Rapid Eye Movement Onset Latency Research Articles

Assessing sleep architecture and cognition in older adults with depressive symptoms attending a memory clinic

BackgroundWhile depression is intrinsically and bidirectionally linked with both sleep disturbance and cognition, the inter-relationships between sleep, cognition, and brain integrity in older people with depression, especially those with late-onset depression are undefined. MethodsOne hundred and seventy-two older adults (mean age 64.3 ± 6.9 years, Depression: n = 66, Control: n = 106) attending a memory clinic underwent a neuropsychological battery of declarative memory, executive function tasks, cerebral magnetic resonance imaging and overnight polysomnography with quantitative electroencephalography. ResultsThe time spent in slow-wave sleep (SWS) and rapid eye movement (REM) sleep, slow-wave activity, sleep spindles, hippocampal volume and prefrontal cortex thickness did not differ between depression and control and depression onset groups. However, sleep onset latency (p = 0.005) and REM onset latency (p = 0.02) were later in the Depression group compared to controls. Less SWS was associated with poorer memory (r = 0.31, p = 0.023) in the depression group, and less SWS was related to better memory in the control group (r = −0.20, p = 0.043; Fishers r-to-z = −3.19). LimitationsLongitudinal studies are needed to determine if changes in sleep in those with depressive symptoms predict cognitive decline and illness trajectory. ConclusionOlder participants with depressive symptoms had delayed sleep initiation, suggestive of delayed sleep phase. The association between SWS and memory suggests SWS may be a useful target for cognitive intervention in older adults with depression symptoms. Reduced hippocampal volumes did not mediate this relationship, indicating a broader distributed neural network may underpin these associations.

The Intersection of Insomnia Disorder and Major Depressive Disorder: A Clinical Perspective

Major depressive disorder (MDD) is associated with profound sleep architectural alterations including reduced slow wave activity, increased delta sleep ratio, REM sleep disinhibition, shortened REM onset latency, and increased REM density. Antidepressants, though mitigating depressive symptoms, often disrupt sleep patterns, highlighting the delicate balance between treatment benefits and sleep-related impacts. Comprehensive assessment and management of insomnia is pivotal due to its significant implications for effective clinical management and treatment outcomes in MDD. Nonpharmacological treatments, notably cognitive-behavioral therapy for insomnia (CBTi), and digital CBTi (dCBTi) should be considered. CBTi unravels maladaptive sleep beliefs and behaviors, yielding improvements in both insomnia and MDD symptoms. Digital CBTi platforms extend accessibility, offering potential relief to a broader demographic. Sedating antidepressants, nonbenzodiazepine hypnotics, and atypical antipsychotics address insomnia within MDD, with cautious consideration for side effects. A combination of pharmacotherapy with CBTi might yield augmented outcomes in patients with MDD and comorbid insomnia. Ketamine, electroconvulsive therapy (ECT), repetitive transcranial magnetic stimulation (rTMS), vagal nerve stimulation (VNS), and deep brain stimulation (DBS) explore novel dimensions in treating treatment-resistant depression, potentially influencing sleep disruptions. [ Psychiatr Ann . 2023;53(11):502–507.]

P096 The Effect of Moderate-Intensity Exercise on Sleep Quality and Quantity in Healthy Adult Males

Abstract Introduction Acute exercise may have the ability to disrupt sleep in healthy adults. Given the popularity of afternoon exercise, it is important to determine how this affects sleep. Therefore, the aim of this study was to investigate the effect of afternoon moderate-intensity cycling exercise on objective and subjective sleep in healthy adult males. Methods To assess the effect of moderate-intensity afternoon exercise on sleep quality and quantity, 12 healthy adult males who were identified as good sleepers completed a repeated-measures, counter-balanced, crossover study design with two conditions (moderate-intensity aerobic exercise or no exercise). The exercise task involved cycling for 40 minutes at 70%HRmax and was completed ~15:30h. Polysomnography was used to measure sleep during a 9-h sleep opportunity (23:00h to 08:00h). Results There were no statistically significant differences in objective or subjective sleep between conditions. Exercise had a medium-sized effect on reducing total sleep time (mean ± SD; control 493.71 ± 12.59 mins vs exercise: 471.46 ± 55.19 mins; Cohen’s d: 0.56), sleep efficiency (mean ± SD; control 91.43 ± 2.33 % vs exercise: 87.31 ± 10.22 %; Cohen’s d: 0.56), and increasing REM onset latency (mean ± SD; control: 76.13 ± 45.10 mins vs exercise: 102.75 ± 46.85 mins; r: -0.33) (all p > 0.05). Discussion Healthy adult males can complete afternoon moderate-intensity exercise without compromising subsequent sleep. Individual responses in objective sleep outcomes may vary after exercise.

