Sudden hearing loss is a common presentation to ENT. In the authors’ practice, patients often wait many weeks for formal hearing testing. This study aimed to assess whether a tablet-based hearing test, hearTest, could aid clinical decision-making within secondary care ENT.

This was a multi-centre, prospective, non-randomised study to assess the feasibility, usability and accuracy of hearTest.

In the sample, hearTest was shown to be an acceptable method of testing for hearing loss by both patients and clinicians. The 0.5–4 kHz range had an average clinical agreement rate of 95.1 per cent when compared with formal pure tone audiometry, deeming it an accurate test to diagnose hearing loss.

The authors propose that hearTest can be used within ENT as a clinical decision support tool when manual audiometry is not immediately available. Within the authors’ practice, hearTest is used to aid diagnosis and management of sudden sensorineural hearing loss.

A seasonal trend of patients with idiopathic sudden sensorineural hearing loss may direct research into possible aetiology.

This study reviewed data from the medical records of patients who presented from 2004 to 2019 and who were diagnosed with new-onset idiopathic sudden sensorineural hearing loss. Seasonal pattern was assessed using chi-square and Rayleigh tests, and further confirmed by Monte Carlo simulation.

The study included 740 patients with a mean age of 48.3 years and a median age of 49 years. There was no statistical evidence for a difference in the distribution of sensorineural hearing loss cases for the four seasons of each year or with the cumulative data. New-onset idiopathic sudden sensorineural hearing loss cases averaged around 11 per month; there was no statistical evidence for a seasonal difference, as determined either by the Rayleigh test or with Monte Carlo simulation.

There was no evidence to support the claim that idiopathic sudden sensorineural hearing loss incidence displays a seasonal pattern. More research is necessary to explore potential external factors such as climate or infection.

This study investigated the characteristics and prognosis of the feeling of ear fullness in patients with unilateral all-frequency sudden sensorineural hearing loss.

Our study included 56 patients with a diagnosis of unilateral all-frequency sudden sensorineural hearing loss accompanied by a feeling of ear fullness and 48 patients without a feeling of ear fullness. The condition of these patients was prospectively observed.

Positive correlations were observed between grading of feeling of ear fullness and hearing loss in patients with a feeling of ear fullness (r = 0.599, p < 0.001). No significant differences were observed in the total effective rate of hearing recovery between patients with and without a feeling of ear fullness after one month of treatment (Z = −0.641, p = 0.521). Eighty-six per cent of patients (48 out of 56) showed complete recovery from the feeling of ear fullness. There was no correlation between feeling of ear fullness recovery and hearing recovery (r = 0.040, p = 0.769).

The prognosis of feeling of ear fullness is good. There was no correlation between feeling of ear fullness recovery and hearing recovery for all-frequency sudden sensorineural hearing loss patients.

The diagnostic value of exploratory tympanotomy in sudden sensorineural hearing loss remains controversial. This study and review were performed to identify the incidence of perilymphatic fistula in patients with sudden sensorineural hearing loss. The effectiveness of tympanotomy for sealing of the cochlear windows in cases with perilymphatic fistula was evaluated.

A search in common databases was performed. Overall, 5034 studies were retrieved. Further, a retrospective analysis on 90 patients was performed.

Eight publications dealing with tympanotomy in patients with sudden sensorineural hearing loss were identified. In 90 patients diagnosed with sudden sensorineural hearing loss and undergoing exploratory tympanotomy, 10 patients (11 per cent) were identified with a perilymphatic fistula, and this corresponds to the results obtained from our review (13.6 per cent).

There was no significant improvement after exploratory tympanotomy and sealing of the membranes for patients with a definite perilymphatic fistula.

Contrast-enhanced magnetic resonance imaging (CEMRI) of the head is frequently employed in investigations of sensorineural hearing loss (SNHL). The yield of these studies is perceptibly low and seemingly at odds with the aims of wise resource allocation and risk reduction within the Canadian healthcare system. The purpose of our study was to audit the use and diagnostic yield of CEMRI for the clinical indication of SNHL in our institution and to identify characteristics that may be leveraged to improve yield and optimize resource utilization.

The charts of 500 consecutive patients who underwent CEMRI of internal auditory canal for SNHL were categorized as cases with relevant positive findings on CEMRI and those without relevant findings. Demographics, presenting symptoms, interventions and responses, ordering physicians, and investigations performed prior to CEMRI testing were recorded. Chi-squared test and t-test were used to compare proportions and means, respectively.

