The diagnosis of RBD was made on the basis of the presence of a clinical history of agitated motor activity occurring repeatedly during sleep for at least 6 months, associated with dream mentation, and the presence of at least one documented episode of abnormal motor behavior occurring during REM sleep in the sleep laboratory. Sixteen patients with “idiopathic” RBD (11 men and 5 women mean age at PSG ± SD, 59.9 ± 7.9 years) were included. The selection process was carried out blind with regard to the presence of abnormal behavior during nocturnal sleep recording. ![]() Narcoleptic patients were randomly selected from our narcoleptic population in order to be sex- and age-matched with patients with “idiopathic” RBD. The presence of hypnagogic hallucinations and sleep paralysis was also noted. The Epworth sleepiness scale (ESS) 18was administered to assess daytime sleepiness, and the mean score was 19.5 ± 2.1. 16, 17 The mean frequency of cataplexy was 3.9 ± 1.0. The frequency of cataplectic attacks was assessed on a scale from 1 to 5, in which 1 represents one or fewer cataplectic attack per year, 2 represents more than one cataplectic attack per year but fewer than one per month, 3 represents more than one cataplectic attack per month but fewer than one per week, 4 represents more than one cataplectic attack per week but fewer than one per day, and 5 represents severe cases with at least one cataplectic attack per day. ![]() All patients had sleep latency <7 min on the MSLT. Results of the MSLT showed a mean sleep latency of 2.7 ± 1.7 min. 16 Mean age at onset of narcolepsy was 24.2 ± 14.1 years, and mean duration of the disease was 36.3 ± 15.7 years. 15 The standard criterion for the diagnosis of narcolepsy is the presence of 2 SOREMPs 6 however, we reported recently that the number of SOREMPs decreases with age, and a substantial number of narcoleptics of more than 50 years of age had only 1 SOREMP. Inclusion criteria for narcolepsy were the presence of both excessive daytime sleepiness and cataplexy, the presence of the HLA-DR2 antigen, and at least one sleep onset REM period (SOREMP) during the multiple sleep latency test (MSLT). Each patient had a clinical evaluation by a sleep specialist followed by at least one night of polysomnographic recording. Sixteen patients with narcolepsy and cataplexy (11 men and 5 women mean age at PSG ± SD, 59.0 ± 6.5 years) were included. The aim of the present study was to assess in narcoleptic patients the REM sleep characteristics known to be impaired in RBD: REM sleep without atonia, REM sleep chin EMG phasic activities, and REM density, and to compare these results with results obtained in patients with RBD and normal controls. 13 As hypocretin neurons are excitatory and active during wakefulness with strong projections to the brainstem structures implicated in REM sleep motor regulation, 14 decreased hypocretinergic tone may cause REM sleep without atonia and RBD in humans. 12 Recent results based on detailed anatomy and lesion experiments in rats have identified independent pathways in brainstem that mediate the atonia and EEG phenomena of REM sleep. 1, 3– 5 The loss of hypocretin neurons within the lateral hypothalamus causes narcolepsy in humans. ![]() Both have increased PLMS at night with a specific increase of PLMS in REM sleep 10– 11 both have dissociated manifestations of REM sleep with a loss of REM sleep muscle atonia in RBD and the inappropriate occurrence of atonia during wakefulness (cataplexy) in narcolepsy. Patients with narcolepsy and those diagnosed with RBD share several common polygraphic features, especially signs of REM sleep dysregulation. 7– 9 In these latter cases, it is termed “secondary RBD.” However, it is often associated with other neurological diseases such as lesions of the brainstem, neurodegenerative disease, especially synucleinopathies, and narcolepsy. 6 RBD may occur alone and is then called “idiopathic” RBD. The presence of REM sleep without atonia associated with prominent motor behavioral manifestations associated with dreaming during REM sleep is the key feature of a condition called REM sleep behavior disorder (RBD). 2 Abnormalities in REM sleep motor regulation have been described in narcolepsy, including persistence of muscle tone, excessive twitching, and periodic leg movements during sleep (PLMS). 1 Normal REM sleep is characterized by tonic features, including cortical EEG desynchronization and muscle atonia, and phasic events, including bursts of rapid eye movements, phasic activities of both chin and limb EMG, and cardiorespiratory variability. ![]() NARCOLEPSY IS CHARACTERIZED BY THE PRESENCE OF EXCESSIVE DAYTIME SLEEPINESS AND CLINICAL MANIFESTATIONS OF DISSOCIATED RAPID EYE MOVEMENT (REM) sleep including cataplexy, hypnagogic and hypnopompic hallucinations, and sleep paralysis.
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