Since the 1993 National Research Council (NRC) report on child abuse and neglect was issued, dramatic advances have been made in understanding the causes and consequences of child abuse and neglect, including advances in the neural, genomic, behavioral, psychologic, and social sciences. These advances have begun to inform the scientific literature, offering new insights into the neural and biological processes associated with child abuse and neglect and in some cases, shedding light on the mechanisms that mediate the behavioral sequelae that characterize children who have been abused and neglected. Research also has expanded understanding of the physical and behavioral health, academic, and economic consequences of child abuse and neglect. Knowledge of sensitive periods—the idea that for those aspects of brain development that are dependent on experience, there are stages in which the normal course of development is more susceptible to disruption from experiential perturbations—also has increased exponentially. In addition, research has begun to explore differences in individual susceptibility to the adverse outcomes associated with child abuse and neglect and to uncover the factors that protect some children from the deleterious consequences explored throughout this chapter. An important message is that factors relating to the individual child and to the familial and social contexts in which the child lives, as well as the severity, chronicity, and timing of abuse and neglect experiences, all conspire to impact, to varying degrees, the neural, biological, and behavioral sequelae of abuse and neglect.
This chapter begins by exploring background topics that are important to an understanding of research on the consequences of child abuse and
neglect, including an ecological framework and methodological attributes of studies in this field. Next is a review of the research surrounding specific outcomes across the neurobiological, cognitive, psychosocial, behavioral, and health domains, many of which can be seen in childhood, adolescence, and adulthood. The chapter then examines outcomes that are specific to adolescence and adulthood, reviews factors that contribute to individual differences in outcomes, and considers the economic burden of child abuse and neglect. The final section presents conclusions.
Newborns are almost fully dependent upon parents to help them regulate physiology and behavior. Under optimal conditions, parents buffer young children from stress and serve as “co-regulators” of behavior and physiology (Hertsgaard et al., 1995; Hofer, 1994, 2006). Over time, children raised by such parents gradually assume these regulatory capacities. They typically enter school well regulated behaviorally, emotionally, and physiologically; thus, being prepared for the tasks of learning to read, write, and interact with peers.
For some children, parents cannot fill these roles as buffer and co-regulator effectively. When children have caregivers who cannot buffer them from stress or who cannot serve as co-regulators, they are vulnerable to the vicissitudes of a challenging environment. Although children can cope effectively with mild or moderate stress when supported by a caregiver, conditions that exceed their capacities to cope adaptively often result in problematic short- or long-term consequences.
Studies conducted with some nonhuman primate species and rodents have shown that the young are dependent on the parent for help in regulating behavior and physiology (Moriceau et al., 2010). Thus, young infants are dependent on parents fulfilling the functions of carrying, holding, and feeding. The period of physical immaturity and dependence lasts an extended time in humans. Even beyond the point at which young children are physically dependent, they remain psychologically dependent throughout childhood and adolescence. Thus, inadequate or abusive care can have considerable consequences in terms of children’s health and social, psychological, cognitive, and brain development.
Children who have experienced abuse and neglect are therefore at increased risk for a number of problematic developmental, health, and mental health outcomes, including learning problems (e.g., problems with inattention and deficits in executive functions), problems relating to peers (e.g., peer rejection), internalizing symptoms (e.g., depression, anxiety), externalizing symptoms (e.g., oppositional defiant disorder, conduct disorder, aggression), and posttraumatic stress
disorder (PTSD). As adults, these children continue to show increased risk for psychiatric disorders, substance use, serious medical illnesses, and lower economic productivity.
This chapter highlights research supporting the association between these outcomes, among others, and experiences of child abuse and neglect. The potential dramatic and pervasive consequences of child abuse and neglect underscore the need for research to illuminate the myriad pathways by which these ill effects manifest in order to guide treatment and intervention efforts. However, it is important to note at the outset that not all abused and neglected children experience problematic outcomes. As discussed in the section on individual differences later in this chapter, a body of research is devoted to uncovering the factors that distinguish children who do not experience problematic outcomes despite facing significant adversity in the form of abuse or neglect. Further, as discussed in Chapter 6, the past two decades have seen substantial growth in proven models for treatment of the consequences of child abuse and neglect, indicating that these effects are potentially reversible and that there is opportunity to intervene throughout the life course.
Several key concepts need to be considered in attempting to understand potential pathways that lead from abuse and neglect to the various consequences discussed in this chapter and the context in which those consequences manifest. First, positive and negative influences found among individual child characteristics, within the family environment, and in the child’s broader social context all interact to predict outcomes related to child abuse and neglect. Second, child abuse and neglect occur in the context of a child’s brain development, and their potential effects on developing brain structures can help explain the onset of certain negative outcomes. Finally, abused and neglected children often are exposed to multiple stressors in addition to experiences of abuse and neglect, and potential consequences may manifest at different points in a child’s development. Therefore, the most rigorous research on this topic attempts to account for the many factors that may be confounded with abuse or neglect.
Since 1993, transactional-bioecological or ecological models have guided attempts to conceptualize the relative contributions of risk and protective factors to children’s developmental outcomes, particularly in relation to child abuse and neglect (Belsky, 1993; Cicchetti and Lynch, 1993; Cicchetti and Toth, 1998). Versions of this approach consider the develop-
ment of the child in the context of the broader social environment in which he or she functions, within the context of a family; in turn, children and families are embedded in a larger social system that includes communities, neighborhoods, and cultures. The assumption underlying these models is that behavior is complex, and development is multiply determined by characteristics of the individual, parents and family, and neighborhood and/or community and their interactions.
In examining the role of contextual factors in the onset of consequences due to child abuse and neglect, Cicchetti and Lynch’s (1993) ecological/transactional model is particularly useful because it successfully incorporates multiple etiological frameworks (Lynch and Cicchetti, 1998). This model is based on Belsky’s (1980, 1993) ecological model and Cicchetti and Rizley’s (1981) transactional model. It expands on these models by highlighting the nature of interaction among risk factors and the ecology in which child maltreatment occurs. The ecological/transactional model describes four interrelated, mutually embedded categories that contribute to abuse and neglect and the potential associated consequences:
• Ontogenic development—Reflects factors within the individual that influence the achievement of competence and adaptation.
• Microsystem—Defined as the “immediate context” (i.e., the family) in which the child experiences abuse or neglect, including the bidirectional influence of parent and child characteristics and other relationships (such as marriage) that may impact parent-child interactions directly or indirectly.
• Exosystem—The exo- and macrosystemic levels reflect social or cultural forces that contribute to and maintain abuse or neglect. The exosystem encompasses the effects of broader societal systems (e.g., employment, neighborhoods) on parent and child functioning.
• Macrosystem—Mirrors temporally driven, sociocultural ideologies (e.g., cultural views of corporal punishment), or a “larger cultural fabric,” that inevitably shape functioning at all other levels. It is represented by social attitudes (such as attitudes toward violence or the value of children).
The model is based on the fact that a child’s multiple ecologies influence one another, affecting the child’s development. Thus, the combined influence of the individual, family, community, and larger culture affect the child’s developmental outcomes. Parent, child, and environmental characteristics combine to shape the probabilistic course of the development of abused and neglected children.
At higher, more distal levels of the ecology, risk factors increase the likelihood of child maltreatment. These environmental systems also influence
what takes place at more proximal ecological levels, such as when risk and protective factors determine the presence or absence of maltreatment within the family environment. Overall, concurrent risk factors at the various ecological levels (e.g., cultural sanction of violence, community violence, low socioeconomic status, loss of job, divorce, parental substance abuse, maladaptation, and/or child psychopathology) act to increase or decrease the likelihood that abuse will occur.
The manner in which children handle the challenges associated with maltreatment is seen in their own ontogenic development, which shapes their ultimate adaptation or maladaptation. Although the overall pattern is that risk factors outweigh protective factors, there are infinite permutations of these risk variables across and within each level of the ecology, providing multiple pathways to the sequelae of child abuse and neglect.
Types of Evidence
Many studies of the consequences of abuse and neglect have been conducted with methodologies ranging from prospective to retrospective designs, from observational measures to self-report, and from experimental to case-controlled designs to no-control designs. The strongest conclusions could be reached with experimental designs whereby children would be randomly assigned to different abusive or neglectful experiences; however, this is obviously neither desirable nor possible.
Nonhuman studies involving primates and other species have allowed experimental assessment of different rearing conditions that may parallel human conditions of neglect and abuse (e.g., Sanchez, 2006; Suomi, 1997). One salient human study involved random assignment of children abandoned to institutions to high-quality foster care (a randomized controlled trial of foster care as an alternative to institutional care) (Nelson, 2007). In this prospective, longitudinal study, known as the Bucharest Early Intervention Project, 136 children abandoned at or around the time of birth and then placed in state-run institutions were extensively studied when they ranged in age from 6 to 31 months (mean age = 21 months), as was a sample of 72 never-institutionalized children who lived with their families in the greater Bucharest community. Following the baseline assessment, half of the institutionalized children were randomly assigned to a high-quality foster care program that the investigators created, financed, and maintained, and half were randomly assigned to remain in care as usual (institutional care). These children were followed extensively through age 12 (for discussion, see Fox et al., 2013; Nelson et al., 2007a,b; Zeanah et al., 2003). Although at first glance it may not be obvious why the study of children reared in institutions is relevant to a report on child abuse and neglect, institutional care, which affects as many as 8 million
children around the world, can involve an extreme and specific form of neglect—broad-spectrum psychosocial deprivation. Therefore, neglectful institutional care settings can serve as a model system for understanding the effects of neglect on brain development. The neglect experienced by children in such settings should not serve as a proxy for the type of neglect experienced by noninstitutionalized children in the United States, who are more likely to experience neglect in such domains as food, shelter, clothing, or medical care rather than broad-spectrum psychosocial deprivation. Nevertheless, this study can provide important insight into the effects of neglect on behavioral and neurological development because of its randomized, controlled, and longitudinal nature.
The discussion in this chapter necessarily relies primarily (although not exclusively) on the strongest nonexperimental studies conducted. These studies involve longitudinal prospective designs, which assess child abuse and neglect objectively at the time of occurrence and assess outcomes longitudinally. A good example is the study of Widom and colleagues (1999), which followed a large cohort of abused and neglected children and a matched comparison sample from childhood into adulthood. Other examples include the studies of Johnson and colleagues (1999, 2000), Noll and colleagues (2007), and Jonson-Reid and colleagues (2012). Retrospective designs that ask participants to recall whether abuse and neglect were experienced are more troublesome because recall of child abuse and neglect can be affected by a variety of factors and open to a number of potential biases (Briere, 1992; Offer et al., 2000; Ross, 1989; Widom, 1988). Results of studies based on treatment samples of adults who experienced maltreatment as children may be potentially biased because not all victims of child abuse and neglect seek treatment as adults, and because people who do seek treatment may have higher rates of problems than people who do not seek treatment (Widom et al., 2007a). When participants are asked to report on conditions such as current depression and previous history of child abuse and neglect, the added problem of shared method variance arises. On the other hand, use of official records raises the problem of underreporting (Gilbert et al., 2009a).
The federal government has supported an effort, launched since the 1993 NRC report was issued—the National Survey of Child and Adolescent Well-Being (NSCAW)—to expand understanding of the consequences of child abuse and neglect. This study includes use of multiple data sources and record reviews, as well as interviews with children and youth who have experienced child abuse and neglect, their caretakers, and child welfare workers. Several of its findings are discussed in Chapter 5.
This chapter contains an extensive review of the more recent biologically based studies of child abuse and neglect because of the important advances that have been made in this area. To the extent possible, the
discussion relies on findings from studies characterized by the greatest methodological rigor.
Despite recent methodological advances, researchers face many challenges in attempting to understand the short- and long-term consequences of the various types of child abuse and neglect (e.g., physical abuse, sexual abuse, neglect from caregivers) for child functioning and development. One of those challenges is teasing apart the impact of child abuse and neglect from that of other co-occurring factors. For example, children involved with child protective services because of neglect or abuse often face a number of overlapping and concurrent risk factors, including poverty, prenatal substance exposure, and parent psychopathology, among others (Dubowitz et al., 1987; Lyons et al., 2005; McCurdy, 2005). These concurrent risk factors can make it particularly difficult to draw causal inferences about the specific consequences of abuse and neglect for children’s functioning, but need to be disentangled from the specific effects of abuse and neglect (Widom et al., 2007a). Controlling for other relevant variables becomes vital, since failure to take such family variables into account may result in reporting spurious relationships (Widom et al., 2007a). Some studies consider and covary other risk factors, and some do not. Considering the course of abuse and neglect may also be particularly important, as Jonson-Reid and colleagues (2012) found that the number of child abuse and neglect reports powerfully predicted adverse outcomes across a range of domains.
Finding: Risk factors that co-occur with child abuse and neglect, such as poverty, prenatal substance exposure, and parent psychopathology, can confound attempts to draw causal inferences about the specific consequences of abuse and neglect for children’s functioning. These factors need to be controlled for in studies seeking to identify the specific consequences of child abuse and neglect.
An adequate caregiver is needed to support developing brain architecture and the developing ability to regulate behavior, emotions, and physiology for young children. When children experience abuse or neglect, such development can be compromised. The effects of abuse and neglect are seen especially in brain regions that are dependent on environmental input for optimal development, and on aspects of functioning especially susceptible to environmental input. Early in development, infants are completely reliant on input from their caregivers for help in regulating arousal, neuroendocrine functioning, temperature, and other basic functions. With time and with successful experiences in co-regulation, children increasingly take over these functions themselves. Abuse and neglect represent the absence
of adequate input (as in the case of neglect) or the presence of threatening input (as in the case of abuse), either of which can compromise development. The following sections present a review of evidence with respect to key neurobiological systems that are altered as a result of abuse and neglect early in life: the hypothalamic-pituitary-adrenal (HPA) axis of the stress response system; the amygdala, involved in emotion processing and emotion regulation; the hippocampus, involved in learning and memory; the corpus callosum, involved in integrating functions between hemispheres; and the prefrontal cortex, involved in higher-order cognitive functions. The discussion begins, however, with a brief overview of brain development.
Overview of Neurobiological Development
The Construction of the Brain
Brain development begins just a few weeks after conception, starting with the construction of the neural tube. This is followed by the generation of different classes of brain cells—neurons and glia. Once formed, these immature neurons begin their migratory phase (generally away from the ventricular zone, which is their point of origin) to build the cerebral cortex. Much of cell migration is completed by the end of the second trimester of pregnancy, eventually leading to the construction of the six-layered cerebral cortex. After these immature cells have migrated to their target destination, they can differentiate; that is, they develop cell bodies and processes (axons and dendrites). Once processes have been formed, synapses begin to form; synapses are the connections between neurons that allow for the transmission of signals across the synaptic cleft, which is the small space that exists between two adjacent brain cells, generally between a dendrite and an axon. The synapse permits one neuron to communicate with another, and eventually, entire circuits are built, followed by neural networks (i.e., organized units). Finally, some axons in the brain develop a coating called myelin that speeds the flow of information along the length of the axon. Sensory and motor pathways begin to myelinate during the last trimester of pregnancy, whereas association areas of the brain, particularly the prefrontal cortex, continue to myelinate through the second decade of life. Neural elements (e.g., axons) that are coated with myelin are referred to as white matter, whereas most of the rest of the brain is referred to as grey matter.
Many aspects of brain development (particularly those that occur before birth) fall under genetic control (although some are affected by experience—prenatal exposure to neurotoxins such as alcohol being but one example). After birth, however, much of brain development be-
comes dependent on experience. For example, although the generation of synapses—which are massively overproduced early in development—is largely under genetic control, the pruning of synapses—which occurs primarily after birth—is largely under experiential control. Thus the prefrontal cortex of the 1-year-old child has many more synapses than the adult brain, but over the next one to two decades, these synapses are pruned back to adult numbers, based largely on experience (Nelson et al., 2011).
Neural Plasticity and Sensitive Periods
Many aspects of brain development depend on experiences occurring during particular time periods, often the first few years of life. These so-called sensitive or critical periods represent vital inflection points in the course of development, such that if specific experiences fail to occur within some narrow window of time (or the wrong experiences occur), development can go awry. This leads to the concept that plasticity “cuts both ways,” meaning that if the child is exposed to good experiences, the brain benefits, but if the child is exposed to bad experiences or inadequate input, the brain may suffer (Nelson et al., 2011). Prenatally, an example of a bad experience is exposure to neurotoxins such as alcohol or drugs of abuse. An example of a good experience is access to good nutrition, including the many micronutrients that facilitate brain development (e.g., iron, zinc). Postnatally, the topic of this report represents examples of bad experience (i.e., abuse and neglect). Conversely, examples of good experiences include providing a child with consistent, sensitive caregiving; a nurturing home in general; and adequate stimulation.
The Time Course of Development
In general, most sensory systems develop early in life; thus the ability to see and to discriminate and recognize faces and speech sounds come on line in the first months and years of life, based on appropriate experiences occurring during that time window (e.g., exposure to faces, to speech). This is not surprising given how vitally important these functions are to subsequent development (e.g., language is not learned until children can discriminate the basic units of sound, such as one consonant from another). Critical to the discussion in this chapter, however, is that the functions subserved by some other regions of the brain, most notably the prefrontal cortex—executive control, planning, cognitive flexibility, emotion regulation—have a much more protracted course of development for the simple reason that both synaptogenesis
FIGURE 4-1 The time course of key aspects of brain development.
SOURCE: Thompson and Nelson, 2001 (reprinted with the permission of American Psychologist).
and myelination of these cortical regions do not mature until mid- to late adolescence, perhaps even a bit later. As a result, the sensitive period for prefrontal cortical functions may be far more prolonged than is the case for sensory functions, extending well into the adolescent period. One example of the differential time course of different brain regions, and perhaps their corresponding sensitive periods, is illustrated in Figure 4-1.
These concepts are important to the study of the neurobiological toll of early childhood abuse and neglect because children who experience considerable adversity early in life may be exposed to environments/experiences that the species has not come to expect (such as abusive caregivers) or worse, environments that are largely lacking in key experiences (i.e., neglect). In both cases, when the expectable environment is violated by either gross alterations in the type of care received or a complete lack of care, subsequent development can be seriously derailed.
Axis and Biological Regulation
There is strong evidence across species that the HPA axis is affected by experiences of early childhood abuse and neglect (e.g., Bruce et al., 2009; Gunnar and Vazquez, 2001; Levine et al., 1993; Shonkoff et al., 2012). Glucocorticoids (cortisol in humans, corticosterone in rodents) are steroid hormones produced as an end product of the HPA system. The HPA axis serves two orthogonal functions: mounting a stress response and maintain-
ing a diurnal rhythm. A cascade of events is designed to promote survival behavior by directing energy to processes that are critical to immediate survival (e.g., metabolism of glucose) and away from processes that are less critical to immediate survival, such as immune functioning, growth, digestion, and reproduction (Gunnar and Cheatham, 2003).
Glucocorticoids also serve an important role in maintaining circadian patterns of daily activity, such as waking up, sleeping, and energy regulation (Gunnar and Cheatham, 2003). Diurnal species, including humans, have a diurnal pattern of cortisol production that enhances the likelihood of being awake at the same time in the day. In humans, diurnal cortisol levels peak about 30 minutes after waking up, decrease sharply by mid-morning, and continue to decrease gradually until bedtime (Gunnar and Donzella, 2002). The higher morning values of cortisol reflect greater metabolism of glucose early in the day, providing energy for the day’s activities.
The HPA axis is highly sensitive to the effects of early experiences. Diurnal effects typically have been examined as wake-up values and bedtime values because those time points allow assessments of change from nearly the highest reliable waking time point (with 30 minutes post wake-up being the highest) to the lowest waking time point. Daytime values are affected by a number of factors, such as exercise, naps, and travel to work (Larson et al., 1991; Watamura et al., 2002). The most consistent findings involve flatter, more blunted patterns of diurnal regulation among abused or neglected children relative to low-risk children (Bernard et al., 2010; Bruce et al., 2009; Dozier et al., 2006; Fisher et al., 2007; Gunnar and Vazquez, 2001). Similar flattened diurnal rhythms have been found in institutionalized children (Bruce et al., 2000; Carlson and Earls, 1997). Flattened diurnal cortisol patterns may reflect down-regulation of HPA axis activity following earlier hyperactivation (Carpenter et al., 2009; Fries et al., 2005).
Cicchetti and colleagues (Cicchetti and Rogosch, 2001a,b) examined changes across the day among abused and neglected children attending summer camp. The time points included when children first arrived at camp (at about 9 AM) and before they left camp for the day (at about 4 PM), likely tapping diurnal change within a challenging environment. The authors report complex findings regarding cortisol in this setting. Differences were found in some studies related to subtype and/or psychopathology and/or aggression (Cicchetti and Rogosch, 2001b; Murray-Close et al., 2008).