CEMRI studies revealed relevant findings in 20 (6.2%) of 324 subjects meeting the inclusion criteria. Pre-CEMRI testing beyond audiometry was conducted in 35% of those with relevant positive findings compared to 7.3% of those without (p < 0.001). Auditory brainstem response/vestibular-evoked myogenic potentials were abnormal in 35% of those with relevant CEMRI findings compared to 6.3% of those without (p < 0.001).

CEMRI is a valuable tool for assessing potential causes of SNHL, but small diagnostic yield at present needs justification for contrast injection for this indication. Our findings suggest preferred referral from otolaryngologists exclusively, and implementation of a non-contrast MRI for SNHL may be a better diagnostic tool.

Sudden sensorineural hearing loss is a rare otological condition with potential for dire outcomes including permanent hearing loss. Although the majority of cases are deemed idiopathic, bilateral sudden sensorineural hearing loss represents a rare subset typically related to systemic conditions, with higher morbidity and mortality. A controversial association with acute otitis media has been reported, with few bilateral cases published in the literature.

A very rare case of bilateral sudden sensorineural hearing loss associated with acute otitis media is described, with a review of the literature.

The limited evidence available suggests that acute otitis media with tinnitus and/or bacterial pathology may have an increased risk of sudden sensorineural hearing loss, which is consistent with the case described. Although there is no sufficiently powered published evidence to provide definitive treatment guidelines, the literature reviewed suggests that early myringotomy and antibiotics may greatly improve treatment outcomes.

Lyme disease is an uncommon tick-borne multisystemic infection caused by Borrelia burgdorferi. The most common clinical manifestation is erythema migrans. In this report, a very unusual presentation of this condition is described, in which sudden onset sensorineural hearing loss was the sole presenting symptom.

Case report and review of English-language literature.

A patient presented with sensorineural hearing loss, with no other symptoms or signs. Acute Lyme infection was detected by laboratory tests. Magnetic resonance imaging showed signs of labyrinthitis of the same inner ear. After hyperbaric oxygen and systemic antibiotic treatment, the patient showed total hearing recovery, and magnetic resonance imaging showed complete resolution of the labyrinthitis.

To our knowledge, this is the first reported case of Lyme disease presenting only with sensorineural hearing loss. Borreliosis should be considered as an aetiological factor in sensorineural hearing loss. Adequate treatment may provide total recovery and prevent more severe forms of Lyme disease.

Sudden sensorineural hearing loss is a true audiological emergency, and its management is much discussed. Currently, no single therapy has been proven effective according to evidence criteria. Recently, intratympanic application of steroids has been increasingly used in refractory cases; however, it has only rarely been reported as first-line therapy.

Twenty consecutive patients with sudden sensorineural hearing loss treated between July 2008 and January 2010 were enrolled in this prospective, case–control study. Ten patients were treated with intratympanic steroids and 10 with systemic ‘shotgun’ therapy (including steroids, pentoxifylline, low molecular weight heparin and vitamin E). The two groups were homogeneous in all respects. Pure tone averages were assessed before and after treatment for both groups.

There were no statistically significant differences between the two groups.

Intratympanic steroids seem to offer a valid alternative to systemic therapy, with few risks, in sudden sensorineural hearing loss patients, and we recommend their use as first-line therapy.

To evaluate the relationship between lipoproteins, fibrinogen and sudden sensorineural hearing loss in a Croatian population. Since pathological derangement of lipoproteins and fibrinogen could be one of the causes of sudden sensorineural hearing loss, we hypothesised that patients with sudden sensorineural hearing loss would have more abnormal fibrinogen and lipoprotein concentrations, compared with subjects with normal hearing.

Plasma concentrations of cholesterol, fibrinogen and triglycerides in patients with sudden sensorineural hearing loss were compared with those in a control group (i.e. subjects with normal hearing function).

Patients with sudden sensorineural hearing loss had significantly higher plasma concentrations of cholesterol and low density lipoprotein cholesterol, compared with controls.

Higher cholesterol and low density lipoprotein cholesterol concentrations were found in patients with sudden sensorineural hearing loss, within a Croatian population. Cholesterol and low density lipoprotein cholesterol concentrations may be important factors in the pathogenesis of sudden sensorineural hearing loss, and should be assessed during the investigation of patients with this condition.

Impaired cochlear perfusion appears to be the most important event in the development of sudden sensorineural hearing loss. Methylenetetrahydrofolate reductase gene mutations at nucleotide 677 cause reduced methylenetetrahydrofolate reductase enzyme activity, resulting in vascular impairment.

Thirty-three patients and 68 control subjects underwent audiological and haematological investigation.

