The studies examined in this review indicate that the MSL is sensitive to conditions expected to increase sleepiness. MSL are generally lower following sleep loss, following use of sedating medications, during wakefulness in the late night or early morning hours, and among patients with sleep disorders associated with excessive sleepiness such as narcolepsy or obstructive sleep apnea. However, the wide range in MSL makes it difficult to establish a specific threshold value for excessive sleepiness or to discriminate patients with sleep disorders from non-patients. Some of this variation may be attributable to methodological differences and some may be attributable to individual differences in sleep tendency (e.g., related to age). The studies analyzed in this review indicate that the MSL on both the MSLT and MWT does not discriminate well between patients with sleep disorders and normal populations. This is due to large SD as well as floor or ceiling effects in the tests. However, the MSL shows appropriate change from initial testing to subsequent testing following treatment or manipulations intended to alter sleepiness or alertness. Additionally the presence of two or more SOREMPs on the MSLT is a common finding in narcolepsy patients. However, SOREMPs are not exclusive to narcolepsy patients but are frequent in untreated sleep apnea

REM sleep behaviour disorder (RBD) is an injurious clinical disorder of attempted dream-enactment ('oneirism') in humans which has a corresponding experimental animal model involving dorsolateral pontine tegmental lesions in cats. To date, our sleep disorders centre has collected data on 96 chronic RBD cases which can be compared with pooled data on 70 chronic RBD cases from other centres contained in 26 reports published in the world literature since 1985, when our initial cases were first reported. The data from our centre and from other centres demonstrate a male predominance in RBD (87.5% vs 63.5%); indicate a similar mean age of RBD onset (52.4 y vs 55.9 y); contain substantial numbers of diverse central nervous system disorders causally associated with RBD (47.9% vs 60.0%); and identify clonazepam treatment as being very effective in controlling both the (violent) dream and sleep behavioural disturbances of RBD. Our centre's data additionally reveal an 80% prevalence of elevated stage 3/4 (slow-wave) sleep% for age in RBD, and reveal a frequent presence of periodic and aperiodic limb movements during NREM sleep. Thus, RBD in humans is a complex syndrome in which there is generalized REM and NREM sleep motor dyscontrol, as was originally observed in the animal RBD model by Jouvet and Delorme in 1965.

Over a 5-yr period, 19 adults presented to our sleep disorders center with histories of involuntary, nocturnal, sleep-related eating that usually occurred with other problematic nocturnal behaviors. Mean age (+/- SD) at presentation was 37.4 (+/- 9.1) yr (range 18-54); 73.7% of the patients (n = 14) were female. Mean age of sleep-related eating onset was 24.7 (+/- 12.9) yr (range 5-44). Eating occurred from sleep nightly in 57.9% (n = 11) of patients. Chief complaints included excessive weight gain, concerns about choking while eating or about starting fires from cooking and sleep disruption. Extensive polysomnographic studies, clinical evaluations and treatment outcome data identified three etiologic categories for the sleep-related eating: (a) sleepwalking (SW), 84.2% (n = 16); (b) periodic movements of sleep (PMS), 10.5% (n = 2) and (c) triazolam abuse (0.75 mg hs), 5.3% (n = 1). DSM-III Axis 1 psychiatric disorders (affective, anxiety) were present in 47.4% (n = 9) of the patients, and only two patients had a daytime eating disorder (anorexia nervosa), each in remission for 3-7 yr. Nearly half of all patients fulfilled established criteria for being overweight, based on the body mass index. Onset of sleep-related eating was linked directly to the onset of SW, PMS, triazolam abuse, nicotine abstinence, chronic autoimmune hepatitis, narcolepsy, encephalitis or acute stress. In the SW group, 72.7% (8/11) of patients had nocturnal eating and other SW behavior suppressed by clonazepam (n = 7) and/or bromocriptine (n = 2) treatment. Both patients with PMS likewise responded to treatment with combinations of carbidopa/L-dopa, codeine and clonazepam. Thus, sleep-related eating disorders can generally be controlled with treatment of the underlying sleep disorder.

Prominent eye movements during NREM sleep and REM sleep behavior disorder associated with fluoxetine treatment of depression and obsessive-compulsive.

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