Animal models have been used to study experimentally the effects of neglect and abuse on HPA functioning (e.g., Levine et al., 1993). Experiences of abuse or neglect, depending on age of pup/infant, duration, chronicity, and subsequent response of dam/mother differentially affect short- and long-term effects on the HPA axis (Sanchez, 2006). Under naturally occurring conditions (about 10 percent of rhesus monkeys abuse their infants), a 1-year-old rhesus monkey that was abused (primarily in the first month of
life) showed higher cortisol levels under basal and stress conditions than a 1-year-old that had not been abused. These effects were not seen at older ages. (The age translation from rhesus to human is about 1 to 4, so a 1-year-old rhesus is developmentally similar to about a 4-year-old human child.) In other studies that have manipulated rearing conditions (such as isolation rearing), differences between conditions of abuse or neglect have been inconsistent. In some studies, higher cortisol values were observed in basal and/or stress conditions; in some, lower basal and/or stress conditions; and in some, no differences between the monkeys that had undergone deprivation and those that had not (Champoux et al., 1989; Clarke, 1993; Higley et al., 1992; Shannon et al., 1998).
Disrupted HPA axis regulation may have negative effects on a number of other biological systems. High levels of circulating cortisol resulting from early life stress may cause damage to developing brain regions (Teicher et al., 2003; Twardosz and Lutzker, 2010). Several brain regions, including limbic regions such as the amygdala and hippocampus and prefrontal regions, may be particularly susceptible to the effects of high levels of circulating cortisol because of the high number of glucocorticoid receptors in these areas (Brake et al., 2000; Schatzberg and Lindley, 2008; Wellman, 2001).
High levels of circulating cortisol may affect telomere length as well. Telomeres are the repeated sequences of DNA that cap the ends of chromosomes. Telomeres shorten each time cells divide, a process generally associated with aging, but also with stress (Epel et al., 2004). If telomeres become too short, the cell may become senescent (grow old) or may become malfunctional, for example, triggering inflammation or tumor development. Children who have been exposed to neglect show shortened telomeres (Asok et al., 2013; Drury et al., 2011). Drury and colleagues (2011) found shorter telomeres among children in institutional care. Similarly, Asok and colleagues (2013) found that children living in highly challenging environments showed shorter telomeres than comparison children, but that mothers could buffer children from the environment challenge. When mothers of neglected children were sensitive to challenging environments, their children’s telomeres were as long as those of low-risk children, but when mothers were insensitive, children’s telomeres were shorter. Clearly, then, sensitive caregiving serves as a protective factor even under difficult conditions of adversity.
There is as yet no compelling empirical evidence among humans that high levels of cortisol result from abuse or neglect and persist long enough to affect brain development adversely, leaving these arguments speculative. Nonetheless, the evidence is compelling that the HPA axis is perturbed in many cases, and perturbations are associated with a range of health and mental health problems (McEwen, 1998; Yehuda et al., 2002).
Studies (e.g., McGowan et al., 2008, 2009, 2011; Meaney and Szyf,
2005; Weaver et al., 2004) have found that the effects of abuse on the stress response are mediated by epigenetic programming of glucocorticoid receptor expression. Differential methylation of the glucocorticoid receptor gene promoter in the hippocampus was found to be associated with different rearing conditions in rodents, and was reversed by changes in caregiving conditions (McGowan et al., 2008). Paralleling these findings among rodents are nonexperimental findings among humans examined in postmortem analyses (McGowan et al., 2009; Szyf and Bick, 2013). Adult suicide victims who had experienced abuse as children differed in glucocorticoid receptor mRNA from adult suicide victims who had not experienced abuse as children and from controls. These findings are consistent with the experimental rodent findings, and suggest that methylation of receptor sites mediates the association between early care and stress responsiveness.
The amygdala performs a primary role in the formation and storage of memories associated with emotional events. The amygdala undergoes rapid development within the first several years of life and is particularly susceptible to early adversity (e.g., Chareyron et al., 2012). Relative to low-risk children, abused and neglected children show behavioral and emotional difficulties that are consistent with effects on the amygdala, such as internalizing problems, heightened anxiety, and emotional reactivity (Ellis et al., 2004; Kaplow and Widom, 2007; Tottenham et al., 2009; van Ijzendoorn and Juffer, 2006; Zeanah et al., 2009) and deficits in emotional processing (Dalgeish et al., 2001; Pollak et al., 2000; Vorria et al., 2006). Figure 4-2 illustrates structures in the medial temporal lobe critically involved in emotion (amygdala) and learning and memory (hippocampus).
Most studies have found no evidence that the structure of the amygdala is affected by abuse or neglect (De Bellis et al., 2001b; Tottenham and Sheridan, 2010; Woon and Hedges, 2008). However, Tottenham and colleagues (2010) and Mehta and colleagues (2009) found that amygdala volume was enlarged among children following institutionalized care, although this finding was not replicated by Sheridan and colleagues (2012) among a similar population. Importantly, both the Mehta et al. and Sheridan et al. studies did find a dramatic reduction in total brain volume, meaning that these children had physically smaller brains.
Functional magnetic resonance imaging (fMRI) studies have shown that early adversity leads to a sensitized amygdala. Relative to comparison children, previously institutionalized children showed heightened amygdala activity in response to fearful faces compared with neutral faces (Tottenham et al., 2011). Similarly, Maheu and colleagues (2010) found that children
FIGURE 4-2 Illustration of brain structures.
with a history of abuse or neglect showed greater activation of the left amygdala in response to fearful and angry relative to neutral faces.
Hippocampus, Learning, and Memory
The hippocampus (see Figure 4-2) plays an important role in learning and memory (Andersen et al., 2007; Ghetti et al., 2010; Otto and Eichenbaum, 1992) and, like the amygdala, matures rapidly over the first months and years of life (Lavenex et al., 2007). The hippocampus appears to be particularly susceptible to stress early in life (Gould and Tanapat, 1999; Sapolsky et al., 1990) and plays a role in modulating the response of the HPA axis to stressors, as binding of cortisol to hippocampal receptors serves to turn off the HPA axis response (Kim and Yoon, 1998). Damage to the hippocampus due to abuse or neglect can have negative consequences for its roles in regulation of the stress response system and in memory formulation (de Quervain et al., 1998; Sheridan et al., 2012).
Most studies have found no evidence of hippocampal volume deficits among abused children compared with healthy, nonabused control children (De Bellis et al., 1999, 2001a, 2002). Among adults, however, decreased hippocampal volume has been linked with the experience of childhood physical and sexual abuse (Andersen and Teicher, 2004; Andersen et al., 2008; Schmahl et al., 2003; Woon and Hedges, 2008). Nonetheless, rela-
tively smaller hippocampal volumes in abused adults may be specific to PTSD rather than abuse itself (Kitayama et al., 2005).
Prefrontal Cortex and Executive Functions
The prefrontal cortex (see Figure 4-2) is responsible for a variety of higher-order “executive” functions (Miller and Cohen, 2001). The development of the prefrontal cortex is protracted, extending from birth into the third decade of life (Gogtay et al., 2004; Rubia et al., 2006; Sowell et al., 2003). Prefrontal systems are especially sensitive to experiences of early adversity (Hart and Rubia, 2012; McLaughlin et al., 2010).
Evidence is mixed with regard to structural changes in the prefrontal cortex following abuse and neglect, with some studies showing smaller volumes of the right orbitofrontal cortex, right ventral-medial prefrontal cortex, and dorsolateral prefrontal cortex (Hanson et al., 2010); some showing decreased grey matter volume in the prefrontal cortex in children with interpersonal trauma and PTSD symptoms (Carrion et al., 2008); some showing the opposite effect (Carrion et al., 2009; Richert et al., 2006); and still others showing no effect after controlling for total brain volume (De Bellis et al., 2002). Despite mixed evidence regarding structural changes in the prefrontal cortex, a number of studies suggest that abuse and neglect are associated with functional changes in the prefrontal cortex and related brain regions. In particular, children with trauma experiences show patterns of neural activation during tasks requiring executive function that are similar to patterns observed in children with attention-deficit hyperactivity disorder (ADHD) (e.g., Carrion et al., 2008).
Consistent with these findings among abused and neglected children, previously institutionalized children and adolescents have been found to demonstrate disruptions in the prefrontal network that is associated with inhibitory control. For example, Mueller and colleagues (2010) found that children with a history of neglect or institutional care showed greater activation in several regions of the prefrontal cortex (e.g., left inferior frontal cortex, anterior cingulate cortex) during response inhibition trials of a go/no-go task compared with children without a history of neglect. Similar findings have been reported by McDermott and colleagues (2012) and Loman and colleagues (2009) among currently and previously institutionalized children.
The corpus callosum facilitates communication between the two hemispheres of the brain (Giedd et al., 1996a,b; Kitterle, 1995). The white matter fibers composing the corpus callosum are myelinated throughout
childhood and adulthood (Giedd et al., 1996a; Teicher et al., 2004), which allows faster, more efficient transmission (Bloom and Hynd, 2005). Myelinated regions such as the corpus callosum are susceptible to the impacts of early exposure to high levels of cortisol, which suppress the glial cell division critical for myelination.
Retrospective/cross-sectional studies have found abuse and neglect to be associated with structural changes in the corpus callosum. Teicher and colleagues (2004) compared corpus callosum volume in adults with different abuse and neglect experiences. The total corpus callosum area of the abused children was smaller than that of both healthy control children and children with psychiatric disorders and no abuse or neglect. Other findings suggest that gender may moderate these effects, with the effects being more pronounced among males than females (De Bellis and Keshavan, 2003; De Bellis et al., 1999, 2002; Teicher et al., 1997). Sheridan and colleagues (2012) performed structural MRIs on children enrolled in the Bucharest Early Intervention Project, described previously in this chapter. In a follow-up of 8- to 11-year-olds, Sheridan and colleagues (2012) found smaller total white and gray matter volume and smaller posterior corpus callosum volume among children who had been institutionalized relative to those who had never been institutionalized. By middle childhood, however, there were no significant differences in total white matter volume or posterior corpus callosum volume between the never-institutionalized (community) children and the foster care children. These early differences in corpus callosum may be associated with less efficient cognitive functioning among children who experience early adversity.
Influence of Early Profound Neglect on Brain Electrical Activity
The influence of profound neglect early in life has been examined using electroencephalography (EEG) and event-related potentials (ERPs).
EEG measurements of the brain’s electrical activity can serve as a coarse metric for brain development. Most work on EEG in the context of neglect has been performed on children with a history of institutional care. The most extensive study of brain electrical activity among children with a history of institutional care was conducted with the children enrolled in the prospective, longitudinal Bucharest Early Intervention Project. At baseline (mean age 20 months), prior to random assignment to continued institutional care or foster care, institutionalized children showed higher levels of theta power (low-frequency brain activity) and lower levels of alpha and beta power (high-frequency activity) compared with children
who were not institutionalized (Marshall et al., 2004). The pattern of activity observed in institutionalized children suggests a maturational delay or deficit in cortical development associated with an extreme form of neglect (Marshall et al., 2004). The profiles are similar to patterns found among children with ADHD (Barry et al., 2003; Harmony et al., 1990).
At follow-up, as a group, children assigned to foster care did not differ from the care-as-usual group (Marshall et al., 2008). However, the subset of children placed in foster care before 2 years of age showed EEG activity that more closely resembled that of the never-institutionalized group than the care-as-usual group. Overall, then, “institutionalization led to dramatic reductions in brain activity (as reflected in the EEG), whereas placement in foster care before 2 years of age led to a more normal pattern of EEG activity” (Nelson et al., 2011, p. 139). This last finding was replicated when the children were 8 years old (Vanderwert et al., 2010). Specifically, previously institutionalized children placed in foster care before about 2 years of age had patterns of brain activity that resembled those of never-institutionalized children, whereas children placed in foster care after 2 years of age had patterns of brain activity that resembled those of children randomly assigned to institutional care.
ERPs measure changes in the brain’s electrical activity in response to an internal or external stimulus or event. The components of the ERP (i.e., positive and negative deflections) can be quantified in terms of latency, amplitude, and location/distribution on the scalp. The P300 (i.e., positive deflection occurring approximately 300 ms after a stimulus) is associated with attention to emotionally evocative visual stimuli, such as emotional faces (Eimer and Holmes, 2007; Olofsson et al., 2008). Whereas nonabused children show similar P300 activity across emotional expressions, abused children show larger P300s to angry target faces (Pollak et al., 1997, 2001), a finding consistent with behavioral evidence of enhanced attention to angry faces among abused children.
Finding: Across human and nonhuman primate studies, perturbations to the HPA system often are seen to be associated with child abuse and neglect. The findings are complex, moderated by a number of factors and seen at some ages and not others. Further, the perturbations sometimes are reflected in atypically high production of cortisol across either basal or reactive contexts and sometimes in atypically low production. Recent work in epigenetics suggests that this may well be an area of future inquiry into the mechanisms whereby abuse or neglect alters gene expression and, in turn, behavior.
Finding: Abused and neglected children show behavioral and emotional difficulties that are consistent with effects on the amygdala, such as internalizing problems, heightened anxiety and emotional reactivity, and deficits in emotional processing. Most studies have found no evidence that the structure of the amygdala is affected by abuse or neglect; however, fMRI studies have shown that early adversity leads to a sensitized amygdala.
Finding: Despite mixed evidence regarding structural changes in the prefrontal cortex, a number of studies suggest that abuse and neglect are associated with functional changes in the prefrontal cortex and associated brain regions, often affecting inhibitory control.
Finding: Examination of patterns of brain electrical activity in institutionalized children suggests that extreme forms of neglect are associated with a maturational delay or deficit in cortical development.
There is a long history of research exploring the effects of child abuse and neglect on cognitive development. Studies have examined executive functioning and attention, as well as academic achievement.
Executive Functioning and Attention
As discussed earlier, some studies have found that child abuse and neglect have effects on the prefrontal cortex, a brain structure centrally involved in executive functioning. Executive functioning refers to higher-order cognitive processes that aid in the monitoring and control of emotions and behavior (Lewis-Morrarty et al., 2012). Included among executive functions are “holding information in working memory, inhibiting impulses, planning, sustaining attention amid distraction, and flexibly shifting attention to achieve goals” (Lewis-Morrarty et al., 2012, p. 2). Executive functioning abilities develop rapidly between the ages of 3 and 6 years, but continue to develop through at least the second decade of life.
Children who experience abuse and neglect appear to be especially at risk for deficits in executive functioning, which have implications for behavioral regulation. Extreme neglect, as seen in institutional care, has been related to executive functioning in a number of studies conducted by the Bucharest Early Intervention Project team (McDermott et al., 2012). For example, McDermott and colleagues (2012) found that children who
were randomly assigned to foster care showed better performance on an executive functioning task (i.e., a go/no-go task requiring inhibitory control) than children who were randomly assigned to treatment as usual. The assessments of executive functioning were conducted when children were 8 years old. Similar findings among comparably aged internationally adopted children (with histories of institutionalization) have been reported (e.g., Loman et al., 2013). These findings suggest that extreme forms of neglect may interfere with the development of executive functioning.
Problems in regulating attention represent one of the most striking deficits seen among children who have experienced severe early deprivation in institutional settings (Gunnar et al., 2007; Kreppner et al., 2001). Gunnar and colleagues (2007) found that problems with inattention or overactivity were more pronounced among children who had experienced early institutional care than among those who had been adopted internationally without early institutional care. Kreppner and colleagues (2007) found that many children who had been adopted following institutional care showed problems with inattention or overactivity, but that such problems were usually seen in combination with reactive attachment disorder, quasi-autistic behaviors, or severe cognitive impairment.
Using NSCAW data, Heneghan and colleagues (2013) examined mental health problems in teens older than age 12 who were the subject of a child welfare agency investigation. They found that 18.6 percent of abused and neglected teens scored positively for ADHD, compared with 5 percent of children and 2.5 percent of adults in the general U.S. population (APA, 2013c). Likewise, Briscoe-Smith and Hinshaw (2006) studied a sample of 228 girls with and without ADHD and with and without a history of abuse and neglect, finding that the girls with ADHD had a statistically significant heightened risk of having a documented history of abuse or neglect, as indicated by substantiated child protective services, parental, or school report. Some studies have found preliminary differences in the characteristics of ADHD displayed by children with and without a history of abuse or neglect (Webb, 2013). For example, Becker-Blease and Freyd (2008) studied a small community sample of 8- to 11-year-old children in which ADHD and abuse history were assessed by parent report. They found that children with a history of abuse displayed more severe impulsivity and inattention than nonabused children with ADHD, but the groups did not differ on measures of hyperactivity (Becker-Blease and Freyd, 2008).
A number of studies have found evidence that children who experience abuse and neglect show deficits in executive functioning and attention (Arseneault et al., 2011; De Bellis et al., 2009; Fisher et al., 2011; Lewis et al., 2007; Spann et al., 2012). Pears and colleagues (2008) found that abuse and neglect were associated with generally lower cognitive functioning among preschoolers. Lewis and colleagues (2007) found that 4-year-old
children who had experienced abuse or neglect and were in foster care showed poorer inhibitory control on a Stroop-like task relative to comparison children, despite similar levels of performance on a control task. Spann and colleagues (2012) found that physical abuse and neglect were associated with diminished cognitive flexibility on the Wisconsin Card Sorting Task among adolescents.
Abuse and neglect increase children’s risk for experiencing academic problems. Several studies suggest that abuse versus neglect matters, with neglect being especially predictive of academic underachievement (Briere et al., 1996; Jonson-Reid et al., 2004; Nikulina et al., 2011). Other studies failed to find differences between abuse and neglect, with both predicting achievement problems (e.g., Barnett et al., 1996; Crozier and Barth, 2005; Eckenrode et al., 1993; Jaffee and Gallop, 2007; Kurtz et al., 1993; Leiter and Johnsen, 1997). On balance, the evidence suggests that both abuse and neglect are predictive of academic problems. Perez and Widom (1994) found that child abuse and neglect had a significant impact on reading ability, IQ scores, and academic achievement. For example, 42 percent of abused and neglected children completed high school, compared with two-thirds of the matched comparison group without histories of abuse and neglect. The average IQ score for the abused and neglected children was about one standard deviation below the average for the control group; this association was significant after controlling for age, race, gender, and social class (Perez and Widom, 1994). Using NSCAW data, Jaffee and Maikovich-Fong (2011) found that chronically abused or neglected children had lower IQ scores than situationally abused or neglected children. The effect of chronic abuse or neglect on IQ scores remained significant after controlling for the effects of caregiver educational level on IQ. Leiter and Johnsen (1997) found that effects of abuse and neglect on school performance were cumulative, with more episodes of abuse and neglect being associated with poorer outcomes. Abuse and neglect predicted entry into special education after controlling for early medical conditions (Jonson-Reid et al., 2004). Jonson-Reid and colleagues (2004) found that 24 percent of the abused and neglected children entered special education, compared with 14 percent of those with no record of abuse or neglect. Further, every additional report of abuse or neglect before the age of 8 led to an increase of 7 percent in entry into special education. Thompson and colleagues (2012) found that expectations of future academic success were adversely affected by previous experiences of abuse and neglect, with these expectations having powerful self-fulfilling possibilities (Ross and Hill, 2002).
Psychosocial and Behavioral Outcomes
Given that child abuse and neglect are social experiences that undermine the ability to trust in caregivers, either because caregivers are frightening (as in cases of abuse) or because they fail to protect or provide care (as in cases of neglect), it makes sense that children who experience abuse and neglect are at risk for interpersonal problems. At the most proximal level, problems are seen in children’s ability to form trusting attachments to their parents. But not surprisingly, the effects also are seen in such areas as children’s processing of emotion (e.g., overly vigilant of angry faces), their attributions of others’ intent (e.g., assuming that intentions are malevolent when they are ambiguous), and difficulties with peers (e.g., being the victim or perpetrator of bullying or violence). Problems also are seen in internalizing symptoms, such as anxiety and depression, and externalizing symptoms, such as conduct disorder and substance use.
Children develop secure attachments to parents who are responsive to them when they are distressed (Ainsworth, 1978). Children typically develop insecure (avoidant or resistant) attachments when parents are unresponsive or inconsistent in responsiveness, but not frightening or bizarre (e.g., Lyons-Ruth et al., 1993; Schuengel et al., 1998). Secure, avoidant, and resistant attachments are referred to as organized attachment strategies because they are organized around the caregiver’s availability and provide a child a template for dealing with distress. On the other hand, disorganized attachment represents a breakdown in or a lack of strategy for dealing with distress when in the parent’s presence (Main and Solomon, 1990). Disorganized attachments are the most problematic in terms of outcomes for children. Relative to organized attachment, disorganized attachment is most predictive of long-term problems, especially externalizing symptoms (Fearon et al., 2010). Fearon and colleagues (2010) found strong evidence for a link between disorganized attachment and later externalizing symptoms through a meta-analysis of 34 studies involving 3,778 participants.
Child abuse and neglect are predictive of disorganized attachment, as well as insecure attachment more generally. A meta-analysis conducted by Cyr and colleagues (2010) included the 10 studies that have examined attachment quality with samples of children who have experienced abuse and neglect. The effect size was large for both disorganized and insecure attachment. Although abuse was more strongly related to disorganized attachment and neglect to insecure attachment, both abuse and neglect were associated with both types of attachment. These results are consistent with theory and with other empirical findings suggesting that when parents are
either frightening or unavailable, children fail to develop a secure attachment to them. Nonetheless, the effects of having more than five socioeconomic risk factors were comparable to those of child abuse and neglect, indicating that multiple challenges to parental functioning had significant effects on attachment regardless of whether these effects were seen in child abuse and neglect.
