SLEEP

Postuma, Ronald B.; Gagnon, Jean-Francois; Tuineaig, Maria; Bertrand, Josie-Anne; Latreille, Veronique; Desjardins, Catherine; Montplaisir, Jacques Y.

doi: 10.5665/sleep.3102pmid: 24179289

AbstractObjectives:Antidepressants, among the most commonly prescribed medications, trigger symptoms of REM sleep behavior disorder (RBD) in up to 6% of users. Idiopathic RBD is a very strong prodromal marker of Parkinson disease and other synuclein-mediated neurodegenerative syndromes. It is therefore critically important to understand whether antidepressant-associated RBD is an independent pharmacologic syndrome or a sign of possible prodromal neurodegeneration.Design:Prospective cohort study.Setting:Tertiary sleep disorders center.Participants:100 patients with idiopathic RBD, all with diagnosis confirmed on polysomnography, stratified to baseline antidepressant use, with 45 matched controls.Measurements/Results:Of 100 patients, 27 were taking antidepressants. Compared to matched controls, RBD patients taking antidepressants demonstrated significant abnormalities of 12/14 neurodegenerative markers tested, including olfaction (P = 0.007), color vision (P = 0.004), Unified Parkinson Disease Rating Scale II and III (P < 0.001 and 0.007), timed up-and-go (P = 0.003), alternate tap test (P = 0.002), Purdue Pegboard (P = 0.007), systolic blood pressure drop (P = 0.029), erectile dysfunction (P = 0.002), constipation (P = 0.003), depression indices (P < 0.001), and prevalence of mild cognitive impairment (13% vs. 60%, P < 0.001). All these abnormalities were indistinguishable in severity from RBD patients not taking antidepressants. However, on prospective follow-up, RBD patients taking antidepressants had a lower risk of developing neurodegenerative disease than those without antidepressant use (5-year risk = 22% vs. 59%, RR = 0.22, 95%CI = 0.06, 0.74).Conclusions:Although patients with antidepressant-associated RBD have a lower risk of neurodegeneration than patients with “purely-idiopathic” RBD, markers of prodromal neurodegeneration are still clearly present. Development of RBD with antidepressants can be an early signal of an underlying neurodegenerative disease.

Petrov, Megan E. Ruiter; Kim, Yongin; Lauderdale, Diane; Lewis, Cora E.; Reis, Jared P.; Carnethon, Mercedes R.; Knutson, Kristen; Glasser, Stephen J.

doi: 10.5665/sleep.3104pmid: 24179290

AbstractStudy Objective:To investigate the longitudinal relationships between actigraph-derived sleep duration, fragmentation, and lipid levels.Design and Setting:Longitudinal data from the Coronary Artery Risk Development in Young Adults Sleep Study (2003-05), an observational cohort at the Chicago site.Participants:There were 503 black and white adults, ages 32-51 years, with no prior history of cardiovascular disease.Interventions:N/A.Measurement and Results:Sleep duration and fragmentation were measured using 6 days of wrist actigraphy. Sleep quality was measured with the Pittsburgh Sleep Quality Index. The outcome variables, measured at 3 examinations over 10 years (Baseline [2000-01], 5-year [2005-06], and 10-year follow-up [2010-11]), were total cholesterol (TC), high-density lipoprotein (HDL), low-density lipoprotein (LDL), triglycerides (TG), and TC/HDL ratio. The associations between each sleep parameter and 10-year change in lipids were analyzed with generalized estimating equation models adjusting for relevant confounders. After adjustment, each hour increase in sleep duration was significantly associated with higher TC (5.2 mg/dL, 95%CI: 1.7, 8.6) and LDL (3.4 mg/dL, 95%CI: 0.2, 6.6) in the total sample, a 1.1 mg/dL increase in TG (95%CI: 1.0, 1.1) among men, and a borderline significant greater odds for a TC/HDL ratio ≥ 5 among men (OR: 1.37, 95%CI: 0.99, 1.90). Overall, sleep fragmentation and sleep quality scores were not associated with change in lipids.Conclusions:Beyond relevant covariates, over a 10-year follow-up, longer objective sleep duration was longitudinally and significantly associated with a poorer lipid profile. Greater objective sleep fragmentation and self-reported poor sleep quality were not related to a poorer lipid profile.

