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Objectives: Providing hearing compensation to patients with aural atresia is considerably challenging. Hearing aid transducers vibrating the aural cartilage (cartilage conduction; CC) have been devised, and hearing aids utilizing them (CC hearing aids) have quickly become a beneficial option for aural atresia in clinical applications. However, it remains unclear which placement (on the aural cartilage or mastoid) is beneficial to signal transmission., Methods: This study included 35 patients (53 ears with an abnormal ear canal and severe conductive hearing loss) who were using CC hearing aids. Thresholds were compared between the transducers on the aural cartilage and on the mastoid., Results: In ears with bony aural atresia, thresholds were significantly improved when the transducer was placed on the aural cartilage compared to when it was placed on the mastoid for frequencies ≤ 500 Hz ( P  < .05). In aural atresia ears with a fibrotic tissue pathway, the aural cartilage stimulation improved the thresholds by approximately 20 dB for frequencies ≤ 1000 Hz ( P  < .05). In non-atretic ears, the aural cartilage locations significantly worsened the threshold at 4000 Hz ( P  < .05)., Conclusion: Our findings demonstrated that placing the transducer at the aural cartilage improved the mid-to-low frequency thresholds compared to mastoid transduction in aural atretic ears. In contrast, no clear improvement to the signal transmission due to the transducer's placement on the aural cartilage was recognized in non-atretic ears., Level of Evidence: 2., Competing Interests: The authors declare no potential conflict of interest., (© 2021 The Authors. Laryngoscope Investigative Otolaryngology published by Wiley Periodicals LLC on behalf of The Triological Society.)

Background and Purpose: Toll-like receptor 4 (TLR4) expressed on spinal microglia and astrocytes has been suggested to play an important role in the regulation of pain signalling. The purpose of the present work was to examine the links between TLR4, glial activation and spinal release of prostaglandin E(2) (PGE(2)) and tumour necrosis factor (TNF), and the role these factors play in TLR4-induced tactile allodynia., Experimental Approach: Toll-like receptor 4 was activated by intrathecal (i.t.) injection of lipopolysaccharide (LPS) and KDO(2)-Lipid A (KDO(2)) to rats. Tactile allodynia was assessed using von Frey filaments and cerebrospinal fluid collected through spinal dialysis and lumbar puncture. PGE(2) and TNF levels were measured by mass spectometry and elisa. Minocycline and pentoxifylline (glia inhibitors), etanercept (TNF-blocker) and ketorolac (COX-inhibitor) were given i.t. prior to injection of the TLR4-agonists, in order to determine if these agents alter TLR4-mediated nociception and the spinal release of PGE(2) and TNF., Key Results: Spinal administration of LPS and KDO(2) produced a dose-dependent tactile allodynia, which was attenuated by pentoxifylline, minocycline and etanercept but not ketorolac. Both TLR4 agonists induced the spinal release of PGE(2) and TNF. Intrathecal pentoxifylline blunted PGE(2) and TNF release, while i.t. minocycline only prevented the spinal release of TNF. The release of PGE(2) induced by LPS and KDO(2) was attenuated by i.t. administration of ketorolac., Conclusions and Implications: Activation of TLR4 induces tactile allodynia, which is probably mediated by TNF released by activated spinal glia.