Pathophysiology of Subjective Tinnitus: Triggers and Maintenance

Abstract

Tinnitus is the conscious perception of a sound without a corresponding external acoustic stimulus, usually described as a phantom perception. One of the major challenges for tinnitus research is to understand the pathophysiological mechanisms triggering and maintaining the symptoms, especially for subjective chronic tinnitus. Our objective was to synthesize the published literature in order to provide a comprehensive update on theoretical and experimental advances and to identify further research and clinical directions. We performed literature searches in three electronic databases, complemented by scanning reference lists from relevant reviews in our included records, citation searching of the included articles using Web of Science, and manual searching of the last 6 months of principal otology journals. One-hundred and thirty-two records were included in the review and the information related to peripheral and central mechanisms of tinnitus pathophysiology was collected in order to update on theories and models. A narrative synthesis examined the main themes arising from this information. Tinnitus pathophysiology is complex and multifactorial, involving the auditory and non-auditory systems. Recent theories assume the necessary involvement of extra-auditory brain regions for tinnitus to reach consciousness. Tinnitus engages multiple active dynamic and overlapping networks. We conclude that advancing knowledge concerning the origin and maintenance of specific tinnitus subtypes origin and maintenance mechanisms is of paramount importance for identifying adequate treatment.

New Onset Tinnitus after High-Frequency Spinal Cord Stimulator Implantation

“…Both conditions are the end results of deafferentiation of nerve signaling pathways [9–11]. In tinnitus, this leads to neuroplastic changes with a subsequent increase in background noise that ultimately leads to a “pure tone” tinnitus [12]. This pure-tone tinnitus has been suggested to be the auditory analog to chronic pain [9].…”

“…Notably, the burst stimulation waveform was originally developed for the treatment for tinnitus via stimulation of the auditory cortex [13]. Anatomically, several recent articles have implicated the basal ganglia and the thalamus as potential generators of pure-tone tinnitus [12, 14, 15]. Additionally, fMRI studies have demonstrated activation of cortical areas of the brain with SCS.…”

Personality Traits, Perceived Stress, and Tinnitus-Related Distress in Patients With Chronic Tinnitus: Support for a Vulnerability-Stress Model

“…Whilst its causes are not always clearly identifiable and closely interlinked, chronic tinnitus has been associated with numerous risk factors (Haider et al, 2018;Trevis et al, 2018;Boecking et al, 2019) that have partly been interpreted within a vulnerabilitystress framework. For example, emotional exhaustion and low emotional well-being were found to predict the risk of developing tinnitus (Hébert et al, 2012) with the former also being shown to predict higher sensitivity to sound following an acute stress task (Hasson et al, 2013).…”

Assessing the Heterogeneity of Complaints Related to Tinnitus and Hyperacusis from an Unsupervised Machine Learning Approach: An Exploratory Study

“…Indeed both ST and HA display a huge heterogeneity in their clinical presentation and may result from a variety of causes involving either peripheral auditory damage or central maladaptive plasticity [Nicolas-Puel et al, 2002;Pienkowski et al, 2014]. Moreover their pathophysiology is not fully understood, even if they most probably share common mechanisms, [Eggermont and Roberts, 2012] and thus far, no objective biomarkers of ST and HA are available that may be used to identify and categorize their countless clinically relevant subtypes [Haider et al, 2018].…”