Loneliness is a risk factor for premature mortality but the mechanics of this relationship remain obscure. A potential mechanism is sleep disturbance. The present study aimed to examine the association between loneliness and sleep disturbance, evaluate loneliness as a risk factor for sleep disturbance and vice-versa, model effects between loneliness and sleep disturbance over time, and evaluate a mediation model of loneliness, sleep disturbance, and health. Data came from the 2006-2012 waves of the Health and Retirement Study, a nationally-representative study of older Americans; participants > 65 were included (n=11,400). Analyses included (i) linear regressions accounting for complex sampling and (ii) path analysis (cross-lagged panel and mediation models). Loneliness and sleep disturbance were correlated and were risk factors for one another. Cross-lagged panel models showed reciprocal effects between loneliness and sleep disturbance. Cross-lagged mediation models showed that loneliness predicted subsequent sleep disturbance, which in turn predicted poor self-reported health. Moreover, there was evidence of a direct and indirect effect of loneliness on sleep disturbance. All associations were weakened— but remained—when accounting for demographics, isolation, and depression. Collectively, these findings are consistent with the theory that sleep disturbance is a mechanism through which loneliness damages health. However, effects between loneliness and sleep are reciprocal, rather than unidirectional. Moreover, longitudinal effects were very small. Further research is necessary to speak to causality, assess daily associations between loneliness and sleep, assess a comprehensive model of the mechanics of loneliness and health, and examine loneliness and sleep in the context of other factors.

During hospitalization, sleep can be interrupted or even elusive. It has been established that quality sleep is essential in neural repair. Previous research has indicated that many nurses are unaware of the impact of sleep disturbance on brain injury recovery and do not understand how to promote sleep in the neurorehabilitation setting. The purpose of this project was to determine whether educational intervention would influence nurses' knowledge and attitudes toward sleep. Benner's (2001) novice to expert theory provided a framework for the project. With the collaboration of a neuropsychologist, this study produced a sleep knowledge and attitudes instrument. Pulmonary sleep specialists, rehabilitation physicians, and neuropsychologists who were experts in the treatment of sleep disorders and brain injury validated the instrument. Following instrument validation, 19 rehabilitation nurses completed the instrument prior to receiving sleep hygiene education. Immediately after education, a posttest was administered. Pretest and posttest data were compared via Wilcoxon signed-rank tests. Results indicated a statistically significant increase nurses' knowledge (p = .015) and attitudes (p = .028) toward sleep. These findings support the use of didactic methods of sleep hygiene education for nurses. Providing nurses with sleep knowledge and improving their attitudes toward sleep may shift nursing focus to sleep as an activity rather than inactivity, and it has the potential to improve quality of patient care by empowering nurses to implement good sleep hygiene practices on inpatient units. Additional research is indicated to determine whether the increase in knowledge and improvement in attitudes will be sustained and ultimately affect patient sleep outcomes.

In mammals, circadian rhythms are controlled by an endogenous clock located in the suprachiasmatic nucleus (SCN). The SCN is part of a wake-promoting pathway in adults involving the dorsomedial hypothalamus (DMH) and locus coeruleus (LC), but little is known about how this circuit develops. Therefore, we examined the neural mechanisms underlying the development of circadian and ultradian sleep-wake rhythms. Circadian rhythms of sleep and wakefulness are exhibited by rats at postnatal day (P)2, but the influence of forebrain structures, including the SCN, has not been examined. In Experiment 1, although precollicular transections at P2 did not alter day-night differences in sleep and wakefulness, transections at P8 did eliminate these differences. In contrast, in Experiment 2, SCN lesions eliminated day-night differences in sleep and wakefulness at P2. These results suggest that the SCN exerts a humoral influence in newborns and gains neural control over brainstem structures over the first postnatal week. Based on the results of Experiments 1 and 2, we hypothesized that neural connections among the SCN, DMH, and LC develop over the first postnatal week. In Experiment 3, we used fluorescent tracers to reveal that connections within this circuit are strengthened and elaborated--and also become bidirectional--between P2 and P8. The results of Experiment 3 indicate that the SCN receives feedback from the LC. To explore the functional mechanisms by which the SCN receives this feedback, in Experiment 4, we deprived pups of sleep at P8 and used cFos to visualize brain areas that became active as a result of forced wakefulness. Our findings in intact pups and those injected with DSP-4, a neurotoxin that targets noradrenergic LC terminals, suggest that forced wakefulness activates the LC, which subsequently activates the DMH and SCN. After connectivity among the SCN, DMH, and LC is established, we tested the functional role of each nucleus in the modulation of sleep and wakefulness. Infants cycle rapidly between states of sleep and wakefulness, resulting in fragmented bouts. Over development, these sleep and wake bouts consolidate and circadian rhythms become evident. Analyses of the statistical distributions of sleep and wake bouts have revealed dramatic changes in the dynamics of sleep-wake activity. Sleep bouts follow an exponential distribution throughout development. In contrast, wake bouts initially follow an exponential distribution, but transition to a power-law distribution around P15. In Experiments 5, 6, and 7, we explored the contributions of the LC, SCN, and DMH, respectively, to this developmental transition. We found that lesions of each area prevented the emergence of power-law wake behavior. Lesions of the SCN and DMH also prevented the expression of nocturnality. Altogether, these findings reveal that neural connections between the SCN and brainstem develop over the first postnatal week. After this connectivity is established, the SCN-DMH-LC pathway is critical for the normal expression of power-law wake behavior and circadian rhythmicity. We suggest that the development of the SCN-DMH-LC circuit is critical for pups to regulate arousal and gain independence from the mother and littermates.

