (Mann–Whitney U test). Wave V latency, III–V interval and I–V interval were negatively associated with T3 serum levels.

Conclusion: The results indicate that clinical caution should be exercised when conducting ABR tests without assessing thyroid hormone levels.