ADHD in Children and Adolescents
Summary and Keywords
Attention-deficit/hyperactivity disorder (ADHD) is a neurodevelopmental disorder characterized by developmentally inappropriate levels of hyperactivity, impulsivity, and/or inattention. ADHD is chronic, may persist into adulthood, and is associated with impairment in social and academic/work domains across the lifespan. Children and adolescents with ADHD often present with executive function deficits and emotion dysregulation, and these deficits may increase impairment and risk for co-occurring disorders. The etiology of ADHD is not yet understood, though research suggests that biological and environmental factors (e.g., family, community) contribute to its development and course. It should be noted that ADHD commonly co-occurs with additional psychiatric disorders, such as oppositional defiant disorder (ODD), conduct disorder (CD), and major depressive disorder.
Evidence-based assessment of ADHD requires information from multiple informants using multiple assessment methods to determine the presence of ADHD symptoms across settings and any co-occurring disorders. The evidence-based treatment options for ADHD are manifold. Pharmacotherapy for ADHD is common, although numerous behavioral interventions are also effective. Stimulant medications are commonly prescribed and are typically effective in ameliorating core ADHD symptoms. There is also evidence that the nonstimulant medication atomoxetine substantially decreases the symptoms of ADHD. Importantly, medication therapy works to reduce symptoms but typically does not alleviate the impairments associated with the disorder. Combined medication and behavioral interventions are more likely to reduce impairments and normalize behavior.
Keywords: Attention-deficit/hyperactivity disorder (ADHD), emotion dysregulation, executive function, pharmacotherapy, etiology, parenting, academic functioning, assessment, evidence-based treatment, psychosocial treatment
Attention deficit hyperactivity disorder (ADHD) is a chronic and impairing neurodevelopmental disorder that has an onset in childhood and typically persists into adulthood (American Psychiatric Association, 2013). As early as the preschool years, very young children with ADHD can be reliably differentiated from their peers on the basis of symptoms and impairments (Lahey et al., 1998). An estimated 10.5% of preschool-aged children meet criteria for ADHD, and approximately 11.4% of children, 8% of adolescents, and 5% of adults meet criteria for the disorder (Willcutt, 2012).
Medical references to a disorder characterized by inattention, impulsivity, and hyperactivity date back to 1775 (Barkley, 2014a). By the 1950s and 1960s, these behaviors were thought to be caused by brain damage to the frontal lobes, and the term minimal brain dysfunction was used to describe these children. This disorder was first described in the Diagnostic and Statistical Manual of Mental Disorders, Second Edition (DSM-II; American Psychiatric Association, 1968) as a hyperkinetic reaction of childhood disorder. Children with this diagnosis had symptoms including inattention, distractibility, and overactivity, but they typically exhibited a reduction in symptoms by adolescence. Subsequent editions of the DSM have had more specific definitions of symptoms and emphasized the important role that neurological and genetic factors play in the etiology of the disorder. Although historically viewed as a childhood disorder, ADHD began to be viewed as a life-course persistent disorder beginning in the 1990s (Barkley, 2014a).
In the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5), ADHD is characterized by developmentally inappropriate levels of hyperactivity, impulsivity, and/or inattention (American Psychiatric Association, 2013) that must be evident across multiple settings (e.g., home and school, with peers). Furthermore, symptoms must be present prior to 12 years of age and must cause impairment (typically in social and academic functioning).
The DSM-5 delineates three presentations of ADHD—predominately hyperactive/impulsive (ADHD-HI), predominately inattentive (ADHD-I), and combined (ADHD-C) (American Psychiatric Association, 2013). ADHD presentations are specified based on symptom clustering. Notably, although a diagnosis of ADHD typically remains stable across development, subtypes or presentations of ADHD are relatively unstable (Lahey, Pelham, Loney, Lee, & Willcutt, 2005). Across the lifespan, the ADHD-HI presentation demonstrates the most instability. Most young children originally diagnosed with ADHD-HI either convert to ADHD-C or no longer meet criteria for ADHD (Lahey et al., 2005). Approximately half of preschoolers with ADHD are diagnosed as ADHD-HI; however, by elementary school, only about 25% of children with ADHD are specified as ADHD-HI, and this number further decreases to 14% in adolescence (Willcutt, 2012). In contrast, about 21% of preschoolers with ADHD present with ADHD-I, but over 70% of adolescents with ADHD are classified as ADHD-I (Willcutt, 2012).
Importantly, ADHD commonly co-occurs with other psychological disorders. Indeed, 67%–80% of clinic-referred children with ADHD meet criteria for at least one other disorder (Barkley, Murphy, & Fischer, 2008). It is not unusual for a child or adolescent diagnosed with ADHD to meet criteria for an externalizing disorder such as oppositional defiant disorder (ODD) or conduct disorder (CD), or an internalizing disorder like depression (MDD) or anxiety (Pliszka, 2014). Furthermore, 30%–45% of youth with ADHD meet criteria for a learning disability (DuPaul & Langberg, 2014). The co-occurrence of ADHD and additional psychopathology is indicative of poorer developmental trajectories and outcomes, a finding that is discussed further throughout this chapter (e.g., Chronis-Tuscano et al., 2010; Mikami, Ransone, & Calhoun, 2011).
Factors Influencing Developmental Trajectory
Gender is one factor that may influence developmental outcomes for children with ADHD. In childhood, the ratio of boys to girls with ADHD is 3:1, but by adulthood, the ratio is 1:1 (Owens, Cardoos, & Hinshaw, 2014). In addition to having a higher prevalence of ADHD in childhood, more boys than girls receive treatment for ADHD. In clinical samples, the ratio of boys to girls ranges from 5:1 to 9:1, suggesting that more boys than girls with ADHD receive treatment (Bruchmüller, Margraf, & Schneider, 2012). With many studies finding that boys and girls with ADHD experience equivalent impairment (Owens et al., 2014), the lower rate of treatment utilization for girls is very concerning. Studies have shown that parents of girls exhibiting ADHD symptoms may recognize the problem but are less likely to request an evaluation; and even when evaluations are requested, girls are less likely to receive a diagnosis of ADHD (Bussing, Zima, Gary, & Garvan, 2003). Some researchers have posited that the lower rate of parental help-seeking and treatment referral for girls with ADHD compared to boys is due to gender differences in co-occurring externalizing disorders. Evidence to support this has been mixed (e.g., Biederman et al., 2002; Ohan & Visser, 2009). Preliminary research has found evidence that the gender difference may be due to the perceptions of parents and teachers that boys with ADHD could benefit more from educational assistance in the classroom than girls with ADHD (Ohan & Visser, 2009).
Compared to girls without ADHD, by adolescence and young adulthood, girls with ADHD are at higher risk for internalizing and externalizing disorders (Biederman et al., 2010; Hinshaw et al., 2012). Hinshaw and colleagues (2012) also found that girls with ADHD demonstrate greater risk for suicide attempts and self-injury, as well as greater impairment in academic achievement and peer relationships, relative to comparison girls. During childhood, boys and girls with ADHD have similar rates of risk for co-occurring internalizing disorders, but girls may have higher risk for later internalizing disorders than boys (Owens et al., 2014). Boys with ADHD may have a higher risk for externalizing disorders than girls with ADHD, but differences are not consistent across studies, and these gender differences may not be specific to ADHD, as they are evident in population samples (Owens et al., 2014). Boys with ADHD also may have more difficulties with school functioning and academic achievement than girls with ADHD, but again findings vary across studies (Owens et al., 2014). In addition to child gender, environmental and community factors may affect risk for ADHD and adverse outcomes associated with ADHD. Environmental risk factors for ADHD include pregnancy complications (e.g., prematurity, breech delivery), exposure to environmental toxins (e.g., lead), and certain childhood illnesses (Millichap, 2008). Children with ADHD are also more likely to have been exposed to maternal substance use in utero. Prenatal maternal smoking, illicit drug use, and alcohol use are all identified risk factors for ADHD (Millichap, 2008). It is important to note that many studies have not controlled for potential confounding factors (e.g., maternal psychopathology), which may explain the relationship between maternal prenatal substance use and offspring ADHD (Linnet et al., 2003). For example, adults with ADHD are more likely to smoke, so it is possible that the relationship between prenatal maternal smoking and offspring ADHD is due to confounding genetic factors (Thapar & Rutter, 2009). Further research is thus needed in this area using genetically informed designs (e.g., Skoglund, Chen, D’Onofrio, Lichtenstein, & Larsson, 2014).
Lower socioeconomic status (SES) also predicts poorer outcomes for children with ADHD (e.g., Biederman, Faraone, & Monuteaux, 2002; Lahey et al., 2016). This may be due to lower-SES families often having fewer resources, poorer school quality, family stress, and limited social support. In addition, child race and ethnicity have been found to affect ADHD diagnosis rates. Although a review paper documented that African-American children may exhibit up to one-half standard deviation more ADHD symptoms than Caucasian children, African-American children are diagnosed with ADHD at rates of 34%–70% less than Caucasian children (Miller, Nigg, & Miller, 2009; Morgan, Hillemeier, Farkas, & Maczuga, 2014). Furthermore, Hispanic children and children of other races/ethnicities are found to be diagnosed with ADHD approximately half as often as Caucasian children (Morgan, Staff, Hillemeier, Farkas, & Maczuga, 2013). Research has found that teacher bias, SES, health insurance status, and English-speaking status do not explain the racial and ethnic differences in diagnosis (Miller et al., 2009; Morgan et al., 2013). Further research in this area is needed to determine if other elements, such as parental beliefs about ADHD, treatment acceptability, and other risk factors, may explain this association (Miller et al., 2009).
Biological and Genetic Underpinnings
The etiology of ADHD is complex and multifaceted. Strong evidence implicates genetic and neurological factors, as well as their interactions with the environment, as core components of the development of ADHD. Although other contributors to the etiology of ADHD have been proposed, including poor parenting and food additives, these factors have limited or mixed evidence supporting them (Barkley, 2014b).
A wealth of research suggests that ADHD is one of the psychiatric disorders most influenced by genetics. The genetic contributions to ADHD are not from aberrant chromosomal structures, mutations, or additional genetic material. Instead, it is the heritable nature of ADHD that accounts for much of the etiology of the disorder (Barkley, 2014b). There is strong support for familial aggregation of ADHD. For example, if a parent has ADHD, there is a 57% risk that a biological offspring also will have the disorder (Biederman et al., 1995), and heritability estimates exceed 0.76 (Faraone et al., 2005).
ADHD is polygenetic, meaning that more than one gene likely contributes to the expression of the disorder. Among the genes that are consistently associated with ADHD across numerous investigations are the D4 and D5 dopamine receptor genes (DRD4 and DRD5), the dopamine transporter gene (DAT1), the serotonin transporter gene (5HTT), the serotonin 1B receptor gene (HTR1B), and the synaptosomal-associated protein 25 gene (SNAP25) (Barkley, 2014b). The latrophilin 3 gene (LPHN3) has also been associated with ADHD (Arcos-Burgos et al., 2010).
