Publications by authors named "Hannah Guest"

Purpose: The Digits-in-Noise (DIN) test is used widely in research and, increasingly, in remote hearing screening. The reported study aimed to provide basic evaluation data for browser-based DIN software, which allows remote testing without installation of an app. It investigated the effects of test language (Arabic vs.

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Musicians are at risk of hearing loss and tinnitus due to regular exposure to high levels of noise. This level of risk may have been underestimated previously since damage to the auditory system, such as cochlear synaptopathy, may not be easily detectable using standard clinical measures. Most previous research investigating hearing loss in musicians has involved cross-sectional study designs that may capture only a snapshot of hearing health in relation to noise exposure.

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Background & Aims: Communicative and sensory differences are core autistic traits, yet speech-perception abilities and difficulties among autistic individuals remain poorly understood. Laboratory studies have produced mixed and inconclusive results, in part because of the lack of input from autistic individuals in defining the hypotheses and shaping the methods used in this field of research. Little in-depth qualitative research on autistic experiences of speech perception has been published, yet such research could form the basis for better laboratory research, for improved understanding of autistic experiences, and for the development of interventions.

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Introduction: The clinical application of listening effort (LE) is challenging due to the lack of consensus regarding measuring the concept. Correlational analysis between different measuring instruments shows conditional and weak relationships, indicating they capture different dimensions of LE. Current research has suggested possible links between LE and downstream consequences such as fatigue, stress and confidence.

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Purpose: Many workers in developing countries are exposed to unsafe occupational noise due to inadequate health and safety practices. We tested the hypotheses that occupational noise exposure and aging affect speech-perception-in-noise (SPiN) thresholds, self-reported hearing ability, tinnitus presence, and hyperacusis severity among Palestinian workers.

Method: Palestinian workers ( = 251, aged 18-70 years) without diagnosed hearing or memory impairments completed online instruments including a noise exposure questionnaire; forward and backward digit span tests; hyperacusis questionnaire; the short-form Speech, Spatial and Qualities of Hearing Scale (SSQ12); the Tinnitus Handicap Inventory; and a digits-in-noise (DIN) test.

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Objective: Patient and public involvement (PPI) in research improves relevance to end users and improves processes including recruitment participants. PPI in our research has gone from being non-existent to ubiquitous over a few years. We provide critical reflections on the benefits and challenges of PPI.

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Noise exposure may damage the synapses that connect inner hair cells with auditory nerve fibers, before outer hair cells are lost. In humans, this cochlear synaptopathy (CS) is thought to decrease the fidelity of peripheral auditory temporal coding. In the current study, the primary hypothesis was that higher middle ear muscle reflex (MEMR) thresholds, as a proxy measure of CS, would be associated with smaller values of the binaural intelligibility level difference (BILD).

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Background And Aims: Humans communicate primarily through spoken language and speech perception is a core function of the human auditory system. Among the autistic community, atypical sensory reactivity and social communication difficulties are pervasive, yet the research literature lacks in-depth self-report data on speech perception in this population. The present study aimed to elicit detailed first-person accounts of autistic individuals' abilities and difficulties perceiving the spoken word.

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Animal research shows that aging and excessive noise exposure damage cochlear outer hair cells, inner hair cells, and the synapses connecting inner hair cells with the auditory nerve. This may translate into auditory symptoms such as difficulty understanding speech in noise, tinnitus, and hyperacusis. The current study, using a novel online approach, assessed and quantified the effects of lifetime noise exposure and aging on (i) speech-perception-in-noise (SPiN) thresholds, (ii) self-reported hearing ability, and (iii) the presence of tinnitus.

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Objectives: We aimed to estimate what proportion of people with SLE attending UK rheumatology clinics would be categorized as being at high risk from coronavirus disease 2019 (COVID-19) and therefore asked to shield, and explore what implications this has for rheumatology clinical practice.

Methods: We used data from the British Society for Rheumatology multicentre audit of SLE, which included a large, representative cross-sectional sample of patients attending UK Rheumatology clinics with SLE. We calculated who would receive shielding advice using the British Society for Rheumatology's risk stratification guidance and accompanying scoring grid, and assessed whether ethnicity and history of nephritis were over-represented in the shielding group.

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Objectives: To assess the baseline care provided to patients with SLE attending UK Rheumatology units, audited against standards derived from the recently published BSR guideline for the management of adults with SLE, the NICE technology appraisal for belimumab, and NHS England's clinical commissioning policy for rituximab.

Methods: SLE cases attending outpatient clinics during any 4-week period between February and June 2018 were retrospectively audited to assess care at the preceding visit. The effect of clinical environment (general vs dedicated CTD/vasculitis clinic and specialized vs non-specialized centre) were tested.

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Musicians are at risk of hearing loss due to prolonged noise exposure, but they may also be at risk of early sub-clinical hearing damage, such as cochlear synaptopathy. In the current study, we investigated the effects of noise exposure on electrophysiological, behavioral and self-report correlates of hearing damage in young adult (age range = 18-27 years) musicians and non-musicians with normal audiometric thresholds. Early-career musicians (n = 76) and non-musicians (n = 47) completed a test battery including the Noise Exposure Structured Interview, pure-tone audiometry (PTA; 0.

