Work at unconventional hours can have both long and short term consequences. Shift workers are often required to perform their duties at times that are not favoured by the body's endogenous clock, or circadian pacemaker. A typical night shift worker, for example, may report reductions in alertness and performance during shifts, or significant difficulty attaining sleep of recuperative value in the day, all the while being more likely to develop health complications. The study of circadian physiology has significantly contributed to our current ability to aid the shift worker deal with atypical schedules. We discuss the usefulness of light treatment as a countermeasure for maladaptation to atypical work schedules.

The efficacy of a light/darkness intervention designed to promote circadian adaptation to night shift work was tested in this combined field and laboratory study. Six full-time night shift workers (mean age ± SD:37.1 ± 8.1 yrs) were provided an intervention consisting of an intermittent exposure to full-spectrum bright white light (∼2000 lux) in the first 6 h of their 8 h shift, shielding from morning light by tinted lenses (neutral gray density, 15% visual light transmission), and regular sleep/darkness episodes in darkened quarters beginning 2 h after the end of each shift. Five control group workers (41.1 ± 9.9 yrs) were observed in the presence of a regular sleep/darkness schedule only. Constant routines (CR) performed before and after a sequence of ∼12 night shifts over 3 weeks revealed that treatment group workers displayed significant shifts in the time of peak cortisol expression and realignment of the rhythm with the night-oriented schedule. Smaller phase shifts, suggesting an incomplete adaptation to the shift work schedule, were observed in the control group. Our observations support the careful control of the pattern of light and darkness exposure for the adaptation of physiological rhythms to night shift work.

The Interactive Neurobehavioral Model integrates Kronauer's and Jewett's latest mathematical model of the resetting effect of light on the human circadian pacemaker. This model is based on several lines of experimental evidence and considers the endogenous circadian pacemaker as a complex oscillatory system that responds dynamically to the resetting effect of light. This model can help us understand the results of an experiment using intermittent bright light exposure in the workplace environment. Intermittent exposure to bright light was effectively used as part of an intervention to promote circadian re-entrainment of a group of nurses to their permanent night work schedule. Regular exposure to lower light levels and darkness also provided a significant phase delay of endogenous circadian rhythms, although the adaptation was incomplete in this group of workers. These last results are consistent with the intensity-dependent component of the model. The development of better tools to measure retinal exposure to light throughout the 24-h day is required to adequately test modeling predictions under field conditions.

STUDY OBJECTIVE:We investigated whether the hypernyctohemeral syndrome (non-24-hour sleep-wake syndrome) may show a clinical association with the delayed sleep phase syndrome (DSPS) in a 39-year-old woman who developed sleep disturbances following a traumatic brain injury.MEASUREMENTS AND RESULTS:Sleep-wake log documentation and wrist-activity recordings for more than 6 consecutive months confirmed the patient's tendency to live on longer-than-24-hour "days." Episodes of relative coordination to the 24-hour day were also noted, suggesting that the patient was transiently in and out of phase with environmental synchronizers too weak to fully entrain her to the geophysical environment. Interestingly, we noted a tendency to initiate sleep between 3:00 am and 5:00 am and wake up from sleep between noon and 1:00 pm.CONCLUSIONS:These results support an association between the hypernyctohemeral syndrome and the DSPS. This association may carry implications for the treatment of circadian rhythms disorders.

The authors report the case of a 39-year-old sighted woman who displayed non-24-hour sleep-wake cycles following a car accident. The phase relationship between endogenous circadian markers such as plasma melatonin and 6-sulfatoxymelatonin rhythms and self-selected sleep times was abnormal. A laboratory investigation indicated that she was sensitive to bright light as a circadian synchronizer. MRI and brain CT scans were normal, but microscopic brain damage in the vicinity of the suprachiasmatic nucleus or its output pathways is plausible.

The acute disruption in sleep quality, vigilance levels, and cognitive and athletic performance observed after transmeridian flights is presumed to be the result of a transient misalignment between the endogenous circadian pacemaker and the shifted sleep schedule. Several laboratory and field experiments have demonstrated that exposure to bright artificial light can accelerate circadian entrainment to a shifted sleep-wake schedule. In the present study, the authors investigated whether the schedule of exposure to indoor room light, to which urban dwellers are typically exposed, can substantially affect circadian adaptation to a simulated eastward voyage. We enrolled 15 healthy young men in a laboratory simulation of a Montreal-to-London voyage. Subjects were exposed to 6 h of room light (mean ± SD: 379 ± 10) prior to bedtime ( n = 7) or when on a progressively advancing schedule ( n = 8) early in the day. The remaining 10 hours of wakefulness were spent in dim light (4 ± 1 lux). Circadian assessments, performed via the constant routine procedure, evaluated the phase of the endogenous circadian rhythms of core body temperature and plasma melatonin before and after 1 week on the shifted schedule. At the end of the study, only subjects exposed to room light on the advancing schedule expressed oscillations of the endogenous circadian pacemaker in phase with the new sleep-wake cycle. In this group, a mean advance shift of the nadir of core body temperature of +5:22 ± 0:15 h was observed, with parallel shifts in plasma melatonin concentration and subjective alertness. The circadian rhythms of subjects exposed to room light later in the day remained much more adjusted to the departure than to the destination time zone. These results demonstrate that the schedule of exposure to room light can substantially affect circadian adaptation to a shifted sleep-wake schedule.

In this combined field and laboratory investigation, the authors tested the efficacy of an intervention designed to promote circadian adaptation to night-shift work. Fifteen nurses working permanent night schedules ([.greaterequal] 8 shifts/ 15 days) were recruited from area hospitals. Following a vacation period of [.greaterequal] 10 days on a regular daytime schedule, workers were admitted to the laboratory for the assessment of circadian phase via a 36-h constant routine. They returned to work ~ 12 night shifts on their regular schedules under one of two conditions. Treatment group workers (n = 10, mean age ± SD = 41.7 ± 8.8 years) received an intervention including 6 h of intermittent bright-light exposure in the workplace (~ 3243 lux) and shielding from bright morning outdoor light with tinted goggles (15% visual light transmission). Control group workers (n = 9, mean age ± SD = 42.0 ± 7.2 years) were observed in their habitual work environments. On work days, participants maintained regular sleep/wake schedules including a single 8-h sleep/darkness episode beginning 2 h after the end of the night shift. A second 36-h constant routine was performed following the series of night shifts. In the presence of the intervention, circadian rhythms of core body temperature and salivary melatonin cycles were delayed by an average (± SEM) of –9.32 ± 1.06 h and –11.31 ± 1.13 h, respectively. These were significantly greater than the phase delays of –4.09 ± 1.94 h and –5.08 ± 2.32 h displayed by the control group (p = 0.03 and p = 0.02, respectively). The phase angle between circadian markers and the shifted schedule was reestablished to its baseline position only in the treatment group of workers. These results support the efficacy of a practical intervention for promoting circadian adaptation to night-shift work under field conditions. They also underline the importance of controlling the overall pattern of exposure to light and darkness in circadian adaptation to shifted sleep/wake schedules.