Pulsed radio frequency radiation affects cognitive performance and the waking electroencephalogram.

We investigated the effects of radio frequency electromagnetic fields on brain physiology. Twenty-four healthy young men were exposed for 30 min to pulse-modulated or continuous-wave radio frequency electromagnetic fields (900 MHz; peak specific absorption rate 1 W/kg), or sham exposed. During exposure, participants performed cognitive tasks. Waking electroencephalogram was recorded during baseline, immediately after, and 30 and 60 min after exposure. Pulse-modulated radio frequency electromagnetic field exposure reduced reaction speed and increased accuracy in a working-memory task. It also increased spectral power in the waking electroencephalogram in the 10.5-11 Hz range 30 min after exposure. No effects were observed for continuous-wave radio frequency electromagnetic fields. These findings provide further evidence for a nonthermal biological effect of pulsed radio frequency electromagnetic fields.

Adenosinergic mechanisms contribute to individual differences in sleep deprivation-induced changes in neurobehavioral function and brain rhythmic activity.

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 (<1 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 caffeine-sensitive 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 <1 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.

Random number generation during sleep deprivation: effects of caffeine on response maintenance and stereotypy.

Neurophysiological and functional imaging studies have demonstrated that frontal regions of the brain are particularly responsive to homeostatic sleep pressure. Previous neuropsychological studies indicate that sleep deprivation causes impairments in prefrontal cortical function. Random number generation (RNG) is thought to provide a sensitive index of executive functions that rely on the prefrontal cortex. The present study tested the hypothesis that sleep deprivation would impair RNG and that caffeine would mitigate this impairment. Healthy young men (n = 21) participated in two 40-h sleep deprivations 1 week apart. During each sleep deprivation period subjects received either caffeine or placebo according to a randomized, double-blind cross-over design, and they completed an oral RNG task at 3-h intervals. Comparison of test sessions at analogous times of day revealed that sleep deprivation was associated with significant drops in the number of responses, a threefold increase in the percentage of rule violations, 59% greater response redundancy and a 20% increase in stereotypy of adjacent response pairs. Sleep deprivation did not consistently alter counting tendency. Caffeine ameliorated the decrease in the number of responses but did not mitigate other deficits in RNG that arose during sleep deprivation. These findings are consistent with prior reports of diminished vigilance and increased perseveration during extended wakefulness. They support the conclusion that caffeine preserves simple aspects of cognitive performance during sleep deprivation, whereas caffeine may not prevent detrimental effects of sleep deprivation on some complex cognitive functions.

Sleep inertia: performance changes after sleep, rest and active waking.

Napping benefits and sustains subsequent performance. Prophylactic naps have been recommended as a means to maintain performance during extended wakefulness, as required during shiftwork. However, napping may cause short-term performance impairments, because awakening from sleep is followed by sleep inertia, a period of hypovigilance and impaired cognitive and behavioral performance. We investigated sleep inertia after an afternoon nap. Healthy 18-28 year-olds (n=50, not sleep deprived) were assigned to sleep, active wake or rest groups for a 2-h experimental phase with polysomnography starting either at 14:00 or 16:00 for half of each group. Before (baseline, 12:30 or 14:30) and in five sessions during the hour after the experimental phase (16:00-17:00 or 18:00-19:00), subjects completed an addition task, an auditory reaction time task, and the Stanford Sleepiness Scale. In session one, addition speed in the sleep group was reduced compared with baseline and with active wake controls, whereas calculation accuracy did not change. Addition speed in the sleep and rest groups increased substantially from session one to session two and reached a level similar to that of the active wake group by the fifth session. In the first session, auditory reaction speed of the sleep group was reduced compared with baseline and with rest controls but did not differ from the active wake group. The slowest reaction times showed significant recovery after 20 min. The groups reported similar increases in subjective sleepiness after the experimental period. These findings provide evidence for performance slowing and recovery during the hour following a 2-h nap opportunity. They highlight the importance of employing multiple control groups and various objective and subjective measures to assess sleep inertia.

Caffeine attenuates waking and sleep electroencephalographic markers of sleep homeostasis in humans.

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.