Functional Hearing Difficulties in Blast-Exposed Service Members With Normal to Near-Normal Hearing Thresholds.

OBJECTIVES: Estimated prevalence of functional hearing and communication deficits (FHCDs), characterized by abnormally low speech recognition and binaural tone detection in noise or an abnormally high degree of self-perceived hearing difficulties, dramatically increases in active-duty service members (SMs) who have hearing thresholds slightly above the normal range and self-report to have been close to an explosive blast. Knowing the exact nature of the underlying auditory-processing deficits that contribute to FHCD would not only provide a better characterization of the effects of blast exposure on the human auditory system, but also allow clinicians to prescribe appropriate therapies to treat or manage patient complaints. DESIGN: Two groups of SMs were initially recruited: (1) a control group (N = 78) with auditory thresholds ≤20 dB HL between 250 and 8000 Hz, no history of blast exposure, and who passed a short FHCD screener, and (2) a group of blast-exposed SMs (N = 26) with normal to near-normal auditory thresholds between 250 and 4000 Hz, and who failed the FHCD screener (cutoffs based on the study by Grant et al.). The two groups were then compared on a variety of audiometric, behavioral, cognitive, and electrophysiological measures. These tests were selected to characterize various aspects of auditory system processing from the cochlear to the cortex. A third, smaller group of blast-exposed SMs who performed within normal limits on the FHCD screener were also recruited (N = 11). This third subject group was unplanned at the onset of the study and was added to evaluate the effects of blast exposure on hearing and communication regardless of performance on the FHCD screener. RESULTS: SMs in the blast-exposed group with FHCD performed significantly worse than control participants on several metrics that measured peripheral and mostly subcortical auditory processing. Cognitive processing was mostly unaffected by blast exposure with the exception of cognitive tests of language-processing speed and working memory. Blast-exposed SMs without FHCD performed similarly to the control group on tests of peripheral and brainstem processing, but performed similarly to blast-exposed SMs with FHCD on measures of cognitive processing. Measures derived from EEG recordings of the frequency-following response revealed that blast-exposed SMs who exhibited FHCD demonstrated increased spontaneous neural activity, reduced amplitude of the envelope-following response, poor internal signal to noise ratio, reduced response stability, and an absent or delayed onset response, compared with the other two participant groups. CONCLUSIONS: Degradation in the neural encoding of acoustic stimuli is likely a major contributing factor leading to FHCD in blast-exposed SMs with normal to near-normal audiometric thresholds. Blast-exposed SMs, regardless of their performance on the FHCD screener, exhibited a deficit in language-processing speed and working memory, which could lead to difficulties in decoding rapid speech and in understanding speech in challenging speech communication settings. Further tests are needed to align these findings with clinical treatment protocols being used for patients with suspected auditory-processing disorders.

Effects of Amplification on Neural Phase Locking, Amplitude, and Latency to a Speech Syllable.

OBJECTIVE: Older adults often have trouble adjusting to hearing aids when they start wearing them for the first time. Probe microphone measurements verify appropriate levels of amplification up to the tympanic membrane. Little is known, however, about the effects of amplification on auditory-evoked responses to speech stimuli during initial hearing aid use. The present study assesses the effects of amplification on neural encoding of a speech signal in older adults using hearing aids for the first time. It was hypothesized that amplification results in improved stimulus encoding (higher amplitudes, improved phase locking, and earlier latencies), with greater effects for the regions of the signal that are less audible. DESIGN: Thirty-seven adults, aged 60 to 85 years with mild to severe sensorineural hearing loss and no prior hearing aid use, were bilaterally fit with Widex Dream 440 receiver-in-the-ear hearing aids. Probe microphone measures were used to adjust the gain of the hearing aids and verify the fitting. Unaided and aided frequency-following responses and cortical auditory-evoked potentials to the stimulus /ga/ were recorded in sound field over the course of 2 days for three conditions: 65 dB SPL and 80 dB SPL in quiet, and 80 dB SPL in six-talker babble (+10 signal to noise ratio). RESULTS: Responses from midbrain were analyzed in the time regions corresponding to the consonant transition (18 to 68 ms) and the steady state vowel (68 to 170 ms). Generally, amplification increased phase locking and amplitude and decreased latency for the region and presentation conditions that had lower stimulus amplitudes-the transition region and 65 dB SPL level. Responses from cortex showed decreased latency for P1, but an unexpected decrease in N1 amplitude. Previous studies have demonstrated an exaggerated cortical representation of speech in older adults compared to younger adults, possibly because of an increase in neural resources necessary to encode the signal. Therefore, a decrease in N1 amplitude with amplification and with increased presentation level may suggest that amplification decreases the neural resources necessary for cortical encoding. CONCLUSION: Increased phase locking and amplitude and decreased latency in midbrain suggest that amplification may improve neural representation of the speech signal in new hearing aid users. The improvement with amplification was also found in cortex, and, in particular, decreased P1 latencies and lower N1 amplitudes may indicate greater neural efficiency. Further investigations will evaluate changes in subcortical and cortical responses during the first 6 months of hearing aid use.

