Association between atherosclerosis, hearing recovery, and hearing in the healthy ear in idiopathic sudden sensorineural hearing loss: a retrospective chart analysis.

Atherosclerosis is reported to be a risk factor for the severity of idiopathic sudden sensorineural hearing loss (ISSNHL). We evaluated the hypothesis that atherosclerosis affects the hearing thresholds of both the affected and healthy sides of ISSNHL patients. We conducted multivariate analyses on retrospectively collected data of patients with ISSNHL (N = 762) to evaluate the relationship between known factors linked to atherosclerosis and hearing thresholds on affected and healthy sides and whether these factors are prognostic for hearing recovery. Older ages, vertigo or dizziness, diabetes mellitus, and congestive heart failure were significantly related to higher hearing thresholds on the affected side. Older ages, male, and vascular disease were significantly related to higher hearing thresholds on the healthy side. Vertigo or dizziness, severe hearing loss and hearing loss at high frequencies on the affected side, higher hearing thresholds on the healthy side, regular anticoagulant medication, and delayed steroid treatment were significantly related to lack of recovery. Since several atherosclerosis-related factors are associated with higher hearing thresholds on both affected and healthy sides in ISSNHL and higher hearing thresholds on the healthy side predict poorer prognosis, diagnosis, and predicting prognosis of ISSNHL may benefit from rigorous evaluation of patients' cardiovascular comorbidities and hearing levels on both the healthy and affected sides.

Severe sudden sensorineural hearing loss related to risk of stroke and atherosclerosis.

The cause of idiopathic sudden sensorineural hearing loss (idiopathic SSNHL)-diagnosed after excluding other causes of hearing loss, such as SSNHL associated with vestibular schwannoma (VS)-is unknown. The presumed pathogenesis of idiopathic SSNHL includes circulatory disorders (e.g., cochlear infarction). We tested the hypothesis that patients with SSNHL who are at high stroke risk will have a lower rate of VS compared to those with low stroke risk. The rationale is that the primary cause of SSNHL in patients with high stroke risk might be a circulatory disturbance. We conducted a retrospective study in six hospitals. Our sampling of SSNHL patients included those diagnosed with idiopathic SSNHL and VS-associated SSNHL. SSNHL patients who had a head MRI were stratified by severity of hearing loss and evaluated for differences in the detection rate of VS between the high-scoring CHADS2 (CHADS2-H-), an index of stroke risk, and low-scoring CHADS2 (CHADS2-L-) groups. We identified 916 patients who met the inclusion criteria. For severe hearing loss, the CHADS2-H group had a significantly lower rate of VS than the CHADS2-L group (OR 0 [95% CI 0.00-0.612]; P = 0.007). These results indirectly support the hypothesis that a primary cause of severe idiopathic SSNHL in those at high risk of stroke might be a circulatory disorder.

Sudden sensorineural hearing loss in patients with vestibular schwannoma.

Clinical features of sudden sensorineural hearing loss (SSNHL) associated with vestibular schwannoma (VS) are not fully understood. Determining a treatment plan and explaining it to patients requires clinicians to clearly understand the clinical features related to the tumor, including SSNHL. To identify the full range of clinical features of VS-associated SSNHL, especially recovery of hearing following multiple episodes of SSNHL and what factors predict recovery and recurrence. A multicenter retrospective chart review was conducted in seven tertiary care hospitals between April 1, 2011, and March 31, 2020. We collected and analyzed dose of administered steroid, pure-tone audiometry results, and brain MRIs of patients diagnosed with VS-associated SSNHL. Seventy-seven patients were included. They experienced 109 episodes of audiogram-confirmed SSNHL. The highest proportion of complete recoveries occurred in patients with U-shaped audiograms. The recovery rates for the first, second, and third and subsequent episodes of SSNHL were 53.5%, 28.0%, and 9.1%, respectively. Recovery rate decreased significantly with increasing number of SSNHL episodes (P =0 .0011; Cochran-Armitage test). After the first episode of SSNHL, the recurrence-free rate was 69.9% over 1 year and 57.7% over 2 years; the median recurrence time was 32 months. Logarithmic approximation revealed that there is a 25% probability that SSNHL would recur within a year. SSNHL in patients with VS is likely to recur within one year in 25% of cases. Also, recovery rate decreases as a patient experiences increasing episodes of SSNHL.

Incidental ethmoidal dural arteriovenous fistula coexisting with a pituitary adenoma exacerbating post-transsphenoidal epistaxis.

A 64 year-old man with pituitary adenoma developed massive epistaxis after an uneventful endoscopic transsphenoidal surgery. Angiography showed extravasation from the sphenopalatine artery, to which embolisation was performed. An incidentally coexisting ethmoidal dural arteriovenous fistula supplied by the ophthalmic artery aberrantly originated from the middle meningeal artery caused increased haemorrhage.