New insights on the peripheral mechanisms and neuroplasticity of tinnitus

Abstract

Tinnitus is a condition characterized by the perception of sound in the head or ears without any external source of sound. It affects over 10% of the global population, with higher prevalence in the elderly. Tinnitus is associated with various symptoms such as concentration difficulties, sleep problems, anxiety, and depression, affecting quality of life. It can be caused by otologic diseases, ototoxic drugs, age-related hearing loss, and neurological conditions like stroke or traumatic brain injury. Tinnitus is a complex and heterogeneous condition, making its classification challenging. Four dimensions of heterogeneity have been identified: clinical profiles (type and laterality of sound), causal risk factors (e.g., hearing loss, temporomandibular joint disorder), comorbidities (e.g., hyperacusis, mood disorders), and treatment responses. Identifying subtypes of tinnitus and its associated conditions can aid in optimizing clinical management and developing effective treatments. While hearing loss is commonly associated with tinnitus, it is not the sole cause. Central auditory and non-auditory pathways are also believed to play a key role. Animal models have contributed to understanding tinnitus, suggesting that cochlear damage and deafferentation of spiral ganglion neurons lead to alterations in the central auditory system. Changes in excitatory, inhibitory, and neuromodulatory networks along the central auditory pathway have been observed, indicating a failure of the central auditory pathway to adapt to peripheral damage. This review aimed to explore the convergence of factors related to peripheral damage and central changes in the brainstem and auditory cortex, leading to maladaptive plasticity and the persistence of tinnitus. Understanding these mechanisms is crucial for developing effective interventions for tinnitus sufferers.