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DOI: 10.1177/074873049501000204 © 1995 SAGE Publications Light Treatment for Sleep Disorders: Consensus ReportII. Basic Properties of Circadian Physiology and Sleep RegulationInstitute of Pharmacology, University of Zürich, Winterthurerstrasse 190, CH-8057, Zürich, Switzerland
Institute for Circadian Physiology, 1 Alewife Center, Cambridge, MA 02140
Biological Rhythms Research Laboratory, Rush-Presbyterian-St. Luke's Medical Center, 1653 West Congress Parkway, Chicago, IL 60612
Department of Psychiatry, Oregon Health Sciences University, 3181 S.W. Sam Jackson Park Road, Portland, OR 97201
Laboratory of Human Chronobiology, New York Hospital, Cornell University Medical College, 21 Bloomingdale Road, White Plains, NY 10605
Department of Psychiatry, Columbia University and New York State Psychiatric Institute, 722 West 168th Street, New York, NY 10032 The rationale for the treatment of sleep disorders by scheduled exposure to bright light in seasonal affective disorder, jet lag, shift work, delayed sleep phase syndrome, and the elderly is, in part, based on a conceptual framework developed by nonclinical circadian rhythm researchers working with humans and other species. Some of the behavioral and physiological data that contributed to these concepts are reviewed, and some pitfalls related to their application to bright light treatment of sleep disorders are discussed. In humans and other mammals the daily light-dark (LD) cycle is a major synchronizer responsible for entrainment of circadian rhythms to the 24-h day, and phase response curves (PRCs) to light have been obtained. In humans, phase delays can be induced by light exposure scheduled before the minimum of the endogenous circadian rhythm of core body temperature (CBT), whereas phase advances are induced when light exposure is scheduled after the minimum of CBT. Since in healthy young subjects the minimum of CBT is located approximately 1 to 2 h before the habitual time of awakening, the most sensitive phase of the PRC to light coincides with sleep, and the timing of the monophasic sleep-wake cycle itself is a major determinant of light input to the pacemaker. The effects of light are mediated by the retinohypothalamic tract, and excitatory amino acids play a key role in the transduction of light information to the suprachiasmatic nuclei. LD cycles have direct "masking" effects on many variables, including sleep, which complicates the assessment of endogenous circadian phase and the interpretation of the effects of light treatment on sleep disorders. In some rodents motor activity has been shown to affect circadian phase, but in humans the evidence for such a feedback of activity on the pacemaker is still preliminary. The endogenous circadian pacemaker is a major determinant of sleep propensity and sleep structure; these, however, are also strongly influenced by the prior history of sleep and wakefulness. In healthy young subjects, light exposure schedules that do not curtail sleep but induce moderate shifts of endogenous circadian phase have been shown to influence the timing of sleep and wakefulness without markedly affecting sleep structure.
Key Words: sleep • circadian rhythms • light • phase response curve • entrainment • sleep homeostasis • nonphotic stimuli • REM sleep • slow-wave sleep • EEG analysis
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