Attention-Deficit Research Paper

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Myth or Mental Disorder?

Attention-deficit/hyperactivity disorder (ADHD) is the current term in the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV-TR; American Psychiatric Association [APA], 2000;) to classify individuals exhibiting persistent, pervasive, developmentally inconsistent, and maladaptive levels of inattention and/or hyperactivity and impulsivity. ADHD is one of the most common referral concerns to health care providers and one of the most common childhood psychiatric disorders (Barkley, 2006). Evidence of ADHD symptomatology persisting beyond childhood has resulted in a dramatic increase in adult referrals and clinical/empirical literature involving this population. Literally hundreds of articles are published each year addressing a vast array of issues pertaining to this intriguing and sometimes controversial disorder.

ADHD: History And Current Diagnostic Conceptualization

The documented historical roots of ADHD date back over 150 years with the descriptions provided by Heinrich Hoffman and George Still, the latter a physician who focused on overactivity arising from deficits in “volitional inhibition” and “moral regulation of behavior.” Through the 1960s, various terms (e.g., “organic driveness,” “minimal brain dysfunction”) were applied to implicate brain damage as the underlying cause of behavioral symptoms now considered to be consistent with ADHD and oppositional defiant disorder (Barkley, 2006).

As research progressed through the 1970s, the work of Douglas (1983) had a profound influence on the disorder being renamed from hyperkinetic reaction of childhood in DSM-II (APA, 1968) to attention deficit disorder with hyperactivity (ADD+H) or without hyperactivity (ADD-H) in DSM-III (APA, 1980). Research on ADD subsequently grew astronomically, including attempts to validate the subtypes of ADD by demonstrating that the patterns of impairment for each subtype were distinct, for which support was minimal at the time of DSM-III. Despite these attempts, DSM-III-R (APA, 1987) reflected a reemergence of placing equal emphasis on hyperactivity, impulsiveness, and inattention as the central characteristics of the disorder, now termed ADHD. Authors of the DSM-III-R subdued the nonhyperactive subtype to a vaguely defined category, Undifferentiated ADD.

With empirical efforts in force during the 1980s, researchers placed considerable energy on developing more research-informed diagnostic criteria accompanied by improved clarity, specificity, and effective operational definitions (Barkley, 2006). Not only did these efforts positively influence the nature of DSM-III-R, they also set the stage for dramatic developments in the areas of social-ecological considerations (e.g., child-environment interactions); theoretical advances; a detailed consideration of the nature, etiology, and course unique to ADHD; advances in the tools of assessment; treatments for ADHD; and increased public awareness (Barkley, 2006). These efforts enabled professionals to view ADHD as a chronic, developmental disorder with a marked heritability accompanied by a pattern of adverse academic and psychosocial outcomes.

However, these gains, along with the tremendous growth of parent support/political action groups (who succeeded in having ADHD included as an educational disability, and therefore eligible for special services through public schools), were dampened by what many view as sensationalized, misinformed, distorted, anecdotal accounts of the dangers of medication therapy and claims of the “myth” of ADHD. The effects of these campaigns continue today. In an attempt to address misunderstandings, the National Institutes of Health sponsored a consensus conference comprising several “nonadvocate, non-federal” experts (National Institutes of Health Consensus Development Conference Statement, 2000). Efforts to inform the professional and lay community; clarify the nature, prevalence, developmental course, and neurological and genetic bases; and develop and evaluate effective treatments for ADHD continue to consume clinical and research agendas.

Diagnostic Criteria

Our current diagnostic criteria reflect decades of effort to incorporate findings from research and clinical experience. Barkley (2006) described the criteria as “some of the most rigorous and most empirically derived criteria ever available in the history of ADHD” (p. 84). Large-scale field trials for DSM-IV resulted in the specification of two major core symptom domains: inattention and hyperactivity/ impulsivity (Lahey et al., 1994). DSM-IV requires that six or more of the nine symptoms of inattention and/or hyperactivity/impulsivity be present for a diagnosis. These symptoms must be more severe, persistent, and pervasive in individuals with ADHD compared to others at a comparable developmental level. Furthermore, impairment from the symptoms must be present in at least two develop-mentally normative settings, the core symptoms that cause impairment must have been present before age 7, and the symptoms must not exclusively occur during the course of other specified disorders or be better accounted for by another mental disorder (APA, 2000). Kamphaus and Campbell (2006) noted,

Methodology of symptom counting and derivation of cut scores associated with the presence of functional impairment, with more emphasis on the number than type of symptoms, represents the influence of dimensional, quantitative, and psychometric methods on the popular psychiatric nosology. (p. 22)

Symptoms and Subtypes

Symptoms of inattention associated with ADHD include difficulty sustaining attention and attending to detail, dis-traction, forgetfulness, organizational difficulties, and problems listening. Symptoms of hyperactive behavior include fidgeting, excess motor activity, loudness, and excessive talking. Symptoms of impulsivity include difficulty waiting for turn, blurting out, and interruptive behavior. Along with its core symptoms, ADHD is often associated with cognitive, behavioral, emotional, physical, interpersonal, and academic difficulties that frequently are the impetus for clinical referral (Barkley, 2006; Pelham, Fabiano, & Massetti, 2005). Derived from the two symptom domains, the DSM-IV differentiates those with ADHD into three different subtypes: predominantly inattentive type (ADHD-I), predominantly hyperactive-impulsive type (ADHD-HI), and combined type (ADHD-C). The latter group includes symptoms of both inattention and hyperactivity/impulsivity.

