Gender and age differences in polysomnography findings and sleep complaints of patients referred to a sleep laboratory

Our objective was to examine the effet of gender on the sleep pattern of patients referred to a sleep laboratory. The data (questionnaires and polysomnographic recordings) were collected from a total of 2365 patients (1550 men and 815 women). The polysomnography permits an objective assessment of the sleep pattern. We included only polysomnography exams obtained with no more than one recording system in order to permit normalization of the data. Men had a significantly higher body mass index than women (28.5 ± 4.8 vs 27.7 ± 6.35 kg/m²) and had a significantly higher score on the Epworth Sleepiness Scale (10.8 ± 5.3 vs 9.5 ± 6.0), suggesting daytime sleepiness. Women had a significantly higher sleep latency than men, as well as a higher rapid eye movement (REM) latency. Men spent more time in stages 1 (4.6 ± 4.1 vs 3.9 ± 3.8) and 2 (57.0 ± 10.5 vs 55.2 ± 10.1) of non-REM sleep than women, whereas women spent significantly more time in deep sleep stages (3 and 4) than men (22.6 ± 9.0 vs 19.9 ± 9.0). The apnea/hypopnea and arousal indexes were significantly higher and more frequent in men than in women (31.0 ± 31.5 vs 17.3 ± 19.7). Also, periodic leg movement index did not differ significantly between genders, but rather differed among age groups. We did not find significant differences between genders in the percentage of REM sleep and sleep efficiency. The results of the current study suggest that there are specific gender differences in sleep pattern.

Systematic head and neck physical examination as a predictor of obstructive sleep apnea in class III obese patients

Our aim was to determine if anatomical abnormalities of the upper airway (UA) and facial skeleton of class III severely obese patients are related to the presence and severity of obstructive sleep apnea syndrome (OSAS). Forty-five patients (69% females, mean age 46.5 ± 10.8 years) with a body mass index (BMI) over 40 kg/m² underwent UA and facial skeletal examinations as well as polysomnography. Mean BMI was 49 ± 7 kg/m² and mean neck circumference was 43.4 ± 5.1 cm. Polysomnographic findings showed that 22% had a normal apnea-hypopnea index (AHI) and 78% had an AHI over 5. The presence of OSAS was associated with younger age (P = 0.02), larger neck circumference (P = 0.004), presence of a voluminous lateral wall (P = 0.0002), posteriorized soft palate (P = 0.0053), thick soft palate (P = 0.0014), long uvula (P = 0.04), thick uvula (P = 0.0052), and inferior turbinate hypertrophy (P = 0.04). A larger neck circumference (P = 0.02), presence of a voluminous lateral wall (P = 0.04), posteriorized soft palate (P = 0.03), and thick soft palate (P = 0.04) were all associated with OSAS severity. The prevalence of OSAS in this group was high. A larger neck circumference and soft tissue abnormalities of the UA were markers for both the presence and severity of OSAS. Conversely, no abnormalities in the facial skeleton were associated with OSAS in patients with morbid obesity.

Effects on prolactin secretion and binding to dopaminergic receptors in sleep-deprived lupus-prone mice

