**1. Introduction**

30 Sleep Disorders

[16] Roy MS, Roy A, Brown S. Increased urinary-free cortisol outputs in diabetic patients. *J* 

[17] Chiodini I, Di Lembo S, Morelli V, Epaminonda P, Coletti F, Masserini B, et al.

[18] Lustman P, Carney R, Amado H. Acute stress and metabolism in diabetes. *Diabetes* 

[19] Spiegel K, Leproult R, Van Cauter E. Impact of sleep debt on metabolic and endocrine

[20] Sandoval DA, Ping L, Neill AR, Morrey S, Davis SN. Cortisol acts through central

[22] Gietzen KF, Virshup DM. Identification of inhibitory autophosphorylation sites in

[23] Jones CR, Campbell SS, Zone SE, Cooper F, DeSano A, Murphy PJ, et al. Familial

[24] Takano A, Uchiyama M, Kajimura N, Mishima K, Inoue Y, Kamei Y, et al. A missense

[25] Vanselow K, Vanselow JT, Westermark PO, Reischl S, Maier B, Korte T, et al.

[27] Tomoda A, Miike T, Yamada E, Honda H, Moroi T, Ogawa M, et al. Chronic fatigue

[28] Tomoda A, Jhodoi T, Miike T. Chronic fatigue and abnormal biological rhythms in

Hypothalamic-pituitary-adrenal activity in type 2 diabetes mellitus: role of

mechanisms to blunt counterregulatory responses to hypoglycemia in conscious

advanced sleep-phase syndrome: A short-period circadian rhythm variant in

variation in human casein kinase I epsilon gene that induces functional alteration and shows an inverse association with circadian rhythm sleep disorders.

Differential effects of PER2 phosphorylation: molecular basis for the human familial advanced sleep phase syndrome (FASPS). *Genes Dev* 2006;20(19):2660-72. [26] Tomoda A, Miike T, Yonamine K, Adachi K, Shiraishi S. Disturbed circadian core body

temperature rhythm and sleep disturbance in school refusal children and

*Diabetes Complications* 1998;12(1):24-7.

function. *Lancet* 1999;354(9188):1435-9.

rats. *Diabetes* 2003;52(9):2198-204.

humans. *Nat Med* 1999;5(9):1062-5.

*Neuropsychopharmacology* 2004;29(10):1901-9.

adolescents. *Biol Psychiatry* 1997;41(7):810-3.

syndrome in childhood. *Brain Dev* 2000;22(1):60-4.

school children. *J Chronic Fatigue Syndrome* 2001;60:607-12.

*Care* 1981;4(6):658-9.

autonomic imbalance. *Metabolism* 2006;55(8):1135-40.

[21] Hastings MH. Central clocking. *Trends Neurosci* 1997;20(10):459-64.

casein kinase I epsilon. *J Biol Chem* 1999;274(45):32063-70.

ADHD is an increasingly prevalent developmental disorder, especially in the western world where prevalence rates are estimated around 12%.

According to both the DSM-IV and the ICD-10 it refers to three major problematic domains: attention, hyperactivity and impulsivity. Subtypes of ADHD have been coded accordingly as a predominantly hyperactive-impulsive type (H), predominantly inattentive (I) and a combined type (C).

Age is an important factor in the clinical/behavioral manifestations of ADHD. Symptoms, in fact, vary according to brain maturation. The hyperactive aspects, for instance, tend to subside with age, even if longitudinal research demonstrated that over 30% of children with ADHD grow up to be adults with significant ADHD related problems.

Gender also plays an important role in ADHD, with a 1:10 male prevalence in clinical samples (Cortese et al., 2006). It also appears to have a strong influence over behavioral symptoms and co-morbid disorders, which appear generally less disruptive in girls.

ADHD holds a high potential for psychiatric and cognitive co-morbidity (mood, anxiety, conduct disorder and learning disability), with a nearly 50% rate of oppositional defiant conduct in males.
