Throughout early development, a child spends more time asleep than in any waking activity. Yet, the specific role of sleep in brain maturation is a complete mystery. In this article, the developmental psychobiology of sleep regulation is conceptualized within the context of close links to the control of arousal, affect, and attention. The interactions among these systems are considered from an ontogenetic and evolutionary biological perspective. A model is proposed for the development of sleep and arousal regulation with the following major tenets:

1. Sleep and vigilance represent opponent processes in a larger system of arousal regulation.

2. The regulation of sleep, arousal, affect, and attention overlap in physiological, neuroanatomical, clinical, and developmental domains.

3. Complex interactions among these regulatory systems are modulated and integrated in regions of the prefrontal cortex (PFC).

4. Changes at the level of PFC underlie maturational shifts in the relative balance across these regulatory systems (such as decreases in the depth/length of sleep and increased capacity for vigilance and attention), which occur with normal development.

5. The effects of sleep deprivation (including alterations in attention, emotions, and goal-directed behaviors) also involve changes at the level of PFC integration across regulatory systems.

This model is then discussed in the context of developmental pathology in the control of affect and attention, with an emphasis on sleep changes in depression.

This study investigated relations between drug exposure, particularly cocaine, and infants' regulation of arousal in response to novelty. Sixty-three infants — 36 cocaine exposed and 27 non-cocaine exposed — participated at 3 months of age in a novel-repeat stimulus presentation procedure. Arousal was operationalized in terms of infant behavioral state, affective expressiveness, and attention to the stimulus. Infants were tested and infant behaviors were scored by experimenters blind to the drug exposure status of the infant. There were no differences between the two groups in baseline behavioral state or affective expression before the presentation of novel stimuli. Compared to the non-cocaine-exposed group, infants exposed prenatally to cocaine and other drugs were more likely to exhibit a crying state and to display negative affect on novel stimulus presentations. There were no group differences in the amount of looking toward the stimulus. Both groups showed less crying and negative affect when stimuli were presented a second time, but decrements were consistently greater for the cocaine-exposed group. These results obtained when group differences were controlled for sociodemographic and perinatal variables. Sources of differences in the regulation of arousal in cocaine-exposed and non-cocainc-exposed infants are discussed, and impairments in the regulation of arousal in cocaine-exposed infants are considered in a framework of predictive implications for children's social and cognitive development.

The model presented identifies the importance of neural regulation of autonomic state as an antecedent substrate for emotional, cognitive, and behavioral regulation. It is proposed that individual differences in neural regulation of autonomic state are related to normal and abnormal development. Establishing nervous system regulation of autonomic state is the infant's initial task of self-regulation. Survival for the high-risk infant is based primarily on physiological self-regulation. Although the methods described focus on the high-risk neonate, the model provides insight into normal development and may be generalized to the study of older children and adults with behavioral and psychological problems. Moreover, the model may contribute to assessment and intervention strategics for normal and abnormal development.

The maturation of corticolimbic systems that neurobiologically mediate essential affective and social regulatory functions is experience dependent. During the first and second years of life, the infant's affective experiences, especially those embedded in the relationship with the primary caregiver, elicit patterns of psychobiological alterations that influence the activity of subcortically produced trophic bioamines, peptides, and steroids that regulate the critical period growth and organization of the developing neocortex. Interactive attachment experiences of psychobiological attunemcnt, stressful misattunement, and stress-regulating repair and reattunement that maximize positive and minimize negative affect are imprinted into the orbitofrontal cortex — the hierarchical apex of the limbic system that is expanded in the early developing right hemisphere. During the critical period of maturation of this system, prolonged episodes of intense and unregulated interactive stress are manifest in disorganizing experiences of heightened negative affect and altered levels of stress hormones, and this chaotic biochemical alteration of the internal environment triggers an extensive apoptotic panellation of corticolimbic circuitries. In this manner less than optimal affect-regulating experiences with the primary caregiver are imprinted into the circuits of this frontolimbic system that is instrumental to attachment functions, thereby producing orbitofrontal organizations that neurobiologically express different patterns of insecure attachments. Such pathomorphogenetic outcomes result in structurally defective systems that, under stress, inefficiently regulate subcortical mechanisms that mediate the physiological processes that underlie emotion. The functional impairments of the cortical-subcortical circuitries of this prefrontal system are implicated in an enduring vulnerability to and the pathophysiology of various later forming psychiatric disorders.

We examined whether the interaction of resting frontal electroencephalogram (EEG) asymmetry and social behavior during peer play was related to the occurrence of maladaptive behavior in preschoolers. Two independent cohorts of children were observed interacting in same-age and -gender play quartets at 4 years of age. Each child was also seen individually for a psychophysiology session during which time measures of EEG activity were recorded. We found that highly sociable children who exhibited greater relative right frontal EEG asymmetry were more likely to exhibit externalizing problems than sociable children who exhibited greater relative left frontal EEG asymmetry. We also found that shy children who exhibited greater relative right frontal EEG asymmetry were more likely to exhibit internalizing problems than shy children who exhibited left frontal EEG asymmetry. These findings suggest that the pattern of frontal EEG asymmetry in combination with social behavioral style is a significant predictor of maladaptive behavior problems during the preschool period.