The DRD4 7-repeat allele decreases the receptor’s sensitivity to dopamine and, in doing so, is thought to increase risk for ADHD. The DRD4 7-repeat allele has been linked to the behavioral, not cognitive, features of ADHD (Banaschewski, Becker, Scherag, Franke, & Coghill, 2010). Allelic variations of the DRD5 receptor gene, which is thought to be involved in long-term potentiation to novel events (Gizer et al., 2009), have also been linked to ADHD. Specifically, the DRD5 148 base-pair allele has been associated with the persistence of ADHD from childhood to adolescence (Banaschewski et al., 2010).
Dopamine transporters (DATs) are responsible for the termination of dopamine signals via rapid reuptake of the dopamine neurotransmitters into presynaptic terminals. Because of their function in dopamine reuptake, DATs are important to the control of dopamine intensity and neurotransmission duration (Turic, Swanson, & Sonuga-Barke, 2010). Alterations in DATs result in changes in dopamine time-course and amplitude (Tripp & Wickens, 2009). Homozygosity for the DAT1 10-repeat allele has been associated with ADHD symptoms and poorer response to treatment with methylphenidate (Turic et al., 2010).
Although dopamine is heavily implicated in the etiology of ADHD, other neurotransmitters are also thought to play a causal role. Serotonin transporter and receptor genes have consistently been associated with ADHD and are involved in the etiology of impulsivity and aggression. Specifically, the 5HTTLPR polymorphism and the rs6296 polymorphism of 5HTR1B are thought to confer risk for ADHD (Gizer et al., 2009).
The SNAP25 gene codes for proteins that are important for synaptic vesicle regulation, axonal growth, and synaptic plasticity (Barkley, 2014b; Gizer, Ficks, & Waldman 2009). The rs3746544 polymorphism evidences significant, albeit modest, associations with the disorder (Gizer et al., 2009).
Lastly, the LPHN3 gene codes for latrophilin receptors in areas of the brain that are implicated in ADHD, including the prefrontal cortex (Arcos-Burgos et al., 2010; Martinez, Muenke, & Arcos-Burgos, 2010). Variants of this gene confer risk for the development of ADHD and have been associated with disruptive behavior disorders and substance use disorders, which often co-occur with ADHD (Martinez et al., 2010). Interestingly, the LPHN3 genotype may predict response to treatment with stimulant medication (Arcos-Burgos et al., 2010).
Although many genes are associated with ADHD, the relative contribution of a given gene to trait variation is minor, and no gene has been found to confer large risk effects for the development of ADHD (Barkley, 2014b). Notably, the genes and variants discussed here represent a small sampling of the genes that have been studied for association with ADHD. Despite the abundance of genes that are associated with the development of ADHD, a fraction of them have been studied for gene-by-environment (GxE) interactions (Nigg, Nikolas, & Burt, 2010). In a review of GxE interactions related to the development of ADHD, Nigg and colleagues (2010) note that the effect sizes for GxE interactions with psychosocial moderators (e.g., low income, parenting, and family conflict) are larger than interactions with prenatal and perinatal risk factors (e.g., cigarette and alcohol exposure). Continued research into GxE interactions will likely provide new insights into the etiology of ADHD and may elucidate how and when environmental factors influence the disorder’s onset and presentation.
Neuroimaging studies using magnetic resonance imaging provide further information about the biological underpinnings of ADHD. Research with pediatric populations has found that groups of children with ADHD can be differentiated from non-ADHD children by brain structure and function. Children with ADHD have less total brain volume, as well as reduced volume in specific areas (Tripp & Wickens, 2009). The caudate nucleus, a region of the brain that is rich in dopamine receptors, is notably smaller in children with ADHD, as is the corpus callosum (Tripp & Wickens, 2009). Reduced cortical volume in regions of the brain associated with executive functioning (EF), such as the cerebellum, and emotion regulation (ER), such as the striatum, has also been associated with ADHD (Barkley, 2014b). In addition, children with ADHD present with aberrant cortical thickness (Shaw et al., 2013). Interestingly, the rate of cortical thinning has been linked with behavioral features of ADHD, such as inattention, as well as with the persistence of the disorder (Shaw et al., 2013). Minimal cortical thinning and, in contrast, cortical thickening are associated with the remission of ADHD (Shaw et al., 2013). Overall, delays in brain maturation are associated with ADHD.
Another form of neuroimaging, diffusion tensor imaging (DTI), has been used to study white matter in the brains of children with ADHD. DTI is an especially useful tool to examine structural connectivity between cortical brain regions and subcortical structures. DTI can also be used to evaluate axonal density, axonal membrane circumference, and myelin sheath thickness. There are considerable differences in white matter tracts and regions between individuals with and without ADHD in the frontal, temporal, parietal, and occipital lobes. DTI research suggests that children with ADHD show delayed myelination, and this delay may persist into adulthood (van Ewijk, Heslenfeld, Zwiers, Buitelaar, & Oosterlaan, 2014). One common measure in DTI is fractional anisotropy (FA), an index of axonal stability and organization. A second common measure is mean diffusion (MD), which is associated with changes in intercellular space. In children, adolescents, and young adults, a number of ADHD symptoms have been linked to more FA and less MD (van Ewijk et al., 2014). In van Ewijk and colleagues (2014), atypical FA and MD were diffuse, and this finding is consistent with other neuroimaging studies that have found abnormalities throughout the brain.
Furthermore, ADHD is associated with specific differences in functional connectivity in brain circuitry essential to EF and ER, which are two areas of dysfunction commonly associated with ADHD. Children show weaker functional connectivity in the executive attention circuit, which is a neural circuitry involved in EF (Posner et al., 2013). The executive attention circuit includes the ventral attention network, which is important for monitoring the environment for stimuli relevant to one’s behavior. It also includes the dorsal attention network, which is implicated in control for attention shifting; and the frontostriatal system, which initiates or inhibits behavioral responses. Deficits in EF contribute to the neuropsychological underpinnings of ADHD (Willcutt, Doyle, Nigg, Faraone, & Pennington, 2005).
Structures involved in the neural circuits that underlie ER include the amygdala, ventral striatum, hippocampus, and subgenual and orbitofrontal cortices. Compared to children without ADHD, children with ADHD have weaker functional connectivity between the orbitofrontal cortex and ventral striatum (Posner et al., 2013). The connection between the ventral striatum and orbitofrontal cortex is inversely related to behavioral outcomes such as emotional lability (Posner et al., 2013). Difficulties with ER are considered in several models of ADHD, and this is important, given that these difficulties can contribute to the development of co-occurring disorders among children with ADHD (Seymour et al., 2012, 2014).
In sum, the biological underpinnings of ADHD are complex and not yet fully understood. Several genes confer risk for the development of the disorder, others are implicated in the persistence of ADHD into adulthood, and still others are associated with the effectiveness of pharmacotherapy. Research on GxE interactions suggests that psychosocial factors may be moderators of ADHD development, but more work on these interactions is needed. At the brain level, children and adolescents with ADHD differ structurally and functionally from their typically developing peers. Many areas of the brain that are structurally or functionally aberrant in individuals with ADHD are associated with behavioral constructs that are known to be problematic in ADHD (i.e., EF and ER).
As previously discussed, children with ADHD tend to have weaker functional connectivity in neural circuits related to ER, and, indeed, children with ADHD often have difficulty self-regulating negative emotions like anger and frustration and positive emotions like excitement. ER can be defined as the use of several cognitive processes to modify emotional states in order to achieve a goal or adapt to the environment (Eisenberg & Spinrad, 2004; Thompson, 1994). Conversely, emotion dysregulation occurs when an individual is unable to exercise ER processes in part or in its entirety (Bunford, Evans, & Wymbs, 2015). Emotion dysregulation includes emotional lability, emotional experiences and expressions that are inappropriate to a situation and that are in excess of social norms, and atypical attention to emotional stimuli (Shaw, Stringaris, Nigg, & Leibenluft, 2014).
Emotion dysregulation occurs in approximately 25%–45% of children with ADHD (Shaw et al., 2014). The combination of ADHD and emotion dysregulation is more impairing than a diagnosis of ADHD alone. Indeed, children with ADHD and emotion dysregulation show more social and academic impairment (Biederman et al., 2012a; Wehmeier, Schacht, & Barkley, 2010). Emotion dysregulation in children with ADHD is also associated longitudinally with the development of additional psychiatric disorders. For example, emotional negativity and lability mediated the association between ADHD and later depressive symptoms in a community sample of youth (Seymour et al., 2014).
Several conceptual models attempt to explain the co-occurrence of ADHD and impairing emotion dysregulation. The core features of ADHD have been historically described as developmentally inappropriate inattention, hyperactivity and impulsivity, or both. However, this conceptualization fails to place any emphasis on the difficulties with effortful inhibition and top-down control of one’s own emotions that are often key characteristics of ADHD, specifically within the combined ADHD (ADHD-C) and predominately hyperactive/impulsive ADHD (ADHD-HI) presentations (Barkley, 2014c). Thus, one model of ADHD and emotion dysregulation conceptualizes emotion dysregulation as a defining feature of ADHD (Barkley, 2014c; Barkley & Murphy, 2010). This model acknowledges that there are close associations between systems that underlie cognitive regulation and ER and suggests that the emotion dysregulation observed in those with ADHD stems from the same neurocognitive deficits that underlie ADHD symptomatology. Notably, the overlap between cognitive regulation and ER systems is far from complete, and approximately half of individuals with ADHD do not demonstrate impairing emotion dysregulation.
A second model views individuals who present with the combination of ADHD and emotion dysregulation to represent a distinct entity (Biederman et al., 2012b; Surman et al., 2011). This group may have a unique etiology and distinct clinical course compared to those with ADHD alone. Evidence for this model comes largely from genetic studies demonstrating co-segregation of ADHD and emotional dysregulation in families. Lastly, a third model conceptualizes symptoms of ADHD and emotion dysregulation as correlated but distinct dimensions stemming from partially overlapping, but dissociable, neurological underpinnings (Nigg & Casey, 2005).
Models of the pathophysiology of ADHD and emotion dysregulation describe dysfunction in both bottom-up and top-down processes that support and underlie ER. The abilities to orient to emotional stimuli and to evaluate signals for reward are two bottom-up processes that are important in ER. The amygdala, ventral striatum, and orbitofrontal cortex are implicated in bottom-up responses to emotional stimuli (Shaw et al., 2014). Individuals with ADHD may overperceive negative stimuli, though they also may have reduced perception of salient positive stimuli. In addition, reward processing tends to be dysfunctional in individuals with ADHD. Individuals with ADHD display a preference for smaller, more immediate rewards over larger, delayed rewards, and this type of dysfunction is thought to contribute to emotion dysregulation (Shaw et al., 2014).
