Misophonia is a relatively new condition, where individuals present with an immediate feeling of irritation and disgust that can easily escalate to an emotion of anger for only specific sound stimuli. These sounds are generally made by human beings (like chewing, lip smacking, loud breathing, tapping sounds, etc.), coined as triggers (Schröder et al., 2013). Misophonic reactions are independent of loudness of trigger stimuli (Swedo et al., 2022). The prevalence of misophonia is reported to fluctuate between 10 % to 50 % across various global populations (Aryal and Prabhu, 2022; Jakubovski et al., 2022; Naylor et al., 2021; Patel et al., 2023; Sarigedik and Gulle, 2021; Sujeeth et al., 2024; Vitoratou et al., 2023).

Research focusing on misophonia has increased over the past two decades, improving understanding and awareness. Yet, currently no globally standardized diagnostic criteria exist for misophonia diagnosis. Neither the fifth edition of the Diagnostic and Statistical Manuel of Mental Disorders (DSM-V) nor the eleventh edition of the International Classification of Diseases (ICD-11) has accepted misophonia as a distinct disease or disorder. Schröder et al. (2013) recognizing misophonia as a new distinct disorder proposed a diagnostic criterion to aid clinical diagnosis and promote research.

The etiology and pathophysiology of misophonia is a mystery. Limited studies are available on misophonia from an audiological viewpoint, having reported normal brainstem functioning (Aryal and Prabhu, 2023), normal temporal auditory processing (Ila et al., 2023) and diminished amplitudes of auditory late latency potentials indicating a central deficit (Aryal and Prabhu, 2024; Patro et al., 2025; Schröder et al., 2014; Schröder et al., 2013). Adline et al. (2025) reported individuals with misophonia performed normally for simple auditory working memory tasks, however performance dropped for more demanding tasks. Suraj et al. (2024) reported that the amplitudes of TEOAE and DPOAE (utilizing conventional clinical protocols) in quiet and contralateral suppression effects were similar between misophonic and non-misophonic groups. Neuro-imaging studies have reported deviant topographical markers (enhanced activity in right insula, right auditory cortex, right anterior cingulate cortex, right superior temporal cortex and left amygdala) in misophonia while listening to trigger sounds (Kumar et al., 2017; Schröder et al., 2015, 2019).

Despite previous findings indicating similar cochlear mechanisms in individuals with and without misophonia, we suspect possible alterations in the cochlear functioning that may go unnoticed based on signal to noise ratio and amplitude analysis of conventional otoacoustic emission (OAE) testing. DPOAE I/O function provides a clearer image on non-linear outer hair cells functioning with different input levels (Neely et al., 2009). To the best of our knowledge, only one other study has assessed cochlear functioning in misophonia using OAE testing. Study of frequency specific DPOAE behaviour at multiple input levels hasn’t been explored in misophonics leaving a void in the literature. Presence of frequency specific differences in peripheral cochlear functioning might indicate altered inputs to higher auditory centres, delineating possible mechanisms in misophonia pathophysiology. We hypothesize alterations in non-linear amplitude growth function in individuals with misophonia. We also suspect a possibility of increased/decreased amplitudes of DPOAE which we intend to explore at different input levels at different frequencies.

Misophonia often coexists with similar sound-related auditory disorders like tinnitus and hyperacusis, being hypothesized to have pathophysiological underpinnings akin to theirs. Sixty percent of tinnitus patients report having misophonia symptoms (Jastreboff and Jastreboff, 2003). Misophonic individuals are also known to have hyperacusis (Ahmmed and Vijayakumar 2024; Jastreboff and Jastreboff, 2023). Individuals with tinnitus having normal hearing sensitivity have shown abnormal amplitudes of transient evoked otoacoustic emissions (TEOAE) (Sarathy and Jaya, 2017; Thabet, 2009), larger DPOAE amplitudes in individuals with tinnitus having hyperacusis (Sztuka et al., 2010), while Alshabory et al. (2022) reported diminished DPOAE amplitudes and steeper DPOAE I/O function. The association of misophonia with tinnitus and hyperacusis, with similarities in their postulated mechanisms further strengthen our reasoning for hypothesising presence of subtle differences in cochlear processing which needs to be researched. The present study attempts to understand the cochlear non-linear functioning at different frequencies for different levels of input through the use of DPOAE I/O function.