Rachael R. Baiduc

Objective: This report documents the effects of hearing treatment in an adult with a history of mild traumatic brain injury (mTBI) and normal peripheral hearing acuity. Design: This report details a case study of a 26-year-old female with a history of mTBI. Study Sample: A 26-year-old female with a history of mTBI presented with auditory symptoms including tinnitus, hyperacusis, listening fatigue, and speech-in-noise (SIN) difficulties despite diagnostic audiological findings showing normal peripheral auditory function and suprathreshold SIN performance within the normal range. The patient was fit with premium-level receiver-in-the-canal (RIC) hearing aids (HAs) using several different mild-gain fitting approaches involving wide dynamic range compression (WDRC) or linearized gain. A combination of objective and subjective methods was utilized to guide clinical decision making on the fitting approach and to verify/validate treatment outcomes. Results: Despite no difference in acutely aided SIN performance between the WDRC or linearized fitting approaches, the patient expressed a clear preference for the HA fitting approach involving application of 2–10 dB of shaped linearized gain > 1.5 kHz for soft, medium, and loud input levels (with greatest gain applied at 3–4 kHz). These settings were preferred in terms of loudness and sound quality even compared to the WDRC fitting approaches previously reported in literature. This fitting approach was verified and validated by SIN testing showing improved performance in the aided condition, as well as high levels of self-reported benefit and satisfaction, reduction in self-reported hearing handicap, reduction in sound sensitivity, and enhanced quality of life with HAs. Conclusions: Results add to the growing body of evidence supporting the benefits of mild-gain HAs for adults with mTBI and self-reported SIN deficits despite normal hearing acuity. Results also support the importance of using a combination of measures (e.g., SIN testing, patient report, outcome questionnaires) to guide the HA fitting process and to verify/validate treatment outcomes. Although findings were derived from a single case study and should be interpreted with caution, the patient's preference for a shaped linearized mild-gain approach is noteworthy. There exists a lack of clinical guidelines and prescriptive fitting methodology for fitting HAs in mTBI adults with SIN difficulty despite normal peripheral hearing acuity. Future research should systematically compare WDRC versus linearized gain approaches of fitting in this population to develop a clinical methodology for HA fitting and optimize outcomes in this special subpopulation.

Purpose: Smith–Magenis syndrome (SMS), a rare, genetically linked complex developmental disorder caused by a deletion or mutation within chromosome 17p11.2, is associated with delays in speech-language development, otopathology, and hearing loss, yet previous studies lack comprehensive descriptions of hearing and communication profiles. Here, analyses of patient registry data expand what is known about speech, language, hearing, and otopathology in SMS. Method: International speech-language and hearing registry survey data for 82 individuals with SMS were analyzed using descriptive and inferential statistics. Hearing loss, history of otitis media and pressure equalization (PE) tubes, communication mode, expressive/receptive language, and vocal quality were analyzed for all subjects and subjects grouped by age. Statistical methods included descriptive statistics and Pearson's chi-square tests of independence to test for differences between age groups for each variable of interest. Association analyses included Pearson's correlations. Results: Hearing and otological analyses revealed that 35% of subjects had hearing loss, 66% had a history of otitis media, and 62% had received PE tubes. Speech-language analyses revealed that 60% of subjects communicated using speech, 79% began speaking words at/after 24 months of age, 92% combined words at/after 36 months, and 41% used sign language before speech. There was a significant association between the age that first words were spoken and the age that PE tubes were first placed. Communication strengths noted in more than 40% of subjects included social interest, humor, and memory for people, past events, and/or facts. Conclusions: Significant delays and impairment in speech-language were common, but the majority of those with SMS communicated using speech by age 6 years. Age was a significant factor for some aspects of hearing loss and communication. Neither hearing loss nor otitis media exacerbated language impairment. These results confirm and extend previous findings about the nature of speech, language, hearing, and otopathology in those with SMS.