In early childhood, abused or neglected children may develop attachment disorders resulting from and following pathogenic care that inhibits a young child’s ability to form selective attachments (Hornor, 2008). Childhood attachment disorders are phenomena distinct from insecure, disorganized, or nonexistent attachment types; they have been redefined in the Diagnostic and Statistical Manual of Mental Disorders, fifth edition (DSM-V) to include two distinct disorders: reactive attachment disorder and disinhibited social engagement disorder (APA, 2013a,b). Reactive attachment disorder involves inhibited or emotionally withdrawn behavior, including rarely seeking and responding to comforting; it results from a lack of or incompletely formed selective attachments to adult caregivers (APA, 2013a). Disinhibited social engagement disorder is marked by a pattern of overly familiar behavior with strangers; it may occur even in children with established or secure attachments. Previously, each attachment disorder was considered the inhibited or disinhibited type of reactive attachment disorder, respectively.
Zeanah and colleagues (2004) studied the prevalence of attachment disorders among 94 toddlers in foster care whose abuse or neglect cases had been substantiated and who were enrolled in an intervention program; they found that the prevalence of attachment disorders reached 38-40 percent. Lyons-Ruth and colleagues (2009) examined socially indiscriminate attachment behavior in a sample of mother-child dyads that included pairs referred to a clinical service because of problematic caregiving and comparison pairs matched on socioeconomic status. They found that 18-month-olds displayed socially indiscriminate attachment behavior only if they had a history of abuse or neglect, or their mother had a history of psychiatric hospitalizations. Both disorders also have been identified in children exposed to neglectful institutional care in Romania who were later adopted into middle-class families in the United Kingdom (Smyke et al., 2002; Zeanah et al., 2002), although the disinhibited type of reactive attachment disorder (as defined in DSM-IV) has been found to be much more prevalent than the inhibited type (O’Connor et al., 2003). Furthermore, findings from the Bucharest Early Intervention Project study indicate that the inhibited type of reactive attachment disorder declined significantly once institutionalized children were placed in foster care, but the disinhibited type proved more persistent (Smyke et al., 2002; Zeanah and Gleason, 2010).
Infants have limited capacities to regulate their own emotions and are dependent on caregivers to help them deal effectively with distress (Tronick, 1989). Indeed, infants and young children are highly attuned and responsive to their parents’ emotions and use parental emotional signals to guide their behavior (Klinnert et al., 1983; Malatesta and Izard, 1984). The scaffolding important for the development of emotion regulation is challenged in abusing or neglecting families. When children feel upset or distressed, parents’ availability and soothing presence can help them feel that they can cope with the strong negative affect, such that they are able to develop autonomous and effective means of regulating emotions over time. When children regulate their emotions well, they react to challenge with flexible and socially acceptable responses (Cole et al., 1994; Kim and Cicchetti, 2010). Abused and neglected children, however, may not have such scaffolding experiences. It is likely that abused and neglected children experience not only a lack of modeling and support and an absence of positive affect but also harsh, inconsistent, and insensitive parenting (Shipman and Zeman, 2001). In the case of abuse, parents often respond in threatening or unpredictable ways to children’s distress (Milner, 2000). In the case of neglect, parents may be unresponsive or nonempathic. As a result of either response, children are at risk of failing to develop effective strategies for regulating emotions (Cicchetti et al., 1995; Kim and Cicchetti, 2010; Rogosch et al., 1995).
An initial, key task in regulating emotions is processing of cues. Studies have examined differences among children who have experienced abuse and neglect in how readily they identify angry, sad, and happy faces (Pollak and Sinha, 2002; Pollak and Tolley-Schell, 2003; Pollak et al., 2000; Shackman et al., 2007). Pollak and Sinha (2002) found that the threshold for detecting anger in the face was lower among abused than nonabused children; there were no differences in processing happy faces. Thus, these children appear to have a bias toward angry faces rather than a general deficit in processing faces. Pollak and Sinha (2002) point out that it is useful to identify emotions in others based on less than full information. Abused children’s bias toward attributing angry or sad affect may be adaptive when living with parents whose anger may be an important threat cue (Belsky et al., 2012); nonetheless, it comes at the cost of assuming hostile intent too readily under benign conditions, leading to aggressive responses that would not have been evoked had attributions been different (Dodge et al., 1995). Neglected children, on the other hand, generally are not as good as nonneglected children at identifying facial expressions, showing a general deficit (Pollak et al., 2000).
Emotion regulation can be seen as key to a number of the constructs
considered in this chapter. Problems in regulating emotion are associated with externalizing behaviors, such as aggression and behavior problems (Eisenberg et al., 2001; Kim and Cicchetti, 2010); internalizing behaviors, such as depression (Cole et al., 2008; Maughan and Cicchetti, 2002); and challenges in peer relations (Kim and Cicchetti, 2010; Rogosch et al., 1995). Emotion regulation can be seen, then, to have effects both on children’s own affect and on their behavioral reactions, which then have implications for their relationships with others.
Children’s relationships with their peers are critical to their sense of well-being. Abused and neglected children have problematic peer relations at disproportionately high rates (Kim and Cicchetti, 2010), as do children with a history of institutional care (Almas et al., 2012). Chronicity of child abuse and neglect predict peer relations, as reported by teachers, at age 8 (Graham et al., 2010). Problematic emotion regulation (Shields and Cicchetti, 2001) and higher levels of aggression and withdrawal (Rogosch et al., 1995) found in abused and neglected children can become apparent to peers when frustrations and challenges arise in school and playground environments.
Externalizing behavior refers to problem behaviors that are manifested externally (rather than internally, as in the case of depression and anxiety). Findings from several studies indicate that children who have experienced abuse and neglect are at greater risk for a number of externalizing behaviors, including conduct disorders, aggression, and delinquency (Lansford et al., 2002, 2009; Lynch and Cicchetti, 1998; Stouthamer-Loeber et al., 2001; Thornberry et al., 2010).
Oppositional defiant disorder and conduct disorder Studies have reported significant associations between a history of childhood abuse or neglect and various conduct problems, including those classified as oppositional defiant disorder or conduct disorder. Oppositional defiant disorder is indicated by a frequent or persistent pattern of angry or irritable mood, argumentative or defiant behavior, and vindictiveness (APA, 2013a). Its symptoms usually first appear during early childhood, and it often precedes conduct disorder, anxiety disorders, or major depressive disorder. Conduct disorder is indicated by a repetitive or persistent pattern of behavior that violates the basic rights of others or major societal norms or rules, including aggression toward people or animals, destruction of property, deceitfulness
or theft, and serious violations of rules (APA, 2013a). Conduct disorder can begin in childhood or adolescence; however, childhood-onset conduct disorder is more often preceded by oppositional defiant disorder, more persistent into adulthood, and more likely to include aggressive behavior than adolescence-onset conduct disorder. Both disorders also frequently co-occur with ADHD.
In a study using a community sample, Dodge and colleagues (1995) found that children who were physically abused before age 5 were 4 times more likely than nonabused children to display externalizing conduct problems in grade 3 and 4. Likewise, Kaplan and colleagues (1998) found that adolescents (aged 12-18) with substantiated cases of physical abuse were more likely to display conduct disorder or oppositional defiant disorder at the time of the study (odds ratio = 5.98) than the matched nonabused comparison group. Fergusson and colleagues (2008) found that childhood sexual abuse was associated with higher rates of conduct disorder in young adulthood. Furthermore, they found that childhood physical abuse was not associated with conduct disorder when sexual abuse was included in the model. Additional environmental and individual factors that interact with abuse or neglect to increase the likelihood of conduct disorder or oppositional defiant disorder include exposure to parental divorce (Afifi et al., 2009), interparental violence (Boden et al., 2010), and community violence (McCabe et al., 2005), as well as gender, with males more likely to display conduct disorder (Boden et al., 2010).
Aggression Manly and colleagues (2001) found that children who had experienced severe emotional abuse only as infants or severe physical abuse only as toddlers were more aggressive and showed more externalizing symptoms as school-aged children than children without a history of abuse or neglect. The severity of abuse experienced predicted aggressiveness and externalizing symptoms in middle childhood. Although abuse experienced only in early childhood had lasting effects, abuse experienced beyond early childhood also had effects on aggression and externalizing symptoms, and the most problematic effects were seen for children subjected to chronic, severe abuse (Manly et al., 2001). Rogosch and colleagues (1995) found that physically abused children showed both aggressive behaviors and social withdrawal during peer interactions. Along these lines, abused and neglected children were disproportionately likely to be both bullies and victims of aggression, effects that were mediated by emotion dysregulation (Shields and Cicchetti, 2001). At odds with these findings, Kotch and colleagues (2008) found that children who experienced neglect in their first 2 years of life showed more aggression toward peers at ages 4, 6, and 8 relative to children without a history of abuse or neglect. Indeed, in that study, other
subgroups (children who were abused or who were neglected at older ages) did not show an increased likelihood of aggression.
Hostile attributional bias refers to the tendency to assume that someone intended harm when circumstances were ambiguous but a negative outcome was experienced. For example, if a peer spilled milk on a child, the child could assume that the action was benign (unintentional) or intentional, with the latter representing a hostile attributional bias. When children assume that such an action was intentional, they are likely to act aggressively in response (Dodge et al., 1995). Physically abused children are more likely than other children to show such attributional biases (Dodge et al., 1995). Price and Glad (2003) found that these effects were seen in boys only and were associated with frequency of abuse. Such biases can lead to a self-fulfilling prophecy whereby children anticipate that someone intends them harm and react in a hostile way, which then elicits a hostile response (Dodge et al., 1995).
Internalizing problems—problems that are manifested internally—include symptoms of depression and anxiety. Child abuse and neglect have been found to put children at increased risk of internalizing symptoms from early childhood through adolescence and adulthood (Dubowitz et al., 2002; Thornberry et al., 2001; Widom et al., 2007a).
Dubowitz and colleagues (2002) found that neglect was associated with internalizing problems for 3- and 5-year-old children. Swanston and colleagues (1997) found that sexually abused children had a significantly higher average score on depression measures than a control group just 5 years after the abuse occurred, after adjusting for individual differences in age and sex, as well as contextual factors such as socioeconomic status, family functioning, mother’s mental health, and number of negative life events. Trickett and colleagues (2001) found that a sample of sexually abused girls had significantly higher rates of self-reported depression than a comparison group of nonabused females. At follow-up, approximately 7 years later, rates of depression were found to be significantly higher among the sexually abused group, excluding a subset whose experience of abuse was characterized chiefly by multiple perpetrators and a relatively short duration.
The heightened risk of depression extends beyond childhood to adolescence and adulthood. Multiple studies have found clear links between child abuse and neglect and depression in adolescence (e.g., Fergusson et al., 2008; Heneghan et al., 2013; Lansford et al., 2002). Brown and colleagues (1999) found that child abuse and neglect were associated with a nearly threefold increase in the rate of depression in adolescence, although this
risk was diminished after controlling for other adverse conditions. Gilbert and colleagues (2009b) cite a body of studies reporting adjusted odds ratios ranging from 1.3 to 2.4 for depression after childhood among those subjected to abuse and neglect as children. Among adults, Brown and colleagues (1999) found that the increased risk of depression associated with child abuse and neglect remained when other factors were covaried, consistent with findings that more than one-third of abused or neglected children show symptoms of major depressive disorder by their late 20s (Gilbert et al., 2009b). Likewise, Widom and colleagues (2007a) followed a group of individuals who had experienced abuse and/or neglect in childhood and a matched comparison group into young adulthood and found that experiencing childhood physical abuse and multiple types of abuse increased the lifetime risk for a diagnosis of major depressive disorder.
A growing body of research examines whether different types and combinations of abuse or neglect in childhood result in different levels of risk for the development of depressive symptoms. The results in this domain are mixed, with strong evidence that sexual and physical abuse in childhood are associated with depression later in life (e.g., Heneghan et al., 2013), but mixed evidence that neglect increases risk for depression independent of contextual factors. Many studies have found child sexual abuse to have large and independent effects on risk for depression later in life. For example, Fergusson and colleagues (2008) found that young adults who reported a history of childhood sexual abuse had mental health disorders, including depression, at a rate 2.4 times higher than that among those not exposed to such abuse. By contrast, Widom and colleagues (2007a) found that child sexual abuse was not associated with an elevated risk of major depressive disorder relative to matched controls, although physical abuse or multiple kinds of abuse did increase the risk for lifetime major depressive disorder. Additional studies have found that physical abuse increased the risk for adult depression (e.g., Brown et al., 1999). Some studies have found that neglect did not increase the risk for depression when statistical models included contextual factors (Nikulina et al., 2011), although Widom and colleagues (2007a) found that neglect increased risk for current major depressive disorder relative to matched controls in adulthood.
As discussed in the section on individual differences later in this chapter, researchers also have examined how the timing (Dunn et al., 2013; Thornberry et al., 2001) and severity (Fergusson et al., 2008) of abuse and neglect affect the risk of developing depression. Other factors throughout the life course, such as the presence or absence of social support (Sperry and Widom, 2013) and exposure to multiple traumas (Banyard et al., 2001) or stressful life events in adulthood (Power et al., 2013), have been found to interact with childhood experiences of abuse and neglect to influence the risk of developing depression later in life.
Dissociation is defined as a “disruption of and/or discontinuity in the normal, subjective integration of one or more aspects of psychological functioning, including—but not limited to—memory, identity, consciousness, perception, and motor control” (Spiegel et al., 2011, p. 19). Dissociation can be measured reliably and validly in children, adolescents, and adults (Briere et al., 2001; Keck Seeley et al., 2004; Lanktree et al., 2008; van Ijzendoorn and Schuengel, 1996; Wherry et al., 2009).
Child abuse and neglect have been associated with dissociation among both preschool-aged and elementary-aged children (Hulette et al., 2008, 2011; Macfie et al., 2001), as well as among adults (van Ikzendoorn and Schuengel, 1996). The existence of a subgroup of PTSD patients with high levels of dissociation has been demonstrated in clinical (Lanius et al., 2013; Putnam, 1997), psychophysiological (Griffin et al., 1997), neuroimaging (Lanius et al., 2013), and epidemiological (Stein et al., 2013) research. As a result, DSM-V is adding a dissociative subtype to the PTSD diagnosis (Spiegel et al., 2011a) (see the discussion of PTSD on p. 139).
High scores on dissociation measures have proven to be a predictor of externalizing behavior in children (Kisiel and Lyons, 2001; Shapiro et al., 2012; Yates et al., 2008). In adults, high levels of dissociation are associated with refractoriness to standard treatments for a number of psychiatric conditions, as well as increased comorbidity (Jans et al., 2008; Kleindienst et al., 2011; Wolf et al., 2012; Zanarini et al., 2011).
A meta-analysis of 55 studies (Cyr et al., 2010) links abuse with disorganized attachment. Grienenberger and colleagues (2005) found that mothers who engaged in disrupted affective communication with their infants at 4 months (as measured using the AMBIANCE scale) were more likely to have toddlers who were classified as disorganized at 14 months. In turn, disorganized attachment at 14 months predicted high dissociation scores at age 20 years (Lyons-Ruth, 2008). Disorganized attachment assessed during the child’s second year predicted elevated levels of self-reported dissociation in mid-adolescence (age 16 years) (Carlson, 1998) and early adulthood (age 19) (Ogawa et al., 1997).
Based on findings from the Minnesota Mother-Child Project, Egeland and Susman-Stillman (1996) propose that dissociation may act as a mediator of child abuse across generations. In a longitudinal study of sexually abused girls followed into parenthood, Kim and colleagues (2010) found that increased dissociation, together with a history of self-reported punitive parenting as a child, predicted whether a mother would parent her own children in a harsh and punitive manner. Thus, a tentative generational loop can be hypothesized in which harsh and abusive parenting increases the risk for higher levels of dissociation in childhood and adolescence,
which in turn increases the risk for impulsive behavior and harsh parenting of offspring. Further research, especially with a longitudinal design, is warranted to determine whether this hypothesized generational pattern of transmission represents an early opportunity for prevention of abuse in the next generation.
Posttraumatic Stress Disorder
In DSM-V, PTSD is classified as a trauma- and stressor-related disorder, a change from its previous classification as an anxiety disorder. PTSD develops following “exposure to actual or threatened death, serious injury, or sexual violation,” including directly experiencing the traumatic event, witnessing the event firsthand, learning that an actual or threatened violent or accidental death occurred to a family member or close friend, and experiencing repeated or extreme firsthand exposure to the details of the traumatic event (APA, 2013c). Behavioral symptoms of PTSD are divided into four categories: intrusion or reexperiencing, avoidance, negative alterations in cognition and mood, and alterations in arousal and reactivity (National Center for PTSD, 2013). Experiences of child abuse and neglect involve traumatic events that are often violent, invasive, and coercive (Kearney et al., 2010). Furthermore, secondary trauma may result from experiences of child abuse and neglect, including separation from family or homelessness, which may also trigger a PTSD response (Wechsler-Zimring et al., 2012).
A number of prospective and retrospective studies have found elevated rates of PTSD among individuals with a history of abuse and neglect (Chen et al., 2010; Kearney et al., 2010; Tolin and Foa, 2006; Weich et al., 2009; Widom, 1999). Numerous studies have found that PTSD was preceded by abuse and neglect; links with sexual abuse were especially strong (Chen et al., 2010; Gregg and Parks, 1995; Kendall-Tackett et al., 1993; Tolin and Foa, 2006; Weich et al., 2009; Widom, 1999). Kearney and colleagues (2010) report PTSD rates of 20-50 percent among youth who had been sexually abused, 50 percent among youth who had been physically abused, and 33-50 percent among youth who had experienced neglect combined with exposure to domestic violence. Kolko (2010) found that nearly 20 percent of youth in out-of-home care showed posttraumatic symptoms. Widom (1999) found increased risk for PTSD among adults who had experienced abuse and neglect as children, with 23 percent of those who had been sexually abused, 19 percent of those who had been physically abused, and 17 percent of those who had been neglected meeting criteria for PTSD at age 29, compared with 10 percent of the comparison group.
Some evidence indicates that PTSD may mediate the association between childhood abuse and neglect and later adverse outcomes. Wolfe
and colleagues (2004) found that boys who had been abused or neglected in childhood and displayed a greater number of PTSD symptoms were at higher risk of perpetrating emotional abuse in a dating relationship compared with abused or neglected boys who displayed fewer trauma symptoms. Weierich and Nock (2008) found that the specific PTSD symptoms of reexperiencing, avoidance, and numbing mediated the relationship between childhood experiences of abuse and neglect and nonsuicidal self-injury. In a study of adult women survivors of childhood sexual abuse, Ginzburg and colleagues (2006) found that severe childhood maltreatment, including sexual abuse as well as other types of abuse or neglect, was significantly associated with experiencing high levels of dissociation in conjunction with PTSD, while less severe childhood maltreatment was not significantly associated with the dissociative subtype. Avery and colleagues (2000) examined PTSD and key areas of functioning based on interviews with sexually abused children and their nonoffending parents. Compared with sexually abused girls with low scores on the Child Posttraumatic Stress Reaction Index, sexually abused girls with higher scores expressed more worries; reported increased problems with sleep, appetite, headaches, and stomachaches; reported increased depression and suicidal ideation; displayed more problems in school functioning; and had higher levels of family disruption.
Evidence links child abuse and neglect with personality disorders. Johnson and colleagues (1999) found that adults with a history of abuse and neglect (as indicated by records and/or self-report) had a fourfold increase in personality disorders relative to those without a history of abuse or neglect. Physical abuse was associated with elevated antisocial and depressive personality disorder symptoms; sexual abuse was associated with elevated borderline personality disorder symptoms; and neglect was associated with elevated symptoms of antisocial, avoidant, borderline, narcissistic, and passive-aggressive personality disorders, as well as with attachment difficulties and other interpersonal and psychological problems. Widom (1998) reports an increase in risk for antisocial personality disorder for both males and females with a history of abuse and neglect. In a subsequent study, Widom and colleagues (2009) report an increase in risk for borderline personality disorder in males only, suggesting that there may be sex differences in the consequences of abuse and neglect. Natsuaki and colleagues (2009) found that personality problems, although not diagnosed personality disorders, worsened as adolescence progressed.
Finding: Abuse and neglect have profound effects on selected aspects of children’s cognitive development. Although many attempts have been
made to disentangle the effects of abuse and neglect, the balance of findings suggests that severe neglect may interfere with the development of executive functioning, and both neglect and abuse increase the risk for attention regulation problems and ADHD, lower IQ, and poorer school performance.
Finding: As a result of abusive or neglectful responses from caregivers, children have a difficult time developing organized and secure attachments. As a result, abused and neglected children are at higher risk for the development of attachment disorders, particularly disinhibited social engagement disorder.
Finding: Abused and neglected children often fail to develop effective strategies for emotion regulation, partly as a result of differences in processing of emotional cues. Difficulties with emotion regulation can lead to further problems, including externalizing and internalizing problems and challenges in peer relations.