0532 Defining Sleep Architecture in Pediatric Patients with Prader Willi Syndrome

Abstract Introduction Prader Willi Syndrome (PWS) is a rare genetic disorder characterized by infantile hypotonia, hyperphagia leading to early childhood obesity, and short stature. PWS patients are at risk for multiple sleep abnormalities including increased risk of obstructive sleep apnea, central sleep apnea, and excessive daytime sleepiness. The limited studies reviewing PSGs in pediatric PWS patients showed varying results. Our study aim is to characterize sleep characteristics in pediatric patients with PWS. Methods We conducted a retrospective chart review of pediatric patients with a genetically confirmed diagnosis of Prader Willi Syndrome from 2007 to 2015. In lab polysomnograms were scored using the AASM criteria for pediatric sleep studies. Data was collected on sleep architecture parameters and compared to normative data available for pediatric polysomnography. Given large variability in sleep architecture during infancy, subjects were divided into two age groups (< 1 years old, 1-19 years old). Results Fifty-one PSGs were reviewed of which 31 (60.7%) belong to males and 20 (39.3%) belong to females. Forty-one PSGs were initial studies and 11 were repeat studies. Age at the time of sleep study ranged from 11 days to 19 years old. 8 (15%) subjects were less than 1 years old and 44 (84%) were 1 year and older. For subjects less than one year old, mean sleep onset latency (min) was 21±33.4, REM onset latency (min) 35±27.2, SWS(%) 43.3±10.2, REM(%) 35.3±7.35, arousal index 9.7±11.9, wake after sleep onset (WASO) (min) 59.5±11.4 and sleep efficiency 82.4±9.4. For the 1-19 year age group, mean sleep onset latency (min) was 24.5±23.1, REM onset latency (min) 104± 59.9, SWS (%) 21.4±7.11, REM (%) 21.3±6.9, arousal index 7.3±5.4, WASO (min) 46.5±36.10 and sleep efficiency was 85.7±9.0. Conclusion In our population of PWS patients, REM onset latency was not decreased as shown in previous studies. Sleep efficiency was decreased. Other sleep parameters fell within normal range. Additional data on signs of excessive daytime sleepiness and sleep disordered breathing in this population is needed to understand if EDS persists with decreased sleep efficiency and otherwise normal sleep parameters and/or with OSA. Support (If Any)

Sleep pattern in a group of patients undergoing hemodialysis compared to control

BackgroundPatients with chronic kidney disease progress regularly every year to end-stage renal disease and have to undergo dialysis. Sleep disturbances have been reported to be frequent among patients receiving dialysis and contributing to the increase of their mortality and morbidity. The present research aimed to study the sleep pattern in hemodialysis patients and the risk factors associated. This cross-sectional case-control study included 40 subjects divided into 2 groups: 20 cases recruited from Ain Shams University Hospital’s dialysis unit and 20 in the control group with normal Pittsburgh Sleep Quality Index score matched for age and sex. Both groups were subjected to overnight polysomnography, and the cases group was assessed by the Pittsburgh Sleep Quality Index to determine their sleep quality.ResultsNearly all polysomnographic parameters were significantly abnormal in the cases group except for sleep onset latency (P > 0.05), showing obstructive sleep apnea and periodic limb movement (P value 0.001). Based on their Pittsburgh Sleep Quality Index score, 30% were classified as good sleepers and 70% as bad sleepers. On comparing both groups, a significant difference was found. Poor sleepers had more worse sleep efficiency (62.9%), spent longer time during their sleep in stage 1 (26.6%) with shorter REM onset latency (113.5 ± 99.5), and had a longer duration of illness with lower serum creatinine level compared to good sleepers.ConclusionsThe prevalence of obstructive sleep apnea and periodic limb movement in hemodialysis patients is high; patients with longer time on dialysis are at more risk of sleep disorders, whereas hemoglobin levels, BUN, and other demographic factors do not seem to play a role in sleep disorder. Hence, patients on hemodialysis need to be screened for sleep disorders so as to improve their mortality and morbidity.

