SUMMAR Y Daytime performance changes were examined during chronic sleep restriction or augmentation and following subsequent recovery sleep. Sixty-six normal volunteers spent either 3 (n ¼ 18), 5 (n¼ 16), 7 (n ¼ 16), or 9 h (n ¼ 16) daily time in bed (TIB) for 7 days (restriction ⁄ augmentation) followed by 3 days with 8 h daily TIB (recovery). In the 3-h group, speed (mean and fastest 10% of responses) on the psychomotor vigilance task (PVT) declined, and PVT lapses (reaction times greater than 500 ms) increased steadily across the 7 days of sleep restriction. In the 7-and 5-h groups speed initially declined, then appeared to stabilize at a reduced level; lapses were increased only in the 5-h group. In the 9-h group, speed and lapses remained at baseline levels. During recovery, PVT speed in the 7-and 5-h groups (and lapses in the 5-h group) remained at the stable, but reduced levels seen during the last days of the experimental phase, with no evidence of recovery. Speed and lapses in the 3-h group recovered rapidly following the first night of recovery sleep; however, recovery was incomplete with speed and lapses stabilizing at a level comparable with the 7-and 5-h groups. Performance in the 9-h group remained at baseline levels during the recovery phase. These results suggest that the brain adapts to chronic sleep restriction. In mild to moderate sleep restriction this adaptation is sufficient to stabilize performance, although at a reduced level. These adaptive changes are hypothesized to restrict brain operational capacity and to persist for several days after normal sleep duration is restored, delaying recovery.k e y w o r d s chronic sleep

The negative effects of sleep deprivation on alertness and cognitive performance suggest decreases in brain activity and function, primarily in the thalamus, a subcortical structure involved in alertness and attention, and in the prefrontal cortex, a region subserving alertness, attention, and higher‐order cognitive processes. To test this hypothesis, 17 normal subjects were scanned for quantifiable brain activity changes during 85 h of sleep deprivation using positron emission tomography (PET) and 18Fluorine‐2‐deoxyglucose (18FDG), a marker for regional cerebral metabolic rate for glucose (CMRglu) and neuronal synaptic activity. Subjects were scanned prior to and at 24‐h intervals during the sleep deprivation period, for a total of four scans per subject. During each 30 min 18FDG uptake, subjects performed a sleep deprivation‐sensitive Serial Addition/Subtraction task. Polysomnographic monitoring confirmed that subjects were awake. Twenty‐four hours of sleep deprivation, reported here, resulted in a significant decrease in global CMRglu, and significant decreases in absolute regional CMRglu in several cortical and subcortical structures. No areas of the brain evidenced a significant increase in absolute regional CMRglu. Significant decreases in relative regional CMRglu, reflecting regional brain reductions greater than the global decrease, occurred predominantly in the thalamus and prefrontal and posterior parietal cortices. Alertness and cognitive performance declined in association with these brain deactivations. This study provides evidence that short‐term sleep deprivation produces global decreases in brain activity, with larger reductions in activity in the distributed cortico‐thalamic network mediating attention and higher‐order cognitive processes, and is complementary to studies demonstrating deactivation of these cortical regions during NREM and REM sleep.

SUMMAR Y As both military and commercial operations increasingly become continuous, 24-h-perday enterprises, the likelihood of operator errors or inefficiencies caused by sleep loss and/or circadian desynchrony also increases. Avoidance of such incidents requires the timely application of appropriate interventions -which, in turn, depend on the ability to measure and monitor the performance capacity of individuals in the operational environment. Several factors determine the potential suitability of candidate measures, including their relative sensitivity, reliability, content validity, intrusiveness and cumbersomeness/fieldability. In the present study, the relative sensitivity (defined as the ratio of effect size to 95% confidence interval) of several measures to the effects of sleep loss was compared in a sleep restriction experiment, in which groups were allowed 3, 5, 7, or 9 h time in bed (TIB) across seven consecutive nights. Of the measures compared, the Psychomotor Vigilance Test was among the most sensitive to sleep restriction, was among the most reliable with no evidence of learning over repeated administrations, and possesses characteristics that make it among the most practical for use in the operational environment.k e y w o r d s effect size, fieldability, performance measures, sleep loss

This field-portable reaction time test and analysis software run on devices using the Palm operating system. It is designed to emulate a test and commercial device widely used in sleep deprivation, shift work, fatigue, and stimulant drug research but provides additional capabilities. Experimental comparisons with the standard commercial device in a 40-hour total sleep deprivation study show it to be comparably sensitive to selected experimental variables. A Pocket PC-compatible version is under developement.

