BackgroundCisplatin, an effective chemotherapy, is a cause of ototoxicity. It enters inner ear cells through Organic Cation Transporter 2 (OCT2). Recently, we identified another cochlear transporter, Multidrug and Toxin Extrusion Protein 1 (MATE1); it allows cisplatin efflux in renal cells. OCT2 and MATE1 appear to work together in eliminating renal toxins. 4-aminopyridine (4-AP), a known blocker of voltage-dependent K+ channels, blocks OCT2 but not MATE1 in the kidney. We hypothesize that 4-AP could prevent cisplatin from entering cochlear cells, without inhibiting the efflux of cisplatin that may have already entered. This could enhance clearance, mitigating ototoxicity.ObjectiveDetermine the otoprotective potential of 4-AP in vitro following cisplatin exposure.MethodsMice cochlear explants were treated with cisplatin (20 μM), with or without 4-AP (500 μM) for 24 h, evaluated for caspase 3/7 activity with Cell Event®, visualized with confocal and phase contrast microscopy. Moreover, HeLa cells and cochlear explants were exposed to cisplatin (75 μM and 30 μM, respectively) with or without 4-AP in the explants and were evaluated for cisplatin-DNA adducts and cleaved caspase-3 immunohistochemistry.ResultsFor cochlear explants exposed to cisplatin, Cell Event® staining occurred in the supporting cells, medial to the hair cells, and in the organ of Corti. No significant differences were found between cisplatin-exposed explants with or without 4-AP. In HeLa cells, consistent cellular staining for cisplatin-DNA adducts and cleaved caspase-3 was observed. However, this was not seen in cochlear explants, and there was no significant decrease in staining levels with 4-AP co-treatment.ConclusionsIn this in vitro study, no otoprotective potential of 4-AP against cisplatin-induced ototoxicity was observed. While 4-AP blocks OCT2, it did not decrease cisplatin-DNA adducts in cochlear cells. Further research into OCT2 and MATE1 transport mechanisms is needed.

OBJECTIVE: Hearing loss is an underrecognized comorbidity in patients with chronic kidney disease (CKD) and chronic liver disease (CLD), particularly among those awaiting solid organ transplantation. Early identification of auditory dysfunction is essential to optimize communication, treatment adherence, and post-transplant care. To describe the prevalence, severity, and audiometric patterns of hearing loss in adult candidates for kidney or liver transplantation. METHODS: A cross-sectional study was conducted in 36 adult patients with advanced CKD or CLD evaluated for kidney or liver transplantation at a tertiary academic center. All participants underwent otomicroscopy, tympanometry, pure-tone audiometry, distortion product otoacoustic emissions (DPOAEs), and tinnitus assessment using the Tinnitus Handicap Inventory. Hearing loss was defined as a pure-tone average >20 dB HL across 0.5-4 kHz in either ear. RESULTS: Hearing loss was identified in 30.6% of patients (CLD: 31.6%; CKD: 29.4%), predominantly mild to moderate, with symmetrical high-frequency sensorineural patterns. Distortion product otoacoustic emissions abnormalities were observed in 56.9% of ears, suggesting subclinical cochlear dysfunction. Tinnitus was reported in 38.2% of participants, with no significant differences between groups. All cases of tinnitus were classified as slight or mild handicap. Use of acetylsalicylic acid was significantly associated with hearing loss among CKD patients (P=.003). CONCLUSIONS: Hearing loss and tinnitus are common in patients with advanced CKD or CLD awaiting transplantation. Comprehensive audiological assessment, including DPOAEs, may improve pre-transplant evaluation by identifying patients at risk for auditory impairment and informing ototoxic medication decisions.