To investigate the associations between self-reported visual functioning (VF) and hearing functioning with cognition in the Hispanic/Latino population. We utilized data from the Miami Ocular Study of Latinos ancillary study to Hispanic Community Health Study/Study of Latinos with 1,056 participants aged 45 and older. The outcomes were cognitive performances assessed by the Digit Symbol Substitution Test (DSST), Word Fluency, Brief-Spanish English Verbal Learning Test-recall (B-SEVLT recall), words recalled over 3 trials, and the Six-Item Screener. VF was measured by National Eye Institute Visual Function Questionnaire (NEI-VFQ), and hearing function was measured by Hearing Handicap Inventory Screening Questionnaire for Adults and Elderly (HHIA/E-S). Multiple regressions were performed for each cognitive outcome while controlling for covariates and complex sampling design. NEI-VFQ was associated with 3 of the 5 cognitive outcomes. A 4-point NEI-VFQ score difference was associated with a 0.56-point difference in DSST (standard error [SE] = 0.27, p < .001), 0.17 in Word fluency (SE = 0.16, p < .01), and 0.08 in B-SEVLT-recall (SE = 0.07, p < .01). HHIA/E-S was not associated with any of the cognitive measures examined. These data suggest that impaired VF is associated with worse cognition in the Hispanic/Latino population. Although previous work in this cohort indicated hearing loss assessed by pure tone audiometry was associated with worse cognition, we found self-perceived hearing function was not associated with cognition, suggesting the potential limitation of self-reported hearing function as a proxy for hearing loss in epidemiological research in Hispanic/Latino populations. Results also imply impaired VF and hearing function may be linked to cognition differently in the Hispanic population, and more research is needed to better understand the underlying linking mechanisms. Visual and hearing impairments are common and treatable and represent important modifiable risk factors that can be treated to preserve cognitive function in Hispanics/Latinos.

Purpose: The purpose of this study is to investigate the association between cardiovascular disease (CVD) risk factors and idiopathic sudden sensorineural hearing loss (ISSNHL) disease severity and recovery. Method: A retrospective medical chart review was performed on 90 patients (n = 48 men; Mage = 59.8 years, SD = 15.8) evaluated for ISSNHL. Major CVD risk factors (current tobacco smoking, diabetes, total cholesterol >= 240 mg/dl or treatment, and hypertension [systolic blood pressure [BP]/diastolic BP >= 140/ >= 90 mmHg or treatment]) determined two CVD risk groups: lower (no major risk factors) and higher (one or more risk factors). Two pure-tone averages (PTAs) were computed: PTA0.5,1,2 and PTA3,4,6,8. Complete recovery of ISSNHL was defined as PTAinitial - PTAfollow-up >= 10 dB. Logistic regression estimated the odds of ISSNHL recovery by CVD risk status adjusting for age, sex, body mass index, noise exposure, and treatment. Results: Most patients (67.8%) had one or more CVD risk factors. Severity of initial low- and high-frequency hearing loss was similar between CVD risk groups. Recovery was 53.2% for PTA0.5,1,2 and 32.9% for PTA3,4,6,8. With multivariable adjustment, current/former smoking was associated with lower odds of PTA0.5,1,2 recovery (OR = 0.27; 95% CI [0.08, 0.92]). Neither higher CVD risk status nor individual CVD risk factors had a significant association with recovery. For every one-unit increase in Framingham Risk Score, odds of PTA3,4,6,8 recovery were 0.95 times lower (95% CI [0.90, 1.00]) after accounting for age, sex, body mass index, noise exposure, and treatment/time-to-treatment grouping (p = .056). Conclusions: The prognosis of low-frequency ISSNHL recovery is worse among current/former smokers than nonsmokers. Other CVD risk factors and aggregate risk are not significantly related to recovery.

