J Otolaryngol Head Neck Surg
November 2022
Background: Squamous cell carcinoma of the external auditory canal (EACSCC) is an uncommon tumor and responsible for no more than 0.2% of all the head and neck malignancies. Although there is remarkable research evidence exhibiting that high-risk human papillomavirus (HPV) accounts for considerable head and neck malignancies, its role in the pathogenesis of EACSCC is yet to be determined.
View Article and Find Full Text PDFTympanosclerosis (TS) is a result of long-standing middle ear inflammation characterized by fibroblasts ossification. Fibrosis is the last revertible stage in the progress of middle ear inflammation to TS. It was hypothesized that chronic hypoxia could be modulating fibrosis, which in turn additionally further aggravated hypoxia via decreasing oxygen diffusion.
View Article and Find Full Text PDFElectric-acoustic stimulation (EAS) uses amplified sound by a hearing aid to stimulate an apical low-frequency region of the cochlea and electrical current from a cochlear implant (CI) to stimulate the basal high-frequency region. EAS recipients had significantly improved speech perception, music appreciation, and hearing function in noise compared to those relying on CI electrical stimulation (ES) alone. However, the interaction between basal ES and apical acoustic stimulation (AS) in the cochlea potentially affects EAS advantages.
View Article and Find Full Text PDFObjectives: Tinnitus has no reliable cure but may be significantly relieved by the usage of cochlear implants. However, not all tinnitus patients necessitate cochlear implantation that can impair hearing. This study was to investigate whether a novel extracochlear electrical stimulation (EES) strategy could relieve tinnitus of guinea pigs without hearing impairment, and the roles of auditory-somatosensory plasticity in the cochlear nucleus in the tinnitus relief.
View Article and Find Full Text PDFIntracochlear electrical stimulation (ES) generated by cochlear implants (CIs) is used to activate auditory nerves to restore hearing perception in deaf subjects and those with residual hearing who use electroacoustic stimulation (EAS) technology. Approximately 1/3 of EAS recipients experience loss of residual hearing a few months after ES activation, but the underlying mechanism is unknown. Clinical evidence indicates that the loss is related to the previous history of noise-induced hearing loss (NIHL).
View Article and Find Full Text PDFWith the development of neural prostheses, neural plasticity including synaptic remodeling under electrical stimulation is drawing more and more attention. Indeed, intracochlear electrical stimulation used to restore hearing in deaf can induce the loss of residual hearing and synapses of the inner hair cells (IHCs). However, the mechanism under this process is largely unknown.
View Article and Find Full Text PDF