BACKGROUND:Vestibular migraine (VM), and probable vestibular migraine (VPM), are frequent causes of vertigo. The objective of this study was to establish the prevalence of hearing loss and cochleovestibular paresis in patients with VM and PVM. METHODS:Retrospective cohort study of adult patients seen between 01/2024 and 12/2025, diagnosed with VM or PVM. Demographics, family history of migraine and results of audiometry, videonystagmography (VNG), and VHIT were evaluated. This study was approved by the local ethics committee. RESULTS:A total of 470 patients we included: 53% had VM, 47% PVM. Overall, most were women (79%), average age 51.1 ± 15.2 years. 61% had a hearing test, and 40% had hearing loss. Most were mild-moderate, 51% had unilateral hearing loss and 6.6% had an event of documented cochleovestibular paresis. There were no differences between prevalence or degree of hearing loss or cochleovestibular paresis between VM and PVM. VNG abnormal findings were seen in 88%, most commonly central positional nystagmus, and 56% had an abnormal VHIT. Family history of migraine was greater in the VM group (64% vs 49%). CONCLUSION:Both VM and PVM patients show a high prevalence of hearing loss and vestibular abnormalities, with no significant differences in severity or clinical presentation between groups. These findings support the concept that VM and PVM represent a single pathophysiology continuum, The family history of migraine remains the most reliable clinical differentiator in the diagnostic spectrum. There appears to be no significant differences between VM and PVM with regards to hearing loss or cochleovestibular paresis. The main differences between both groups is family history of migraine.

Bilateral vestibulopathy (BV) is a known cause of chronic vestibular syndrome. With the video head impulse test (VHIT), we can now evaluate all six semicircular canals independently and establish BV subgroups based on canal gain patterns. Background/objectives: To assess canal gain patterns for BV with VHIT, and evaluate subgroups with regard to sex, age, and hearing loss. Methods: A retrospective chart review was performed of all patients who underwent a VHIT between January 2021 and July 2024. Patients with decreased lateral canal gains, bilaterally, were included. Results of canal gains, VHIT patterns, audiometry, and videonystagmography (VNG) results were reviewed. Results: 101 cases were included. Patients were 75.5 ± 13.1 years old and 64.4% were women. Various VHIT patterns were observed; the most frequent being decreased canal gains across all six canals (44.6%), followed by a mix of canals with decreased gains with no clear pattern (34.7%). Decreased gains limited to the lateral canals were rare. We did not observe any significant difference between subgroups with regard to gender or age. Concomitant hearing loss was common (89.6%). A trend was noted, suggesting that severity of hearing loss increased with the number of affected canals. An abnormal VNG test was common (73.3%). Conclusions: Various patterns of canal gains were observed for patients with BV. Audiometry and VNG should be considered as part of BV studies since abnormalities are commonly found. Further research is needed to understand VHIT patterns in BV.

The aging population is increasingly affected by both diabetes mellitus and hearing loss, two conditions that often coexist and can significantly impact quality of life. As the prevalence of diabetes rises with age, so does the incidence of hearing impairment, with both conditions contributing to cognitive decline and functional limitations. The interplay between diabetes, hearing loss, and cognition highlights the need for comprehensive healthcare strategies that address the unique challenges faced by older adults. This review explores the mechanisms underlying the interplay between these three conditions, including mitochondrial dysfunction, neuroinflammation, oxidative stress, and microangiopathy.

La parálisis o paresia facial alternobárica es una neuropraxia del séptimo nervio cra-neal debido a cambios de presión. Se produce en el contexto de una disfunción de la trompa de Eustaquio, una dehiscencia canal del nervio facial y cambios en la presión atmosférica. Se considera una rara complicación de barotrauma. Su prevalencia es difícil de estimar y, probablemente, se encuentre subreportada. La forma de presentación más habitual incluye paresia facial, plenitud aural, hipoacusia, otalgia, parestesias faciales y linguales. La mayoría de los episodios son transitorios, con una duración entre minutos y algunas horas, con recuperación posterior completa. Entre los diagnósticos diferenciales se encuentran causas periféricas y centrales de paresia facial, las cuales hay que sospechar ante la persistencia de los síntomas en el tiempo o ante la presencia de otros signos o síntomas neurológicos. La evaluación inicial debe incluir un examen otoneurológico completo. La tomografía computarizada de hueso temporal favorece la visualización de posibles dehiscencias del canal del facial. La prevención de nuevos episodios incluye la práctica de ecualización efectiva, la resolución de la disfunción de la trompa de Eustaquio y en algunos casos específicos, métodos alternativos de ventilación del oído medio como la colocación de tubos de ventilación. Una vez instalada la parálisis facial, si no se produce recuperación espontánea, el uso de corticoides es una opción. Se presenta un caso de paresia facial alternobárica recurrente y una revisión de literatura.

