Subjective Sleep Onset Research Articles

Rumination Predicts Longer Sleep Onset Latency After an Acute Psychosocial Stressor

Rumination has been linked to self-reported sleep quality. However, whether rumination is related to an objective sleep parameter has not been tested. This study examined whether rumination predicts sleep onset latency (SOL) on the night after an acute psychosocial stressor. We hypothesized that those who ruminate (assessed with both trait and stressor-specific measures) would have longer SOL (assessed with objective and subjective methods). Seventy participants delivered a 5-minute speech in front of an evaluative panel during an afternoon laboratory session. Trait rumination was assessed before the stressor. Stressor-specific rumination was captured with the frequency of task-related thoughts participants experienced during a 10-minute rest period after the stressor. Participants wore actigraphs on their wrists on the night after the laboratory session to measure objective sleep onset latency (SOL-O). Subjective sleep onset latency was estimated by participants on the subsequent morning. Consistent with hypotheses, trait and stressor-specific rumination predicted longer SOL-O and subjective sleep onset latency, respectively. In addition, trait and stressor-specific rumination interacted to predict longer SOL-O. SOL-O was longest among those who engaged in more stressor-specific rumination and had greater trait rumination scores. Neither rumination measure was related to sleep duration or wakefulness after sleep onset. The findings from this study are consistent with previous research linking rumination to subjective sleep quality. The results also suggest that post-stressor ruminative thought may predict delayed sleep onset for those with a propensity for rumination.

Paradoxical insomnia: The role of CAP and arousals in sleep misperception

Objective The relationship between CAP parameters and subjective time perception during sleep in primary insomnia was investigated. Patients and methods Data collected from all-night PSG recordings of 20 patients with a diagnosis of paradoxical insomnia (misperceptors) were compared with those of 20 normal gender- and age-matched subjects (controls). Besides sleep staging, scoring measures included CAP parameters and EEG arousals. Results Patients and controls presented non-significant differences in the amounts of objective sleep time (464 min vs. 447 min) and objective sleep latency (9 min vs. 8 min). Compared to controls, misperceptors reported a significantly shorter time of perceived sleep (285 min vs. 461 min) and a significantly longer duration of perceived sleep latency (51 min vs. 22 min). In spite of the 11 objective awakenings, misperceptors reported only 4 subjective awakenings, while controls described 2 of the 5 objective awakenings. Arousal index (31.7/h vs. 18.6/h) and total CAP rate (58.1% vs. 35.5%) were significantly higher in misperceptors. In the sleep period between objective and subjective sleep onset, CAP rate was 64.4% in misperceptors and 45.1% in controls ( p < 0.002). Insomniacs showed significantly higher amounts of CAP rate in stage 1 (62.7% vs. 37.5%) and in stage 2 (53.3% vs. 33.1%), but not in slow wave sleep. CAP phase A2 subtypes were significantly increased in misperceptors (31% vs. 24%). Conclusions The study points out the topical role of enhanced activation and arousal instability not only in the first part of the night (mismatch between objective and subjective sleep onset) but also in the misperception of consecutive objective awakenings which are subjectively grouped together as a single prolonged event.

Zolpidem Extended-Release Improves Sleep and Next-Day Symptoms in Comorbid Insomnia and Generalized Anxiety Disorder

A multicenter, double-blind, parallel-group study was designed to assess the efficacy and safety of zolpidem extended-release coadministered with escitalopram in patients with insomnia and comorbid generalized anxiety disorder. Patients (N = 383) received open-label escitalopram 10 mg/d and were randomized to either adjunct zolpidem extended-release 12.5 mg or placebo. The primary efficacy measure was change from baseline to week 8 in subjective total sleep time. Secondary efficacy measures included subjective sleep onset latency, number of awakenings, wake time after sleep onset, sleep quality, the Hamilton Rating Scale for Anxiety, the Beck Anxiety Inventory, the Sleep Impact Scale, the Massachusetts General Hospital Cognitive and Physical Functioning Questionnaire, and the Sheehan Disability Scale. The last-observation-carried-forward method was used to impute missing values for most efficacy measures. Safety was monitored at each visit. At week 8 and all time points, there was a significant improvement in the zolpidem extended-release/escitalopram group compared with placebo/escitalopram for total sleep time (P < 0.0001). Most of the secondary efficacy measures also significantly favored zolpidem at most visits (P < 0.0001). The most common treatment-emergent adverse events in both groups were nausea, dizziness, headache, fatigue, and dry mouth. Concurrent zolpidem extended-release/escitalopram, compared with placebo/escitalopram, significantly improved insomnia and sleep-related next-day symptoms, but not anxiety symptoms, in patients with comorbid insomnia and generalized anxiety disorder.