Finding: Children who experience abuse or neglect have been found to be at higher risk for the development of externalizing behavior problems, including oppositional defiant disorder, conduct disorder, and aggressive behaviors. Abused and neglected children also have been found to be at increased risk for internalizing problems, particularly depression, in childhood, adolescence, and adulthood.
Finding: Among preschool- and elementary school–aged children, as well as adults, a history of childhood abuse and neglect has been associated with dissociation, which increases the risk for externalizing behavior in childhood and resistance to treatment for psychiatric conditions later in life. It has been suggested that dissociation may act as a mediator of harsh or abusive parenting across generations, although this hypothesis requires further research.
Finding: A number of studies have found elevated rates of PTSD among individuals with a history of abuse and neglect. PTSD has been associated with physical, cognitive, psychological, social, and behavioral problems among youth who were abused or neglected in childhood.
Child abuse and neglect have effects on a number of health outcomes, from growth to illness to obesity. Connections have been found between problematic neurobiological outcomes of child abuse and neglect and
health. One plausible mechanism for these effects relates to the purported frequent or chronic activation of the HPA axis. As discussed previously, the HPA axis is designed for responding in crises.
Growth and Motor Development
In their most extreme forms, abuse and neglect are associated with stunted growth. Children living in institutional environments (Johnson et al., 2010) or adopted from highly neglecting institutional environments (Johnson and Gunnar, 2011) sometimes show very delayed growth in height and head circumference. Olivan (2003) found that children placed in foster care between ages 24 and 48 months were significantly below normal for height, weight, and head circumference. Similarly, Chernoff and colleagues (1994) found that most children entering foster care had an abnormal physical screen involving at least one body system, and on average weighed less and were shorter than comparison children.
Gross motor development often is delayed among children with a history of institutional care who have then been adopted internationally (Dobrova-Krol et al., 2008; Roeber et al., 2012). Roeber and colleagues (2012) found that children adopted from institutional settings showed motor system delays, with greater balance delays being predicted by length of time institutionalized and bilateral coordination delays being predicted by severity of deprivation. Rapid gains are seen after placement in adoptive homes, however (Pomerleau et al., 2005). Although somewhat canalized (less responsive to genetic or environmental variations), the development of these gross motor abilities is dependent upon opportunities to engage in motor activities. Note that these findings regarding motor delays may be limited in their application to extreme cases of neglect in which young children are left alone in their cribs or otherwise neglected for extended periods of time.
Child abuse and neglect have been linked to various forms of physical illness as well as various indicators of physical health problems. Adolescents with a history of childhood abuse or neglect report a lower rating of their own health compared with low-risk peers (Bonomi et al., 2008; Hussey et al., 2006). Likewise, more gastrointestinal symptoms were reported by adults who reported having been abused or neglected as children (Walker et al., 1999). To examine whether this association resulted from shared method variance, van Tilburg and colleagues (2010) used data collected from multiple informants among a sample of 845 children enrolled in the longitudinal, prospective Longitudinal Studies of Child Abuse and Neglect.
Across informants, youth who had experienced abuse or neglect had an increased likelihood of gastrointestinal symptoms, which often followed or coincided with sexual abuse.
In a longitudinal prospective study, childhood abuse and neglect predicted health indices among middle-aged adults (Widom et al., 2012). Both physical abuse and neglect predicted hemoglobin A1C (a biomarker for diabetes) and albumin (a biomarker for liver and kidney function); physical abuse uniquely predicted malnutrition and blood urea nitrogen (a marker for kidney function); neglect uniquely predicted poor peak airflow; and sexual abuse uniquely predicted hepatitis C (Widom et al., 2012).
Findings from the Adverse Childhood Experiences study indicate a heightened risk for liver disease, lung cancer, and ischemic heart disease among adults who report multiple adverse experiences in childhood (Brown et al., 2010; Dong et al., 2003, 2004). The adverse experiences measured in the study include emotional abuse, physical abuse, sexual abuse, emotional neglect, and physical neglect, as well as indicators of household dysfunction, such as domestic violence, parental divorce or separation, household member mental illness, household member substance abuse, and household member incarceration. Dong and colleagues (2003) found that the adjusted odds ratio for ever having liver disease ranged from 1.4 to 1.6 for different types of abuse and neglect; among individuals with more than 6 adverse childhood experiences, the adjusted odds ratio was 2.6. Notably, the risk of liver disease was substantially mediated by risk behaviors for liver disease, such as alcohol and drug use and various sexual behaviors. Brown and colleagues (2010) found an association between adverse childhood experiences and an increased risk of lung cancer, which was partially mediated by smoking behavior. In particular, exposure to a large number of adverse childhood experiences was strongly associated with premature death from lung cancer; among individuals who died from lung cancer, those with 6 or more adverse childhood experiences died an average of 13 years earlier than those with no adverse childhood experiences. Likewise, Dong and colleagues (2004) found that adverse childhood experiences increased the likelihood of ischemic heart disease. The association was substantially mediated by both traditional (diabetes, hypertension, physical inactivity, smoking, and obesity) and psychological (anger and depressed affect) risk factors, but the psychological risk factors of anger (adjusted odds ratio of 2.1) and depression (adjusted odds ratio of 2.5) had stronger associations with heart disease than the traditional risk factors.
In various studies, different forms of child abuse and neglect have been linked with increased body mass index and higher rates of obesity in
childhood, adolescence, and adulthood. Some studies link neglect but not abuse to obesity (e.g., Johnson et al., 2002; Lissau and Sorensen, 1994), and some link physical abuse but not neglect (Bentley and Widom, 2009). These differences may be the result of differences in the time points at which obesity is assessed, in sample characteristics, or in the adequacy of controls, or other factors. Knutson and colleagues (2010) found that specific types of neglect (supervisory versus care) predicted obesity at different ages. Care neglect, defined as inattention to such things as provision of adequate food and clothing, predicted body mass index at younger ages, whereas supervisory neglect, defined as parental lack of availability, predicted body mass index at older ages.
Finding: Experiences of child abuse and neglect have effects on many health outcomes, including risks for long-term chronic and debilitating diseases and, in extreme cases, stunted growth.
While a number of the consequences of child abuse and neglect discussed previously in this chapter can be present across childhood, adolescence, and adulthood, this section focuses on behavioral outcomes that manifest specifically in either adolescence or adulthood.
Delinquency and Violence
Maxfield and Widom (1996) found that abuse and neglect experienced in childhood predicted violence and arrests in early adulthood. Adults with a history of abuse and neglect were more likely than adults without such a history to have committed nontraffic offenses (49 percent versus 38 percent) and violent crimes (18 percent versus 14 percent). Victims of childhood physical abuse and neglect were more likely to be arrested for violence (odds ratios 1.9 and 1.6, respectively) after controlling for age, race, and sex. These authors also found that abused and neglected girls were at increased risk for being arrested for violence relative to girls who had not been abused and neglected, with an odds ratio of 1.9. Smith and colleagues (2005) also found that abuse and neglect increase the risk of violent offending in late adolescence and early adulthood. Jonson-Reid and colleagues (2012) found a powerful effect for the number of child abuse reports predicting violent delinquency, with the association being linear for up to three reports. Two of these prospective longitudinal studies also found that sexual abuse increased the risk for general offending, but not violent offending (Smith et al., 2005). Physical abuse appears to be strongly
related to violence in girls, as demonstrated in a meta-analysis (Hubbard and Pratt, 2002).
There is evidence that childhood abuse increases the risk for crime and delinquency. A number of large prospective investigations in different parts of the United States have documented a relationship between childhood abuse and neglect and juvenile and/or young adult crime (English et al., 2002; Lansford et al., 2007; Maxfield and Widom, 1996; Smith and Thornberry, 1995; Stouthamer-Loeber et al., 2001; Widom, 1989; Widom and Maxfield, 2001; Zingraff et al., 1993). Despite differences in geographic region, time period, youths’ age and sex, definition of child maltreatment, and assessment technique, these prospective investigations provide evidence that childhood maltreatment increases later risk for delinquency and violence. Replication of this relationship across a number of well-designed studies supports the generalizability of and increases confidence in the results.
Alcohol and Substance Use
As adolescents and adults, those with a history of abuse and neglect have higher rates of alcohol abuse and alcoholism than those without a history of abuse and neglect (Gilbert et al., 2009b; Jonson-Reid et al., 2012). The effects tend to be stronger for women, being seen even when other factors are covaried (Simpson and Miller, 2002; Widom et al., 1995). For example, Widom and colleagues (1995) found no association between a history of abuse and neglect and alcohol use by young men, but found an association for women even after controlling for parental substance use and other correlated variables. A similar pattern of results emerged in a follow-up with these participants about 10 years later, when they were approximately 40 years old. Women with a documented history of child abuse and/or neglect were more likely to drink excessively in middle adulthood than those without such a history (Widom et al., 2007b); again, this difference was not seen in men. Girls with a history of physical abuse tend to start using substances (including alcohol, marijuana, tobacco, etc.) at younger ages than youth without such a history (Lansford et al., 2010). Work by Lansford and colleagues (2010) suggests that this early initiation serves as the mechanism for later substance use in adulthood.
Evidence linking abuse and neglect to substance abuse in adulthood is mixed (Gilbert et al., 2009b; Widom et al., 1999), with retrospective and prospective findings differing. For example, Widom and colleagues (1999) describe findings based on defining child abuse and neglect prospectively and retrospectively using self-reports (i.e., following their sample forward and asking adults whether they had been abused or neglected as children). The findings based on these two types of data differed dramatically. The
prospective data showed no increase in risk of substance abuse at age 29, whereas the retrospective data showed significant differences. Interestingly, a later follow-up with this sample (Widom et al., 2006) found that in middle adulthood, abused and neglected individuals compared with controls were about 1.5 times more likely to report using any illicit drug (in particular, marijuana) during the past year, and reported use of a greater number of illicit drugs and more substance use–related problems. Findings such as these provide support for the importance of longitudinal studies because without the subsequent follow-up, there would have appeared to be no increase in risk for adults who had experienced childhood abuse or neglect; these findings also illustrate the importance of contextual factors in understanding consequences.
Experiences of abuse and neglect in childhood have a large effect on suicide attempts in adolescence and adulthood (Brown et al., 1999; Fergusson et al., 2008; Gilbert et al., 2009b; Widom, 1998). Among adults in their late 20s, Widom (1998) found that 19 percent of those with a history of abuse or neglect had made at least one suicide attempt, as compared with 8 percent of a matched community sample. Fergusson and colleagues (2008) found high rates of suicide among a New Zealand sample as well. These effects are seen for physical and sexual abuse even after accounting for other associated risk factors (Fergusson et al., 2008). Trickett and colleagues (2011) found, through a prospective design, more incidents of self-harm and suicidal behaviors among women who had been sexually abused than among a control group of women who had not been sexually abused.
Studies have investigated the association between child abuse and neglect and several aspects of sexual behavior, including early sexual initiation and sexual risk behavior, teen pregnancy, and prostitution and the risk for commercial sexual exploitation of children and adults.
Early Sexual Initiation and Sexual Risk Behavior
Children who experience abuse and neglect may initiate sexual activity at earlier ages than other children (Lodico and DiClemente, 1994; Noll et al., 2003; Springs and Friedrich, 1992; Wilson and Widom, 2008). In addition, there is limited evidence of an association between child abuse and neglect and increased risky sexual behaviors (Jones et al., 2010; Senn et al., 2008). This association has been studied most frequently for sexual
abuse; however, Jones and colleagues (2010) found that physical and emotional abuse, but not neglect, contributed to risky behaviors over and above the effects of sexual abuse. Trickett and colleagues (2011) undertook one of the most extensive longitudinal studies of developmental outcomes for female victims of sexual abuse. The majority had experienced severe sexual abuse, defined by the type of abuse (with vaginal and anal penetrative abuse seen as most severe), the length of time over which the abuse occurred, and the relationship of the abuser to the victim. In addition to earlier initiation of sexual activity among women who had been sexually abused in childhood, the authors found less use of birth control (Noll et al., 2003). For both abused and nonabused women, having a large number of male peers in childhood networks was associated with a lack of birth control use in adolescence (Trickett et al., 2011). For abused females, however, having high-quality relationships with male peers and nonpeers in childhood was associated with greater birth control use in adolescence; in the comparison group, this association was not found.
Evidence linking childhood sexual abuse and increased risk for teen pregnancy has been mixed. Trickett and colleagues (2011) found that severely sexually abused females reported significantly higher rates of teen pregnancy and teen motherhood than nonabused females (abused = 39 percent, nonabused = 15 percent). In a meta-analysis of previously published studies of sequelae of child sexual abuse, Noll and colleagues (2009) found an increased risk for early pregnancy among girls who had been sexually abused. In contrast, using a prospective cohort design that followed children with documented cases of abuse and neglect into young adulthood, Widom and Kuhns (1996) found no evidence that childhood sexual abuse was a significant risk factor for multiple early sexual partners or teenage pregnancy.
Prostitution and Risk for Commercial Sexual Exploitation of Children and Adults
In a prospective study, Widom and Kuhns (1996) found that sexual abuse and neglect, but not physical abuse, were associated with later prostitution. In a subsequent study, Wilson and Widom (2010) examined the role of problem behaviors as a pathway to adult prostitution and found that adult victims who had experienced child abuse and neglect were more likely than nonvictims to report having been involved in prostitution as adults or prostituted as juveniles (Wilson and Widom, 2008). Stoltz and colleagues (2007) found a significant relationship between child abuse and
neglect (sexual, physical, and emotional) and later involvement in prostitution among a sample of 361 drug-using, street-involved youth in Canada.
While an important topic, evidence that child abuse and neglect increase the risk for commercial sexual exploitation of children is very limited and comes primarily from retrospective studies of sexually exploited youth. Some older studies have reported that experiences of childhood sexual abuse influenced the decision of young women to become involved in commercial sex work (Bagley and Young, 1987; Silbert and Pines, 1983). A comprehensive look at those issues will be presented in a forthcoming Institute of Medicine report from the Committee on Commercial Sexual Exploitation and Sex Trafficking of Minors in the United States.
Finding: Experiences of abuse and neglect in childhood have a large effect on delinquency, violence, and suicide attempts in adolescence and adulthood.
Finding: Adolescents and adults with a history of child abuse and neglect have higher rates of alcohol abuse and alcoholism than those without a history of abuse and neglect, although this relationship has been found most frequently in women.
Finding: Children who experience abuse and neglect may initiate sexual activity at earlier ages than comparison groups. Childhood sexual abuse also has been found to be associated with heightened risks for a range of adverse outcomes related to sexual risk-taking behaviors.
Finding: Studies seeking an association between child abuse and neglect and teen pregnancy or adult prostitution have reported mixed results.
This chapter has presented extensive evidence that children who are abused or neglected, as a group, are at increased risk for a variety of problematic outcomes. However, not all children who experience abuse or neglect experience these negative consequences. Not surprisingly (given what is known about typical development), children vary in the outcomes they experience even when exposed to the same type of abuse or neglect, with outcomes ranging from the most problematic to functioning well across domains. As discussed earlier in this chapter, an ecological-transactional model is helpful for understanding outcomes related to abuse and neglect as influenced by the interplay of risk and protective factors that occur at multiple levels of a child’s ecology. Through examination of compensatory resources in children and their environment, an ecological-transactional
framework can aid in understanding children who exhibit resilient outcomes despite having been abused or neglected (Cicchetti and Toth, 2009; Luthar et al., 2000). Factors that influence resilience among abused and neglected children have been identified at the level of the individual child, the family, and the child’s broader social context. However, neither a child’s individual strengths nor the surrounding environment alone can predict resilient outcomes. As noted by Jaffee and colleagues (2007, p. 233), “the fit between the child and the environment is the best predictor of children’s psychological well-being.” The following sections describe research examining explanatory factors for differences in outcomes related to child abuse and neglect.
Characteristics of Abuse or Neglect Experiences
Characteristics of a child’s exposure to abuse or neglect have been shown to influence the risk for problematic outcomes. Such characteristics include the point within the course of a child’s development at which an experience of abuse or neglect occurs; the chronicity of abuse or neglect experiences, taking into account their duration and frequency; the severity of the experiences; and the type of abuse or neglect (Bulik et al., 2001; Collishaw et al., 2007; Keiley et al., 2001; Manly et al., 2001).
Among a sample of adult female twins, Bulik and colleagues (2001) found an association between characteristics of the abuse experience (e.g., a high level of severity of child sexual abuse, such as attempted or completed intercourse and the use of force or threats) and certain psychiatric disorders. In examining the effect of timing on outcomes related to child physical abuse, Keiley and colleagues (2001) found that children who experienced such abuse while under the age of 5 were at higher risk for negative outcomes than those who experienced the same type of abuse at age 5 or older. Jonson-Reid and colleagues (2012) found that nearly all children who experienced chronic, persisting abusing or neglect showed adverse outcomes in adulthood: 91.9 percent of children showed at least one negative outcome if they had 12 or more reports of abuse or neglect (Jonson-Reid et al., 2012).
The concept of resilience serves as a useful lens for evaluating the differing outcomes of children exposed to abuse and neglect. By examining factors that contribute to whether children experience maladaptive outcomes in response to abuse or neglect, researchers can gain a better understanding of how better to prevent and treat these consequences. While resilience has been defined in various ways, it can be understood as “a good outcome in
spite of high risk, sustained competence under stress, and recovery from trauma” (McGloin and Widom, 2001, p. 1022).
The study of resilience in the context of child abuse and neglect must take into account several factors. First, as shown throughout this chapter, consequences of child abuse and neglect can manifest in multiple domains of functioning. Therefore, a child’s subsequent adaptation or maladaptation following abuse or neglect must be assessed in terms of multiple outcomes rather than a single indicator, such as depression (Afifi and Macmillan, 2011; McGloin and Widom, 2001). Second, resilience is not a static construct, meaning that a child can exhibit resilient outcomes at a certain point in the course of development but may still experience problematic outcomes at a later time. It follows that analysis of resilience in abused and neglected children should include a temporal component (McGloin and Widom, 2001). Third, many factors believed to promote resilience in response to child abuse and neglect can also serve to promote positive adaptation more generally in response to other childhood stressors, making it imperative for studies to include a comparison group that has not been abused or neglected (Collishaw et al., 2007). Finally, resilience might usefully be considered from the perspective of allostatic load (Danese and McEwen, 2012). That is, some children who experience abuse or neglect do not show problematic outcomes, but as abuse, neglect, and other adverse childhood experiences accumulate, they challenge children’s ability to cope with the negotiation of life tasks.
Results from a study of adults who were the subjects of substantiated cases of child abuse or neglect as children indicate that 22 percent of abused and neglected individuals met the criteria for resilience, which required successful functioning in 6 of 8 domains (McGloin and Widom, 2001). A study by Collishaw and colleagues (2007) examined resilience to adult psychopathology within a representative community sample, finding that 44 percent of adults who reported abuse during childhood reported no psychiatric problems in adulthood and demonstrated positive adaptation in other domains.
Protective factors supporting resilience have been examined at the levels of the individual, family, and social environment, with resilience being measured in childhood, adolescence, and early adulthood. In a review of protective factors for resilience following child abuse and neglect, Afifi and Macmillan (2011) identify three protective factors that are best supported by findings from longitudinal and cross-sectional studies: a stable family environment, supportive familial relationships, and personality traits that support social skills.
Individual-level protective factors identified among those displaying resilience following child abuse and neglect include personality traits (e.g., high ego control, high self-esteem, internal locus of control, external at-
tributions of blame, and attribution of success to own efforts); gender (females more resilient than males); and relationship capabilities (Afifi and Macmillan, 2011; Collishaw et al., 2007; Jaffee and Gallop, 2007; Jaffee et al., 2007). There is some evidence that intelligence or cognitive ability functions as a protective factor (Masten and Tellegen, 2012), but it has not always been found to be significant in supporting resilience (Afifi and Macmillan, 2011; Collishaw et al., 2007). Jaffee and colleagues (2007) found that children with protective individual-level characteristics were likely to be resilient in low-stress environments (59 percent), but children with the same protective individual-level characteristics were less likely to be resilient in highly challenging environments.
Family-level protective factors include a caring and safe home environment; positive changes in family structure (e.g., intervention, cessation of visiting rights, or removal to foster care); and supportive familial relationships at the time of abuse (Afifi and Macmillan, 2011; Collishaw et al., 2007; Jaffee et al., 2007). In a sample of sexually abused girls in foster care, family support was not found to be a protective factor, but peer influences, school plan certainty, and positive future orientation were (Edmond et al., 2006). Other social-level protective factors include supportive relationships with non-family members, such as teachers or camp counselors, and supportive relationships with peers in adolescence (Flores et al., 2005; Jaffee et al., 2007).