Inattention and impulsivity are heterogeneous constructs, which partly contributes to inconsistencies in the literature. In order to substantiate the diagnostic existence of a subtype, one must determine that groups within each subtype share common but distinctive characteristics—symptoms, etiology, problem severity, or outcome (Mash & Wolfe, 2005). With regard to inattention, the primary attention deficit in ADHD is difficulty maintaining persistence over time (i.e., sustained attention; Douglas, 1983) and is often associated with the following functional impairments: shyness, withdrawal, lack of assertiveness, peer rejection, underachievement in math, and enrollment in special education for a learning disability. Individuals diagnosed with ADHD-I, relative to those with ADHD-C or ADHD-HI, appear to have distinct associated symptoms, family histories, outcomes, and treatment responses (Barkley, 2006). Adding to the complexity is the informed speculation that a subset of individuals diagnosed with ADHD-I show sluggish cognitive tempo and behavioral passivity (e.g., described as drowsy, daydreamy, spacey, in a fog, or easily confused), perhaps making them distinct from others diagnosed with ADHD-I (Carlson & Mann, 2002; McBurnett, Pfiffner, & Frick, 2001). Thus, in the current diagnostic system, the ADHD-I group is quite diverse, is distinct from the other subtypes (Milich, Balentine, & Lynam, 2001), and may itself contain a distinct subgroup.

The primary impairment in hyperactivity/impulsivity is significant difficulty with voluntarily inhibiting an ongoing or dominant response and is frequently associated with accidental injuries, lack of self-control, aggressiveness, and disruptiveness. Relative to those diagnosed with ADHD-I, individuals with ADHD-HI and ADHD-C tend to have significant problems with inhibiting behavior and behavioral persistence (Nigg, Blaskey, Huang-Pollack, & Rappley, 2002). Individuals diagnosed with ADHD-C tend to be referred more often and tend to have a higher rate of coexisting conduct problems.

We know the least about the least prevalent subtype, ADHD-HI, which includes primarily preschool children. Preliminary evidence suggests that these children may, in later years, no longer meet criteria for ADHD or mostly shift to ADHD-C (Lahey, Pelham, Loney, Lee, & Willcutt, 2005). A more detailed presentation of subtype distinctions can be found in Barkley (2006).

Classification Caveats

The DSM, as a classification system and the diagnostic criteria for all mental disorders, undergoes continual review and revision. We provide salient factors related to DSM-IV generally and ADHD specifically that are important to keep in mind (Barkley, 2006; Mash & Wolfe, 2005):

The DSM-IV applies the same criteria for ADHD across all ages and genders, both in terms of specific symptoms and cutoff criteria. This application poses a problem with the developmental sensitivity of the applied criteria to individuals younger or older than those included in the original field trials (ages 4-16). Subsequent research supports consideration of adjusting the criteria to be more developmentally sensitive.
The DSM-IV follows a categorical model of classification (diagnosis either applies or does not, given the number of documented symptoms), which necessitates an arbitrary diagnostic cutoff. Therefore, meeting criteria for ADHD may fluctuate over time, while serious impairment stemming from core ADHD symptoms may be present continuously. Research supports the dimensional view of ADHD (symptoms occur on a continuum, with all individuals possessing them to a certain degree), consistent with the developmental psychopathology and multivariate-statistical approach to classification (Achenbach & Edelbrock, 1983; Hudziak et al., 1998; Hudziak, Wadsworth, Heath, & Achenbach, 1999; Levy, Hay, McStephen, Wood, & Waldman, 1997).
Empirical support is lacking for requiring symptom onset before age seven. Its utility may depend on the subtype under consideration because symptoms of inattention show a later age of onset than those of hyperactivity and impulsivity.
Empirical support is lacking for the duration requirement of six months for symptom presence. This criterion partially guards against the diagnosis being given in the case of transient developmental changes, although the duration poses problems for preschoolers, whose symptoms often remit. A longer duration may improve detecting true cases of the disorder.
The requirement of symptom pervasiveness may present confounds between setting and individuals providing symptom reports. Current criteria require that ADHD symptoms occur in more than one setting. However, it is often the case that informants disagree in their ratings or show modest levels of agreement (Achenbach, McConaughy, & Howell, 1987). This matter may be due to real differences in situational demands, individual differences among raters, or both. Although this criterion guards against applying the diagnosis to highly context-specific scenarios, research does not support sole use of one informant over the other. A more appropriate strategy may be to blend informant reports, rather than requiring agreement (Crystal, Ostrander, Chen, & August, 2001). Considering the utility of all informants’ perspectives provides a richer clinical picture of child-environment factors and reminds us that diagnosis is a mean to an end (e.g., the relief of suffering), not the end in itself (Barkley, 2006).

