Sleep and Developmental Psychopathology

Lisa J. Meltzer

• Publisher: Routledge
• Year: 2018
• Print ISBN: 9781138542389
• eBook ISBN: 9781351008907
• Edition: 1
• Topic: Psychology
• Subtopic: Developmental Psychology
• Index: Psychology

Sleep plays a critical role in child development, with insufficient sleep or sleep disorders linked to poorer physical health, increased weight gain, academic deficits, behavior problems, and difficulties with emotion regulation. This book examines the complex and dynamic relationship between sleep and developmental psychopathology. By focusing on broad topics such as social and emotional development or child well-being, as well as specific disorders including ADHD, anxiety, and bipolar, many different aspects of developmental psychopathology are considered. In addition, a breadth of studies examine different measurement approaches and sleep as an underlying mechanism for the development of behavior, social, and emotional problems. This collection of novel research studies exploring the intersection between sleep and developmental outcomes is essential for clinicians and researchers who work with children and adolescents.

This book was first published as a special issue of the Journal of Clinical Child and Adolescents Psychology.

Sleep Architecture Relates to Daytime Affect and Somatic Complaints in Clinically Anxious but Not Healthy Children

Cara A. Palmer and Candice A. Alfano

It is increasingly clear that seminal sleep-affective relationships begin to take root in childhood, yet studies exploring how nighttime sleep characteristics relate to daytime affective symptoms, both in clinical and healthy populations of children, are lacking. The current study sought to explore these relationships by investigating whether trait-like and/or daily reports of affective and somatic symptoms of children with generalized anxiety disorder and matched controls relate to sleep architecture. Sixty-six children (ages 7–11; 54.4% female; 56.1% Caucasian; 18.2% biracial; 6.1% African American; 3% Asian; 16.7% Hispanic) participated including 29 with primary generalized anxiety disorder (without comorbid depression) and 37 healthy controls matched on age and race/ethnicity. Participants underwent structured diagnostic assessments including child-report measures and subsequently reported on their negative affect and somatic symptoms over the course of 1 week. Children also completed 1 night of polysomnography. Among children with generalized anxiety disorder only, greater amounts of slow wave sleep corresponded with less negative affect, and greater amounts of rapid eye movement sleep was related to more somatic complaints across the week. Similarly, for trait-like measures, more rapid eye movement sleep and shorter latency to rapid eye movement sleep were related to greater depressive symptoms in the anxious group only. The current findings suggest that physiologic sleep characteristics may contribute in direct ways to the symptom profiles of clinically anxious children. The functional relevance of such findings (e.g., how specific sleep characteristics serve to either increase or reduce long-term risk) is a vital direction for future research.

Although sleep complaints are prevalent across various types of child internalizing disorders (Alfano & Gamble, 2009) differences in sleep architecture (i.e., the basic structural organization of sleep) as compared to typically developing children are far less commonly observed. For example, during the pre-pubertal years, youth with anxiety disorders and major depressive disorder exhibit objective sleep patterns largely similar to those of healthy youth (for reviews, see Ivanenko, Crabtree, & Gozal, 2005; McMakin & Alfano, 2015). These findings stand in contrast to reliable evidence of sleep abnormalities in adult patients, particularly those with depression (Palagini, Baglioni, Ciapparelli, Gemignani, & Riemann, 2013). Notwithstanding the fact that child-based studies are fewer overall and often comprised of broad age ranges of youth, lack of sleep-based differences in child patients may well be attributable to maturational differences (e.g., stronger homeostatic sleep pressure) that override sleep-based expression of affective illness (Carskadon, 2002; Dahl, 1996). Still, as the vast majority of children with anxiety disorders and depression complain of poor sleep (Alfano, Ginsburg, & Kingery, 2007; Alfano, Patriquin, & De Los Reyes, 2015; Chorney, Detweiler, Morris, & Kuhn, 2008) and early sleep problems reliably presage the later onset of these disorders (Gregory et al., 2005; Kelly & El-Sheikh, 2014; Ong, Wickramaratne, Tang, & Weissman, 2006), it is clear that critical sleep-affective relationships begin to take root in childhood. Thus, there is need for research to move beyond group-based comparisons of sleep in favor of exploring how nighttime sleep characteristics relate to daytime emotional functioning in both clinical and healthy populations of children.