Killgore, William D. S.

doi: 10.5665/sleep.3106pmid: 24179291

AbstractStudy Objectives:Prior research suggests that sleep deprivation is associated with declines in some aspects of emotional intelligence and increased severity on indices of psychological disturbance. Sleep deprivation is also associated with reduced prefrontal-amygdala functional connectivity, potentially reflecting impaired top-down modulation of emotion. It remains unknown whether this modified connectivity may be observed in relation to more typical levels of sleep curtailment. We examined whether self-reported sleep duration the night before an assessment would be associated with these effects.Design:Participants documented their hours of sleep from the previous night, completed the Bar-On Emotional Quotient Inventory (EQ-i), Mayer-Salovey-Caruso Emotional Intelligence Test (MSCEIT), and Personality Assessment Inventory (PAI), and underwent resting-state functional magnetic resonance imaging (fMRI).Setting:Outpatient neuroimaging center at a private psychiatric hospital.Participants:Sixty-five healthy adults (33 men, 32 women), ranging in age from 18-45 y.Interventions:N/A.Measurements and Results:Greater self-reported sleep the preceding night was associated with higher scores on all scales of the EQ-i but not the MSCEIT, and with lower symptom severity scores on half of the psychopathology scales of the PAI. Longer sleep was also associated with stronger negative functional connectivity between the right ventromedial prefrontal cortex and amygdala. Moreover, greater negative connectivity between these regions was associated with higher EQ-i and lower symptom severity on the PAI.Conclusions:Self-reported sleep duration from the preceding night was negatively correlated with prefrontal-amygdala connectivity and the severity of subjective psychological distress, while positively correlated with higher perceived emotional intelligence. More sleep was associated with higher emotional and psychological strength.

Ward, Andrew M.; McLaren, Donald G.; Schultz, Aaron P.; Chhatwal, Jasmeer; Boot, Brendon P.; Hedden, Trey; Sperling, Reisa A.

doi: 10.5665/sleep.3108pmid: 24179292

AbstractStudy Objectives:Sleep deprivation and daytime somnolence impair numerous aspects of physical, cognitive, and memory performance. However, most studies examining the effect of somnolence on brain function focus on acute sleep restriction in young adults. We examine the relationship between chronic daytime somnolence and connectivity in six brain networks in both young and elderly subjects using stimulus-free resting-state functional magnetic resonance imaging.Design:Cross-sectional.Setting:Outpatient research at the Massachusetts General Hospital.Participants:Young (n = 27) and elderly (n = 84) healthy, cognitively normal volunteers.Interventions:None.Measurements and Results:Compared with young subjects, cognitively normal elderly adults report less daytime somnolence on the Epworth Sleepiness Scale (ESS) (P = 0.019) and display reduced default mode network (DMN) connectivity (P = 0.004). Across all subjects, increasing daytime sleepiness was associated with decreasing functional connectivity in the DMN (P = 0.003, partial r of ESS = -0.29). There was no difference in the slope of this relationship between young adults and elderly subjects. No other cortical networks were correlated with daytime sleepiness. Daytime sleepiness and DMN connectivity were not related to sex, brain structure, or body mass index.Conclusions:These findings suggest that daytime sleepiness is associated with impaired connectivity of the DMN in a manner that is distinct from the effects of aging. This association is important to consider in any study using DMN connectivity as a biomarker. Additionally, these results may help identify those subjects at risk for future memory decline.

Burke, Tina M.; Markwald, Rachel R.; Chinoy, Evan D.; Snider, Jesse A.; Bessman, Sara C.; Jung, Christopher M.; Wright, Kenneth P.

doi: 10.5665/sleep.3110pmid: 24179293

AbstractStudy Objectives:Photic and non-photic stimuli have been shown to shift the phase of the human circadian clock. We examined how photic and non-photic time cues may be combined by the human circadian system by assessing the phase advancing effects of one evening dose of exogenous melatonin, alone and in combination with one session of morning bright light exposure.Design:Randomized placebo-controlled double-blind circadian protocol. The effects of four conditions, dim light (∼1.9 lux, ∼0.6 Watts/m2)-placebo, dim light-melatonin (5 mg), bright light (∼3000 lux, ∼7 Watts/m2)-placebo, and bright light-melatonin on circadian phase was assessed by the change in the salivary dim light melatonin onset (DLMO) prior to and following treatment under constant routine conditions. Melatonin or placebo was administered 5.75 h prior to habitual bedtime and 3 h of bright light exposure started 1 h prior to habitual wake time.Setting:Sleep and chronobiology laboratory environment free of time cues.Participants:Thirty-six healthy participants (18 females) aged 22 ± 4 y (mean ± SD).Results:Morning bright light combined with early evening exogenous melatonin induced a greater phase advance of the DLMO than either treatment alone. Bright light alone and melatonin alone induced similar phase advances.Conclusion:Information from light and melatonin appear to be combined by the human circadian clock. The ability to combine circadian time cues has important implications for understanding fundamental physiological principles of the human circadian timing system. Knowledge of such principles is important for designing effective countermeasures for phase-shifting the human circadian clock to adapt to jet lag, shift work, and for designing effective treatments for circadian sleep-wakefulness disorders.

