Ten to fifteen percent of the population experience tinnitus. It is necessary to develop effective treatments for patients suffering from tinnitus. This study aimed to explore the effectiveness of an internet-based treatment consisting of tinnitus retraining therapy and cognitive behavioral therapy for patients with primarily tinnitus. The secondary aims were to investigate changes in hyperacusis (hypersensitivity to sounds), misophonia (strong emotional reaction to a sound), depression, and anxiety.

Background: Hyperacusis is a common, but often underrecognized comorbidity in patients with chronic subjective tinnitus. Reduced sound tolerance is associated with a greater tinnitus-related burden, impaired communication, reduced social participation, and poorer daily functioning. However, published data regarding its prevalence and clinical impact remain limited and inconsistent. Objectives: To determine the prevalence of hyperacusis in patients with chronic subjective tinnitus and to assess its association with tinnitus-related handicap, uncomfortable loudness levels, and degree of hearing loss and daily functioning. Methods: This cross-sectional study included 194 patients aged 21-85 years with chronic subjective tinnitus. Hyperacusis was assessed using a structured clinical interview that included questions on decreased sound tolerance and sound-induced ear pain and uncomfortable loudness level measurements (ULLs). Patients were categorized into two groups: tinnitus with hyperacusis (T + H; n = 32) and tinnitus without hyperacusis (T; n = 162). The impact of tinnitus on daily functioning was evaluated using a standardized and clinically validated questionnaire-the Tinnitus Handicap Inventory (THI). Data were analyzed using appropriate parametric and nonparametric statistical tests. Results: Hyperacusis was identified in 32 of 194 patients with chronic tinnitus (16.5%). Patients with tinnitus and hyperacusis (T + H) had significantly higher THI scores than those with isolated tinnitus, indicating greater tinnitus-related handicap (76.3 vs. 41.9; p < 0.001). Patients with hyperacusis also demonstrated significantly lower ULL values than those without hyperacusis (p < 0.001). Conclusions: Although the reported prevalence of hyperacusis among patients with tinnitus varies across the literature, our findings indicate that hyperacusis is a common comorbidity associated with significantly greater tinnitus-related handicap. Routine assessment of hyperacusis, including ULL measurements, should be incorporated into the clinical evaluation of patients with tinnitus to facilitate comprehensive diagnosis and optimize management. These findings highlight the importance of systematic assessment of hyperacusis in patients with tinnitus in routine audiological practice.

Hyperacusis describes the condition in which mid-level sounds are perceived as uncomfortably loud. This study assessed 36 listeners (mean age = 25.75 years) with low noise-exposure history (Noise Exposure Structured Interview, NESI) and no tinnitus, to investigate the association between assessed hyperacusis scores (Hyperacusis Questionnaire, HQ), measured uncomfortable loudness levels (ULLs), and speech intelligibility in noise (Matrix Speech test). Thresholds were ≤ 20 dB HL, for the standard audiometric signal frequencies (0.25-8 kHz). ULLs were measured for signal frequencies of 0.5-, 2-, and 4-kHz. Extended high-frequency (EHF) audiometric thresholds were also measured for signal frequencies up to 16 kHz. Cluster analysis identified three groups based on EHF audiometric threshold and slope. The cluster EHF thresholds for the three groups were 5.2 dB HL (LOW-hf), 18.3 dB HL (MED-hf), and 45.7 dB HL (HIGH-hf). Results indicated that the MED-hf group exhibited significantly higher HQ scores compared to the HQ scores associated with LOW-hf and HIGH-hf groups. Also, elevated EHF thresholds were generally unrelated to speech-in-noise intelligibility scores, and there was no significant relationship between HQ and NESI scores. For young listeners with relatively low noise exposure, normal or mildly-elevated EHF thresholds (8-16 kHz) may be associated with mid-range HQ scores.

Humans can experience sound-evoked pain, either from extremely loud sounds or in cases of pain hyperacusis from typically tolerable sounds. However, the mechanisms underlying sound-evoked pain remain poorly understood. Developing behavioral methods to measure sound-evoked pain in animal models is critical for elucidating these mechanisms. Here, a machine learning-based approach was developed to measure sound-evoked pain in freely moving mice of both sexes by analyzing facial grimace and body position from video recordings during sound exposure. Facial grimace, a commonly used method to detect pain in mice, and body position, which can be used to measure postural and movement changes that also indicate pain, were both quantified using a deep neural network model trained to extract established facial and body features from video recorded by a single camera. To validate the model's capability to detect pain, a known painful state, migraine induced by the injection of the neuropeptide calcitonin gene-related peptide (CGRP), was used. Using this machine learning-based approach, the ability to quantify a pain response from CGRP-induced migraine, distinct from baseline behavior, was demonstrated, resulting in a defined pain threshold. Sound exposures at high intensities elicited significant changes in facial grimace and body position, in comparison, surpassing the pain threshold calculated from CGRP-induced migraine. These behavioral changes were absent in Tmie-knock-out mice, which lack functional sound transduction in the cochlea. This automated, high-throughput framework enables objective and sensitive analysis of pain-related behavior providing a foundation for future studies investigating the peripheral and central mechanisms of sound-evoked pain.

Cochlear damage triggers compensatory primary auditory cortex (A1) plasticity that amplifies responses to residual sensory inputs, thereby contributing to the restoration of both cortical responsiveness to sound and perceptual sound detection threshold. However, this adaptation can become maladaptive, producing neuronal hyperactivity that contributes to tinnitus and hyperacusis. The neuromodulatory mechanisms governing these adaptive and maladaptive changes remain unknown. Here, we demonstrate that noise-induced cochlear injury triggers bidirectional synaptic zinc signaling plasticity that potentiates activity in excitatory principal neurons and parvalbumin-expressing interneurons, while suppressing activity in somatostatin-expressing interneurons. These cell-type-specific effects of synaptic zinc plasticity contribute to restoring A1 responsiveness to sound and perceptual detection thresholds, while being necessary for neural hyperactivity. Together, our findings establish synaptic zinc as a pivotal neuromodulator that shapes both adaptive and maladaptive cortical plasticity and identify a promising therapeutic target for improving perceptual recovery after cochlear damage and mitigating tinnitus and hyperacusis.

Misophonia is a sound sensitivity disorder characterized by heightened emotional, physiological, and behavioral reactions to specific auditory stimuli. Although prior research has linked misophonia to maladaptive personality traits and internalizing symptoms, the role of early maladaptive schemas (EMSs) remains underexplored. The present study examined the associations between misophonia severity, EMSs, personality trait domains, and psychological symptoms, and tested whether EMSs accounted for incremental variance beyond these factors. A total of 144 adults (72 with misophonia and 72 matched controls) completed self-report measures of misophonia, EMSs, personality traits, depression, and anxiety. Misophonia severity was positively associated with most EMSs, as well as with negative affectivity, detachment, psychoticism, and symptoms of depression and anxiety. Individuals with misophonia reported significantly higher levels across all EMSs, personality domains, and psychological symptoms compared to controls. Regression analyses indicated that several EMSs predicted misophonia severity, with Entitlement and Emotional Inhibition emerging as the strongest independent predictors. In a hierarchical regression model, EMSs accounted for additional variance beyond personality traits and psychological symptoms. In the final model, Entitlement and Negative Affectivity remained significant predictors. These findings support a hierarchical framework in which personality trait domains reflect a broad dispositional vulnerability, whereas EMSs represent more specific cognitive-emotional processes that may shape the appraisal and perceived meaning of trigger sounds. Targeting EMSs may enhance psychological interventions by addressing maladaptive appraisals and emotional regulation difficulties underlying misophonic responses.