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.

Modulation of hyperacusis and tinnitus loudness in tinnitus patients with and without hearing loss following 3 weeks of acoustic stimulation: A proof-of-concept study.

Tinnitus and hyperacusis are two debilitating conditions that are highly comorbid. It has been postulated that they may originate from similar pathophysiological mechanisms such as an increase in central gain. Interestingly, sound stimulation has been shown to reduce central gain and is currently used for the treatment of both conditions. This study investigates the effect of sound stimulation on both tinnitus and hyperacusis in the same patients. Two distinct series of tinnitus participants were tested: one with normal or near-normal hearing (n=16) and one with hearing loss (n=14). A broadband noise shaped to cover most of the tinnitus frequency spectrum was delivered through hearing aids using the noise generator feature (no amplification) and verified through real-ear measurements. Participants received sound stimulation for 3 weeks and were tested before (at baseline), then after 1 week and at the end of the 3 weeks of sound stimulation. There was also a 1-month follow-up after the end of the stimulation protocol. The measurements included self-reported measures of tinnitus and hyperacusis (VAS), validated questionnaires (THI, HQ) and psychoacoustic measurements (tinnitus battery and loudness functions). On both self-assessment (VAS of sound tolerance and tinnitus loudness) and psychoacoustic measures (loudness function and tinnitus loudness in dB), about 50% of tinnitus participants had a synchronous (either a decrease or an increase) modulation of hyperacusis and tinnitus loudness after 1 week and 3 weeks of acoustic stimulation and up to about 70% of participants at 1-M follow-up. The decrease of hyperacusis and tinnitus loudness was more prevalent in normal-hearing participants. There was a significant increase in tinnitus loudness during and following the stimulation in the group with hearing loss. Hyperacusis improvement as assessed by loudness function was significantly correlated with the intensity level of the acoustic stimulation (dB level of the noise produced by the noise generator) in tinnitus participants with normal/near-normal hearing thresholds. Our study partly supports the central gain hypothesis by showing synchronous modulation of hyperacusis and tinnitus loudness. It also shows beneficial effects of acoustic stimulation in some tinnitus individuals, in particular those with normal or near-normal hearing, while highlighting the importance of a careful fitting of sound generators to prevent increase. Since the amplification feature was not turned on in our study, future work should determine whether amplification alone, or in addition to acoustic stimulation (sound generators), would benefit to those with hearing loss.

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.

Hyperacusis in tinnitus patients relates to enlarged subcortical and cortical responses to sound except at the tinnitus frequency.

Hyperacusis, a hypersensitivity to sounds of mild to moderate intensity, has been related to increased neural gain along the auditory pathway. To date, there is still uncertainty on the neural correlates of hyperacusis. Since hyperacusis often co-occurs with hearing loss and tinnitus, the effects of the three conditions on cortical and subcortical structures are often hard to separate. In this fMRI study, two groups of hearing loss and tinnitus participants, with and without hyperacusis, were compared to specifically investigate the effect of the latter in a group that often reports hyperacusis. In 35 participants with hearing loss and tinnitus, with and without hyperacusis as indicated by a cut-off score of 22 on the Hyperacusis Questionnaire (HQ), subcortical and cortical responses to sound stimulation were investigated. In addition, the frequency tuning of cortical voxels was investigated in the primary auditory cortex. In cortical and subcortical auditory structures, sound-evoked activity was higher in the group with hyperacusis. This effect was not restricted to frequencies affected by hearing loss but extended to intact frequencies. The higher subcortical and cortical activity in response to sound thus appears to be a marker of hyperacusis. In contrast, the response to the tinnitus frequency was reduced in the group with hyperacusis. This increase in subcortical and cortical activity in hyperacusis can be related to an increase in neural gain along the auditory pathway, and the reduced response to the tinnitus frequency to differences in attentional resources allocated to the tinnitus sound.

Acoustic startle stimuli inhibit pain but do not alter nociceptive flexion reflexes to sural nerve stimulation.