The previous section outlined a brief historical perspective and articulation of the current diagnostic criteria for ADHD, and caveats that serve as future research agendas. In the next section and in the context of ADHD, we discuss the frameworks for defining “disorder.” Such frameworks have served the clinical field well in addressing critics who may be quick to discount consistent group differences, patterns of concurrent and subsequent maladjustment, findings of potential etiological factors, and positive results of intervention strategies.

Evidence For The Validity Of ADHD

To advocate for the validity of ADHD (or any other disorder), a framework is needed to demonstrate that (a) clinicians and researchers utilize specific criteria for establishing a mental disorder as valid and (b) ADHD meets the criteria of the validation framework. Two frameworks for establishing a disorder’s validity have dominated the field of psychology, one proposed by Robins and Guze (1970) and another offered by Wakefield (1992, 1999). Some clinical researchers have explicitly applied these frameworks to argue for the validity of ADHD (Antshel, Phillips, Gordon, Barkley, & Faraone, 2006; Barkley, 2006; Faraone, 2005; Nigg, 2006), whereas others have implicitly applied variants of these frameworks (Lahey & Willcutt, 2002). In this section, we apply both Robins and Guze’s and Wakefield’s frameworks explicitly to ADHD in order to demonstrate the validity of ADHD as a mental disorder.

Robins and Guze’s Validation Criteria

Robins and Guze’s (1970) framework for the validation of a mental disorder emerged during the revolution in psychology that discarded theory-bound diagnoses (DSM-II) in favor of empirically based diagnoses (DSM-III), which entail a neurobiological account of a disorder’s conceptualization. Thus, Robins and Guze’s framework dually assumes that all evidence is empirically derived and that some of this empirical evidence examines the neurobiological basis for a disorder. Robins and Guze’s criteria assert that diagnostic validity may be established when a disorder (a) includes well-defined clinical correlates (in addition to symptoms), (b) displays a characteristic course and outcome, (c) has neurobiological correlates as demonstrated in laboratory studies, (d) shows evidence of heritability, (e) can be delimited from other disorders, and (f) displays a characteristic response to treatment.

Clinical Correlates

Robins and Guze (1970) posited that a valid disorder not only must be identified reliably through a consistent constellation of symptoms, but also must be associated with a consistent pattern of clinically significant impairments. The reliability of ADHD assessment is quite high when using structured diagnostic interviews (typically involving parents) and parent and teacher diagnostic rating scales (Faraone, 2005; Lahey & Willcutt, 2002). For example, standard measures of reliability for these ADHD assessment instruments, such as Cohen’s kappa (i.e., inter-rater reliability) and Cronbach’s alpha (i.e., internal consistency), typically exceed 0.80 (Faraone, 2005).

The fact that the ADHD symptom set “hangs together” well and that different raters typically arrive at the same diagnostic conclusion provides considerable evidence for the internal validity of ADHD. Numerous studies support the current two-factor internal structure and further bolster the internal validity of ADHD (e.g., Lahey & Willcutt, 2002). Multiple research teams have shown that the DSM-IV two-dimensional structure of inattention and hyperactivity/impulsivity offers the best account for the pattern of symptom covariation compared to the DSM-III three-dimensional structure (i.e., inattention, hyperactivity, and impulsivity) or the DSM-III-R single-dimension structure.

A valid disorder must also demonstrate a reliable association between its symptom pattern and clinically meaningful impairments. Of the various lines of evidence presented in this research-paper within Robins and Guze’s validation framework, the strength of support is likely highest for the breadth and depth of impairment experienced by children and adolescents with ADHD. Compared to peers without ADHD, youths with ADHD demonstrate significant impairment in multiple domains (Barkley, 2006; Faraone, 2005, Hinshaw, 2002; Lahey & Willcutt, 2002). For example, ADHD is associated with impairments in academic achievement and school performance (e.g., academic underachievement, increased need for special education, greater rates of grade retention, suspension, and dropout), family interactions and home life (e.g., decreased parent harmony, increased parenting distress, negative parent-child interactions), peer relationships (e.g., deficits in social skill performance, overall peer rejection with evidence for differential peer rejection for ADHD-C and ADHD-H vs. peer neglect for ADHD-I), self-esteem and self-image (e.g., lower self-esteem, paradoxically coupled with inflated self-perceptions and expectations possibly due to deficits in social information processing), occurrence of accidental injuries (e.g., higher rates of broken limbs, head injuries, accidental poisonings, and hospitalizations), and adaptive functioning (e.g., decreased independence, ability for self-care), among other domains (Barkley, 2006; Faraone, 2005, Hinshaw, 2002; Lahey & Willcutt, 2002).

