SLEEP

Jensen, Chad D; Duraccio, Kara M; Barnett, Kimberly A; Carbine, Kaylie A; Stevens, Kimberly S; Muncy, Nathan M; Kirwan, C Brock

doi: 10.1093/sleep/zsz001pmid: 30649528

Study ObjectivesSleep is an important behavior that affects appetite and eating in adolescents. Our study examined food-related neural activation in brain regions associated with food reward and inhibition in adolescents under sleep-restricted and well-rested conditions.MethodsIn this within-subjects study, 52 adolescents (ages 12–18; 46% female; M age = 15.96 years, SD = 1.56) with normal weight (NW; N = 29, M body mass index % [BMI%] = 54.55, SD = 24.54) or overweight/obesity (OV/OB; N = 23, M BMI% = 93.78, SD = 4.60) spent 5 hours in bed at home each night for five consecutive nights and 9 hours in bed at home each night for 5 consecutive nights, with the first day of each condition occurring 4 weeks apart. The morning following each sleep modification period, functional magnetic resonance imaging (fMRI) data were collected while participants performed an inhibitory (go/no-go) task with food stimuli.ResultsWe found significantly greater activation in brain regions associated with inhibition in adolescents with NW in response to food cues when sleep restricted. No increase in inhibition-related neural activation was observed in adolescents with OV/OB when sleep restricted. We also found neural activation consistent with greater reward processing associated with food cues following sleep restriction regardless of weight status.ConclusionsThese findings suggest that chronic sleep restriction may increase the likelihood of suboptimal dietary behavior for adolescents with OV/OB because they do not experience increased inhibition-related neural responding to counter possible increased reward-related neural responding following sleep restriction.

Cox, Simon R; Ritchie, Stuart J; Allerhand, Mike; Hagenaars, Saskia P; Radakovic, Ratko; Breen, David P; Davies, Gail; Riha, Renata L; Harris, Sarah E; Starr, John M; Deary, Ian J

doi: 10.1093/sleep/zsz019pmid: 30668819

We examined associations between self-reported sleep measures and cognitive level and change (age 70–76 years) in a longitudinal, same-year-of-birth cohort study (baseline N = 1091; longitudinal N = 664). We also leveraged GWAS summary data to ascertain whether polygenic scores (PGS) of chronotype and sleep duration related to self-reported sleep, and to cognitive level and change. Shorter sleep latency was associated with significantly higher levels of visuospatial ability, processing speed, and verbal memory (β ≥ |0.184|, SE ≤ 0.075, p ≤ 0.003). Longer daytime sleep duration was significantly associated slower processing speed (β = −0.085, SE = 0.027, p = 0.001), and with steeper 6-year decline in visuospatial reasoning (β = −0.009, SE = 0.003, p = 0.008), and processing speed (β = −0.009, SE = 0.002, p < 0.001). Only longitudinal associations between longer daytime sleeping and steeper cognitive declines survived correction for important health covariates and false discovery rate (FDR). PGS of chronotype and sleep duration were nominally associated with specific self-reported sleep characteristics for most SNP thresholds (standardized β range = |0.123 to 0.082|, p range = 0.003 to 0.046), but neither PGS predicted cognitive level or change following FDR. Daytime sleep duration is a potentially important correlate of cognitive decline in visuospatial reasoning and processing speed in older age, whereas cross-sectional associations are partially confounded by important health factors. A genetic propensity toward morningness and sleep duration were weakly, but consistently, related to self-reported sleep characteristics, and did not relate to cognitive level or change.