No statistically significant association was found between sudden sensorineural hearing loss and the methylenetetrahydrofolate reductase C677T gene mutation. Mean homocysteine and cholesterol concentrations were significantly higher in patients than in controls. Mean folate levels were significantly lower in patients than in controls. Amongst patients with sudden sensorineural hearing loss, no significant differences in mean cholesterol, homocysteine or folate concentration were found, comparing patients with methylenetetrahydrofolate reductase C677T mutation genotypes with those without.

No statistically significant association was found between the methylenetetrahydrofolate reductase C677T gene mutation and sudden sensorineural hearing loss. There was a statistically significant difference between the homocysteine, folate and cholesterol concentrations of sudden sensorineural hearing loss patients, compared with controls. However, there was no statistically significant difference in these levels, comparing patients with and without the methylenetetrahydrofolate reductase C677T mutation.

We report a young man with bilateral enlarged internal auditory canals who developed sudden sensorineural hearing loss following weight-lifting exercise.

We present a detailed clinical history, including the patient's high resolution computed tomography and magnetic resonance imaging scans.

The patient reported left-sided hearing loss immediately following weight-lifting exercise. He had no vestibular disturbance. He was treated with a combined regimen of steroids and an antiviral drug, but his profound hearing loss did not resolve. During another session of weight-lifting exercise, he suffered another episode of sudden hearing loss.

To the best of our knowledge, this is the first report of a patient with patulous internal auditory canals, with no other anomalies, who developed bilateral sudden hearing loss after weight-lifting exercise. Although no definitive conclusions can be drawn, close surveillance and lifestyle warnings should be considered in such patients, even if they are clinically asymptomatic.

The management of sudden sensorineural hearing loss has not yet been standardised. Hyperbaric oxygen therapy influences recovery from sudden sensorineural hearing loss, but the underlying mechanism is unknown and the appropriate indications and protocols undetermined.

Nineteen patients affected by sudden sensorineural hearing loss were treated after unsuccessful medical therapy, either in an acute or chronic setting. Pure oxygen inhalation at 2.5 atmospheres absolute pressure was administered for 90 minutes, for 30 sessions. Frequency-specific and average pure tone hearing thresholds were determined before and after hyperbaric oxygen therapy. The number of hyperbaric oxygen therapy sessions, the patient's age and any therapeutic delay were considered as quantitative variables possibly influencing outcome. Stepwise multivariate analysis was performed.

Salvage hyperbaric oxygen therapy appeared to improve patients' pure tone hearing thresholds, particularly at low frequencies. Positive results were more likely with increased patient age and reduced delay in receiving hyperbaric oxygen therapy.

Hyperbaric oxygen therapy has a strong scientific rationale, and improves pure tone hearing thresholds in cases of sudden sensorineural hearing loss unresponsive to medical therapy. Further research may be able to identify those patients with sudden sensorineural hearing loss for whom hyperbaric oxygen therapy would be most cost-effective.

To evaluate the results of vestibular evoked myogenic potential testing in patients with idiopathic sudden hearing loss, and to correlate these results with the findings of caloric testing, the clinical appearance of vertigo and the influence of age.

Eighty-six patients with unilateral idiopathic sudden hearing loss and 35 healthy controls underwent a standard protocol of neurotological evaluation. Vestibular evoked myogenic potential responses were measured and compared with caloric responses.

On the affected side, 30.2 per cent of patients showed abnormal vestibular evoked myogenic potential responses, while 52.3 per cent had abnormal caloric responses. A statistically significant relationship was found between the results of these two tests. A statistically significant relationship was also found between the type of vestibular lesion and the occurrence of vertigo. Advancing age correlated statistically with more extensive labyrinthic lesions.

A combination of vestibular evoked myogenic potential and electronystagmography testing indicated the existence of vestibular involvement in many patients with idiopathic sudden hearing loss. Both tests are necessary in order to obtain a more thorough and in-depth knowledge of the pathophysiology of idiopathic sudden hearing loss.

To evaluate the effectiveness of hyperbaric oxygen therapy in the management of sudden hearing loss.

Patients with sudden hearing loss were divided into study and control groups. The 36 patients in the study group were treated with hyperbaric oxygen therapy in addition to standard medical therapy, whereas the 21 patients in the control group were treated with only standard medical therapy.

Both groups were treated with standard therapy, comprising prednisolone starting at a dose of 1 mg/kg and reducing over three weeks. Patients in the study group received hyperbaric oxygen therapy in addition to standard drug therapy.