Efficacy and hypnotic effects of melatonin in shift-work nurses: double-blind, placebo-controlled crossover trial

BackgroundNight work is associated with disturbed sleep and wakefulness, particularly in relation to the night shift. Circadian rhythm sleep disorders are characterized by complaints of insomnia and excessive daytime sleepiness that are primarily due to alterations in the internal circadian timing system or a misalignment between the timing of sleep and the 24-h social and physical environment.MethodsWe evaluated the effect of oral intake of 5 mg melatonin taken 30 minutes before night time sleep on insomnia parameters as well as subjective sleep onset latency, number of awakenings, and duration of sleep. A double-blind, randomized, placebo-controlled crossover study with periods of 1 night and washouts of 4 days comparing melatonin with placebo tablets was conducted. We tried to improve night-time sleep during recovery from night work. Participants were 86 shift-worker nurses aged 24 to 46 years. Each participant completed a questionnaire immediately after awakening.ResultsSleep onset latency was significantly reduced while subjects were taking melatonin as compared with both placebo and baseline. There was no evidence that melatonin altered total sleep time (as compared with baseline total sleep time). No adverse effects of melatonin were noted during the treatment period.ConclusionMelatonin may be an effective treatment for shift workers with difficulty falling asleep.

Long-Term Efficacy and Safety of Zolpidem Extended-Release 12.5 mg, Administered 3 to 7 Nights Per Week for 24 Weeks, in Patients With Chronic Primary Insomnia: A 6-Month, Randomized, Double-Blind, Placebo-Controlled, Parallel-Group, Multicenter Study

To evaluate long-term efficacy and safety of zolpidem extended-release 3 to 7 nights/week for chronic primary insomnia. Multicenter, 25-week, phase IIIb, randomized, double-blind, placebo-controlled, parallel-group. Outpatient; visits every 4 weeks. Aged 18 to 64 years; DSM-IV criteria for chronic primary insomnia; > or =3 months of difficulty initiating or maintaining sleep or experiencing nonrestorative sleep. Single-dose zolpidem extended-release 12.5 mg (n = 669) or placebo (n = 349), self-administered from a minimum of 3 nights/week to a maximum of 7 nights/week. Patient's Global Impression (PGI) and Clinical Global Impression-Improvement (CGI-I) were assessed every 4 weeks up to week 24. Patient Morning Questionnaire (PMQ), recorded daily, assessed subjective sleep measures-sleep onset latency (SOL), total sleep time (TST), number of awakenings (NAW), wake time after sleep onset (WASO), and quality of sleep (QOS)-and next-day functioning. At week 12, PGI, Item 1 (aid to sleep), the primary endpoint, was scored as favorable (i.e., "helped me sleep") by 89.8% of zolpidem patients vs. 51.4% of placebo patients (P < 0.0001, based on rank score) and at week 24 by 92.3% of zolpidem extended-release patients vs. 59.7% of placebo patients. Zolpidem extended-release also was statistically significantly superior to placebo at every time point for PGI (Items 1-4) and CGI-I (P < 0.0001, rank score), TST, WASO, QOS (P < 0.0001), and SOL (P < or = 0.0014); NAW (Months 2-6; P < 0.0001). Sustained improvement (P < 0.0001, all time points) was observed in morning sleepiness and ability to concentrate (P = 0.0014, month 6) with zolpidem extended-release compared with placebo. Most frequent adverse events for zolpidem extended-release were headache, anxiety and somnolence. No rebound effect was observed during the first 3 nights of discontinuation. These findings establish the efficacy of 3 to 7 nights per week dosing of zolpidem extended-release 12.5 mg for up to 6 months. Treatment provided sustained and significant improvements in sleep onset and maintenance and also improved next-day concentration and morning sleepiness.

Meta‐analysis of sleep changes in control groups of insomnia treatment trials

A meta-analysis assessing the magnitude of sleep changes from baseline in placebo-treated (psychological and pharmacological placebo) and untreated groups issued from independent trials was conducted. Comparisons were then performed to assess if the magnitude of sleep changes in the placebo control groups were significantly different than those of the untreated group. Medline, PsychInfo and Current Contents databases (1990-2004) were searched for primary insomnia treatment studies using a randomized controlled parallel-group design. Effect sizes were computed for each end-point variable based on subjective (patient-reported) and polysomnographic measures. Thirty-four studies (n = 1392 subjects) met inclusion criteria; twenty-three used a pharmacological placebo (n = 1163), four used a psychological placebo (n = 81), and seven used a waitlist condition (n = 148). Between-group comparisons were performed using a random effects model analysis. Significant pre-post changes were observed in the pharmacological placebo condition on several sleep parameters, both on objectively and subjectively measured outcomes [objective and subjective sleep onset latency (SOL) and total sleep time (TST) and subjective wake after sleep onset]. Although a tendency was observed for objective SOL, only the changes on subjective SOL and TST in the pharmacological placebo condition were significantly different from the corresponding changes in the untreated group. No differences were significant for the psychological placebo groups. Although the present findings suggest that sleep may significantly change in response to a pharmacological placebo, conclusions remain tentative because of possible confounds that may arise when comparing groups issued from different trials. Further research directly comparing placebo groups and untreated groups from the same randomized trials remains necessary.