Clearly, children and adolescents with ADHD experience significant impairments in crucial areas of life, thereby illustrating the concurrent validity and supporting the external validity of ADHD.

In addition to the significant impairments associated with ADHD, comorbidity is the rule rather than the exception for individuals with ADHD (Faraone, 2005; Hinshaw, 2002; Lahey & Willcutt, 2002; Milberger, Biederman, Faraone, Murphy, & Tsuang, 1995; Sroufe, 1997). Accordingly, ADHD comorbid with other disorders (e.g., oppositional defiant disorder, depression) typically results in greater impairment compared to ADHD alone. Importantly, comorbidity does not account for the myriad domains of impairment associated with ADHD, such that research has controlled for comorbidity and found the continued significant association between ADHD and clinically meaningful impairments (Hinshaw, 2002).

Course and Outcome

According to Robins and Guze (1970), the characteristic course and outcome of a disorder allows greater confidence to be placed in the validity of the disorder. Characteristic course and outcome may be defined as individuals continuing to meet diagnostic criteria, demonstrating significant clinical symptoms, and experiencing impairment over time. Considerable evidence supports the claim of persistent impairment over time.

Longitudinal studies show that ADHD in childhood persists into adolescence and adulthood, although these findings are mixed and require interpretation (Barkley, 2002; Faraone, 2005; Lahey & Willcutt, 2002). Levels of hyperactivity decline and attention problems predominate (but improve over time) as ADHD in childhood transitions to adolescence and adulthood. Despite this developmental change in ADHD symptomatology, overall findings from longitudinal studies indicate that 70 to 80 percent of children with ADHD continue to show significant levels of ADHD symptoms in adolescence, with 30 to 80 percent of children with ADHD continuing to experience impairment or meet current diagnostic criteria for ADHD in adolescence (Barkley, 2006). Longitudinal study of ADHD into adulthood demonstrates an even wider range of persistence in terms of endorsing symptoms, experiencing impairment, and meeting full diagnostic criteria, with rates ranging from 4 to 90 percent (Barkley, 2006; Faraone, 2005).

However, careful interpretation is warranted. Nearly all longitudinal studies of ADHD have included significant methodological limitations (Barkley, 2002). For example, all longitudinal studies initially assessed children with ADHD using pre-DSM-IV criteria, and most changed diagnostic criteria (e.g., from DSM-III to DSM-III-R) as well as information sources (e.g., using parent report in childhood and adolescence but self-report in adulthood) during follow-up assessments in adolescence and adulthood.

Employing different diagnostic criteria, even for the same disorder, makes it difficult to determine accurately the true persistence of ADHD. It also is well established that individuals with ADHD underestimate their level of impairment compared to parents and teachers, and thus make poor informants as to the true level of symptomatology, impairment, and diagnostic persistence (Barkley, Fischer, Smallish, & Fletcher, 2002). Moreover, the wording of the DSM-IV diagnostic criteria is geared for children ages 5 to 12 (e.g., getting up from seat, failure to complete schoolwork) rather than adults. Thus, the diagnostic criteria are not developmentally appropriate for adults, such that individuals with childhood ADHD may not actually outgrow the disorder as adults but, rather, may outgrow the diagnostic criteria.

Clinical researchers have taken into account these methodological limitations of the existing longitudinal studies and found that ADHD symptoms persist and continue to cause significant life impairments for about 60 percent of adults diagnosed with ADHD in childhood (Barkley, 2006; Faraone, 2005; Lahey & Willcutt, 2002). In fact, the variety and degree of impairments observed in adult ADHD largely mirror those seen in childhood and adolescent ADHD (Barkley, 2006). For example, compared to individuals without ADHD, adults with ADHD are at greater risk for lower educational attainment, occupational underachievement, deficits in neuropsychological functioning (e.g., measures of inhibition, working memory), driving accidents and traffic violations, contraction of a sexually transmitted disease, deficits in adaptive functioning, substance abuse, antisocial and criminal activities, and comorbid diagnoses (e.g., conduct problems, antisocial personality disorder, depression, anxiety).

In summary, substantial evidence documents ADHD’s predicted course and outcome, providing evidence for the validity of ADHD as a chronic disorder. ADHD is a life span developmental disorder that persists into adulthood in the majority of childhood cases and, similar to its presentation in childhood and adolescence, carries considerable risk for significant life impairments.

Laboratory Studies

Robins and Guze (1970) proposed that an important criterion for validating a mental disorder is the demonstration of reliable laboratory findings that distinguish individuals with the disorder and reflect the disorder’s neurobiological underpinnings. Robins and Guze acknowledged that goldstandard (i.e., providing diagnostic confirmation) laboratory tests do not exist for most mental disorders. However, significant research in the areas of neuropsychology and neuroimaging has elucidated key neurobiological correlates of ADHD.

