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Background Understanding the pathophysiology of sudden sensorineural hearing loss (SSNHL) and identifying its clinical symptoms and associated risk factors are crucial for doctors in order to create effective prevention and therapeutic methods for this prevalent otolaryngologic emergency. Methods This study focuses on investigating the correlation between the C-reactive protein/albumin ratio (CAR) and SSNHL complicated by hypertension. In this study, 120 patients diagnosed with SSNHL were divided into groups with and without hypertension, and propensity score matching was used to compare and analyze the severity, type, prognosis, and CAR levels in SSNHL. Results The results showed that the SSNHL group with hypertension had significantly higher CAR levels, age, hearing curve abnormalities, and more severe hearing loss compared to the control group with isolated SSNHL. These differences were statistically significant ( p  < 0.001). Among different subtypes of SSNHL, CAR levels increased progressively with the advancement of the condition, and these differences were also statistically significant ( p  < 0.001). Conclusion In summary, in patients with SSNHL, those with hypertension had higher CAR levels than those without a history of hypertension, and they experienced more severe hearing loss. Moreover, there was a clear correlation between CAR levels and the extent of SSNHL, indicating that greater CAR levels in patients with SSNHL are connected to more severe hearing loss in various hearing patterns and perhaps indicative of a poorer prognosis.

•A relatively inactive dynamic brain status occurred more often in SSNHL participants. Early-stage SSNHL participants showed decreased brain status transition number.•Disturbed neurovascular coupling restricted to the primary auditory cortex occurred in the intermediate- and late-stage SSNHL patients.•A significant shrinkage of the left medial superior frontal gyrus developed at the late stage.•Our study offered neuroimaging evidence for evolvement from functional to structural brain alterations of SSNHL patients with disease duration less than 1 month. A cortical plasticity after long-duration single side deafness (SSD) is advocated with neuroimaging evidence while little is known about the short-duration SSDs. In this case-cohort study, we recruited unilateral sudden sensorineural hearing loss (SSNHL) patients and age-, gender-matched health controls (HC), followed by comprehensive neuroimaging analyses. The primary outcome measures were temporal alterations of varied dynamic functional network connectivity (dFNC) states, neurovascular coupling (NVC) and brain region volume at different stages of SSNHL. The secondary outcome measures were pure-tone audiograms of SSNHL patients before and after treatment. A total of 38 SSNHL patients (21 [55%] male; mean [standard deviation] age, 45.05 [15.83] years) and 44 HC (28 [64%] male; mean [standard deviation] age, 43.55 [12.80] years) were enrolled. SSNHL patients were categorized into subgroups based on the time from disease onset to the initial magnetic resonance imaging scan: early- (n = 16; 1-6 days), intermediate- (n = 9; 7-13 days), and late- stage (n = 13; 14-30 days) groups. We first identified slow state transitions between varied dFNC states at early-stage SSNHL, then revealed the decreased NVC restricted to the auditory cortex at the intermediate- and late-stage SSNHL. Finally, a significantly decreased volume of the left medial superior frontal gyrus (SFGmed) was observed only in the late-stage SSNHL cohort. Furthermore, the volume of the left SFGmed is robustly correlated with both disease duration and patient prognosis. Our study offered neuroimaging evidence for the evolvement from functional to structural brain alterations of SSNHL patients with disease duration less than 1 month, which may explain, from a neuroimaging perspective, why early-stage SSNHL patients have better therapeutic responses and hearing recovery. [Display omitted]