Acoustic startle stimuli inhibit pain, but whether this is due to a cross-modal inhibitory process or some other mechanism is uncertain. To investigate this, electrical stimulation of the sural nerve either preceded or followed an acoustic startle stimulus (by 200 ms) or was presented alone in 30 healthy participants. Five electrical stimuli, five acoustic startle stimuli, 10 startle + electrical stimuli, and 10 electrical + startle stimuli were presented in mixed order at intervals of 30-60 s. Effects of the startle stimulus on pain ratings, pupillary dilatation and nociceptive flexion reflexes to the electric shock were assessed. The acoustic startle stimulus inhibited electrically evoked pain to the ensuing electric shock (p < .001), and the electrical stimulus inhibited the perceived loudness of a subsequent acoustic startle stimulus (p < .05). However, the startle stimulus did not affect electrically evoked pain when presented 200 ms after the electric shock, and electrically evoked pain did not influence the perceived loudness of a prior startle stimulus. Furthermore, stimulus order did not influence the pupillary responses or nociceptive flexion reflexes. These findings suggest that acoustic startle stimuli transiently inhibit nociceptive processing and, conversely, that electrical stimuli inhibit subsequent auditory processing. These inhibitory effects do not seem to involve spinal gating as nociceptive flexion reflexes to the electric shock were unaffected by stimulus order. Thus, cross-modal interactions at convergence points in the brainstem or higher centers may inhibit responses to the second stimulus in a two-stimulus train.

The effect of insular cortex lesion on hyperacusis-like behavior in rats.

Background and objectives: Hyperacusis is hypersensitivity and extreme response to the intensity of sound that is tolerable in normal subjects. The mechanisms underlying hyperacusis has not been well understood, specially the role of insular cortex. The aim of this study is to investigate the role of insular cortex in hyperacusis like behavior. Material and methods: The number of 33 male wistar rats weighting 170-250 gr were allocated randomly in three groups; control, sham, and insular lesion. Auditory startle responses (ASR) to different intensities of stimuli (70, 80, 90, 100, and110 dB without background noise as well as 110 dB in the presence of 70, 80 dB background noise) were measured before and up to four weeks after intervention. Results: Data analyses showed an increase in ASR to 100 dB stimulus without background noise one week after insular lesion, and increased responses to other intensities two weeks after lesion. Furthermore, there was a decrease in ASR to 110 dB stimulus with 80 dB background noise two weeks after insular lesion. However, no significant difference was observed in 70 dB background noise. The changes in ASR lasts at least four weeks.Conclusion: The findings indicated that there was an increase in ASR in the absence of background noise following cortical excititoxic lesion limited to insular cortex, while there was a decrease in responses in the presence of background noise which suggests possible increased sensitivity to sound loudness as a hyperacusis-like phenomenon. The study showed a significant relationship between insular cortex lesion and ASR in rats.

Functional magnetic resonance imaging of enhanced central auditory gain and electrophysiological correlates in a behavioral model of hyperacusis.

Hyperacusis is a debilitating hearing condition in which normal everyday sounds are perceived as exceedingly loud, annoying, aversive or even painful. The prevalence of hyperacusis approaches 10%, making it an important, but understudied medical condition. To noninvasively identify the neural correlates of hyperacusis in an animal model, we used sound-evoked functional magnetic resonance imaging (fMRI) to locate regions of abnormal activity in the central nervous system of rats with behavioral evidence of hyperacusis induced with an ototoxic drug (sodium salicylate, 250 mg/kg, i.p.). Reaction time-intensity measures of loudness-growth revealed behavioral evidence of salicylate-induced hyperacusis at high intensities. fMRI revealed significantly enhanced sound-evoked responses in the auditory cortex (AC) to 80 dB SPL tone bursts presented at 8 and 16 kHz. Sound-evoked responses in the inferior colliculus (IC) were also enhanced, but to a lesser extent. To confirm the main results, electrophysiological recordings of spike discharges from multi-unit clusters were obtained from the central auditory pathway. Salicylate significantly enhanced tone-evoked spike-discharges from multi-unit clusters in the AC from 4 to 30 kHz at intensities ≥60 dB SPL; less enhancement occurred in the medial geniculate body (MGB), and even less in the IC. Our results demonstrate for the first time that non-invasive sound-evoked fMRI can be used to identify regions of neural hyperactivity throughout the brain in an animal model of hyperacusis.

Auditory brainstem function in women with vestibular migraine: a controlled study.

