The effects of nicotine on distractor interference are modulated synergistically by cholinergic and dopaminergic genetic variations. Hence, both genes may contribute to the often reported individual variability in cognitive and neural effects of nicotine.
Recently, evidence has been accumulating that untreated hearing loss can lead to neurophysiological changes that affect speech processing abilities in noise. To shed more light on how aiding may impact these effects, this study explored the influence of hearing aid (HA) experience on the cognitive processes underlying speech comprehension. Eye-tracking and functional magnetic resonance imaging (fMRI) measurements were carried out with acoustic sentence-in-noise (SiN) stimuli complemented by pairs of pictures that either correctly (target picture) or incorrectly (competitor picture) depicted the sentence meanings. For the eye-tracking measurements, the time taken by the participants to start fixating the target picture (the ‘processing time’) was measured. For the fMRI measurements, brain activation inferred from blood-oxygen-level dependent responses following sentence comprehension was measured. A noise-only condition was also included. Groups of older hearing-impaired individuals matched in terms of age, hearing loss, and working memory capacity with (eHA;
N
= 13) or without (iHA;
N
= 14) HA experience participated. All acoustic stimuli were presented via earphones with individual linear amplification to ensure audibility. Consistent with previous findings, the iHA group had significantly longer (poorer) processing times than the eHA group, despite no differences in speech recognition performance. Concerning the fMRI measurements, there were indications of less brain activation in some right frontal areas for SiN relative to noise-only stimuli in the eHA group compared to the iHA group. Together, these results suggest that HA experience leads to faster speech-in-noise processing, possibly related to less recruitment of brain regions outside the core sentence-comprehension network. Follow-up research is needed to substantiate the findings related to changes in cortical speech processing with HA use.
Low frequency noise (LFS) and infrasound (IS) are controversially discussed as potential causes of annoyance and distress experienced by many people. However, the perception mechanisms for IS in the human auditory system are not completely understood yet. In the present study, sinusoids at 32 Hz (at the lower limit of melodic pitch for tonal stimulation), as well as 8 Hz (IS range) were presented to a group of 20 normal hearing subjects, using monaural stimulation via a loudspeaker sound source coupled to the ear canal by a long silicone rubber tube. Each participant attended two experimental sessions. In the first session, participants performed a categorical loudness scaling procedure as well as an unpleasantness rating task in a sound booth. In the second session, the loudness scaling procedure was repeated while brain activation was measured using functional magnetic resonance imaging (fMRI). Subsequently, activation data were collected for the respective stimuli presented at fixed levels adjusted to the individual loudness judgments. Silent trials were included as a baseline condition. Our results indicate that the brain regions involved in processing LFS and IS are similar to those for sounds in the typical audio frequency range, i.e., mainly primary and secondary auditory cortex (AC). In spite of large variation across listeners with respect to judgments of loudness and unpleasantness, neural correlates of these interindividual differences could not yet be identified. Still, for individual listeners, fMRI activation in the AC was more closely related to individual perception than to the physical stimulus level.
The findings suggest that nicotine acts primarily as a stimulus filter that prevents irrelevant stimuli from entering awareness in situations of high distractor interference.
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