Williams, Paula G; Curtis, Brian J; Anderson, Jeffrey S

doi: 10.1093/sleep/zsz035pmid: 30946470

In an insightful Letter to the Editor (this issue), Massar and Chee elaborate on one interpretation of the findings of our recent report indicating that self-reported habitual short sleep duration is associated with increased delay discounting [1]. They accurately note that habitual short sleep duration may result from a tendency to choose instant gains over long-term benefits, in addition to or as an alternative to short sleep leading to increased delay discounting. We greatly appreciate their thoughtful elaborations on the mechanistic and clinical implications that result from a greater understanding of the directional association between sleep and impulsivity/self-control. In general agreement with Massar and Chee, we believe that there is almost certainly a reciprocal feed-forward association between cognitive individual differences (including delay discounting/impulsivity) and habitual short sleep. Indeed, the discussion can be broadened to highlight other possible (and related) cognitive-motivational tendencies underlying individual differences in habitual short sleep. An individual differences perspective would allow for more precise explication of mechanisms—an endeavor that, in turn, has implications for targeted intervention. Importantly, these “subtypes” of habitual short sleepers may all exhibit delay discounting, but the direction of effect, as well as the mechanisms underlying the association may be quite different. The distinction between habitual short sleepers who do not report daytime dysfunction and those that do is a critical one. In the case of the former, there is reason to believe that behavioral motivation characterized by high reward drive—along with impulsivity—may underlie the development and perpetuation of short sleep. Indeed, there is evidence that these habitual short sleepers are higher in extraversion [2], thought to reflect individual differences in the dopamine incentive reward system [3]. Related, these short sleepers exhibit tendencies consistent with a vigilance regulation model of ADHD and mania [4] whereby routinely seeking out stimulating activities may be both a behavioral strategy to override underlying daytime fatigue and sleepiness, as well as a manifestation of high reward drive and activity level. Further, there is a hypothesized feed-forward, reciprocal association—high activity, high reward-related impulsivity, and lack of perceived negative consequences (i.e., no subjective daytime dysfunction) drive habitual short sleep, which, in turn, leads to further decrements in cognitive functioning. Critically, as cognitive functioning declines, these habitual short sleepers may be increasingly inaccurate in their judgment of functional abilities. This is a variation of the Dunning–Kruger effect—that individuals with demonstrably poorer cognitive or intellectual functioning tend to erroneously assess their abilities as greater than they are [5]. For this reason, self-report measures of functionality, including trait measures of self-control, may be inaccurate. Massar and Chee refer to empirical work characterizing people who report “needlessly and voluntarily delaying going to bed, despite foreseeably being worse off as a result,” a behavioral tendency termed “bedtime procrastination [6].” For this subgroup of habitual short sleepers, there may be the appearance of bedtime procrastination, however the lack of foreseeable dysfunction means there are fewer intervention targets. That is, a focus on the negative outcomes that will result from inadequate sleep would not likely be effective because these individuals do not experience the fatigue or dysfunction that most other short sleepers experience. Indeed, our experience phenotyping short sleepers not reporting dysfunction [7] suggests that if these individuals come for sleep assessment and intervention at all, it is often at the insistence of concerned family members rather than out of distress over their lack of sleep. Given the hypothesized behavioral motivation tendencies and the lack of perceived negative consequences, intervention for this group of habitual short sleepers would likely require regimented, structured removal of access to stimulating nighttime activities. On the other hand, habitual short sleepers who experience the expected daytime dysfunction are likely a heterogeneous group. Some may routinely get short sleep for purely environmental reasons (e.g., multiple jobs, small children) and would, left to their own devices, get more sleep. For these short sleepers, associations with impulsivity are likely a consequence rather than a predictor of short sleep duration. Other habitual short sleepers with reported dysfunction, however, may have