Objectives: Evaluate the relationship between cardiovascular disease (CVD) risk factors and cochlear function in African Americans.Methods: Relationships between hearing loss, cochlear function, and CVD risk factors were assessed in a cross‐sectional analysis of 1106 Jackson Heart Study participants. Hearing loss was defined as puretone average (PTA_0.5,1,2,4) > 15 dB HL. Distortion product otoacoustic emissions (DPOAEs) were collected for f₂ = 1.0–8.0 kHz. Two amplitude averages were computed: DPOAE_low (f₂ ≤ 4 kHz) and DPOAE_high (f₂ ≥ 6 kHz). Based on major CVD risk factors (diabetes, current smoking, total cholesterol ≥240 mg/dL or treatment, and systolic blood pressure [BP]/diastolic BP ≥ 140/≥90 mmHg or treatment), four risk groups were created: 0, 1, 2, and ≥3 risk factors. Logistic regression estimated the odds of hearing loss and absent/reduced DPOAE_low and DPOAE_high by CVD risk status adjusting for age, sex, education, BMI, vertigo, and noise exposure.Results: With multivariable adjustment, diabetes was associated with hearing loss (OR = 1.48 [95% CI: 1.04–2.10]). However, there was not a statistically significant relationship between CVD risk factors (individually or for overall risk) and DPOAEs.Conclusion: Diabetes was associated with hearing loss. Neither individual CVD risk factors nor overall risk showed a relationship to cochlear dysfunction.Level of Evidence: 2b.

Hearing loss has been associated with individual cardiovascular disease (CVD) risk factors and, to a lesser extent, CVD risk metrics. However, these relationships are understudied in clinical populations. We conducted a retrospective study of electronic health records to evaluate the relationship between hearing loss and CVD risk burden. Hearing loss was defined as puretone average (PTA_0.5,1,2,4) > 20 dB hearing level (HL). Optimal CVD risk was defined as nondiabetic, nonsmoking, systolic blood pressure (SBP) < 120 and diastolic (D)BP < 80 mm Hg, and total cholesterol < 180 mg/dL. Major CVD risk factors were diabetes, smoking, hypertension, and total cholesterol ≥ 240 mg/dL or statin use. We identified 6332 patients (mean age = 62.96 years; 45.5% male); 64.0% had hearing loss. Sex-stratified logistic regression adjusted for age, noise exposure, hearing aid use, and body mass index examined associations between hearing loss and CVD risk. For males, diabetes, hypertension, smoking, and ≥ 2 major CVD risk factors were associated with hearing loss. For females, diabetes, smoking, and ≥ 2 major CVD risk factors were significant risk factors. Compared to those with no CVD risk factors, there is a higher likelihood of hearing loss in patients with ≥ 2 major CVD risk factors. Future research to better understand sex dependence in the hearing loss-hypertension relationship is indicated.

