Background The origin of tinnitus has been attributed to a peripheral auditory lesion, inducing bottom‐up changes and resulting in the perception of a “phantom sound.” However, non‐auditory factors can co‐exist as well, and can even lie at the origin of tinnitus development. An increasing body of literature focuses on psychological, (neuro)muscular, cardiovascular and many other influences and their respective associations with tinnitus prevalence. Objective of review The purpose of this study was to provide a comprehensive description of these non‐otologic risk factors, and to summarise the evidence in literature about their link with tinnitus. Type of review A narrative systematic review was conducted, following the Preferred Reporting Items for Systematic reviews and Meta‐Analyses statement. Search strategy The MEDLINE, Embase and Web of Science databases were systematically searched for eligible articles, supplemented with manual search methods and grey literature search. Epidemiological studies reporting on the relationship between various non‐otologic risk factors and tinnitus were included. Evaluation method Quality assessment was performed using the Hoy & Brooks tool. Results Fifty‐five studies were included. Studies were of variable quality, with poor tinnitus definitions and evaluations or questionable sampling of the study population as main contributing factors for high risk of bias. Multiple associated factors have been identified, including cardiovascular, psychological, neurological, musculoskeletal and dietary factors. Conclusions The current literature review identified multiple risk factors that could be of significant importance for tinnitus development, maintenance or aggravation. While causality remains uncertain, this systematic elaboration of possible tinnitus comorbidities/risk factors can help provide direction for future research, and can direct clinicians to identify patients at risk and treat relevant symptoms accordingly.

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Purpose Functional imaging is often used to try to elucidate the pathophysiological mechanism of tinnitus. Residual inhibition, the temporary suppression of tinnitus after application of a masking noise, could be an interesting technique to modulate tinnitus perception in functional imaging paradigms. The purposes of this study were to primarily assess reproducibility of the (partial) positive residual inhibition response duration in patients with tinnitus and to explore its utility in experimental designs. Method Patients with tinnitus exhibiting a (partial) positive residual inhibition response or tinnitus reduction after a 1-min white noise presentation were selected from a broad consulting tinnitus population. In 27 patients, this response was tested 4 times: twice during initial testing and twice during a retest of the psychoacoustic tinnitus measures, 4–8 weeks after initial consultation. In 17 patients with stable residual inhibition responses, reproducibility of response duration, the duration of tinnitus reduction up to pretesting state, was analyzed. Results Initial testing showed a residual inhibition duration of 29.5 s on average. Test–retest reproducibility of response duration was shown to be reliable with an ICC(3, 4) of .871 (95% CI [0.733, 0.948]) and a standard error of measurement of 6.64 s. Conclusions This study indicates the good test–retest reproducibility of residual inhibition duration in our subset of 17 patients with stable (partial) positive residual inhibition. Residual inhibition is, therefore, a technique that can potentially be used for temporary tinnitus manipulation in experimental paradigms to unravel tinnitus pathophysiology.