Sleep disturbances have far-reaching effects on the neuroendocrine and immune systems and may be linked to disease manifestation. Sleep deprivation can accelerate the onset of lupus in NZB/NZWF1 mice, an animal model of severe systemic lupus erythematosus. High prolactin (PRL) concentrations are involved in the pathogenesis of systemic lupus erythematosus in human beings, as well as in NZB/NZWF1 mice. We hypothesized that PRL could be involved in the earlier onset of the disease in sleep-deprived NZB/NZWF1 mice. We also investigated its binding to dopaminergic receptors, since PRL secretion is mainly controlled by dopamine. Female NZB/NZWF1 mice aged 9 weeks were deprived of sleep using the multiple platform method. Blood samples were taken for the determination of PRL concentrations and quantitative receptor autoradiography was used to map binding of the tritiated dopaminergic receptor ligands [³H]-SCH23390, [³H]-raclopride and [³H]-WIN35,428 to D1 and D2 dopaminergic receptors and dopamine transporter sites throughout the brain, respectively. Sleep deprivation induced a significant decrease in plasma PRL secretion (2.58 ± 0.95 ng/mL) compared with the control group (25.25 ± 9.18 ng/mL). The binding to D1 and D2 binding sites was not significantly affected by sleep deprivation; however, dopamine transporter binding was significantly increased in subdivisions of the caudate-putamen - posterior (16.52 ± 0.5 vs 14.44 ± 0.6), dorsolateral (18.84 ± 0.7 vs 15.97 ± 0.7) and ventrolateral (24.99 ± 0.5 vs 22.54 ± 0.7 µCi/g), in the sleep-deprived mice when compared to the control group. These results suggest that PRL is not the main mechanism involved in the earlier onset of the disease observed in sleep-deprived NZB/NZWF1 mice and the reduction of PRL concentrations after sleep deprivation may be mediated by modifications in the dopamine transporter sites of the caudate-putamen.

Sleep, ageing and night work

Studies have shown that the frequency or worsening of sleep disorders tends to increase with age and that the ability to perform circadian adjustments tends to decrease in individuals who work the night shift. This condition can cause consequences such as excessive sleepiness, which are often a factor in accidents that occur at work. The present study investigated the effects of age on the daytime and nighttime sleep patterns using polysomnography (PSG) of long-haul bus drivers working fixed night or day shifts. A total of 124 drivers, free of sleep disorders and grouped according to age (<45 years, N = 85, and ≥45 years, N = 39) and PSG timing (daytime (D) PSG, N = 60; nighttime (N) PSG, N = 64) participated in the study. We observed a significant effect of bedtime (D vs N) and found that the length of daytime sleep was shorter [D: <45 years (336.10 ± 73.75 min) vs N: <45 years (398 ± 78.79 min) and D: ≥45 years (346.57 ± 43.17 min) vs N: ≥45 years (386.44 ± 52.92 min); P ≤ 0.05]. Daytime sleep was less efficient compared to nighttime sleep [D: <45 years (78.86 ± 13.30%) vs N: <45 years (86.45 ± 9.77%) and D: ≥45 years (79.89 ± 9.45%) and N: ≥45 years (83.13 ± 9.13%); P ≤ 0.05]. An effect of age was observed for rapid eye movement sleep [D: <45 years (18.05 ± 6.12%) vs D: ≥45 years (15.48 ± 7.11%) and N: <45 years (23.88 ± 6.75%) vs N: ≥45 years (20.77 ± 5.64%); P ≤ 0.05], which was greater in younger drivers. These findings are inconsistent with the notion that older night workers are more adversely affected than younger night workers by the challenge of attempting to rest during the day.

A link between sleep loss, glucose metabolism and adipokines

The present review evaluates the role of sleep and its alteration in triggering problems of glucose metabolism and the possible involvement of adipokines in this process. A reduction in the amount of time spent sleeping has become an endemic condition in modern society, and a search of the current literature has found important associations between sleep loss and alterations of nutritional and metabolic contexts. Studies suggest that sleep loss is associated with problems in glucose metabolism and a higher risk for the development of insulin resistance and type 2 diabetes mellitus. The mechanism involved may be associated with the decreased efficacy of regulation of the hypothalamus-pituitary-adrenal axis by negative feedback mechanisms in sleep-deprivation conditions. In addition, changes in the circadian pattern of growth hormone (GH) secretion might also contribute to the alterations in glucose regulation observed during sleep loss. On the other hand, sleep deprivation stress affects adipokines - increasing tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) and decreasing leptin and adiponectin -, thus establishing a possible association between sleep-debt, adipokines and glucose metabolism. Thus, a modified release of adipokines resulting from sleep deprivation could lead to a chronic sub-inflammatory state that could play a central role in the development of insulin resistance and type 2 diabetes mellitus. Further studies are necessary to investigate the role of sleep loss in adipokine release and its relationship with glucose metabolism.