Sleep and affective functioning are also recognized to share bidirectional associations (see Alvaro, Roberts, & Harris, 2013), yet differential relationships are evident across clinical and non-clinical samples. Sleep deprivation, particularly loss of rapid eye movement (REM) sleep, produces reliable, albeit transient improvements in mood in a majority of clinically depressed patients, whereas a worsening of mood is typically observed in nondepressed samples (see Giedke & Schwärzler, 2002). Other research has found affective responses to sleep deprivation to be predicted by degree of diurnal mood variation more specifically (Haug, 1992). Sleep deprivation studies are infrequent in child samples, but other research highlights the bidirectionality of nighttime sleep and daytime affect in youth both with and without internalizing psychopathology. For the most part, this growing body of research reveals stronger pathways from sleep to affect/mood than the reverse relationship (McMakin & Alfano, 2015). For example, using three waves of data over a 5-year period (8–13 years) Kelly and El-Sheikh (2014) showed shorter sleep duration and worse sleep quality to predict increased anxiety and depressive symptoms, whereas less robust associations were identified in the opposite direction. Similarly, in a study among youth ages 9–16, subjective sleep complaints predicted a later diagnosis of generalized anxiety disorder (GAD; Shanahan, Copeland, Angold, Bondy, & Costello, 2014). In one of the only studies to include youth with anxiety and depressive disorders as well as healthy children, 1 week of actigraphy and daily affect monitoring revealed more time spent asleep at night to predict greater positive affect the next day in the clinical groups only (Cousins et al., 2011). These findings in particular highlight the presence of differential relationships between nighttime sleep patterns and daytime affect in clinical versus healthy children.

Building on this burgeoning area of research, the current study was interested in whether, irrespective of quantitative differences in sleep, the daytime symptoms of youth with anxiety disorders might show distinct relationships with sleep architecture. Our study focuses on children with GAD specifically for several reasons. Most prominently, the vast majority (up to 90%) of children with GAD and/or their parents report sleep to be problematic (Alfano, Beidel, Turner, & Lewin, 2006; Alfano et al., 2007; Alfano, Pina, Zerr, & Villalta, 2010). Second, defining features of the disorder, including chronic worry and hypervigilance for threat, are inherently counterproductive to achieving and maintaining sleep (Dahl, 1996). A large proportion of children with GAD also eventually develop depressive disorders (Brown & Barlow, 1992; Kessler et al., 1994; Pine, Cohen, & Brook, 2001), vulnerability for which is marked by sleep-related disruptions (Palagini et al., 2013). Third, examinations of sleep architecture in this population, which are notably limited, have produced equivocal findings. In a sleep lab setting, children with GAD evidenced prolonged sleep onset and reduced latency to REM sleep compared to controls (Alfano, Reynolds, Scott, Dahl, & Mellman, 2013), but results were not replicated using home-based polysomnography (PSG; Patriquin, Mellman, Glaze, & Alfano, 2014). Understanding whether and how the underlying structure of sleep maps onto the daytime symptoms of children with GAD may provide greater insight into these discrepancies, early sleep-affective relationships in general, and the role of sleep in the symptom profiles of anxious youth.

We begin with an overview of normal sleep architecture including seminal relationships between specific sleep stages and aspects of affect and psychopathology as a basis for the current investigation, which includes children with a primary GAD diagnosis and a healthy control sample.

SLEEP ARCHITECTURE AND AFFECTIVE LINKS IN CHILDHOOD

PSG, which includes electroencephalography (EEG), electrooculography (EOG), and electromyography (EMG), is considered the “gold standard” for assessing sleep architecture. In general, sleep consists of two main types—REM sleep and non-rapid eye movement (NREM) sleep—each with unique neurobiological and physiological characteristics. NREM sleep is further divided into three stages (N1–N3) corresponding with increasing depth of sleep as determined by progressive dominance of high-voltage, low-frequency EEG activity. NREM sleep stages are also marked by parasympathetic dominance, including decreased muscle tone, reductions in blood pressure/heart rate, and slowed and rhythmic respiration. N1, sometimes referred to as “relaxed wakefulness,” characterizes the transition from wake to sleep and occupies the smallest percentage of total sleep time. In contrast, N2 occupies approximately 50% of the nighttime sleep period and is characterized as light sleep. N3 is the deepest and most restorative of all sleep stages, marked by slow, delta brain waves, and thus is referred to as slow wave sleep (SWS).

As compared to other stages of sleep, dramatic changes in N3 are observed in late childhood as children transition into adolescence, including an approximate 40% decrease in SWS (Campbell & Feinberg, 2009; Carskadon & Dement, 2011; Colrain & Baker, 2011). This significant decline primarily accounts for observable reductions in total sleep time during adolescence compared to the childhood years (Karacan, Anch, Thornby, Okawa, & Williams, 1975). Studies experimentally disrupting SWS find increased daytime sleep propensity (Dijk, Groeger, Stanley, & Deacon, 2006) and subsequent increases in SWS (Dijk, Beersma, Daan, Bloem, & Van Den Hoofdakker, 1987; Ferrara, De Gennaro, & Bertini, 1999), highlighting its functional significance. SWS enhances various daytime functions and is believed to be important for learning and memory consolidation (Walker, 2009). During childhood, SWS is theorized to play a critical role in brain maturation and development, including increased synaptic density (Campbell & Feinberg, 2009; Kurth et al., 2010).

