Evidence of a Neuroinflammatory Model of Tinnitus

Abstract

Emerging literature has highlighted the relationship between inflammatory and neuroinflammatory biomarkers and tinnitus. Neuroinflammation may help to explain the mechanisms underpinning hyperactivity in the cochlea, cochlear nucleus, inferior colliculus, medial geniculate body, and the auditory cortex in those with tinnitus. Glial activation and pro-inflammatory cytokines may cause excitatory-inhibitory synaptic imbalance. Advancing our understanding of these mechanisms may help elucidate the pathogenesis of tinnitus and lead to improvement in subtyping subjective tinnitus. The chapter explores our current understanding of the neuroinflammatory model within the context of the classical auditory pathway and what we can infer about the underlying mechanisms based on these studies.