trait tendencies that predict and perpetuate short sleep duration over time. In particular, these short sleepers are likely prone to anxiety (i.e., high in neuroticism), sensitive to punishment cues (i.e., behavioral inhibition), and have high interoceptive awareness (i.e., feel fatigue and poor restoration resulting from short sleep). These individuals may meet criteria for insomnia and are at higher risk for the development of depression. Importantly, this collection of individual differences is also related to delay discounting/impulsivity but for different reasons than their high reward-drive counterparts. Impulsivity is hypothesized to be driven by negative affect, is worsened under conditions of life stress, and is sometimes termed “urgency” (see ref. [8]). Indeed, clinical depression is associated with delay discounting [9]. In individuals with these tendencies, bedtime procrastination and/or behaviors characteristic of poor sleep hygiene may be (maladaptive) efforts to manage anxiety. Intervention along the lines of those suggested by Massar and Chee may be useful for these short sleepers, given that they experience the negative consequences of short sleep duration. However, strategies to lower anxiety and presleep arousal may also be needed. In summary, we believe an individual differences framework would inform our understanding of the development and perpetuation of habitual short sleep duration. As others have described [10], careful examination of habitual short sleeper phenotypes would fill an important gap in the study of short sleep duration which has been studied predominantly through either experimental manipulation or large-scale epidemiology research. Given the growing list of adverse outcomes prospectively associated with short sleep duration, understanding the mechanisms underlying habitual short sleep seems imperative. Most crucially, is it the case that habitual short sleepers who do not report dysfunction are at the same risk as those that do? Can some people “get away” with less sleep than everyone else? Only by differentiating these groups, examining objective indicators of functioning in longitudinal studies, and as suggested by Massar and Chee, implementing mechanism-informed intervention studies, will we achieve clarity on this issue. Conflict of interest statement. None declared. References 1. Curtis BJ , et al. Objective cognitive functioning in self-reported habitual short sleepers not reporting daytime dysfunction: examination of impulsivity via delay discounting . Sleep . 2018 ; 41 ( 9 ): 1 – 9 . doi:10.1093/sleep/zsy115. Google Scholar Crossref Search ADS 2. Williams PG , et al. Are short sleepers who deny dysfunction more dysfunctional than normal sleepers ? Poster Present Annu Meet Assoc Res Personal Sacramento, CA . 2017 . 3. Wacker J , et al. Investigating the dopaminergic basis of extraversion in humans: a multilevel approach . J Pers Soc Psychol. 2006 ; 91 ( 1 ): 171 – 187 . Google Scholar Crossref Search ADS PubMed 4. Hegerl U , et al. The vigilance regulation model of affective disorders and ADHD . Neurosci Biobehav Rev . 2014 ; 44 : 45 – 57 . Google Scholar Crossref Search ADS PubMed 5. Kruger J , et al. Unskilled and unaware of it: how difficulties in recognizing one’s own incompetence lead to inflated self-assessments . J Pers Soc Psychol. 1999 ; 77 ( 6 ): 1121 – 1134 . Google Scholar Crossref Search ADS PubMed 6. Kroese FM , et al. Bedtime procrastination: a behavioral perspective on sleep insufficiency . In: Sirois FM, Pychyl TA, eds. Procrastination, Health, and Well-Being . Cambridge, MA: Academic Pres; 2016: 93 – 119 . 7. Curtis BJ , et al. Short sleeper syndrome (SSS): a possible sleep-duration, circadian, metabolic, affective, pain-tolerance, normal variant in humans . Sleep . 2011 ; 34 : A259 – A260 . 8. Whiteside SP , et al. The five factor model and impulsivity: using a structural model of personality to understand impulsivity . Pers Individ Dif . 2001 ; 30 ( 4 ): 669 – 689 . Google Scholar Crossref Search ADS 9. Pulcu E , et al. Temporal discounting in major depressive disorder . Psychol Med . 2014 ; 44 ( 9 ): 1825 – 1834 . Google Scholar Crossref Search ADS PubMed 10. Grandner MA , et al. Pack AI. Problems associated with short sleep: bridging the gap between laboratory and epidemiological studies . Sleep Med Rev . 2010 ; 14 ( 4 ): 239 – 247 . Google Scholar Crossref Search ADS PubMed © Sleep Research Society 2019. Published by Oxford University Press on behalf of the Sleep Research Society. All rights reserved. For permissions, please e-mail [email protected]. This article is published and distributed under the terms of the Oxford University Press, Standard Journals Publication Model (https://academic.oup.com/journals/pages/open_access/funder_policies/chorus/standard_publication_model)

