Individual 'fingerprints' in human sleep EEG topography.

The sleep EEG of eight healthy young men was recorded from 27 derivations during a baseline night and a recovery night after 40 h of waking. Individual power maps of the nonREM sleep EEG were calculated for the delta, theta, alpha, sigma and beta range. The comparison of the normalized individual maps for baseline and recovery sleep revealed very similar individual patterns within each frequency band. This high correspondence was quantified and statistically confirmed by calculating the Manhattan distance between all pairs of maps within and between individuals. Although prolonged waking enhanced power in the low-frequency range (0.75-10.5 Hz) and reduced power in the high-frequency range (13.25-25 Hz), only minor effects on the individual topography were observed. Nevertheless, statistical analysis revealed frequency-specific regional effects of sleep deprivation. The results demonstrate that the pattern of the EEG power distribution in nonREM sleep is characteristic for an individual and may reflect individual traits of functional anatomy.

Unihemispheric enhancement of delta power in human frontal sleep EEG by prolonged wakefulness.

EEG power spectra exhibit site-specific and state-related differences in specific frequency bands. In the present study we investigated the effect of total sleep deprivation on sleep EEG topography. Eight healthy, young, right-handed subjects were recorded during baseline sleep and recovery sleep after sleep deprivation. Forty hours of sleep deprivation affected power spectra in all derivations. However, hemispheric asymmetries were observed in the delta range. Sleep deprivation enhanced the anterior predominance of delta activity in the left hemisphere but not in the right one. This effect may reflect a functional asymmetry between the dominant and non-dominant hemisphere. The results provide further evidence for the presence of both global and local aspects of sleep regulation.

Revisiting the identity issue in anorexia.

Anorexia nervosa is considered an enigmatic disease with a multitude of predisposing factors and no empirically confirmed effective treatment. However, all people with the disease relentlessly pursue a common idealized goal--the state of severe emaciation. In this article, the perspective that this condition epitomizes a life-time struggle for self-acceptance and self-definition is reexamined. People afflicted with anorexia come to define themselves through their emaciated form, and maintenance of this form becomes their major focus and primary means of fulfillment. Therapy must address the identity issue, which is fundamental to the onset and perpetuation of the disease. Use of interpersonal techniques is advocated as most appropriate in serving this purpose.

Functional topography of the human nonREM sleep electroencephalogram.

The sleep EEG of healthy young men was recorded during baseline and recovery sleep after 40 h of waking. To analyse the EEG topography, power spectra were computed from 27 derivations. Mean power maps of the nonREM sleep EEG were calculated for 1-Hz bins between 1.0 and 24.75 Hz. Cluster analysis revealed a topographic segregation into distinct frequency bands which were similar for baseline and recovery sleep, and corresponded closely to the traditional frequency bands. Hallmarks of the power maps were the frontal predominance in the delta and alpha band, the occipital predominance in the theta band, and the sharply delineated vertex maximum in the sigma band. The effect of sleep deprivation on EEG topography was determined by calculating the recovery/baseline ratio of the power spectra. Prolonged waking induced an increase in power in the low-frequency range (1-10.75 Hz) which was largest over the frontal region, and a decrease in power in the sigma band (13-15.75 Hz) which was most pronounced over the vertex. The topographic pattern of the recovery/baseline power ratio was similar to the power ratio between the first and second half of the baseline night. These results indicate that changes in sleep propensity are reflected by specific regional differences in EEG power. The predominant increase of low-frequency power in frontal areas may be due to a high 'recovery need' of the frontal heteromodal association areas of the cortex.

Dual electroencephalogram markers of human sleep homeostasis: correlation between theta activity in waking and slow-wave activity in sleep.

To investigate the relationship between markers of sleep homeostasis during waking and sleep, the electroencephalogram of eight young males was recorded intermittently during a 40-h waking episode, as well as during baseline and recovery sleep. In the course of extended waking, spectral power of the electroencephalogram in the 5-8Hz band (theta activity) increased. In non-rapid eye movement sleep, power in the 0.75-4.5Hz band (slow-wave activity) was enhanced in the recovery night relative to baseline. Comparison of individual records revealed a positive correlation between the rise rate of theta activity during waking and the increase in slow-wave activity in the first non-rapid eye movement sleep episode. A topographic analysis based on 27 derivations showed that both effects were largest in frontal areas. From these results, we suggest that theta activity in waking and slow-wave activity in sleep are markers of a common homeostatic sleep process.