Disruptions in several top-down regulatory processes are thought to contribute to emotion dysregulation. Compared to peers without ADHD, children with ADHD demonstrate reduced autonomic nervous system regulatory responses to negative stimuli (Musser, Galloway-Long, Frick, & Nigg, 2013) and regulatory abilities that are less flexible to stimulus valence (Musser et al., 2011). Abnormal attention to emotional stimuli may stem from aberrant functioning of the medial prefrontal cortex and ventrolateral prefrontal cortex (Shaw et al., 2014).
In sum, a nonnegligible percentage of individuals with ADHD experience significant emotion dysregulation. The co-occurrence of ADHD and emotion dysregulation is indicative of increased impairment and is associated with poorer developmental outcomes. Several conceptual models have been developed in attempts to explain the overlap between ADHD and emotion dysregulation. Studies and models of the pathophysiology of ADHD and emotion dysregulation point to disruptions in networks involved in bottom-up and top-down responses to emotional stimuli.
Executive functioning (EF) is defined as self-regulation through the use of multiple cognitive processes for the purposes of organizing and directing behavior in order to achieve a goal (Barkley, 2011). Several theories of ADHD propose that symptoms of the disorder arise from deficits in EF (see Willcutt et al., 2005), and many neural regions that have been associated with ADHD are also implicated in EF (e.g., executive attention circuit; Posner et al., 2013).
Approximately 30%–50% of children and adolescents with ADHD exhibit deficits in EF (Biederman et al., 2004; Lambek et al., 2011; Loo et al., 2007; Nigg, Willcutt, Doyle, & Sonuga-Barke, 2005). Among children with ADHD, EF deficits have been associated with disruptive classroom behavior, poor academic functioning, and poor social functioning (Barkley, 1997; Tseng & Gau, 2013). Importantly, EF deficits may persist into adulthood (Hervey, Epstein, & Curry, 2004; Seidman, 2006).
EF tasks requiring the use of inhibition, such as stop-signal reaction time or flanker inhibitory control tasks, are particularly challenging for children with ADHD, and research shows that they perform more poorly on these tasks than children without ADHD (e.g., Barkley, 1997; Sjöwall, Roth, Lindqvist, & Thorell, 2013; Willcutt et al., 2005). Children with ADHD also demonstrate poor task performance on measures of cognitive flexibility and on tasks that tap working memory (Fried et al., 2015). Additional domains of EF difficulty in individuals with ADHD have been found with measures of spatial working memory, planning, organization, and vigilance (Fried et al., 2015; Willcutt et al., 2005).
Despite the variety of EF domains in which individuals with ADHD tend to perform more poorly than individuals without the disorder, research suggests that deficits in EF are not necessary and sufficient in and of themselves to lead to ADHD. Correlations between EF task scores and ADHD symptoms tend to be small, although statistically significant (Willcutt et al., 2005), and effect sizes of EF task performance between groups with and without ADHD are medium (Willcutt et al., 2005). Furthermore, impairing deficits in EF occur in less than half of children with ADHD (Nigg et al., 2005). These findings suggest that EF deficits have demonstrated associations with ADHD but are unlikely the root cause of the disorder. However, it is important to consider that these conclusions rest on the assumption that the tasks used to measure EF can validly indicate dysfunction in different EF constructs. As Barkley and Murphy (2011) note, EF tasks have limited to no ecological validity, as assessed by correlating EF task performance with ratings of EF in daily life.
Although many tasks typically used to assess EF lack ecological validity, children with ADHD and EF deficits still display more impairment in real-world functioning. Several studies have found that, among children with ADHD, poor EF is associated with poorer school functioning. Biederman and colleagues (2004) found that children with ADHD and EF deficits achieved less academically and were at greater risk for grade retention. Indeed, EF deficits partially mediate the relation between ADHD symptoms and mathematics skills, as well as the relation between ADHD symptoms and language skills (Thorell, 2007). Furthermore, working memory deficits among children with ADHD predict poorer reading ability, and global EF deficits predict higher rates of school suspensions and expulsions (Miller, Nevado-Montenegro, & Hinshaw, 2012).
In sum, many (but not all) children and adolescents with ADHD demonstrate deficits in EF, and these deficits may persist into adulthood. These deficits span a wide range of EF domains. Although it is argued that the tasks used to assess these domains often do not correlate with real-world behavior or functioning, children and adolescents with ADHD and EF deficits demonstrate poorer functioning than those without EF deficits.
Family factors affect both the persistence of child ADHD symptoms and the development of co-occurring disorders. These factors include parent characteristics (e.g., parental psychopathology), the parent-child relationship, the marital or co-parenting relationship, and the sibling relationship (Johnston & Chronis-Tuscano, 2014). They interact with child characteristics, including genetic vulnerabilities to ADHD and child temperament, to contribute to either more adaptive or more adverse child outcomes.
In regard to parent characteristics, parents of children with ADHD have higher rates of psychopathology than parents of children without ADHD. Furthermore, maternal psychopathology has been found to predict the continuation of ADHD in childhood to adulthood (e.g., Biederman, Petty, Clarke, Lomedico, & Faraone, 2011). Almost half of children with ADHD have a parent with high levels of ADHD symptoms, and parent ADHD symptoms are associated with more severe child ADHD, higher levels of disruptive behaviors, and more social problems (Johnston & Chronis-Tuscano, 2014). Parent ADHD also may affect parenting quality, as parents with higher levels of ADHD symptoms are found to use more inconsistent and overreactive discipline and more negative control, as well as experiencing more parenting stress (Johnston, Mash, Miller, & Ninowski, 2012).
Depression is the most common psychological disorder among mothers of children with ADHD, with rates around 40%–50% (Chronis et al., 2003). Maternal depression independently predicts the development of conduct problems in children with ADHD, as well as later child depression and suicidal behavior (Chronis et al., 2007; Chronis-Tuscano et al., 2010). Less is known about paternal depression, but studies have found it to be related to child ADHD symptoms and persistence of ADHD from childhood into adulthood (Johnston & Chronis-Tuscano, 2014).
Furthermore, children with ADHD are more likely to experience lower parenting quality than children without ADHD. Parents of children with ADHD are more likely to have a parenting style that is lower in warmth and positivity and higher in directiveness (Johnston & Chronis-Tuscano, 2014). Negative parenting practices, such as overreactive discipline, have been found to predict later levels of disruptive behavior problems in preschool-aged children with ADHD (Harvey, Metcalfe, Herbert, & Fanton, 2011). Positive parenting practices, including parental warmth, monitoring, and appropriate limit-setting, reduce the likelihood of children with ADHD developing disruptive behavior problems and later substance use (e.g., Chronis et al., 2007; Harvey et al., 2011; Molina et al., 2012). Parents of children with ADHD experience more parenting stress than parents of children without ADHD, and parenting stress is associated with ADHD symptom severity (Theule, Wiener, Tannock, & Jenkins, 2013). Importantly, children’s ADHD symptoms and parenting behavior have been found to be bidirectional, where children’s disruptive and inattentive behaviors evoke maladaptive parenting behaviors, and these negative parenting behaviors in turn intensify child disruptive behaviors (Johnston & Chronis-Tuscano, 2014). For instance, a study of adoptive mothers and their unrelated children with ADHD found that early childhood ADHD symptoms predicted parenting quality, and then that parenting quality predicted the course of child ADHD symptoms over time (Harold et al., 2013).
In addition, children who have experienced abuse or neglect exhibit a higher rate of ADHD than the general population (e.g., Ackerman, Newton, McPherson, Jones, & Dykman, 1998). This may be partially explained by the effects of child maltreatment on brain development (McCrory, De Brito, & Viding, 2012). Children with ADHD are also more likely to experience child maltreatment than are children without ADHD (Ouyang, Fang, Mercy, Perou, & Grosse, 2008).
Compared to children without ADHD, children with ADHD also experience more family conflict and are exposed to more interparental conflict (Johnston & Chronis-Tuscano, 2014). Parents of children with ADHD are more likely to divorce and have shorter time to divorce than parents of children without the disorder (Wymbs et al., 2008). As with the association between parenting behavior and children’s ADHD symptoms, interparental conflict and children’s disruptive behavior problems influence each other in a bidirectional pattern. Research demonstrates that interparental conflict predicts child behavioral and emotional regulation problems over a 1-year period, and the child dysregulated behavior was related to later interparental conflict (Schermerhorn, Cummings, DeCarlo, & Davies, 2007). Children’s perceptions of interparental conflict are also related to parent and teacher ratings of child ADHD symptoms (Counts, Nigg, Stawicki, Rappley & Von Eye, 2005). In addition, in families where multiple siblings had a diagnosis of ADHD, family conflict was higher than in normative samples and explained 40% of the siblings’ similarity in impairment as rated by clinicians and parents (Pressman et al., 2006). Interparental conflict and children’s ADHD symptoms likely influence each other indirectly through reductions in parenting quality, though these pathways are not well understood. Parental psychopathology and other family conflicts also affect interparental conflicts, contributing to the developmental outcomes of children with ADHD.
Little research has examined the effect of sibling relationships on developmental outcomes for children with ADHD, but research suggests that these sibling relationships are higher in conflict than sibling relationships of children without ADHD (Mikami & Pfiffner, 2008). Findings also indicate that co-occurring internalizing and externalizing behavior problems affect the warmth and closeness of the sibling relationship and conflict levels (Mikami & Pfiffner, 2008).
Overall, children with ADHD are more likely to experience parental psychopathology, maladaptive parenting, interparental conflict, and family conflict. These family factors have reciprocal interactions with children’s ADHD symptoms and disruptive behavior to affect the course of children’s ADHD and other developmental outcomes.
The prevalence of learning and academic problems in children with ADHD ranges from 50% to 80% and often persists into adolescence (DuPaul & Langberg, 2014). Compared to youth without ADHD, youth with ADHD exhibit lower grades, higher rates of grade retention, and are more likely to drop out of high school (DuPaul & Stoner, 2014). Children and adolescents with ADHD also are more likely to qualify for a learning disability, with rates ranging from 30% to 45% (DuPaul & Langberg, 2014). Importantly, negative academic outcomes are better predicted by children’s inattentive symptoms than by their hyperactivity-impulsivity symptoms (Massetti et al., 2008).
The academic impairment of children with ADHD is evident as early as the preschool years. Preschoolers with ADHD have significant difficulties with early literacy and numeracy skills and have lower academic readiness skills in general (DuPaul & Langberg, 2014). Preschool ADHD symptoms predict later adolescent performance in math, spelling, and reading (Spira & Fischel, 2005). It is possible that preschool ADHD symptoms may hinder the development of literacy skills that serve as the foundation for later academic abilities. Also, transitions in academic settings, including the transition from elementary school to middle school and from middle school to high school, can be difficult for children with ADHD. These transitions often result in additional academic impairment and increased ADHD symptom severity due to a reduction in structure (e.g., more long-term assignments, less teacher support) and an increased need to self-regulate planning and organization (DuPaul & Langberg, 2014). Importantly, children with ADHD who perceive themselves to have stronger academic abilities may be protected against negative outcomes. For instance, childhood self-perceived academic competence was associated with fewer substance abuse and internalizing problems during adolescence for girls with ADHD (Mikami & Hinshaw, 2006).