A large body of research has demonstrated general relations of sleep complaints with psychological disorders, including anxiety, depression, and dissociation/schizotypy. In contrast, very few studies have focused on the specificity of sleep complaints to daytime symptoms. Identifying sleep disturbances that show evidence of specificity is important for differential diagnosis and assessment. This study used the structure of self-reported sleep complaints as a framework for examining specificity. Comprehensive questionnaire and interview measures of sleep disturbance were submitted to factor analyses in students and psychiatric patients. These analyses revealed the presence of three well defined higher order factors: Lassitude, Insomnia, and Unusual Sleep Experiences. These factors were then correlated with interview and questionnaire measures of daytime symptoms. Lassitude was specific to dysphoria, whereas Insomnia had weaker, nonspecific relations with daytime symptoms. Fatigue, a component of Lassitude, showed the strongest evidence of specificity. Unusual Sleep Experiences was specific to symptoms of posttraumatic stress disorder (PTSD) and dissociation. In particular, the Nightmares component of Unusual Sleep Experiences was strongly related to PTSD and the Sleep Hallucinations component of Unusual Sleep Experiences was strongly related to dissociation.

There are numernus social, emotional, and behavioral problems toddlers and preschool children can exhibit. Some of the more common problems reported by parents of young children are daytime behavior problems and sleep disturbances. This study investigated sleep difficulties in toddler and preschool-age children with (n = 31) and without (n = 59) significant behavior problems. Furthermore, the current study investigated the relationship between sleep difficulties and other psychological constructs (i.e., maternal general stress, maternal depression, and parenting stress), which might be related to sleep and behavior problems. Mothers of clinically referred children with behavior problems and nonclinically referred children without behavior problems completed measures regarding their children's sleep and behavior as well as their own general stress, parenting stress, and depressive symptomology. Overall, children with behavior problems showed significantly more sleep difficulties than children without behavior problems. Specifically, when compared to children without behavior problems, children with behavior problems took more time to initiate sleep, showed increased bedtime resistance, had more night wakings, and had shorter sleep durations. Additionally, the results showed that other factors (i.e., maternal depression, family stress, parent-child relationship stress) likely contribute to and/or maintain sleep disturbances in children. The findings from this study suggest a complex relationship between childhood sleep, daytime externalizing behaviors, and maternal health. Potential clinical implications of these findings and future directions for research are discussed.

Abstract not available

Doctor of Philosophy (Medicine) / Sleepiness is an important source of morbidity in the community, with potentially catastrophic consequences of occupational or driving injuries or accidents. Although many measures of sleepiness exist, there is no gold standard. The electroencephalograph (EEG) has been studied as an indicator of sleep pressure in the waking organism, or sleep depth. A mathematical model has been developed, relating the observed EEG to interactions between groups of neurons in the cortex and thalamus (Robinson, Rennie, Rowe, O'Connor, & Gordon, 2005; Robinson, Rennie, & Wright, 1997). These interactions are thought to be important in the transition from wake to sleep. Sleepiness is common in obstructive sleep apnea (OSA). The measurement of sleepiness would have great utility in quantifying the disease burden, measuring treatment response, or determining fitness for work or driving. This study will evaluate parameters derived from the EEG mathematical model as a measure of sleepiness. It is divided into the following four parts: 1. Subjects with likely OSA based on symptoms and demographics from an international database were compared with matched non-OSA controls. The OSA group showed deficits in executive function and abnormalities on evoked response potential testing. 2. Outcomes from a cross-sectional study in a sleep-clinic OSA population were aggregated by factor analysis into a five summary variables relevant to sleepiness: subjective sleepiness, mood & anxiety, memory & learning, driving, and executive functioning. 3. EEG mathematical model parameters from wake EEG recordings were related to the five summary outcomes. Executive function correlated with a parameter Z, representing the negative feedback loop between the thalamic reticular nucleus and the thalamocortical relay nuclei. 4. EEG model parameters during first NREM sleep cycle of 8 subjects with regular sleep architecture were studied. Net cortical excitation (parameter X) is predicted to increase across the cycle, while there was, as predicted, a greater inhibitory effect of the thalamic reticular nucleus upon thalamocortical relay cells (parameter Z). In this preliminary assessment, EEG model parameters reflecting thalamocortical interactions are sensitive to prefrontal lobe tasks such as executive function, which are known to be vulnerable to sleep loss and sleepiness, and these parameters also show variation with increasing sleep depth.