Genetic influence on externalizing problems, internalizing problems, and attentional/activity problems in 5-year-olds was consistently identified across informants and assessment contexts. Effects of the shared environment were identified as well but with less consistency (i.e., only from parents, not teachers, and more from father than mother reports). Correlations between observed patterns of regulation at ages 3, 4, and 5 years and behavior problems at age 5 years were often significant, but low in magnitude and specific to teacher reports. Adaptive internalization of control at each age (e.g., frustration tolerance, capacity to attend and focus, good impulse control) predicted fewer externalizing problems. Internalization of standards, reflected in children's moral themes, understanding of reciprocity, and constructive social problem solving, also were sometimes associated with fewer problems. Significant correlations were low in magnitude and again specific to teacher reports. Externalizing problems were more prevalent for boys than girls, and regulation (i.e., internalization of control and standards) was more characteristic of girls than boys.

Emotional security is a central concept in many accounts of normal development and the development of psychopathology. However, the construct has rarely been subject to precise explication, and the conceptualization of emotional security as deriving from qualities of family functioning as a whole requires development. Emotional security as a regulatory system is defined and related to current approaches to emotions as regulatory processes. Although our model is built upon attachment theory, the emphasis is shifted from the evolutionary/ethological origins of attachment theory to the regulation of emotional well being and security as a goal in itself. Emotional security is conceptualized from a contextualistic perspective, emphasizing the interplay between socioemotional and biological processes. Felt-security as a goal is defined from an organizational perspective, reflecting the entire pattern of the individual's reactions to events in relation to emotional security as a goal, as opposed to simply those reactions that are “conscious” or reported as “feelings.” Component regulatory systems are specified (e.g., processes of emotion regulation, regulation of exposure to family affect), with illustrations centering on the impact of marital and parent-child relations on children's security.

The relations of regulation and emotionality to elementary school children's problem behavior was examined. Parents and teachers reported on children's problem behavior. One parent and teachers rated children on various measures of regulation (including resiliency) and emotionality; children's baseline heart rate and facial reactivity were assessed; and physiological and facial distress and gaze aversion while viewing a distress film sequence were measured. In general, low regulation, negative emotionality, and general and positive emotional intensity predicted problem behaviors. Teachers' reports of negative emotionality and regulation interacted in their relation to problem behaviors, with regulation apparently buffering the effects of moderate and high negative emotionality. Baseline heart rate and facial distress were related to low levels of problem behavior, and gaze aversion during the distress film segment was associated with low levels of problem behavior.

The capacity to manage emotion is based on the growth of self-regulatory capacities in the early years, but is also affected by situational demands, influences from other people, and the child's goals for regulating emotion in a particular setting. For most children growing up in supportive contexts, the growth of emotional regulation is associated with enhanced psychosocial well-being and socioemotional competence. But for children who are at risk for the development of psychopathology owing to environmental stresses or intrinsic vulnerability (or their interaction), emotional regulation often entails inherent trade-offs that make nonoptimal strategics of managing emotion expectable, perhaps inevitable, in a context of difficult environmental demands and conflicting emotional goals. This analysis discusses how emotional regulation in children at risk may simultaneously foster both resiliency and vulnerability by considering how emotion is managed when children (a) are living with a parent who is depressed, (b) witness or experience domestic violence, or (c) are temperamentally inhibited when encountering novel challenges. In each case, the child's efforts to manage emotion may simultaneously buffer against certain stresses while also enhancing the child's vulnerability to other risks and demands. This double-edged sword of emotional regulation in conditions of risk for children cautions against using “optimal” emotional regulation as an evaluative standard for such children or assuming that emotional regulation necessarily improves psychosocial well-being. It also suggests how the study of emotional regulation must consider the goals for regulating emotion and the contexts in which those goals are sought.

Norepinephrine (NE), dopamine (DA), and serotonin (5HT) are three of the more than thirty neurotransmitters (NTs) in the brain. Axons from a relatively small number of cell bodies located in the midbrain and brainstem branch out to connect with virtually all areas of the brain. Via these connections, these three NTs participate in the regulation of several behavioral systems that help modulate the interaction of the individual with his/her environment. Because the NT systems continue to develop after birth, interactions between the individual and his/her environment after birth may affect the development of these systems and have long-term effects on the individual's behavior. Animal studies indicate that early experience affects behavior and biogenic amine systems in the adult. For instance, one study showed that maternal deprivation, which is analogous to human neglect, affects the NE system in monkeys and may have a long-lasting effect on its development and function. In a previous study, similar relationships between early neglect and the NE system in humans were examined. Our results show that emotionally disturbed children with a history of neglect have lower dopamine-β-hydroxylase (DβH) activity, an enzyme involved in the synthesis of NE, than do children with no history of neglect. Additionally, the children with a history of neglect have lower systolic and diastolic blood pressure, both of which are functions mediated by the NE system, than the other children studied. These results support findings in animal studies that neglect affects the development of the NE system in a long-lasting, if not permanent way.