Compared to same-age peers, children with ADHD demonstrate more difficulties with peer relationships and more deficits in overall social functioning (Mikami, 2010). Children with ADHD are more likely to experience peer rejection, have fewer friendships that are reciprocated, and have less stable friendships. Among children with ADHD, peer rejection develops rapidly, is resistant to change, and is not easily reversed (McQuade & Hoza, 2014). During peer interactions, higher rates of disruptive, intrusive, and annoying behavior are observed in children with the hyperactive-impulsive and combined presentations of ADHD. Children with the predominantly inattentive presentation of ADHD also face peer rejection because they are more likely to be socially withdrawn and passive during peer interactions (McQuade & Hoza, 2014).
There is evidence that children with ADHD are both more likely to be victimized within peer relationships and to engage in bullying behavior (Wiener & Mak, 2009). Some research has found that the higher risk for bullying may be explained by co-occurring ODD symptoms (e.g., Wiener & Mak, 2009). Although studies have shown that boys and girls with ADHD have similar difficulties with peer relationships, some posit that girls with ADHD may experience additional problems due to the greater levels of emotional intimacy and reciprocity that typify female friendships (Mikami, 2010).
Peer relationships also play an important role in the developmental trajectories of children with ADHD. Childhood peer problems and peer rejection have been found to predict increased risk for adolescent delinquency, substance abuse, depression, anxiety, and global impairment for children with ADHD (Mikami, 2010; Mrug et al., 2012). Research indicates that these effects may attenuate during later adolescence (Mrug et al., 2012). Although little research exists on the possible buffering effect of friendships for children with ADHD, one study found that having one or more friends protected against peer victimization among girls with and without ADHD (Cardoos & Hinshaw, 2011). In contrast, another study found that having a reciprocal friend did not protect children with ADHD from any long-term negative effects of peer rejection (Mrug et al., 2012).
The assessment of ADHD in children and adolescents requires a comprehensive evaluation comprised of multiple assessment methods and information from multiple informants, including the child’s caregiver, the child, and the child’s teacher or day-care provider. Evidence-based assessment places an emphasis on both evaluating symptom criteria for ADHD and assessing cross-situational impairments in functioning (e.g., disruptions in school, home, or social settings) related to ADHD symptoms (Pelham, Fabiano, & Massetti, 2005). Symptom rating scales, structured interviews, global impairment measures, and behavioral observations are considered evidence-based ADHD assessment methods (Pelham et al., 2005). Assessment of ADHD also requires ruling out other childhood behavioral or emotional disorders that can present with similar symptoms or co-occur with ADHD. A psychoeducational evaluation is also recommended to determine if learning problems or intellectual or developmental delays are present and require attention due to the high prevalence of these issues in this population.
The parent or caregiver interview is an important source of information regarding ADHD symptoms and child functioning. It is recommended to obtain information regarding frequency, severity, and duration of ADHD symptoms according to DSM criteria, and to gather contextual information regarding these symptoms in line with a functional analytic approach (Pliszka & AACAP Work Group on Quality Issues, 2007). In addition to ADHD symptoms, interviews should assess the child’s developmental, medical, and mental health history. Family functioning, including parent psychopathology, peer relations, and cultural background, also needs to be assessed, as these factors may influence the course of treatment and may indicate possible co-occurring disorders (Barkley, 2014d). Parent rating scales, including ADHD symptom rating scales and broadband rating scales, are also typically administered to gain additional information (Pliszka et al., 2007).
In addition to information from the child’s parent, obtaining teacher reports of ADHD symptoms and functioning in the school setting is an essential part of the assessment of ADHD. Teacher rating scales have a solid evidence base and can be used to obtain information about both child ADHD symptoms and global impairment in the school setting. Teachers provide valuable information about how children are behaving in the classroom compared to their same-age peers. Studies also support the use of structured classroom observations in the assessment process (DuPaul & Stoner, 2014). Although children and adolescents often do not provide accurate reports of their own ADHD symptoms (Sibley et al., 2012), interviewing older children and adolescents can be helpful to obtain information about possible co-occurring conduct and internalizing disorders (Pliszka et al., 2007). Self-report measures can also be useful in this respect, providing information about difficulties associated with ADHD, including problems with peer relationships.
A medical examination may be indicated if the child’s physical examination is out of date, if another medical condition may account for the symptoms, or if medication may be used to treat the disorder (Barkley, 2014d). If the child’s medical history is normal, medical laboratory and neurological testing are not necessary (Pliszka et al., 2007). In addition, laboratory measures of attention and impulsivity are not currently considered valid for diagnosing ADHD, predicting child functioning, or measuring treatment response outside the laboratory setting (e.g., Edwards et al., 2007).
Assessment of ADHD often involves not only diagnosis, but also treatment planning, and later, evaluating treatment outcomes. A comprehensive, evidence-based assessment of ADHD that includes data from multiple informants and uses multiple assessment methods will provide the necessary information to determine whether a child meets diagnostic criteria for ADHD and has the requisite cross-situational impairment needed to make the diagnosis. This information and additional reports and observations regarding co-occurring disorders and family functioning provide the foundation for treatment planning and evaluating later treatment outcomes.
Evidence-Based Psychosocial Interventions
ADHD is a chronic disorder that often calls for intervention and management throughout childhood and adolescence and into adulthood as well. ADHD treatment often aims to improve both ADHD symptoms and child functioning across multiple settings in which the child is impaired (i.e., at home, at school, with peers). The following section delineates psychosocial interventions available to treat ADHD in children and is based on several evidence-based reviews, including one by Evans, Owens, and Bunford (2014). This section is organized by the evidence level for each intervention, starting with interventions that demonstrate the most research support (Well-Established Treatments) and concluding with interventions where research demonstrates no beneficial effect (Treatments of Questionable Efficacy) (see Evans et al., 2014 for additional information).
Behavioral Parent Training (BPT)
Behavioral parent training (BPT) teaches parents how to manage their child’s behavior using operant conditioning and social learning principles. Maladaptive parenting practices are one of the strongest predictors of negative developmental outcomes for children with problem behaviors. Thus, BPT targets changing these parenting behaviors to improve child outcomes (Pelham, Wheeler, & Chronis, 1998). Parents are taught specific skills, including how to set up the environment in a way that will enhance the child’s ability to be successful (e.g., recognizing antecedents), rewarding prosocial behavior with positive attention/praise, planned ignoring of minor misbehaviors, giving effective commands, and utilizing nonphysical discipline techniques such as timeout and privilege removal (Chronis, Jones, & Raggi, 2006). The efficacy of BPT has been well established by numerous studies that support both group and individual BPT formats (Pelham & Fabiano, 2008; Evans et al., 2014). Studies demonstrate that BPT results in reductions of child problem behavior and improvements in observed negative parenting (Daley et al., 2014).
Behavioral Classroom Management (BCM)
Behavioral classroom management (BCM) consists of instructing teachers to use behavior modification strategies to address problematic child behavior in the school setting. Specific strategies taught include the use of positive attention, a Daily Report Card (DRC), effective commands, and point systems to manage classroom behavior (Chronis et al., 2006). The DRC involves setting specific, individualized behavioral goals in the classroom setting (e.g., keeping your hands to yourself) and rewarding the child for achieving the behavioral goals (Fabiano et al., 2010). Shaping is used to make the behavioral goals progressively more difficult until the child’s classroom behavior is within the developmentally normative range. A number of efficacy studies have demonstrated very large improvement in child classroom behavior resulting from BCM (Pelham & Fabiano, 2008; Evans et al., 2014), but these studies have been conducted only with children in elementary school. Therefore, the efficacy of BCM with adolescents is not known, warranting further research in this area.
Behavioral Peer Intervention (BPI)
Behavioral peer intervention (BPI) involves adult (e.g., paraprofessional counselors, parents) manipulation of environmental contingencies to improve the social functioning and peer relationships of children with ADHD (Evans et al., 2014). Impaired social functioning increases the risk for children with ADHD to exhibit negative developmental outcomes, and BPI directly addresses these social behaviors. The Summer Treatment Program (STP) provides intensive behavioral intervention in a recreational camp setting with other children over an eight-week period (Pelham et al., 2010). In the STP, paraprofessional counselors implement strategies that include a token or point system, effective commands, a DRC, and social skills training. Parent Friendship Coaching (PFC), in which parents work to increase appropriate social behavior through coaching children and manipulating contingencies in the social environment (Mikami et al., 2013), is another BPI. The efficacy of BPI in recreational settings (e.g., STP) and clinic settings (e.g., PFC) on multiple outcomes, including child behavior and social skills, has been established through several studies (Evans et al., 2014).
Combined Behavior Management Interventions
These interventions combine BPT, BCM, and/or BPI to treat children with ADHD and improve their functioning in a number of areas. In one study, Pfiffner and colleagues (2007) implemented a combined BPT and BCM intervention with a skills training group for children with ADHD-I and found significant improvements in inattentive symptoms, organization skills, and social skills compared to a control group. Overall, studies demonstrate that combining these efficacious treatments results in positive child outcomes and may improve functioning in certain domains better than any single behavior management intervention (Evans et al., 2014).
Combined Behavioral Interventions and Medication
Several studies have compared combined behavioral interventions and medication to stimulant medication alone, and others have also compared the two groups to behavior therapy. In the Multimodal Treatment Study for Children with ADHD (MTA Cooperative Group, 1999), a combination of BPI, BCM, and BPI was compared to (1) stimulant medication only, (2) combined behavioral interventions and stimulant medication, and (3) a community comparison control group. Results indicated that the combined behavioral management and stimulant medication group had better functional impairment outcomes in areas including social skills and parent-child relationships than with stimulant medication alone. Combined behavioral interventions and medication may also result in a lower dosage of medication (MTA Cooperative Group, 1999).
The optimal sequence of stimulant medication and behavior therapy to treat children with ADHD has recently been investigated. In a study by Pelham and colleagues (2016), children were randomized to either receive behavioral intervention or stimulant medication, and at a later time, children demonstrating insufficient response to the initial treatment were randomized a second time to either increase the intensity or dose of the initial intervention or begin the other treatment. The specific treatment protocol with the best response was for children who began with the behavioral intervention and then were given stimulant medication if they demonstrated insufficient response (Pelham et al., 2016). Overall, results indicate that children who received behavioral intervention initially demonstrated better overall outcomes than children who began with stimulant medication (Pelham et al., 2016).
Organizational Skills Training (OST)
Organizational skills training (OST) teaches children with ADHD strategies to improve their organizational skills, including organizational rules and how to track assignments (Evans et al., 2014). As reviewed herein, children with ADHD often have difficulty with EF, which affects organization skills, and OST directly addresses these children’s organizational difficulties with school materials. Two randomized controlled trials (RCTs) have been conducted on OST with children and early adolescents and demonstrated significant benefits in child organization, homework, and family conflict (Abikoff et al., 2013; Langberg, Epstein, Becker, Girio-Herrera, & Vaughn, 2012).