Bedsharing between infants and parents interacts with many factors to increase the risk of SIDS, eg maternal smoking, alcohol or drug consumption, overtiredness, excessive bedding and younger infant. However, bedsharing also encourages breastfeeding, settles babies, reduces parental tiredness and increases mother-baby interactions. We studied infants in the natural setting of their own home, in their usual situation (bedsharing or cot-sleeping) to identify risks and benefits, and to understand how bedsharing could be made safer for all infants. Methods: Overnight home video and physiological recordings of 40 bedshare infants (5-27 weeks), were compared with 40 cot infants matched for age and study season. Video data provided a log of infant/parent sleep positions, movements and interactions. The physiological recordings measured respiratory pattern, respiratory airflow, inspired CO2, oxygen saturation (SaO2), heart rate and core, peripheral and environmental temperatures. Results: All infants maintained normal core temperatures overnight although bedshare infants had a higher shin temperature [35.43 vs 34.60°C at 2hrs after sleep onset (difference 0.83, 95% CI: 0.18 to 1.49)]. Bedshare infants had thicker bedding (RR:2.35 (95% CI:1.76 to 3.14) and more face covered time [0.9h/night vs 0.2 (RR:5.62, 95% CI: 3.08 to 10.25)]. Awakenings in the bedshare group were more common, of shorter duration, and caused less change in infant temperatures. Exposure to >3% CO2 occurred in 18 bedshare infants and 1 swaddled, cot-sleep infant. The maximum exposure time was the same for both groups (60mins). These levels of CO2 significantly (p<0.05) elevated breathing rate and maintained normal SaO2. Central apnoeas of 5-10 seconds resulted in drops in SaO2 <90% (BS mean 6.8/night vs cot: 3.1, p<0.001). SaO2 rarely fell below 85% and heart rate did not ever fall below 90bpm. Bedshare infants commonly slept on their side, while cot infants slept supine. Prone sleeping was rare (BS:5 infants, 1.6-3.5h/night vs cot:2, 8.9-10.2) and for bedshare infants involved sleeping on mother�s chest. Bedshare infants woke and fed more frequently (mean wake times/night: 4.6 vs 2.5), but total sleep time was not different. Maternal checks were more frequent in the bedshare group (median:10, IQ range:7-23, max:55) than cot ( 4, 3-6, 16) and bedshare mothers frequently responded to infant initiated movements. During bedsharing baby and mother usually slept facing each other, touching, with infants at mothers� breast level. Father (or sibling) contact was rare. Conclusions: Bedshare infants sleep in a warmer environment and experience more potentially dangerous events such as head-covering and rebreathing. However, all infants in this study maintained normal rectal temperature and SaO2 suggesting they were protected by homeostatic responses. Infant safety is also facilitated by frequent maternal checking and maternal responses to infant movements. The mother-infant proximity during bedsharing allows prompt responses, reduces time infants are upset, and minimises disruption from frequent breast feeding - aspects valued by many. It is not known if infants of smoking mothers or parents with impaired responses eg due to alcohol, respond adequately to the potentially dangerous situations identified. Outcome: The results of this study will be used to formulate recommendations to parents for improving the safety of bedsharing.