P120 The Relationship Between Sleep Architecture And Cognition In Late-Life Depression

Abstract Introduction Depression in older people is associated with changes in sleep, however associations between sleep architecture and cognition have not yet been delineated. We examined sleep architecture in older people with and without depressive symptoms, and relationships with neuropsychological performance. Methods Adults over 50 years underwent overnight polysomnography and memory and executive function tests. Depression and controls groups were defined by a Geriatric Depression Scale-15 cut off score of 6. Sleep architectural outcomes included amount of slow wave sleep (SWS), rapid eye movement (REM) sleep, REM onset latency (ROL), NREM slow wave activity (SWA, 0.5–4 Hz), N2 sleep spindle density and REM density. Results The sample comprised of 71 participants with depressive symptoms and 101 controls (mean age both groups = 64, mean GDS-15 dep= 9.3, con= 1.8). There were no significant group differences in time spent in SWS, REM, REM density or SWA. Those with depressive symptoms had later ROL (p=.008) and less N2 sleep spindles (p=.03) compared to controls. A differential association was observed with less SWS being associated with poor memory recall in the depression group only (z=.342, p=0.008). No associations between sleep and executive function performance were observed. Discussion The link between less time in SWS and poorer memory in those with depressive symptoms could suggest that SWS is particularly pertinent for cognition in depression or that both sleep and cognition mechanisms are influenced by depressive state. Further studies are needed to determine if changes in sleep are linked with underlying neurobiological changes.

EEG and Sleep Effects of Tramadol Suggest Potential Antidepressant Effects with Different Mechanisms of Action.

Tramadol is a widely used, centrally acting, opioid analgesic compound, with additional inhibitory effects on the synaptic reuptake of serotonin and noradrenaline, as well as on the 5-HT2 and NMDA receptors. Preclinical and clinical evidence also suggests its therapeutic potential in the treatment of depression and anxiety. The effects of most widely used antidepressants on sleep and quantitative electroencephalogram (qEEG) are well characterized; however, such studies of tramadol are scarce. Our aim was to characterize the effects of tramadol on sleep architecture and qEEG in different sleep–wake stages. EEG-equipped Wistar rats were treated with tramadol (0, 5, 15 and 45 mg/kg) at the beginning of the passive phase, and EEG, electromyogram and motor activity were recorded. Tramadol dose-dependently reduced the time spent in rapid eye movement (REM) sleep and increased the REM onset latency. Lower doses of tramadol had wake-promoting effects in the first hours, while 45 mg/kg of tramadol promoted sleep first, but induced wakefulness thereafter. During non-REM sleep, tramadol (15 and 45 mg/kg) increased delta and decreased alpha power, while all doses increased gamma power. In conclusion, the sleep-related and qEEG effects of tramadol suggest antidepressant-like properties, including specific beneficial effects in selected patient groups, and raise the possibility of a faster acting antidepressant action.

Underutilization of the MSLT in sleepy patients with a short onset REM period (SOREMP) in the sleep clinic

Objective/BackgroundA nocturnal sleep onset REM period (defined as REM onset latency ≤ 15 min; SOREMP) occurs rarely and research has shown that the phenomenon is specific for type 1 and 2 narcolepsy. However, little is known about the meaningfulness of the phenotype in general sleep clinic patients because those that exhibit the phenomenon often present with few traditional narcolepsy symptoms. As such, this study aimed to (1) evaluate the rate of eventual MSLT testing for those with a SOREMP on routine PSG when the phenomenon occurred in the absence of potential explanatory factors and (2) quantify the stability of the SOREMP phenotype. Patients/MethodsThis was a retrospective analysis of a large repository of de-identified PSG and MSLT test results from 2008 to 2015. Patient records were retrieved from a repository of studies completed at a variety of sleep laboratories across the USA. A total of 118,046 baseline polysomnograms were evaluated for a PSG SOREMP (occurred in 0.7% of the sample). Patients were excluded if they indicated working either shift or night work at the time of the SOREMP or if their self-reported habitual weekday time in bed was less than 7 h. A final sample of 391 cases with a SOREMP were sequestered and previous or consecutive studies were searched for each individual. ResultsThe vast majority of patients (n = 347/391; 89%) with a PSG SOREMP never received MSLT testing. Patients that were evaluated by MSLT (n = 44; 11%) were typically very sleepy and 82% ended up with a diagnosis of narcolepsy or had MSLTs consistent with current narcolepsy criteria (ie, including the nocturnal SOREMP). Only seven of the 140 patients (n = 5%) that with OSA that first underwent one or more PAP titrations were subsequently seen for an MSLT. Compared to those that eventually received an MSLT, patients that did not receive MSLT testing were older (52 vs. 41 years, p < 0.001), more likely to have moderate to severe OSA (AHI ≥ 15; 39% vs. 16%, p < 0.001), and were generally less likely to report severe sleepiness (ESS ≥ 16; 25% vs. 55%, p < 0.001) and vehicle or workplace accidents or injuries. However, 12% of those that never received an MSLT reported such extreme sleepiness that they endorsed a near-miss car accident due to sleepiness, almost twice as prevalent than that found in a random sample of matched moderate-to-severe OSA patients (p < 0.01). Overall, the reliability of the SOREMP phenotype was low at 9.8%, but was much higher for those diagnosed with type 2 narcolepsy (31%) compared to those without narcolepsy (IH or normal MSLTs; 0%; p < 0.01) or where narcolepsy status was unknown because an MSLT was not conducted (7%; p < 0.01). ConclusionsThe MSLT has been historically underutilized for those exhibiting a SOREMP on diagnostic PSG, a potential marker of narcolepsy. This is presumably because patients with a PSG SOREMP reported variable levels of sleepiness (although some severe) and many had some degree of OSA, which may either be a partial factor in symptomology or even obscure true narcolepsy. Some patients with a PSG SOREMP were very sleepy and most, when an MSLT was conducted, received a diagnosis of type 2 narcolepsy despite few presenting with some of the associated features of narcolepsy. Well-controlled longitudinal studies with high quality data on cataplexy and hypocretin status are needed to understand where the PSG SOREMP phenomenon falls on the hypersomnolence spectrum and to establish which comorbidities share variance with and/or potentially mask narcolepsy. However because untreated narcolepsy can have high social, functional, and financial burden, until such studies are done, physicians should consider a narcolepsy workup when a SOREMP is observed (especially if multiple are seen) as well as close follow-up for symptom resolution when, for example, a patient is treated for sleep apnea.