The present study aimed to explore the pathogenesis of the ascending sudden sensorineural hearing (SSNHL) loss by comparing the clinical characteristics and prognosis of acute low-frequency hearing loss (ALFHL) and ascending SSNHL. A total of 43 patients with ALFHL and 122 patients with ascending SSNHL were enrolled in this study. First, the prognosis of patients with ALFHL and ascending SSNHL were compared, and the prognostic factors of AFHL and ascending SSNHL were analyzed. Acute low-frequency hearing loss and ascending SSNHL have no remarkable difference in complete recovery rate. Compared to ascending SSNHL, ALFHL has younger onset age, female prevalence, lower hearing threshold, shorter time from onset to recovery, and a lower proportion of combined tinnitus. The PTA at admission and delay from onset to therapy were significantly related to the prognosis of patients with ascending SSNHL, while only delay from onset to therapy was significantly related to the prognosis of patients with ALFHL. The majority of patients with ascending SSNHL and ALFHL recovered completely within 10 days from onset. Audiogram shape plays a critical role in the prognosis of SSNHL. Ascending SSNHL and ALFHL may share a common pathological mechanism.

Objective There was disagreement over the association between serum/plasma homocysteine (HCY) levels and sudden sensorineural hearing loss (SSNHL). Through the use of a meta-analysis, this study aims to determine whether there is a significant difference in serum homocysteine levels between the SSNHL group and the control group. Design The Cochrane Library, EMBASE, and PubMed databases were all thoroughly searched. The two independent reviewers thoroughly examined the initially searched articles. The data results were calculated by standard mean difference (SMD) or odds ratios (OR). Review Manager (version 5.3) was applied to statistical data. Study sample There were 766 participants in the 6 trials with continuous outcomes that were part of the meta-analysis A. In addition, meta-analysis B, which included 961 people, contained a total of 3 studies with dichotomous results. Results Both meta-analyses revealed the same conclusion that serum/plasma HCY levels in the SSNHL patients are higher than those in the controls (SMD 0.41, 95 % confidence interval (CI) 0.11 to 0.72, P  < 0.01; OR 3.27, 95 % CI 2.16 to 4.94, P  < 0.01). Conclusion This study demonstrated that the SSNHL patients' serum/plasma HCY levels were greater than those of the control group.

Sudden sensorineural hearing loss (SSNHL) is defined as a sensorineural hearing loss of 30 dB or greater on at least three contiguous audiometric frequencies occurring within a 72 h period. Although SSNHL is commonly encountered in clinical audiology and otolaryngology practice, its etiopathogenesis continues to be poorly understood. Scientific investigations have highlighted the vulnerability of cochlear microcirculation to blood flow alterations. Even mild hypoperfusion can lead to immediate dysfunction in the organ of Corti, given the heightened susceptibility of cochlear hair cells to hypoxia and ischemic damage. The purpose of this review paper is to present evidence of endothelial and vascular involvement in SSNHL and the risk factors, such as metabolic syndrome, that may negatively impact the inner ear’s vascular supply, influencing the onset pattern, incidence, and prognosis of SSNHL. By addressing these variables, we can deepen our comprehension of the mechanisms underlying SSNHL and potentially uncover strategies for prevention.

Background The association between exposure to air pollution and sudden sensorineural hearing loss (SSNHL) has not been extensively discussed in the literature. Therefore, we conducted this nationwide study to evaluate the risk of SSNHL in Taiwanese residents with exposure to air pollution. Methods We enrolled subjects aged older than 20 years with no history of SSNHL from 1998 to 2010, and followed up until developing SSNHL, withdrawn from the National Health Insurance program, and the end of the database (2011/12/31). The air quality data are managed by Taiwan Environmental Protection Administration. The annual concentrations of PM 2.5 , SO 2 , CO, NO, and NO 2 from 1998 to 2010 were classified into the three levels according to tertiles. We calculated the annual average of pollutants from baseline until the end of the study, and classified into tertiles. The adjusted hazard ratio (aHR) was estimated by using the multivariate Cox proportional hazard model. Results When considered continuous air pollutants concentration, subjects who exposed with higher concentration of CO (aHR = 2.16, 95% CI 1.50–3.11), NO (aHR = 1.02, 95% CI 1.01–1.03), and NO 2 (aHR = 1.02, 95% CI 1.01–1.04) developing significant higher risk of SSNHL. When classified air pollutants concentration into low, moderate and high level by tertiles, and selected low level as reference, patients exposed with moderate (aHR = 1.56, 95% CI 1.20–2.04) or high level (aHR = 1.33, 95% CI 1.01–1.75) of PM 2.5 showed significant higher risk of developing SSNHL. Conclusion This study indicated an increased risk of SSNHL in residents with long-term exposure to air pollution. Nevertheless, further experimental, and clinical studies are needed to validate the study findings.