This study assessed the ability of high doses of caffeine to reverse changes in alertness and mood produced by prolonged sleep deprivation. Fifty healthy, nonsmoking males between the ages of 18 and 32 served as volunteers. Following 49 h without sleep, caffeine (0, 150, 300, or 600 mg/70 kg, PO) was administered in a double-blind fashion. Measures of alertness were obtained with sleep onset tests, the Stanford Sleepiness Scale (SSS), and Visual Analog Scales (VAS). Sleep deprivation decreased onset to sleep from a rested average of 19.9 min to 7 min. Following the highest dose of caffeine tested, sleep onset averaged just over 10 min; sleep onset for the placebo group averaged 5 min. Scores on the SSS increased from a rested mean of 1.6-4.8 after sleep deprivation. Caffeine reduced this score to near rested values. Caffeine reversed sleep deprivation-induced changes in three subscales of the POMS (vigor, fatigue, and confusion) and produced values close to fully rested conditions on several VAS. Serum caffeine concentrations peaked 90 min after ingestion and remained elevated for 12 h. This study showed that caffeine was able to produce significant alerting and long-lasting beneficial mood effects in individuals deprived of sleep for 48 h.

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Sleep deprivation impairs alertness and cognitive performance, and these deficits suggest decreases in brain activity and function, particularly in the prefrontal cortex, a region subserving alertness, attention, and higher-order cognitive processes and in the thalamus, a subcortical structure involved in alertness and attention. To substantiate this premise, we characterized the effects of 24, 48, and 72 h of progressive sleep deprivation on brain activity by assessing regional cerebral metabolic rate for glucose (CMRglu) during complex cognitive task performance in 17 young, normal, healthy male volunteers using positron emission tomography (PET) and l8 Fluoro-2-deoxyglucose ( 18 FDG). The results of prolonged sleep deprivation, 48 and 72 h, are reported here. Compared to rested baseline (RB), global CMRglu decreased by 6% at 48 and 72 h sleep deprivation (SD) and approximated the 8% decrease seen at 24 h SD. Absolute and relative regional CMRglu decreased at 48 and 72 h SD primarily in the prefrontal and parietal cortices and in the thalamus, the same areas that showed decreases at 24 h SD. Compared to 24 h SD, relative regional CMRglu decreased further in the prefrontal cortex and dorsal thalamus at 48 and 72 h, and at 72 h SD in a limited area of medial visual cortex. Relative regional CMRglu increased in lateral superior occipital cortices, lingual and fusiform gyri, anterior cerebellum, and in primary and supplementary motor cortices at 48 and 72 h SD, indicating a rebound CMRglu activity response from 24 h SD. Polysomnographic monitoring confirmed that subjects were awake. Behavioral outcomes showed continuing decreases in alertness, cognitive performance, and saccadic velocity (a measure of oculomotor response) with prolonged sleep deprivation. Progressive decreases in relative CMRglu values in prefrontal, thalamic, and primary visual areas were correlated positively with the impairments in cognitive performance and saccadic velocity across the 72 h sleep deprivation period. Relative thalamic activity was also correlated with the alterations in alertness. The prefrontal and thalamic regions were positively correlated, suggesting that sleep deprivation impacted these areas together as a functional network.We propose that the decreases in CMRglu induced in the prefrontal-thalamic network by prolonged sleep deprivation underlie the decline in alertness and cognitive performance and signify the brain's involuntary progression toward sleep onset, while the increases in visual and motor areas express the brain's exertion of voluntary control to remain awake and perform. This exertion of voluntary control is manifest in increased subject effort and physical movement, and the recruitment of additional brain regions may reflect an attempt to sustain alertness and cognitive performance despite a continuing decline in prefrontal-thalamic activity. Our findings provide support for the notion of a specific sensitivity of the prefrontal cortex to, and a pivotal role of the thalamus in, sleepiness.