Quantitative sleep EEG and polysomnographic predictors of driving simulator performance in obstructive sleep apnea

ObjectivesTo improve identification of obstructive sleep apnea (OSA) patients at risk of driving impairment, this study explored predictors of driving performance impairment in untreated OSA patients using clinical PSG metrics, sleepiness questionnaires and quantitative EEG markers from routine sleep studies. MethodsSeventy-six OSA patients completed sleepiness questionnaires and driving simulator tests in the evening of their diagnostic sleep study. All sleep EEGs were subjected to quantitative power spectral analysis. Correlation and multivariate linear regression were used to identify the strongest predictors of driving simulator performance. ResultsAbsolute EEG spectral power across all frequencies (0.5–32Hz) throughout the entire sleep period and separately in REM and NREM sleep, (r range 0.239–0.473, all p<0.05), as well as sleep onset latency (r=0.273, p<0.017) positively correlated with driving simulator steering deviation. Regression models revealed that amongst clinical and qEEG variables, the significant predictors of worse steering deviation were greater total EEG power during NREM and REM sleep, greater beta EEG power in NREM and greater delta EEG power in REM (range of variance explained 5–17%, t range 2.29–4.0, all p<0.05) and sleep onset latency (range of variance explained 4–9%, t range 2.15–2.5, all p<0.05). ConclusionsIn OSA patients, increased EEG power, especially in the faster frequency (beta) range during NREM sleep and slower frequency (delta) range in REM sleep were associated with worse driving performance, while no relationships were observed with clinical metrics e.g. apnea, arousal or oxygen indices. SignificanceQuantitative EEG analysis in OSA may provide useful markers of driving impairment risk. Future studies are necessary to confirm these findings and assess the clinical significance of quantitative EEG as predictors of driving impairment in OSA.

Differentiated effects of the multimodal antidepressant vortioxetine on sleep architecture: Part 2, pharmacological interactions in rodents suggest a role of serotonin-3 receptor antagonism.

Antidepressants often disrupt sleep. Vortioxetine, a multimodal antidepressant acting through serotonin (5-HT) transporter (SERT) inhibition, 5-HT3, 5-HT7 and 5-HT1D receptor antagonism, 5-HT1B receptor partial agonism, and 5-HT1A receptor agonism, had fewer incidences of sleep-related adverse events reported in depressed patients. In the accompanying paper a polysomnographic electroencephalography (sleep-EEG) study of vortioxetine and paroxetine in healthy subjects indicated that at low/intermediate levels of SERT occupancy, vortioxetine affected rapid eye movement (REM) sleep differently than paroxetine. Here we investigated clinically meaningful doses (80–90% SERT occupancy) of vortioxetine and paroxetine on sleep-EEG in rats to further elucidate the serotoninergic receptor mechanisms mediating this difference. Cortical EEG, electromyography (EMG), and locomotion were recorded telemetrically for 10 days, following an acute dose, from rats receiving vortioxetine-infused chow or paroxetine-infused water and respective controls. Sleep stages were manually scored into active wake, quiet wake, and non-REM or REM sleep. Acute paroxetine or vortioxetine delayed REM onset latency (ROL) and decreased REM episodes. After repeated administration, vortioxetine yielded normal sleep-wake rhythms while paroxetine continued to suppress REM. Paroxetine, unlike vortioxetine, increased transitions from non-REM to wake, suggesting fragmented sleep. Next, we investigated the role of 5-HT3 receptors in eliciting these differences. The 5-HT3 receptor antagonist ondansetron significantly reduced paroxetine’s acute effects on ROL, while the 5-HT3 receptor agonist SR57227A significantly increased vortioxetine’s acute effect on ROL. Overall, our data are consistent with the clinical findings that vortioxetine impacts REM sleep differently than paroxetine, and suggests a role for 5-HT3 receptor antagonism in mitigating these differences.

