SUMMAR Y Usage of mobile phones is rapidly increasing, but there is limited data on the possible effects of electromagnetic field (EMF) exposure on brain physiology. We investigated the effect of EMF vs. sham control exposure on waking regional cerebral blood flow (rCBF) and on waking and sleep electroencephalogram (EEG) in humans. In Experiment 1, positron emission tomography (PET) scans were taken after unilateral head exposure to 30-min pulse-modulated 900 MHz electromagnetic field (pm-EMF).In Experiment 2, night-time sleep was polysomnographically recorded after EMF exposure. Pulse-modulated EMF exposure increased relative rCBF in the dorsolateral prefrontal cortex ipsilateral to exposure. Also, pm-EMF exposure enhanced EEG power in the alpha frequency range prior to sleep onset and in the spindle frequency range during stage 2 sleep. Exposure to EMF without pulse modulation did not enhance power in the waking or sleep EEG. We previously observed EMF effects on the sleep EEG

Prolonged wakefulness increases electroencephalogram (EEG) low-frequency activity (< 10 Hz) in waking and sleep, and reduces spindle frequency activity (approximately 12-16 Hz) in non-rapid-eye-movement (nonREM) sleep. These physiologic markers of enhanced sleep propensity reflect a sleep-wake-dependent process referred to as sleep homeostasis. We hypothesized that caffeine, an adenosine receptor antagonist, reduces the increase of sleep propensity during waking. To test this hypothesis, we compared the effects of caffeine and placebo on EEG power spectra during and after 40 h of wakefulness. A total of 12 young men underwent two periods of sleep deprivation. According to a randomized, double-blind, crossover design, they received two doses of caffeine (200 mg) or placebo after 11 and 23 h of wakefulness. Sleep propensity was estimated at 3-h intervals by measuring subjective sleepiness and EEG theta (5-8 Hz) activity, and polysomnographic recordings of baseline and recovery nights. Saliva caffeine concentration decreased from 15.7 micromol/l 16 h before the recovery night, to 1.8 micromol/l 1 h before the recovery night. Compared with placebo, caffeine reduced sleepiness and theta activity during wakefulness. Compared with sleep under baseline conditions, sleep deprivation increased 0.75-8.0 Hz activity and reduced spindle frequency activity in nonREM sleep of the recovery nights. Although caffeine approached undetectable saliva concentrations before recovery sleep, it significantly reduced EEG power in the 0.75-2.0 Hz band and enhanced power in the 11.25-20.0 Hz range relative to placebo. These findings suggest that caffeine attenuated the build-up of sleep propensity associated with wakefulness, and support an important role of adenosine and adenosine receptors in the homeostatic regulation of sleep.

Brainstem and thalamic structures are known to play a critical role in modulating sleep-wake cycles, but the extent to which the cerebral hemispheres are involved remains unclear. To study the role of the cerebral hemispheres in generating sleep EEG patterns, all-night polysomnographic recordings were collected in subjects with brain damage (n = 30) caused by hemispheric stroke and in hospitalized controls (n = 12). Recordings were made in the acute (< or =10 days post-stroke), subchronic (11-35 days post-stroke) and chronic (>60 days post-stroke) phases of stroke. Bipolar and referential EEG derivations were recorded. Standard sleep stage scoring was conducted using the referential derivation placed opposite the lesion. Sleep stage 2 power and coherence spectra were calculated based on recordings from bipolar derivations. In the mean spectra, the highest spindle frequency peak was identified and its size was calculated relative to the background spectrum. Analysis of visually scored EEG data indicated that, compared with controls, acute phase brain-damaged subjects had lower sleep efficiency and increased waking after sleep onset. The durations of rapid eye movement and non-rapid eye movement sleep stages did not differ significantly between brain-damaged subjects and hospitalized controls. Spectral analyses revealed that, compared with hospitalized controls, brain-damaged subjects had significantly reduced spindle peak sizes in the power and coherence spectra from derivations ipsilateral to the lesion. Within-subject comparisons across time demonstrated that the power and coherence of sleep spindle frequency activity increased significantly from the acute to the chronic phases of stroke, suggesting that plastic mechanisms allowed the possibility of recovery. Our findings provide novel evidence that the cerebral hemispheres are important in generating coherent sleep spindles in humans, and they are consonant with prior empirical and theoretical evidence that corticothalamic projections modulate the generation of synchronous spindle oscillations. Because spindle oscillations are thought to be involved in blocking sensory input to the cortex during sleep, the decrease in synchronous spindle frequency activity following hemispheric stroke may contribute to the observed reduction in sleep continuity.

Large individual differences characterize the changes induced by sleep deprivation on neurobehavioral functions and rhythmic brain activity. To investigate adenosinergic mechanisms in these differences, we studied the effects of prolonged waking and the adenosine receptor antagonist caffeine on sustained vigilant attention and regional electroencephalogram (EEG) power in the ranges of theta activity (6.25-8.25 Hz) in waking and the slow oscillation (Ͻ1 Hz) in sleep. Activity in these frequencies is functionally related to sleep deprivation. In 12 subjectively caffeine-sensitive and 10 -insensitive young men, psychomotor vigilance task (PVT) performance and EEG were assessed at 3 h intervals before, during, and after one night without sleep. After 11 and 23 h waking, subjects received 200 mg caffeine and placebo in double-blind, cross-over manner. In the placebo condition, sleep deprivation impaired PVT speed more in caffeinesensitive than in caffeine-insensitive men. This difference was counteracted by caffeine. Theta power in waking increased more in a frontal EEG derivation than in a posterior derivation. Caffeine attenuated this power gradient in caffeine sensitive subjects. Sleep loss also differently affected the power distribution Ͻ1 Hz in non-rapid eye movement sleep between caffeine sensitive and insensitive subjects. Also, this difference was mirrored by the action of caffeine. The effects of sleep deprivation and caffeine on sustained attention and regional EEG power in waking and sleep were inversely related. These findings suggest that adenosinergic mechanisms contribute to individual differences in waking-induced impairment of neurobehavioral performance and functional aspects of EEG topography associated with sleep deprivation.