The Influence of Biological Rhythms on Sleep-Wake Regulation
The timing of major night-time sleep is governed in a large part by the endogeneous circadian pacemaker. Under conditions of normal daily life, such dependence is reflected in the tendency for major nocturnal sleep to be initiated five to six hours prior to the temperature minimum and terminated shortly after the minimum. For most people, this corresponds roughly to sleep onset times of between 11 pm and midnight, and wake-up times of between about 6 am to 7 am. Because most humans exhibit similar timing in sleep-wake behavior, societal demands have evolved to accommodate such biological timetables. For a small percentage of the population, however, there is a misalignment between the endogeneous clock that governs sleep and the sleep/wake schedule that is desired, or which is regarded as the societal norm. These individuals are said to have circadian rhythm sleep disorders. This class of sleep disorders can be grouped further into two general categories – extrinsic and intrinsic types. Extrinsic types are those in which the disorder is brought on by an alteration in the environment relative to sleep timing, for example, jet lag, or shift work sleep disorder. Circadian rhythm sleep disorders of the intrinsic type are those that occur as a result of the endogeneous clock being altered relative to the (social) environment. That the biological clock can be reset to conform to social schedules, without markedly improving sleep quality, has etiologic implications as well. Alleviation of the rhythm disturbance in the absence of enhanced sleep quality clearly suggests that the sleep disorder aspect of circadian rhythm sleep disorders may include pathophysiology beyond their relationship to the circadian timing system. A current model of sleep regulation hypothesizes that the timing and composition of sleep are controlled by two interacting processes. It is quite likely that circadian rhythm sleep disorders are the result not only of alterations in circadian factors, but also disturbances in so-called Process S, the non-circadian factor proposed by the model. It is also likely that the reverse is true. That is, in sleep disorders such as primary insomnia, it has to be taken into account that these disorders may also be affected by a circadian dysfunctioning. This would suggest that not only Process S is altered but the possible deviations of the course of Process C should be considered as a contributing factor to insomnia. As such, a clear differentiation between classification of sleep disorders such as insomnia and as circadian rhythm disorders becomes less evident.