Neural and behavioral changes after the use of hearing aids.

OBJECTIVE: Individuals with age-related hearing loss (ARHL) can restore some loss of the auditory function with the use of hearing aids (HAs). However, what remains unknown are the physiological mechanisms that underlie how the brain changes with exposure to amplified sounds though the use of HAs. We aimed to examine behavioral and physiological changes induced by HAs. METHODS: Thirty-five older-adults with moderate ARHL with no history of hearing aid use were fit with HAs tested in aided and unaided conditions, and divided into experimental and control groups. The experimental group used HAs during a period of six months. The control group did not use HAs during this period, but were given the opportunity to use them after the completion of the study. Both groups underwent testing protocols six months apart. Outcome measures included behavioral (speech-in-noise measures, self-assessment questionnaires) and electrophysiological brainstem recordings (frequency-following responses) to the speech syllable /ga/ in two quiet conditions and in six-talker babble noise. RESULTS: The experimental group reported subjective benefits on self-assessment questionnaires. Significant physiological changes were observed in the experimental group, specifically a reduction in fundamental frequency magnitude, while no change was observed in controls, yielding a significant time × group interaction. Furthermore, peak latencies remained stable in the experimental group but were significantly delayed in the control group after six months. Significant correlations between behavioral and physiological changes were also observed. CONCLUSIONS: The findings suggest that HAs may alter subcortical processing and offset neural timing delay; however, further investigation is needed to understand cortical changes and HA effects on cognitive processing. SIGNIFICANCE: The findings of the current study provide evidence for clinicians that the use of HAs may prevent further loss of auditory function resulting from sensory deprivation.

Pilot Study Comparing Nasal vs Oral Intubation for Dental Surgery by Physicians, Nurse Anesthetists, and Trainees.

The purpose of this article was to determine if pediatric dental treatment under general anesthesia utilizing orotracheal intubation takes longer than using nasotracheal intubation techniques. Twenty-six American Society of Anesthesiologists Physical Status Classification I and II pediatric dental patients, ages 2-8 years treated under general anesthesia, were assigned to 1 of 2 groups: (a) nasotracheal intubation (control, n = 13), (b) orotracheal intubation (experimental, n = 13). Times for intubation, radiographic imaging, and dental procedures, as well as total case time were quantified. Data were collected on airway difficulty, numbers of providers needed for intubation, intubation attempts, and intubation trauma. There was a significant difference in mean intubation time (oral = 2.1 minutes versus nasal = 6.3 minutes; p < .01). There was no difference in mean radiograph time (oral = 4.2 minutes versus nasal = 3.4 minutes; p = .144), and overall radiograph image quality was not affected. There was no difference in dental procedure time ( p = .603) or total case time ( p = .695). Additional providers were needed for intubation and more attempts were required for nasotracheal intubation versus orotracheal intubation (6 additional providers/22 attempts vs 0 additional providers/15 attempts, p < .01 and p < .05, respectively). Nine of 13 nasotracheal intubations were rated as traumatic (69%) versus 0 of 13 for orotracheal intubations (0%) ( p < .01). In 7/9 orotracheal intubation cases (78%), the tube was not moved during treatment ( p < .01). Orotracheal intubation does not increase case time, does not interfere with radiographic imaging, and is less traumatic for the patient when performed by physician anesthesiologists, emergency and pediatric medicine physician residents, certified registered nurse anesthetists, and student nurse anesthetists, all with variable nasotracheal intubation experience.

Loss of dysbindin-1 in mice impairs reward-based operant learning by increasing impulsive and compulsive behavior.

The dystrobrevin-binding protein 1 (DTNBP1) gene, which encodes the dysbindin-1 protein, is a potential schizophrenia susceptibility gene. Polymorphisms in the DTNBP1 gene have been associated with altered cognitive abilities. In the present study, dysbindin-1 null mutant (dys-/-), heterozygous (dys+/-), and wild-type (dys+/+) mice, on a C57BL/6J genetic background, were tested in either a match to sample or nonmatch to sample visual discrimination task. This visual discrimination task was designed to measure rule learning and detect any changes in response timing over the course of testing. Dys-/- mice displayed significant learning deficits and required more trials to acquire this task. However, once criterion was reached, there were no differences between the genotypes on any behavioral measures. Dys-/- mice exhibited increased compulsive and impulsive behaviors compared to control littermates suggesting the inability to suppress incorrectly-timed responses underlies their increased time to acquisition. Indeed, group comparisons of behavior differences between the first and last day of testing showed that only dys-/- mice consistently decreased measures of perseverative, premature, timeout, and total responses. These findings illustrate how some aspects of altered cognitive performance in dys-/- mice might be related to increased impulsive and compulsive behaviors, analogous to cognitive deficits in some individuals with psychiatric disorders.