Vozoris, Nicholas T

doi: 10.1093/sleep/zsy264pmid: 30657987

Study ObjectivesThe study objectives were to explore trends in prevalence of couse of benzodiazepine receptor modulators and opioids, and nonselective and selective (i.e. Z-drugs) benzodiazepine receptor modulators, in the United States, as well as risk factors for these drug utilization patterns.MethodsThis was a multiyear, cross-sectional, population-level study, using US health survey data. Data from eight National Health and Nutrition Examination Survey (NHANES) cycles were analyzed, from 1999–2000 until 2013–2014, with each survey cycle containing information on ~10 000 individuals. The main measure was prevalent prescription drug use within 30 days preceding survey administration. Drug usage was objectively confirmed for a large majority of participants though direct inspection of prescription bottles.ResultsThe estimated prevalence of concurrent benzodiazepine receptor modulator and opioid use in the United States was 0.39% in 1999–2000 and 1.36% in 2013–2014, reflecting absolute and relative changes of +0.97% and +249%. The estimated prevalence of nonselective and selective benzodiazepine receptor modulator couse steadily rose in the United States from 0.05% in 1999–2000 to 0.47% in 2013–2014, reflecting absolute and relative increases of +0.42% and +840%. Independent risk factors for these two forms of psychoactive medication polypharmacy were identified.ConclusionsIn this exploratory analysis, concurrent use of benzodiazepine receptor modulators and opioids, and nonselective and selective benzodiazepine receptor modulators, was found to have progressively risen in the United States. The progressive increases in these two forms of psychoactive medication polypharmacy are concerning, given that these drug use patterns are associated with increased risk for serious adverse outcomes.

Bliwise, Donald L

doi: 10.1093/sleep/zsz013pmid: N/A

Thirty-three years ago, in this very journal, Carlos H. Schenck, Mark W. Mahowald and colleagues published a now seminal paper describing Rapid Eye Movement Behavior Disorder (RBD) [1]. Initially viewed as perhaps nothing more than a curiosity among the somewhat dark and mysterious world of parasomnias, this condition now encompasses a huge body of clinical and scientific interest (with about 2000 PubMed citations as of January 2019). Components of this impressive mass of work have now been coalesced into the first scientific textbook about the topic, co-edited, not surprisingly, by Dr. Schenck of the University of Minnesota, along with Drs. Birgit Högl of the Medical University of Innsbruck and Aleksandar Videnovic of Massachusetts General Hospital/Harvard Medical School. This volume is rich in diversity and depth, covering topics ranging from the basic science underpinnings of RBD to technical considerations in the measurement of the condition to the now well-recognized potential of RBD as a harbinger of human alpha-synuclein neurodegenerative diseases, like Parkinsonism, from years to perhaps several decades in advance. Related to the latter, the book also deals forthrightly with the admittedly somewhat limited knowledge base related to treatment of RBD, not only as a symptomatic condition leading to potentially injurious behavior but also from the perspective of neuroprotection. Whether early identification of synucleinopathic conditions via RBD might be the first step towards successful prevention trials of late-life neurodegenerative diseases is certainly one of the most relevant and significant topics here. In fact, this issue has led recently to the federally funded North American Prodromal Synucleinopathy (NAPS) consortium, a first-of-its-kind group of investigators mandated with the establishment of a cohort of individuals with RBD, potentially eligible for enrollment in the future with such neuroprotective agents. An international focus is clearly present in the book, with active research groups from Austria, Canada, Denmark, France, Germany, Hong Kong, India, Italy, Japan, The Netherlands, Spain, and the United States all contributing substantially. Some of the more intriguing topics of current interest involve autonomic correlates of RBD, involving both heart and gut, as well as newer developments in brain neuroimaging, which attempt to link RBD to regional abnormalities involving specific ligand-derived SPECT and PET measurements or network-based connectivity dysfunction. Topics about which less certainty exists (RBD in paraneoplastic conditions, RBD in children and young adults) also get coverage, which speaks favorably regarding the Contributors and Editors wish to address not only what is known, but also what remains lesser known or unknown, about the condition. Textual material is well-presented with well-documented, primary source reference lists, a staple for others pursuing research in these areas. Non-textual material is presented clearly with good graphics, figures and tables, and whenever possible, photography, although, admittedly, it is difficult to fully capture the dynamics of full-blown dream enactment with still visual images. At 678 pages, the book is comprehensive, and one is hard-pressed to find topics that are not covered adequately. There are few topics in Sleep Medicine as engaging as RBD. Not only does the topic fully occupy an enticing interface between basic and clinical research, but it also “anchors” the field in a particular historical way. The modern field of Sleep Medicine takes origin in the discovery of REM sleep in the 1950s and the hundreds of studies on dreaming and its correlates published in the 1960s and 1970s. When a person acts out their dreams with ideation of events current and past and when we observe them doing so, it reminds us partially of the fascination with dreaming that beguiled so many of the early pioneers in the arena of Sleep Medicine, not to mention the “inveterate” topic of dreaming that has enchanted philosophers from the time of Aristotle and Plato [2]. For the many current researchers and clinicians studying RBD, the topic remains no less vexing, and just as enigmatic. References 1. Schenck CH , et al. Chronic behavioral disorders of human REM sleep: a new category of parasomnia . Sleep . 1986 ; 9 ( 2 ): 293 – 308 . Google Scholar Crossref Search ADS PubMed 2. Schiller F . The inveterate paradox of dreaming . Arch Neurol . 1985 ; 42 ( 9 ): 903 – 906 . Google Scholar Crossref Search ADS PubMed © Sleep Research Society 2019. Published by Oxford University Press on behalf of the Sleep Research Society. All rights reserved. For permissions, please e-mail [email protected]. This article is published and distributed under the terms of the Oxford University Press, Standard Journals Publication Model (https://academic.oup.com/journals/pages/open_access/funder_policies/chorus/standard_publication_model)