Alcohol and Sleep Review: Sound Statistics and Valid Conclusions

HANK YOU FOR forwarding to us the letter fromPressman and colleagues (2015) and for inviting ourresponse.The role of alcohol and its impact on sleep has been stud-ied for more than a century, and a substantial knowledgebase has been created. The studies, like most scientific stud-ies, are dependent on the technology available at the timeandtheavailabilityofdata.Thisissomethingwetookintoconsiderationwhenprepar-ing our qualitative review on the impact of alcohol on nor-malsleep.Theissuesraisedcanbesummarizedasfollows:1. The use of percentages to represent the difference inthe mean values of sleep architecture variables in ourtables,2. Our results and conclusions as they pertain to the impactofalcohol onslowwavesleep(SWS),3. Ourinclusion–exclusioncriteriaforstudies,and4. Alcohol, N3, sleepwalking, and medico-legal conse-quences.1. The use of the mean value as a percentage to representsleeparchitecturevariables:1.1. In our article, we made clear how we have presentedthedata:Valuesforsleep architecturevariablesareprovidedinper-centage terms only. Where the researchers have reportedsleep stage data in minutes we have converted these intopercentages. Some variables, such as sleep onset latencyand rapid eye movement onset latency are reported inminutes only. Only the mean value is displayed for allvariables in the tables to enable a uniform approachthroughout(Ebrahimet al.,2013).1.2. This was accepted by the Journal and the peerreviewers as this review was based on highlighting 2specificareas:1.2.1. The impact of various alcohol doses and their tim-ing on nocturnal sleep in healthy controls and nor-mal populations.1.2.2. The impact of these alcohol doses on various sleepstages.1.3. Asthis was a qualitative reviewand not a quantitativemeta-analysis, it was our aim to provide a broadunderstanding to the “nonsleep specialist”readershipoftheimpactofalcoholonsleep.1.4. Furthermore, in routine clinical practice, sleepstages are reported both in actual time and as apercentage of total sleep, a simple difference in themeans between alcohol and placebo nights wasthought to be the best way to demonstrate theeffect.2. Alcohol andSWS:2.1. Alcohol andfirsthalfofnightSWS(N3):2.1.1. Low dose alcohol studies—Of the 4 studiesreported, 2 showed a significant increase in SWS(MacLean and Cairns, 1982; Van Reen et al., 2011)and the other 2 studies failed to find a significantdifference;2.1.2. Moderatedose studies—Ofthe 5 studies reported,2studies demonstrated a significant increase in SWS(Roehrs et al., 1999; Williams et al., 1983). Theother3 studiesfailedtodemonstrateany significantfindings;2.1.3. High dose studies—Five of the 9 studies reported astatistically significant increase in SWS with alco-hol (Arnedt et al., 2011; Feige et al., 2006;MacLean and Cairns, 1982; Prinz et al., 1980; Wil-liams et al., 1983) and 4 studies did not show anysignificantdifferences.The direction of evidence confirms that at low and moder-ate doses alcohol is not clearly associated with increased

Endurance exercise, tryptophan availability to the brain, and sleep electrophysiology in older men