A multitude of evidence reveals the presence of decreased N3 sleep in adults with depression as compared to healthy individuals (Berger, Van Calker, & Riemann, 2003; Palagini et al., 2013; Riemann, Berger, & Voderholzer, 2001; Tsuno, Besset, & Ritchie, 2005). This robust finding is also evident in the first-degree relatives of those who are depressed and observed even after a depressive episode has remitted (Lauer, Schreiber, Holsboer, & Krieg, 1995; Pillai, Kalmbach, & Ciesla, 2011). In childhood, N3 sleep may be distinctly protective against the later onset of depression in at-risk children. In a longitudinal study of nondepressed pre-pubertal children (ages 6–11) at genetic risk for depression, participants completed diagnostic assessments annually through early adulthood (18–29 years) to examine risk and protective factors (Silk et al., 2007). Participants who did not develop depressive disorders in adulthood (i.e., resilient at-risk participants) evidenced greater amounts of SWS in childhood.

In contrast to NREM sleep, REM sleep is often referred to as “paradoxical sleep” due to the presence of low-amplitude mixed-frequency EEG activity (e.g., theta and alpha waves) that resembles brain activity during wakefulness. Increased eye movements, irregular respiration, and rapid changes in heart rate and blood pressure are also seen during REM sleep. This is the stage during which most dreaming activity occurs, with concomitant muscle atonia inhibiting motor activity so cortical signals during dreaming do not create bodily responses. REM sleep accounts for approximately 25% of nighttime sleep (Anders, Sadeh, & Appareddy, 1995) with mild decreases observed after the transition to adolescence. Unlike N3 sleep, however, REM sleep percentage does not change significantly in relation to total sleep time (Ohayon, Carskadon, Guilleminault, & Vitiello, 2004). Also, whereas N3 sleep dominates the first half of the night, REM sleep is dominant during the second half, with REM periods becoming progressively longer and denser across the night.

REM sleep shows intimate relations with emotional learning and memory (Goldstein & Walker, 2014; Walker & Van Der Helm, 2009). At a basic neurobiological level, increased activity in emotion-related brain regions are observed during REM sleep, including the amygdala, striatum, hippocampus, insula, and the medial prefrontal cortex, along with reductions in levels of various neurotransmitters (e.g., noradrenaline; Hobson & Pace-Schott, 2002; Walker & Van Der Helm, 2009). During REM, the activation of these emotion-related brain structures in the absence of noradrenergic changes is believed to provide the backdrop for consolidating emotional events experienced during the day into memory while attenuating the intensity of associated emotions (Walker & van der Helm, 2009). For example, in a study that selectively deprived healthy adults of REM sleep, subsequent increases in reactivity to emotional stimuli were found in comparison to an NREM sleep-deprived group (Rosales-Lagarde et al., 2012).

REM sleep is also heavily implicated in depressive symptomology. Among the most reliable sleep alterations observed in depressed patients are decreased latency to the first REM sleep period and increased time spent in REM (Palagini et al., 2013), which have been replicated in some samples of youth (Arana-Lechuga et al., 2008; Dahl et al., 1991; Emslie, Rush, Weinberg, Rintelmann, & Roffwarg, 1990; Lahmeyer, Poznanski, & Bellur, 1983). Several studies among those at risk for depression have found alterations in REM sleep to be present even before onset of the disorder (Giles, Roffwarg, & Rush, 1987). REM sleep abnormalities are therefore considered among the most robust biomarkers for depressive illness (Palagini et al., 2013).

To a lesser extent, REM sleep has been implicated in somatic/physiological hyperarousal processes. Sleep disturbance generally is associated with somatic complaints in youth (e.g., Lewandowski, Ward, & Palermo, 2011; Miller, Palermo, Powers, Scher, & Hershey, 2003), but research among depressed patients suggests relationships between REM sleep specifically and inflammatory markers/disease (Motivala, Sarfatti, Olmos, & Irwin, 2005). For exam...

Table of contents

• Cover
• Half Title
• Title Page
• Copyright Page
• Contents
• Citation Information
• Notes on Contributors
• Introduction: Sleep and Developmental Psychopathology: Introduction to the Special Issue
• 1 Sleep Architecture Relates to Daytime Affect and Somatic Complaints in Clinically Anxious but Not Healthy Children
• 2 Stage 2 Sleep EEG Sigma Activity and Motor Learning in Childhood ADHD: A Pilot Study
• 3 A Preliminary Multimethod Comparison of Sleep Among Adolescents With and Without Generalized Anxiety Disorder
• 4 Does an Online CBT Program for Anxiety Impact Upon Sleep Problems in Anxious Youth?
• 5 Sleep Moderates the Association Between Response Inhibition and Self-Regulation in Early Childhood
• 6 Sleep and Social-Emotional Development in Infants and Toddlers
• 7 Sleep in Adolescents With Bipolar I Disorder: Stability and Relation to Symptom Change
• 8 Sleep Duration and Child Well-Being: A Nonlinear Association
• 9 Tracking Effects of Problematic Social Networking on Adolescent Psychopathology: The Mediating Role of Sleep Disruptions
• 10 ADHD and Sleep Quality: Longitudinal Analyses From Childhood to Early Adulthood in a Twin Cohort
• 11 Future Directions in Sleep and Developmental Psychopathology
• Index