Temporal dynamics of ocular indicators of sleepiness across sleep restriction.

The current study characterized the temporal dynamics of ocular indicators of sleepiness during extended sleep restriction. Ten male participants (mean age ± SD = 23.3 ± 1.6 years) underwent 40 h of continuous wakefulness under constant routine (CR) conditions; they completed the Karolinska Sleepiness Scale (KSS) and a 10-min auditory psychomotor vigilance task (aPVT) hourly. Waking electroencephalography (EEG) and ocular measures were recorded continuously throughout the CR. Infrared-reflectance oculography was used to collect the ocular measures positive and negative amplitude-velocity ratio, mean blink duration, the percentage of eye closure, and a composite score of sleepiness levels (Johns Drowsiness Scale). All ocular measures, except blink duration, displayed homeostatic and circadian properties. Only circadian effects were detected in blink duration. Significant, phase-locked cross-correlations (p < 0.05) were detected between ocular measures and aPVT reaction time (RT), aPVT lapses, KSS, and EEG delta-theta (0.5-5.5 Hz), theta-alpha (5.0-9.0 Hz), and beta (13.0-20.0 Hz) activity. Receiver operating characteristic curve analysis demonstrated reasonable sensitivity and specificity of ocular measures in correctly classifying aPVT lapses above individual baseline thresholds (initial 16 h of wakefulness). Under conditions of sleep restriction, ocular indicators of sleepiness paralleled performance impairment and self-rated sleepiness levels, and demonstrated their potential to detect sleepiness-related attentional lapses. These findings, if reproduced in a larger sample, will have implications for the use of ocular-based sleepiness-warning systems in operational settings.

Evaluation of a single-channel nasal pressure device to assess obstructive sleep apnea risk in laboratory and home environments.

STUDY OBJECTIVES: To evaluate the sensitivity and specificity of a portable single-channel (intra-nasal pressure) sleep apnea device (ApneaLink) in both the laboratory and at home for assessment of sleep apnea risk in comparison with standard polysomnography (PSG). METHODS: Fifty-five participants underwent simultaneous recordings of standard PSG and ApneaLink in the laboratory. Of these, 38 participants also used the ApneaLink device in their own homes for one night. PSG respiratory events were scored using standard criteria. Intra-nasal pressure signals were analyzed using the ApneaLink automated computerized algorithm provided to yield estimates of airflow for detection of apneas and hypopneas. Apnea-hypopnea indices (AHI) were compared. RESULTS: There was high sensitivity and specificity for the ApneaLink AHI when compared to simultaneous PSG at comparable AHI levels (AHI ≥ 15 events/h; sensitivity 100%, specificity 92%; positive and negative predictive values 70% and 100%, respectively). Home-measured ApneaLink AHI sensitivity and specificity were also reliable when compared with PSG (AHI ≥ 5, 81% and 77%, respectively; AHI ≥ 15, 67% and 91%), and improved slightly when two nights' data were used (AHI ≥ 5, 88% and 85%; AHI ≥ 15, 67% and 93%). CONCLUSIONS: The ApneaLink demonstrated good sensitivity and specificity in quantifying AHI when compared to PSG in a population with and without confirmed OSA. This simple, easy-to-use device may be useful in de novo large-scale occupational or underserved community OSA diagnostic programs to identify those with unambiguous disease who need immediate treatment or indicate those who may be at increased risk of OSA.

Frontally mediated inhibitory processing and white matter microstructure: age and alcoholism effects.

RATIONALE: The NOGO P3 event-related potential is a sensitive marker of alcoholism, relates to EEG oscillation in the δ and θ frequency ranges, and reflects activation of an inhibitory processing network. Degradation of white matter tracts related to age or alcoholism should negatively affect the oscillatory activity within the network. OBJECTIVE: This study aims to evaluate the effect of alcoholism and age on δ and θ oscillations and the relationship between these oscillations and measures of white matter microstructural integrity. METHODS: Data from ten long-term alcoholics to 25 nonalcoholic controls were used to derive P3 from Fz, Cz, and Pz using a visual GO/NOGO protocol. Total power and across trial phase synchrony measures were calculated for δ and θ frequencies. DTI, 1.5 T, data formed the basis of quantitative fiber tracking in the left and right cingulate bundles and the genu and splenium of the corpus callosum. Fractional anisotropy and diffusivity (λL and λT) measures were calculated from each tract. RESULTS: NOGO P3 amplitude and δ power at Cz were smaller in alcoholics than controls. Lower δ total power was related to higher λT in the left and right cingulate bundles. GO P3 amplitude was lower and GO P3 latency was longer with advancing age, but none of the time-frequency analysis measures displayed significant age or diagnosis effects. CONCLUSIONS: The relation of δ total power at CZ with λT in the cingulate bundles provides correlational evidence for a functional role of fronto-parietal white matter tracts in inhibitory processing.

Sleep evoked delta frequency responses show a linear decline in amplitude across the adult lifespan.