Gene x Environment Interactions
Historically, those working in the field of child abuse and neglect were unable to examine whether such adverse experiences interacted with biological risk or protective factors (e.g., so-called risk or protective genes)—specifically, whether experience interacted with underlying genetics. This situation has changed over the past 20 years as advances in molecular genetics have enabled a search for gene x environment (GxE) interactions. A number of such interactions have been studied in the last several decades in relation to early adversity generally and child abuse and neglect in particular. Critics of these approaches charge, among other things, that examining single gene and single environment combinations in interactions capitalizes on chance. In addition, some experts in genetics argue that the action of any single gene is likely to be very small, and to detect its effects will likely require very large sample sizes. Nonetheless, some GxE findings have emerged as robust and apparently replicable.
The 5-HTT gene is perhaps at the top of this list. This gene regulates reuptake of serotonin (a neurotransmitter that has various functions, including regulation of mood and sleep and some cognitive functions, such as memory and learning) at the synaptic cleft. The gene has long and short
allelic variants that confer differential reuptake efficiency. Rodent, nonhuman primate, and human studies (e.g., Caspi et al., 2003) have shown that two alleles confer advantage among animals raised in stressful environments. Caspi and colleagues (2003) found that adults who had experienced stressful life events as children were more likely to have a major depressive disorder if they had one or two short alleles. Those who had two long alleles were no more likely to develop depression than individuals who had not experienced stressful life events.
A second genetic polymorphism that has received much attention is a functional polymorphism in the promoter region of the monoamine oxidase A (MAOA) gene. MAOA encodes the MAOA enzyme and selectively degrades serotonin, norepinephrine, and dopamine. Abused and neglected boys with the genotype conferring low levels of MAOA expression were found to be more likely to develop a range of externalizing behaviors, including conduct disorder, antisocial personality disorder, and violent criminality (Caspi et al., 2002). However, subsequent studies have failed to replicate these findings or have demonstrated only partial replications (Huizinga et al., 2006; Widom and Brzustowicz, 2006). For a recent review of the GxE literature concerned with child depression and abuse, see Dunn and colleagues (2011).
Finding: Not all children who experience abuse or neglect show problematic outcomes. Factors that influence resilience among abused and neglected children have been identified at the level of the individual child, the family, and the child’s broader social context. These factors, along with risks and stressors at each level, interact with one another to predict resilient outcomes.
Finding: There is a positive association between the number of risk factors for abuse and neglect to which a child is exposed and the likelihood of experiencing adverse outcomes.
Finding: The timing, chronicity, and severity of child abuse and neglect, as well as the context in which they occur, have been shown to impact the associated outcomes.
Although the total costs of child abuse and neglect are difficult to gauge because much abuse is unreported (Waters et al., 2004), a number of studies over the last few decades have attempted to document the economic burden of child abuse and neglect on society (Corso and Fertig, 2010; Fang et al., 2012; Wang and Holton, 2007; Waters et al., 2004). Economic burden or
economic impact analyses typically quantify burden by aggregating the direct medical expenditures resulting from a condition, the direct nonmedical expenditures associated with a condition, and the subsequent indirect losses in productivity potential for society. These analyses often are called cost of illness/injury analyses.
Examples of direct medical expenditures include inpatient and outpatient hospital care, mental health care, medical transport required in the event of an emergency, medications and medical devices, and the medical treatment of chronic conditions resulting from the abuse. Multiple studies since the 1993 NRC report was issued have assessed the direct medical costs associated with child abuse and neglect (Brown et al., 2011), particularly the inpatient costs associated with severe abuse (Courtney, 1999; Evasovich et al., 1998; Irazuzta et al., 1997; Libby et al., 2003; New and Berliner, 2000; Rovi et al., 2004).
Direct nonmedical expenditures include use of the child welfare system, law enforcement, and the criminal justice system. Studies have included nonmedical costs in their assessment of the economic burden of child abuse and neglect (Staudt, 2003; Zagar et al., 2009).
Productivity losses include the child’s missing school or performing at subpar levels in school because of the abuse, parents missing work or performing at subpar levels at work because of the abuse situation or having to deal with child welfare and criminal justice services, and permanent losses in lifetime productivity potential because of premature death. Productivity losses and economic well-being have been incorporated into a number of analyses of the economic burden of child abuse and neglect (Brown et al., 2011; Corso and Fertig, 2010; Corso et al., 2011; Currie and Widom, 2010; Fang et al., 2012).
Gelles and Perlman (2012) estimate that cases of abuse or neglect impose a cumulative cost to society of $80.2 billion each year—$33.3 billion in direct costs and $46.9 billion in indirect costs. An analysis by the Centers for Disease Control and Prevention found that the average lifetime cost of a case of nonfatal child abuse and neglect is $210,012 in 2010 dollars, most of this total ($144,360) due to lost productivity but also encompassing the costs of child and adult health care, child welfare, criminal justice, and special education (Fang et al., 2012). The average lifetime cost of a case of fatal child abuse and neglect is $1.27 million, due mainly to loss of productivity.
Currie and Widom (2010) found that adults who had experienced abuse and neglect in childhood had lower levels of education, employment, and earnings and fewer assets than adults without a history of abuse and neglect. A higher percentage of adults who had been abused or neglected as children worked in menial, semiskilled positions at age 29 compared with adults who had not been abused or neglected—62 versus 45 percent, respectively. More of the abused and neglected group has been unemployed at
some point during the previous 5 years (41 versus 58 percent, respectively). And fewer of those from the abused or neglected group were currently employed or had a bank account, owned a car, or owned their home. Larger effects were seen for women than for men.
Analyses of the economic burden of child abuse and neglect could be strengthened by greater transparency in the study methods, including a full accounting of all cost categories that may be impacted by abuse and neglect and transparency in the unit cost estimates for each cost category, as well as a methodologically sound choice of study design for estimating economic burden (Corso and Fertig, 2010; Corso and Lutzker, 2006; Fang et al., 2012). Several approaches could be taken to estimate economic burden, each of which has advantages and disadvantages that could potentially result in overestimating or underestimating the true economic cost of child abuse and neglect. Options include using cross-sectional data to compare the medical costs for an abused/neglected population compared with a nonabused/nonneglected population, including only those health care costs that can be explicitly linked to diagnosis-specific health care utilization (and costs) through the use of diagnosis and external cause codes used in inpatient settings, and supplementing either of these two approaches by including the costs of the fraction of other health conditions attributed to child abuse and neglect.
Finding: Although the total costs of child abuse and neglect are difficult to gauge, a number of studies have attempted to document the economic burden of child abuse and neglect on society, including such measures as direct medical and nonmedical expenditures and productivity losses. One study estimates that cases of abuse or neglect impose a cumulative cost to society of $80.2 billion annually (Gelles and Perlman, 2012).
Finding: Some studies have shown that adults who experienced abuse and neglect in childhood have lower levels of education, employment, and earnings and fewer assets than adults without a history of abuse and neglect.
Child abuse and neglect appear to influence the course of development by altering many elements of biological, cognitive, psychosocial, and behavioral development; in other words, child abuse and neglect “get under the skin” (Hertzman and Boyce, 2010) to have a profound and often lasting impact on development. Brain development is affected, as is the ability to make decisions as carefully as one’s peers, or executive functioning; the
ability to regulate physiology, behavior, and emotions is impaired; and the trajectory toward more problematic outcomes is impacted. Effects are seen across domains, with the interplay across brain and behavioral systems being particularly striking.
Risk and protective factors across multiple levels of a child’s ecology interact to influence outcomes related to child abuse and neglect. Factors that influence resilience across these domains are important to an understanding of how to protect children from the adverse outcomes discussed in this chapter. Evidence suggests that the timing, chronicity, and severity of the abuse or neglect matter in terms of outcomes. The more times children experience abuse or neglect, the worse are the outcomes (Jonson-Reid et al., 2012). As Jonson-Reid and colleagues (2012) point out, it is not enough to know whether an event happened; one must also know how ongoing the problem is. The committee sees as hopeful the evidence that changing environments can change brain development, health, and behavioral outcomes. There is a window of opportunity, with developmental tasks becoming increasingly more challenging to negotiate with continued abuse and neglect over time.
Future research in this area needs to focus on disentangling the effects of child abuse and neglect from those of other conditions. There is a need to explore beneath the surface to understand the behavioral, neurobiological, social, and environmental mechanisms that mediate the association between exposure to abuse and neglect and their behavioral and neurobiological sequelae.
Afifi, T. O., and H. L. Macmillan. 2011. Resilience following child maltreatment: A review of protective factors. Canadian Journal of Psychiatry 56(5):266-272.
Afifi, T. O., J. Boman, W. Fleisher, and J. Sareen. 2009. The relationship between child abuse, parental divorce, and lifetime mental disorders and suicidality in a nationally representative adult sample. Child Abuse & Neglect 33(3):139-147.
Ainsworth, M. D. S. 1978. Patterns of attachment: A psychological study of the strange situation. Hillsdale, NJ: Lawrence Erlbaum Associates.
Almas, A. N., K. A. Degnan, A. Radulescu, C. A. Nelson, 3rd, C. H. Zeanah, and N. A. Fox. 2012. Effects of early intervention and the moderating effects of brain activity on institutionalized children’s social skills at age 8. Proceedings of the National Academy of Sciences of the United States of America 109(Suppl. 2):17228-17231.
Andersen, P., R. Morris, D. Amaral, T. Bliss, and J. O’Keefe. 2007. The hippocampus book. New York: Oxford University Press.
Andersen, S. L., and M. H. Teicher. 2004. Delayed effects of early stress on hippocampal development. Neuropsychopharmacology: Official Publication of the American College of Neuropsychopharmacology 29(11):1988-1993.
Andersen, S. L., A. Tomada, E. S. Vincow, E. Valente, A. Polcari, and M. H. Teicher. 2008. Preliminary evidence for sensitive periods in the effect of childhood sexual abuse on regional brain development. Journal of Neuropsychiatry and Clinical Neurosciences 20(3):292-301.
APA (American Psychiatric Association). 2013a. Diagnostic and statistical manual of mental disorders: DSM-5. Washington, DC: APA.
APA. 2013b. Highlights of changes from DSM-IV-TR to DSM-V. Washington, DC: APA.
APA. 2013c. Posttraumatic stress disorder—DSM-V. Washington, DC: APA.
Arseneault, L., M. Cannon, H. L. Fisher, G. Polanczyk, T. E. Moffitt, and A. Caspi. 2011. Childhood trauma and children’s emerging psychotic symptoms: A genetically sensitive longitudinal cohort study. American Journal of Psychiatry 168(1):65-72.
Asok, A., K. Bernard, T. L. Roth, J. B. Rosen, and M. Dozier. 2013. Parental responsiveness moderates the association between early-life stress and reduced telomere length. Development and Psychopathology 25(3):577-585.
Avery, L., C. R. Massat, and M. Lundy. 2000. Posttraumatic stress and mental health functioning of sexually abused children. Child and Adolescent Social Work Journal 17(1):19-34.
Bagley, C., and L. Young. 1987. Juvenile prostitution and child sexual abuse: A controlled study. Canadian Journal of Community Mental Health 6(1):5-26.
Banyard, V. L., L. M. Williams, and J. A. Siegel. 2001. The long-term mental health consequences of child sexual abuse: An exploratory study of the impact of multiple traumas in a sample of women. Journal of Traumatic Stress 14(4):697-715.
Barnett, D., J. I. Vondra, and S. M. Shonk. 1996. Self-perceptions, motivation, and school functioning of low-income maltreated and comparison children. Child Abuse & Neglect 20(5):397-410.
Barry, R. J., S. J. Johnstone, and A. R. Clarke. 2003. A review of electrophysiology in attention-deficit/hyperactivity disorder: II. Event-related potentials. Journal of Clinical Neurophysiology 114(2):184-198.
Becker-Blease, K. A., and J. J. Freyd. 2008. A preliminary study of ADHD symptoms and correlates: Do abused children differ from nonabused children? Journal of Aggression, Maltreatment and Trauma 17(1):133-140.
Belsky, J. 1980. Child maltreatment: An ecological integration. American Psychologist 35(4): 320-335.
Belsky, J. 1993. Etiology of child maltreatment: A developmental-ecological analysis. Psychological Bulletin 114(3):413-434.
Belsky, J., G. L. Schlomer, and B. J. Ellis. 2012. Beyond cumulative risk: Distinguishing harshness and unpredictability as determinants of parenting and early life history strategy. Developmental Psychology 48(3):662-673.
Bentley, T., and C. S. Widom. 2009. A 30-year follow-up of the effects of child abuse and neglect on obesity in adulthood. Obesity (Silver Spring) 17(10):1900-1905.
Bernard, K., Z. Butzin-Dozier, J. Rittenhouse, and M. Dozier. 2010. Cortisol production patterns in young children living with birth parents vs children placed in foster care following involvement of child protective services. Archives of Pediatrics and Adolescent Medicine 164(5):438-443.
Bloom, J. S., and G. W. Hynd. 2005. The role of the corpus callosum in interhemispheric transfer of information: Excitation or inhibition? Neuropsychology Review 15(2):59-71.
Boden, J. M., D. M. Fergusson, and L. J. Horwood. 2010. Risk factors for conduct disorder and oppositional/defiant disorder: Evidence from a New Zealand birth cohort. Journal of the American Academy of Child and Adolescent Psychiatry 49(11):1125-1133.
Bonomi, A. E., M. L. Anderson, F. P. Rivara, E. A. Cannon, P. A. Fishman, D. Carrell, R. J. Reid, and R. S. Thompson. 2008. Health care utilization and costs associated with childhood abuse. Journal of Genernal Internal Medicine 23(3):294-299.
Brake, W. G., R. M. Sullivan, and A. Gratton. 2000. Perinatal distress leads to lateralized medial prefrontal cortical dopamine hypofunction in adult rats. Journal of Neuroscience 20(14):5538-5543.
Briere, J. N. 1992. Child abuse trauma: Theory and treatment of the lasting effects. Newbury Park, CA: Sage Publications.
Briere, J., M. F. Erickson, and B. Egeland. 1996. The APSAC handbook on child maltreatment. Thousand Oaks, CA: Sage Publications.
Briere, J., K. Johnson, A. Bissada, L. Damon, J. Crouch, E. Gil, R. Hanson, and V. Ernst. 2001. The Trauma Symptom Checklist for Young Children (TSCYC): Reliability and association with abuse exposure in a multi-site study. Child Abuse & Neglect 25(8):1001-1014.
Briscoe-Smith, A. M., and S. P. Hinshaw. 2006. Linkages between child abuse and attention-deficit/hyperactivity disorder in girls: Behavioral and social correlates. Child Abuse & Neglect 30(11):1239-1255.
Brown, D. S., X. Fang, and C. S. Florence. 2011. Medical costs attributable to child maltreatment: A systematic review of short- and long-term effects. American Journal of Preventive Medicine 41(6):627-635.
Brown, D. W., R. F. Anda, V. J. Felitti, V. J. Edwards, A. M. Malarcher, J. B. Croft, and W. H. Giles. 2010. Adverse childhood experiences are associated with the risk of lung cancer: A prospective cohort study. BMC Public Health 10:20.
Brown, J., P. Cohen, J. G. Johnson, and E. M. Smailes. 1999. Childhood abuse and neglect: Specificity of effects on adolescent and young adult depression and suicidality. Journal of the American Academy of Child and Adolescent Psychiatry 38(12):1490-1496.
Bruce, J., M. Kroupina, S. Parker, and M. R. Gunnar. 2000. The relationships between cortisol patterns, growth retardation, and developmental delay in post-institutionalized children. Paper presented at International Conference on Infant Studies, Brighton, England.
Bruce, J., P. A. Fisher, K. C. Pears, and S. Levine. 2009. Morning cortisol levels in preschool-aged foster children: Differential effects of maltreatment type. Developmental Psychobiology 51(1):14-23.
Bulik, C. M., C. A. Prescott, and K. S. Kendler. 2001. Features of childhood sexual abuse and the development of psychiatric and substance use disorders. British Journal of Psychiatry 179(5):444-449.
Carlson, E. A. 1998. A prospective longitudinal study of attachment disorganization/disorientation. Child Development 69(4):1107-1128.
Carlson, M., and F. Earls. 1997. Psychological and neuroendocrinological sequelae of early social deprivation in institutionalized children in Romania. Annals of the New York Academy of Sciences 807:419-428.
Carpenter, L. L., A. R. Tyrka, N. S. Ross, L. Khoury, G. M. Anderson, and L. H. Price. 2009. Effect of childhood emotional abuse and age on cortisol responsivity in adulthood. Biological Psychiatry 66(1):69-75.
Carrion, V. G., A. Garrett, V. Menon, C. F. Weems, and A. L. Reiss. 2008. Posttraumatic stress symptoms and brain function during a response-inhibition task: An fMRI study in youth. Depression and Anxiety 25(6):514-526.
Carrion, V. G., C. F. Weems, C. Watson, S. Eliez, V. Menon, and A. L. Reiss. 2009. Converging evidence for abnormalities of the prefrontal cortex and evaluation of midsagittal structures in pediatric posttraumatic stress disorder: An MRI study. Psychiatry Research 172(3):226-234.
Caspi, A., J. McClay, T. E. Moffitt, J. Mill, J. Martin, I. W. Craig, A. Taylor, and R. Poulton. 2002. Role of genotype in the cycle of violence in maltreated children. Science 297(5582): 851-854.
Caspi, A., K. Sugden, T. E. Moffitt, A. Taylor, I. W. Craig, H. Harrington, J. McClay, J. Mill, J. Martin, A. Braithwaite, and R. Poulton. 2003. Influence of life stress on depression: Moderation by a polymorphism in the 5-HTT gene. Science 301(5631):386-389.
Champoux, M., C. L. Coe, S. M. Schanberg, C. M. Kuhn, and S. J. Suomi. 1989. Hormonal effects of early rearing conditions in the infant rhesus monkey. American Journal of Primatology 19(2):111-117.
Chareyron, L. J., P. B. Lavenex, D. G. Amaral, and P. Lavenex. 2012. Postnatal development of the amygdala: A stereological study in macaque monkeys. Journal of Comparative Neurology 520(9):1965-1984.
Chen, L. P., M. H. Murad, M. L. Paras, K. M. Colbenson, A. L. Sattler, E. N. Goranson, M. B. Elamin, R. J. Seime, G. Shinozaki, L. J. Prokop, and A. Zirakzadeh. 2010. Sexual abuse and lifetime diagnosis of psychiatric disorders: Systematic review and meta-analysis. Mayo Clinic Proceedings 85(7):618-629.
Chernoff, R., T. Combs-Orme, C. Risley-Curtiss, and A. Heisler. 1994. Assessing the health status of children entering foster care. Pediatrics 93(4):594-601.
Cicchetti, D., and M. Lynch. 1993. Toward an ecological/transactional model of community violence and child maltreatment: Consequences for children’s development. Psychiatry-Interpersonal and Biological Processes 56(1):96-118.
Cicchetti, D., and R. Rizley. 1981. Developmental perspectives on the etiology, intergenerational transmission, and sequelae of child maltreatment. New Directions for Child and Adolescent Development 1981(11):31-55.
Cicchetti, D., and F. A. Rogosch. 2001a. Diverse patterns of neuroendocrine activity in maltreated children. Developmental Psychopathology 13(3):677-693.
Cicchetti, D., and F. A. Rogosch. 2001b. The impact of child maltreatment and psychopathology on neuroendocrine functioning. Developmental Psychopathology 13(4):783-804.
Cicchetti, D., and S. L. Toth. 1998. Perspectives on research and practice in developmental psychopathology. In Handbook of child psychology, 5th ed., Vol. 4, edited by W. Damon, I. E. Sigel, and K. A. Renninger. Hoboken, NJ: John Wiley & Sons, Inc. Pp. 479-583.
Cicchetti, D., and S. L. Toth. 2009. The past achievements and future promises of developmental psychopathology: The coming of age of a discipline. Journal of Child Psychology and Psychiatry 50(1-2):16-25.
Cicchetti, D., B. P. Ackerman, and C. E. Izard. 1995. Emotions and emotion regulation in developmental psychopathology. Development and Psychopathology 7(1):1-10.
Clarke, A. S. 1993. Social rearing effects on HPA axis activity over early development and in response to stress in rhesus monkeys. Developmental Psychobiology 26(8):433-446.
Cole, P. M., M. K. Michel, and L. O. D. Teti. 1994. The development of emotion regulation and dysregulation: A clinical perspective. Monographs of the Society for Research in Child Development 59(2-3):73-102.
Cole, P. M., J. Luby, and M. W. Sullivan. 2008. Emotions and the development of childhood depression: Bridging the gap. Child Development Perspectives 2(3):141-148.
Collishaw, S., A. Pickles, J. Messer, M. Rutter, C. Shearer, and B. Maughan. 2007. Resilience to adult psychopathology following childhood maltreatment: Evidence from a community sample. Child Abuse & Neglect 31(3):211-229.
Corso, P. S., and A. R. Fertig. 2010. The economic impact of child maltreatment in the United States: Are the estimates credible? Child Abuse & Neglect 34(5):296-304.
Corso, P. S., and J. R. Lutzker. 2006. The need for economic analysis in research on child maltreatment. Child Abuse & Neglect 30(7):727-738.
Corso, P. S., X. Fang, and J. A. Mercy. 2011. Benefits of preventing a death associated with child maltreatment: Evidence from willingness-to-pay survey data. American Journal of Public Health 101(3):487-490.