More is becoming known about the importance of sleep to health, with inadequate sleep recognised as a significant public health issue. Sleep clinics have reported disproportionate numbers of Māori and Pacific peoples with more severe obstructive sleep apnoea syndrome (OSAS), raising concerns about accessibility of services and possible differences in prevalence between ethnic groups. Prevalence information on sleep disorders in Aotearoa is needed to assess its public health impact and plan for population health care needs. This thesis presents a national study examining the prevalence of OSAS symptoms and risk factors among Maori and non-Maori adults in Aotearoa. This project is also situated within the wider scope of ethnic inequalities in health between Maori and non-Maori and is concerned with making a positive contribution to Maori health and the elimination of disparities. Kaupapa Maori Research (KMR) is the underlying methodology that drives this study. As such, it assumes a Maori norm, and prioritises Maori needs. A Maori/non-Maori analytical framework is used that distinguishes Maori as tangata whenua, addresses Maori health needs as well as non-Maori, and enables the monitoring of guarantees as outlined by the Treaty of Waitangi. The goals of this thesis were to estimate the prevalence of OSAS symptoms and risk factors among Maori and non-Maori adults in New Zealand, and to examine independent predictive variables for specific OSAS symptoms. An objective was also to contribute to KMR through designing and undertaking a KMR project using a quantitative method, with the development of concepts for use in other areas of research. In April 1999, a short questionnaire was sent to a sample of 10000 New Zealands (5500 of Maori descent and 4500 non-Maori participants to enable research questions to be examined with equal statistical power for both groups. The results demonstrate that the prevalence of OSAS symptoms and risk factors, particularly among non-Maori, are comparable to other international studies, indicating that OSAS is likely to be a common problem among adults in Aotearoa. Furthermore, the results suggest that Maori are significantly more likely to suffer from OSAS than non-Maori, with higher rates of symptoms and risk factors of OSAS among both men and women. As an area of medicine that is under-serviced in Aotearoa, the results provide important information with which to plan for population needs. There are a number of health implications from this study, relating specifically to the diagnosis and management of OSAS in Aotearoa, and to Maori health and the elimination of disparities. These are multi-levelled and include health service implications across the continuum of care, from specialist sleep services to primary care; public health implications that involve preventive measures and broader determinants of health; and KMR principles that can be applied to interventions and health research in general. As a KMR project the implications and recommendations focus on Maori health research in general. As a KMR project the implications and recommendations focus on Maori health gain and addressing disparities in health. This is consistent with Maori health rights, and a population approach that considers health inequalities and the role of wider determinants of health and health services.

Major Depressive Disorder (MDD) is exceedingly prevalent and considered to be one of the leading cause of disability worldwide. Depression is also a heterogeneous disorder characterized by complex diagnotic approaches with a lack of diagnostic biomarker, an inconsistent response to treatment, no established mechanism, and affecting multiple physiological systems such as endocrine, immunological and cardiovasular as well. The growing impact of the analysis of complex signals on biology and medicine is fundamentally changing our view of living organisms, physiological systems, and disease processes. In this endeavour, the basic challenge is to reveal how the coordinated, dynamical behavior of cells and tissues at the macroscopic level, emerges from the vast number of random molecular interactions at the microscopic level. In this way, the fundamental questions could be: (i) how physiological systems function as a whole, (ii) how they transduce and process dynamical information, (iii) how they respond to external stimuli, and mostly (iv), how they change during a pathological processus. These challenges are of interest from a number of perspectives including basic modeling of physiology and practical bedside approaches to medical and risk stratification. The general purpose of this thesis, therefore, is to study physiological time series to provide a new understanding of sleep dynamics in health, specifically as they apply to the pathological condition of MDD. More precisely: (1) to quantitatively characterize the complex, nonlinear behaviour of cardiovascular (ECG) and electroencephalographic (EEG) time series during sleep, in health and in MDD. This project will test the hypotheses that both the sleep EEG and ECG detects reorganization in the system dynamics in patient suffering from depression. (2) To develop new diagnostic and prognostic tests for MDD, by detecting and extracting “hidden information” in the ECG and EEG datasets. Three different methods are introduced in this thesis for the analysis of dynamical systems. The first one, detrended fluctuation analysis, can reveal the presence of long-term correlations ("memory" in the physiological system) even when embedded in non-stationary time series. Graph theoretical measures were then applied to test whether disrupting an optimal pattern ["small-world network"] of functional brain connectivity underlies depression. Finally, multiscale entropy method, which is aimed at quantifying the complexity of the systems' output resulting from the presence of irregular structures on multiple scales, was applied on the ECG signal. The results indicate that healthy physiologic systems, measured through the EEG and the ECG signals, are the most complex. According to the decomplexification theory, the depressive disease model exhibits a loss of system complexity, with potential important applications in the development and testing of basic physiologic models, of new diagnostic and prognostic tools in psychiatry, and of clinical risk stratification.