Neuropsychological research in the last decade has greatly influenced the shift in conceptualization of ADHD from a disorder of attentional processing to a disorder of self-regulation—the effortful and automatic mechanisms that allow behavioral adaptation to the changing environment (Nigg, 2005). Neuropsychological studies demonstrate that individuals with ADHD exhibit deficits in executive functioning (e.g., response inhibition, vigilance, working memory, planning) compared to those without ADHD (Hervey, Epstein, & Curry, 2004; Nigg, 2005; Willcutt, Doyle, Nigg, Faraone, & Pennington, 2005). Executive functioning is likely the best-developed arena of ADHD neuropsychological research (Willcutt et al., 2005). Accordingly, a current and influential theory of ADHD concerns deficits in executive functioning (Barkley, 2006). However, despite executive functioning deficits observed at the group level, moderate group differences and lack of universality of executive functioning deficits at the individual level indicate that executive functioning is neither a necessary nor a sufficient cause of all ADHD cases. In fact, parsing out the presence or absence of these deficits has been suggested as an important step in clarifying etiological models for ADHD (Nigg, 2006).

Recent research has also shed light on other potentially important neuropsychological domains related to ADHD (Nigg, 2005). For example, ADHD is associated with arousal deficits, illustrated by poor initial performance on a novel task or failure to maintain performance (i.e., vigilance) on an extended-time task. ADHD is also associated with motivation deficits, such that individuals display poor ability to delay reinforcement, leading to impulsive behavior to obtain proximal rewards.

Given ADHD’s association with deficits in executive functioning, much interest has been given to neuroimaging the brain region most associated with these deficits, the prefrontal cortex. In addition, the success of psychostimulant medications for treating ADHD and their known effects in prefrontal cortex has bolstered interest in this brain region. Accordingly, significant structural neuroimaging (e.g., magnetic resonance imaging, positron emission tomography, and computerized tomography) research in children and adolescents with ADHD has revealed a decreased volume in prefrontal cortex compared to youths without ADHD (Seidman, Valera, & Makris, 2005). However, neuroimaging studies have found that ADHD is associated with decreases in total cerebral volume as well as in other brain regions such as the caudate, palladium, corpus callosum, and cerebellum, indicating that ADHD is associated with more widespread brain differences than previously thought (Seidman et al., 2005). However, these results pertain only to children and adolescents with ADHD, as many neuroimaging studies exist for youths with ADHD compared to far fewer involving adults with ADHD.

Neuropsychology and neuroimaging are promising avenues for helping to understand ADHD, but clearly more research is needed. Nevertheless, laboratory evidence provides considerable support toward satisfying Robins and Guze’s (1970) validation criterion for distinguishing individuals with ADHD and reflecting its neurobiological underpinnings.

Heritability

Considerable evidence from family, twin, and adoption studies, and more recent molecular genetic research, substantiates Robins and Guze’s (1970) view that a valid disorder must be heritable. The rationale of family studies is that, if there is a genetic contribution for a given disorder, relatives of individuals with the disorder should be at a higher risk for having the disorder. Indeed, research shows this notion to be the case for ADHD. Parents and siblings of children with ADHD have a two- to eightfold increase in risk for the disorder (Faraone, 2005; Faraone & Doyle, 2001). One estimate places the risk of ADHD for siblings of children with ADHD at 37 percent, and if a parent has ADHD, the risk for his or her children is 57 percent (Barkley, 2006). Consistent with the genetic influence of ADHD, second-degree relatives have a lower risk compared to first-degree relatives (Faraone & Doyle, 2001).

Family studies support the genetic foundation for a disorder, but social learning or other environmental factors cannot be ruled out as causal influences for transmitting ADHD (see Nigg, 2006). Therefore, twin and adoption studies must be used to separate genetic and environmental influences. To do so, twin studies compare the heritability of ADHD between identical (monozygotic, or MZ, sharing all their genes) and fraternal (dizygotic, or DZ, sharing half their genes) twins, assuming that the twins are reared together and thus experience the same shared environment (e.g., socioeconomic status, child-rearing practices, family nutrition). Given this difference in genetic contributions with the similarity in environmental influences, the finding that ADHD occurs more often in MZ than DZ twins would support the genetic influence of ADHD. Results from twin studies support this conclusion, as concordance for ADHD in MZ twins has ranged from 67 to 100 percent, compared to 0 to 29 percent for DZ twins (Barkley, 2006), resulting in an average heritability of 80 percent for ADHD symptoms (Barkley, 2006; Faraone et al., 2005). Additionally, twin studies show that the shared environment plays a negligible role in the causation and expression of ADHD, which is why researchers and clinicians place little emphasis on environmental or social causes of ADHD (Barkley, 2006). Instead, focus is placed on genetics and environmental factors that are specific and unique (nonshared) to an individual with ADHD.