Background Individual cardiovascular disease (CVD) risk factors (RFs) have been associated with hearing loss (HL). The relationship to aggregate risk is poorly understood and has not been explored in the Hispanic/Latino population. Purpose The aim of this study was to characterize the association between aggregate CVD RF burden and hearing among Hispanics/Latinos. Research Design Cross-sectional examination. Study Sample Participants (18‐74 years; n = 12,766) in the Hispanic Community Health Study/Study of Latinos. Data Collection and Analysis Thresholds (0.5‐8 kHz) were obtained, and HL was defined dichotomously as pure-tone average (PTA_{0.5,1, 2,4}) > 25 dB HL. Optimal CVD risk burden was defined as follows: systolic blood pressure (SBP) < 120 mm Hg and diastolic blood pressure (DBP) < 80 mm Hg; total cholesterol < 180 mg/dL; nonsmoking; and no diabetes. Major CVD RFs were diabetes, currently smoking, SBP >160 or DBP > 100 mm Hg (or antihypertensives), and total cholesterol > 240 mg/dL (or statins). Thresholds were estimated by age (18‐44 and ≥45 years) and sex using linear regression. The association between CVD risk burden and HL was assessed using multivariable logistic regression. Models were adjusted for age, sex, Hispanic/Latino background, center, education, income, alcohol use, body mass index, and noise exposure. Results In the target population, 53.03% were female and 18.81% and 8.52% had all RFs optimal and ≥2 major RFs, respectively. Elevated BP (SBP 120‐139 mm Hg or DBP 80‐89 mm Hg) was associated with HL in females < 45 years (odds ratio [OR], 2.18; 95% confidence interval [CI], 1.14‐4.16). Diabetes (OR, 1.37; 95% CI, 1.01‐1.84) and tobacco smoking (OR, 1.44; 95% CI, 1.03‐2.01) were associated with HL in females ≥ 45 years. The odds of HL were higher for females ≥ 45 years with ≥2 RFs versus those with all RFs optimal (OR, 1.99; 95% CI, 1.12‐3.53). Elevated BP (SBP 140‐159 mm Hg or DBP 90‐99 mm Hg), but not aggregate risk burden, was associated with HL in males ≥ 45 years (OR, 1.49; 95% CI, 1.02‐2.19). No relationships with major CVD RFs were significant in males < 45 years. Conclusions HL is associated with elevated BP in females < 45 years, with diabetes and hypertension in males ≥ 45 years, and with diabetes, smoking, and having ≥2 major CVD RFs in females ≥ 45 years. Future studies are needed to examine if these factors are associated with incident HL.

Introduction: A relationship between tobacco smoking and hearing loss has been reported; associations with cannabis smoking are unknown. In this cross-sectional population-based study, we examined relationships between hearing loss and smoking (tobacco, cannabis, or co-drug use). Methods: We explored the relationship between hearing loss and smoking among 2705 participants [mean age = 39.41 (SE: 0.36) years] in the National Health and Nutrition Examination Survey (2011 to 12; 2015 to 16). Smoking status was obtained via questionnaire; four mutually exclusive groups were defined: nonsmokers, current regular cannabis smokers, current regular tobacco smokers, and co-drug users. Hearing sensitivity (0.5 to 8 kHz) was assessed, and two puretone averages (PTAs) computed: low- (PTA_0.5,1,2) and high-frequency (PTA_3,4,6,8). We defined hearing loss as threshold >15 dB HL. Multivariable logistic regression was used to examine sex-specific associations between smoking and hearing loss in the poorer ear (selected based on PTA_0.5,1,2) adjusting for age, sex, race/ethnicity, hypertension, diabetes, education, and noise exposure with sample weights applied. Results: In the age-sex adjusted model, tobacco smokers had increased odds of low- and high-frequency hearing loss compared with non-smokers [odds ratio (OR) = 1.58, 95% confidence ratio (CI): 1.05 to 2.37 and OR = 1.97, 95% CI: 1.58 to 2.45, respectively]. Co-drug users also had greater odds of low- and high-frequency hearing loss [OR = 2.07, 95% CI: 1.10 to 3.91 and OR = 2.24, 95% CI: 1.27 to 3.96, respectively]. In the fully adjusted multivariable model, compared with non-smokers, tobacco smokers had greater odds of high-frequency hearing loss [multivariable adjusted odds ratio = 1.64, 95% CI: 1.28-2.09]. However, in the fully adjusted model, there were no statistically significant relationships between hearing loss (PTA_0.5,1,2 or PTA_3,4,6,8) and cannabis smoking or co-drug use. Discussion: Cannabis smoking without concomitant tobacco consumption is not associated with hearing loss. However, sole use of cannabis was relatively rare and the prevalence of hearing loss in this population was low, limiting generalizability of the results. This study suggests that tobacco smoking may be a risk factor for hearing loss but does not support an association between hearing loss and cannabis smoking. More definitive evidence could be derived using physiological measures of auditory function in smokers and from longitudinal studies.