Pain-related diseases and sleep disorders

Pain and sleep share mutual relations under the influence of cognitive and neuroendocrine changes. Sleep is an important homeostatic feature and, when impaired, contributes to the development or worsening of pain-related diseases. The aim of the present review is to provide a panoramic view for the generalist physician on sleep disorders that occur in pain-related diseases within the field of Internal Medicine, such as rheumatic diseases, acute coronary syndrome, digestive diseases, cancer, and headache.

Sleep pattern and learning in knockdown mice with reduced cholinergic neurotransmission

Impaired cholinergic neurotransmission can affect memory formation and influence sleep-wake cycles (SWC). In the present study, we describe the SWC in mice with a deficient vesicular acetylcholine transporter (VAChT) system, previously characterized as presenting reduced acetylcholine release and cognitive and behavioral dysfunctions. Continuous, chronic ECoG and EMG recordings were used to evaluate the SWC pattern during light and dark phases in VAChT knockdown heterozygous (VAChT-KDHET, n=7) and wild-type (WT, n=7) mice. SWC were evaluated for sleep efficiency, total amount and mean duration of slow-wave, intermediate and paradoxical sleep, as well as the number of awakenings from sleep. After recording SWC, contextual fear-conditioning tests were used as an acetylcholine-dependent learning paradigm. The results showed that sleep efficiency in VAChT-KDHET animals was similar to that of WT mice, but that the SWC was more fragmented. Fragmentation was characterized by an increase in the number of awakenings, mainly during intermediate sleep. VAChT-KDHET animals performed poorly in the contextual fear-conditioning paradigm (mean freezing time: 34.4±3.1 and 44.5±3.3 s for WT and VAChT-KDHET animals, respectively), which was followed by a 45% reduction in the number of paradoxical sleep episodes after the training session. Taken together, the results show that reduced cholinergic transmission led to sleep fragmentation and learning impairment. We discuss the results on the basis of cholinergic plasticity and its relevance to sleep homeostasis. We suggest that VAChT-KDHET mice could be a useful model to test cholinergic drugs used to treat sleep dysfunction in neurodegenerative disorders.

Poor sleep in middle-aged women is not associated with menopause per se

Whether sleep problems of menopausal women are associated with vasomotor symptoms and/or changes in estrogen levels associated with menopause or age-related changes in sleep architecture is unclear. This study aimed to determine if poor sleep in middle-aged women is correlated with menopause. This study recruited women seeking care for the first time at the menopause outpatient department of our hospital. Inclusion criteria were an age ≥40 years, not taking any medications for menopausal symptoms, and no sleeping problems or depression. Patients were assessed with the Pittsburgh Sleep Quality Index (PSQI), modified Kupperman Index (KI), and Menopause Rating Scale (MRS). A PSQI score of <7 indicated no sleep disorder and ≥7 indicated a sleep disorder. Blood specimens were analyzed for follicle-stimulating hormone and estradiol levels. A total of 244 women were included in the study; 103 (42.2%) were identified as having a sleep disorder and 141 as not having one. In addition, 156 (64%) women were postmenopausal and 88 (36%) were not menopausal. Follicle-stimulating hormone and estradiol levels were similar between the groups. Patients with a sleep disorder had a significantly higher total modified KI score and total MRS score (both, P<0.001) compared with those without a sleep disorder. Correlations of the PSQI total score with the KI and MRS were similar in menopausal and non-menopausal women. These results do not support that menopause per se specifically contributes to sleep problems.

