La malveille. Hypersomnie, somnolence, clinophilie

Abstract

Excessive daytime sleepiness (EDS) is a very frequent symptom and can be considered as a semiotic interface between psychiatry, neurology, pneumology, endocrinology an internal medicine. Whenever a patient enters the psychiatrist office with an EDS complain, the practitioner has to cautiously evaluate the various conditions possibly responsible for this symptom and must integrate the treatment of EDS in his global therapeutic strategy. In both cases, the psychiatrist may find considerably helpful the intervention of a sleep medicine specialist. If clinical investigation is usually sufficient to diagnose the origin of EDS, polysomnography is mandatory to evaluate the severity of an obstructive sleep apnoea syndrome (OSAS) or a narcolepsy. Hypersomnia, frequently mixed up with sleepiness, is so common and its definition is so fuzzy that most of psychiatrists do not further investigate this aspect during the initial assessment. Some differences must be made between hypersomnia (increased sleep time >10 h per day), sleepiness (intermediate state between sleep and wakefulness, occurring usually during daytime), clinophily (the subject does not sleep even lying) and affective withdrawal (the subject is prostrated but can be very anxious or delusional). In the general population the frequency of hypersomnia varies between 0.5 and 8.7% depending on the definition. The best tool to evaluate hypersomnia is the sleep log: sleep time is self-recorded daily during one month. In the psychiatric field it is impossible to simply get rid of the somatic causes of EDS. In fact EDS can be secondary to a depression, but a real depression can commonly be the consequence of an OSAS even if the treatment of respiratory events is rarely sufficient to cure the depression. Moreover, OSAS can be associated to impotence, alcoholism, behaviour or memory disorders that are matters of concern for the psychiatrist. Narcolepsy and idiopathic hypersomnia are both associated to depression due to the decrease of the cognitive and social activities induced by the reduction of wakefulness during daytime. EDS is obviously a symptom of atypical and seasonal affective disorders (SAD). Atypical depression associates personality and mood disorders when SAD associates sadness, hypersomnia and bulimia (mainly for carbo-hydrates). Usually sleep polysomnography reveals less sleep than expected and the symptomatology is intermediary between hypersomnia and clinophily. Here clinophily is associated with an illusion of sleep called “agrypnagnosia”. Last but not least, most of the psychotropic drugs have sedative side effects, especially antidepressants and anxiolytics. The use, and abuse, of these drugs is a common cause of EDS and must be investigated systematically. If the “true” hypersomnia is relatively rare, a reduction of the daytime vigilance and an increase of the time spent in bed are common in psychiatry, although few studies have been specifically dedicated to this topic. These symptoms are frequently associated with resistant depression and decreased quality of life. Moreover, EDS can cause traffic accidents or occupational injuries and the psychiatrist engages his legal responsibility on this point.