COVID-19 Vaccination Effects on Tinnitus and Hyperacusis: Longitudinal Case study.

The case study explores COVID-19 vaccination connection to tinnitus and hyperacusis, considering its onset and exacerbation post vaccination. The subject is a 47-year-old woman with a history of bilateral tinnitus, and her hearing history was tracked from 2014 to 2023. An intense episode of tinnitus occurred in 2021, distinct from previous experiences post COVID-19 vaccination, second dose. Symptoms manifested as sudden onset of hyperacusis, pronounced "roar" type tinnitus, and a sudden decline in hearing. Audiometric results showed reduce thresholds in low frequencies and lower speech scores in the left ear. This escalation significantly affects speech understanding in group conditions and noisy environments. There was a gradual improvement in tinnitus and hyperacusis severity, but the subject has a greater problem with speech understanding. The subject's journey involved visits to specialists, multiple testing including neuroimaging, naturopath consultations, and anxiety medication. It emphasizes the importance of healthcare practitioners recognizing and documenting these issues and need for timely multidisciplinary intervention and support. Further research is necessary to better understand the relationship between COVID-19, vaccination, and auditory symptoms.

Sensory hypersensitivities are associated with post-traumatic headache-related disability.

OBJECTIVE: To examine whether sensory hypersensitivity contributes to headache-related disability in a secondary analysis of patients with post-traumatic headache. BACKGROUND: Up to one-third of individuals with traumatic brain injuries report persistent headache 3 months post-injury. High rates of allodynia and photophobia have been observed in clinical studies and animal models of post-traumatic headache, but we do not fully understand how sensory amplifications impact post-traumatic headache-related disability. METHODS: We identified a cross-sectional sample of patients from the American Registry for Migraine Research database with new or worsening headaches post-head injury from 2016 to 2020 and performed a secondary analysis of those data. We modeled the relationship between sensory sensitivity and Migraine Disability Assessment scores using questionnaires. Candidate variables included data collection features (study site and year), headache-related and general clinical features (headache frequency, migraine diagnosis, abuse history, sex, age, cognitive and affective symptom scores), and sensory symptoms (related to light, sound, and touch sensitivity). RESULTS: The final sample included 193 patients (median age 46, IQR 22; 161/193, 83.4% female). Migraine Disability Assessment scores ranged from 0 to 260 (median 47, IQR 87). The final model included allodynia, hyperacusis, photosensitivity, headache days per month, abuse history, anxiety and depression, cognitive dysfunction, and age (R2 = 0.43). An increase of one point in allodynia score corresponded to a 3% increase in headache disability (95% CI: 0%-7%; p = 0.027), an increase of one-tenth of a point in the photosensitivity score corresponded to a 12% increase (95% CI: 3%-25%; p = 0.002), and an increase of one point in the hyperacusis score corresponded to a 2% increase (95% CI: 0%-4%; p = 0.016). CONCLUSIONS: Increased photosensitivity, allodynia, and hyperacusis were associated with increased headache-related disability in this sample of patients with post-traumatic headache. Symptoms of sensory amplification likely contribute to post-traumatic headache-related disability and merit an ongoing investigation into their potential as disease markers and treatment targets.

Hyperacusis is associated with smaller gray matter volumes in the supplementary motor area.

Hyperacusis is a disorder in loudness perception characterized by increased sensitivity to ordinary environmental sounds and associated with otologic conditions, including hearing loss and tinnitus (the phantom perception of sound) as well as neurologic and neuropsychiatric conditions. Hyperacusis is believed to arise centrally in the brain; however, the underlying causes are unknown. To gain insight into differences in brain morphology associated with hyperacusis, we undertook a retrospective case-control study comparing whole-brain gray matter morphology in participants with sensorineural hearing loss and tinnitus who either scored above or below the threshold for hyperacusis based on a standard questionnaire. We found that participants reporting hyperacusis had smaller gray matter volumes and cortical sheet thicknesses in the right supplementary motor area (SMA), independent of anxiety, depression, tinnitus burden, or sex. In fact, the right SMA volumes extracted from an independently defined volume of interest could accurately classify participants. Finally, in a subset of participants where functional data were also available, we found that individuals with hyperacusis showed increased sound-evoked responses in the right SMA compared to individuals without hyperacusis. Given the role of the SMA in initiating motion, these results suggest that in hyperacusis the SMA is involved in a motor response to sounds.