O'Brien, Louise M.; Bullough, Alexandra S.; Owusu, Jocelynn T.; Tremblay, Kimberley A.; Brincat, Cynthia A.; Chames, Mark C.; Kalbfleisch, John D.; Chervin, Ronald D.

doi: 10.5665/sleep.3112pmid: 24179294

AbstractStudy Objective:This cohort study examined the impact of maternal snoring on key delivery outcomes such as mode of delivery, infant birth centile, and small-for-gestational age.Design:Cohort study.Setting:A large tertiary medical center.Patients or Participants:Pregnant women in their third trimester were recruited between March 2007 and December 2010.Measurements and Results:Women were screened for habitual snoring, as a known marker for sleep disordered breathing. Outcome data were obtained from medical records following delivery and birth centiles were calculated. Of 1,673 women, a total of 35% reported habitual snoring (26% with pregnancy-onset snoring and 9% with chronic snoring). After adjusting for confounders, chronic snoring was associated with small-forgestational age (OR 1.65, 95%CI 1.02-2.66, P = 0.041) and elective cesarean delivery (OR 2.25, 95%CI 1.22-4.18, P = 0.008). Pregnancy-onset snoring was associated with emergency cesarean delivery (OR 1.68, 95%CI 1.22-2.30, P = 0.001).Conclusion:Maternal snoring during pregnancy is a risk factor for adverse delivery outcomes including cesarean delivery and small-for-gestational age. Screening pregnant women for symptoms of SDB may provide an early opportunity to identify women at risk of poor delivery outcomes.Clinical Trials Registration:Identifier: NCT01030003.

Alexopoulos, Emmanouel I.; Theologi, Vasiliki; Malakasioti, Georgia; Maragozidis, Panagiotis; Tsilioni, Irene; Chrousos, George; Gourgoulianis, Konstantinos; Kaditis, Athanasios G.

doi: 10.5665/sleep.3114pmid: 24179295

AbstractBackground:Obstructive sleep apnea (OSA) has been associated with increased frequency of excessive daytime sleepiness (EDS). Increased plasma TNF-α levels may mediate this association in adults, but conflicting results have been reported in children. We hypothesized that: (i) the higher the OSA severity in childhood, the higher the frequency of EDS and morning plasma TNF-α levels; and (ii) high TNF-α levels predict presence of EDS.Methods:Children without and with snoring underwent polysomnography. EDS was determined by parental response to specific questions, and plasma TNF-α levels were measured.Results:Children with moderate-to-severe OSA (n = 24; 5.7 ± 2 years; apnea-hypopnea index [AHI] 11.5 ± 5.1/h), but not participants with mild OSA (n = 22; 6 ± 2.5 years; AHI 2.1 ± 1/h) were at significantly higher risk for EDS than controls (n = 22; 6.8 ± 2.1 years; AHI 0.5 ± 0.3/h) (OR [95% CI] adjusted for age, gender, and obesity: 9.2 [1.7-50.2] and 3.8 [0.7-21.8], respectively). The 3 groups did not differ regarding TNF-α concentration (0.63 ± 0.2 vs 0.65 ± 0.18 vs 0.63 ± 0.17 pg/mL; P > 0.05). TNF-α levels were associated significantly with body mass index z-score (P < 0.05) and not with polysomnography indices (P > 0.05). Subjects with high TNF-α levels (> 0.57 pg/mL) were not at higher risk for EDS than participants with low levels (OR [95% CI] adjusted for age, gender, and obesity: 1.7 [0.5-5.7]).Conclusions:Increasing severity of OSA is associated with increasing frequency of EDS, but not with elevated plasma TNF-α concentration. High TNF-α levels cannot be used as predictor for the presence of EDS in children with sleep apnea.