Aging is associated with many changes in sleep, with one of the most prominent being a reduction in slow wave sleep. Traditional measures of this phenomenon rely on spontaneous activity and typically confound the incidence and amplitude of delta waves. The measurement of evoked K-complexes during sleep, enable separate assessment of incidence and amplitude taken from the averaged K-complex waveform. The present study describes data from 70 normal healthy men and women aged between 19 and 78 years. K-Complexes were evoked using short auditory tones and recorded from a midline array of scalp sites. Significant reductions with age were seen in the amplitude of the N550 component of the averaged waveform, which represents the amplitude of the K-complex, with linear regression analysis indicating approximately 50% of the variance was due to age. Smaller, yet still significant reductions were seen in the ability to elicit K-complexes. The data highlight the utility of evoked K-complexes as a sensitive marker of brain aging in men and women.

The impact of alcoholism on sleep evoked Delta frequency responses.

BACKGROUND: K-complexes (KCs) are evoked delta frequency electroencephalogram (EEG) responses during sleep that occur when large numbers of healthy cortical cells burst fire in a synchronized manner. The KC amplitude and incidence are sensitive measures of normal healthy brain aging. Given the known neurodegenerative consequences of alcohol abuse it was hypothesized that alcoholism would be associated with further KC amplitude and incidence reductions. METHODS: Eighty-four subjects (42 alcoholics) screened for medical, psychiatric, and sleep problems participated. The protocol involved the presentation of auditory stimuli during stage 2 sleep throughout a night in the laboratory. The KCs were identified and averaged, to enable measurement of the P2, N550, and P900 peaks. RESULTS: Compared with control subjects, alcoholic men and women had lower KC incidence (p < .001) and P2 (p < .001), N550 (p < .05), and P900 (p < .05) amplitudes. There was a significant diagnosis x site interaction (p < .001), indicating the group difference was largest at frontal sites. Longer sobriety correlated with increased N550 amplitude (p < .01). CONCLUSIONS: The KC incidence and amplitude were negatively impacted in alcoholic men and women with exacerbation of the normal aging effects, particularly over frontal scalp regions. The observed relationship between improvements in KC measures and increased time of abstinence suggests that these measures might provide a useful marker of brain recovery with continued abstinence from alcohol.

The impact of slow wave sleep proximity on evoked K-complex generation.

During human stage 2 non-rapid eye movement (NREM) sleep, spontaneous K-complexes are more likely to occur prior to transitions to stage 3 or stage 4 sleep (referred to as slow wave sleep or SWS) compared to transitions to REM sleep, suggesting that the K-complex may be the 'forerunner' of SWS. The present study investigated the impact of SWS or REM sleep proximity on the probability of evoking a K-complex (pKC) during stage 2 and on components of the NREM sleep averaged evoked potential. Ten subjects spent three nights in the laboratory. On either the second or third night tones were presented continuously during sleep. Evoked K-complexes and sleep-evoked potentials were assessed for the 10 min of stage 2 prior to SWS (SWS-10) or REM (REM-10) sleep episodes as well as for all of SWS. pKC did not differ between SWS-10 (0.88) and SWS (0.91) but was significantly larger in SWS-10 than REM-10 (0.63). Amplitude effects were seen for the P2, N350, P900 NREM sleep-evoked potential components but not for the K-complex related N550. In each case where amplitude effects were found, SWS-10 was larger than REM-10. No latency differences were seen between conditions for the earlier components (P2, N350) however, both N550 and P900 were significantly shorter during SWS-10 compared to REM-10. These results are consistent with previous spontaneous K-complex studies and are supportive of a relationship between the K-complex and delta activity. They also indicate that stage 2 may consist of a continuum of microstates between SWS and REM sleep that are indicative of different brain stem, diecephalic and cortical patterns of activation.

A review of the evidence for P2 being an independent component process: age, sleep and modality.

This article reviews the event-related potential (ERP) literature in relation to the P2 waveform of the human auditory evoked potential. Within the auditory evoked potential, a positive deflection at approximately 150-250 ms is a ubiquitous feature. Unlike other cognitive components such as N1 or the P300, remarkably little has been done to investigate the underlying neurological correlates or significance of this waveform. Indeed until recently, many researchers considered it to be an intrinsic part of the 'vertex potential' complex, involving it and the earlier N1. This review seeks to describe the evidence supportive of P2 being the result of independent processes and highlights several features, such as its persistence from wakefulness into sleep, the general consensus that unlike most other EEG phenomena it increases with age, and the fact that it can be generated using respiratory stimuli.

Evoked potential components unique to non-REM sleep: relationship to evoked K-complexes and vertex sharp waves.

Following the loss of wakeful consciousness, the averaging of responses to stimuli produce evoked potential waveforms with prominent components either unique to or greatly enhanced by non-REM sleep. In the sleep onset periods (stage 1) these are the P2 and N350. Following the establishment of stable sleep (stage 2 and SWS), the N550 and P900 are also prominent. Investigation of the EEG associated with individual responses indicates that a good proportion of stimuli elicit, K-complexes or vertex sharp waves (VSWs) and occasionally will elicit both. Recent work has indicated that the N550 in the averaged response is due to the presence of K-complexes and that the N350 is at least largely due to the presence of VSWs. The large size of these grapho-elements indicates that they are probably produced by a synchronized discharge of multiple neural units. Both are readily observed in the absence of external stimulation and occur as normal components of sleep, indeed the K-complex is used as one of the identifying features of the onset of stable non-REM sleep. The present review details the investigation of these features and their associated evoked potential components, in terms of stimulus features, brain states associated with their production, their scalp topography, and changes as a function of age.