The electrophysiological markers of hyperacusis: a scoping review.

OBJECTIVE: Hyperacusis is known as a reduced tolerance to sounds perceived as normal to the majority of the population. There is currently no agreed definition, diagnostic tool, or objective measure of its occurrence. The purpose of this review is to catalogue the research to date on the use of auditory evoked potentials (AEP) to assess hyperacusis. DESIGN: A step-by-step methodology was conducted following guidelines. Four databases were searched. A total of 3343 papers were identified. A final yield of 35 articles were retained for analysis. RESULTS: The analysis identified four types of aetiologies to describe the hyperacusic population in AEP studies; developmental disorders (n = 19), neurological disorders (n = 3), induced hearing damage (n = 8) and idiopathic aetiology (n = 5). Electrophysiological measures were of short (n = 16), middle (n = 13) and long (n = 19) latencies, believed to reflect the activity of the ascending and descending pathways of the auditory system from periphery to cortex. CONCLUSIONS: The results of this review revealed the potential use of electrophysiological measures for further understanding the mechanisms of hyperacusis. However, according to the disparity of concepts to define hyperacusis, definitions and populations need to be clarified before biomarkers specific to hyperacusis can be identified.

Auditory disturbances in patients with complex regional pain syndrome.

ABSTRACT: Complex regional pain syndrome (CRPS) is often associated with reduced sound tolerance (hyperacusis) on the affected side, but the mechanism of this symptom is unclear. As compensatory increases in central auditory activity after cochlear injury may trigger hyperacusis, hearing and discomfort thresholds to pure tones (250, 500, 1000, 2000, 3000, 4000, 6000, and 8000 Hz) were assessed in 34 patients with CRPS and 26 pain-free controls. In addition, in 31 patients and 17 controls, auditory-evoked potentials to click stimuli (0.08 ms duration, 6 Hz, 60 dB above the hearing threshold) were averaged across 2000 trials for each ear. Auditory discomfort thresholds were lower at several pitches on the CRPS-affected than contralateral side and lower at all pitches on the affected side than in controls. However, ipsilateral hyperacusis was not associated with psychophysical or physiological signs of cochlear damage. Instead, neural activity in the ipsilateral brainstem and midbrain was greater when repetitive click stimuli were presented on the affected than contralateral side and greater bilaterally than in controls. In addition, click-evoked potentials, reflecting thalamo-cortical signal transfer and early cortical processing, were greater contralaterally in patients than controls. Together, these findings suggest that hyperacusis originates in the ipsilateral brainstem and midbrain rather than the peripheral auditory apparatus of patients with CRPS. Failure of processes that jointly modulate afferent auditory signalling and pain (eg, inhibitory influences stemming from the locus coeruleus) could contribute to ipsilateral hyperacusis in CRPS.

Sound Therapy to Reduce Auditory Gain for Hyperacusis and Tinnitus.

PURPOSE: Hyperacusis is the most common of the different types of sound tolerance conditions. It has been defined as physical discomfort or pain when any sound reaches a certain level of loudness that would be comfortable for most people. Because hyperacusis and tinnitus occur together so often, it has been theorized that they have a common neural mechanism. A leading contender for that mechanism is enhancement of auditory gain. The purpose of this tutorial is to review the evidence that sound/acoustic therapy can reduce auditory gain and, thereby, can increase loudness tolerance for people with hyperacusis and/or suppress the percept of tinnitus. METHOD: The scientific literature was informally reviewed to identify and elucidate relationships between tinnitus, hyperacusis, sound therapy, and auditory gain. RESULTS: Evidence exists, both in animal and human studies, that enhanced auditory gain is associated with hyperacusis and tinnitus. Further evidence supports the theory that certain forms of sound therapy can reduce neural hyperactivity, thereby reducing auditory gain. The evidence for sound therapy reducing auditory gain is stronger for hyperacusis than it is for tinnitus. CONCLUSIONS: Based on results from numerous studies, sound therapy clearly has application as a method of desensitization for hyperacusis. Enhanced auditory gain might be responsible for tinnitus, but other mechanisms have been theorized. A review of the relevant literature leads to the conclusion that some form(s) of sound therapy has the potential to suppress or eliminate tinnitus on a long-term basis. Systematic research is needed to evaluate this premise.