Adoption studies provide another avenue for untangling genetic versus environmental contributions to a disorder. Parents confer risk for a disorder to their biological children through both genetic and environmental means, whereas parents of adopted children confer risk through only environmental means. Higher rates of a disorder in biological compared to adoptive (nonbiological) relatives would provide evidence for a primarily genetic rather than an environmental etiology. Consistent with twin studies of ADHD, two adoption studies indicated higher rates of hyperactivity and associated disorders in biological parents and relatives compared to adoptive parents and relatives of children with hyperactivity (Barkley, 2006; Faraone & Doyle, 2001). Biological relatives of nonadopted children with ADHD also have higher rates of ADHD (18 percent) compared to both adoptive relatives of adopted children with ADHD (6 percent) and biological relatives of nonadopted children without ADHD (3 percent; Barkley, 2006; Faraone & Doyle, 2001).

Given the extensive support from family, twin, and adoption studies for the heritability of ADHD, research has also found fruitful beginnings for the molecular genetic basis of ADHD. Research groups have conducted few genome-wide scans, which have not produced converging results (Faraone et al., 2005). In contrast, research teams (for a review, see Faraone et al., 2005) have conducted many candidate gene studies—using either a case-control (comparing frequencies of alternative gene forms [alleles] between individuals with and without ADHD) or a family-based (comparing alleles that parents transmit and do not transmit to their children with ADHD) design—that have examined eight specific genes of interest. Importantly,seven of the eight genes (i.e., DRD4, DRD5, DAT, DBH, 5-HTT, HTR1B, SNAP-25) show statistically significant associations to ADHD, indicating that the genetic contribution to ADHD is quite complex (Faraone et al., 2005). Thus, family, twin, adoption, and molecular genetic studies provide substantial evidence for the heritability of ADHD.

Delimitation From Other Disorders

Comorbidity is the rule rather than the exception for all mental disorders, including ADHD. Having one mental disorder increases the risk of having one or more other mental disorders. However, Robins and Guze (1970) understood that for a mental disorder to be considered valid, its clinical features and associated impairments could not be accounted for by another disorder. The occurrence of comorbidity does not invalidate one of the co-occurring disorders, although this validation criterion requires that the diagnosis of one disorder is not an artifact due to overlapping diagnostic criteria of another disorder.

To address this concern, Milberger et al. (1995) examined the influence of symptom overlap on the diagnoses of ADHD and disorders that are frequently comorbid: major depression, bipolar disorder, and generalized anxiety disorder. The study included three groups: clinically referred children and adolescents, the nonreferred parents of these youths, and clinically referred adults with ADHD. Milberger et al. diagnosed the groups using a full DSM diagnostic algorithm, and then rediagnosed each person by subtracting the overlapping symptoms from the diagnostic algorithm. For all three groups, the majority of individuals diagnosed with ADHD and comorbid major depression, bipolar disorder, or generalized anxiety disorder continued to meet criteria for ADHD when overlapping symptoms were subtracted. An average of 79 percent, 56 percent, and 75 percent of individuals maintained their respective diagnosis of major depression, bipolar disorder, and generalized anxiety disorder when overlapping symptoms were removed. These findings show that ADHD is not an artifact of symptom overlap from comorbid disorders, and also that the comorbid disorders are not an artifact of overlapping ADHD symptoms.

In addition to Milberger et al. (1995), clinical researchers have made significant efforts to demonstrate that other factors do not explain the findings reported in previous sections of this chapter (Barkley, 2002; Hinshaw, 2002; Lahey & Willcutt, 2002). For example, clinical researchers have controlled for and thus ruled out a variety of factors (e.g., comorbidity, intellectual functioning, academic achievement, parent psychopathology, family dysfunction) as being possible explanations for the multiple domains of impairment, characteristic course and outcome, neurobiological correlates, and heritability associated with ADHD. In brief, ADHD can be delimited from its frequent comorbid conditions, and a host of factors have been ruled out as causes of ADHD’s clinical features and impairments.

Characteristic Response to Treatment

Given that the eventual goal in assigning a diagnosis is to provide effective treatment, Robins and Guze (1970) understood treatment response to be an important criterion for determining the validity of a disorder. However, various interventions may be effective at treating several different disorders, such that treatment response cannot decisively distinguish disorders. Therefore, in determining the validity of a disorder, treatment response cannot be the sole criterion but remains a valuable piece of converging evidence.

Extensive evidence exists for the effective treatment of ADHD using pharmacological, psychosocial, and combined approaches (Barkley, 2006; Chronis, Jones, & Raggi, 2006). The majority of the following results apply to children age 12 and under. Stimulant medication (e.g., amphetamine, methylphenidate) is first-line treatment and is effective for approximately 70 percent of children with ADHD at reducing symptoms of hyperactivity, impulsivity, and inattention (Barkley, 2006; Chronis et al., 2006; MTA Cooperative Group, 1999). Stimulant medication has been shown to reduce negative social behaviors (e.g., aggression, inappropriate peer interactions), negative parent-child interactions, and classroom disruption as well as increase compliance, on-task behavior, and academic productivity.