Background Sudden sensorineural hearing loss (SSNHL) is an abrupt loss of hearing, still idiopathic in most of cases. Several mechanisms have been proposed including genetic and epigenetic interrelationships also considering iron homeostasis genes, ferroptosis and cellular stressors such as iron excess and dysfunctional mitochondrial superoxide dismutase activity. Results We investigated 206 SSNHL patients and 420 healthy controls for the following genetic variants in the iron pathway: SLC40A1 − 8CG (ferroportin; FPN1), HAMP − 582AG (hepcidin; HEPC), HFE C282Y and H63D (homeostatic iron regulator), TF P570S (transferrin) and SOD2 A16V in the mitochondrial superoxide dismutase-2 gene. Among patients, SLC40A1 − 8GG homozygotes were overrepresented (8.25% vs 2.62%; P  = 0.0015) as well SOD2 16VV genotype (32.0% vs 24.3%; P  = 0.037) accounting for increased SSNHL risk (OR = 3.34; 1.54–7.29 and OR = 1.47; 1.02–2.12, respectively). Moreover, LINE-1 methylation was inversely related ( r 2  = 0.042; P  = 0.001) with hearing loss score assessed as pure tone average (PTA, dB HL), and the trend was maintained after SLC40A1 − 8CG and HAMP − 582AG genotype stratification (Δ SLC40A1  = + 8.99 dB HL and Δ HAMP  = − 6.07 dB HL). In multivariate investigations, principal component analysis (PCA) yielded PC1 (PTA, age, LINE-1, HAMP , SLC40A1 ) and PC2 (sex, HFE C282Y , SOD2, HAMP ) among the five generated PCs, and logistic regression analysis ascribed to PC1 an inverse association with moderate/severe/profound HL (OR = 0.60; 0.42–0.86; P  = 0.0006) and with severe/profound HL (OR = 0.52; 0.35–0.76; P  = 0.001). Conclusion Recognizing genetic and epigenetic biomarkers and their mutual interactions in SSNHL is of great value and can help pharmacy science to design by pharmacogenomic data classical or advanced molecules, such as epidrugs, to target new pathways for a better prognosis and treatment of SSNHL.

The link between Vitamin D (Vit D) deficiency and sudden sensorineural hearing loss (SSNHL), especially regarding recurrence and age‐related disparities, remains unclear. Recurrence and age‐specific risks of SSNHL are under addressed, limiting preventive strategies. This study investigated if Vit D deficiency increases SSNHL onset and recurrence risks, with a focus on age‐specific associations. In this prospective cohort study, 80 adult SSNHL patients and 60 matched controls were enrolled. All patients received standard therapy. Baseline serum 25(OH)D was measured, Vit D deficiency or insufficient patients were randomized in a single‐blind manner to receive 3‐month Vit D supplementation. We monitored Vit D levels, hearing recovery (pure‐tone audiometry at 10 days and 3 months), recurrence, and associated symptoms. Vit D deficiency was more prevalent in SSNHL patients than controls (38.8% vs. 10.0%, p = 0.000). Recurrent SSNHL patients had significantly lower Vit D levels (18.4 ± 4.1 ng/mL) than first‐onset patients (24.9 ± 9.7 ng/mL). The highest deficiency rate (60.0%) was in patients under 30 years. Multivariate analysis identified audiometric subtype, not Vit D status, as an independent outcome predictor. Vit D supplementation did not significantly improve recovery rates (75.7% vs. 68.2%) or alleviate symptoms. Vit D deficiency is a significant, modifiable risk factor for SSNHL onset and recurrence, with the strongest association in patients under 30 years old. However, short‐term Vit D supplementation initiated after SSNHL diagnosis failed to improve clinical outcomes, underscoring that long‐term maintenance of adequate Vit D levels, rather than acute post‐symptom intervention, may be critical for reducing SSNHL risk in high‐risk populations. Pure‐tone audiometry (0–120 dB HL) identified patients with sudden sensorineural hearing loss (SSNHL). Serum 25‐hydroxyvitamin D levels revealed deficient (< 20 ng/mL), insufficient (20–30 ng/mL), or sufficient (≥ 30 ng/mL) status. Novel findings demonstrate low vitamin D correlates with higher SSNHL onset/recurrence, particularly elevating risk in younger populations (< 30 years). Preventive vitamin D supplementation is proposed as a strategic intervention for high‐risk groups, emphasizing its potential role in mitigating auditory morbidity. HL, hearing level; SSNHL, sudden sensorineural hearing loss; VD, Vitamin D.