Probably Efficacious Treatments
Combined Training Interventions
The Challenging Horizons Program (CHP) is a school-based training intervention for adolescents with ADHD that targets organizational, social, and academic skills training (Evans, Schultz, DeMars, & Davis, 2011). Studies report benefits in a variety of areas, including school adjustment, classroom functioning, hyperactivity/impulsivity symptoms, and delinquency. This intervention has not yet been evaluated with an RCT conducted by an independent research group (Evans et al., 2014).
Possibly Efficacious Treatments
Neurofeedback (NF) Training
Neurofeedback (NF) training aims to teach children to control certain brain activity patterns to improve ADHD symptoms and functioning in multiple settings (Evans et al., 2014). For children with ADHD, two training protocols are usually implemented: (1) training of slow cortical potentials and (2) theta/beta training (Gevensleben et al., 2009). Most research published on NF training has not utilized randomized control design or subject blinding (Lofthouse et al., 2012). One methodologically rigorous RCT, conducted by Gevensleben and colleagues (2009), found significant improvements in both parent and teacher ratings of ADHD symptoms, but no improvements in child functioning in school, home, or peer settings.
Cognitive Training (CogT)
Cognitive training (CogT) utilizes home practice with computerized exercises to target deficits in cognitive flexibility, working memory, and behavioral inhibition. CogT views ADHD as an EF disorder and may work through altering brain regions and neural systems affected by ADHD (Rutledge et al., 2012). Results from RCTs have demonstrated child symptom improvement on parent rating scales but little to no improvement per teacher reporting (Evans et al., 2014). Generalization to nontrained tasks and improvement in academic functioning is also very limited (Chacko et al., 2013).
Treatments of Questionable Efficacy
Therapy provided individually to children, including play therapy, does not have research support for reducing ADHD symptoms and improving child functioning in the home and school settings. Although some research on play therapy for children with ADHD has demonstrated some improvements in child symptoms, none have shown improvement in impairment associated with ADHD relative to a comparison group (e.g., Ray, Schottelkorb, & Tsai, 2007).
Social Skills Training (SST)
Social skills training (SST) typically involves a clinician teaching children social skills in an office setting (either in an individual or group format), but in general, the social skills learned fail to generalize to social settings outside the clinic (Evans et al., 2014).
Several dietary interventions have been investigated to determine whether eliminating certain foods or increasing certain foods affects ADHD symptoms. A meta-analysis examining the effects of eliminating fatty acid supplementation and food coloring from the diet found modest improvements in ADHD symptoms but no improvement in children’s daily functioning (Sonuga-Barke et al., 2013). Another meta-analysis found that omega-3 can help to augment ADHD medication and that 8% of children demonstrate a relationship between ADHD symptoms and food coloring (Nigg, Lewis, Edinger, & Falk, 2012). Overall, although there is some research that supports the effect of certain dietary interventions on ADHD symptoms, there is no evidence that dietary interventions can improve the functioning of children with ADHD or have greater effects than the well-established treatments discussed previously.
Psychopharmacology and Medication Treatment
Stimulant medications (e.g., methylphenidate and amphetamine) are commonly prescribed for the treatment of ADHD in childhood and adolescence. Decades of research support the safety and effectiveness of stimulants in reducing symptoms of ADHD. The mechanisms by which stimulant medications relieve ADHD symptoms are not well understood, but researchers believe that stimulant medications help to improve dopamine levels in the brain (Durston, 2003). As previously discussed, ADHD symptoms are associated with the aberrant structure and function of numerous brain regions, notably brain regions that are dense with dopamine receptors (Tripp & Wickens, 2009). Inattentive symptoms are hypothesized to be due in part to hypodopaminergic states in the prefrontal cortices (Durston, 2003). On the other hand, hyperdopaminergic states in the striatum may result in hyperactivity (Durston, 2003).
The compounds found in stimulant medication include d,l-methylphenidate, d-methylphenidate, or d-amphetamine. These compounds act as endogenous catecholamines (Connor, 2014). Although both methylphenidates (e.g., Ritalin) and amphetamines (e.g., Adderall) affect the amount of dopamine available in the brain, the mechanisms by which they operate on synaptic dopamine differ. Methylphenidate is a dopamine reuptake inhibitor, and amphetamine inhibits the reuptake of dopamine and aids in the release of dopamine (Faraone & Buitelaar, 2010). Both drugs produce significant and robust reductive effects on ADHD symptoms (Faraone & Buitelaar, 2010). Although effective, stimulant medications carry the risk of (mostly minor) side effects, including loss of appetite, upset stomach, sleep disturbance, tachycardia, irritability, headaches, and increased psychosis and tics. Long-term side effects may include reduced height and weight gain (Faraone et al., 2008; Poulton et al., 2012). Studies are mixed with respect to which drug, methylphenidate or amphetamine, is associated with worse side effects (Faraone & Buitelaar, 2010). Notably, up to 30% of children who are prescribed stimulant medication do not tolerate or do not respond to the drug (Connor, 2014). If a second stimulant medication is prescribed, response rates increase to 80%–90% (Greenhill, Pliszka, & Dulcan, 2002; Pliszka et al., 2007).
Although stimulant medications are the first-line medication treatment, many nonstimulant drugs have been developed and may be effective alternatives for the treatment of ADHD. Atomoxetine (e.g., Strattera) is a norepinephrine reuptake inhibitor. In the United States, the Food and Drug Administration (FDA) approved the use of atomoxetine for the treatment of ADHD in children as young as age 6. Several meta-analyses comparing atomoxetine to methylphenidate found that both drugs significantly reduce core symptoms of ADHD, and that atomoxetine fares equally as well as methylphenidate in reducing ADHD symptoms in noninferiority analyses (Gibson, Bettinger, Patel, & Crismon, 2006; Hazell et al., 2011). More research is needed to better understand how these medications compare with respect to reducing impairment. Side effects of atomoxetine include decreased appetite, nausea, headaches, constipation, vomiting, insomnia, fatigue, and mood swings (Banaschewski, Roessner, Dittman, Santosh, & Rothenberger, 2004).
Guanfacine (e.g., Intuniv) and clonidine (e.g., Kapvay) are extended-release, alpha-2-adrenergic agonists that have been approved by the FDA for the treatment of ADHD in children 6 years of age and older. These drugs are thought to have effects on the prefrontal cortex. Extended-release, alpha-2-adrenergic agonists may be effective for the treatment of ADHD, but the treatment effects are not as great as those of stimulant medications (Banaschewski et al., 2004). Children presenting with both ADHD and aggression may benefit from the co-administration of stimulants and clonidine to reduce problematic behavior (Banaschewski et al., 2004). Clonidine has also been studied as an add-on medication therapy for children who do not respond to stimulant medication alone (Kollins et al., 2011). Common side effects of guanfacine and clonidine include drowsiness, depression, and sedation. In addition, clonidine carries with it cardiovascular risks, including conduction delays and slowed sinus rates (Banaschewski et al., 2004).
Several other drugs (e.g., bupropion and tricyclic antidepressants) have been studied and are utilized in the treatment of ADHD, but they have not been approved by the FDA (Banaschewski et al., 2004; Faraone, 2009).
Pharmacotherapy is used to treat inattention, hyperactivity, and impulsivity due to ADHD (Connor, 2014). However, pharmacotherapy shows reduced effects on the impairments associated with ADHD (Epstein et al., 2010). To improve functional impairment, it is important to reduce symptoms and develop skills within areas of impairment (i.e., academic or social) (Epstein et al., 2010). Because medication targets the reduction of symptoms and behavioral treatments aim to decrease impairment, as discussed previously, a multimodal treatment approach that combines medication and evidence-based behavioral treatments may best address the needs of children with ADHD (Epstein et al., 2010).
ADHD is a neurodevelopmental disorder linked to significant functional impairments throughout childhood and adolescence, and often into adulthood as well. Genetic and neuroimaging studies suggest strong biological underpinnings for the disorder, although many of these biological factors are likely influential only when they interact with specific environments. Environmental factors (e.g., family environment and sociodemographic factors) also contribute significantly to the developmental trajectories of children with ADHD. Fortunately, numerous evidence-based psychosocial (i.e., behavioral) interventions and medications exist to treat children with ADHD and improve their developmental trajectories. Although there is no “cure” for ADHD, treating the disorder with evidence-based approaches can ameliorate many of the impairments seen in academic, social, and family settings and reduce risk for co-occurring conditions.
This material is based upon work supported by the National Science Foundation Graduate Research Fellowship under Grant No. DGE1322106 awarded to the first author.