Bargiotas, Panagiotis; Lachenmayer, M Lenard; Schreier, David R; Mathis, Johannes; Bassetti, Claudio L

doi: 10.1093/sleep/zsz004pmid: 30649557

Study ObjectivesThe main objective of the study was to assess the prevalence, the severity, and the daytime course of excessive daytime sleepiness (EDS) in advanced Parkinson’s disease (PD) and to explore how people with PD perceive the degree and onset of their sleepiness during objective sleepiness tests. In addition, the occurrence of early-onset rapid eye movement (REM) periods (sleep-onset REM periods [SOREMPs]) in PD was assessed.MethodsWe analyzed data from 46 people with PD (26 males, mean age 63.5 years, mean UPDRS-III-OFF 34.7). The sleep–wake assessment included Epworth sleepiness scale (ESS), Karolinska sleepiness scale (KSS), and objective (polysomnography, multiple sleep latency test [MSLT], and maintenance of wakefulness tests [MWT]) measures.ResultsSubjective (ESS ≥ 10) and objective (mean sleep latency, MSL < 5 min in MSLT) EDS were present in 43% and 41% of patients, respectively. The MSL in MSLT and MWT remained unchanged throughout the day and significantly correlated with KSS during the trial but not with KSS shortly before it. In MWT, about one-fourth of patients failed to signal their sleepiness before falling asleep. SOREMPs, usually (83%) arising from NREM1 or wake, were recorded in 24% of the patients. People with SOREMPs had significantly lower MSL in MSLT and MWT and higher AHI compared with those without SOREMPs.ConclusionsPatients with PD exhibit daylong increased EDS but they underestimate its degree and often fail to signal its onset. SOREMPs in PD have a “narcoleptic” character in sleep-stage sequencing and are associated with the presence of sleep-disturbed breathing. These results add to our understanding of sleepiness and sleepiness perception in PD and have important implications for its diagnosis and management.

Nordstrand, Sebjørg Elizabeth Hesla; Hansen, Berit Hjelde; Rootwelt, Terje; Karlsen, Tor-Ivar; Swanson, David; Nilsen, Kristian Bernhard; Knudsen, Stine

doi: 10.1093/sleep/zsz008pmid: 30649483

Study ObjectivesSeveral studies have reported psychiatric comorbidity in patients with narcolepsy type 1 (NC1). The primary aim of this study was to explore the extent of psychiatric symptoms in a cohort of Norwegian NC1 patients, most of whom were H1N1-vaccinated. We also wanted to explore possible causes of the psychiatric symptoms seen in NC1.MethodsCross-sectional study. Psychiatric symptoms were assessed by the Achenbach System of Empirically Based Assessment (ASEBA) Child Behavior Check List (CBCL) in children and by Adult Self Report (ASR) in adults.ResultsThe mean (SD) total T-scores were 58.6 (9.2) for children and 57.0 (9.8) for adults, these being mainly driven by internalizing problems. Internalizing symptom T-scores showed that 37.5% of the children and 33.3% of the adults were in the clinical range of concern. T-scores were lower when the questionnaire’s sleep-related items were excluded. However, 27.5% of children and 22.2% of adults still remained within the total psychiatric symptoms clinical range. Psychiatric symptoms and excessive daytime sleepiness were not associated. However, in children fragmented sleep, measured by sleep-stage shift index was significantly negatively associated with all the psychiatric summary scores (all p ≤ 0.020), and awakening index was negatively associated with externalizing (p = 0.042) and total summary scores (p = 0.042). In adults, awakening index, but not sleep-stage shift index, was positively associated with internalizing score (p = 0.015). Hypocretin-1 levels showed no association with psychiatric symptoms.ConclusionsWe found a high prevalence of psychiatric symptoms in NC1 patients. Fragmented sleep was significantly associated with psychiatric symptoms.