BACKGROUND: Vestibular migraine (VM) has been recognized as a diagnostic entity over the past three decades. It affects up to 1% of the general population and 7% of patients seen in dizziness clinics. It is still underdiagnosed; consequently, it is important to conduct clinical studies that address diagnostic indicators of VM. The aim of this study was to assess auditory brainstem function in women with vestibular migraine using electrophysiological testing, contralateral acoustic reflex and loudness discomfort level. METHODS: The study group consisted of 29 women with vestibular migraine in the interictal period, and the control group comprised 25 healthy women. Auditory brainstem response, frequency following response, binaural interaction component and assessment of contralateral efferent suppression were performed. The threshold of loudness discomfort and the contralateral acoustic reflex were also investigated. The results were compared between the groups. RESULTS: There was a statistically significant difference between the groups in the frequency following response and the loudness discomfort level. CONCLUSIONS: The current study suggested that temporal auditory processing and loudness discomfort levels are altered in VM patients during the interictal period, indicating that these measures may be useful as diagnostic criteria.

Does 5, 7-Dihydroxytryptamine injection into nucleus accumbens cause hyperacusis?

Hyperacusis may be defined as diminishing tolerance to moderate and high intensity sounds in people with normal hearing sensitivity. Serotonin plays a critical role in some of auditory tasks including startle reflex and prepulse inhibition. Serotonin deficiency can cause some diseases which can coincide with hyperacusis. The aim of the present study was to investigate the probable influence of serotonergic depletion in nucleus accumbens (NAcc) on the startle reflex. The startle reflexes were examined in Wistar rats (n: 48) in different intensities with and without the background noise. The amplitude of startle reflex significantly increased in NAcc-injected rats without background noise, while this difference disappeared in the presence of background noise in all intensities. These data proposed that the injection of 5, 7-Dihydroxytryptamine (5, 7-DHT) into nucleus accumbens will cause hyperacusis-like behavior, and strengthens the possibility of the role of serotonin and nucleus accumbens in hyperacusis.

Enhanced Central Neural Gain Compensates Acoustic Trauma-induced Cochlear Impairment, but Unlikely Correlates with Tinnitus and Hyperacusis.

For successful future therapeutic strategies for tinnitus and hyperacusis, a subcategorization of both conditions on the basis of differentiated neural correlates would be of invaluable advantage. In the present study, we used our refined operant conditioning animal model to divide equally noise-exposed rats into groups with either tinnitus or hyperacusis, with neither condition, or with both conditions co-occurring simultaneously. Using click stimulus and noise burst-evoked Auditory Brainstem Responses (ABR) and Distortion Product Otoacoustic Emissions, no hearing threshold difference was observed between any of the groups. However, animals with neither tinnitus nor hyperacusis responded to noise trauma with shortened ABR wave I and IV latencies and elevated central neuronal gain (increased ABR wave IV/I amplitude ratio), which was previously assumed in most of the literature to be a neural correlate for tinnitus. In contrast, animals with tinnitus had reduced neural response gain and delayed ABR wave I and IV latencies, while animals with hyperacusis showed none of these changes. Preliminary studies, aimed at establishing comparable non-invasive objective tools for identifying tinnitus in humans and animals, confirmed reduced central gain and delayed response latency in human and animals. Moreover, the first ever resting state functional Magnetic Resonance Imaging (rs-fMRI) analyses comparing humans and rats with and without tinnitus showed reduced rs-fMRI activities in the auditory cortex in both patients and animals with tinnitus. These findings encourage further efforts to establish non-invasive diagnostic tools that can be used in humans and animals alike and give hope for differentiated classification of tinnitus and hyperacusis.

Vestibular myogenic potentials evoked by air-conducted stimuli at safe acoustic intensity levels retain optimal diagnostic properties for superior canal dehiscence syndrome.

BACKGROUND: Vestibular-evoked myogenic potential (VEMP) is commonly conducted with air-conducted (AC) stimuli whose intensity may exceed the prudential levels of acoustic exposure in susceptible subjects. OBJECTIVES: To determine the diagnostic accuracy of AC VEMP for superior canal dehiscence syndrome (SCDS) at lowered acoustic stimulation levels. MATERIAL AND METHODS: VEMP was tested in 10 SCDS patients and in 10 age/sex matched control subjects. VEMP were recorded on cervical muscles (cVEMP) and extraocular muscles (oVEMP) in response to short AC tone bursts at 500, 1000 and 2000 Hz delivered at 80 dB nHL (103 dB peSPL). Parameters of interest were the response amplitude and the frequency tuning. RESULTS: VEMP evoked by AC stimuli at safe acoustic stimulation levels did effectively separate SCDS patients from healthy controls. The separation was optimal at all the frequencies tested, however 500 Hz resulted the best VEMP tuning frequency, especially at oVEMP. CONCLUSIONS: Lowering the AC stimulation to the levels compatible with testing of patients susceptible to acoustic exposure didn't affect the VEMP diagnostic properties for SCDS. SIGNIFICANCE: SCDS may be screened by VEMP even among subjects susceptible for acoustic exposure.