Background Numerous cardiometabolic factors may underlie risk of hearing loss. Modifiable risk factors such as non-optimal blood pressure (BP) are of interest. Purpose To investigate early auditory evoked potentials (AEPs) in persons with nonoptimal BP. Research Design A cross-sectional nonexperimental study was performed. Study Sample Fifty-two adults (18‐55 years) served as subjects. Individuals were classified as having optimal (systolic [S] BP < 120 and diastolic [D] BP < 80 mm Hg, n = 25) or non-optimal BP (SBP ≥=120 or DBP ≥=80 mm Hg or antihypertensive use, n = 27). Thirteen subjects had hypertension (HTN) (SBP ≥130 or DBP ≥80 mm Hg or use of antihypertensives). Data Collection and Analysis Behavioral thresholds from 0.25 to 16 kHz were collected. Threshold auditory brain stem responses (ABRs) were recorded using rarefaction clicks (17.7/second) from 80 dB nHL to wave V threshold. Electrocochleograms were obtained with 90 dB nHL 7.1/second alternating clicks and assessed for summating and compound action potentials (APs). Outcomes were compared via independent samples t tests. Linear mixed effects models for behavioral thresholds and ABR wave latencies were constructed to account for potential confounders. Results Wave I and III latencies were comparable between optimal and non-optimal BP groups. Wave I was prolonged in hypertensive versus optimal BP subjects at stimulus level 70 dB nHL (p = 0.016). ABR wave V latencies were prolonged in non-optimal BP at stimulus level 80 dB nHL (p = 0.048) and in HTN at levels of 80, 50, and 30 dB nHL (all p < 0.050). DBP was significantly correlated with wave V latency (r = 0.295; p = 0.039). No differences in ABR amplitudes were observed between optimal and non-optimal BP subjects. Electrocochleographic study showed statistically comparable action and summating potential amplitudes between optimal and non-optimal BP subjects. AP latencies were also similar between the groups. Analysis using a set baseline amplitude of 0 μV showed that hypertensive subjects had higher summating (p = 0.038) and AP (p = 0.047) amplitudes versus optimal BP subjects; AP latencies were comparable. Conclusion Elevated BP and more specifically, HTN was associated with subtle AEP abnormalities. This study provides preliminary evidence that nonoptimal BP, and more specifically HTN, may be related to auditory neural dysfunction; larger confirmatory studies are warranted.

Purpose: Cannabis is widely used for medicinal and recreational purposes. Studies have evaluated its health benefits and consequences, although there is limited work on its effects on the auditory system. In this exploratory study, we evaluate the effects of cannabis smoking on early auditory evoked potentials. Method: We investigated auditory brainstem response (ABR) and electrocochleography waveforms in 18 cannabis smokers (44% women, 54% men; M _age = 23.06 years, range: 21–28 years) and 19 nonsmoker controls (63% women, 37% men; M _age = 23.74 years, range: 21–33 years). Threshold ABRs were recorded using rarefaction clicks at a rate of 17.7/s from 80 dB nHL to Wave V threshold. Resulting amplitudes and latencies for Waves I, III, and V were compared via independent-samples t tests. Electrocochleograms obtained with 90 dB nHL (7.1/s) alternating clicks were assessed for summating and compound action potentials, which were compared between groups using independent-samples t tests. Results: ABR Wave I amplitudes were significantly lower in smokers ( M = 0.14 μV, SD = 0.11) compared to nonsmokers ( M = 0.21 μV, SD = 0.10, p = .039) at 80 dB nHL. Wave V latencies were significantly delayed in smokers at 80 dB nHL. Wave I and III latencies did not differ significantly between the two groups. Summating potential/compound action potential ratios were significantly elevated in smokers ( M = 0.30, SD = 0.04) versus nonsmokers ( M = 0.21, SD = 0.05, p = .042). Conclusion: We identified significant differences in electrophysiological outcomes between cannabis smokers and nonsmokers. Cannabis smoking may have a subtle neurotoxic effect on the auditory system. Larger confirmatory studies are warranted.