Alcántara, Carmela; Gallo, Linda C; Wen, Jia; Dudley, Katherine A; Wallace, Douglas M; Mossavar-Rahmani, Yasmin; Sotres-Alvarez, Daniela; Zee, Phyllis C; Ramos, Alberto R; Petrov, Megan E; Casement, Melynda D; Hall, Martica H; Redline, Susan; Patel, Sanjay R

DelRosso, Lourdes M; Jackson, Caroline V; Trotter, Kimberly; Bruni, Oliviero; Ferri, Raffaele

doi: 10.1093/sleep/zsy269pmid: 30602036

Study ObjectivesChildren with “restless sleep disorder” (RSD) were previously identified clinically and polysomnographically. In this study, we attempt to characterize their sleep-related movements and describe them in terms of type of movement, duration, and timing.MethodsVideo-polysomnography (vPSG) from 15 school-aged children with RSD, 15 sex- and age-matched children with restless legs syndrome (RLS), and 15 controls was reviewed for identification of sleep-related movements. Data obtained included the routine data collected during PSG and the video assessment of the movements which included time of the night when the movement occurred, type of movement (arms, legs, and body position change), and duration of the movement.ResultsvPSG recordings from 15 children with RLS (12 males, 3 females) with a mean age of 11.9 (SD: 3.52), 15 participants with RSD (11 males, 4 females) with a mean age of 9.5 (SD: 3.18), and 15 controls (9 males, 6 females) with a mean age of 10. The total movement index, obtained by summing together all types of movements in each participant and dividing it by the total sleep time, was prominent in children with RSD in all sleep stages. Five movements per hour gave 100% accuracy vs. controls and 90% vs. RLS. Movements occurred all night.ConclusionsWe have characterized the sleep-related movements of children with RSD in comparison to the movements in children with RLS and in controls. We identified that children with RSD move all night and an index of 5 per hour accurately separates RSD from other disorders.

Leong, Ruth L F; Koh, Shirley Y J; Chee, Michael W L; Lo, June C

doi: 10.1093/sleep/zsz003pmid: 30649558

Study ObjectivesPrevious studies have shown that sleep benefits prospective memory by facilitating spontaneous retrieval processes. Here, we investigated the sleep features supporting such a benefit.MethodsForty-nine young adults (mean age ± SD: 22.06 ± 1.71 years; 18 males) encoded intentions comprising four related (phone-unplug earphones) and four unrelated (mirror-close the book) cue–action pairs. They were instructed to remember to perform these actions in response to cue words presented during a semantic categorization task 12 h later. The retention interval involved either a period of wakefulness (09:30–21:30; n = 24) or overnight sleep with polysomnographic monitoring (21:30–09:30; n = 25).ResultsWe found a significant Group × Relatedness interaction for prospective memory accuracy (F = 8.35, p < 0.01). The sleep group successfully executed a significantly higher percentage of related intentions compared to the wake group (mean ± standard error of the mean (SEM): 94.00 ± 2.61% vs 66.67 ± 6.84%, p < 0.001). This benefit for related intentions was associated with longer post-learning slow wave sleep (r = 0.46, p < 0.05). In contrast, the percentage of unrelated intentions successfully executed did not differ between groups (82.00 ± 5.10% vs 72.92 ± 6.88%, p = 0.29).ConclusionSlow wave sleep after memory encoding may strengthen the preexisting associations between semantically related cues and actions, thereby facilitating subsequent spontaneous retrieval processes.