Diane B. Boivin

As the thermoregulation centres are deep in the brain, the cerebral temperature is one of the most important markers of fever, circadian rhythms physical and mental activities. However due to a lack of accessibility, the brain temperature is not easily measured. The axillary, buccal, tympanic and rectal temperatures do not reflect exactly the cerebral temperature. Nevertheless the rectal temperature is used as probably the most reliable indicator of the core body temperature. The brain temperature can be measured using NMR spectroscopy, microwave radiometry, near infrared spectroscopy, ultra-sound thermometry. However none of those methods are amenable to long term ambulatory use outside of the laboratory or of the hospital during normal daily activities, sport, etc. The brain core temperature "BCT" sensor, developed by the Biomedical Microsensors dpt of LPM at INSA-Lyon is a flexible active sensor using "zero-heat-flow" principle. The sensor has been used for experimental measurement: brain temperature during mental activity, and in hospital for the study of circadian rhythms. The results are in agreement with the measurement by the rectal probe. There are 2 versions of this sensor: a non ambulatory for the use in hospitals, and an ambulatory version using teletransmission. We are working for improving the autonomy of the ambulatory version up to several days. This wearable biomedical sensor (WBS) can be used for circadian assessment for chronobiology studies and in medical therapies

As the thermoregulation centres are deep in the brain, the cerebral temperature is one of the most important markers of fever, circadian rhythms physical and mental activities. However due to a lack of accessibility, the brain temperature is not easily measured. The axillary, buccal, tympanic and rectal temperatures do not reflect exactly the cerebral temperature. Nevertheless the rectal temperature is used as probably the most reliable indicator of the core body temperature. The brain temperature can be measured using NMR spectroscopy, microwave radiometry, near infrared spectroscopy, ultra-sound thermometry. However none of those methods are amenable to long term ambulatory use outside of the laboratory or of the hospital during normal daily activities, sport, etc. The brain core temperature "BCT" sensor, developed by the Biomedical Microsensors dpt of LPM at INSA-Lyon is a flexible active sensor using "zero-heat-flow" principle. The sensor has been used for experimental measurement: brain temperature during mental activity, and in hospital for the study of circadian rhythms. The results are in agreement with the measurement by the rectal probe. There are 2 versions of this sensor: a non ambulatory for the use in hospitals, and an ambulatory version using teletransmission. We are working for improving the autonomy of the ambulatory version up to several days. This wearable biomedical sensor (WBS) can be used for circadian assessment for chronobiology studies and in medical therapies

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. 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. 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 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.

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 ...

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.

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.

Recent evidence shows that the temporal alignment between the sleep-wake cycle and the circadian pacemaker affects self-assessment of mood in healthy subjects. Despite the differences in affective state between healthy subjects and patients with psychiatric disorders, these results have implications for analyzing diurnal variation of mood in unipolar and bipolar affective disorders and sleep disturbances in other major psychiatric conditions such as chronic schizophrenia. In a good proportion of patients with depression, mood often improves over the course of the day; an extension of waking often has an antidepressant effect. Sleep deprivation has been described as a treatment for depression for more than 30 years, and approximately 50% to 60% of patients with depression respond to this approach, especially those patients who report that their mood improves over the course of the day. The mechanisms by which sleep deprivation exerts its antidepressant effects are still controversial, but a reduction in rapid eye movement sleep (REM sleep), sleep pressure and slow-wave sleep (SWS), or a circadian phase disturbance, have been proposed. Although several studies support each of these hypotheses, none is sufficient to explain all observations reported to date. Unfortunately, the disturbed sleep-wake cycle or behavioural activities of depressed patients often explain several of the abnormalities reported in the diurnal rhythms of these patients. Thus, protocols that specifically manipulate the sleep-wake cycle to unmask the expression of the endogenous circadian pacemaker are greatly needed. In chronic schizophrenia, significant disturbances in sleep continuity, REM sleep, and SWS have been consistently reported. These disturbances are different from those observed in depression, especially with regard to REM sleep. Circadian phase abnormalities in schizophrenic patients have also been reported. Future research is expected to clarify the nature of these abnormalities.