Courtney, M. E. 1999. National call to action: Working toward the elimination of child maltreatment. The economics. Child Abuse & Neglect 23(10):975-986.
Crozier, J. C., and R. P. Barth. 2005. Cognitive and academic functioning in maltreated children. Children & Schools 27(4):197-206.
Currie, J., and C. S. Widom. 2010. Long-term consequences of child abuse and neglect on adult economic well-being. Child Maltreatment 15(2):111-120.
Cyr, C., E. M. Euser, M. J. Bakermans-Kranenburg, and M. H. van Ijzendoorn. 2010. Attachment security and disorganization in maltreating and high-risk families: A series of meta-analyses. Development and Psychopathology 22(1):87-108.
Dalgeish, T., A. R. Moradi, M. R. Taghavi, H. T. Neshat-Doost, and W. Yule. 2001. An experimental investigation of hypervigilance for threat in children and adolescents with post-traumatic stress disorder. Psychological Medicine 31(3):541-547.
Danese, A., and B. S. McEwen. 2012. Adverse childhood experiences, allostasis, allostatic load, and age-related disease. Physiology & Behavior 106(1):29-39.
De Bellis, M. D., and M. S. Keshavan. 2003. Sex differences in brain maturation in maltreatment-related pediatric posttraumatic stress disorder. Neuroscience and Biobehavioral Reviews 27(1-2):103-117.
De Bellis, M. D., M. S. Keshavan, D. B. Clark, B. J. Casey, J. N. Giedd, A. M. Boring, K. Frustaci, and N. D. Ryan. 1999. Developmental traumatology. Part II: Brain development. Biological Psychiatry 45(10):1271-1284.
De Bellis, M. D., J. Hall, A. M. Boring, K. Frustaci, and G. Moritz. 2001a. A pilot longitudinal study of hippocampal volumes in pediatric maltreatment-related posttraumatic stress disorder. Biological Psychiatry 50(4):305-309.
De Bellis, M. D., M. S. Keshavan, S. R. Beers, J. Hall, K. Frustaci, A. Masalehdan, J. Noll, and A. M. Boring. 2001b. Sex differences in brain maturation during childhood and adolescence. Cerebral Cortex 11(6):552-557.
De Bellis, M. D., M. S. Keshavan, H. Shifflett, S. Iyengar, S. R. Beers, J. Hall, and G. Moritz. 2002. Brain structures in pediatric maltreatment-related posttraumatic stress disorder: A sociodemographically matched study. Biological Psychiatry 52(11):1066-1078.
De Bellis, M. D., S. R. Hooper, E. G. Spratt, and D. P. Woolley. 2009. Neuropsychological findings in childhood neglect and their relationships to pediatric PTSD. Journal of the International Neuropsychological Society 15(6):868-878.
de Quervain, D. J., B. Roozendaal, and J. L. McGaugh. 1998. Stress and glucocorticoids impair retrieval of long-term spatial memory. Nature 394(6695):787-790.
Dobrova-Krol, N. A., M. H. van Ijzendoorn, M. J. Bakermans-Kranenburg, C. Cyr, and F. Juffer. 2008. Physical growth delays and stress dysregulation in stunted and non-stunted Ukrainian institution-reared children. Infant Behavior and Development 31(3):539-553.
Dodge, K. A., G. S. Pettit, J. E. Bates, and E. Valente. 1995. Social information-processing patterns partially mediate the effect of early physical abuse on later conduct problems. Journal of Abnormal Psychology 104(4):632-643.
Dong, M., S. R. Dube, V. J. Felitti, W. H. Giles, and R. F. Anda. 2003. Adverse childhood experiences and self-reported liver disease: New insights into the causal pathway. Archives of Internal Medicine 163(16):1949-1956.
Dong, M., W. H. Giles, V. J. Felitti, S. R. Dube, J. E. Williams, D. P. Chapman, and R. F. Anda. 2004. Insights into causal pathways for ischemic heart disease: Adverse childhood experiences study. Circulation 110(13):1761-1766.
Dozier, M., M. Manni, M. K. Gordon, E. Peloso, M. R. Gunnar, K. C. Stovall-McClough, D. Eldreth, and S. Levine. 2006. Foster children’s diurnal production of cortisol: An exploratory study. Child Maltreatment 11(2):189-197.
Drury, S. S., K. Theall, M. M. Gleason, A. T. Smyke, I. De Vivo, J. Y. Y. Wong, N. A. Fox, C. H. Zeanah, and C. A. Nelson. 2011. Telomere length and early severe social deprivation: Linking early adversity and cellular aging. Molecular Psychiatry 17:719-727.
Dubowitz, H., R. L. Hampton, W. G. Bithoney, and E. H. Newberger. 1987. Inflicted and noninflicted injuries: Differences in child and familial characteristics. American Journal of Orthopsychiatry 57(4):525-535.
Dubowitz, H., M. A. Papas, M. M. Black, and R. H. Starr, Jr. 2002. Child neglect: Outcomes in high-risk urban preschoolers. Pediatrics 109(6):1100-1107.
Dunn, E. C., M. Uddin, S. V. Subramanian, J. W. Smoller, S. Galea, and K. C. Koenen. 2011. Research review: Gene-environment interaction research in youth depression—a systematic review with recommendations for future research. Journal of Child Psychology and Psychiatry 52(12):1223-1238.
Dunn, E. C., K. A. McLaughlin, N. Slopen, J. Rosand, and J. W. Smoller. 2013. Developmental timing of child maltreatment and symptoms of depression and suicidal ideation in young adulthood: Results from the national longitudinal study of adolescent health. Depression and Anxiety 30(10):955-964.
Eckenrode, J., M. Laird, and J. Doris. 1993. School performance and disciplinary problems among abused and neglected children. Developmental Psychology 29(1):53-62.
Edmond, T., W. Auslander, D. Elze, and S. Bowland. 2006. Signs of resilience in sexually abused adolescent girls in the foster care system. Journal of Child Sexual Abuse 15(1):1-28.
Egeland, B., and A. Susman-Stillman. 1996. Dissociation as a mediator of child abuse across generations. Child Abuse & Neglect 20(11):1123-1132.
Eimer, M., and A. Holmes. 2007. Event-related brain potential correlates of emotional face processing. Neuropsychologia 45(1):15-31.
Eisenberg, N., E. T. Gershoff, R. A. Fabes, S. A. Shepard, A. J. Cumberland, S. H. Losoya, I. K. Guthrie, and B. C. Murphy. 2001. Mother’s emotional expressivity and children’s behavior problems and social competence: Mediation through children’s regulation. Developmental Psychology 37(4):475.
Ellis, B. H., P. A. Fisher, and S. Zaharie. 2004. Predictors of disruptive behavior, developmental delays, anxiety, and affective symptomatology among institutionally reared romanian children. Journal of American Academy of Child and Adolescent Psychiatry 43(10):1283-1292.
English, D. J., C. S. Widom, and C. Brandford. 2002. Childhood victimization and delinquency, adult criminality, and violent criminal behavior: A replication and extension, final report (document no. 192291). https://www.ncjrs.gov/pdffiles1/nij/grants/192291.pdf (accessed September 16, 2013).
Epel, E. S., E. H. Blackburn, J. Lin, F. S. Dhabhar, N. E. Adler, J. D. Morrow, and R. M. Cawthon. 2004. Accelerated telomere shortening in response to life stress. Proceedings of the National Academy of Sciences of the United States of America 101(49):17312-17315.
Evasovich, M., R. Klein, F. Muakkassa, and R. Weekley. 1998. The economic effect of child abuse in the burn unit. Burns 24(7):642-645.
Fang, X., D. S. Brown, C. S. Florence, and J. A. Mercya. 2012. The economic burden of child maltreatment in the United States and implications for prevention. Child Abuse & Neglect 36:156-165.
Fearon, R. P., M. J. Bakermans-Kranenburg, M. H. van Ijzendoorn, A.-M. Lapsley, and G. I. Roisman. 2010. The significance of insecure attachment and disorganization in the development of children’s externalizing behavior: A meta-analytic study. Child Development 81(2):435-456.
Fergusson, D. M., J. M. Boden, and L. J. Horwood. 2008. Exposure to childhood sexual and physical abuse and adjustment in early adulthood. Child Abuse & Neglect 32(6):607-619.
Fisher, P. A., M. Stoolmiller, M. R. Gunnar, and B. O. Burraston. 2007. Effects of a therapeutic intervention for foster preschoolers on diurnal cortisol activity. Psychoneuroendocrinology 32(8-10):892-905.
Fisher, P. A., B. M. Lester, D. S. DeGarmo, L. L. Lagasse, H. Lin, S. Shankaran, H. S. Bada, C. R. Bauer, J. Hammond, T. Whitaker, and R. Higgins. 2011. The combined effects of prenatal drug exposure and early adversity on neurobehavioral disinhibition in childhood and adolescence. Development and Psychopathology 23(3):777-788.
Flores, E., D. Cicchetti, and F. A. Rogosch. 2005. Predictors of resilience in maltreated and nonmaltreated Latino children. Developmental Psychology 41(2):338-351.
Fox, N. A., C. A. Nelson, III, and C. H. Zeanah, Jr. 2013. The effects of early severe psychosocial deprivation on children’s cognitive and social development: Lessons from the Bucharest Early Intervention Project. In Families and child health, edited by N. S. Landale, S. M. McHale, and A. Booth. New York: Springer. Pp. 33-41.
Fries, E., J. Hesse, J. Hellhammer, and D. H. Hellhammer. 2005. A new view on hypocortisolism. Psychoneuroendocrinology 30(10):1010-1016.
Gelles, R. J., and S. Perlman. 2012. Estimated annual cost of child abuse and neglect. Chicago: Prevent Child Abuse America.
Ghetti, S., D. M. DeMaster, A. P. Yonelinas, and S. A. Bunge. 2010. Developmental differences in medial temporal lobe function during memory encoding. Journal of Neuroscience 30(28):9548-9556.
Giedd, J. N., J. M. Rumsey, F. X. Castellanos, J. C. Rajapakse, D. Kaysen, A. Catherine Vaituzis, Y. C. Vauss, S. D. Hamburger, and J. L. Rapoport. 1996a. A quantitative MRI study of the corpus callosum in children and adolescents. Developmental Brain Research 91(2):274-280.
Giedd, J. N., J. W. Snell, N. Lange, J. C. Rajapakse, B. J. Casey, P. L. Kozuch, A. C. Vaituzis, Y. C. Vauss, S. D. Hamburger, D. Kaysen, and J. L. Rapoport. 1996b. Quantitative magnetic resonance imaging of human brain development: Ages 4-18. Cerebral Cortex 6(4):551-559.
Gilbert, R., A. Kemp, J. Thoburn, P. Sidebotham, L. Radford, D. Glaser, and H. L. Macmillan. 2009a. Recognising and responding to child maltreatment. Lancet 373(9658):167-180.
Gilbert, R., C. S. Widom, K. Browne, D. Fergusson, E. Webb, and S. Janson. 2009b. Burden and consequences of child maltreatment in high-income countries. Lancet 373(9657):68-81.
Ginzburg, K., C. Koopman, L. Butler, O. Palesh, H. Kraemer, C. Classen, and D. Spiegel. 2006. Evidence for a dissociative subtype of post-traumatic stress disorder among help-seeking childhood sexual abuse survivors. Journal of Trauma and Dissociation 7(2):7-27.
Gogtay, N., J. N. Giedd, L. Lusk, K. M. Hayashi, D. Greenstein, A. C. Vaituzis, T. F. Nugent, III, D. H. Herman, L. S. Clasen, A. W. Toga, J. L. Rapoport, and P. M. Thompson. 2004. Dynamic mapping of human cortical development during childhood through early adulthood. Proceedings of the National Academy of Sciences of the United States of America 101(21):8174-8179.
Gould, E., and P. Tanapat. 1999. Stress and hippocampal neurogenesis. Biological Psychiatry 46(11):1472-1479.
Graham, J., D. English, A. Litrownik, R. Thompson, E. Briggs, and S. Bangdiwala. 2010. Maltreatment chronicity defined with reference to development: Extension of the social adaptation outcomes findings to peer relations. Journal of Family Violence 25(3):311-324.
Gregg, G. R., and E. D. Parks. 1995. Selected Minnesota Multiphasic Personality Inventory-2 scales for identifying women with a history of sexual abuse. Journal of Nervous and Mental Disease 183(1):53-56.
Grienenberger, J. F., K. Kelly, and A. Slade. 2005. Maternal reflective functioning, mother-infant affective communication, and infant attachment: Exploring the link between mental states and observed caregiving behavior in the intergenerational transmission of attachment. Attachment and Human Development 7(3):299-311.
Griffin, M. G., P. A. Resick, and M. B. Mechanic. 1997. Objective assessment of peritraumatic dissociation: Psychophysiological indicators. American Journal of Psychiatry 154(8):1081-1088.
Gunnar, M. R., and C. L. Cheatham. 2003. Brain and behavior interface: Stress and the developing brain. Infant Mental Health Journal 24(3):195-211.
Gunnar, M. R., and B. Donzella. 2002. Social regulation of the cortisol levels in early human development. Psychoneuroendocrinology 27(1-2):199-220.
Gunnar, M. R., and D. M. Vazquez. 2001. Low cortisol and a flattening of expected daytime rhythm: Potential indices of risk in human development. Developmental Psychopathology 13(3):515-538.
Gunnar, M. R., M. H. van Dulmen, T. Achenbach, E. Ames, E. Ames, M. Berry, R. Barth, G. Bohlin, L. Janols, and M. Bohman. 2007. Behavior problems in postinstitutionalized internationally adopted children. Development and Psychopathology 19(1):129-148.
Hanson, J. L., M. K. Chung, B. B. Avants, E. A. Shirtcliff, J. C. Gee, R. J. Davidson, and S. D. Pollak. 2010. Early stress is associated with alterations in the orbitofrontal cortex: A tensor-based morphometry investigation of brain structure and behavioral risk. Journal of Neuroscience 30(22):7466-7472.
Harmony, T., E. Marosi, A. E. Diaz de Leon, J. Becker, and T. Fernandez. 1990. Effect of sex, psychosocial disadvantages and biological risk factors on EEG maturation. Electroencephalography and Clinical Neurophysiology 75(6):482-491.
Hart, H., and K. Rubia. 2012. Neuroimaging of child abuse: A critical review. Frontiers in Human Neuroscience 6:52.
Heneghan, A., R. E. K. Stein, M. S. Hurlburt, J. Zhang, J. Rolls-Reutz, E. Fisher, J. Landsverk, and S. M. Horwitz. 2013. Mental health problems in teens investigated by U.S. child welfare agencies. Journal of Adolescent Health 52(5):634-640.
Hertsgaard, L., M. Gunnar, M. F. Erickson, and M. Nachmias. 1995. Adrenocortical responses to the strange situation in infants with disorganized/disoriented attachment relationships. Child Development 66(4):1100-1106.
Hertzman, C., and T. Boyce. 2010. How experience gets under the skin to create gradients in developmental health. Annual Review of Public Health 31:329-347.
Higley, J. D., S. J. Suomi, and M. Linnoila. 1992. A longitudinal study of CSF monoamine metabolite and plasma cortisol concentrations in young rhesus monkeys: Effects of early experience, age, sex and stress on continuity of interindividual differences. Biological Psychiatry 32:127-145.
Hofer, M. A. 1994. Hidden regulators in attachment, separation, and loss. Monographs of the Society for Research in Child Development 59(2/3):192-207.
Hofer, M. A. 2006. Psychobiological roots of early attachment. Current Directions in Psychological Science 15(2):84-88.
Hornor, G. 2008. Reactive attachment disorder. Journal of Pediatric Health Care 22(4):234-239.
Hubbard, D. J., and T. C. Pratt. 2002. A meta-analysis of the predictors of delinquency among girls. Journal of Offender Rehabilitation 34(3):1-13.
Huizinga, D., B. C. Haberstick, A. Smolen, S. Menard, S. E. Young, R. P. Corley, M. C. Stallings, J. Grotpeter, and J. K. Hewitt. 2006. Childhood maltreatment, subsequent antisocial behavior, and the role of monoamine oxidase a genotype. Biological Psychiatry 60(7):677-683.
Hulette, A. C., J. J. Freyd, K. C. Pears, H. K. Kim, P. A. Fisher, and K. A. Becker-Blease. 2008. Dissociation and posttraumatic symptoms in maltreated preschool children. Journal of Child & Adolescent Trauma 1(2):93-108.
Hulette, A. C., J. J. Freyd, and P. A. Fisher. 2011. Dissociation in middle childhood among foster children with early maltreatment experiences. Child Abuse & Neglect 35(2):123-126.
Hussey, J. M., J. J. Chang, and J. B. Kotch. 2006. Child maltreatment in the United States: Prevalence, risk factors, and adolescent health consequences. Pediatrics 118(3):933-942.
Irazuzta, J., J. E. McJunkin, K. Danadian, F. Arnold, and J. Zhang. 1997. Outcome and cost of child abuse. Child Abuse & Neglect 21(8):751-757.
Jaffee, S. R., and R. Gallop. 2007. Social, emotional, and academic competence among children who have had contact with child protective services: Prevalence and stability estimates. Journal of the American Academy of Child and Adolescent Psychiatry 46(6):757-765.
Jaffee, S. R., and A. K. Maikovich-Fong. 2011. Effects of chronic maltreatment and maltreatment timing on children’s behavior and cognitive abilities. Journal of Child Psychology and Psychiatry and Allied Disciplines 52(2):184-194.
Jaffee, S. R., A. Caspi, T. E. Moffitt, M. Polo-Tomás, and A. Taylor. 2007. Individual, family, and neighborhood factors distinguish resilient from non-resilient maltreated children: A cumulative stressors model. Child Abuse & Neglect 31(3):231-253.
Jans, T., S. Schneck-Seif, T. Weigand, W. Schneider, H. Ellgring, C. Wewetzer, and A. Warnke. 2008. Long-term outcome and prognosis of dissociative disorder with onset in childhood or adolescence. Child and Adolescent Psychiatry and Mental Health 2(1):19.
Johnson, D. E., and M. R. Gunnar. 2011. IV. Growth failure in institutionalized children. Monographs of the Society for Research in Child Development 76(4):92-126.
Johnson, D. E., D. Guthrie, A. T. Smyke, S. F. Koga, N. A. Fox, C. H. Zeanah, and C. A. Nelson, III. 2010. Growth and associations between auxology, caregiving environment, and cognition in socially deprived Romanian children randomized to foster vs ongoing institutional care. Archives of Pediatrics and Adolescent Medicine 164(6):507-516.
Johnson, J. G., P. Cohen, J. Brown, E. M. Smailes, and D. P. Bernstein. 1999. Childhood maltreatment increases risk for personality disorders during early adulthood. Archives of General Psychiatry 56(7):600-608.
Johnson, J. G., E. M. Smailes, P. Cohen, J. Brown, and D. P. Bernstein. 2000. Associations between four types of childhood neglect and personality disorder symptoms during adolescence and early adulthood: Findings of a community-based longitudinal study. Journal of Personality Disorders 14(2):171-187.
Johnson, J. G., P. Cohen, S. Kasen, and J. S. Brook. 2002. Childhood adversities associated with risk for eating disorders or weight problems during adolescence or early adulthood. American Journal Psychiatry 159(3):394-400.
Jones, D. J., D. K. Runyan, T. Lewis, A. J. Litrownik, M. M. Black, T. Wiley, D. E. English, L. J. Proctor, B. L. Jones, and D. S. Nagin. 2010. Trajectories of childhood sexual abuse and early adolescent HIV/AIDS risk behaviors: The role of other maltreatment, witnessed violence, and child gender. Journal of Clinical Child and Adolescent Psychology 39(5):667-680.
Jonson-Reid, M., B. Drake, J. Kim, S. Porterfield, and L. Han. 2004. A prospective analysis of the relationship between reported child maltreatment and special education eligibility among poor children. Child Maltreatment 9(4):382-394.
Jonson-Reid, M., P. L. Kohl, and B. Drake. 2012. Child and adult outcomes of chronic child maltreatment. Pediatrics 129(5):839-845.
Kaplan, S. J., D. Pelcovitz, S. Salzinger, M. Weiner, F. S. Mandel, M. L. Lesser, and V. E. Labruna. 1998. Adolescent physical abuse: Risk for adolescent psychiatric disorders. American Journal of Psychiatry 155(7):954-959.
Kaplow, J. B., and C. S. Widom. 2007. Age of onset of child maltreatment predicts long-term mental health outcomes. Journal of Abnormal Psychology 116(1):176-187.
Kearney, C. A., A. Wechsler, H. Kaur, and A. Lemos-Miller. 2010. Posttraumatic stress disorder in maltreated youth: A review of contemporary research and thought. Clinical Child and Family Psychology Review 13(1):46-76.
Keck Seeley, S. M., S. L. Perosa, and L. M. Perosa. 2004. A validation study of the adolescent dissociative experiences scale. Child Abuse & Neglect 28(7):755-769.
