As

the nights pass by, sleep debt increases. The insufficient sleep syndrome causes 5% to 10% of consultations for excessive daytime sleepiness.27 The subject is generally an active or overactive 40-year-old man, with responsibilities and a high social status. The syndrome can also be related to shift work or frequent transmeridian airplane trips. As the sleep debt develops, the individual starts suffering from excessive somnolence in the afternoon, Inhibitors,research,lifescience,medical in the evening, or after meals. Patients report that they sleep 5 to 6 h nightly on weekdays, and 9 h during the weekends. They have difficulty rising in the morning and sometimes experience sleep drunkenness-like episodes. Work and cognitive performance, as well as Inhibitors,research,lifescience,medical decision-making, may be impaired. The patient may also find protocol complain of increasing levels of subjective fatigue, mood deterioration, muscular pain, gastrointestinal upset, and visual disturbances. Symptoms disappear on weekends and during the holidays. The diagnosis is mainly performed during interview. However, in cases of a suspected associated pathology, such as respiratory disturbances during sleep, a polysomnographic recording may be indicated. In the case of insufficient Inhibitors,research,lifescience,medical sleep syndrome, this recording will show a good sleep efficiency (>90%) and short sleep latency, indicative of a sleep rebound. Medication- and toxin-dependent sleepiness Numerous medications are

potentially responsible for excessive daytime sleepiness, such as hypnotic, anxiolytic, antidepressant, neuroleptic, antihistaminic, Inhibitors,research,lifescience,medical antiepileptic (except for lamotrigine), and antiparkinsonian drugs. Alcohol presents sedative or stimulant effects, which depend on dosage and individual susceptibility.28 Acute alcohol consumption may delay or, in contrast, advance sleep induction. REM sleep is postponed to the second half of the night and SWS increases in the first half. Discontinuation of alcohol consumption is often reported to be followed by an REM sleep Inhibitors,research,lifescience,medical rebound. Chronic alcoholics

sleep poorly, with a reduced amount of REM sleep, sleep being composed almost exclusively of nonREM sleep. Acute withdrawal is accompanied by more frequent REM sleep episodes determining a shortening of REM-non-REM sleep cycles with decreased SWS. Hallucinations occurring in this condition have been hypothesized to be related to REM sleep fragmentation and/or rebound. In chronic alcoholics who become sober, shortened REM latency, elevated REM percentages, Ribonucleotide reductase and high REM density,29 as well as lowered SWS percentages,30 have been reported as predictors of relapse. Interview should eliminate such drug-sleep interactions. In the case of drug-induced hypersomnia, careful and progressive withdrawal and/or substitution must be undertaken. Treatment withdrawal from stimulants could in fact be expected to lead to a rebound of sleep, as is the well-known case in sleep deprivation.31 Such a rebound is not observed.