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Dalhoff, E.

Publications and source records attributed to Dalhoff, E..

3 recordsLinked to original sources

Extended high frequency hearing influences cortical response amplitudes to speech

Since young adults hear sounds up to 20 kHz, the loss of extended high-frequency hearing (EHF; above 8 kHz) is a hallmark of age-related hearing loss, often progressing from early lifetime. However, this deficit frequently goes undetected because routine clinical hearing tests and most hearing aids are currently limited mostly up to 8 kHz. EHF hearing has been linked to deficits in speech perception in noise and to self-reported hearing. However, it remains elusive how EHF hearing influences speech intelligibility. Here we recorded neuromagnetic brain responses using magnetoencephalography (MEG) within a frequency-tagging speech paradigm designed to probe hierarchical levels of attention and memory-dependent speech processing and recognition. Auditory evoked cortical magnetic field (AEF) responses were significantly reduced in both left and right brain hemispheres in individuals with impaired EHF hearing compared to those subjects with rather preserved EHF hearing. A gradual reinforcement of left-hemispheric AEF seen over age was not observed in young adults (19-29 y) with preserved EHF hearing. This was linked to stronger auditory brainstem responses (ABR), reflecting better neural synchronized auditory responses at stimulus onset. The reinforced left hemispheric dominance in young adults with impaired EHF hearing, in contrast, was linked to lower ABRs. Our findings suggest that sound energy above 8 kHz contributes through its impact on stimulus-onset synchrony to phase locking of oscillations in the auditory cortex to intelligible speech. Together, the results highlight the need to reconsider the neglect of EHF hearing in both audiological assessment and hearing aid design. SignificanceWe show here that deficits in extended high-frequency (EHF) hearing, up to now neglected in routine clinical audiometry and hearing aid technology, lead to reduced cortical evoked auditory field (AEF) response amplitudes to attended and unattended speech, even at a young age. A gradual increase in reinforced left-hemispheric AEF responses during attended speech does not occur in young people with good EHF hearing; this is linked to better synchronization of neural responses at the onset of sound. This suggests a crucial role of sounds containing energy above 8kHz in minimizing the need for cognitive resources during active listening. Collectively, our results challenge current clinical practices and underscore the need to incorporate EHF hearing into audiological assessment and hearing aid design.

neuroscience↗

Phase coding in phoneme processing slows with age

The comprehension of phonemes is a fundamental component of speech processing which relies on both, temporal fine structure (TFS) and temporal envelope (TE) coding. EEG amplitude in response to phonemes has been identified as indicator of speech performance in hearing aid users. Presbyacusis may also alter neuro-electric responses to phonemes, even with minimally or unaffected hearing thresholds. Elevated speech reception thresholds (SRT) in absence of pure-tone threshold (PTT) elevation suggest central processing deficits. We therefore collected audiometric data (PTT, SRT) and EEG during passive listening in 80 subjects, ranging in age from 18 to 76 years. We confirm phoneme-evoked EEG response amplitude (PEA) as indicator of speech comprehension. Specifically, PEA decreased with elevated SRT, PTT and increased age. As novel observation, we report the temporal delay of phoneme-evoked EEG responses (PED) to increase with age and PTT. The absolute duration of PED, its age-correlation, and the lack of PEA-lateralization combined with the frequency of phoneme stimuli used here suggest a predominantly thalamic generator of phoneme-evoked EEG responses. Hearing loss in extended high-frequencies affects PED more than PEA. In our sample, neural compensation for increased PTT came at the cost of decreased temporal processing speed. Most importantly, PED correlates with SRT and explains SRT-variance in quiet and in ipsilateral noise that PTT cannot. PED was a better predictor of TFS coding in quiet and of TE coding in ipsilateral noise. As PED reflects both TFS and TE coding, thalamic activity may provide integrated information at the gate of neocortex. Significance StatementIntact speech comprehension is essential for social participation which protects against depression and dementia. Age-related hearing loss is a growing problem in aging societies, as hearing deficits constitute the third most important modifiable risk factor for cognitive decline. This work uses electrical brain responses to phonemes in a cohort covering age 18 to 76 years. As the temporal delay of phoneme responses showed the most significant correlations with age and high-frequency thresholds, we demonstrated that speed of neural processing seems essential for speech comprehension. The observed neural signals likely originate from thalamus which receives feedback from neocortex and is embedded in cognitive processing. Developing objective markers for speech processing is key for ensuring cognitive fitness in aging.

systems biology↗

Neural adaptation at stimulus onset and speed of neural processing as critical contributors to speech comprehension independent of hearing threshold or age

Loss of afferent auditory fiber function (cochlear synaptopathy) has been suggested to occur before a clinically measurable deterioration of subjective hearing threshold. This so-called "hidden" hearing loss is characterized by speech comprehension difficulties. We examined young, middle-aged, and older individuals with and without hearing loss using pure-tone (PT) audiometry, short-pulsed distortion-product otoacoustic emissions (DPOAE), auditory brainstem responses (ABR), auditory steady state responses (ASSR), speech comprehension (OLSA), and syllable discrimination in quiet and noise. After normalizing OLSA thresholds for PT thresholds ("PNOT"), differences in speech comprehension still remained and showed no significant dependence on age, allowing us to categorize participants into groups with good, standard, and poor speech comprehension. Listeners with poor speech comprehension in quiet exhibited smaller firing rate adaptions at stimulus onset (as measured by the difference between DPOAE threshold and pure-tone threshold) and delayed supra-threshold ABR waves I-V, suggesting high spontaneous rate low threshold fiber cochlear synaptopathy. In contrast, when speech comprehension was tested in noise, listeners with poor speech comprehension had larger DPOAEs acceptance rate, putatively resulting from altered basilar membrane compression (recruitment). This was linked with higher uncomfortable loudness levels and larger ASSR amplitudes. Moreover, performance in phoneme discrimination was significantly different below (/o/-/u/) and above the phase-locking limit (/i/-/y/), depending on whether vowels were presented in quiet or ipsilateral noise. This suggests that neural firing rate adaptation at stimulus onset is critical for speech comprehension, independent of hearing threshold and age, whereas the recruitment phenomenon counterbalances the loss in speech-in-noise discrimination due to impaired threshold. Significance StatementAge-related hearing loss is the third largest modifiable risk factor for cognitive decline. It has been suggested that the link between hearing loss and cognitive decline is not fully explained by hearing threshold loss. We here suggest that language comprehension deficits may be used as an early indication of future hearing loss and therefore cognitive decline. We found that, independent of age and pure-tone thresholds, speech comprehension in quiet and ipsilateral noise depend on different onset firing-rate adaptations of inner hair cells (measured by DPOAE threshold), along with cochlear synaptopathy of high spontaneous rate auditory nerve fibers and neural spiking synchronicity. These measures may be used as possible future indicators of risk for cognitive decline.

neuroscience↗