Effect of repeated gaboxadol administration on night sleep and next-day performance in healthy elderly subjects

Aging is associated with dramatic reductions in sleep continuity and sleep intensity. Since gaboxadol, a selective GABA(A) receptor agonist, has been demonstrated to improve sleep consolidation and promote deep sleep, it may be an effective hypnotic, particularly for elderly patients with insomnia. In the present study, we investigated the effects of subchronic gaboxadol administration on nocturnal sleep and its residual effects during the next days in elderly subjects. This was a randomized, double-blind, placebo-controlled, balanced crossover study in 10 healthy elderly subjects without sleep complaints. The subjects were administered either placebo or 15 mg gaboxadol hydrochloride at bedtime on three consecutive nights. Sleep was recorded during each night from 2300 to 0700 h and tests assessing attention (target detection, stroop test) and memory function (visual form recognition, immediate word recall, digit span) were applied at 0900, 1400, and 1700 h during the following days. Compared with placebo, gaboxadol significantly shortened subjective sleep onset latency and increased self-rated sleep intensity and quality. Polysomnographic recordings showed that it significantly decreased the number of awakenings, the amount of intermittent wakefulness, and stage 1, and increased slow wave sleep and stage 2. These effects were stable over the three nights. None of the subjects reported side effects. Next-day cognitive performance was not affected by gaboxadol. Gaboxadol persistently improved subjective and objective sleep quality and was devoid of residual effects. Thus, at the employed dose, it seems an effective hypnotic in elderly subjects.

Effect of Repeated Gaboxadol Administration on Night Sleep and Next-Day Performance in Healthy Elderly Subjects

Aging is associated with dramatic reductions in sleep continuity and sleep intensity. Since gaboxadol, a selective GABA(A) receptor agonist, has been demonstrated to improve sleep consolidation and promote deep sleep, it may be an effective hypnotic, particularly for elderly patients with insomnia. In the present study, we investigated the effects of subchronic gaboxadol administration on nocturnal sleep and its residual effects during the next days in elderly subjects. This was a randomized, double-blind, placebo-controlled, balanced crossover study in 10 healthy elderly subjects without sleep complaints. The subjects were administered either placebo or 15 mg gaboxadol hydrochloride at bedtime on three consecutive nights. Sleep was recorded during each night from 2300 to 0700 h and tests assessing attention (target detection, stroop test) and memory function (visual form recognition, immediate word recall, digit span) were applied at 0900, 1400, and 1700 h during the following days. Compared with placebo, gaboxadol significantly shortened subjective sleep onset latency and increased self-rated sleep intensity and quality. Polysomnographic recordings showed that it significantly decreased the number of awakenings, the amount of intermittent wakefulness, and stage 1, and increased slow wave sleep and stage 2. These effects were stable over the three nights. None of the subjects reported side effects. Next-day cognitive performance was not affected by gaboxadol. Gaboxadol persistently improved subjective and objective sleep quality and was devoid of residual effects. Thus, at the employed dose, it seems an effective hypnotic in elderly subjects.

Short-term stimulus control treatment of insomnia in older adults

A 4-week stimulus control treatment was administered in small groups to 16 ambulatory, noninstitutionalized older adults with sleep onset insomnia. Nine subjects received immediate treatment, and 7 received delayed treatment. Subjective sleep onset latency was collected at baseline, at termination of treatment, and at a 6-week follow-up. Results showed a strong treatment effect which was replicated with the delayed treatment group; both groups maintained their gains through the 6-week follow-up period. The effectiveness of these procedures with the older insomniac is especially encouraging, since it is a much safer intervention than sedative-hypnotic medications.

The threshold of sleep: perception of sleep as a function of time asleep and auditory threshold.

A number of studies have found that many subjects have reported being awake when awakened during various periods of electroencephalographically (EEG)-defined sleep. These observations have led to an examination of the perception of sleep after periods when EEG-defined sleep was experimentally varied between 1 and 140 min. Twelve normal young adult subjects slept in the laboratory for 5 consecutive nights. Each subject was briefly awakened five times on each night, and subjective state, auditory arousal threshold, and sleep/wake time estimation data were collected. The threshold of sleep onset (i.e., the point at which a report of sleep was given 50% of the time) occurred 2-4 min after the first sleep spindle. In contrast, auditory thresholds rose rapidly within 1 min of the first sleep spindle. The threshold data corroborate the appearance of a sleep spindle as an objective measure of sleep onset. However, subjective sleep onset appears to be a relatively lengthy period during which perception of state is blurred and uncertain.