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Sheppard A, Hayes SH, Chen GD, et al. Review of salicylate-induced hearing loss, neurotoxicity, tinnitus and neuropathophysiology. Acta Otorhinolaryngol Ital. 2014;34(2):79-93
Sheppard, A., Hayes, S. H., Chen, G. D., Ralli, M., & Salvi, R. (2014). Review of salicylate-induced hearing loss, neurotoxicity, tinnitus and neuropathophysiology. Acta otorhinolaryngologica Italica : organo ufficiale della Societa italiana di otorinolaringologia e chirurgia cervico-facciale, 34(2), 79-93.
Sheppard, A, et al. "Review of salicylate-induced hearing loss, neurotoxicity, tinnitus and neuropathophysiology." Acta otorhinolaryngologica Italica : organo ufficiale della Societa italiana di otorinolaringologia e chirurgia cervico-facciale vol. 34,2 (2014): 79-93.
Sheppard A, Hayes SH, Chen GD, Ralli M, Salvi R. Review of salicylate-induced hearing loss, neurotoxicity, tinnitus and neuropathophysiology. Acta Otorhinolaryngol Ital. 2014 Apr;34(2):79-93. PMID: 24843217; PMCID: PMC4025186.
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Acta Otorhinolaryngol Ital. 2014 Apr;34(2):79-93.

Review of salicylate-induced hearing loss, neurotoxicity, tinnitus and neuropathophysiology.

Acta otorhinolaryngologica Italica : organo ufficiale della Societa italiana di otorinolaringologia e chirurgia cervico-facciale

A Sheppard, S H Hayes, G-D Chen, M Ralli, R Salvi

Affiliations

  1. Center for Hearing and Deafness, SUNY at Buffalo, Buffalo, USA.
  2. Institute of Otolaryngology, Catholic University of Sacred Heart Rome, Italy.

PMID: 24843217 PMCID: PMC4025186

Abstract

Salicylate's ototoxic properties have been well established, inducing tinnitus and a sensory hearing loss when administered in high doses. Peripherally, acute dosing of salicylate causes frequency dependent reductions in DPOAEs and CAP amplitudes in low (<10 kHz) and high (>20 kHz) frequencies more than mid frequencies (10-20 kHz), which interestingly corresponds to the pitch of behaviourally-matched salicylate-induced tinnitus. Chronic salicylate dosing affects the peripheral system by causing a compensatory temporary enhancement in DPOAE amplitudes and up-regulation of prestin mRNA and protein expression. Despite salicylate's antioxidant properties, cultured cochlea studies indicate it also impairs spiral ganglion neurons (SGNs) by paradoxically causing an upsurge of superoxide radicals leading to apoptosis. Centrally, salicylate alters γ-aminobutyric acid (GABA) and serotonin mediated neurotransmission in the central nervous system (CNS), which results in classical and non-classical auditory regions showing hyperactivity after salicylate administration. In the auditory cortex (AC) and lateral amygdala (LA), neuron characteristic frequencies (CF) shift upward and downward to mid frequencies (10-20 kHz) altering tonotopy following salicylate administration. Additionally, current source density (CSD) analysis showed enhanced current flow into the supergranular layer of the auditory cortex after a high systemic dose of salicylate. In humans, auditory perception changes following salicylate or aspirin, including decreased word discrimination and temporal integration ability. The results of previous studies have partially identified the mechanisms that are involved in salicylate-induced tinnitus and hearing loss, however to date some interactions remain convoluted. This review discusses current knowledge of salicylate ototoxicity and interactions.

Keywords: Auditory cortex (AC); Characteristic frequency (CF); Compound action potential (CAP); Current source density (CSD); Distortion product otoacoustic emissions (DPOAE); Inferior colliculus (IC),; Lateral amygdala (LA); Sodium salicylate (SS)

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