Keiley, M. K., T. R. Howe, K. A. Dodge, J. E. Bates, and G. S. Petti. 2001. The timing of child physical maltreatment: A cross-domain growth analysis of impact on adolescent externalizing and internalizing problems. Development and Psychopathology 13(4):891-912.
Kendall-Tackett, K. A., L. M. Williams, and D. Finkelhor. 1993. Impact of sexual abuse on children: A review and synthesis of recent empirical studies. Psychological Bulletin 113(1):164-180.
Kim, J., and D. Cicchetti. 2010. Longitudinal pathways linking child maltreatment, emotion regulation, peer relations, and psychopathology. Journal of Child Psychology and Psychiatry 51(6):706-716.
Kim, J. J., and K. S. Yoon. 1998. Stress: Metaplastic effects in the hippocampus. Trends in Neurosciences 21(12):505-509.
Kim, K., P. K. Trickett, and F. W. Putnam. 2010. Childhood experiences of sexual abuse and later parenting practices among non-offending mothers of sexually abused and comparison girls. Child Abuse & Neglect 34(8):610-622.
Kisiel, C. L., and J. S. Lyons. 2001. Dissociation as a mediator of psychopathology among sexually abused children and adolescents. American Journal of Psychiatry 158(7):1034-1039.
Kitayama, N., V. Vaccarino, M. Kutner, P. Weiss, and J. D. Bremner. 2005. Magnetic resonance imaging (MRI) measurement of hippocampal volume in posttraumatic stress disorder: A meta-analysis. Journal of Affective Disorders 88(1):79-86.
Kitterle, F. L. 1995. Hemispheric communication: Mechanisms and models. Hillsdale, NJ: Lawrence Erlbaum Associates.
Kleindienst, N., M. F. Limberger, U. W. Ebner-Priemer, J. Keibel-Mauchnik, A. Dyer, M. Berger, C. Schmahl, and M. Bohus. 2011. Dissociation predicts poor response to dialectial behavioral therapy in female patients with borderline personality disorder. Journal of Personality Disorders 25(4):432-447.
Klinnert, M., J. Campos, J. Sorce, R. Emde, and M. Svejda. 1983. Emotions as behavior regulators in infancy: Social referencing in infancy. In Emotion: Theory, research and experience, edited by R. P. H. Kellerman. New York: Academic Press. Pp. 57-86.
Knutson, J. F., S. M. Taber, A. J. Murray, N.-L. Valles, and G. Koeppl. 2010. The role of care neglect and supervisory neglect in childhood obesity in a disadvantaged sample. Journal of Pediatric Psychology 35(5):523-532.
Kolko, D. J. 2010. Posttraumatic stress symptoms in children and adolescents referred for child welfare investigation a national sample of in-home and out-of-home care. Child Maltreatment 15(1):48-63.
Kotch, J. B., T. Lewis, J. M. Hussey, D. English, R. Thompson, A. J. Litrownik, D. K. Runyan, S. I. Bangdiwala, B. Margolis, and H. Dubowitz. 2008. Importance of early neglect for childhood aggression. Pediatrics 121(4):725-731.
Kreppner, J. M., T. G. O’Connor, and M. Rutter. 2001. Can inattention/overactivity be an institutional deprivation syndrome? Journal of Abnormal Child Psychology 29(6):513-528.
Kreppner, J. M., M. Rutter, C. Beckett, J. Castle, E. Colvert, C. Groothues, A. Hawkins, T. G. O’Connor, S. Stevens, and E. J. Sonuga-Barke. 2007. Normality and impairment following profound early institutional deprivation: A longitudinal follow-up into early adolescence. Developmental Psychology 43(4):931-946.
Kurtz, P. D., J. M. Gaudin, Jr., J. S. Wodarski, and P. T. Howing. 1993. Maltreatment and the school-aged child: School performance consequences. Child Abuse & Neglect 17(5):581-589.
Lanius, R., M. Miller, E. Wolf, B. Brand, P. Frewen, E. Vermetten, and D. Spiegel. 2013. Dissociative subtype of PTSD. Washington, DC: U.S. Department of Veterans Affairs.
Lanktree, C. B., A. M. Gilbert, J. Briere, N. Taylor, K. Chen, C. A. Maida, and W. R. Saltzman. 2008. Multi-informant assessment of maltreated children: Convergent and discriminant validity of the TSCC and TSCYC. Child Abuse & Neglect 32(6):621-625.
Lansford, J. E., K. A. Dodge, G. S. Pettit, J. E. Bates, J. Crozier, and J. Kaplow. 2002. A 12-year prospective study of the long-term effects of early child physical maltreatment on psychological, behavioral, and academic problems in adolescence. Archives of Pediatrics and Adolescent Medicine 156(8):824-830.
Lansford, J. E., S. Miller-Johnson, L. J. Berlin, K. A. Dodge, J. E. Bates, and G. S. Pettit. 2007. Early physical abuse and later violent delinquency: A prospective longitudinal study. Child Maltreatment 12(3):233-245.
Lansford, J. E., M. M. Criss, K. A. Dodge, D. S. Shaw, G. S. Pettit, and J. E. Bates. 2009. Trajectories of physical discipline: Early childhood antecedents and developmental outcomes. Child Development 80(5):1385-1402.
Lansford, J. E., K. A. Dodge, G. S. Pettit, and J. E. Bates. 2010. Does physical abuse in early childhood predict substance use in adolescence and early adulthood? Child Maltreatment 15(2):190-194.
Larson, M. C., M. R. Gunnar, and L. Hertsgaard. 1991. The effects of morning naps, car trips, and maternal separation on adrenocortical activity in human infants. Child Development 62(2):362-372.
Lavenex, P., P. Banta Lavenex, and D. G. Amaral. 2007. Postnatal development of the primate hippocampal formation. Developmental Neuroscience 29(1-2):179-192.
Leiter, J., and M. C. Johnsen. 1997. Child maltreatment and school performance declines: An event-history analysis. American Educational Research Journal 34(3):563-589.
Levine, S., S. G. Wiener, and C. L. Coe. 1993. Temporal and social factors influencing behavioral and hormonal responses to separation in mother and infant squirrel monkeys. Psychoneuroendocrinology 18(4):297-306.
Lewis, E. E., M. Dozier, J. Ackerman, and S. Sepulveda-Kozakowski. 2007. The effect of placement instability on adopted children’s inhibitory control abilities and oppositional behavior. Developmental Psychology 43(6):1415-1427.
Lewis-Morrarty, E., M. Dozier, K. Bernard, S. M. Terracciano, and S. V. Moore. 2012. Cognitive flexibility and theory of mind outcomes among foster children: Preschool follow-up results of a randomized clinical trial. Journal of Adolescent Health 51(2 Suppl.):S17-S22.
Libby, A. M., M. R. Sills, N. K. Thurston, and H. D. Orton. 2003. Costs of childhood physical abuse: Comparing inflicted and unintentional traumatic brain injuries. Pediatrics 112(1):58-65.
Lissau, I., and T. I. Sorensen. 1994. Parental neglect during childhood and increased risk of obesity in young adulthood. Lancet 343(8893):324-327.
Lodico, M. A., and R. J. DiClemente. 1994. The association between childhood sexual abuse and prevalence of HIV-related risk behaviors. Clinical Pediatrics 33(8): 498-502.
Loman, M. M., K. L. Wiik, K. A. Frenn, S. D. Pollak, and M. R. Gunnar. 2009. Postinstitutionalized children’s development: Growth, cognitive, and language outcomes. Journal of Developmental and Behavioral Pediatrics 30(5):426-434.
Loman, M. M., A. E. Johnson, A. Westerlund, S. D. Pollak, C. A. Nelson, and M. R. Gunnar. 2013. The effect of early deprivation on executive attention in middle childhood. Journal of Child Psychology and Psychiatry 54(1):37-45.
Luthar, S. S., D. Cicchetti, and B. Becker. 2000. The construct of resilience: A critical evaluation and guidelines for future work. Child Development 71(3):543-562.
Lynch, M., and D. Cicchetti. 1998. An ecological-transactional analysis of children and contexts: The longitudinal interplay among child maltreatment, community violence, and children’s symptomatology. Developmental Psychopathology 10(2):235-257.
Lyons, S. J., J. R. Henly, and J. R. Schuerman. 2005. Informal support in maltreating families: Its effect on parenting practices. Children and Youth Services Review 27(1): 21-38.
Lyons-Ruth, K. 2008. Contributions of the mother-infant relationship to dissociative, borderline, and conduct symptoms in young adulthood. Infant Mental Health Journal 29(3):203-218.
Lyons-Ruth, K., L. Alpern, and B. Repacholi. 1993. Disorganized infant attachment classification and maternal psychosocial problems as predictors of hostile-aggressive behavior in the preschool classroom. Child Development 64(2):572-585.
Lyons-Ruth, K., J. F. Bureau, C. D. Riley, and A. F. Atlas-Corbett. 2009. Socially indiscriminate attachment behavior in the strange situation: Convergent and discriminant validity in relation to caregiving risk, later behavior problems, and attachment insecurity. Development and Psychopathology 21(2):355-372.
Macfie, J., D. Cicchetti, and S. L. Toth. 2001. Dissociation in maltreated versus nonmaltreated preschool-aged children. Child Abuse & Neglect 25(9):1253-1267.
Maheu, F. S., M. Dozier, A. E. Guyer, D. Mandell, E. Peloso, K. Poeth, J. Jenness, J. Y. Lau, J. P. Ackerman, D. S. Pine, and M. Ernst. 2010. A preliminary study of medial temporal lobe function in youths with a history of caregiver deprivation and emotional neglect. Cognitive, Affective, and Behavioral Neuroscience 10(1):34-49.
Main, M., and J. Solomon. 1990. Procedures for identifying infants as disorganized/disoriented during the Ainsworth Strange Situation. Attachment in the Preschool Years: Theory, Research, and Intervention 1:121-160.
Malatesta, C. Z., and C. E. Izard. 1984. The ontogenesis of human social signals: From biological imperative to symbol utilization. In The psychobiology of affective development, edited by N. A. Fox and R. J. Davidson. Hillsdale, NJ: Psychology Press. Pp. 161-206.
Manly, J. T., J. E. Kim, F. A. Rogosch, and D. Cicchetti. 2001. Dimensions of child maltreatment and children’s adjustment: Contributions of developmental timing and subtype. Development and Psychopathology 13(4):759-782.
Marshall, P. J., N. A. Fox, and Bucharest Early Intervention Project Core Group. 2004. A comparison of the electroencephalogram between institutionalized and community children in Romania. Journal of Cognitive Neuroscience 16(8):1327-1338.
Marshall, P. J., B. C. Reeb, N. A. Fox, C. A. Nelson, and C. H. Zeanah. 2008. Effects of early intervention on EEG power and coherence in previously institutionalized children in Romania. Developmental Psychopathology 20(3):861-880.
Masten, A. S., and A. Tellegen. 2012. Resilience in developmental psychopathology: Contributions of the project competence longitudinal study. Development and Psychopathology 24(2):345-361.
Maughan, A., and D. Cicchetti. 2002. Impact of child maltreatment and interadult violence on children’s emotion regulation abilities and socioemotional adjustment. Child Development 73(5):1525-1542.
Maxfield, M. G., and C. S. Widom. 1996. The cycle of violence: Revisited 6 years later. Archives of Pediatrics & Adolescent Medicine 150(4):390-395.
McCabe, K. M., R. L. Hough, M. Yeh, S. E. Lucchini, and A. Hazen. 2005. The relation between violence exposure and conduct problems among adolescents: A prospective study. American Journal of Orthopsychiatry 75(4):575-584.
McCurdy, K. 2005. The influence of support and stress on maternal attitudes. Child Abuse & Neglect 29(3):251-268.
McDermott, J. M., A. Westerlund, C. H. Zeanah, C. A. Nelson, and N. A. Fox. 2012. Early adversity and neural correlates of executive function: Implications for academic adjustment. Developmental Cognitive Neuroscience 2(Suppl. 1):S59-S66.
McEwen, B. S. 1998. Stress, adaptation, and disease. Allostasis and allostatic load. Annals of the New York Academy of Sciences 840:33-44.
McGloin, J. M., and C. S. Widom. 2001. Resilience among abused and neglected children grown up. Development and Psychopathology 13(4):1021-1038.
McGowan, P. O., A. Sasaki, T. C. T. Huang, A. Unterberger, M. Suderman, C. Ernst, M. J. Meaney, G. Turecki, and M. Szyf. 2008. Promoter-wide hypermethylation of the ribosomal RNA gene promoter in the suicide brain. PLoS ONE 3(5).
McGowan, P. O., A. Sasaki, A. C. D’Alessio, S. Dymov, B. Labonte, M. Szyf, G. Turecki, and M. J. Meaney. 2009. Epigenetic regulation of the glucocorticoid receptor in human brain associates with childhood abuse. Nature Neuroscience 12(3):342-348.
McGowan, P. O., M. Suderman, A. Sasaki, T. C. T. Huang, M. Hallett, M. J. Meaney, and M. Szyf. 2011. Broad epigenetic signature of maternal care in the brain of adult rats. PLoS ONE 6(2).
McLaughlin, K. A., N. A. Fox, C. H. Zeanah, M. A. Sheridan, P. Marshall, and C. A. Nelson. 2010. Delayed maturation in brain electrical activity partially explains the association between early environmental deprivation and symptoms of attention-deficit/hyperactivity disorder. Biological Psychiatry 68(4):329-336.
Meaney, M. J., and M. Szyf. 2005. Environmental programming of stress responses through DNA methylation: Life at the interface between a dynamic environment and a fixed genome. Dialogues in Clinical Neuroscience 7(2):103-123.
Mehta, M. A., N. I. Golembo, C. Nosarti, E. Colvert, A. Mota, S. C. R. Williams, M. Rutter, and E. J. S. Sonuga-Barke. 2009. Amygdala, hippocampal and corpus callosum size following severe early institutional deprivation: The English and Romanian adoptees study pilot. Journal of Child Psychology and Psychiatry 50(8):943-951.
Miller, E. K., and J. D. Cohen. 2001. An integrative theory of prefrontal cortex function. Annual Review of Neuroscience 24:167-202.
Milner, J. S. 2000. Social information processing and child physical abuse: Theory and research. Motivation and Child Maltreatment 46:39-84.
Moriceau, S., T. L. Roth, and R. M. Sullivan. 2010. Rodent model of infant attachment learning and stress. Developmental Psychobiology 52(7):651-660.
Mueller, S. C., F. S. Maheu, M. Dozier, E. Peloso, D. Mandell, E. Leibenluft, D. S. Pine, and M. Ernst. 2010. Early-life stress is associated with impairment in cognitive control in adolescence: An fMRI study. Neuropsychologia 48(10):3037-3044.
Murray-Close, D., G. Han, D. Cicchetti, N. R. Crick, and F. A. Rogosch. 2008. Neuroendocrine regulation and physical and relational aggression: The moderating roles of child maltreatment and gender. Developmental Psychology 44(4):1160-1176.
National Center for PTSD. 2013. DSM-5 criteria for PTSD. Washington, DC: U.S. Department of Veterans Affairs.
Natsuaki, M. N., D. Cicchetti, and F. A. Rogosch. 2009. Examining the developmental history of child maltreatment, peer relations, and externalizing problems among adolescents with symptoms of paranoid personality disorder. Development and Psychopathology 21(4):1181-1193.
Nelson, C. A. 2007. A neurobiological perspective on early human deprivation. Child Development Perspectives 1(1):13-18.
Nelson, C. A., III, C. H. Zeanah, and N. A. Fox. 2007a. The effects of early deprivation on brain-behavioral development: The Bucharest Early Intervention Project. In Adolescent psychopathology and the developing brain: Integrating brain and prevention science, edited by D. Romer and E. F. Walker. New York: Oxford University Press. Pp. 197-215.
Nelson, C. A., C. H. Zeanah, N. A. Fox, P. J. Marshall, A. T. Smyke, and D. Guthrie. 2007b. Cognitive recovery in socially deprived young children: The Bucharest Early Intervention Project. Science 318(5858):1937-1940.
Nelson, C. A., K. Bos, M. R. Gunnar, and E. J. S. Sonuga-Barke. 2011. V. The neurobiological toll of early human deprivation. Monographs of the Society for Research in Child Development 76(4):127-146.
New, M., and L. Berliner. 2000. Mental health service utilization by victims of crime. Journal of Traumatic Stress 13(4):693-707.
Nikulina, V., C. S. Widom, and S. Czaja. 2011. The role of childhood neglect and childhood poverty in predicting mental health, academic achievement and crime in adulthood. American Journal of Community Psychology 48(3-4):309-321.
Noll, J. G., P. K. Trickett, and F. W. Putnam. 2003. A prospective investigation of the impact of childhood sexual abuse on the development of sexuality. Journal of Consulting and Clinical Psychology 71(3):575-586.
Noll, J. G., M. H. Zeller, P. K. Trickett, and F. W. Putnam. 2007. Obesity risk for female victims of childhood sexual abuse: A prospective study. Pediatrics 120(1):e61-e67.
Noll, J. G., C. E. Shenk, and K. T. Putnam. 2009. Childhood sexual abuse and adolescent pregnancy: A meta-analytic update. Journal of Pediatric Psychology 34(4):366-378.
NRC (National Research Council). 1993. Understanding child abuse and neglect. Washington, DC: National Academy Press.
O’Connor, T. G., R. S. Marvin, M. Rutter, J. T. Olrick, P. A. Britner, C. Beckett, M. Brophy, J. Castle, E. Colvert, C. Croft, J. Dunn, C. Groothues, and J. Kreppner. 2003. Child-parent attachment following early institutional deprivation. Development and Psychopathology 15(1):19-38.
Offer, D., M. Kaiz, K. I. Howard, and E. S. Bennett. 2000. The altering of reported experiences. Journal of the American Academy of Child and Adolescent Psychiatry 39(6):735-742.
Ogawa, J. R., L. A. Sroufe, N. S. Weinfield, E. A. Carlson, and B. Egeland. 1997. Development and the fragmented self: Longitudinal study of dissociative symptomatology in a nonclinical sample. Development and Psychopathology 9(4):855-879.
Olivan, G. 2003. Catch-up growth assessment in long-term physically neglected and emotionally abused preschool age male children. Child Abuse & Neglect 27(1):103-108.
Olofsson, J. K., S. Nordin, H. Sequeira, and J. Polich. 2008. Affective picture processing: An integrative review of ERP findings. Biological Psychology 77(3):247-265.
Otto, T., and H. Eichenbaum. 1992. Neuronal activity in the hippocampus during delayed non-match to sample performance in rats: Evidence for hippocampal processing in recognition memory. Hippocampus 2(3):323-334.
Pears, K. C., H. K. Kim, and P. A. Fisher. 2008. Psychosocial and cognitive functioning of children with specific profiles of maltreatment. Child Abuse & Neglect 32(10): 958-971.
Perez, C. M., and C. S. Widom. 1994. Childhood victimization and long-term intellectual and academic outcomes. Child Abuse & Neglect 18(8):617-633.
Pollak, S. D., and P. Sinha. 2002. Effects of early experience on children’s recognition of facial displays of emotion. Developmental Psychology 38(5):784-791.
Pollak, S. D., and S. A. Tolley-Schell. 2003. Selective attention to facial emotion in physically abused children. Journal of Abnormal Psychology 112(3):323-338.
Pollak, S. D., D. Cicchetti, R. Klorman, and J. T. Brumaghim. 1997. Cognitive brain event-related potentials and emotion processing in maltreated children. Child Development 68(5):773-787.
Pollak, S. D., D. Cicchetti, K. Hornung, and A. Reed. 2000. Recognizing emotion in faces: Developmental effects of child abuse and neglect. Developmental Psychology 36(5):679-688.
Pollak, S. D., R. Klorman, J. E. Thatcher, and D. Cicchetti. 2001. P3b reflects maltreated children’s reactions to facial displays of emotion. Psychophysiology 38(2):267-274.
Pomerleau, A., G. Malcuit, J.-F. Chicoine, R. Séguin, C. Belhumeur, P. Germain, I. Amyot, and G. Jéliu. 2005. Health status, cognitive and motor development of young children adopted from China, East Asia, and Russia across the first 6 months after adoption. International Journal of Behavioral Development 29(5):445-457.
Power, R. A., L. Lecky-Thompson, H. L. Fisher, S. Cohen-Woods, G. M. Hosang, R. Uher, G. Powell-Smith, R. Keers, M. Tropeano, A. Korszun, L. Jones, I. Jones, M. J. Owen, N. Craddock, I. W. Craig, A. E. Farmer, and P. McGuffin. 2013. The interaction between child maltreatment, adult stressful life events and the 5-HTTLPR in major depression. Journal of Psychiatric Research 47(8):1032-1035.
Price, J. M., and K. Glad. 2003. Hostile attributional tendencies in maltreated children. Journal of Abnormal Child Psychology 31(3):329-343.
Putnam, F. W. 1997. Dissociation in children and adolescents: A developmental perspective. New York: Guilford Press.
Richert, K. A., V. G. Carrion, A. Karchemskiy, and A. L. Reiss. 2006. Regional differences of the prefrontal cortex in pediatric PTSD: An MRI study. Depression and Anxiety 23(1):17-25.