Postmastoidectomy Hyperacusis Syndrome: Clinical Features and Treatment.

OBJECTIVE: We report a novel postmastoidectomy hyperacusis syndrome (PMHS) in patients who have had cortical mastoidectomies and experience hyperacusis to stimuli involving touch of the pinna and periauricular area. This report aims to describe the clinical characteristics of patients predisposed to this disabling complication after mastoid surgery and describes surgical treatment with mastoid cortex resurfacing with hydroxyapatite bone cement. PATIENTS: Three patients who have undergone intact canal wall mastoidectomies for nonchronic middle ear-related pathologies all reported a similar constellation of postoperative symptoms. None of the patients had any ossicular chain or middle ear abnormalities, and none had preoperative conductive hearing loss. All patients reported disabling hyperacusis related to light touch stimuli in the periauricular area. On examination, all three patients demonstrated synchronous movement of the tympanic membrane when the postauricular area was palpated. INTERVENTIONS: After a period of observation, none of the patients noted any improvement to their symptoms. Resurfacing of the mastoid cortex with hydroxyapatite bone cement was performed in all patients. MAIN OUTCOME MEASURES: Presence of touch-induced hyperacusis and audiometry was assessed postoperatively. Patients were also examined for synchronous movement of the tympanic membrane with palpation of the postauricular area. RESULTS: All patients experienced complete resolution of touch-induced hyperacusis postoperatively. Pure-tone audiometric hearing thresholds remained unchanged after mastoid cortex resurfacing, and there was no longer tympanic membrane movement with palpation of the postauricular area. CONCLUSIONS: PMHS can occur in patients after cortical mastoidectomy when there is no history of ossicular chain or history of chronic middle ear disease or middle ear abnormalities. PMHS can cause significant distress to patients and remain underrecognized unless synchronous tympanic membrane movement is specifically examined for. Treatment via mastoid cortex surfacing with hydroxyapatite bone cement is safe and effective.

Clinical and investigational tools for monitoring noise-induced hyperacusis.

Hyperacusis is a recognized perceptual consequence of acoustic overexposure that can lead to debilitating psychosocial effects. Despite the profound impact of hyperacusis on quality of life, clinicians and researchers lack objective biomarkers and standardized protocols for its assessment. Outcomes of conventional audiologic tests are highly variable in the hyperacusis population and do not adequately capture the multifaceted nature of the condition on an individual level. This presents challenges for the differential diagnosis of hyperacusis, its clinical surveillance, and evaluation of new treatment options. Multiple behavioral and objective assays are emerging as contenders for inclusion in hyperacusis assessment protocols but most still await rigorous validation. There remains a pressing need to develop tools to quantify common nonauditory symptoms, including annoyance, fear, and pain. This review describes the current literature on clinical and investigational tools that have been used to diagnose and monitor hyperacusis, as well as those that hold promise for inclusion in future trials.

Exploring the middle ear function in patients with a cluster of symptoms including tinnitus, hyperacusis, ear fullness and/or pain.

Middle ear muscle (MEM) abnormalities have been proposed to be involved in the development of ear-related symptoms such as tinnitus, hyperacusis, ear fullness, dizziness and/or otalgia. This cluster of symptoms have been called the Tonic Tensor Tympani Syndrome (TTTS) because of the supposed involvement of the tensor tympani muscle (TTM). However, the putative link between MEM dysfunction and the symptoms has not been proven yet and the detailed mechanisms (the causal chain) of TTTS are still elusive. It has been speculated that sudden loud sound (acoustic shock) may impair the functioning of the MEM, specifically the TTM, after an excessive contraction. This would result in inflammatory processes, activation of the trigeminal nerve and a change of the MEMs state into a hypersensitive one, that may be associated to the cluster of symptoms listed above. The goal of this study is to provide further insights into the mechanisms of TTTS. The middle ear function of 11 patients who reported TTTS symptoms has been investigated using either admittancemetry and/or measurement of air pressure in the sealed external auditory canal. While the former method measured the middle ear stiffness the latter provides an estimate of the tympanic membrane displacement. Most patients displayed results consistent with phasic contractions of the TTM (n = 9) and/or Eustachian Tube (ET) dysfunction (n = 6). The MEM contraction or ET dysfunction could be evoked by acoustic stimulation (n = 3), somatic maneuvers (n = 3), or pressure changes in the ear canal (n = 3). Spontaneous TTM contraction (n = 1) or ET opening (n = 1) could also be observed. Finally, voluntary contraction of MEM was also reported (n = 5). On the other hand, tonic contraction of the TTM could not be observed in any patient. The implications of these results for the mechanisms of TTTS are discussed.