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In animal models, exposure to high noise levels can cause permanent damage to hair-cell synapses (cochlear synaptopathy) for high-threshold auditory nerve fibers without affecting sensitivity to quiet sounds. This has been confirmed in several mammalian species, but the hypothesis that lifetime noise exposure affects auditory function in humans with normal audiometric thresholds remains unconfirmed and current evidence from human electrophysiology is contradictory. Here we report the auditory brainstem response (ABR), and both transient (stimulus onset and offset) and sustained functional magnetic resonance imaging (fMRI) responses throughout the human central auditory pathway across lifetime noise exposure.

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Although there is strong histological evidence for age-related synaptopathy in humans, evidence for the existence of noise-induced cochlear synaptopathy in humans is inconclusive. Here, we sought to evaluate the relative contributions of age and noise exposure to cochlear synaptopathy using a series of electrophysiological and behavioral measures. We extended an existing cohort by including 33 adults in the age range 37 to 60, resulting in a total of 156 participants, with the additional older participants resulting in a weakening of the correlation between lifetime noise exposure and age.

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The acoustic reflex (AR), a longstanding component of the audiological test battery, has received renewed attention in the context of noise-induced cochlear synaptopathy-the destruction of synapses between inner hair cells and auditory nerve fibers. Noninvasive proxy measures of synaptopathy are widely sought, and AR thresholds (ARTs) correlate closely with synaptic survival in rodents. However, measurement in humans at high stimulus frequencies-likely important when testing for noise-induced pathology-can be challenging; reflexes at 4 kHz are frequently absent or occur only at high stimulus levels, even in young people with clinically normal audiograms.

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Investigations of cochlear synaptopathy in living humans rely on proxy measures of auditory nerve function. Numerous procedures have been developed, typically based on the auditory brainstem response (ABR), envelope-following response (EFR), or middle-ear-muscle reflex (MEMR). Validation is challenging, due to the absence of a gold-standard measure in humans.

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The acoustic middle-ear-muscle reflex (MEMR) has been suggested as a sensitive non-invasive measure of cochlear synaptopathy, the loss of synapses between inner hair cells and auditory nerve fibers. In the present study, clinical MEMR thresholds were measured for 1-, 2-, and 4-kHz tonal elicitors, using a procedure shown to produce thresholds with excellent reliability. MEMR thresholds of 19 participants with tinnitus and normal audiograms were compared to those of 19 age- and sex-matched controls.

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Lifetime noise exposure is generally quantified by self-report. The accuracy of retrospective self-report is limited by respondent recall but is also bound to be influenced by reporting procedures. Such procedures are of variable quality in current measures of lifetime noise exposure, and off-the-shelf instruments are not readily available.

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The auditory brainstem response (ABR) is a sub-cortical evoked potential in which a series of well-defined waves occur in the first 10 ms after the onset of an auditory stimulus. Wave V of the ABR, particularly wave V latency, has been shown to be remarkably stable over time in individual listeners. However, little attention has been paid to the reliability of wave I, which reflects auditory nerve activity.

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In rodents, noise exposure can destroy synapses between inner hair cells and auditory nerve fibers ("cochlear synaptopathy") without causing hair cell loss. Noise-induced cochlear synaptopathy usually leaves cochlear thresholds unaltered, but is associated with long-term reductions in auditory brainstem response (ABR) amplitudes at medium-to-high sound levels. This pathophysiology has been suggested to degrade speech perception in noise (SPiN), perhaps explaining why SPiN ability varies so widely among audiometrically normal humans.

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Background: Rodent studies indicate that noise exposure can cause permanent damage to synapses between inner hair cells and high-threshold auditory nerve fibers, without permanently altering threshold sensitivity. These demonstrations of what is commonly known as hidden hearing loss have been confirmed in several rodent species, but the implications for human hearing are unclear.

Objective: Our Medical Research Council-funded program aims to address this unanswered question, by investigating functional consequences of the damage to the human peripheral and central auditory nervous system that results from cumulative lifetime noise exposure.

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An estimate of lifetime noise exposure was used as the primary predictor of performance on a range of behavioral tasks: frequency and intensity difference limens, amplitude modulation detection, interaural phase discrimination, the digit triplet speech test, the co-ordinate response speech measure, an auditory localization task, a musical consonance task and a subjective report of hearing ability. One hundred and thirty-eight participants (81 females) aged 18-36 years were tested, with a wide range of self-reported noise exposure. All had normal pure-tone audiograms up to 8 kHz.

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In rodents, exposure to high-level noise can destroy synapses between inner hair cells and auditory nerve fibers, without causing hair cell loss or permanent threshold elevation. Such "cochlear synaptopathy" is associated with amplitude reductions in wave I of the auditory brainstem response (ABR) at moderate-to-high sound levels. Similar ABR results have been reported in humans with tinnitus and normal audiometric thresholds, leading to the suggestion that tinnitus in these cases might be a consequence of synaptopathy.

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