Functional neuroanatomy of human sleep states after zolpidem and placebo: a H215O-PET study.

Changes in the functional organization of the brain during the course of sleep and waking are reflected by different patterns of regional cerebral blood flow (rCBF). To investigate the effect of the hypnotic zolpidem, a benzodiazepine receptor agonist, drug or placebo were administered to eight young, healthy men prior to bedtime. The subjects were sleep-deprived to promote sleep during the 4-h recording period in the positron emission tomography scanner. Intravenous injections of labelled water were administered during pre-drug wakefulness, and during Stage 2, Stage 4 and rapid eye movement (REM) sleep, each injection being followed by an emission scan. Statistical parametric mapping was used to investigate the effects of treatment and sleep states. During sleep (combined Stages 2 and 4, and REM sleep) relative rCBF was lower after zolpidem than after placebo in the basal ganglia and insula, and higher in the parietal cortex. A 'multiple study' analysis of REM sleep revealed that rCBF in the anterior cingulum was lower after zolpidem than after placebo, whereas rCBF in the occipital and parietal cortex, parahippocampal gyrus and cerebellum was higher. When the pooled data (drug and placebo) of Stages 2 and 4 were compared with wakefulness, rCBF was lower in prefrontal cortex and insula, and higher in the occipital and parietal cortex. The results indicate that some differences in rCBF from wakefulness to non-REM sleep are further augmented by zolpidem.

Zolpidem and sleep deprivation: different effect on EEG power spectra.

To study the role of GABA-ergic mechanisms in sleep regulation, the combined action of 40 h sleep deprivation and either 20 mg zolpidem or placebo on the sleep electroencephalogram (EEG) were investigated by quantitative EEG analysis in eight young men who participated in a positron emission tomography study. Compared with baseline, sleep deprivation increased low-frequency (1.25-7.0 Hz) EEG power in non-rapid eye movement (NREM) sleep in the placebo night. After administration of zolpidem, power in the 3.75-10.0 Hz range and 14. 25-16.0 Hz band was reduced. The largest decrease was observed in the theta band. Comparison with placebo revealed that zolpidem attenuated power in the entire 1.75-11.0 Hz range. The plasma concentration of zolpidem at 4.5 h after intake showed a positive correlation with the drug-induced difference in power from placebo in the 14.25-16.0 Hz band. Regional EEG analysis based on bipolar derivations along the antero-posterior axis disclosed, for NREM sleep, a drug-induced posterior shift of power in the frequency range of 7.75-9.75 Hz. Zolpidem did not affect rapid eye movemnt sleep spectra. We conclude that sleep deprivation and agonistic modulation of GABAA receptors have separate and additive effects on power spectra and that their effects are mediated by different neurophysiological mechanisms.

Serotonin-2 receptors and human sleep: effect of a selective antagonist on EEG power spectra.

To investigate the effect on the sleep EEG, a 1-mg oral dose of SR 46349B, a novel 5-HT2 antagonist, was administered three hours before bedtime. The drug enhanced slow wave sleep (SWS) and reduced stage 2 without affecting subjective sleep quality. In nonREM sleep (NREMS) EEG slow-wave activity (SWA; power within 0.75-4.5 Hz) was increased and spindle frequency activity (SFA; power within 12.25-15 Hz) was decreased. The relative NREMS power spectrum showed a bimodal pattern with the main peak at 1.5 Hz and a secondary peak at 6 Hz. A regional analysis based on bipolar derivations along the antero-posterior axis revealed significant 'treatment' x 'derivation' interactions within the 9-16 Hz range. In enhancing SWA and attenuating SFA, the 5-HT2 receptor antagonist mimicked the effect of sleep deprivation, whereas the pattern of the NREMS spectrum differed.