However, due to limitations in obtaining accurate levels of loudness discomfort or sometimes hearing thresholds, particularly in severe cases of ASD, clinicians rely on behavioral observation strategies and case history. Īssessment of hyperacusis typically will involve extensive case history taking, pure tone audiometry, measurement of uncomfortable loudness levels (ULLs), and self-report questionnaires such as the hyperacusis questionnaire (HQ). Other theories propose the role of central gain enhancement in hyperacusis and the possibility of hyperacusis to be an indication of problems with the limbic system or auditory pathway. Utilizing Magnetic Resonance Imaging (MRI), scientists have seen elevated auditory activity in the auditory midbrain, thalamus and cortex, as well as enlarged subcortical and cortical responses to sound in subjects with hyperacusis. Theories include the idea that hyperacusis is the result of increased neural synchrony and reorganization of the tonotopic structure of the auditory cortex as well as the possibility that neurons that would typically respond to loud sounds start to respond to lower intensity sounds. The precise cause of hyperacusis still remains unknown. It can impact one’s emotional wellbeing, sleep, concentration, and can cause anxiety. Hyperacusis can affect an individual at various degrees depending on the severity. These reactions are in response to general sounds, rather than specific sounds (such as chewing and sniffling), as would be the case with misophonia. Hyperacusis is a class of decreased sound tolerance disorders in which a negative or incongruous reaction is triggered from exposure to sounds that are not described as threatening or uncomfortable by a neurotypical individual. The most common types of DSTD are hyperacusis and misophonia. Decreased Sound Tolerance Disorders (DSTD) are routinely observed in autism spectrum disorder (ASD).
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