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Objectives: This study examined the relationships between electrophysiological measures of the electrically evoked auditory brainstem response (EABR) with speech perception measured in quiet after cochlear implantation (CI) to identify the ability of EABR to predict postoperative CI outcomes.

Methods: Thirty-four patients with congenital prelingual hearing loss, implanted with the same manufacturer's CI, were recruited. In each participant, the EABR was evoked at apical, middle, and basal electrode locations.

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Background: Exposures to hazardous noise causes irreversible injury to the structures of the inner ear, leading to changes in hearing and balance function with strong links to age-related cognitive impairment. While the role of noise-induced hearing loss in long-term health consequences, such as progression or development of Alzheimer's Disease (AD) has been suggested, the underlying mechanisms and behavioral and cognitive outcomes or therapeutic solutions to mitigate these changes remain understudied. This study aimed to characterize the association between blast exposure, hearing loss, and the progression of AD pathology, and determine the underlying mechanisms.

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Background: Alzheimer's disease is a progressive form of dementia where cognitive capacities deteriorate due to neurodegeneration. Interestingly, Alzheimer's patients exhibit cognitive fluctuations during all stages of the disease. Though it is thought that contextual factors are critical for unlocking these hidden memories, understanding the neural basis of cognitive fluctuations has been hampered due to the lack of behavioral approaches to dissociate memories from contextual-performance.

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The N1 auditory evoked potential amplitude depends heavily on the inter-stimulus interval (ISI). Typically, shorter ISIs result in reduced N1 amplitudes, suggesting a decreased neural response with high stimulus presentation rates. However, an exception known as N1 facilitation occurs with very brief ISIs (∼150-500 ms), where the N1 amplitude increases.

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Loss of Fascin2 increases susceptibility to cisplatin-induced hearing impairment and cochlear cell apoptosis in mice.

J Otol

July 2024

Department of Biochemistry and Molecular Biology, and Key Laboratory for Genetic Hearing Disorders in Shandong, Binzhou Medical University, 346 Guanhai Road, Yantai, 264003, Shandong, PR China.

Objectives: Deletion of gene in mice has been linked to progressive hearing loss and degeneration of cochlear cells. Cisplatin, an antitumor drug, can cause various side effects, including ototoxicity. The aim of this study was to investigate the effects of on cisplatin-induced hearing impairment in mice and to explore the possible mechanism.

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