Asleep or not asleep? Evaluation of the Quality of Patients’ Sleep in Critical Care Nursing

Sleep is important for the recovery of a critically ill patient, as lack of sleep is known to influence negatively a person’s cardiovascular system, mood, orientation, and metabolic and immune function and thus, it may prolong patients’ intensive care unit (ICU) and hospital stay. Intubated and mechanically ventilated patients suffer from fragmented and light sleep. However, it is not known well how non-intubated patients sleep. The evaluation of the patients’ sleep may be compromised by their fatigue and still position with no indication if they are asleep or not. The purpose of this study was to evaluate ICU patients’ sleep evaluation methods, the quality of non-intubated patients’ sleep, and the sleep evaluations performed by ICU nurses. The aims were to develop recommendations of patients’ sleep evaluation for ICU nurses and to provide a description of the quality of non-intubated patients’ sleep. The literature review of ICU patients’ sleep evaluation methods was extended to the end of 2014. The evaluation of the quality of patients’ sleep was conducted with four data: A) the nurses’ narrative documentations of the quality of patients’ sleep (n=114), B) the nurses’ sleep evaluations (n=21) with a structured observation instrument C) the patients’ self-evaluations (n=114) with the Richards-Campbell Sleep Questionnaire, and D) polysomnographic evaluations of the quality of patients’ sleep (n=21). The correspondence of data A with data C (collected 4–8/2011), and data B with data D (collected 5–8/2009) were analysed. Content analysis was used for the nurses’ documentations and statistical analyses for all the other data. The quality of non-intubated patients’ sleep varied between individuals. In many patients, sleep was light, awakenings were frequent, and the amount of sleep was insufficient as compared to sleep in healthy people. However, some patients were able to sleep well. The patients evaluated the quality of their sleep on average neither high nor low. Sleep depth was evaluated to be the worst and the speed of falling asleep the best aspect of sleep, on a scale 0 (poor sleep) to 100 (good sleep). Nursing care was mostly performed while the patients were awake, and thus the disturbing effect was low. The instruments available for nurses to evaluate the quality of patients’ sleep were limited and measured mainly the quantity of sleep. Nurses’ structured observatory evaluations of the quality of patients’ sleep were correct for approximately two thirds of the cases, and only regarding total sleep time. Nurses’ narrative documentations of the patients’ sleep corresponded with patients’ self-evaluations in just over half of the cases. However, nurses documented several dimensions of sleep that are not included in the present sleep evaluation instruments. They could be classified according to the components of the nursing process: needs assessment, sleep assessment, intervention, and effect of intervention. Valid, more comprehensive sleep evaluation methods for nurses are needed to evaluate, document, improve and study patients’ quality of sleep.

Electrophysiological analysis of the sleep onset period : a comparison between subjects with long term insomnia complaints associated with mild traumatic brain injury and matched controls /

The purpose of the current undertaking was to study the electrophysiological properties of the sleep onset period (SOP) in order to gain understanding into the persistent sleep difficulties of those who complain of insomnia following mild traumatic brain injury (MTBI). While many believe that symptoms of post concussion syndrome (PCS) following MTBI resolve within 6 to 12 months, there are a number of people who complain of persistent sleep difficulty. Two models were proposed which hypothesize alternate electrophysiological presentations of the insomnia complaints of those sustaining a MTBI: 1) Analyses of standard polysomnography (PSG) sleep parameters were conducted in order to determine if the sleep difficulties of the MTBI population were similar to that of idiopathic insomniacs (i.e. greater proportion ofREM sleep, reduced delta sleep); 2) Power spectral analysis was conducted over the SOP to determine if the sleep onset signature of those with MTBI would be similar to psychophysiological insomniacs (characterized by increased cortical arousal). Finally, exploratory analyses examined whether the sleep difficulties associated with MTBI could be explained by increases in variability of the power spectral data. Data were collected from 9 individuals who had sustained a MTBI 6 months to 5 years earlier and reported sleep difficulties that had arisen within the month subsequent to injury and persisted to the present. The control group consisted of 9 individuals who had experienced neither sleep difficulties, nor MTBI. Previous to spending 3 consecutive uninterrupted nights in the sleep lab, subjects completed questionnaires regarding sleep difficulties, adaptive functioning, and personality.