Jackman, Angela R.; Biggs, Sarah N.; Walter, Lisa M.; Embuldeniya, Upeka S.; Davey, Margot J.; Nixon, Gillian M.; Anderson, Vicki; Trinder, John; Horne, Rosemary S. C.

doi: 10.5665/sleep.3116pmid: 24179296

AbstractObjectives:To characterize health-related quality of life (QOL) in preschool children with sleep disordered breathing (SDB) and their families compared with nonsnoring control patients in the community. It was hypothesized that children with SDB and their families would have poorer QOL than control children, that a relationship would be found between SDB severity and QOL, and that even children with mild SDB and their families would have reduced QOL.Participants and Methods:A clinical sample of preschool children (3-5 y) with SDB diagnosed by gold standard polysomnography (primary snoring, PS = 56, mild obstructive sleep apnea, OSA = 35, moderate/severe OSA = 24) and control children recruited from the community (n = 38) were studied. Parents completed health-related QOL and parenting stress questionnaires.Results:Children and families in the PS and mild OSA groups had consistently poorer QOL than control children (both P < 0.05-0.001), based on parent ratings, and parents of children with PS had elevated stress ratings relative to control children (P < 0.05-0.001). The moderate/severe OSA group differed from the control group on select measures of parent and family QOL (worry, P < 0.001 and total family impact, P < 0.05).Conclusions:Our findings demonstrate that sleep disordered breathing is associated with reduced quality of life in preschool children and their families. These results support previous quality of life findings in older children and in samples with broader age ranges. Furthermore, clinically referred preschool children with mild forms of sleep disordered breathing may be at greatest risk.

Bartlett, Delwyn; Wong, Keith; Richards, Dianne; Moy, Emma; Espie, Colin A.; Cistulli, Peter A.; Grunstein, Ronald

doi: 10.5665/sleep.3118pmid: 24179297

AbstractObjective:To examine whether a social cognitive therapy (SCT) intervention increases continuous positive airway pressure (CPAP) use compared to equivalent social interaction (SI) time.Participants:Individuals with obstructive sleep apnea (OSA) referred for CPAP therapy.Intervention:Participants received a 30-min group education session regarding OSA and CPAP. Groups of three to four participants were then randomly assigned to an SCT session or social interaction.Measurements:CPAP usage was assessed at 7 nights, then 1, 3, and 6 months. The two primary outcomes were adherence, usage ≥ 4 h per night at 6 months, and uptake of CPAP. Questionnaires were given pretreatment and posttreatment.Results:Two hundred six individuals were randomized to SI (n = 97) or SCT (n = 109). CPAP uptake was not different between groups (82% in SI, 88% in SCT groups, P = 0.35). There were no differences between groups in adherence: 63-66% at 1 week, and at 6 months 55-47% (P = 0.36). Higher pretreatment apnea-hypopnea index, higher baseline self-efficacy, and use of CPAP (≥ 4 h) at 1 week were independent predictors of CPAP adherence at 6 months. CPAP adherence increased by a factor of 1.8 (odds ratio = 1.8, 95% confidence interval 1.1-3.0) for every one-unit increase in self-efficacy. There was no difference between groups postintervention in self-efficacy scores, sleepiness, mood, or sleep quality.Conclusions:In this randomized trial, a single SCT application did not increase adherence when compared with SI time. Although self-efficacy scores prior to CPAP predicted adherence, self-efficacy was not increased by the interventions. Increasing intensity and understanding of SCT interventions may be needed to improve CPAP adherence.Clinical Trials Registration:Australian New Zealand Clinical Trials Registry, ACTRN12607000424404.

Aloia, Mark S.; Arnedt, J. Todd; Strand, Matthew; Millman, Richard P.; Borrelli, Belinda

doi: 10.5665/sleep.3120pmid: 24179298

AbstractBackground:Obstructive sleep apnea (OSA) is associated with a variety of medical conditions. Positive airway pressure (PAP) is an effective treatment for improving sleep, yet adherence rates are low. The aim of the current study is to test two treatments versus standard care in improving adherence to PAP.Method:Two hundred twenty-seven patients with OSA were randomized to standard care (SC), education (ED) and motivational enhancement therapy (MET). Adherence was measured objectively and the first week of adherence (prior to the intervention) was used as an a priori moderator of the effect of the various interventions. Mediators of treatment response were also examined using theory-based measures of decisional balance and self-efficacy.Results:Adherence declined over time for all three groups. There was a significant interaction between level of adherence during the first week of treatment and treatment group. Those who had moderate levels of adherence during their first week of PAP were more likely to adhere to treatment at follow-up if they had MET; those who had high levels of adherence during their first week of PAP were more likely to adhere to treatment at follow-up if they had ED. MET treatment increased the perception of the positive aspects of PAP, but ED did not.Conclusions:Initial adherence to positive airway pressure could help guide subsequent treatment plans. The results also support social cognitive theory in that educational approaches might be best suited for those who are ready for change whereas more motivational approaches might be best for those who are ambivalent about change.