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Sleep Initiation and Maintenance Disorders: HELP
Articles by Emmanuel Mignot
Based on 4 articles published since 2009
(Why 4 articles?)
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Between 2009 and 2019, Emmanuel Mignot wrote the following 4 articles about Sleep Initiation and Maintenance Disorders.
 
+ Citations + Abstracts
1 Article Familial Kleine-Levin Syndrome: A Specific Entity? 2016

Nguyen, Quang Tuan Remy / Groos, Elisabeth / Leclair-Visonneau, Laurène / Monaca-Charley, Christelle / Rico, Tom / Farber, Neal / Mignot, Emmanuel / Arnulf, Isabelle. ·National Reference Center for Narcolepsy, Idiopathic Hypersomnia and Kleine-Levin Syndrome, Sleep Disorders Unit and Hospital-University Institute of Neuroscience, Pitié-Salpêtrière Hospital (APHP), Pierre and Marie Curie University, Paris, France. · Regional Competence Center for Narcolepsy, Idiopathic Hypersomnia and Kleine-Levin Syndrome, Laennec University Hospital, Nantes, France. · Regional Competence Center for Narcolepsy, Idiopathic Hypersomnia and Kleine-Levin Syndrome, Salengro University Hospital, Lille, France. · Center for Sleep Sciences and Medicine, Stanford University, Palo Alto, CA. · Kleine-Levin Syndrome Foundation, Boston, MA. ·Sleep · Pubmed #27253765.

ABSTRACT: STUDY OBJECTIVES: Kleine-Levin syndrome (KLS) is a rare, mostly sporadic disorder, characterized by intermittent episodes of hypersomnia plus cognitive and behavior disorders. Although its cause is unknown, multiplex families have been described. We contrasted the clinical and biological features of familial versus sporadic KLS. METHODS: Two samples of patients with KLS from the United States and France (n = 260) were studied using clinical interviews and human leukocyte antigen (HLA) genotyping. A multiplex family contained two or more first- or second-degree affected relatives (familial cases). RESULTS: Twenty-one patients from 10 multiplex families (siblings: n = 12, including two pairs of monozygotic twins; parent-child: n = 4; cousins: n = 2; uncle-nephews: n = 3) and 239 patients with sporadic KLS were identified, yielding to 4% multiplex families and 8% familial cases. The simplex and multiplex families did not differ for autoimmune, neurological, and psychiatric disorders. Age, sex ratio, ethnicity, HLA typing, karyotyping, disease course, frequency, and duration of KLS episodes did not differ between groups. Episodes were less frequent in familial versus sporadic KLS (2.3 ± 1.8/y versus 3.8 ± 3.7/y, P = 0.004). Menses triggered more frequently KLS onset in the nine girls with familial KLS (relative risk, RR = 4.12, P = 0.03), but not subsequent episodes. Familial cases had less disinhibited speech (RR = 3.44, P = 0.049), less combined hypophagia/hyperphagia (RR = 4.38, P = 0.006), more abrupt termination of episodes (RR = 1.45, P = 0.04) and less postepisode insomnia (RR = 2.16, P = 0.008). There was similar HLA DQB1 distribution in familial versus sporadic cases and no abnormal karyotypes. CONCLUSION: Familial KLS is mostly present in the same generation, and is clinically similar to but slightly less severe than sporadic KLS.

2 Article Physiology. The perfect hypnotic? 2013

Mignot, Emmanuel. ·Center for Sleep Sciences, Stanford University, Palo Alto, CA 94304, USA. mignot@stanford.edu ·Science · Pubmed #23559238.

ABSTRACT: -- No abstract --

3 Article Faster REM sleep EEG and worse restedness in older insomniacs with HLA DQB1*0602. 2011

Zeitzer, Jamie Marc / Fisicaro, Ryan Anthony / Grove, Megan Elizabeth / Mignot, Emmanuel / Yesavage, Jerome Albert / Friedman, Leah. ·Department of Psychiatry and Behavioral Sciences, Stanford University, Stanford CA, United States. jzeitzer@stanford.edu ·Psychiatry Res · Pubmed #21292329.

ABSTRACT: HLA DQB1*0602 is found in most individuals with hypocretin-deficient narcolepsy, a disorder characterized by a severe disruption of sleep and wake. Population studies indicate that DQB1*0602 may also be associated with normal phenotypic variation of rapid eye movement (REM) sleep. Disruption of REM sleep has been linked to specific symptoms of insomnia. We here examine the relationship of sleep and DQB1*0602 in older individuals (n=46) with primary insomnia, using objective (polysomnography, wrist actigraphy) and subjective (logs, scales) measures. DQB1*0602 positivity was similarly distributed in the older individuals with insomnia (24%) as in the general population (25%). Most sleep variables were statistically indistinguishable between DQB1*0602 positive and negative subjects except that those with the allele reported that they were significantly less well rested than those without it. When sleep efficiencies were lower than 70%, DQB1*0602 positive subjects reported being less well rested at the same sleep efficiency than those without the allele. Examination of EEG during REM sleep also revealed that DQB1*0602 positive subjects had EEG shifted towards faster frequencies compared with negative subjects. Thus, DQB1*0602 positivity is associated with both a shift in EEG power spectrum to faster frequencies during REM sleep and a diminution of restedness given the same sleep quantity.

4 Article DQB1*0602 predicts interindividual differences in physiologic sleep, sleepiness, and fatigue. 2010

Goel, Namni / Banks, Siobhan / Mignot, Emmanuel / Dinges, David F. ·Division of Sleep and Chronobiology, Unit for Experimental Psychiatry, Department of Psychiatry, University of Pennsylvania School of Medicine, 1013 Blockley Hall, Philadelphia, PA 19104-6021, USA. goel@mail.med.upenn.edu ·Neurology · Pubmed #20975052.

ABSTRACT: OBJECTIVE: The human leukocyte antigen (HLA) DQB1*0602 allele is closely associated with narcolepsy, a neurologic disorder characterized by excessive daytime sleepiness, fragmented sleep, and shortened REM sleep latency. We evaluated whether DQB1*0602 was a novel marker of interindividual differences by determining its relationship to sleep homeostatic, sleepiness, and cognitive responses to baseline and chronic partial sleep deprivation (PSD) conditions. METHODS: Ninety-two DQB1*0602-negative and 37 DQB1*0602-positive healthy adults participated in a protocol of 2 baseline 10 hours time in bed (TIB) nights followed by 5 consecutive 4 hours TIB nights. DQB1*0602 allelic frequencies did not differ significantly between Caucasians and African Americans. RESULTS: During baseline, although DQB1*0602-positive subjects were subjectively sleepier and more fatigued, they showed greater sleep fragmentation, and decreased sleep homeostatic pressure and differentially sharper declines during the night (measured by non-REM EEG slow-wave energy [SWE]). During PSD, DQB1*0602-positive subjects were sleepier and showed more fragmented sleep, despite SWE elevation comparable to negative subjects. Moreover, they showed differentially greater REM sleep latency reductions and smaller stage 2 reductions, along with differentially greater increases in fatigue. Both groups demonstrated comparable cumulative decreases in cognitive performance. CONCLUSIONS: DQB1*0602 positivity in a healthy population may represent a continuum of some sleep-wake features of narcolepsy. DQB1*0602 was associated with interindividual differences in sleep homeostasis, physiologic sleep, sleepiness, and fatigue-but not in cognitive measures-during baseline and chronic PSD. Thus, DQB1*0602 may represent a genetic biomarker for predicting such individual differences in basal and sleep loss conditions.