This study aimed to determine the probability of hearing recovery in patients with idiopathic sudden sensorineural hearing loss following salvage intratympanic steroids

A retrospective review of all patients receiving salvage intratympanic steroid injections for idiopathic sudden sensorineural hearing loss was performed (January 2014 to December 2019). Twenty-two patients were identified, of whom 15 met inclusion criteria. Pre- and post-treatment audiograms were compared with the unaffected ear. Hearing recovery was categorised based on American Academy of Otolaryngology Head and Neck Surgery criteria.

Only 1 patient out of 15 (6.7 per cent) made a partial recovery, and the remainder were non-responders. The median duration of time between symptom onset and first salvage intratympanic steroid treatment was 52 days (range, 14–81 days). No adverse reactions were observed.

‘Real world’ patients with idiopathic sudden sensorineural hearing loss present differently to those in the literature. Sudden sensorineural hearing loss should be diagnosed with care and intratympanic steroid injections initiated early if considered appropriate. Patients should make an informed decision on treatment based on prognostic factors and local success rates.

To assess the Framingham risk score as a prognostic tool for idiopathic sudden sensorineural hearing loss patients.

Medical records were reviewed for unilateral idiopathic sudden sensorineural hearing loss patients between January 2010 and October 2017. The 10-year risk of developing cardiovascular disease was calculated. Patients were subdivided into groups: group 1 – Framingham risk score of less than 10 per cent (n = 28); group 2 – score of 10 to less than 20 per cent (n = 6); and group 3 – score of 20 per cent or higher (n = 5).

Initial pure tone average and Framingham risk score were not significantly associated (p = 0.32). Thirteen patients in group 1 recovered completely (46.4 per cent), but none in groups 2 and 3 showed complete recovery. Initial pure tone average and Framingham risk score were significantly associated in multivariable linear regression analysis (R2 = 0.36). The regression coefficient was 0.33 (p = 0.003) for initial pure tone average and −0.67 (p = 0.005) for Framingham risk score.

Framingham risk score may be useful in predicting outcomes for idiopathic sudden sensorineural hearing loss patients, as those with a higher score showed poorer hearing recovery.

This study evaluated tumour necrosis factor-α, interleukins 10 and 12, and interferon-γ levels, peripheral blood mononuclear cells, and clusters of differentiation 17c and 86 expression in unilateral sudden sensorineural hearing loss.

Twenty-four patients with unilateral sudden sensorineural hearing loss, and 24 individuals with normal hearing and no history of sudden sensorineural hearing loss (who were attending the clinic for other problems), were enrolled. Peripheral blood mononuclear cells, and clusters of differentiation 11c and 86 were isolated and analysed. Plasma and supernatant levels of tumour necrosis factor-α, interferon-γ, and interleukins 10 and 12 were measured.

There were no significant differences with respect to age and gender. Monocyte population, mean tumour necrosis factor-α level and cluster of differentiation 86 expression were significantly increased in the study group compared to the control group. However, interferon-γ and interleukin 12 levels were significantly decreased. The difference in mean interleukin 10 level was not significant.

Increases in tumour necrosis factor-α level and monocyte population might play critical roles in sudden sensorineural hearing loss. This warrants detailed investigation and further studies on the role of dendritic cells in sudden sensorineural hearing loss.

To evaluate the plasma levels of endothelial cell-specific molecule-1 (ESM-1) and pentraxin-3 (PTX-3) in patients with idiopathic sudden sensorineural hearing loss, and to compare the pre- and post-treatment levels in patients responsive and non-responsive to therapy.

The study included 108 subjects: 51 with idiopathic sudden sensorineural hearing loss and 57 controls. For ESM-1 and PTX-3 analyses, blood samples were collected before and three months after treatment initiation in the idiopathic sudden sensorineural hearing loss group and once for the control group. Treatment response was evaluated three months after therapy initiation with pure tone audiometry, and the patients were divided into two groups: responsive and non-responsive to treatment.

Serum ESM-1 levels were significantly higher in the idiopathic sudden sensorineural hearing loss group than the control group, whereas the difference was not significant for PTX-3. In the responsive and non-responsive groups, ESM-1 and PTX-3 levels were not statistically different before and after treatment.

To our knowledge, this is the first study investigating plasma ESM-1 and PTX-3 levels in idiopathic sudden sensorineural hearing loss. Increased plasma ESM-1 levels may confirm endothelial dysfunction involvement in idiopathic sudden sensorineural hearing loss pathogenesis, which could be associated with vascular impairment.

Recent studies found that mobile phone users had a significantly greater risk of having elevated thresholds in speech frequencies. This study investigated the correlation between the laterality of sudden sensorineural hearing loss, handedness and the preferred ear for mobile phone use.