Hiperacusia en trastornos del espectro autista: una revisión de la literatura / Hyperacusis in autism spectrum disorders: a review of the literature

Resumen La hiperacusia se define como la intolerancia a ciertos sonidos cotidianos que causa angustia y discapacidad significativas en las actividades sociales, ocupacionales, recreativas y otras actividades cotidianas. Los sonidos pueden percibirse como incómodamente fuertes, desagradables, atemorizantes o dolorosos. Se encuentra presente en aproximadamente un 3% población general, y aumenta significativamente en trastornos del espectro autista (TEA), alcanzando entre un 15% a 40%. Los mecanismos fisiopatológicos no son del todo claros, pero se ha propuesto, una alteración en el funcionamiento de mecanismos reflejos y de regulación, tanto a nivel de la vía auditiva periférica, como central, incluyendo estructuras no relacionadas directamente con la vía auditiva. El siguiente texto tiene como objetivo analizar la relación entre hiperacusia y TEA, enfatizando en la frecuencia en que se presentan como comorbilidades, en los posibles mecanismos fisiopatológicos, y en actualizaciones en el abordaje diagnóstico y terapéutico. Se realiza una revisión bibliográfica cualitativa en Pubmed con artículos entre los años 2008-2020 utilizando los términos: "hyperacusis autism", "sistema olivococlear", arrojando 39 artículos, de los cuales se seleccionaron en base a la temática de cada uno, evaluada por los autores. A pesar de una significativa relación entre hiperacusia y TEA, los mecanismos fisiopatológicos de ambas patologías siguen siendo un misterio. Existen estudios que sugieren pruebas de screening no invasivas que relacionan ambas patologías, pero debido a los sesgos de selección, todavía no son factibles de usar en forma universal. El abordaje terapéutico ha sido poco explorado, y no se dispone de fármacos que hayan demostrado su efectividad, por el contrario, algunos de ellos empeoran la sintomatología. Se recomienda al tratante, seguir un camino largo, en conjunto con el paciente, donde las terapias no farmacológicas como la terapia cognitivo conductual han mostrado tener buenos resultados.

Abstract Hyperacusis is defined as intolerance to certain sounds that causes significant distress and disability in social, occupational, recreational and other activities. Sounds can be perceived as uncomfortably loud, unpleasant, frightening, or painful. It is present in approximately 3% of the general population, and increases significantly in autism spectrum disorders (ASD), between 15% and 40%. The pathophysiological mechanisms are not entirely clear, but an alteration in the functioning of reflex and regulatory mechanisms has been proposed, both at the peripheral and central auditory pathways, including structures not directly related to the auditory pathway. The therapeutic approach has been little explored as there are no drugs that have demonstrated their effectiveness, on the contrary, some of them worsen the symptoms. The practitioner is recommended to follow a long path, in conjunction with the patient, where non-pharmacological therapies such as cognitive behavioral therapy have been shown to have good results. The following text shows a review of the literature with articles referring to the subject between the years 2008-2019.

Tinnitus, sound intolerance, and mental health: the role of long-term occupational noise exposure.