This study examined the effects of stressful environments on physiological and affective functioning among 131 maltreated school-aged children attending a summer day camp. Sixty-six nonmaltreated children also attending the camp served as a comparison group. Salivary Cortisol measures were obtained daily at 10:00 a.m. and at 4:00 p.m. Depression was measured using the Child Depression Inventory. Children with scores of 19 or higher were classified as depressed. Internalizing and externalizing behavior problems were determined from the Teacher Report Form of the Child Behavior Checklist. Children with t scores of 70 or higher were classified as having clinical levels of these problems. Maltreated children had slightly elevated afternoon Cortisol concentrations, but their morning concentrations did not differ significantly from those of nonmaltreated children. Neither clinical levels of depression, internalizing, or externalizing problems were predictive of the elevated afternoon values. Depression among maltreated children was, however, associated with altered activity of the hypothalamic-pituitary-adrenocortical (HPA) axis. Depressed maltreated children had lower morning Cortisol concentrations compared to nondepressed maltreated children and were more likely to show a rise rather than the expected decrease in Cortisol from morning to afternoon. These data replicated earlier findings. There was no evidence that depressed, nonmaltreated children exhibited this change in diurnal Cortisol activity.

Although the construct of regulation is usually applied to ongoing behavior, it also has implications for ongoing cognition and the development of cognitive representations. We propose that subcortical motivational systems influence cortical representations in two general ways. First, they regulate response processes, promoting a general selection of information to which the child is exposed. Second, motivational systems regulate attention, promoting a more selective stabilization of representations for motivationally relevant sources of information. Together with the environment, these regulatory processes shape the child's developing representations. Individual differences in these processes result in cortical representational systems that enhance the motivational systems* ability to detect relevant inputs and to guide behavior in light of them. Examples are provided that focus on fearful children, discussing how their self-representation may contribute to anxious psychopathology.

An important regulatory process in the development of behavior is cognition. However, cognition as a blanket term is far too broad to be useful. Rather, specific types of cognition need to be examined separately. One proposal is that one type of human reasoning evolved in a social context, to solve social problems. Here, we report two experiments that use autism to test a prediction from that theory: that social intelligence should be independent of nonsocial intelligence. Autism was chosen because deficits in social reasoning (“theory of mind”) are well known. The question we tested was whether their theory of mind deficit was dissociable from abstract and relational reasoning ability. In particular, we expected that the abnormalities in the behavioral development of children with autism would be regulated by abnormalities in theory of mind reasoning rather than other forms of reasoning. Children with autism and matched controls were given tests of abstracting reasoning, which did not involve mental state understanding. Results showed that children with autism performed comparably to the control groups, both on a test of transitive inferential reasoning and on a test of analogical reasoning. These results lend support to the specificity of the theory of mind hypothesis for autism and to Cosmides' theory of the evolution of social intelligence. They also show that cognition as a regulatory process in development needs to be examined in highly specific ways.

A general theory of personality and its development is described in terms of four quantitative dimensions of temperament and three quantitative dimensions of character. The four temperament dimensions (harm avoidance, novelty seeking, reward dependence, and persistence) are moderately heritable, moderately stable throughout life, and invariant despite sociocultural influences. The three character dimensions (self-directedness, cooperativeness, and self-transcendence) mature in a stepwise manner from early childhood throughout adulthood. Transitions between levels of maturity are nonlinear functions of temperament, specific genetic influences, social learning, and random life events. Personality development is quantitatively formulated in terms of nonlinear dynamics of a complex adaptive system. The psychosocial interpretation of personality as a fitness-optimizing process is described and illustrated in terms of available data about the development of different personality configurations. Several quantitative predictions of this theory of personality development are tested, including the sequence of emergence of the different character dimensions, individual differences in the development of stable temperament configurations, and the effects of sociocultural influences. The theoretical predictions agree with available empirical data and suggest many hypotheses for future developmental research, including etiological, dynamic, and therapeutic studies.

The recurrent affective disorders are discussed from the perspective of accumulating inherited and experiential effects on gene expression. Stress and episodes of affective illness are viewed as leaving biochemical and microstructural residues in the central nervous system (CNS) in relation to their patterning, severity, and recurrence. Comorbid factors such as substance abuse and developmental disturbances may also interact with these illness-related variables. In addition to the primary pathological processes, secondary adaptive changes can also be induced, which, in concert with pharmacological interventions, may be sufficient to counter episode occurrences and illness progression. We postulate that the balance of primary pathological and secondary adaptive changes at multiple levels of CNS regulation accounts for recurrence and cyclicity in the affective disorders. The importance of early, effective, long-term interventions in the recurrent affective disorders and the therapeutic potential of several new treatment modalities including repeated transcranial magnetic stimulation (rTMS) are discussed.