First-line psychosocial interventions for ADHD involve behavior modification—namely behavioral parent training and behavioral classroom management—and have also garnered significant empirical support. Similar to pharmacotherapy, behavior modification is effective at treating about 70 percent of children to reduce ADHD symptoms (Chronis et al., 2006). Other psychosocial treatments such as academic interventions (e.g., task and instructional modifications, peer tutoring, study strategies) and peer interventions (e.g., social skills training, summer treatment programs) have also gained support, and ongoing research shows them to be promising interventions (Chronis et al., 2006).

Combined behavioral-pharmacological treatment is the most common form of intervention for children with ADHD (Barkley, 2006; Chronis et al., 2006). Although results for combined treatment are generally equivalent to pharmacotherapy for reducing ADHD symptoms, combined treatment shows significantly better outcomes compared to medication alone for addressing impairments associated with ADHD (e.g., reduction in oppositional/aggressive symptoms, internalizing symptoms, and harsh and ineffective parenting; increase in parent-child relations, teacher-rated social skills, and reading achievement; Chronis et al., 2006; MTA Cooperative Group, 1999). A likely reason for the expanded and enhanced treatment scope of the combined approach is that, in contrast to medications alone, combined treatment offers active techniques for parents and children to use in addressing the challenges of ADHD. That is, “pills alone do not teach skills,” but the combined approach may reduce ADHD symptom via pharmacotherapy and alleviate ADHD sequelae via behavior modification.

The evidence base for treatment of adolescents and adults with ADHD is lacking, largely due to a lack of research with these populations (Barkley, 2006; Chronis et al., 2006). Preliminary evidence shows that pharmacotherapy is effective for treating ADHD symptoms in adolescents and adults, although much work remains to adapt psychosocial treatments that are effective for children with ADHD for use in these later developmental periods (Barkley, 2006; Chronis et al., 2006). In brief, research evidence provides substantial support for the robust treatment effectiveness for children with ADHD and emerging support for the effective treatment of ADHD in adolescence and adulthood, which in effect supports the validation criterion of characteristic treatment response for ADHD.

Wakefield’s Validation Criteria

If Robins and Guze’s (1970) validation framework has provided a compelling rationale for establishing a mental disorder due to its comprehensive criteria, then Wakefield’s validation framework has exerted wide influence on the classification of mental disorders due to its eloquent parsimony. Wakefield (1992, 1999) advocated that a disorder is valid if it demonstrates “harmful dysfunction” in an individual. Dysfunction is a scientific (factually objective) term that refers to the failure of a mental mechanism to perform a natural function that evolution has selected for its survival value. The harmful component is a value (socially subjective) term referring to the significant harm to an individual (e.g., impaired major life activities, mortality) that is caused by the dysfunction. Applying Wakefield’s validation framework to ADHD, the substantial evidence for deficits in self-regulation and executive functioning associated with ADHD satisfies the criterion for a failure of a mental mechanism that has evolutionary value. Thus, self-regulation and executive functioning abilities have important survival value because they help individuals direct all aspects of their behavior (e.g., navigating social interactions, acquiring and managing resources, avoiding danger), and individuals with ADHD have demonstrated deficits in these domains. Deficits in self-regulation and executive functioning lead to a host of major life impairments, which satisfies the criterion for the dysfunction conferring harm to the individual. In short, ADHD confers a harmful dysfunction to individuals affected by this disorder and thus meets Wakefield’s standard for validity as a mental disorder.

Addressing The “Myth” Of ADHD

Decades of research have focused on understanding the construct of ADHD, defining its core symptoms, elucidating causal factors, and establishing effective treatment practices. This continued focus perhaps reflects ongoing controversies along several dimensions crucial to our understanding of ADHD. However, serious empirical considerations of numerous aspects of ADHD may be warranted given the notion that diagnostic categories are social constructions (Bandura, 1969), and thus are prone to reification with serious consequences. ADHD is not well understood by the general public, perhaps because of sensationalized media attention and misconceptions fostered by groups relying on destructive propaganda (Barkley, 2006). Indeed, confusion exists among professional circles as well. Consensus statements and their responses provide good examples of our current state of knowledge, an articulation of needed research agendas, and fiery exchanges fueled by ADHD (Barkley et al., 2002; Barkley et al., 2004; Jensen & Cooper, 2002; National Institutes of Health Consensus Development Conference Statement, 1999; Timimi & Taylor, 2004; Timimi et al., 2004). This section summarizes some of the primary issues that relate to questioning the validity of ADHD and its treatment.