A dose-response investigation of the attentional blink during sleep restriction /

Recent dose-response sleep restriction studies, in which nightly sleep is curtailed to varying degrees (e.g., 3-, 5-, 7-hours), have found cumulative, dose-dependent changes in sleepiness, mood, and reaction time. However, brain activity has typically not been measured, and attentionbased tests employed tend to be simple (e.g., reaction time). One task addressing the behavioural and electrophysiological aspects of a specific attention mechanism is the Attentional Blink (AB), which shows that the report accuracy of a second target (T2) is impaired when it is presented soon after a first target (Tl). The aim of the present study was to examine behavioural and electrophysioiogical responses to the AB task to elucidate how sleep restriction impacts attentional capacity. Thirty-six young-adults spent four consecutive days and nights in a sleep laboratory where sleep, food, and activity were controlled. Nightly sleep began with a baseline sleep (8 hours), followed by two nights of sleep restriction (3,5 or 8 hours of sleep), and a recovery sleep (8 hours). An AB task was administered each day at 11 am. Results from a basic battery oftests (e.g., sleepiness, mood, reaction time) confirmed the effectiveness of the sleep restriction manipulation. In terms of the AB, baseline performance was typical (Le., T2 accuracy impaired when presented soon after Tl); however, no changes in any AB behavioural measures were observed following sleep restriction for the 3- or 5-hour groups. The only statistically significant electrophysiological result was a decrease in P300 amplitude (for Tl) from baseline to the second sleep restriction night for the 3-hour group. Therefore, following a brief, two night sleep restriction paradigm, brain functioning was impaired for the TI of the AB in the absence of behavioural deficit. Study limitations and future directions are discussed.

Information processing in sleep-onset insomnia : a test of the neurocognitive model /

The present thesis study is a systematic investigation of information processing at sleep onset, using auditory event-related potentials (ERPs) as a test of the neurocognitive model of insomnia. Insomnia is an extremely prevalent disorder in society resulting in problems with daytime functioning (e.g., memory, concentration, job performance, mood, job and driving safety). Various models have been put forth in an effort to better understand the etiology and pathophysiology of this disorder. One of the newer models, the neurocognitive model of insomnia, suggests that chronic insomnia occurs through conditioned central nervous system arousal. This arousal is reflected through increased information processing which may interfere with sleep initiation or maintenance. The present thesis employed event-related potentials as a direct method to test information processing during the sleep-onset period. Thirteen poor sleepers with sleep-onset insomnia and 1 2 good sleepers participated in the present study. All poor sleepers met the diagnostic criteria for psychophysiological insomnia and had a complaint of problems with sleep initiation. All good sleepers reported no trouble sleeping and no excessive daytime sleepiness. Good and poor sleepers spent two nights at the Brock University Sleep Research Laboratory. The first night was used to screen for sleep disorders; the second night was used to investigate information processing during the sleep-onset period. Both groups underwent a repeated sleep-onsets task during which an auditory oddball paradigm was delivered. Participants signalled detection of a higher pitch target tone with a button press as they fell asleep. In addition, waking alert ERPs were recorded 1 hour before and after sleep on both Nights 1 and 2.As predicted by the neurocognitive model of insomnia, increased CNS activity was found in the poor sleepers; this was reflected by their smaller amplitude P2 component seen during wake of the sleep-onset period. Unlike the P2 component, the Nl, N350, and P300 did not vary between the groups. The smaller P2 seen in our poor sleepers indicates that they have a deficit in the sleep initiation processes. Specifically, poor sleepers do not disengage their attention from the outside environment to the same extent as good sleepers during the sleep-onset period. The lack of findings for the N350 suggest that this sleep component may be intact in those with insomnia and that it is the waking components (i.e., Nl, P2) that may be leading to the deficit in sleep initiation. Further, it may be that the mechanism responsible for the disruption of sleep initiation in the poor sleepers is most reflected by the P2 component. Future research investigating ERPs in insomnia should focus on the identification of the components most sensitive to sleep disruption. As well, methods should be developed in order to more clearly identify the various types of insomnia populations in research contexts (e.g., psychophysiological vs. sleep-state misperception) and the various individual (personality characteristics, motivation) and environmental factors (arousal-related variables) that influence particular ERP components. Insomnia has serious consequences for health, safety, and daytime functioning, thus research efforts should continue in order to help alleviate this highly prevalent condition.