Introducción: El traumatismo craneoencefálico (TCE) puede generar vértigo, mareo e inestabilidad. Posibles causas otorrinolaringológicas son el vértigo postural paroxístico benigno (VPPB) que constituye el diagnóstico más frecuente, y la hipofunción vestibular.

BackgroundCisplatin appears to enter the cochlear cells through the organic cation transporter 2 (OCT2). There is recent evidence that multidrug and toxin extrusion protein 1 (MATE1) is involved in cisplatin-induced nephrotoxicity. Its presence and role in the ear are unknown.Aims/ObjectivesEvaluate the presence and localization of MATE1, and determine the localization of OCT2, in the cochlea. Evaluate cisplatin uptake with regard to MATE1 and OCT2 expression.Material and MethodsMurine cochlear explants and paraffin-embedded cochleae were evaluated with immunohistochemistry for OCT2 and MATE1. Explant cultures were also treated with Texas Red cisplatin to determine their cellular uptake.ResultsMATE1 is present in the cochlea. Most intense labeling of MATE1 and OCT2 was seen in the outer hair cells (OHCs) and pillar cells, respectively. Both transporters were observed in the spiral ganglion neurons and stria vascularis. Expression levels of OCT2 and MATE1 decreased following cisplatin exposure. Texas Red cisplatin staining was strong in OHCs and pillar cells.Conclusions and SignificanceTo the best of our knowledge, this is the first study demonstrating the presence and localization of MATE1 in the cochlea. OCT2 labeling was seen in pillar cells. Consistently, OHCs and pillar cells uptake Texas Red cisplatin.

BACKGROUND: Lindsay-Hemenway syndrome was first described as an acute unilateral peripheral vestibulopathy followed by positional vertigo. A vascular etiology was proposed. An association between cardiovascular risk factors and benign paroxysmal positional vertigo secondary to acute unilateral peripheral vestibulopathy has been described with contradictory evidence. The study aimed to evaluate the prevalence of cardiovascular risk factors in patients with benign paroxysmal positional vertigo secondary to acute unilateral peripheral vestibulopathy and analyze differences in prior history of benign paroxysmal positional vertigo, affected semicircular canals, and response to repositioning maneuvers between patients with idiopathic benign paroxysmal positional vertigo and secondary to acute unilateral peripheral vestibulopathy. METHODS: We performed a retrospective, descriptive study of all cases of benign paroxysmal positional vertigo between January/2017 and June/2020, with or without a history of acute unilateral peripheral vestibulopathy within the previous year. Cases secondary to trauma or otoneurological causes and acute unilateral peripheral vestibulopathy without confirmatory tests and cases with auditory symptoms were excluded. RESULTS: In total, 242 cases were obtained; 158 idiopathic benign paroxysmal positional vertigo and 84 secondary to acute unilateral peripheral vestibulopathy. No statistically significant differences were found in relation to age: 61.2 +/- 14.6 versus 62.4 +/- 16.2 years (P =.55), sex: female 78.5% versus 73.8% (P =.41), presence of cardiovascular risk factors: 52.5% versus 54.8% (P =.67), prior history of benign paroxysmal positional vertigo: 22.2% versus 27.7% (P =.43), affected semicircular canals (P =.16) or number of repositioning maneuvers (P =.57). CONCLUSION: Associations between age, cardiovascular risk factors, and benign paroxysmal positional vertigo secondary to acute unilateral peripheral vestibulopathy have been described with conflicting evidence. This is the first study to evaluate cardiovascular risk factors specifically for Lindsay-Hemenway syndrome, and we did not observe any differences between idiopathic benign paroxysmal positional vertigo cases and those secondary to acute unilateral peripheral vestibulopathy.