Normal aging entails significant changes in serotonergic activity and function. Noteworthy, these alterations might predispose older individuals to develop depressive symptoms and contribute to age-related changes in sleep. This study verified if exercise increases tryptophan (Trp) availability to the brain and affects sleep depth and architecture in older men. Nineteen men (aged 64 ± 3 years) undertook a series of 4 tests, which was repeated at follow-up (after 16 weeks of training) as follows: (i) dual-energy X-ray absorptiometry (body composition); (ii) peak O2 consumption, ventilatory threshold, and respiratory compensation point (cardiopulmonary testing); (iii) blood withdrawals immediately before, during, and after exercise for analysis of glucose, lactate, ammonia, free fatty acids (FFA), total proteins, albumin, prolactin, valine, leucine, isoleucine, adiponectin, leptin, free and total Trp, and calculated variable: branched-chain amino acids (BCAA); and (iv) sleep electrophysiology (wake, stage 1, stage 2, stages 3+4 or slow-wave sleep (SWS), stage 5 or rapid eye movements, movement time, leg movements during sleep, apneas, hypopneas, and derivative variables). The intervention consisted of supervised exercise (3× per week × 45 min, 65%–70% peak oxygen uptake (V̇O2peak) whereas experimental exercise consisted of 1 h of inclined treadmill (∼68% V̇O2peak). Variations in serum prolactin and free Trp/BCAA served as proxies of 5-hydroxytryptamine activity and synthesis rate, respectively. A series of 3 nights was assessed before and after training using laboratory-based sleep electrophysiology (polysomnography: electroelectroencephalography and electromyography and electro-oculography) as follows: (i) familiarization, (ii) inactive trial, and (iii) exercise trial. Aerobic taining increased oxygen uptake at both ventilatory thresholds, whereas body mass decreased. Acute exercise increased free Trp/BCAA ratio by more than 100% of that at rest and remained elevated postexercise. This ratio shared a positive association with FFA levels. After 1 h of exercise, prolactin was higher than that at rest and was positively associated with free Trp/BCAA. However, the acute response to exercise was attenuated following training for many compounds, including free Trp/BCAA, prolactin, lactate, and FFA. Analyses revealed significant main effects of exercise on wake after sleep onset, rapid eye movement onset latency, and time awake overnight. As compared with the inactive trial at baseline, a higher proportion of SWS was observed during the night subsequent to exercise following training. In addition, we found a positive association between resting adiponectin and SWS. The results support the hypothesis that increases in serotonin synthesis and activity might be involved in the antidepressant outcome of exercise in older men. Inasmuch as training lowered the increase in Trp supply during exercise, Trp requirement by the brain in response to exercise might be attenuated by training. Despite gains in cardiorespiratory fitness after training, a day without exercise led to SWS values similar to those at baseline. However, exercise increased the proportion of SWS during subsequent sleep but this could only be found after training. These results provide evidence that not only sleep quantity (duration) but also quality (SWS) could affect circulating adiponectin levels. Finally, a positive correlation was found between sleep depth and circulating adiponectin levels.

Sleep depth and continuity before and after chronic exercise in older men: Electrophysiological evidence

During later life sleep depth (slow-wave sleep, SWS) and maintenance exhibit deleterious changes, with possible negative effects on daytime function. This study assessed the effect of chronic, supervised exercise on sleep using laboratory-based polysomnography (PSG) and repeated measures in older adults. Thirteen men aged 64±3served as their own controls and had their sleep measured for a total of 6 nights: 3 before and 3 after the 16-week training intervention. Each sequence involved 1 familiarization trial followed by 2 experimental nights (exercise night; nonexercise night) measured using 13-channel PSG (combined electroencephalography, electromyography, and electro-oculography). The exercise challenges consisted of inclined treadmill brisk walking (60min, 68–69% V˙O2peak). The intervention successfully improved some parameters of aerobic fitness, i.e. ventilatory thresholds 1 and 2 (P<0.05). Acute exercise triggered increases in circulating free fatty acids and lactate levels both at baseline and after the intervention (P<0.05). Noteworthy, acute exercise following training resulted in a 71% increase in SWS during subsequent sleep in comparison with the nonexercise condition before training, respectively 2.4% and 1.4% (P<0.05). Following training, acute exercise reduced total wake time by 30% and REM onset latency by 14% (P<0.05). Acute exercise improved sleep continuity by decreasing total wake time. These results show that aerobic training could increase sleep depth and continuity, during active days, in elderly men. In habitual exercisers, these effects of aerobic exercise on sleep, although modest, might counteract those resulting from aging.

EPA-0169 – Effects of antidepressants on sleep architecture

Introduction Sleep disturbances are an integral part of the biological syndrome of depression and relief from this is often essential to enhance compliance with medications and psychological treatments. Anti-depressants, which are the mainstay of treatment of depressive illnesses, have varying effects on our sleep architecture. It is important for researchers and clinicians to be aware of these effects. Objectives We looked at the available literature on how antidepressants affect sleep patterns and tried to synthesize the findings in this poster. Aims The primary aim of our effort was to look at how antidepressants alter our sleeping behaviour and how they affect the different stages of sleep. Methods We tried to look at the available literature and product summary sheets of various antidepressants and have attempted to summarize how they alter our sleep architecture. Results SSRIs and TCAs have marked dose-dependent effects on REM sleep in both healthy volunteers and depressed patients, with increased REM-onset latency and decreased REM sleep. Other antidepressants have modest or minimal effects on REM sleep. The effects on sleep are most likely mediated by 5-HT1 receptors. Conclusions Most antidepressants affect sleep and the physiological patterns of different sleep stages. These effects are greatest and most consistent on rapid eye movement (REM) sleep, and tend to be in the opposite direction to the sleep abnormalities found in depression.

