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Hypersomnia is characterized by a propensity to fall asleep in situations when one is expected to be awake and alert. It may present with prolonged sleep episodes coupled with excessive daytime sleepiness (EDS) and frequent napping. It is described in narcolepsy, a neurological disorder characterized by EDS occurring with or without cataplexy; in idiopathic hypersomnia, also of central origin, characterized by EDS and episodes of prolonged nocturnal sleep; in recurrent hypersomnias, rare disorders manifesting with recurrent episodes of more or less continuous sleep (average duration of 1 week), recurring at highly variable intervals (one to several months), such as, Kleine–Levin syndrome and menstrual-related hypersomnia. Chronic sleep loss and/or poor sleep quality may be underlying reasons for EDS; these occur in numerous sleep disorders, such as obstructive sleep apnea (OSA) and in psychiatric disorders, particularly depression. Approximately 80% of depressive states are associated with insomnia; patients do not necessarily have a higher propensity to fall asleep in daytime but report subjective sleepiness that differs from the EDS encountered in narcolepsy and OSA. There are also hypersomnias attributable to other medical conditions, drugs, or substances, as well as behaviorally induced hypersomnia caused by insufficient time to sleep.
Transition between sleep and wakefulness is simply described as oscillations between two opponent processes, one promoting sleep, another promoting wakefulness. The complex neurobiological mechanisms and the neurotransmitters and neuromodulators underlying these processes, including noradrenergic, serotonergic, cholinergic, adenosinergic, and histaminergic systems and more recently, the hypocretin/orexin and dopamine systems, have been established. The mechanisms of action of some vigilance-promoting agents are as follows: psychostimulants act through enhanced dopamine action (amphetamines, methylphenidate) or acetylcholine action (caffeine); modafinil may act through enhanced central histamine, hypocretin, and possibly dopamine action; ? -hydroxybutyrate (GHB), acts on GABA and GHB receptors. EDS in narcolepsy is traditionally treated with psychostimulants; these are rarely effective in idiopathic hypersomnia, although this was not examined through randomized controlled trials. Modafinil, a first-line wakefulness-promoting medication, is a useful alternative to psychostimulants for EDS in narcolepsy (Level I evidence). It may be effective for EDS due to idiopathic hypersomnia (one Level IV study and expert consensus). It is not associated with rebound hypersomnolence, cardiovascular problems, or abuse potential, as may be seen with amphetamines. Modafinil alleviates sleepiness and fatigue in shift work disorders, residual sleepiness in treated sleep apnea syndrome, multiple sclerosis, Parkinson's disease and depression. It is promising as an alternative to psychostimulants for excessive fatigue associated with medical and psychiatric disorders and as an augmentation medication for treatment-resistant depression. Due to rare serious complications (allergic and psychiatric), the EMA concluded that its benefit/risk balance was positive for narcolepsy but negative for other sleep disorders and neurological diseases, including idiopathic hypersomnia. The FDA has approved it for EDS in narcolepsy, shift work sleep disorder, and OSA. In narcolepsy, GHB at bedtime reduces nocturnal awakenings, increases stage 3 and 4 sleep, and consolidates REM sleep periods; these effects coincide with improvement in daytime symptoms, including cataplexy.