PURPOSE: Whereas chronic noise exposure (CNE) is a known risk factor for tinnitus, little is known about how a history of CNE impacts tinnitus characteristics and its comorbid symptoms. METHODS: Seventy-five participants with chronic tinnitus (59m/16f, 22-78 years, 48 with sensory-neural hearing loss, and 27 with a normal audiogram) including 43 individuals with (Tin-CNE group) and 32 without (Tin group) a history of long-term occupational noise exposure were studied. Tinnitus characteristics were rated by a visual analog scale, and tinnitus comorbid symptoms were scored using self-assessment questionnaires. RESULTS: The Tin-CNE group showed reduced uncomfortable loudness level (ULL), sound tolerance, and quality of life (QoL), and increased tinnitus loudness, tinnitus handicap, anxiety, depression, insomnia severity, and tinnitus annoyance scores compared to the Tin group. Higher tinnitus loudness and a lower anxiety score were observed in participants with hearing loss relative to those without. Using a stepwise regression model also showed that tinnitus-related characteristics, hyperacusis, and tinnitus comorbid symptoms enhance one another. CONCLUSIONS: The findings were in support of accumulative evidence indicating the adverse auditory and non-auditory effects of CNE, including exacerbated sound intolerance and tinnitus-related psychiatric symptoms. The results also showed that tinnitus alone can affect mental health regardless of hearing loss.

Relación entre hiperacusia y desorden del procesamiento auditivo central: Una revisión de la literatura / Relationship between hyperacusis and auditory processing disorder: a literature review

Resumen La hiperacusia corresponde a la excesiva sensibilidad auditiva o intolerancia a ciertos sonidos cotidianos que para la mayoría de las personas parecerían habituales. Considerando los mecanismos fisiológicos involucrados en el origen de la hiperacusia, es lógico pensar que su presencia podría afectar algunas habilidades del procesamiento auditivo central, sin embargo, la evidencia en torno al tema es escasa y no existe actualmente una revisión de la literatura que agrupe las investigaciones sobre esta temática. Por ello, el presente estudio pretende identificar y analizar la evidencia científica disponible sobre la relación entre hiperacusia y desorden del procesamiento auditivo central. Se realizó una revisión de la literatura guiada por protocolo PRISMA en las bases de datos Proquest, Ebsco, Pubmed, ScienceDirect, Cochrane Library y Scielo de acuerdo con términos claves. Fueron incluidos artículos originales de investigación, revisiones sistemáticas y metaanálisis, publicados desde el año 2010, realizados en animales y humanos, escritos en idiomas inglés, español y portugués. Se encontraron 323 estudios relacionados con los términos claves utilizados, de los cuales 13 cumplieron con los criterios de inclusión y fueron analizados. Se puede concluir que la evidencia científica en torno al tema es escasa e incipiente. Estructuras de la vía auditiva central como núcleos cocleares, lemnisco lateral, colículos inferiores, cuerpo geniculado medial y corteza auditiva primaria estarían relacionadas con la hiperacusia, así como también habilidades de procesamiento auditivo de figura/fondo, ordenación temporal y transferencia interhemisférica se verían afectadas.

Abstract Hyperacusis has been defined as the excessive auditory sensitivity or intolerance to certain everyday sounds that seem common for most people. Considering the underlying physiological mechanisms of hyperacusis, it is reasonable to think that it could affect some abilities involved in the central auditory processing. However, there is lack of evidence about this topic, and there is no literature review that gathers all the existing research. Therefore, the current study intends to identify and analyze the available scientific evidence regarding the relationship between hyperacusis and central auditory processing disorder. The review of the literature followed the PRISMA protocol, using key words in Proquest, Ebsco, Pubmed, ScienceDirect, Cochrane Library and Scielo databases. Original research articles, systematic reviews and meta-analyses of studies made with human and animals that have been published since 2010 in English, Spanish and Portuguese were included. Among them, 323 studies were related to the key terms, out of which 13 met the inclusion criteria and were analyzed. It is possible to conclude that there is little and incipient scientific evidence on the topic. Structures of the central auditory pathway such as cochlear nuclei, lateral lemniscus, inferior colliculi, medial geniculate body and primary auditory cortex seem to be related to hyperacusis; auditory processing skills such as figure/ground discrimination, temporal ordering and interhemispheric transfer appear to be affected as well.

Premonitory and Accompanying Symptoms in Childhood Migraine.

PURPOSE OF REVIEW: To review the literature on the clinical characteristics of the symptoms other than headache that occurs during a migraine attack in childhood and adolescence. RECENT FINDINGS: Premonitory symptoms (42-67%) and postdrome phase (82%) are frequent. The most frequent auras were visual. There was no association between age or sex and the occurrence of auras. Cranial autonomic symptoms are also frequent (40-70%) and are most often bilateral. Most studies suggest that age is not associated with the frequency of nausea, vomiting, photophobia, and phonophobia. Cephalic cutaneous allodynia (15-37%) and osmophobia (20-53%) are common symptoms in children with migraine. Osmophobia has low sensitivity and high specificity for the diagnosis of migraine and is associated with the severity of the migraine. Migraine is a complex disease, and although headache is its best-known symptom, other symptoms also occur frequently during migraine attacks in children and adolescents.