Stapedial reflex threshold predicts individual loudness tolerance for people with autistic spectrum disorders.

People with autism spectrum disorder (ASD) frequently show the symptoms of oversensitivity to sound (hyperacusis). Although the previous studies have investigated methods for quantifying hyperacusis in ASD, appropriate physiological signs for quantifying hyperacusis in ASD remain poorly understood. Here, we investigated the relationship of loudness tolerance with the threshold of the stapedial reflex and with contralateral suppression of the distortion product otoacoustic emissions, which has been suggested to be related to hyperacusis in people without ASD. We tested an ASD group and a neurotypical group. The results revealed that only the stapedial reflex threshold was significantly correlated with loudness tolerance in both groups. In addition to reduced loudness tolerance, people with lower stapedial reflex thresholds also exhibited higher scores on the Social Responsiveness Scale-2.

Testing the Central Gain Model: Loudness Growth Correlates with Central Auditory Gain Enhancement in a Rodent Model of Hyperacusis.

The central gain model of hyperacusis proposes that loss of auditory input can result in maladaptive neuronal gain increases in the central auditory system, leading to the over-amplification of sound-evoked activity and excessive loudness perception. Despite the attractiveness of this model, and supporting evidence for it, a critical test of the central gain theory requires that changes in sound-evoked activity be explicitly linked to perceptual alterations of loudness. Here we combined an operant conditioning task that uses a subject's reaction time to auditory stimuli to produce reliable measures of loudness growth with chronic electrophysiological recordings from the auditory cortex and inferior colliculus of awake, behaviorally-phenotyped animals. In this manner, we could directly correlate daily assessments of loudness perception with neurophysiological measures of sound encoding within the same animal. We validated this novel psychophysical-electrophysiological paradigm with a salicylate-induced model of hearing loss and hyperacusis, as high doses of sodium salicylate reliably induce temporary hearing loss, neural hyperactivity, and auditory perceptual disruptions like tinnitus and hyperacusis. Salicylate induced parallel changes to loudness growth and evoked response-intensity functions consistent with temporary hearing loss and hyperacusis. Most importantly, we found that salicylate-mediated changes in loudness growth and sound-evoked activity were correlated within individual animals. These results provide strong support for the central gain model of hyperacusis and demonstrate the utility of using an experimental design that allows for within-subject comparison of behavioral and electrophysiological measures, thereby making inter-subject variability a strength rather than a limitation.

Uncomfortable loudness levels among children and adolescents seeking help for tinnitus and/or hyperacusis.

OBJECTIVE: To assess the prevalence of hyperacusis and severe hyperacusis among children and adolescents seen at an audiology outpatient tinnitus and hyperacusis service. DESIGN: This was a retrospective study. Hyperacusis was considered as present if the average uncomfortable loudness level (ULL) at 0.25, 0.5, 1, 2, 4 and 8 kHz for the ear with the lower average ULL, which is denoted as ULLmin, was ≤77 dB HL. Severe hyperacusis was considered as present if the ULL was 30 dB HL or less for at least one of the measured frequencies for at least one ear. STUDY SAMPLE: There were 62 young patients with an average age of 12 years (SD = 4.1 years, range 4-18 years). RESULTS: Eighty-five percent of patients had hyperacusis and 17% had severe hyperacusis. On average, ULLs at 8 kHz were 9.3 dB lower than ULLs at 0.25 kHz. For 33% of patients, ULLs were at least 20 dB lower at 8 than at 0.25 kHz. CONCLUSIONS: Among children and adolescents seen at an audiology outpatient clinic for tinnitus and hyperacusis, hyperacusis diagnosed on the basis of ULLs is very prevalent and it is often characterised by lower ULLs at 8 than at 0.25 kHz.

Tinnitus and temporary hearing loss result in differential noise-induced spatial reorganization of brain activity.

