Multiple auditory steady state response thresholds to bone conduction stimuli in adults with normal and elevated thresholds.

OBJECTIVE: Auditory steady state responses (ASSRs) to multiple air conduction (AC) stimuli modulated at ∼80 Hz have been shown to provide reasonable estimates of the behavioral audiogram. To distinguish the type of hearing loss (i.e., conductive, sensorineural, or mixed), bone conduction (BC) results are necessary. There are few BC-ASSR data, especially for individuals with hearing loss. The present studies aimed to (1) determine multiple ASSR thresholds to BC stimuli in adults with normal hearing, masker-simulated hearing loss, and sensorineural hearing loss (SNHL) and (2) determine how well BC-ASSR distinguishes normal versus elevated thresholds to BC stimuli in adults with normal hearing or SNHL. DESIGN: Multiple ASSR and behavioral thresholds for BC stimuli were determined in two studies. Study A assessed 16 normal-hearing adults with relatively flat threshold elevations produced by 50, 60, and 70 dB SPL AC masking noise, as well as no masking. Study B assessed 10 adults with normal hearing and 40 adults with SNHL. In both studies, the multiple (500 to 4000 Hz) ASSR stimuli were modulated between 77 and 101 Hz and varied in intensity from 0 to 50 dB HL in 10-dB steps. Stimuli were presented using a B71 bone oscillator held on the temporal bone by an elastic band while participants relaxed or slept. RESULTS: Study A: Correlations (r) between behavioral and ASSR thresholds for all conditions combined were 0.77, 0.87, 0.90, and 0.87 for 500, 1000, 2000, and 4000 Hz, respectively. ASSR minus behavioral threshold difference scores for all frequencies combined for the no-masker, 50, 60, and 70 dB SPL masker conditions were 14.3 ± 9.2, 12.1 ± 10.4, 12.7 ± 7.7, and 11.4 ± 8.1 dB, respectively. Study B: The difference scores for 500, 1000, 2000, and 4000 Hz were, on average, 15.7 ± 12.3, 10.3 ± 10.7, 9.7 ± 10.3, and 5.7 ± 7.9 dB, respectively, with correlations of 0.73, 0.84, 0.87, and 0.94 for the normal-hearing and SNHL groups combined. The ASSR minus behavioral difference scores were significantly larger for 500 Hz and significantly smaller for 4000 Hz compared with 1000 and 2000 Hz. Across all frequencies, the BC-ASSR correctly classified 89% of thresholds as "normal" or "elevated" (92% correct for 1000, 2000, and 4000 Hz). CONCLUSIONS: The threshold difference scores and correlations in individuals with SNHL are similar to those in normal listeners with simulated SNHL. These difference scores are also similar to those shown by previous studies for the AC-ASSR in individuals with SNHL, at least for 1000 to 4000 Hz. The BC-ASSR provides a reasonably good estimate of BC behavioral threshold in adults, especially between 1000 and 4000 Hz. Further research is required in infants with hearing loss.

CNS arousal and neurobehavioral performance in a short-term sleep restriction paradigm.

Few studies have investigated waking electrophysiological measures of arousal during sleep restriction. This study examined electroencephalogram (EEG) activity and performance during a 96-hour laboratory protocol where participants slept a baseline night (8 h), were randomly assigned to 3-, 5-, or 8-hour sleep groups for the next two nights sleep restriction (SR1, SR2), and then slept a recovery night (8 h). There were dose-dependent deficits on measures of mood, sleepiness, and reaction time that were apparent during this short-term bout of sleep restriction. The ratio of alpha to theta EEG recorded at rest indicated dose-dependent changes in CNS arousal. At 9:00 hours, both the 3- and 5-hour groups showed EEG slowing (sleepiness) during restriction, with the 3-hour group exhibiting greater deficits. Later in the day at 13:00 hours, the 5-hour group no longer exhibited EEG slowing, but the extent of slowing was more widespread across the scalp for the 3-hour group. High-frequency EEG, a measure of effort, was greater on the mornings following sleep restriction. The 5-hour group had increased beta EEG at central-parietal sites following both nights of restriction, whereas the 3-hour group had increased beta and gamma EEG at occipital regions following the first night only. Short-term sleep restriction leads to deficits in performance as well as EEG slowing that correspond to the amount and duration of sleep loss. High-frequency EEG may be a marker of effort or compensation.

Sensory gating impairments in poor sleepers during presleep wakefulness.

The neurocognitive model of insomnia predicts information processing deficits in poor sleepers. There is some evidence for deficits in later cognitive processing, but earlier sensory processing remains to be investigated. Paired-click stimuli were delivered to good and poor sleepers in a single night. P50 amplitude to stimuli provided an index of sensory gating in presleep wake, rapid eye movement sleep and stage 2 sleep. Poor sleepers exhibited sensory gating impairments during wake. For both groups, gating was intact in rapid eye movement sleep but absent in stage 2 sleep. These data show that poor sleepers experience enhanced sensory processing in the waking period before sleep. Further study is needed to explore sensory gating in chronic primary insomnia, sleep maintenance insomnia, and across multiple recording nights.

Physiological arousal and attention during a week of continuous sleep restriction.

Waking brain physiology underlying deficits from continuous sleep restriction (CSR) is not well understood. Fourteen good sleepers participated in a 21-day protocol where they slept their usual amount in a baseline week, had their time in bed restricted by 33% in a CSR week, and slept the desired amount in a recovery week. Participants slept at home, completing diaries and wearing activity monitors to verify compliance. Each day participants completed an RT task and mood and sleepiness ratings every 3 h. Laboratory assessment of electrophysiology and performance took place at the end of baseline, three times throughout the CSR week, and at the beginning of recovery. Participants reported less sleep during CSR which was confirmed by activity monitors. Correspondingly, well-being and neurobehavioural performance was impaired. Quantitative EEG analysis revealed significantly reduced arousal between the 1st and 7th days of restriction and linear effects at anterior sites (Fp2, Fz, F8, T8). At posterior sites (P4, P8), reductions occurred only later in the week between the 4th and 7th nights of restriction. Both the immediate linear decline in arousal and precipitous drop later in the week were apparent at central sites (C4, Cz). Thus, frontal regions were affected immediately, while parietal regions showed maintenance of function until restriction was more severe. The P300 ERP component showed evidence of reduced attention by the 7th day of restriction (at Pz, P4). EEG and ERPs deficits were more robust in the right-hemisphere, which may reflect greater vulnerability to sleep loss in the non-dominant hemisphere.