Success rates were 78.95 per cent in the study group and 71.30 per cent in the control group. However, this difference was not statistically significant (p > 0.05).

Considering the cost of hyperbaric oxygen therapy and its inconvenience to patients, this treatment should only be considered in patients suffering sudden hearing loss if there are contraindications to standard medical treatment.

To investigate the safety and efficacy of ozone therapy in adult patients with sudden sensorineural hearing loss.

Prospective, randomised, double-blinded, placebo-controlled, parallel group, clinical trial.

Forty-five adult patients presented with sudden sensorineural hearing loss, and were randomly allocated to receive either placebo (15 patients) or ozone therapy (auto-haemotherapy; 30 patients). For the latter treatment, 100 ml of the patient's blood was treated immediately with a 1:1 volume, gaseous mixture of oxygen and ozone (from an ozone generator) and re-injected into the patient by intravenous infusion. Treatments were administered twice weekly for 10 sessions. The following data were recorded: pre- and post-treatment mean hearing gains; air and bone pure tone averages; speech reception thresholds; speech discrimination scores; and subjective recovery rates.

Significant recovery was observed in 23 patients (77 per cent) receiving ozone treatment, compared with six (40 per cent) patients receiving placebo (p < 0.05). Mean hearing gains, pure tone averages, speech reception thresholds and subjective recovery rates were significantly better in ozone-treated patients compared with placebo-treated patients (p < 0.05).

Ozone therapy is a significant modality for treatment of sudden sensorineural hearing loss; no complications were observed.

To evaluate the vestibular aqueduct in patients with sudden sensorineural hearing loss.

We evaluated 19 patients (12 men and seven women; age range, 22−79 years) with unilateral sudden sensorineural hearing loss, using computed tomography and magnetic resonance imaging. All these patients had unilateral sudden sensorineural hearing loss. We also evaluated 47 control subjects (22 men and 25 women; age range, 22–79 years).

In sensorineural hearing loss affected ears, the width of the vestibular aqueduct at the midpoint and at the operculum was significantly greater than that in contralateral ears or in control ears. The width of the vestibular aqueduct at the midpoint and the operculum did not correlate with the audiometric threshold or the audiogram configuration. Contrast enhancement of the ipsilateral endolymphatic sac was observed in 17 of 19 patients with sudden sensorineural hearing loss (89 per cent). Eleven of these 17 patients also showed enhancement on the contralateral side, but no patient showed enhancement only on the contralateral side. In sensorineural hearing loss affected ears, the width of the vestibular aqueduct did not differ significantly between those patients with and without enhancement.

The vestibular aqueducts of sudden sensorineural hearing loss affected ears are wider than those of controls. Precise imaging and evaluation of the inner ear is essential when investigating the pathological conditions responsible for sudden sensorineural hearing loss.

To define the impact of patient-related and audiovestibular parameters on the prognosis of sudden hearing loss.

Eighty-three patients were included in this retrospective study. All were treated medically. We recorded the patients' demographic parameters, systemic diseases, time elapsed between onset of sudden hearing loss and initiation of treatment, tinnitus, vestibular symptoms, type of initial audiogram, pure tone averages and speech discrimination scores. For all patients, audiological measurements were performed on initial admission and at the completion of treatment on the 10th day.

There was no correlation between the hearing gain and recovery rate scores and patients' gender or age (p>0.05). However, a correlation was found between gender and relative hearing gain. Vertigo was not correlated with hearing gain and recovery rate scores (p<0.05). However, relative hearing gain correlated negatively with the presence of vertigo (−r=0.05, 81 degrees of freedom, p=0.043). Patients with <40 dB hearing loss on admission showed a better relative hearing gain (r=0.55, 81 degrees of freedom, p=0.03). Relative hearing gain correlated positively with better pre-treatment speech discrimination scores (r=0.82, 81 degrees of freedom, p=0.009) and negatively with poorer pre-treatment pure tone averages (−r=0.082, 81 degrees of freedom, p=0.009). There was no correlation between the scores for hearing gain, relative hearing gain and recovery rate and: systemic diseases (p>0.05); time elapsed between onset of sudden hearing loss and initiation of treatment (p>0.05); type of audiogram on initial admission (p>0.05), except for midfrequency type of audiogram; and tinnitus (p>0.05).

The outcome of sudden hearing loss was unaffected by systemic disease, tinnitus or type of audiogram (except for midfrequency type). The following were poor prognostic factors in the outcome of sudden hearing loss: female gender, presence of vertigo, initiation of treatment more than seven days after onset of hearing loss, and >40 dB hearing loss on admission.