The study included all patients who presented with sudden sensorineural hearing loss to the Department of Otolaryngology – Head and Neck Surgery in our tertiary referral medical centre between 2014 and 2016. Patients were asked to indicate their dominant hand and preferred ear for mobile phone use.

The study comprised 160 patients. No correlation was found between the dominant hand or preferred ear for mobile phone use and the side of sudden sensorineural hearing loss. There was no correlation between the side of the sudden sensorineural hearing loss (preferable or non-preferable for mobile phone use) and audiometric characteristics.

No correlation was found between the laterality of ears used for mobile phone and sudden sensorineural hearing loss.

Sudden sensorineural hearing loss in divers may be caused by either inner-ear barotrauma or inner-ear decompression sickness. There is no consensus on the best treatment option. This study aimed to evaluate the therapeutic value of hyperbaric oxygen therapy for sudden sensorineural hearing loss in divers.

A literature review and three cases of divers with sudden sensorineural hearing loss treated with hyperbaric oxygen therapy are presented.

Hyperbaric oxygen therapy resulted in hearing improvement in 80 per cent of patients: 39 per cent had hearing improvement and 41 per cent had full recovery.

Hyperbaric oxygen therapy improved hearing in divers with sudden sensorineural hearing loss.

To investigate of the efficacy of hyperbaric oxygen therapy as a salvage treatment after unsuccessful oral corticosteroid therapy.

Case notes of patients who were followed up because of idiopathic sudden sensorineural hearing loss between 2005 and 2011 in a tertiary care centre were examined retrospectively. Audiograms from before and after hyperbaric oxygen therapy were examined in terms of mean gains in pure tone average and at 0.25, 0.5, 1, 2, 4 and 8 kHz. In addition, recovery according to Siegel's criteria was noted.

Mean gain in pure tone average was 10.55 ± 13.56 dB. Mean gains at 0.25, 0.5, 1, 2, 4 and 8 kHz were 16.66 ± 18.43 dB, 16.94 ± 19.93 dB, 12.63 ± 16.71 dB, 7.36 ± 15.28 dB, 5.27 ± 11.58 dB and 2.91 ± 12.44 dB, respectively. Three patients had complete recovery, 1 had partial recovery, 5 had slight recovery and 25 had no improvement.

Hyperbaric oxygen utilised as a salvage therapy after failed corticosteroid therapy may be beneficial in some patients. Studies with more patients are needed.

This study aimed to evaluate the association of chronic rhinosinusitis with sudden sensorineural hearing loss using a population-based database.

Sampled subject data were obtained from the Taiwan Longitudinal Health Insurance Database 2000. A total of 3325 patients with sudden sensorineural hearing loss were identified and 9975 controls were randomly selected. A conditional logistic regression was used to calculate the odds ratio for having been previously diagnosed with chronic rhinosinusitis, for cases and controls.

The adjusted odds ratio of having prior chronic rhinosinusitis among cases compared to controls was 1.36 (95 per cent confidence interval = 1.16–1.60). The significant relationship between sudden sensorineural hearing loss and chronic rhinosinusitis was most pronounced among those patients aged 44 years or less (compared to controls) (odds ratio = 2.18; 95 per cent confidence interval = 1.63–2.92). However, the significant relationship between sudden sensorineural hearing loss and prior chronic rhinosinusitis was not sustained for patients older than 60 years compared to controls.

To evaluate a small cohort of patients who presented with symptoms and signs consistent with acute infective sensorineural hearing loss who were treated with intratympanic steroids.

Seven patients received a 7-day course of oral antibiotics and oral prednisolone followed by 3 intratympanic injections of methylprednisolone and 1 week of topical dexamethasone drops.

Hearing improved in 57 per cent of patients (four out of seven). The mean improvement in this group was 24 dB (range, 10–52 dB). The magnitude of the sensorineural hearing loss at presentation was less in those who responded to intratympanic steroid therapy than in non-responders (mean pure tone average of 30 dB versus 65 dB pre-intratympanic steroids, and 14 dB versus 83 dB post-intratympanic steroids, respectively).

The results of our study suggest that intratympanic steroids provide a valuable contribution to the treatment of acute infective sensorineural hearing loss and may provide additional benefit by virtue of a concentrated local steroid effect in patients who do not respond to antibiotics.

To investigate a novel oxidative stress marker, thiol/disulphide literature homeostasis, in patients with idiopathic sudden sensorineural hearing loss, and to compare the results with healthy controls for the first time.

Thirty-two patients with idiopathic sudden sensorineural hearing loss and 30 healthy individuals were included in the study. Serum native thiol, total thiol and disulphide levels were measured, and disulphide/native thiol and disulphide/total thiol ratios were determined in all subjects.