Roeber, B. J., C. L. Tober, D. M. Bolt, and S. D. Pollak. 2012. Gross motor development in children adopted from orphanage settings. Developmental Medicine and Child Neurology 54(6):527-531.
Rogosch, F. A., D. Cicchetti, and J. L. Aber. 1995. The role of child maltreatment in early deviations in cognitive and affective processing abilities and later peer relationship problems. Development and Psychopathology 7(4):591-609.
Ross, L. T., and E. M. Hill. 2002. Childhood unpredictability, schemas for unpredictability, and risk taking. Social Behavior and Personality: An International Journal 30(5): 453-473.
Ross, M. 1989. Relation of implicit theories to the construction of personal histories. Psychological Review 96(2):341-357.
Rovi, S., P. H. Chen, and M. S. Johnson. 2004. The economic burden of hospitalizations associated with child abuse and neglect. American Journal of Public Health 94(4):586-590.
Rubia, K., A. B. Smith, J. Woolley, C. Nosarti, I. Heyman, E. Taylor, and M. Brammer. 2006. Progressive increase of frontostriatal brain activation from childhood to adulthood during event-related tasks of cognitive control. Human Brain Mapping 27(12):973-993.
Sanchez, M. M. 2006. The impact of early adverse care on HPA axis development: Nonhuman primate models. Hormones and Behavior 50(4):623-631.
Sapolsky, R. M., H. Uno, C. S. Rebert, and C. E. Finch. 1990. Hippocampal damage associated with prolonged glucocorticoid exposure in primates. Journal of Neuroscience 10(9):2897-2902.
Schatzberg, A. F., and S. Lindley. 2008. Glucocorticoid antagonists in neuropsychiatric [corrected] disorders. European Journal of Pharmacology 583(2-3):358-364.
Schmahl, C. G., E. Vermetten, B. M. Elzinga, and J. Douglas Bremner. 2003. Magnetic resonance imaging of hippocampal and amygdala volume in women with childhood abuse and borderline personality disorder. Psychiatry Research 122(3):193-198.
Schuengel, C., I. H. V. Marinus, M. J. Bakermans-Kranenburg, and M. Blom. 1998. Frightening maternal behaviour, unresolved loss, and disorganized infant attachment: A pilot-study. Journal of Reproductive and Infant Psychology 16(4):277-283.
Senn, T., M. P. Carey, and P. A. Vanable. 2008. Childhood and adolescent sexual abuse and subsequent sexual risk behavior: Evidence from controlled studies, methodological critique, and suggestions for research. Clinical Psychology Review 28(5):711-735.
Shackman, J. E., A. J. Shackman, and S. D. Pollak. 2007. Physical abuse amplifies attention to threat and increases anxiety in children. Emotion 7(4):838.
Shannon, C., M. Champoux, and S. J. Suomi. 1998. Rearing condition and plasma cortisol in rhesus monkey infants. American Journal of Primatology 46(4):311-321.
Shapiro, D. N., J. B. Kaplow, L. Amaya-Jackson, and K. A. Dodge. 2012. Behavioral markers of coping and psychiatric symptoms among sexually abused children. Journal of Traumatic Stress 25(2):157-163.
Sheridan, M. A., N. A. Fox, C. H. Zeanah, K. A. McLaughlin, and C. A. Nelson, III. 2012. Variation in neural development as a result of exposure to institutionalization early in childhood. Proceedings of the National Academy of Sciences of the United States of America 109(32):12927-12932.
Shields, A., and D. Cicchetti. 2001. Parental maltreatment and emotion dysregulation as risk factors for bullying and victimization in middle childhood. Journal of Clinical Child Psychology 30(3):349-363.
Shipman, K. L., and J. Zeman. 2001. Socialization of children’s emotion regulation in mother-child dyads: A developmental psychopathology perspective. Development and Psychopathology 13(2):317-336.
Shonkoff, J. P., A. S. Garner, B. S. Siegel, M. I. Dobbins, M. F. Earls, A. S. Garner, L. McGuinn, J. Pascoe, and D. L. Wood. 2012. The lifelong effects of early childhood adversity and toxic stress. Pediatrics 129(1):e232-e246.
Silbert, M. H., and A. M. Pines. 1983. Early sexual exploitation as an influence in prostitution. Social Work 28(4):285-289.
Simpson, T. L., and W. R. Miller. 2002. Concomitance between childhood sexual and physical abuse and substance use problems. A review. Clinical Psychology Review 22(1):27-77.
Smith, C., and T. P. Thornberry. 1995. The relationship between childhood maltreatment and adolescent involvement in delinquency. Criminology 33(4):451-481.
Smith, C. A., T. O. Ireland, and T. P. Thornberry. 2005. Adolescent maltreatment and its impact on young adult antisocial behavior. Child Abuse & Neglect 29(10):1099-1119.
Smyke, A. T., A. Dumitrescu, and C. H. Zeanah. 2002. Attachment disturbances in young children. I: The continuum of caretaking casualty. Journal of the American Academy of Child and Adolescent Psychiatry 41(8):972-982.
Sowell, E. R., B. S. Peterson, P. M. Thompson, S. E. Welcome, A. L. Henkenius, and A. W. Toga. 2003. Mapping cortical change across the human life span. Nature Neuroscience 6(3):309-315.
Spann, M. N., L. C. Mayes, J. H. Kalmar, J. Guiney, F. Y. Womer, B. Pittman, C. M. Mazure, R. Sinha, and H. P. Blumberg. 2012. Childhood abuse and neglect and cognitive flexibility in adolescents. Child Neuropsychology 18(2):182-189.
Sperry, D. M., and C. S. Widom. 2013. Child abuse and neglect, social support, and psychopathology in adulthood: A prospective investigation. Child Abuse & Neglect 37(6): 415-425.
Spiegel, D., R. J. Loewenstein, R. Lewis-Fernández, V. Sar, D. Simeon, E. Vermetten, E. Cardeña, and P. F. Dell. 2011. Dissociative disorders in DSM-5. Depression and Anxiety 28(12):E17-E45.
Springs, F. E., and W. N. Friedrich. 1992. Health risk behaviors and medical sequelae of childhood sexual abuse. Mayo Clinic Proceedings 67(6):527-532.
Staudt, M. M. 2003. Mental health services utilization by maltreated children: Research findings and recommendations. Child Maltreatment 8(3):195-203.
Stein, D. J., K. C. Koenen, M. J. Friedman, E. Hill, K. A. McLaughlin, M. Petukhova, A. M. Ruscio, V. Shahly, D. Spiegel, G. Borges, B. Bunting, J. M. Caldas-de-Almeida, G. de Girolamo, K. Demyttenaere, S. Florescu, J. M. Haro, E. G. Karam, V. Kovess-Masfety, S. Lee, H. Matschinger, M. Mladenova, J. Posada-Villa, H. Tachimori, M. C. Viana, and R. C. Kessler. 2013. Dissociation in posttraumatic stress disorder: Evidence from the world mental health surveys. Biological Psychiatry 73(4):302-312.
Stoltz, J. A., K. Shannon, T. Kerr, R. Zhang, J. S. Montaner, and E. Wood. 2007. Associations between childhood maltreatment and sex work in a cohort of drug-using youth. Social Science & Medicine 65(6):1214-1221.
Stouthamer-Loeber, M., R. Loeber, D. L. Homish, and E. Wei. 2001. Maltreatment of boys and the development of disruptive and delinquent behavior. Development and Psychopathology 13(4):941-955.
Suomi, S. J. 1997. Early determinants of behaviour: Evidence from primate studies. British Medical Bulletin 53(1):170-184.
Swanston, H. Y., J. S. Tebbutt, B. I. O’Toole, and R. K. Oates. 1997. Sexually abused children 5 years after presentation: A case-control study. Pediatrics 100(4):600-608.
Szyf, M., and J. Bick. 2013. DNA methylation: A mechanism for embedding early life experiences in the genome. Child Development 84(1):49-57.
Teicher, M. H., S. L. Andersen, A. Polcari, C. M. Anderson, C. P. Navalta, and D. M. Kim. 2003. The neurobiological consequences of early stress and childhood maltreatment. Neuroscience and Biobehavioral Reviews 27(1-2):33-44.
Teicher, M. H., N. L. Dumont, Y. Ito, C. Vaituzis, J. N. Giedd, and S. L. Andersen. 2004. Childhood neglect is associated with reduced corpus callosum area. Biological Psychiatry 56(2):80-85.
Thompson, R. A., and C. A. Nelson. 2001. Developmental science and the media. Early brain development. American Psychologist 56(1):5-15.
Thompson, R., T. R. A. Wiley, T. Lewis, D. J. English, H. Dubowitz, A. J. Litrownik, P. Isbell, and S. Block. 2012. Links between traumatic experiences and expectations about the future in high risk youth. Psychological Trauma: Theory, Research, Practice, and Policy 4(3):293-302.
Thornberry, T. P., T. O. Ireland, and C. A. Smith. 2001. The importance of timing: The varying impact of childhood and adolescent maltreatment on multiple problem outcomes. Development and Psychopathology 13(4):957-979.
Thornberry, T. P., K. L. Henry, T. O. Ireland, and C. A. Smith. 2010. The causal impact of childhood-limited maltreatment and adolescent maltreatment on early adult adjustment. Journal of Adolescent Health 46(4):359-365.
Tolin, D. F., and E. B. Foa. 2006. Sex differences in trauma and posttraumatic stress disorder: A quantitative review of 25 years of research. Psychological Bulletin 132(6):959-992.
Tottenham, N., and M. A. Sheridan. 2010. A review of adversity, the amygdala and the hippocampus: A consideration of developmental timing. Frontiers in Human Neuroscience 3(68).
Tottenham, N., J. W. Tanaka, A. C. Leon, T. McCarry, M. Nurse, T. A. Hare, D. J. Marcus, A. Westerlund, B. Casey, and C. Nelson. 2009. The NimStim set of facial expressions: Judgments from untrained research participants. Psychiatry Research 168(3):242-249.
Tottenham, N., T. A. Hare, B. T. Quinn, T. W. McCarry, M. Nurse, T. Gilhooly, A. Millner, A. Galvan, M. C. Davidson, I. Eigsti, K. M. Thomas, P. J. Freed, E. S. Booma, M. R. Gunnar, M. Altemus, J. Aronson, and B. J. Casey. 2010. Prolonged institutional rearing is associated with atypically large amygdala volume and difficulties in emotion regulation. Developmental Science 13(1):46-61.
Tottenham, N., T. A. Hare, A. Millner, T. Gilhooly, J. D. Zevin, and B. J. Casey. 2011. Elevated amygdala response to faces following early deprivation. Developmental Science 14(2):190-204.
Trickett, P. K., J. G. Noll, A. Reiffman, and F. W. Putnam. 2001. Variants of intrafamilial sexual abuse experience: Implications for short- and long-term development. Development and Psychopathology 13(4):1001-1019.
Trickett, P. K., J. G. Noll, and F. W. Putnam. 2011. The impact of sexual abuse on female development: Lessons from a multigenerational, longitudinal research study. Development and Psychopathology 23(2):453-476.
Tronick, E. Z. 1989. Emotions and emotional communication in infants. American Psychologist 44(2):112-119.
Twardosz, S., and J. R. Lutzker. 2010. Child maltreatment and the developing brain: A review of neuroscience perspectives. Aggression and Violent Behavior 15(1):59-68.
van Ijzendoorn, M. H., and F. Juffer. 2006. The Emanuel Miller memorial lecture 2006: Adoption as intervention. Meta-analytic evidence for massive catch-up and plasticity in physical, socio-emotional, and cognitive development. Journal of Child Psychology and Psychiatry 47(12):1228-1245.
van Ijzendoorn, M. H., and C. Schuengel. 1996. The measurement of dissociation in normal and clinical populations: Meta-analytic validation of the Dissociative Experiences Scale (DES). Clinical Psychology Review 16(5):365-382.
van Tilburg, M. A., D. K. Runyan, A. J. Zolotor, J. C. Graham, H. Dubowitz, A. J. Litrownik, E. Flaherty, D. K. Chitkara, and W. E. Whitehead. 2010. Unexplained gastrointestinal symptoms after abuse in a prospective study of children at risk for abuse and neglect. Annals of Family Medicine 8(2):134-140.
Vanderwert, R. E., P. J. Marshall, C. A. Nelson, C. H. Zeanah, and N. A. Fox. 2010. Timing of intervention affects brain electrical activity in children exposed to severe psychosocial neglect. PLoS ONE 5(7):e11415.
Vorria, P., Z. Papaligoura, J. Sarafidou, M. Kopakaki, J. Dunn, M. H. van Ijzendoorn, and A. Kontopoulou. 2006. The development of adopted children after institutional care: A follow-up study. Journal of Child Psychology and Psychiatry 47(12):1246-1253.
Walker, E. A., A. Gelfand, W. J. Katon, M. P. Koss, M. Von Korff, D. Bernstein, and J. Russo. 1999. Adult health status of women with histories of childhood abuse and neglect. American Journal of Medicine 107(4):332-339.
Wang, C.-T., and J. Holton. 2007. Total estimated cost of child abuse and neglect in the United States. Chicago: Prevent Child Abuse America.
Watamura, S. E., A. M. Sebanc, and M. R. Gunnar. 2002. Rising cortisol at childcare: Relations with nap, rest, and temperament. Developmental Psychobiology 40(1):33-42.
Waters, H., A. Hyder, Y. Rajkotia, S. Basu, J. A. Rehwinkel, and A. Butchart. 2004. The economic dimensions of interpersonal violence. Geneva: Department of Injuries and Violence Prevention, World Health Organization.
Weaver, I. C., N. Cervoni, F. A. Champagne, A. C. D’Alessio, S. Sharma, J. R. Seckl, S. Dymov, M. Szyf, and M. J. Meaney. 2004. Epigenetic programming by maternal behavior. Nature Neuroscience 7(8):847-854.
Webb, E. 2013. Poverty, maltreatment and attention deficit hyperactivity disorder. Archives of Disease in Childhood 98(6):397-400.
Wechsler-Zimring, A., C. A. Kearney, H. Kaur, and T. Day. 2012. Posttraumatic stress disorder and removal from home as a primary, secondary, or disclaimed trauma in maltreated adolescents. Journal of Family Violence 27(8):813-818.
Weich, S., J. Patterson, R. Shaw, and S. Stewart-Brown. 2009. Family relationships in childhood and common psychiatric disorders in later life: Systematic review of prospective studies. British Journal of Psychiatry 194(5):392-398.
Weierich, M. R., and M. K. Nock. 2008. Posttraumatic stress symptoms mediate the relationship between childhood sexual abuse and nonsuicidal self-injury. International Journal of Emergency Mental Health 10(2):156-158.
Wellman, C. L. 2001. Dendritic reorganization in pyramidal neurons in medial prefrontal cortex after chronic corticosterone administration. Journal of Neurobiology 49(3):245-253.
Wherry, J. N., D. A. Neil, and T. N. Taylor. 2009. Pathological dissociation as measured by the child dissociative checklist. Journal of Child Sexual Abuse 18(1):93-102.
Widom, C. S. 1988. Sampling biases and implications for child abuse research. American Journal of Orthopsychiatry 58(2):260-270.
Widom, C. S. 1989. The cycle of violence. Science 244(4901):160-166.
Widom, C. S. 1998. Childhood victimization: Early adversity and subsequent psychopathology. Adversity, Stress, and Psychopathology 81-95.
Widom, C. S. 1999. Posttraumatic stress disorder in abused and neglected children grown up. American Journal of Psychiatry 156(8):1223-1229.
Widom, C. S., and L. M. Brzustowicz. 2006. MAOA and the “cycle of violence”: Childhood abuse and neglect, MAOA genotype, and risk for violent and antisocial behavior. Biological Psychiatry 60(7):684-689.
Widom, C. S., and J. B. Kuhns. 1996. Childhood victimization and subsequent risk for promiscuity, prostitution, and teenage pregnancy: A prospective study. American Journal of Public Health 86(11):1607-1612.
Widom, C. S., and M. G. Maxfield. 2001. An update on the “cycle of violence.” Washington, DC: U.S. Department of Justice, Office of Justice Programs, National Institute of Justice.
Widom, C. S., T. Ireland, and P. J. Glynn. 1995. Alcohol abuse in abused and neglected children followed-up: Are they at increased risk? Journal of Studies on Alcohol 56(2): 207-217.
Widom, C. S., B. L. Weiler, and L. B. Cottler. 1999. Childhood victimization and drug abuse: A comparison of prospective and retrospective findings. Journal of Consulting and Clinical Psychology 67(6):867-880.
Widom, C. S., N. R. Marmorstein, and H. Raskin White. 2006. Childhood victimization and illicit drug use in middle adulthood. Psychology of Addictive Behaviors 20(4):394-403.
Widom, C. S., K. DuMont, and S. J. Czaja. 2007a. A prospective investigation of major depressive disorder and comorbidity in abused and neglected children grown up. Archives of General Psychiatry 64(1):49-56.
Widom, C. S., H. R. White, S. J. Czaja, and N. R. Marmorstein. 2007b. Long-term effects of child abuse and neglect on alcohol use and excessive drinking in middle adulthood. Journal of Studies on Alcohol and Drugs 68(3):317-326.
Widom, C. S., S. J. Czaja, and J. Paris. 2009. A prospective investigation of borderline personality disorder in abused and neglected children followed up into adulthood. Journal of Personality Disorders 23(5):433-446.
Widom, C. S., S. J. Czaja, T. Bentley, and M. S. Johnson. 2012. A prospective investigation of physical health outcomes in abused and neglected children: New findings from a 30-year follow-up. American Journal of Public Health 102(6):1135-1144.
Wilson, H. W., and C. S. Widom. 2008. An examination of risky sexual behavior and HIV in victims of child abuse and neglect: A 30-year follow-up. Health Psychology 27(2):149-158.
Wilson, H. W., and C. S. Widom. 2010. The role of youth problem behaviors in the path from child abuse and neglect to prostitution: A prospective examination. Journal of Research on Adolescence 20(1):210-236.
Wolf, E. J., C. A. Lunney, M. W. Miller, P. A. Resick, M. J. Friedman, and P. P. Schnurr. 2012. The dissociative subtype of PTSD: A replication and extension. Depression and Anxiety 29(8):679-688.
Wolfe, D. A., C. Wekerle, K. Scott, A.-L. Straatman, and C. Grasley. 2004. Predicting abuse in adolescent dating relationships over 1 year: The role of child maltreatment and trauma. Journal of Abnormal Psychology 113(3):406-415.
Woon, F. L., and D. W. Hedges. 2008. Hippocampal and amygdala volumes in children and adults with childhood maltreatment-related posttraumatic stress disorder: A meta-analysis. Hippocampus 18(8):729-736.
Yates, T. M., E. A. Carlson, and B. Egeland. 2008. A prospective study of child maltreatment and self-injurious behavior in a community sample. Development and Psychopathology 20(2):651-671.
Yehuda, R., S. L. Halligan, and L. M. Bierer. 2002. Cortisol levels in adult offspring of holocaust survivors: Relation to PTSD symptom severity in the parent and child. Psychoneuroendocrinology 27(1-2):171-180.
Zagar, A. K., R. J. Zagar, B. Bartikowski, and K. G. Busch. 2009. Cost comparisons of raising a child from birth to 17 years among samples of abused, delinquent, violent, and homicidal youth using victimization and justice system estimates. Psychological Reports 104(1):309-338.
Zanarini, M. C., C. S. Laudate, F. R. Frankenburg, D. B. Reich, and G. Fitzmaurice. 2011. Predictors of self-mutilation in patients with borderline personality disorder: A 10-year follow-up study. Journal of Psychiatric Research 45(6):823-828.
Zeanah, C. H., and M. M. Gleason. 2010. Reactive attachment disorder: A review for DSM-V. Washington, DC: APA.
Zeanah, C. H., A. T. Smyke, and A. Dumitrescu. 2002. Attachment disturbances in young children. II: Indiscriminate behavior and institutional care. Journal of the American Academy of Child and Adolescent Psychiatry 41(8):983-989.
Zeanah, C. H., C. A. Nelson, N. A. Fox, A. T. Smyke, P. Marshall, S. W. Parker, and S. Koga. 2003. Designing research to study the effects of institutionalization on brain and behavioral development: The Bucharest Early Intervention Project. Developmental Psychopathology 15(4):885-907.
Zeanah, C. H., M. Scheeringa, N. W. Boris, S. S. Heller, A. T. Smyke, and J. Trapani. 2004. Reactive attachment disorder in maltreated toddlers. Child Abuse & Neglect 28(8):877-888.
Zeanah, C. H., H. L. Egger, A. T. Smyke, C. A. Nelson, N. A. Fox, P. J. Marshall, and D. Guthrie. 2009. Institutional rearing and psychiatric disorders in Romanian preschool children. American Journal of Psychiatry 166(7):777-785.
Zingraff, M. T., J. Leiter, K. A. Myers, and M. C. Johnsen. 1993. Child maltreatment and youthful problem behavior. Criminology 31(2):173-202.