Effect of Evening Postexercise Cold Water Immersion on Subsequent Sleep

This study investigated the effect of cold water immersion after evening exercise on subsequent sleep quality and quantity in trained cyclists. In the evenings (~1900 h) on three separate occasions, male cyclists (n = 11) underwent either no exercise (control, CON), exercise only (EX), or exercise followed by cold water immersion (CWI). EX comprised cycling for 15 min at 75% peak power, then a 15-min maximal time trial. After each condition, a full laboratory-based sleep study (polysomnography) was performed. Core and skin temperature, heart rate, salivary melatonin, ratings of perceived fatigue, and recovery were measured in each trial. No differences were observed between conditions for any whole night sleep measures, including total sleep time, sleep efficiency, sleep onset latency, rapid eye movement onset latency, wake after sleep onset, or proportion of the night spent in different sleep stages. Core temperature in EX and CWI trials was higher than CON, until it decreased below that of EX and CON until bedtime in CWI. After bedtime, core temperature was similar for all conditions throughout the night, except for a 90-min period where it was lower for CWI than EX and CON (3.5-4.5 h postexercise). Heart rates for EX and CWI were both significantly higher than CON postexercise until bedtime, whereas skin temperature after CWI was significantly lower than EX and CON, remaining lower than EX until 3 h postexercise. Melatonin levels and recovery ratings were similar between conditions. Fatigue ratings were significantly elevated after exercise in both CWI and EX conditions, with EX still being elevated compared with CON at bedtime. Whole night sleep architecture is not affected by evening exercise alone or when followed by CWI.

Retrograde effects of triazolam and zolpidem on sleep-dependent motor learning in humans

Drugs that act as allosteric activators at the benzodiazepine site of the gamma-aminobutyric acid (GABA(A)) receptor complex are used commonly to treat insomnia but relatively little is known of how such use affects learning and memory. Although anterograde effects on memory acquisition have been shown, possible retrograde effects on consolidation are more relevant when such agents are administered at bedtime. We tested the effects of two GABA(A) allosteric activators on sleep-dependent motor skill memory consolidation in 12 healthy male subjects. Subjects slept in a sleep laboratory for four consecutive nights (one accommodation night followed by three experimental nights). Placebo, triazolam 0.375 mg, and zolpidem 10 mg were given to each subject in counterbalanced order on the experimental nights. Polysomnographic (PSG) sleep measurement and sleep-dependent motor learning were assessed at each condition. Triazolam was associated with longer total sleep time and increased Stage 2 sleep. Both zolpidem and triazolam were associated with increased latency to rapid eye movement (REM) sleep. Overnight motor learning correlated with total sleep time in the placebo condition but not in the triazolam or zolpidem conditions. A statistically significant impairment in motor performance occurred overnight in the triazolam condition only. Triazolam, given in sufficient doses to prolong sleep in healthy people, affected overnight motor learning adversely. Zolpidem, in a dose sufficient to prolong REM onset latency but without other effects on PSG-measured sleep, degraded the relationship between total sleep time and overnight motor learning. These data indicate that non-selective or alpha1-preferring benzodiazepine site allosteric activators can interfere with sleep-dependent memory consolidation.

Serotonin and Sleep: Molecular, Functional, and Clinical Aspects

Serotonin and Sleep: Molecular, Functional, and Clinical Aspects

Impact of orthodontic appliances on sleep quality

Many young patients are asked to wear headgear or functional appliances during sleep as part of their orthodontic treatment. The objective of this clinical study was to assess the impact of these appliances on sleep quality. Twenty-two subjects (8 boys, 14 girls) between 10 and 15 years of age wearing either a headgear or a removable appliance for 3 to 12 months were enrolled in a sleep study. Each subject participated in 2 overnight sleep studies with and without the appliance. There was a 1-week interval after an adaptation night. The studies were performed at the Sleep Research Laboratory at Toronto Western Hospital in Canada. Each subject served as his or her own control. Twelve subjects had an extraoral headgear appliance, and 10 had intraoral functional (5 Fränkel, 5 Twin-block) appliances. No subject reported any sleep or medical disorder. The primary outcome variable was sleep efficiency. Sleep efficiencies were 90.7% (SD, 7.9) and 91.6% (SD, 4.3) with and without the appliances, respectively. When sleep quality was compared with and without appliances, analysis of variance (ANOVA) showed no significant difference in sleep efficiency or other sleep variables such as sleep onset latency, rapid eye movement onset latency, rapid eye movement percentage, short-wave sleep percentage, or respiratory disturbance index. Sex and body mass index were not confounding variables. In addition, the use of extraoral or intraoral appliances did not affect sleep quality. In young orthodontic patients, there appears to be no difference in sleep quality with or without the overnight use of these appliances after they have been worn for a minimum of 3 months.