Serum native thiol and total thiol levels were significantly lower in patients with sudden sensorineural hearing loss compared with controls (p < 0.05). Of the 32 patients, 25 had lower native thiol levels than controls (333.2 ± 73.9 vs 381.8 ± 35.6 μmol/l, p = 0.002) and 24 had lower total thiol levels (375.1 ± 74.3 vs 426.1 ± 39.3 μmol/l, p = 0.002).

The changes in oxidative markers evident in a significant number of patients may be associated with oxidative stress, which may, in turn, have caused sudden sensorineural hearing loss in those patients.

Unilateral sudden sensorineural hearing loss due to an infarct in the vertebrobasilar system has been widely reported. Most patients have a background of traditional coronary risk factors related to these cerebrovascular episodes.

A 32-year-old male, a regular user of anabolic steroids, presented to the emergency department with unilateral sensorineural hearing loss and symptoms suggestive of an infarct of the anterior inferior cerebellar artery but in the absence of risk factors for ischaemic stroke.

Magnetic resonance imaging confirmed the presence of infarction in the region supplied by the anterior inferior cerebellar artery. Polycythaemia was found on haematological analysis, which we believe was secondary to the use of anabolic steroids. The patient was commenced on aspirin as per the stroke management protocol. There was resolution of neurological symptomatology six weeks after the episode, but no improvement in hearing.

To our knowledge, this is the first case report of unilateral sensorineural hearing loss secondary to the use of anabolic steroids causing polycythaemia. This cause should be considered in the differential diagnosis of patients presenting with sensorineural hearing loss, especially in young males, when no other risk factors can be identified.

To evaluate the incidence rates and risk of sudden sensorineural hearing loss among patients with depressive disorders.

Data for 27 547 patients with newly diagnosed depressive disorders and 27 547 subjects without depressive disorders between 2001 and 2008 were yielded from the Taiwan National Health Insurance Research Database. Sudden sensorineural hearing loss incidence at the end of 2011 was determined. Cumulative incidence and adjusted hazard ratio were computed.

Sudden sensorineural hearing loss incidence was 1.45 times higher in the depressive disorders group compared to the non-depressive disorders group (p = 0.0041), with an adjusted hazard ratio of 1.460. A significant increased risk of developing sudden sensorineural hearing loss was noted in patients with diabetes mellitus, chronic kidney disease and hyperlipidaemia (p < 0.05).

The results suggest an increased risk of developing sudden sensorineural hearing loss in patients with depressive disorders. Co-morbidities such as diabetes mellitus, chronic kidney disease and hyperlipidaemia significantly aggravated the risk. Depressive disorders might be considered a risk factor for sudden sensorineural hearing loss. It remains to be seen whether control of depressive disorders can decrease the incidence of sudden sensorineural hearing loss in patients with depressive disorders.

Although other blood dyscrasias are known to cause sudden sensorineural hearing loss, macrocytosis has not previously been implicated in the absence of another causative agent.

We present a case of bilateral sequential sudden sensorineural hearing loss in a patient with significant macrocytosis (mean corpuscular volume at presentation 124 fl) secondary to alcohol-induced liver dysfunction.

A possible pathophysiological mechanism linking macrocytosis and sudden sensorineural hearing loss was identified, suggesting areas for further investigation.

Spinal anaesthesia is one of the most widely used regional anaesthesia techniques. Sudden bilateral hearing loss following spinal anaesthesia has only been reported in a few cases.

This paper reports the case of a 50-year-old woman who developed sudden bilateral hearing loss following spinal anaesthesia for hallux valgus orthopaedic surgery. This is followed by a literature review.

The patient's hearing improved almost completely on the morning of the 3rd day following surgery. No recurrence of hearing loss, tinnitus or vertigo was reported during the six-month follow-up period.

Some complications regarding hearing may emerge after spinal anaesthesia. The possibility of hearing loss after spinal anaesthesia should be taken into consideration. Complaints such as hearing loss, tinnitus or vertigo should be taken seriously when reported, and the patient should be referred to an ENT clinic. This will ensure early diagnosis and treatment.

Three-dimensional fluid-attenuated inversion recovery magnetic resonance imaging has been used to detect alterations in the composition of inner-ear fluid. This study investigated the association between hearing level and the signal intensity of pre- and post-contrast three-dimensional fluid-attenuated inversion recovery magnetic resonance imaging in patients with sudden-onset sensorineural hearing loss.

Three-dimensional fluid-attenuated inversion recovery magnetic resonance imaging was performed in 18 patients with sudden-onset sensorineural hearing loss: 12 patients with mild-to-moderate sensorineural hearing loss (baseline hearing levels of 60 dB or less) and 6 patients with severe-to-profound sensorineural hearing loss (baseline hearing levels of more than 60 dB).

High-intensity signals in the inner ear were observed in two of the six patients (33 per cent) with severe-to-profound sensorineural hearing loss, but not in those with mild-to-moderate sensorineural hearing loss (mid-p test, p = 0.049). These signals were observed on magnetic resonance imaging scans 6 or 18 days after sensorineural hearing loss onset.

