Abstract

Recurrent depressions that begin late in the fall and resolve in the spring have been called winter seasonal affective disorder (SAD) (Rosenthal et al., 1984). Typically, this clinical syndrome is characterized by predominance of «atypicab> depressive symptoms, such as hyperpliagia, carbohydrate craving, hypersomnolence and fatigue. Accumulating evidence indicates that bright light treatment (BLT) induces considerable improvement of psychic and vegetative functions in winter depression (Rosenthal et al., 1984). Whereas there has been extensive study on biological basis of SAD, it still remains uncertain what are the physiological mechanisms which produce the therapeutic effect of bright light exposure. According to the phase-shift hypothesis (Lewy et al., 1988), endogenous circadian rhythms in most SAD patients are abnormally phase-delayed with respect to real time or sleep time and bright light in the morning can correct this phase disturbance by an advance shift of circadian pacemaker. Antidepressant effects of treatments administered at times other than morning were explained by an energizing effect of bright light (which may partly or wholly be a nonspecific placebo effect). The energizing effect of BLT could be either additive to the antidepressant phase-advancing effect of morning light, or opposite to the depressant effect of phase delay with evening light (Lewy et al., 1988). Earlier we reported that clinical response to BLT is related to such chronopliysiological effects as phase advance (Putilov et al., 1996) and intensification of non-rapid eye movement sleep (Palchikov et al., 1997).

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