Abikoff, H. B., Gallagher, R., Wells, K., Murray, D. W., Huang, L., Lu, F., et al. (2013). Remediating organizational functioning in children with ADHD: Immediate and long-term effects from a randomized controlled trial. Journal of Consulting and Clinical Psychology, 81, 113–128.Find this resource:
Ackerman, P. T., Newton, J. O., McPherson, W. B., Jones, J. G., & Dykman, R. A. (1998). Prevalence of post traumatic stress disorder and other psychiatric diagnoses in three groups of abused children (sexual, physical, and both). Child Abuse & Neglect, 22(8), 759–774.Find this resource:
American Psychiatric Association. (1968). Diagnostic and statistical manual of mental disorders: DSM-II (2d ed.). Washington, DC: Author.Find this resource:
American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders: DSM-5™ (5th ed.). Arlington, VA: American Psychiatric Publishing.Find this resource:
Arcos-Burgos, M., Jain, M., Acosta, M. T., Shively, S., Stanescu, H., Wallis, D., et al. (2010). A common variant of the latrophilin 3 gene, LPHN3, confers susceptibility to ADHD and predicts effectiveness of stimulant medication. Molecular Psychiatry, 15, 1053–1066.Find this resource:
Banaschewski, T., Becker, K., Scherag, S., Franke, B., & Coghill, G. (2010). Molecular genetics of attention-deficit/hyperactivity disorder: An overview. European Child & Adolescent Psychiatry, 19, 237–257.Find this resource:
Banaschewski, T., Roessner, V., Dittman, R. W., Santosh, P. J., & Rothenberger, A. (2004). Non-stimulant medications in the treatment of ADHD. European Child & Adolescent Psychiatry, 13(1), 102–116.Find this resource:
Barkley, R. A. (1997). Behavioral inhibition, sustained attention, and executive functions: Constructing a unifying theory of ADHD. Psychological Bulletin, 121, 65–94.Find this resource:
Barkley, R. A. (2011). Barkley Deficits in Executive Functioning Scale (BDEFS). New York: Guilford Press.Find this resource:
Barkley, R. A. (2014a). History of ADHD. In R. A. Barkley (Ed.), Attention-deficit hyperactivity disorder: A handbook for diagnosis and treatment (4th ed., pp. 3–50). New York: Guilford Press.Find this resource:
Barkley, R. A. (2014b). Etiologies of ADHD. In R. A. Barkley (Ed.), Attention-deficit/hyperactivity disorder: A handbook for diagnosis and treatment (4th ed., pp. 356–390). New York: Guilford Press.Find this resource:
Barkley, R. A. (2014c). Emotion dysregulation is a core component of ADHD. In R. A. Barkley (Ed.), Attention-deficit/hyperactivity disorder: A handbook for diagnosis and treatment (4th ed., pp. 85–115). New York: Guilford Press.Find this resource:
Barkley, R. A. (2014d). Psychological assessment of children with ADHD. In R. A. Barkley (Ed.), Attention-deficit hyperactivity disorder: A handbook for diagnosis and treatment (4th ed., pp. 455–474). New York: Guilford Press.Find this resource:
Barkley, R. A., & Murphy, K. R. (2010). Deficient emotional self-regulation in adults with attention-deficit/hyperactivity disorder (ADHD): The relative contributions of emotional impulsiveness and ADHD symptoms to adaptive impairments in major life activities. Journal of ADHD & Related Disorders, 1(4), 5–28.Find this resource:
Barkley, R. A., & Murphy, K. R. (2011). The nature of executive function (EF) deficits in daily life activities in adults with ADHD and their relationship to performance on EF tests. Journal of Psychopathology and Behavioral Assessment, 33, 137–158.Find this resource:
Barkley, R. A., Murphy, K. R., & Fischer, M. (2008). Adult ADHD: What the science says. New York: Guilford Press.Find this resource:
Biederman, J., Faraone, S. V., Mick, E., Spencer, T., Wilens, T., Kiely, K., et al. (1995). High risk for attention deficit hyperactivity disorder among children of parents with childhood onset of the disorder: A pilot study. American Journal of Psychiatry, 152(3), 431–435.Find this resource:
Biederman, J., Faraone, S. V., & Monuteaux, M. C. (2002). Differential effect of environmental adversity by gender: Rutter’s index of adversity in a group of boys and girls with and without ADHD. American Journal of Psychiatry, 159(9), 1556–1562.Find this resource:
Biederman, J., Mick, E., Faraone, S. V., Braaten, E., Doyle, A., Spencer, T., et al. (2002). Influence of gender on attention deficit hyperactivity disorder in children referred to a psychiatric clinic. American Journal of Psychiatry, 159, 36–42.Find this resource:
Biederman, J., Monuteaux, M. C., Doyle, A. E., Seidman, L. J., Wilens, T. E., Ferrero, F., et al. (2004). Impact of executive function deficits and attention-deficit/hyperactivity disorder (ADHD) on academic outcomes in children. Journal of Consulting and Clinical Psychology, 72, 757–766.Find this resource:
Biederman, J., Petty, C. R., Clarke, A., Lomedico, A., & Faraone, S. V. (2011). Predictors of persistent ADHD: An 11-year follow-up study. Journal of Psychiatric Research, 45(2), 150–155.Find this resource:
Biederman, J., Petty, C. R., Monuteaux, M. C., Fried, R., Byrne, D., Mirto, T., et al. (2010). Adult psychiatric outcomes of girls with attention deficit hyperactivity disorder: 11-year follow-up in a longitudinal case-control study. American Journal of Psychiatry, 167(4), 409–417.Find this resource:
Biederman, J., Spencer, T., Lomedico, A., Day, H., Petty, C. R., & Faraone, S. V. (2012b). Deficient emotional self-regulation and pediatric attention deficit hyperactivity disorder: a family risk analysis. Psychological Medicine, 42, 639–646.Find this resource:
Biederman, J., Spencer, T. J., Petty, C., Hyder, L. L., O’Connor, K. B., Surman, C. B., et al. (2012a). Longitudinal course of deficient emotional self-regulation CBCL profile in youth with ADHD: Prospective controlled study. Neuropsychiatric Disease and Treatment, 8, 267–276.Find this resource:
Bruchmüller, K., Margraf, J., & Schneider, S. (2012). Is ADHD diagnosed in accord with diagnostic criteria? Overdiagnosis and influence of client gender on diagnosis. Journal of Consulting and Clinical Psychology, 80(1), 128.Find this resource:
Bunford, N., Evans, S. W., & Wymbs, F. (2015). ADHD and emotion dysregulation among children and adolescents. Clinical Child and Family Psychology Review, 18, 185–217.Find this resource:
Bussing, R., Zima, B. T., Gary, F. A., & Garvan, C. W. (2003). Barriers to detection, help-seeking, and service use for children with ADHD symptoms. Journal of Behavioral Health Services & Research, 30(2), 176–189.Find this resource:
Cardoos, S. L., & Hinshaw, S. P. (2011). Friendship as protection from peer victimization for girls with and without ADHD. Journal of Abnormal Child Psychology, 39(7), 1035–1045.Find this resource:
Chacko, A., Feirsen, N., Bedard, A. C., Marks, D., Uderman, J. Z., & Chimiklis, A. (2013). Cogmed Working Memory Training for youth with ADHD: A closer examination of efficacy utilizing evidence-based criteria. Journal of Clinical Child & Adolescent Psycholo-gy, 42(6), 769–783.Find this resource:
Chronis, A. M., Jones, H. A., & Raggi, V. L. (2006). Evidence-based psychosocial treatments for children and adolescents with attention-deficit/hyperactivity disorder. Clinical Psychology Review, 26(4), 486–502.Find this resource:
Chronis, A. M., Lahey, B. B., Pelham, W. E., Kipp, H. L., Baumann, B. L., & Lee, S. S. (2003). Psychopathology and substance abuse in parents of young children with attention-deficit/hyperactivity disorder. Journal of the American Academy of Child & Adolescent Psychiatry, 42(12), 1424–1432.Find this resource:
Chronis, A. M., Lahey, B. B., Pelham Jr., W. E., Williams, S. H., Baumann, B. L., Kipp, H., et al. (2007). Maternal depression and early positive parenting predict future conduct problems in young children with attention-deficit/hyperactivity disorder. Developmental Psychology, 43(1), 70–82.Find this resource:
Chronis-Tuscano, A., Molina, B. G., Pelham, W. E., Applegate, B., Dahlke, A., Overmyer, M., et al. (2010). Very early predictors of adolescent depression and suicide attempts in children with attention-deficit/hyperactivity disorder. Archives of General Psychiatry, 67, 1044–1051.Find this resource:
Connor, D. F. (2014). Stimulant and non-stimulant medications for childhood ADHD. In R. A. Barkley (Ed.), Attention-deficit/hyperactivity disorder: A handbook for diagnosis and treatment (4th ed., pp. 666–685). New York: Guilford Press.Find this resource:
Counts, C. A., Nigg, J. T., Stawicki, J. A., Rappley, M. D., & Von Eye, A. (2005). Family adversity in DSM-IV ADHD combined and inattentive subtypes and associated disruptive behavior problems. Journal of the American Academy of Child & Adolescent Psychiatry, 44(7), 690–698.Find this resource:
Daley, D., Van der Oord, S., Ferrin, M., Danckaerts, M., Doepfner, M., Cortese, S., et al. (2014). Behavioral interventions in attention-deficit/hyperactivity disorder: A meta-analysis of randomized controlled trials across multiple outcome domains. Journal of the American Academy of Child & Adolescent Psychiatry, 53(8), 835–847.Find this resource:
DuPaul, G. J., & Langberg, J. M. (2014). Educational impairments in children with ADHD. In R. A. Barkley (Ed.), Attention-deficit/hyperactivity disorder: A handbook for diagnosis and treatment (4th ed., pp. 169–190). New York: Guilford Press.Find this resource:
DuPaul, G. J., & Stoner, G. (2014). ADHD in the schools: Assessment and intervention strategies. New York: Guilford Publications.Find this resource:
Durston, S. (2003). A review of the biological bases of ADHD: What have we learned from imaging studies?Mental Retardation and Developmental Disabilities Research Reviews, 9, 184–195.Find this resource:
Edwards, M. C., Gardner, E. S., Chelonis, J. J., Schulz, E. G., Flake, R. A., & Diaz, P. F. (2007). Estimates of the validity and utility of the Conners’ Continuous Performance Test in the assessment of inattentive and/or hyperactive-impulsive behaviors in children. Journal of Abnormal Child Psychology, 35(3), 393–404.Find this resource:
Eisenberg, N., & Spinrad, T. L. (2004). Emotion-related regulation: Sharpening the definition. Child Development, 75, 334–339.Find this resource:
Epstein, J. N., Langberg, J. M., Lichtenstein, P. K., Altaye, M., Brinkman, W. B., House, K., et al. (2010). Attention-deficit/hyperactivity disorder outcomes for children treated in community-based pediatric settings. Archives of Pediatrics & Adolescent Medicine, 164, 160–165.Find this resource:
Evans, S. W., Owens, J. S., & Bunford, N. (2014). Evidence-based psychosocial treatments for children and adolescents with attention-deficit/hyperactivity disorder. Journal of Clinical Child & Adolescent Psychology, 43(4), 527–551.Find this resource:
Evans, S. W., Schultz, B. K., DeMars, C. E., & Davis, H. (2011). Effectiveness of the Challenging Horizons After-School Program for young adolescents with ADHD. Behavior Therapy, 42, 462–474.Find this resource:
Fabiano, G. A., Vujnovic, R. K., Pelham, W. E., Waschbusch, D. A., Massetti, G. M., Pariseau, M. E., et al. (2010). Enhancing the effectiveness of special education programming for children with attention deficit hyperactivity disorder using a daily report card. School Psychology Review, 39(2), 219–239.Find this resource:
Faraone, S. V. (2009). Using meta-analysis to compare the efficacy of medications for attention-deficit/hyperactivity disorder in youths. Pharmacy and Therapeutics, 34(12), 678–694.Find this resource:
Faraone, S. V., Biederman, J., Morley, C. P., & Spencer, T. J. (2008). Effect of stimulants on height and weight: A review of the literature. Journal of the American Academy of Child & Adolescent Psychiatry, 47, 994–1009.Find this resource:
Faraone, S. V., & Buitelaar, J. (2010). Comparing the efficacy of stimulants for ADHD in children and adolescents using meta-analysis. European Child & Adolescent Psychiatry, 19, 353–364.Find this resource:
Faraone, S. V., Perlis, R. H., Doyle, A. E., Smoller, J. W., Goralnick, J. J., Holmgren, M. A., et al. (2005). Molecular genetics of attention-deficit/hyperactivity disorder. Biological Psychiatry, 57, 1313–1323.Find this resource:
Fried, R., Hirshfeld-Becker, D., Petty, C., Batchelder, H., & Biederman, J. (2015). How informative is the CANTAB to assess executive functioning in children with ADHD? A controlled study. Journal of Attention Disorders, 19, 468–475.Find this resource:
Gevensleben, H., Holl, B., Albrecht, B., Schlamp, D., Kratz, O., Studer, P., et al. (2009). Distinct EEG effects related to neurofeedback training in children with ADHD: A randomized controlled trial. International Journal of Psychophysiology, 74(2), 149–157.Find this resource:
Gibson, A. P., Bettinger, T. L., Patel, N. C., & Crismon, M. L. (2006). Atomoxetine versus stimulants for treatment of attention deficit/hyperactivity disorder. Annals of Pharmacotherapy, 40, 1134–1142.Find this resource:
Gizer, I. R., Ficks, C., & Waldman, I. D. (2009). Candidate gene studies of ADHD: A meta-analytic review. Human Genetics, 126, 51–90.Find this resource:
Greenhill, L. L., Pliszka, S., & Dulcan, M. K. (2002). Practice parameter for the use of stimulant medications in the treatment of children, adolescents, and adults. Journal of the American Academy of Child & Adolescent Psychiatry, 41, 26–49.Find this resource:
Harold, G. T., Leve, L. D., Barrett, D., Elam, K., Neiderhiser, J. M., Natsuaki, M. N., et al. (2013). Biological and rearing mother influences on child ADHD symptoms: Revisiting the developmental interface between nature and nurture. Journal of Child Psychology and Psychiatry, 54(10), 1038–1046.Find this resource:
Harvey, E. A., Metcalfe, L. A., Herbert, S. D., & Fanton, J. H. (2011). The role of family experiences and ADHD in the early development of oppositional defiant disorder. Journal of Consulting and Clinical Psychology, 79(6), 784–795.Find this resource:
Hazell, P. L., Kohn, M. R., Dickson, R., Walton, R. J., Granger, R. E., & van Wyk, G. W. (2011). Core ADHD symptom improvement with atomoxetine versus methylphenidate: A direct comparison meta-analysis. Journal of Attention Disorders, 15, 674–683.Find this resource:
Hervey, A. S., Epstein, J. N., & Curry, J. F. (2004). Neuropsychology of adults with attention-deficit/hyperactivity disorder: A meta-analytic review. Neuropsychology, 18, 485–503.Find this resource:
Hinshaw, S. P., Owens, E. B., Zalecki, C., Huggins, S. P., Montenegro-Nevado, A. J., Schrodek, E., et al. (2012). Prospective follow-up of girls with attention-deficit/hyperactivity disorder into early adulthood: Continuing impairment includes elevated risk for suicide attempts and self-injury. Journal of Consulting and Clinical Psychology, 80(6), 1041–1051.Find this resource:
Johnston, C., & Chronis-Tuscano, A. M. (2014). Families and ADHD. In R. A. Barkley (Ed.), Attention-deficit hyperactivity disorder: A handbook for diagnosis and treatment (4th ed., pp. 191–209). New York: Guilford Press.Find this resource:
Johnston, C., Mash, E. J., Miller, N., & Ninowski, J. E. (2012). Parenting in adults with attention-deficit/hyperactivity disorder (ADHD). Clinical Psychology Review, 32(4), 215–228.Find this resource:
Kollins, S. H., Jain, R., Brams, M., Segal, S., Findling, R. L., Wigal, S. B., et al. (2011). Clonidine extended-release tablets as add-on therapy to psychostimulants in children and adolescents with ADHD. Pediatrics, 127, e1406–e1413.Find this resource:
Lahey, B. B., Lee, S. S., Sibley, M. H., Applegate, B., Molina, B. S., & Pelham, W. E. (2016). Predictors of adolescent outcomes among 4–6-year-old children with attention-deficit/hyperactivity disorder. Journal of Abnormal Psychology, 125(2), 168–181.Find this resource:
Lahey, B. B., Pelham, W. E., Loney, J., Lee, S. S., & Willcutt, E. (2005). Instability of the DSM-IV subtypes of ADHD from preschool through elementary school. Archives of General Psychiatry, 62, 896–902.Find this resource:
Lahey, B. B., Pelham, W. E., Stein, M. A., Loney, J., Trapani, C., Nugent, K., et al. (1998). Validity of DSM-IV attention-deficit/hyperactivity disorder for younger children. Journal of the American Academy of Child & Adolescent Psychiatry, 37, 695–702.Find this resource:
Lambek, R., Tannock, R., Dalsgaard, S., Trillingsgaard, A., Damm, D., & Thomsen, P. H. (2011). Executive dysfunction in school-age children with ADHD. Journal of Attention Disorders, 15, 646–655.Find this resource:
Langberg, J. M., Epstein, J. N., Becker, S. P., Girio-Herrera, E., & Vaughn, A. J. (2012). Evaluation of the Homework, Organization, and Planning Skills (HOPS) intervention for middle school students with ADHD as implemented by school mental health providers. School Psychology Review, 41, 342–364.Find this resource:
Linnet, K. M., Dalsgaard, S., Obel, C., Wisborg, K., Henriksen, T. B., Rodriguez, A., et al. (2003). Maternal lifestyle factors in pregnancy risk of attention deficit hyperactivity disorder and associated behaviors: Review of the current evidence. American Journal of Psychiatry, 160(6), 1028–1040.Find this resource:
Lofthouse, N., Arnold, L. E., & Hurt, E. (2012). Current status of neurofeedback for attention-deficit/hyperactivity disorder. Journal of Attention Disorders, 14(5), 536–542.Find this resource:
Loo, S. K., Humphrey, L. A., Tapio, T., Moilanen, I. K., McGough, J. J., McCracken, J. T., et al. (2007). Executive functioning among Finnish adolescents with attention-deficit/hyperactivity disorder. Journal of the American Academy of Child & Adolescent Psychiatry, 46, 1594–1604.Find this resource:
Martinez, A. F., Muenke, M., & Arcos-Burgos, M. (2010). From the black widow spider to human behavior: Latrophilins, a relatively unknown class of G protein-coupled receptors, are implicated in psychiatric disorders. American Journal of Medical Genetics Part B: Neuropsychiatric Genetics, 156, 1–10.Find this resource:
Massetti, G. M., Lahey, B. B., Pelham, W. E., Loney, J., Ehrhardt, A., Lee, S. S., et al. (2008). Academic achievement over 8 years among children who met modified criteria for attention-deficit/hyperactivity disorder at 4–6 years of age. Journal of Abnormal Child Psychology, 36(3), 399–410.Find this resource:
McCrory, E., De Brito, S. A., & Viding, E. (2012). The link between child abuse and psychopathology: A review of neurobiological and genetic research. Journal of the Royal Society of Medicine, 105(4), 151–156.Find this resource:
McQuade, J. D., & Hoza, B. (2014). Peer relationships of children with ADHD. In R. A. Barkley (Ed.), Attention-deficit hyperactivity disorder: A handbook for diagnosis and treatment (4th ed., pp. 210–222). New York: Guilford Press.Find this resource:
Mikami, A. Y. (2010). The importance of friendship for youth with attention-deficit/hyperactivity disorder. Clinical Child and Family Psychology Review, 13(2), 181–198.Find this resource:
Mikami, A. Y., Griggs, M. S., Lerner, M. D., Emeh, C. C., Reuland, M. M., Jack, A., et al. (2013). A randomized trial of a classroom intervention to increase peers’ social inclusion of children with attention-deficit/hyperactivity disorder. Journal of Consulting and Clinical Psychology, 81(1), 100–112.Find this resource:
Mikami, A. Y., & Hinshaw, S. P. (2006). Resilient adolescent adjustment among girls: Buffers of childhood peer rejection and attention-deficit/hyperactivity disorder. Journal of Abnormal Child Psychology, 34(6), 823–837.Find this resource:
Mikami, A. Y., & Pfiffner, L. J. (2008). Sibling relationships among children with ADHD. Journal of Attention Disorders, 11(4), 482–492.Find this resource:
Mikami, A. Y., Ransone, M. L., & Calhoun, C. D. (2011). Influence of anxiety on the social functioning of children with and without ADHD. Journal of Attention Disorders, 15, 473–484.Find this resource:
Miller, M., Nevado-Montenegro, A. J., & Hinshaw, S. P. (2012). Childhood executive function continues to predict outcomes in young adult females with and without childhood-diagnosed ADHD. Journal of Abnormal Child Psychology, 40, 657–668.Find this resource:
Miller, T. W., Nigg, J. T., & Miller, R. L. (2009). Attention deficit hyperactivity disorder in African American children: What can be concluded from the past ten years?Clinical Psychology Review, 29(1), 77–86.Find this resource:
Millichap, J. G. (2008). Etiologic classification of attention-deficit/hyperactivity disorder. Pediatrics, 121(2), 358–365.Find this resource:
Molina, B. S., Pelham Jr., W. E., Cheong, J., Marshal, M. P., Gnagy, E. M., & Curran, P. J. (2012). Childhood attention-deficit/hyperactivity disorder (ADHD) and growth in adolescent alcohol use: The roles of functional impairments, ADHD symptom persistence, and parental knowledge. Journal of Abnormal Psychology, 121(4), 922–935.Find this resource:
Morgan, P. L., Hillemeier, M. M., Farkas, G., & Maczuga, S. (2014). Racial/ethnic disparities in ADHD diagnosis by kindergarten entry. Journal of Child Psychology and Psychiatry, 55(8), 905–913.Find this resource:
Morgan, P. L., Staff, J., Hillemeier, M. M., Farkas, G., & Maczuga, S. (2013). Racial and ethnic disparities in ADHD diagnosis from kindergarten to eighth grade. Pediatrics, 132(1), 85–93.Find this resource:
Mrug, S., Molina, B. S., Hoza, B., Gerdes, A. C., Hinshaw, S. P., Hechtman, L., et al. (2012). Peer rejection and friendships in children with attention-deficit/hyperactivity disorder: contributions to long-term outcomes. Journal of Abnormal Child Psychology, 40(6), 1013–1026.Find this resource:
MTA Cooperative Group. (1999). A 14-month randomized clinical trial of treatment strategies for attention-deficit/hyperactivity disorder. Archives of General Psychiatry, 56(12), 1073–1086.Find this resource:
Musser, E. D., Backs, R. W., Schmitt, C. F., Ablow, J. C., Measelle, J. R., & Nigg, J. T. (2011). Emotion regulation via the autonomic nervous system in children with attention-deficit/hyperactivity disorder (ADHD). Journal of Abnormal Child Psychology, 39, 841–852.Find this resource:
Musser, E. D., Galloway-Long, H. S., Frick, P. J., & Nigg, J. T. (2013). Emotion regulation and heterogeneity in attention-deficit/hyperactivity disorder. Journal of the American Academy of Child and Adolescent Psychiatry, 52, 163–171.Find this resource:
