Adolescents with Sleep Disturbance: Causes and Diagnosis

Abstract

In our previous study, circadian rhythm sleep disorders have been reported in pediatric and adolescent populations (Tomoda, Miike, Uezono, & Kawasaki, 1994). Pediatric practitioners now commonly encounter sleep disturbance in previously healthy children and adolescents (Boergers, Hart, Owens, Streisand, & Spirito, 2007; Giannotti, Cortesi, Sebastiani, & Ottaviano, 2002; Stein, Mendelsohn, Obermeyer, Amromin, & Benca, 2001). The characteristic clinical features are well known, but the specific causes remain unknown. New types of circadian rhythm sleep disorders, such as familial advanced sleep phase syndrome (ASPS) and delayed sleep phase syndrome (DSPS), non-24-h sleep-wake syndrome (non-24), and morningnesseveningness have been described during the last decade. Such disorders are probably caused by various disturbances of circadian expression of the clock gene (Archer et al., 2003; Ebisawa et al., 2001; Iwase et al., 2002; Pirovano et al., 2005; Takimoto et al., 2005; Toh et al., 2001; Wijnen, Boothroyd, Young, & Claridge-Chang, 2002). Polymorphisms in clock genes are known to induce circadian rhythm sleep disorders. For example, mutations in the period2 (Per2) gene (S662G) or casein kinase1 d (CK16) gene (T44A) cause familial ASPS; furthermore, missense polymorphisms in the Per3 (V647G) and CK1e (S408N) genes increase or decrease the risk of developing DSPS. In our clinical practices, we recognized that the majority of our patients have a circadian rhythm disorder even though they usually do not mention or recognize this problem at the first interview. We hypothesized that there could be certain relationship between biological rhythm disorders in these patients and their indefinite symptoms as well as their sleep disturbances. This chapter introduces sleep patterns, circadian rhythms of core body temperature (CBT), glucose metabolism, and human clock gene profile in children and adolescents with sleep disturbance.