Background/Objectives: Vestibular dysfunction is one of the main complications after cochlear implant (CI) surgery, and there are currently no standardized protocols for vestibular assessment in CI candidates. Our objectives were to investigate the incidence of vestibular impairment after CI surgery, anamnestic (age, known systemic pathologies and cause of deafness) and surgical (intraoperative complications, malposition of the CI) risk factors, and the role of vestibular assessment in the selection of the suitable ear for implantation. Methods: We included 68 adult patients (80 ears) affected by moderate-to-profound SNHL undergoing CI. The dizziness handicap inventory (DHI), the video head impulse test (VHIT), the caloric test, and dynamic posturography (DP) were used to study the vestibular function and balance before and one month after CI. The DHI was also administered 24 h after surgery. Results: Despite significative impairment 24 h after surgery (29.6 ± 30), the mean DHI score returned to preoperative values (17.9 ± 26) after one month. Dizziness persisted in case of age ≥ 65 years old, surgical difficulties, simultaneous bilateral CI, Meniere’s disease and otosclerosis, comorbidities ≥ 3, anxiety/depression, and neurological diseases. The VHIT significantly worsened in 25% of ears, while the caloric test SPV nystagmus significantly decreased in 30% of ears. In cases of preoperative unilateral weakness, the implantation of the better ear was significantly related to higher DHI scores. Only 4/68 patients had a significant persistent reduction in the postural composite score after surgery, with an increased risk of falls. Conclusions: Medical history and vestibular assessment predict the risk of vestibular damage and help to choose the CI’s side and to manage vertigo after surgery.

Background/Objectives: Sudden sensorineural hearing loss (SSNHL) represents a challenging clinical entity with variable prognosis. Audiometric curve configuration has been proposed as a predictor of recovery. This study aimed to evaluate the association between audiogram morphology at onset and hearing outcome in patients with idiopathic unilateral SSNHL treated with standardized therapy. Methods: We retrospectively analyzed 156 patients with idiopathic SSNHL. Hearing thresholds at key frequencies were measured at baseline and 4 weeks post-treatment. Patients were categorized into upsloping, flat, downsloping, or U-shaped audiogram subgroups. Recovery was classified into four levels. Comparisons were made across subgroups for audiometric and laboratory data using ANOVA and chi-square tests. Results: Baseline PTA values were comparable across audiogram subgroups (p = 0.12). Hearing recovery differed significantly according to audiogram configuration (chi-square, p < 0.001), with upsloping and U-shaped patterns showing the best outcomes. Flat and downsloping curves were associated with poorer recovery, lower HDL, and elevated NLR values. Conclusions: Audiogram configuration is a relevant prognostic marker in SSNHL. Patterns linked to adverse metabolic and inflammatory profiles may benefit from tailored treatment strategies in a personalized medicine framework.

Cisplatin-induced ototoxicity is a permanent, bilateral sensorineural hearing loss occurring in up to 80% of treated patients. Its defining and clinically challenging feature is the progressive worsening of auditory function that continues well after chemotherapy has ended, a trajectory that cannot be explained by cumulative dose alone. This article is a comprehensive review of the present research studies on mechanisms that are responsible for this post-treatment progression. The cochlea, unlike other organs, appears to be unable to eliminate platinum (the active divalent metal ion released from cisplatin and responsible for its cytotoxic and ototoxic effects): traces of it can be found in human temporal bone tissue even more than 18 months after last infusion, and bone might serve as a long-term systemic reservoir. Within the inner ear, platinum accumulates preferentially in the stria vascularis, impairing endocochlear potential and outer hair cell function. Retained platinum sustains cascading effects including sustained NOX3-dependent oxidative stress, mitochondrial dysfunction, ongoing genotoxic injury to non-regenerative cells, and the early loss of ribbon synapses that precipitates delayed spiral ganglion neurodegeneration. Pharmacogenetic variability in platinum transport and antioxidant metabolism further modulates individual susceptibility. These findings support lifelong audiological surveillance and provide a basis for designing strategies that can protect hearing without compromising the essential anticancer efficacy of cisplatin therapy.