The results indicate that three-dimensional fluid-attenuated inversion recovery magnetic resonance imaging is not a useful tool for detecting inner-ear abnormalities in patients with mild sensorineural hearing loss.

To determine the efficacy of intratympanic methylprednisolone injections for treating sudden sensorineural hearing loss.

A retrospective chart review was performed to identify patients suffering from sudden sensorineural hearing loss with no recovery after oral steroids. Patients were given up to three intratympanic methylprednisolone injections at one-week intervals. They were classified according to their functional hearing class, remission was monitored and potential factors affecting prognosis were analysed.

Intratympanic injections provide effective salvage therapy for sudden sensorineural hearing loss (p = 0.039). Changes in pure tone average and speech discrimination score were analysed following intratympanic methylprednisolone injections. The pure tone average reached a plateau after the second injection; however, the speech discrimination score improved until after the third injection. Hearing improvement after intratympanic injections mainly occurred at low frequencies. The interval between symptoms appearing and intratympanic injections starting was not significantly associated with remission (p = 0.680).

A delay between symptom onset and the first intratympanic methylprednisolone injection does not seem to affect prognosis.

Sudden sensorineural hearing loss rarely occurs in patients with chronic myeloid leukaemia.

We present a case report of a patient who presented with sudden sensorineural hearing loss as the first manifestation of chronic myeloid leukaemia, and review the mechanisms responsible for sudden sensorineural hearing loss in leukaemic patients.

A 31-year-old female presented to our clinic with unilateral sudden sensorineural hearing loss and tinnitus. Pure tone audiometry revealed profound sensorineural hearing loss in the left ear at all frequencies. During an investigation into her hearing loss, the patient was found to have chronic myeloid leukaemia.

Every case of sudden sensorineural hearing loss must be carefully evaluated, and haematological disorders must be considered in the differential diagnosis of sudden hearing loss.

This paper reports on two patients with posterior inferior cerebellar artery infarction whose only presenting complaint was acute unilateral hearing loss.

In the two cases reported, sudden hearing loss was an initial symptom, with no other neurological signs. Infarction in the territory of the posterior inferior cerebellar artery was diagnosed using brain magnetic resolution imaging. The patients had some degree of hearing improvement 3 or 4 days after initial treatment.

In this article, new cases of posterior inferior cerebellar artery infarction presenting as sudden deafness, without prominent neurological signs, are described. Otologists should be aware that hearing loss can sometimes appear as a warning sign of impending posterior inferior cerebellar artery infarction.

To evaluate the long-term stability of intratympanic steroids and investigate the ‘real’ impact of sudden sensorineural hearing loss on patients.

A total of 14 patients treated with intratympanic steroids were evaluated by audiometric and vestibular examinations. The modified Glasgow Benefit Inventory was used to evaluate quality of life changes after intratympanic steroid treatment.

There was no significant difference between pure tone average post-intratympanic steroids and at follow up. The general Glasgow Benefit Inventory score was not significantly associated with the presence of tinnitus or dizziness, or with patient age. The change in pure tone average after intratympanic steroid treatment did not correlate with social or physical scores, but correlated strongly with the general Glasgow Benefit Inventory score (p = 0.0023). Intratympanic steroid administration led to a stable improvement in hearing. Quality of life assessment showed that patients can feel satisfaction regardless of the hearing outcome. Patients who regained a social hearing level expressed greater satisfaction than patients without serviceable hearing. Overall, quality of life improvement was not related to hearing improvement.

Sudden sensorineural hearing loss is devastating. Considering the audiological effects alone ignores the ‘human’ perspective. Audiological success can correlate with poor quality of life outcome.

Unilateral and bilateral sudden sensorineural hearing loss represent different disease entities. The unilateral condition is more common and predominantly idiopathic, and up to 65 per cent of patients spontaneously recover hearing. Conversely, the bilateral condition is rare, mostly associated with serious systemic conditions, and has a higher prevalence of morbidity and mortality.

A literature search using the PubMed database was conducted using the MeSH terms ‘sudden’, ‘bilateral’ and ‘sensorineural hearing loss’.

One hundred and three reported cases of bilateral sudden sensorineural hearing loss were identified. The condition is most often associated with toxic, autoimmune, neoplastic and vascular conditions. A younger age of onset, with a bimodal age distribution, was seen for bilateral sudden sensorineural hearing loss, compared with the unilateral condition. Patients with the bilateral condition had more profound hearing loss, with poorer recovery and a 35 per cent mortality rate. Vestibular symptoms were also less common than in the unilateral condition.

The presentation of bilateral sudden onset sensorineural hearing loss is a medical emergency requiring thorough and urgent investigation to exclude life-threatening and reversible conditions.