Background and Objectives: Sudden Sensorineural Hearing Loss (SSNHL) is a quite common clinical finding in otolaryngology. Most cases are classified as idiopathic and there is a dearth of information on factors able to predict the response to treatment and hearing recovery. The main aim of this systematic review and meta-analysis was to assess and critically discuss the role of circulating inflammatory biomarkers in SSNHL. Materials and Methods: A search was conducted of the English literature published between 1 January 2009 and 7 July 2022 on Pubmed, Scopus, Web of Science, ScienceDirect, and Cochrane following PRISMA guidelines. Results: A total of 256 titles were retrieved from the search. After full-text screening and application of inclusion/exclusion criteria, 13 articles were included. Twelve out of thirteen studies reported significant differences in biomarkers values in SSNHL patients, of which Tumor Necrosis Factor alpha (TNF-α) and C-reactive Protein (CRP) were the most analyzed. Our meta-analysis for CRP’s mean values in SSNHL groups vs. controls showed significantly higher CRP levels with a pooled overall difference of 1.07; confidence interval (CI) at 95%: 0.03; 2.11. For TNF-α, discordant results were found: three studies showed significantly higher levels in SSNHL patients vs. controls, whereas other three investigations showed lower levels in the SSNHL groups (overall pooled difference 1.97; 95% CI: −0.90; 4.84). A high between-study heterogeneity was found. Conclusions: This systematic review pointed out that, although there exists a growing literature in the field of circulatory biomarkers identification in SSNHL, there is a high heterogeneity of results and low quality of evidence. CRP resulted to be higher in SSNHL patients than in controls, while TNF-α showed more heterogeneous behavior. The data reported herein needs to be confirmed in well-designed prospective multicenter randomized studies, with the objective of improving SSNHL treatment and outcome and thereby reducing the social burden of hearing loss.

Background: There is growing evidence of otoneurological involvement of SARS-CoV-2, such as tinnitus and balance disorders and smell and taste disorders, but HL in COVID-19 patients has still been marginally studied. Investigating the role of SARS-CoV-2 as an aetiological factor of Sudden Sensorineural Hearing Loss (SSNHL) may offer the opportunity to address treatment strategies to maximize clinical recovery and avoid side effects. Methods and results: For this purpose, we will present case studies of five patients who experienced SSNHL during COVID-19. Patients were selected from COVID-19 positive adult subjects with mild clinical presentation, admitted to the outpatient Ear Nose and Throat Department of Cardarelli Hospital due to the onset of SSNHL during the infection. All underwent a complete audio-vestibular investigation before and after SSNHL treatment protocol. Each patient is described with a detailed analysis. Conclusions: SSNHL could be an occasional symptom of COVID-19, even in mild manifestations of the disease. Our experience leads us to underline the value of promptly recognizing and addressing this and other uncommon symptoms, giving patients the opportunity to receive early treatment.