Current topics in hearing research: Deafferentation and threshold independent hearing loss.

Hearing research findings in recent years have begun to change how we think about hearing loss and how we consider the risk of auditory damage from noise exposure. These findings include evidence of noise-induced cochlear damage in the absence of corresponding permanent threshold elevation or evidence of hair cell loss. Animal studies in several species have shown that noise exposures that produce robust but only temporary threshold shifts can permanently damage inner hair cell synaptic ribbons. This type of synaptic degeneration has also been shown to occur as a result of aging in animals and humans. The emergence of these data has motivated a number of clinical studies aimed at identifying the perceptual correlates associated with synaptopathy. The deficits believed to arise from synaptopathy include poorer hearing in background noise, tinnitus and hyperacusis (loudness intolerance). However, the findings from human studies have been mixed. Key questions remain as to whether synaptopathy reliably produces suprathreshold perceptual deficits or whether it serves as an early indicator of auditory damage with suprathreshold deficits emerging later as a function of further cochlear damage. Here, we provide an overview of both human and animal studies that explore the relationship among inner hair cell damage, including loss of afferent synapses, auditory thresholds, and suprathreshold measures of hearing.

A randomized study of IV prochlorperazine plus diphenhydramine versus IV hydromorphone for migraine-associated symptoms: A post hoc analysis.

OBJECTIVE: We conducted a randomized trial among emergency department patients with migraine to determine the relative impact on migraine-associated symptoms of hydromorphone, an opioid, versus prochlorperazine, an antidopaminergic antiemetic. METHODS: This was a post hoc analysis of data from a double-blind study registered at http://clinicaltrials.gov (NCT02389829). Patients who met International Classification of Headache Disorders, 3rd edition criteria for migraine without aura or for probable migraine without aura were eligible for participation. Participants received either hydromorphone 1 mg IV or prochlorperazine 10 mg IV plus diphenhydramine 25 mg IV and could receive a second dose of the same medication 1 h later if needed. The outcomes were sustained relief of nausea, photophobia, and phonophobia. RESULTS: A total of 127 patients were enrolled, of whom 63 received prochlorperazine and 64 received hydromorphone. Of 49 patients in the prochlorperazine arm who reported nausea at baseline, 34 (69.4%) reported complete resolution without relapse versus 15/49 (30.6%) in the hydromorphone arm (absolute risk reduction [ARR] = 38.8%, 95% CI: 20.5%-57.0%, p < 0.001). Of 55 patients in the prochlorperazine arm who reported photophobia at baseline, 23 (41.8%) reported complete resolution without relapse versus 13/62 (20.9%) patients treated with hydromorphone (ARR = 20.8%, 95% CI: 4.3%-37.3%, p = 0.014). Of 56 patients in the prochlorperazine arm who reported phonophobia at baseline, 25 (44.6%) reported complete resolution without relapse versus 16/59 (27.1%) in the hydromorphone arm (ARR = 17.5%, 95% CI: 0.3%-34.8%, p = 0.049). For adverse events, three patients in the prochlorperazine arm reported anxiety or restlessness, and nine patients in the hydromorphone arm reported dizziness or weakness. CONCLUSIONS: Prochlorperazine plus diphenhydramine is more efficacious than hydromorphone for the treatment of migraine-associated symptoms.

Auditory hypersensitivity in Williams syndrome.

