Misophonia is an affective sensory processing disorder characterized by intense negative emotions in response to particular sounds; these responses are recognised by sufferers to feel unreasonably excessive [1,2]. Triggers tend to be idiosyncratic but are often human-made noises that originate in the mouth (lip-smacking, crunching, chewing, breathing). They can also include repetitive noises (e.g., clicking, tapping) and sometimes include sounds made by animals or inanimate objects (e.g., clocks, fans etc.). While most people perceive such triggers as moderately irritating or might even fail to notice them, the emotional reactions experienced by misophonics include anger, disgust, panic, and the feeling of being trapped [3, 4]. Co-occurring physical reactions – for example as measured by increased skin conductance [5] - have been likened to a ‘flight or fight’ response. Although little is known about its epidemiology, misophonia is thought to be relatively common. Wu et al. [6] found that 20% of a predominantly female undergraduate sample reported clinically significant misophonia. The condition also seems to present in other family members, with one study finding that 55% of their sample had misophonic family members [5] and another detailing a family in which 15 out of 34 members were affected by the condition across three generations [7]. Misophonia is often comorbid with other clinical disorders and symptoms such as generalised anxiety [6], and obsessive compulsive personality traits [3,8,9]. These profiling studies represent important first steps but what is lacking is a mechanistic understanding of how and why these features co-occur. Similarly, there is little understanding of how misophonia might arise out of individual differences in affective (i.e. emotional) processing or in sensory and attentional processing [36]. The few neuroscientific studies conducted to date suggest that both are likely to be important with a diminished EEG signature for early auditory change detection in misophonics [10] and differences in functional connectivity amongst regions of the brain involved in computing emotional salience [11]. Misophonia can be regarded as a heightened form of sensory sensitivity. As such it belongs, at least superficially, to a family of potentially related conditions that share this trait including hyperacusis, autism, migraine, synaesthesia (e.g. sounds evoking colours), amongst others [12]. All of these conditions are accompanied by heightened levels of discomfort to certain sensory stimuli. Whether there are any deeper similarities – in terms of underlying mechanisms – remains to be established. But the advantage of exploring this line of enquiry is that there are already substantial research efforts into all of these domains, with research into misophonia somewhat ‘behind the curve’. As such, we can leverage ideas and methods that have been applied in these other domains. The most obvious difference between misophonia and these other conditions is that misophonia is defined by atypical responsiveness to sounds in particular, whereas other conditions are defined by a broader sensitivity profile. Our testable hypothesis is that misophonic triggers (typically limited to a small set of auditory stimuli) may be the ‘tip-of-the-iceberg’ below which lies a pattern of less extreme (but nonetheless heightened) sensory sensitivities to a wider range of stimuli including to senses other than hearing. There is some preliminary evidence consistent with this in misophonia [6], and we will use additional scales that have been validated in conditions such as autism. Our proposal here is that broad sensory sensitivities may act as a type of ‘start-up kit’ from which misophonia later emerges. Hence, broad low-level sensory sensitivities may conspire with other traits (e.g., anxiety) as a catalyst towards the emergence of the more specific auditory sensitivities of misophonia (e.g., chewing). Given this hypothesis, we will examine more closely the sensory, attentional and cognitive profiles of misophonics. We will be careful to assess characteristics of misophonia that distinguish it from hyperacusis including the nature of the trigger (e.g. sound type, loudness) and response (e.g. emotion, pain) [14]. AIMS & HYPOTHESES The first three hypotheses are more confirmatory in nature (motivated by prior research) and the last three take a more exploratory and data-driven approach: 1) People with misophonia will have increased clinical traits in the domain of anxiety (measured by Anxiety Sensitivity Index (ASI-3) [45]), autism spectrum traits (measured by the Autism Quotient (AQ) [18]), obsessive-compulsive tendencies (measured by the Obsessive-Compulsive Inventory (OCI) [21]), and increased headache/migraine (measured by the Penn Online Evaluation of Migraine (POEM) [37]). 2) People with misophonia will have heightened sensory sensitivity outside of their set of particular misophonic triggers as measured by the Glasgow Sensory Questionnaire (GSQ) [17] and visual pattern glare test (where mid spatial frequency gratings elicit discomfort and visual distortions) [48, 49]. 3) Interoceptive sensibility can be regarded as a particular form of (embodied) sensory sensitivity and we expect misophonics to have higher scores than control participants on MAIA [22] subscales of Noticing, Emotional Awareness, and Body Listening. Given evidence of heightened emotional salience/reactivity in misophonia coupled with increased interoceptive awareness [11], we also expect that individuals with misophonia will score lower on the subscales of MAIA that measure regulation of internal states, such as Not-Distracting, Not-Worrying, Attention-Regulation, Self-Regulation, and Trusting, relative to controls. 4) To determine whether misophonia has different subtypes as indicated by cluster analysis of the five factors of the Sussex Misophonia Scale [46] and, if so, whether these subtypes are linked to a different profile on the clinical measures and sensory sensitivity measures that are linked to misophonia more generally (see the measures above). 5) To create a symptom network profile of misophonia that incorporates the relationship between different symptoms of their misophonia and co-occurring clinically-relevant traits. 6) To determine which sounds (e.g. apple crunching, tapping) and which responses to sounds (e.g. annoyance, pain) discriminate people with misophonia from those who lack it. 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