Gender differences on polysomnographic findings in Greek subjects with obstructive sleep apnea syndrome

Background and purposeStudies from North American clinics have reported that females with obstructive sleep apnea syndrome (OSAS) are about the same age as males but are heavier, have less severe apnea and make up a much smaller proportion of cases. We examined polysomnographic differences between Greek men and women with OSAS in order to study the influence of gender on clinical presentation and laboratory findings. Patients and methodsThis retrospective study included a cohort of 1010 Greek patients (844 males, 166 females) diagnosed with OSAS by overnight polysomnography (PSG), who were referred to the Sleep Disorders Center of Evangelismos Hospital, Athens Medical School, University of Athens. All patients were studied over a period of three consecutive years, during which time clinical and polysomnography (PSG) findings were compared. ResultsBody mass index (BMI) was similar in men and women with OSAS (BMI=31.6±5.5kg/m2 in men versus BMI=32.5±8.1 (SD) kg/m2 in women). Female patients were significantly older than male patients (56.9±10.6 versus 50.6±11.7 year, P=0.001). The mean apnea–hypopnea index (AHI) during total sleep time was higher in men than in women (42.4±28.2 versus 33.2±27.7 events/h, P<0.001). The AHI in non-rapid eye movement (NREM) sleep was higher in men than in women (42.9±28.9 versus 32.6±28.7 events/h, P<0.001), but in rapid eye movement (REM) sleep AHI was similar in men and women (36.0±23.3 versus 34.9±25.4 events/h). Forty percent of men had AHI–REM sleep >AHI–NREM compared to 62% of women, and the difference between REM and NREM–AHI was significantly less in men than in women (14.21±11.18 versus 19.76±13.43 events/h, P<0.001)). Several aspects of sleep were worse in women versus men: sleep efficiency index was lower (79.4±16.1% versus 85.1±12.5%, P<0.001); sleep onset latency (27.7±27.7 versus 17.9±18.1min, P<0.001), and REM onset latency (161.5±76.2 versus 145.7±71.4min, P<0.018) were longer; wake time after sleep onset (WASO) was also greater in women (42.6±46.5 versus 30.7±34.9min, P<0.003). ConclusionsIn Greek subjects with OSAS, there was no difference in BMI, and female patients were significantly older than male patients. OSAS was diagnosed in men five times more often than in women. AHI was greater in men than in women, but women are more likely than men to have a higher AHI in REM than NREM. Sleep quality is worse in female than in male patients.

Reduced sleep efficiency in cervical spinal cord injury; association with abolished night time melatonin secretion.

Case-controlled preliminary observational study. Melatonin is usually secreted only at night and may influence sleep. We previously found that complete cervical spinal cord injury (SCI) interrupts the neural pathway required for melatonin secretion. Thus, we investigated whether the absence of night time melatonin in cervical SCI leads to sleep disturbances. General Clinical Research Center, Brigham and Women's Hospital, Boston, USA. In an ancillary analysis of data collected in a prior study, we assessed the sleep patterns of three subjects with cervical SCI plus absence of nocturnal melatonin (SCI levels: C4A, C6A, C6/7A) and two control patients with thoracic SCI plus normal melatonin rhythms (SCI levels: T4A, T5A). We also compared those results to the sleep patterns of 10 healthy control subjects. The subjects with cervical SCI had significantly lower sleep efficiency (median 83%) than the control subjects with thoracic SCI (93%). The sleep efficiency of subjects with thoracic SCI was not different from that of healthy control subjects (94%). There was no difference in the proportion of the different sleep stages, although there was a significantly increased REM-onset latency in subjects with cervical SCI (220 min) as compared to subjects with thoracic SCI (34 min). The diminished sleep in cervical SCI was not associated with sleep apnea or medication use. We found that cervical SCI is associated with decreased sleep quality. A larger study is required to confirm these findings. If confirmed, the absence of night time melatonin in cervical SCI may help explain their sleep disturbances, raising the possibility that melatonin replacement therapy could help normalize sleep in this group.