Nigg, J. T., & Casey, B. J. (2005). An integrative theory of attention-deficit/hyperactivity disorder based on the cognitive and affective neurosciences. Development and Psychopathology, 17, 785–806.Find this resource:
Nigg, J. T., Lewis, K., Edinger, T., & Falk, M. (2012). Meta-analysis of attention-deficit/hyperactivity disorder or attention-deficit/hyperactivity disorder symptoms, restriction diet, and synthetic food color additives. Journal of the American Academy of Child & Adolescent Psychiatry, 51(1), 86–97.Find this resource:
Nigg, J., Nikolas, M., & Burt, S. A. (2010). Measured gene-by-environment interaction in relation to attention-deficit/hyperactivity disorder. Journal of the American Academy of Child & Adolescent Psychiatry, 49, 863–873.Find this resource:
Nigg, J. T., Willcutt, E. G., Doyle, A. E., & Sonuga-Barke, E. J. S. (2005). Causal heterogeneity in attention-deficit/hyperactivity disorder: Do we need neuropsychologically impaired subtypes?Biological Psychiatry, 57, 1224–1230.Find this resource:
Ohan, J. L., & Visser, T. W. (2009). Why is there a gender gap in children presenting for attention deficit/hyperactivity disorder services?Journal of Clinical Child and Adolescent Psychology, 38(5), 650–660.Find this resource:
Ouyang, L., Fang, X., Mercy, J., Perou, R., & Grosse, S. D. (2008). Attention-deficit/hyperactivity disorder symptoms and child maltreatment: A population-based study. Journal of Pediatrics, 153(6), 851–856.Find this resource:
Owens, E., Cardoos, S., & Hinshaw, S. (2014). Developmental progression and gender differences among individuals with ADHD. In R. A. Barkley (Ed.), Attention-deficit hyperactivity disorder: A handbook for diagnosis and treatment (pp. 223–255). New York: Guilford Press.Find this resource:
Pelham Jr., W. E., & Fabiano, G. A. (2008). Evidence-based psychosocial treatments for attention-deficit/hyperactivity disorder. Journal of Clinical Child & Adolescent Psychology, 37(1), 184–214.Find this resource:
Pelham Jr., W. E., Fabiano, G. A., & Massetti, G. M. (2005). Evidence-based assessment of attention deficit hyperactivity disorder in children and adolescents. Journal of Clinical Child and Adolescent Psychology, 34(3), 449–476.Find this resource:
Pelham, W. E, Gnagy, E. M., Greiner, A. R., Waschbusch, D. A., Fabiano, G. A., & Burrows-MacLean, L. (2010). Summer treatment programs for attention deficit/hyperactivity disorder. In A. E. Kazdin & J. R. Weisz (Eds.), Evidence-based psychotherapies for children and adolescents (2d ed., pp. 277–292). New York: Guilford Press.Find this resource:
Pelham, W. E., Fabiano, G. A., Waxmonsky, J. G., Greiner, A. R., Gnagy, E. M., Pelham, W. E., et al. (2016). Treatment sequencing for childhood ADHD: A multiple-randomization study of adaptive medication and behavioral interventions. Journal of Clinical Child & Adolescent Psychology, 45(4), 396–415.Find this resource:
Pelham, W. E., Wheeler, T., & Chronis, A. (1998). Empirically supported psychosocial treatments for ADHD. Journal of Clinical Child Psychology, 27, 190–205.Find this resource:
Pfiffner, L. J., Mikami, A. Y., Huang-Pollock, C., Easterlin, B., Zalecki, C., & McBurnett, K. (2007). A randomized, controlled trial of integrated home-school behavioral treatment for ADHD, predominantly inattentive type. Journal of the American Academy of Child & Adolescent Psychiatry, 46(8), 1041–1050.Find this resource:
Pliszka, S., & AACAP Work Group on Quality Issues. (2007). Practice parameter for the assessment and treatment of children and adolescents with attention-deficit/hyperactivity disorder. Journal of the American Academy of Child and Adolescent Psychiatry, 46, 894–921.Find this resource:
Pliszka, S. R. (2014). Comorbid psychiatric disorders in children with ADHD. In R. A. Barkley (Ed.), Attention-deficit/hyperactivity disorder: A handbook for diagnosis and treatment (4th ed., pp. 140–168). New York: Guilford Press.Find this resource:
Posner, J., Rauh, V., Gruber, A., Gat, I., Wang, Z., & Peterson, B. (2013). Dissociable attentional and affective circuits in medication-naïve children with attention-deficit/hyperactivity disorder. Psychiatry Research: Neuroimaging, 213, 24–30.Find this resource:
Poulton, A., Briody, J., McCorquodale, T., Melzer, E., Herrmann, M., Baur, L. A., et al. (2012). Weight loss on stimulant medication: How does it affect body composition and bone metabolism? A prospective longitudinal study. International Journal of Pediatric Endocrinology, 30, 1–9.Find this resource:
Pressman, L. J., Loo, S. K., Carpenter, E. M., Asarnow, J. R., Lynn, D., McCracken, J. T., et al. (2006). Relationship of family environment and parental psychiatric diagnosis to impairment in ADHD. Journal of the American Academy of Child & Adolescent Psychiatry, 45(3), 346–354.Find this resource:
Ray, D. C., Schottelkorb, A., & Tsai, M. H. (2007). Play therapy with children exhibiting symptoms of attention deficit hyperactivity disorder. International Journal of Play Therapy, 16(2), 95–111.Find this resource:
Rutledge, K. J., van den Bos, W., McClure, S. M., & Schweitzer, J. B. (2012). Training cognition in ADHD: Current findings, borrowed concepts, and future directions. Neurotherapeutics, 9(3), 542–558.Find this resource:
Schermerhorn, A. C., Cummings, E. M., DeCarlo, C. A., & Davies, P. T. (2007). Children’s influence in the marital relationship. Journal of Family Psychology, 21(2), 259–269.Find this resource:
Seidman, L. J. (2006). Neuropsychological functioning in people with ADHD across the lifespan. Clinical Psychology Review, 26, 466–485.Find this resource:
Seymour, K., Chronis-Tuscano, A., Halldorsdottir, T., Stupica, B., Owens, K., & Sacks, T. (2012). Emotion regulation mediates the relationship between ADHD and depressive symptoms in youth. Journal of Abnormal Child Psychology, 40, 595–606.Find this resource:
Seymour, K. E., Chronis-Tuscano, A. M., Iwamoto, D. K., Kurdziel, G., & MacPherson, L. (2014). Emotion regulation mediates the association between ADHD and depressive symptoms in a community sample of youth. Journal of Abnormal Child Psychology, 42, 611–621.Find this resource:
Shaw, P., Malek, M., Watson, B., Greenstein, D., de Rossi, P., & Sharp, W. (2013). Trajectories of cerebral cortical development in childhood and adolescence and adult attention-deficit/hyperactivity disorder. Biological Psychiatry, 74, 599–606.Find this resource:
Shaw, P., Stringaris, A., Nigg, J., & Leibenluft, E. (2014). Emotion dysregulation in attention deficit hyperactivity disorder. American Journal of Psychiatry, 171, 276–293.Find this resource:
Sibley, M. H., Pelham, W. J., Molina, B. G., Gnagy, E. M., Waschbusch, D. A., Garefino, A. C., et al. (2012). Diagnosing ADHD in adolescence. Journal of Consulting and Clinical Psychology, 80(1), 139–150.Find this resource:
Sjöwall, D., Roth, L., Lindqvist, S., & Thorell, L. B. (2013). Multiple deficits in ADHD: Executive dysfunction, delay aversion, reaction time variability, and emotional deficits. Journal of Child Psychology and Psychiatry, 54, 619–627.Find this resource:
Skoglund, C., Chen, Q., D’Onofrio, B. M., Lichtenstein, P., & Larsson, H. (2014). Familial confounding of the association between maternal smoking during pregnancy and ADHD in offspring. Journal of Child Psychology and Psychiatry, 55(1), 61–68.Find this resource:
Sonuga-Barke, E. J., Brandeis, D., Cortese, S., Daley, D., Ferrin, M., Holtmann, M., et al. (2013). Nonpharmacological interventions for ADHD: Systematic review and meta-analyses of randomized controlled trials of dietary and psychological treatments. American Journal of Psychiatry, 170(3), 275–289.Find this resource:
Spira, E. G., & Fischel, J. E. (2005). The impact of preschool inattention, hyperactivity, and impulsivity on social and academic development: A review. Journal of Child Psychology and Psychiatry, 46(7), 755–773.Find this resource:
Surman, C. B. H., Biederman, J., Spencer, T., Yorks, D., Miller, C. A., Petty, C. R., et al. (2011). Deficient emotional self-regulation and adult attention deficit hyperactivity disorder: A family risk analysis. American Journal of Psychiatry, 168, 617–623.Find this resource:
Thapar, A., & Rutter, M. (2009). Do prenatal risk factors cause psychiatric disorder? Be wary of causal claims. British Journal of Psychiatry, 195(2), 100–101.Find this resource:
Theule, J., Wiener, J., Tannock, R., & Jenkins, J. M. (2013). Parenting stress in families of children with ADHD: A meta-analysis. Journal of Emotional and Behavioral Disorders, 21(1), 3–17.Find this resource:
Thompson, R. A. (1994). Emotion regulation: A theme in search of definition. Monographs of the Society for Research in Child Development, 59, 25–52.Find this resource:
Thorell, L. B. (2007). Do delay aversion and executive function deficits make distinct contributions to the functional impact of ADHD symptoms? A study of early academic skill deficits. Journal of Child Psychology and Psychiatry, 48, 1061–1070.Find this resource:
Tripp, G., & Wickens, J. R. (2009). Neurobiology of ADHD. Neuropharmacology, 57, 579–589.Find this resource:
Tseng, W. L., & Gau, S. S. F. (2013). Executive function as a mediator in the link between attention-deficit/hyperactivity disorder and social problems. Journal of Child Psychology and Psychiatry, 54, 996–1004.Find this resource:
Turic, D., Swanson, J., & Sonuga-Barke, E. (2010). DRD4 and DAT1 in ADHD: Functional neurobiology to pharmacogenetics. Pharmacogenomics and Personalized Medicine, 3, 61–78.Find this resource:
van Ewijk, H., Heslenfeld, D. J., Zwiers, M. P., Faraone, S. V., Luman, M., Hartman, C. A., et al. (2014). Different mechanisms of white matter abnormalities in attention-deficit/hyperactivity disorder: A diffusion tensor imaging study. Journal of the American Academy of Child & Adolescent Psychiatry, 53, 790–799.e3.Find this resource:
Wehmeier, P. M., Schacht, A., & Barkley, R. A. (2010). Social and emotional impairment in children and adolescents with ADHD and the impact on quality of life. Journal of Adolescent Health, 46, 209–217.Find this resource:
Wiener, J., & Mak, M. (2009). Peer victimization in children with Attention‐Deficit/Hyperactivity Disorder. Psychology in the Schools, 46(2), 116–131.Find this resource:
Willcutt, E. G. (2012). The prevalence of DSM-IV attention-deficit/hyperactivity disorder: A meta-analytic review. Neurotherapeutics, 9, 490–499.Find this resource:
Willcutt, E. G., Doyle, A. E., Nigg, J. T., Faraone, S. V., & Pennington, B. F. (2005). Validity of the executive theory of attention-deficit/hyperactivity disorder: A meta-analytic review. Biological Psychiatry, 57, 1336–1346.Find this resource:
Wymbs, B. T., Pelham Jr., W. E., Molina, B. S., Gnagy, E. M., Wilson, T. K., & Greenhouse, J. B. (2008). Rate and predictors of divorce among parents of youths with ADHD. Journal of Consulting and Clinical Psychology, 76(5), 735–744.Find this resource: