CHRONOBIOLOGICAL ASPECTS OF CYCLOTHYMIA

Abstract

The paradoxical effect of sleep deprivation in endogenous depression has renewed the traditional interests of psychiatrists in the rhythmic phenomena associated with the symptomatology and course of cyclothymia. The development of clinical research on sleep, neuroendocrinology, chronobiology and chronopathology in conjunction with important developments of methodology and statistical procedures have enabled a modern reconceptualization of the relationship between cyclothymia and disturbances in biological rhythms. Chronobiological aspects of sleep disturbances were examined to differentiate those disturbances which are specific to cyclothymia from those which are more generally characteristic of serious sleep disorders. Sleep disturbances in depressives are similar to those in healthy subjects who have experienced experimental sleep reversal, suggesting an hypothesis that sleep disturbance in cyclothymia is of a similar character. To test this hypothesis, 24-h studies of sleep-waking cycles and longitudinal studies of the course of manic-depressive cycles are recommended. Among the many psychometric, endocrinological, biochemical and physiological studies, a few merit special attention because they are methodologically suggestive of productive avenues of research, e.g., the studies on episodic secretion of cortisol, 24-h EEG recordings with appropriate frequency analyses, and 24-h registration of psychomotor activity. Investigations of these parameters indicate a disturbance in the rather complex temporal organization of circadian and ultradian rhythmical phenomena. This new conceptualization of pathogenetic aspects of cyclothymia was derived from empirical data and current theory about the temporal regulation of biological rhythms in the organism. An insufficiency of the mechanisms of internal synchronization is considered to be the basic genetic disturbance. The manifestation of depression is associated primarily with quantifiable internal and external desynchronizations, and secondarily, with instability of ultradian rhythms as well as with infradian rhythms detectable in the temporal course of cyclothymia. The times in which cyclothymic phases are manifest with highest probability are conceptualized as periods of increased risk of desynchronization. This conceptualization of cyclothymia may be related to the catecholamine and serotonin hypotheses, since monoaminergic neurons play a central role in the temporal regulation of sleep-waking cycles, in the neuroendocrinological regulation, and in other mechanisms of internal and external synchronization. Thus, for example, an insufficiency of internal mechanisms of synchronization could be the manifestation of an insufficiency in the functions of certain groups of serotonergic or noradrenergic neurons. The chronobiological model introduced may help to explain the therapeutic effect of sleep deprivation, and simultaneously provide a new starting point for the investigation of cyclothymia and its treatment. Methodological presupposition and difficulties connected with clinical chronobiological research are outlined.