OBJECTIVES: The objective of this study was to investigate auditory hypersensitivity in WS and to evaluate hyperacusis through standardized protocols, checking if it can be associated with the absence of acoustic reflexes in people with WS. METHOD: The study was performed in 17 individuals with WS, aged between seven and 17 years old (10 males and seven females), and 17 individuals with typical development age- and gender-matched to individuals with WS. Statistical tests were used to analyze the responses collected with the Loudness Discomfort Level (LDL) test as well as ipsilateral and contralateral reflex responses. RESULTS: Auditory hypersensitivity was commonly found. Individuals with WS had phonophobia and were less tolerant to high sound intensity, presenting a reduced discomfort threshold compared to those with typical development. However, hyperacusis was found in 35.29% of individuals with WS and was mild in 50% of cases. There was an association between hyperacusis and acoustic reflex responses, and individuals with absence of the contralateral acoustic reflex were more likely to have hyperacusis. CONCLUSIONS: Individuals with WS have a high prevalence of auditory hypersensitivity, with the presence of phonophobia; however, hyperacusis was not as prevalent and may be associated with the absence of contralateral acoustic reflexes.

Metabolic changes in the brain and blood of rats following acoustic trauma, tinnitus and hyperacusis.

It has been increasingly recognized that tinnitus is likely to be generated by complex network changes. Acoustic trauma that causes tinnitus induces significant changes in multiple metabolic pathways in the brain. However, it is not clear whether those metabolic changes in the brain could also be reflected in blood samples and whether metabolic changes could discriminate acoustic trauma, hyperacusis and tinnitus. We analyzed brain and serum metabolic changes in rats following acoustic trauma or a sham procedure using metabolomics. Hearing levels were recorded before and after acoustic trauma and behavioral measures to quantify tinnitus and hyperacusis were conducted at 4 weeks following acoustic trauma. Tissues from 11 different brain regions and serum samples were collected at about 3 months following acoustic trauma. Among the acoustic trauma animals, eight exhibited hyperacusis-like behavior and three exhibited tinnitus-like behavior. Using Gas chromatography-mass spectrometry and multivariate statistical analysis, significant metabolic changes were found in acoustic trauma animals in both the brain and serum samples with a number of metabolic pathways significantly perturbated. Furthermore, metabolic changes in the serum were able to differentiate sham from acoustic trauma animals, as well as sham from hyperacusis animals, with high accuracy. Our results suggest that serum metabolic profiling in combination with machine learning analysis may be a promising approach for identifying biomarkers for acoustic trauma, hyperacusis and potentially, tinnitus.

Loud Music and Leisure Noise Is a Common Cause of Chronic Hearing Loss, Tinnitus and Hyperacusis.

High sound levels capable of permanently damaging the ear are experienced not only in factories and war zones but in concert halls, nightclubs, sports stadiums, and many other leisure environments. This review summarizes evidence that loud music and other forms of "leisure noise" are common causes of noise-induced hearing loss, tinnitus, and hyperacusis, even if audiometric thresholds initially remain within clinically normal limits. Given the huge global burden of preventable noise-induced hearing loss, noise limits should be adopted in a much broader range of settings, and education to promote hearing conservation should be a higher public health priority.

Fibromyalgia Patients Are Not Only Hypersensitive to Painful Stimuli But Also to Acoustic Stimuli.

Fibromyalgia is a chronic widespread pain syndrome associated with hypersensitivity to nociceptive stimuli. This increased sensitivity of FM patients has been associated with central sensitization of dorsal horn neurons. Increasing evidence, however, suggests that the mechanisms of FM hypersensitivity not only affect pain but include light, smell, and sound. We hypothesized that supraspinal augmentation of sensory input including sound represent a hallmark of FM. We tested 23 FM patients and 28 healthy controls (HC) for sensory augmentation of nociceptive and non-nociceptive sensations: For assessment of nociceptive augmentation we used sensitivity adjusted mechanical and heat ramp & hold stimuli and for assessment of sound augmentation, we applied wideband noise stimuli using a random-staircase design. Quantitative sensory testing demonstrated increased heat and mechanical pain sensitivity in FM participants (P < .001). The sound pressures needed to report mild, moderate, and intense sound levels were significantly lower in FM compared to HC (P < .001), consistent with auditory augmentation. FM patients are not only augmenting noxious sensations but also sound, suggesting that FM augmentation mechanisms are not only operant in the spinal cord but also in the brain. Whether the central nervous system mechanisms for auditory and nociceptive augmentation are similar, needs to be determined in future studies. PERSPECTIVE: This study presents QST evidence that the hypersensitivity of FM patients is not limited to painful stimuli but also to innocuous stimuli like sound. Our results suggest that abnormal brain mechanisms may be responsible for the increased sensitivity of FM patients.