Loud noise frequently results in hyperacusis or hearing loss (i.e., increased or decreased sensitivity to sound). These conditions are often accompanied by tinnitus (ringing in the ears) and changes in spontaneous neuronal activity (SNA). The ability to differentiate the contributions of hyperacusis and hearing loss to neural correlates of tinnitus has yet to be achieved. Towards this purpose, we used a combination of behavior, electrophysiology, and imaging tools to investigate two models of noise-induced tinnitus (either with temporary hearing loss or with permanent hearing loss). Manganese (Mn2+) uptake was used as a measure of calcium channel function and as an index of SNA. Manganese uptake was examined in vivo with manganese-enhanced magnetic resonance imaging (MEMRI) in key auditory brain regions implicated in tinnitus. Following acoustic trauma, MEMRI, the SNA index, showed evidence of spatially dependent rearrangement of Mn2+ uptake within specific brain nuclei (i.e., reorganization). Reorganization of Mn2+ uptake in the superior olivary complex and cochlear nucleus was dependent upon tinnitus status. However, reorganization of Mn2+ uptake in the inferior colliculus was dependent upon hearing sensitivity. Furthermore, following permanent hearing loss, reduced Mn2+ uptake was observed. Overall, by combining testing for hearing sensitivity, tinnitus, and SNA, our data move forward the possibility of discriminating the contributions of hyperacusis and hearing loss to tinnitus.

Prolonged Exposure of CBA/Ca Mice to Moderately Loud Noise Can Cause Cochlear Synaptopathy but Not Tinnitus or Hyperacusis as Assessed With the Acoustic Startle Reflex.

Hearing loss changes the auditory brain, sometimes maladaptively. When deprived of cochlear input, central auditory neurons become more active spontaneously and begin to respond more strongly and synchronously to better preserved sound frequencies. This spontaneous and sound-evoked central hyperactivity has been postulated to trigger tinnitus and hyperacusis, respectively. Localized hyperactivity has also been observed after long-term exposure to noise levels that do not damage the cochlea. Adult animals exposed to bands of nondamaging noise exhibited suppressed spontaneous and sound-evoked activity in the area of primary auditory cortex (A1) stimulated by the exposure band but had increased spontaneous and evoked activity in neighboring A1 areas. We hypothesized that the cortically suppressed frequencies should for some time after exposure be perceived as less loud than before (hypoacusis), whereas the hyperactivity outside of the exposure band might lead to frequency-specific hyperacusis or tinnitus. To investigate this, adult CBA/Ca mice were exposed for >2 months to 8 to 16 kHz noise at 70 or 75 dB sound pressure level and tested for hypo-/hyperacusis and tinnitus using tone and gap prepulse inhibition of the acoustic startle reflex. Auditory brainstem responses and distortion product otoacoustic emissions showed evidence of cochlear synaptopathy after exposure at 75 but not 70 dB, putting a lower bound on damaging noise levels for CBA/Ca mice. Contrary to hypothesis, neither exposure significantly shifted startle results from baseline. These negative findings nevertheless have implications for startle test methodology and for the putative role of central hyperactivity in hyperacusis and tinnitus.

Tinnitus and sound intolerance: evidence and experience of a Brazilian group / Zumbido e intolerância a sons: evidência e experiência de um grupo brasileiro

Abstract Introduction Tinnitus and sound intolerance are frequent and subjective complaints that may have an impact on a patient's quality of life. Objective To present a review of the salient points including concepts, pathophysiology, diagnosis and approach of the patient with tinnitus and sensitivity to sounds. Methods Literature review with bibliographic survey in LILACS, SciELO, Pubmed and MEDLINE database. Articles and book chapters on tinnitus and sound sensitivity were selected. The several topics were discussed by a group of Brazilian professionals and the conclusions were described. Results The prevalence of tinnitus has increased over the years, often associated with hearing loss, metabolic factors and inadequate diet. Medical evaluation should be performed carefully to guide the request of subsidiary exams. Currently available treatments range from medications to the use of sounds with specific characteristics and meditation techniques, with variable results. Conclusion A review on tinnitus and auditory sensitivity was presented, allowing the reader a broad view of the approach to these patients, based on scientific evidence and national experience.