EDITORIAL article Front. Pediatr., 28 July 2023Sec. Pediatric Otolaryngology Volume 11 - 2023 | https://doi.org/10.3389/fped.2023.1231803

La migraña vestibular es una de las etiologías más frecuentes del síndrome vestibular episódico a nivel mundial. Presenta varias hipótesis de patofisiología, principalmente a nivel de sistema vestibular central y genético. Su diagnóstico es fundamentalmente clínico, pero se han observado alteraciones a nivel de la función vestibular y de las pruebas oculomotoras. Los hallazgos clínicos no solo están presentes en el momento de la crisis, sino también se han observado en intervalos asintomáticos. La paresia unilateral en la prueba calórica suele ser más frecuente que una ganancia baja del reflejo vestíbulo-ocular del canal lateral en la videonistagmografía, sin embargo, existe una tasa elevada de discordancia entre ambas pruebas. Respecto a la prueba de estudio del movimiento ocular, se han observado alteraciones en el seguimiento pendular, movimiento sacádico, nistagmo optocinético, nistagmo evocado por la mirada, nistagmo espontáneo y nistagmo posicional. Es frecuente observar que el nistagmo provocado por cambios posicionales presenta características centrales durante la crisis de migraña vestibular, pero también se pueden presentar en periodos libres de síntomas en este grupo de pacientes.

Background: Ototoxicity is a side effect of drugs and medications that usually leads to bilateral and symmetric sensorineural hearing loss that commonly affects the high-frequency range initially, with or preceded by tinnitus. Possible ototoxic side effects of calcineurin inhibitor immunosuppressants have been suggested, but this remains unclear. Therefore, this study aims to evaluate audiological changes in patients undergoing transplantation receiving immunosuppressive treatment with calcineurin inhibitors. Methods: Prospective cohort study. Adult patients undergoing liver or kidney transplantation treated with calcineurin inhibitors were included. Pure-tone audiometry, distortion product otoacoustic emissions, and the Tinnitus Handicap Inventory questionnaire were completed at baseline, one, three, and six months after transplantation. Hearing thresholds were compared and correlated with plasma concentrations of calcineurin inhibitors. Results: Seventeen patients were included, 59% males, with a median age of 54.7 years (29-68 years). Twelve patients underwent liver transplantation, four underwent kidney transplantation, and one patient underwent both. The median follow-up was 5.8 months (4-8 months). Significant pure-tone average shifts were observed in two patients. Both cases presented fluctuations in their hearing levels, which were not bilateral or symmetrical and affected the higher frequencies. All patients received tacrolimus within the therapeutic range during the follow-up period. Three different patients exceeded the expected range once; however, they were rapidly corrected and did not correlate with any changes in hearing. Conclusions: It appears that tacrolimus does not cause hearing loss when levels are within the therapeutic range for a follow-up period of six months post-transplantation.

BACKGROUND:Vestibular migraine (VM) is the most frequent etiology of recurrent spontaneous episodic vertigo. Vestibular and oculomotor abnormalities have been described in VM; however, the diagnosis is currently based on symptoms. The objective of this study was to determine the most frequent abnormalities in videonystagmography (VNG), caloric testing (Cal) and video head impulse test (vHIT) in patients with VM.METHODS:A retrospective cohort study was conducted, including all VM and probable VM patients seen from January 2021 to July 2022. Demographics, auditory symptoms and results via VNG, Cal and vHIT were evaluated. VNG results were compared with a control group.RESULTS:Sixty patients, 81.7% with VM and 18.3% with probable vestibular migraine, were included. VNG revealed the following abnormalities: 21.7% spontaneous nystagmus; 33.3% positional nystagmus, mostly central; 26.7% optokinetic nystagmus; 56.7% smooth pursuit abnormalities and 70% saccade test abnormalities, mostly velocity and latency. An abnormal unilateral caloric response was seen in 22.9%, while vHIT revealed a low gain in at least one canal in 21.7%, and saccades were seen in at least one canal with normal gains in 18.3%. Concordant results between Cal and lateral vHIT were seen in 77.1% of cases.CONCLUSIONS:Although VM is a clinical diagnosis, vestibular and oculomotor abnormalities are commonly seen. The most frequent oculomotor findings were an abnormal saccade test, abnormal smooth pursuit and central positional nystagmus.