Neuroinflammation in Tinnitus

Abstract

Abstract Purpose of Review The current review aims to explore recent studies that have illustrated a link between neuroinflammation and tinnitus and the consequential effect on neuronal functioning. We explore parallels amongst pain and tinnitus pathologies and a novel treatment option. Recent Findings Genetic and pharmacological blockage of pro-inflammatory cytokines mitigates the physiological and behavioral tinnitus phenotype in acute rodent models. In addition, recent pain studies target a signaling pathway to prevent the transition from acute to chronic neuropathic pain, which could translate to tinnitus. Summary Neuroinflammation likely mediates hyperexcitability of the auditory pathway, driving the development of acute tinnitus. In chronic tinnitus, we believe translational regulation plays a role in maintaining persistent tinnitus signaling. We therefore propose this pathway as a potential therapeutic strategy.