Resumo Introdução Zumbido e intolerância a sons são queixas frequentes e subjetivas que podem ter impacto na qualidade de vida do paciente. Objetivo Apresentar uma revisão dos principais pontos, inclusive conceitos, fisiopatologia, diagnóstico e abordagem do paciente com zumbido e sensibilidade a sons. Método Revisão da literatura com levantamento bibliográfico na base de dados da LILACS, SciELO, Pubmed e MEDLINE. Foram selecionados artigos e capítulos de livros sobre zumbido e sensibilidade a sons. Os diversos tópicos foram discutidos por um grupo de profissionais brasileiros e as conclusões, descritas. Resultado A prevalência de zumbido tem aumentado ao longo dos anos, muitas vezes associado a perda auditiva, fatores metabólicos e erros alimentares. A avaliação médica deve ser feita minuciosamente no sentido de orientar a solicitação de exames subsidiários. Os tratamentos disponíveis atualmente variam de medicamentos ao uso de sons com características específicas e técnicas de meditação, com resultados variáveis. Conclusão Foi apresentada uma revisão sobre os temas que permitindo ao leitor uma visão ampla da abordagem dos pacientes com zumbido e sensibilidade auditiva baseada em evidências científicas e experiência nacional.

[Smartphone app-supported approaches to tinnitus therapy]. / Smartphone-App-gestützte Ansätze in der Tinnitusbehandlung.

In recent years, applications (apps) for medical purposes have been developed and introduced, including apps that perform diagnostics and documentation for hearing loss and tinnitus in combination with smartphones. Even therapeutic apps, particularly for chronic tinnitus, have been launched. This review discusses the existing scientific literature for these smartphone applications. For tinnitus, Internet-based cognitive behavioral therapy has been developed and evaluated. For tinnitus therapy, introduced apps combine acoustic stimulation and music, or serve acoustic stimulation of cortical regions around the tinnitus frequency. Although these apps appear very innovative, their effectiveness has not yet been scientifically proven. A general problem associated with using smartphone apps lies in their safety in terms of possible side effects and personal data protection. However, Internet programs and apps can be a useful supplement to multimodal tinnitus therapies.

Tinnitus and sound intolerance: evidence and experience of a Brazilian group.

INTRODUCTION: Tinnitus and sound intolerance are frequent and subjective complaints that may have an impact on a patient's quality of life. OBJECTIVE: To present a review of the salient points including concepts, pathophysiology, diagnosis and approach of the patient with tinnitus and sensitivity to sounds. METHODS: Literature review with bibliographic survey in LILACS, SciELO, Pubmed and MEDLINE database. Articles and book chapters on tinnitus and sound sensitivity were selected. The several topics were discussed by a group of Brazilian professionals and the conclusions were described. RESULTS: The prevalence of tinnitus has increased over the years, often associated with hearing loss, metabolic factors and inadequate diet. Medical evaluation should be performed carefully to guide the request of subsidiary exams. Currently available treatments range from medications to the use of sounds with specific characteristics and meditation techniques, with variable results. CONCLUSION: A review on tinnitus and auditory sensitivity was presented, allowing the reader a broad view of the approach to these patients, based on scientific evidence and national experience.

Effect of sound generator on tinnitus and hyperacusis.

OBJECTIVE: Sound generator (SG) plays a role as effective sound therapy of tinnitus retaining therapy (TRT) in patients with severe tinnitus (Category 1) or hyperacusis (Category 3). This study was performed to evaluate the therapeutic effect of SGs. METHODS: A total of 120 tinnitus patients who visited our tinnitus clinic and were treated with SG along with TRT from January 2008 to December 2016 were included. The patients were divided into two groups by tinnitus category; 78 patients of category 1 and 42 patients of category 3. Their medical records including questionnaires regarding tinnitus severity were retrospectively reviewed to evaluate the therapeutic effect of SGs on tinnitus and hyperacusis. RESULTS: Category 3 patients included more female patients, were younger than category 1 patients (p = .001), and were prescribed SG earlier due to their severe symptom of hyperacusis. (p = .004) All patients showed significant improvements on all categories of tinnitus visual analogue scale (VAS) scores and tinnitus handicap inventory (THI) scores after six months use of SG (p < .05). Loudness discomfort levels measured by pure tone audiometry were significantly improved in category 3 group after six months use of SGs. CONCLUSION: SG with TRT seems to be an effective treatment modality for all tinnitus patients, especially those with comorbid hyperacusis.