A comparison of electrophysiological changes during the sleep onset period of psychophysiological insomniacs, psychiatric insomniacs and normal sleepers

The EEG of the sleep onset period of psychophysiological insomniacs, psychiatric insomniacs and controls was compared using power spectral analysis (FFT). Eighteen drug-free subjects were equally divided into three groups according to their responses in the Brock Sleep and Insomnia Questionnaire, the Minnesota Multiphasic Personality Inventory and the Sleep Disorders Questionnaire. Group 1 consisted of psychophysiological insomniacs, group 2 included insomniacs with an indication of psychiatric disturbances, and group 3 was a control group. EEG, EOG and EMG were recorded for two consecutive nights. Power spectral analysis (FFT) of EEG at C4 from the sleep onset period (defined as lights out to the first five minutes of stage 2) was performed on all standard frequency bands, delta: .5-4 Hz; theta: 4-8 Hz; alpha: 8-12 Hz; sigma: 12-15 Hz beta: 15-25 Hz. Psychophysiological insomniacs had less alpha during wakefulness than the other two groups and did not show the dramatic drop in alpha across the sleep onset period, which characterizes normal sleep. They also had less delta, especially during stage 2 on night 2. They also showed less delta in the last quartile of the chronological analysis of the sleep onset period. Psychiatric insomniacs showed lower relative beta power values overall while psychophysiological insomniacs showed higher relative beta power values during wakefulness. This microanalysis 11 confirms that the sleep onset period is generally similar for psychiatric insomniacs and normal sleepers. This may be due to the sample of psychiatric insomniacs being heterogeneous or may reflect a sleep onset system that is essentially intact. Psychophysiological insomniacs have higher cortical arousal during the sleep onset period than do the psychiatric insomniacs and the controls. Clear differences in the sleep onset period of psychophysiological insomniacs exist. The dramatic changes in power values in these two groups are not seen in the psychophysiological insomniacs, which may make the discrimination between wakefulness and sleep more difficult.

Subjective, behavioural and electrophysiological measurements of the time-course and intensity of sleep inertia after a full night of sleep /

Several recent studies have described the period of impaired alertness and performance known as sleep inertia that occurs upon awakening from a full night of sleep. They report that sleep inertia dissipates in a saturating exponential manner, the exact time course being task dependent, but generally persisting for one to two hours. A number of factors, including sleep architecture, sleep depth and circadian variables are also thought to affect the duration and intensity. The present study sought to replicate their findings for subjective alertness and reaction time and also to examine electrophysiological changes through the use of event-related potentials (ERPs). Secondly, several sleep parameters were examined for potential effects on the initial intensity of sleep inertia. Ten participants spent two consecutive nights and subsequent mornings in the sleep lab. Sleep architecture was recorded for a fiiU nocturnal episode of sleep based on participants' habitual sleep patterns. Subjective alertness and performance was measured for a 90-minute period after awakening. Alertness was measured every five minutes using the Stanford Sleepiness Scale (SSS) and a visual analogue scale (VAS) of sleepiness. An auditory tone also served as the target stimulus for an oddball task designed to examine the NlOO and P300 components ofthe ERP waveform. The five-minute oddball task was presented at 15-minute intervals over the initial 90-minutes after awakening to obtain six measures of average RT and amplitude and latency for NlOO and P300. Standard polysomnographic recording were used to obtain digital EEG and describe the night of sleep. Power spectral analyses (FFT) were used to calculate slow wave activity (SWA) as a measure of sleep depth for the whole night, 90-minutes before awakening and five minutes before awakening.