There are many situations in which it would be useful to know the phase state of the biological clock. It is recognized that measurement of melatonin levels can provide this information, but traditionally blood has been used for the analysis, and there are many problems in extending the measurements into the home or field situations. The aim of this study was to develop and validate a salivary melatonin radioimmunoassay and to compare results obtained against a plasma assay for determining the onset of melatonin secretion. The assay developed was sensitive (4.3 pM) and required only 200 microliters of sample. A rhythm in melatonin was detected in saliva, peaking at approximately 120 pM or 30% of the plasma levels. Using an objective criterion for determining the onset of secretion (mean +/- 2 standard deviations of three daytime samples), the time of onset was shown to exhibit low intraindividual variability (coefficient of variation = 1.5%-4.3%). The time of onset determined using saliva was significantly correlated with the plasma onset (r = .70, p < .05). The onsets determined were 22:30 h +/- 22 min for the saliva and 21:50 h +/- 16 min for plasma for 17 subjects. Similarly, the acrophases of the saliva and plasma melatonin rhythms were significantly correlated. Neither posture alone nor changes in posture affected the calculation of the onset of melatonin secretion using the saliva approach. Very high saliva flow rates induced by citric acid resulted in lower melatonin concentrations compared to the gentle chewing on parafin film. These results firmly establish the use of salivary melatonin measurements for phase typing of the melatonin rhythm in humans.
Sleep disordered breathing in children is a common but largely underdiagnosed problem. It ranges in severity from primary snoring to obstructive sleep apnea syndrome (OSAS). Preliminary evidence suggests that children with severe OSAS show reduced neurocognitive performance, however, less is known about children who snore but do not have severe upper airway obstruction. Participants included 16 children referred to the Ear, Nose and Throat/Respiratory departments of a Children's Hospital for evaluation of snoring and 16 non-snoring controls aged 5-10 years. Overnight polysomnography (PSG) was carried out in 13 children who snored and 13 controls. The PSG confirmed the presence of primary snoring in seven and very mild OSAS (as evidenced by chest wall paradox) in eight children referred for snoring while controls showed a normal sleep pattern. To test for group differences in neurocognitive functioning and behavior, children underwent one day of testing during which measures of intelligence, memory, attention, social competency, and problematic behavior were collected. Compared to controls, children who snored showed significantly impaired attention and, although within the normal range, lower memory and intelligence scores. No significant group differences were observed for social competency and problematic behavior. These findings suggest that neurocognitive performance is reduced in children who snore but are otherwise healthy and who do not have severe OSAS. They further imply that the impact of mild sleep disordered breathing on daytime functioning may be more significant than previously realized with subsequent implications for successful academic and developmental progress.
These studies confirm the mediating role of intershift-shift recovery in the evolution of adaptive end-of-shift fatigue states to maladaptive persistent fatigue traits. The OFER scale is suggested as a potentially valuable new tool for use in work-related fatigue research.
The 10-min psychomotor vigilance task (PVT) has often been used to assess the impact of sleep loss on performance. Due to time constraints, however, regular testing may not be practical in field studies. The aim of the present study was to examine the suitability of tests shorter than 10 min. in duration. Changes in performance across a night of sustained wakefulness were compared during a standard 10-min PVT, the first 5 min of the PVT, and the first 2 min of the PVT. Four performance metrics were assessed: (1) mean reaction time (RT), (2) fastest 10% of RT, (3) lapse percentage, and (4) slowest 10% of RT. Performance during the 10-min PVT significantly deteriorated with increasing wakefulness for all metrics. Performance during the first 5 min and the first 2 min of the PVT deteriorated in a manner similar to that observed for the whole 10-min task, with all metrics except lapse percentage displaying significant impairment across the night. However, the shorter the task sampling time, the less sensitive the test is to sleepiness. Nevertheless, the 5-min PVT may provide a viable alternative to the 10-min PVT for some performance metrics.
The findings demonstrate the effectiveness of timed exposure to bright light in the treatment of age-related sleep maintenance insomnia. With further refinement of treatment regimens, this non-drug intervention may prove useful in a large proportion of sleep disturbed elderly.
Early studies on the physiological effects of melatonin typically reported hypnotic 'side-effects' . Later studies, specifically addressing this action, failed to reliably replicate hypnotic effects using standard polysomnography . This difference may be related to differences in the basic physiological action of melatonin compared with more conventional hypnotics. It is suggested that melatonin exerts a hypnotic effect through thermoregulatory mechanisms. By lowering core body temperature, melatonin reduces arousal and increases sleep-propensity. Thus, in humans, one role of melatonin is to transduce the light-dark cycle and define a window-of-opportunity in which sleep-propensity is enhanced. As such, melatonin is likely to be an effective hypnotic agent for sleep disruption associated with elevated temperature due to low circulating melatonin levels. The combined circadian and hypnotic effects of melatonin suggest a synergistic action in the treatment of sleep disorders related to the inappropriate timing of sleep and wakefulness. Adjuvant melatonin may also improve sleep disruption caused by drugs known to alter normal melatonin production ( e g , P-blockers and benzodiazepines). If melatonin is to be developed as a successful clinical treatment, differences between the pharmacological profile following exogenous administration and the normal endogenous rhythm should be minimized. Continued development as a useful clinical tool requires control of both the amplitude and duration of the exogenous melatonin pulse. There is a need to develop novel drug delivery systems that can reliably produce a square-wave pulse of melatonin at physiological levels for 8-10 hr duration.
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