Issue 1: ADHD and the Range of Normal Behavior; Environmental Contributions

Carey (2002) suggested that ADHD is a form of inherited temperamental traits for which there is no demarcation between normality and abnormality. Carey argued that high activity, impulsiveness, and inattention are not clearly distinguishable from normal temperamental variations. Reflecting concerns over the categorical model of psychiatric classification, he noted difficulties arising from DSM’s use of cutpoints to define abnormality, particularly in light of research to suggest that ADHD is best conceived as a continuous function. Carey advocated for considering temperament theory in the DSM system:

[A]lthough pathology in the environment, child or both can be responsible for malfunction in the child, there are occasions when the pathogenic influence is to be found primarily in the dissonant interaction between a normal child and a normal but incompatible environment.. .[Thus,] what appears to matter for the generation of dysfunction in the child is not the number of normal yet challenging temperament traits but, rather, the ‘goodness of fit’ between any number of potentially aversive traits and the particular requirements of the environment. (pp. 3-6)

Carey also stated that many studies of ADHD are based on self-referred or self-selected subjects, an approach that fails to appreciate the frequency with which these traits occur in normal individuals. Treatment, therefore, would focus on resolving the “misfit” between the individual’s temperament and environmental demands or addressing the interaction between genetic predisposition and social learning phenomenon (Conners & Jensen, 2002). Carey also noted children’s low adaptability as an important predisposing factor of ADHD.

The preceding critique raises many important and relevant issues, such as debating the utility of a categorical classification system, the use of cutpoints, and gene-by-environment interactions. Noting the need for additional research on temperament and ADHD, some acknowledge the utility of the above argument. Indeed, Nigg and colleagues (see Nigg, 2006) discussed findings that may serve to stimulate this line of research—both in terms of defining temperament characteristics among individuals with ADHD and viewing heritability as a liability to, rather than a determinant of, a disorder—thus advocating for efforts to increase our understanding of gene-by-environment interactions and correlations. At a more fundamental level, though, we must remember that ADHD is accompanied by serious immediate and long-term consequences. Jensen and colleagues (Conners & Jensen, 2002; Jensen & Cooper, 2002) offered the analogy of benign essential hypertension or elevated blood pressure, noting that it is the negative medical sequelae, based on group statistics, that “medicalize” this problem. With ADHD, current evidence of impairment, as well as serious long-term consequences, compels professionals to diagnose and treat.

With regard to ADHD being a dimension or category, Barkley (2006) cited that the development of the DSM-IV criteria (Lahey et al., 1994) used both models. He also pointed out,

The DSM-IV (as well as preceding editions) emphasized the use of items from empirically-established rating scales, which are dimensional;
Symptom lists and cutoffs were evaluated along a threshold of interrater agreement, severity, and functional impairment;
Professional organizations formally recommend the use of standardized dimensional measures to assess deviancy from normative standards;
Diagnostic correspondence between individuals scoring high on dimensional measures and structured diagnostic interviews (which apply DSM-IV criteria) is high. (p. 96)

Thus, the dimensional approach “seems most consistent with the available evidence, whereas the categorical approach remains one of convenience, parsimony, and tradition…dimensions can be carved into categories when the purpose of decision making necessitates dichotomous choices” (Barkley, 2006, p. 96).

Issue 2: Current ADHD Diagnostic Criteria Lack Specificity

It is certainly the case that symptoms of hyperactivity, impulsivity, and inattention are common to other psychiatric conditions besides ADHD. Decisional challenges arise when forming clinical and comparison groups for clinical research. Does the researcher recruit individuals representing commonly occurring comorbid patterns, or ones that show “pure” though somewhat atypical symptom patterns from an epidemiological standpoint? Intriguing theoretical and etiological models (see Barkley, 2006; Nigg, 2006) may help to clarify the intrinsic or core symptoms, but they are at various stages of elucidation and validation. There are likely several etiological pathways, which will make it difficult to determine if ADHD is best conceptualized as “one disorder, a disorder of several types, or several different disorders” (Conners & Jensen, 2002, p. P1-1). We will likely see evidence-based consideration given to further diagnostic subtyping in subsequent diagnostic classification systems and/or refined delineation of more homogeneous research samples, which will allow for clarification of the nature and treatment of ADHD.

Issue 3: Support for ADHD as a Neurodevelopmental Disorder Is Premature; the Pattern of Genetic Heritability Is “Open to Question”

Carey (2002) and others (e.g., Timimi et al., 2004) commented that much of the published literature assumes that ADHD arises from abnormal brain function, neuro-imaging results are overinterpreted and inconsistent, and genetic research is too preliminary to substantiate any definitive conclusions. Carey cited some lines of research that conflict with the presumed neurological link, including the nonspecific nature of brain insults; the lack of a consistent structural, functional, or chemical neurological marker for ADHD; and dangers equating differences with dysfunction.

A review of the genetic and pathophysiological literature related to ADHD is prohibitive here, particularly given the volume of research generated in a short period of time. In responding to Timimi et al. (2004), Barkley (2004) stated that ADHD and its symptoms are “among the most genetically influenced psychiatric conditions across multiple studies in multiple countries” (see also Levy & Hay, 2001). Yet, Jensen and Cooper (2002) outline the dauntingly complex task ahead of us:

Unless we . . . understand that genes might work quite differently in different kinds of environments, we run the risk of underestimating the role of environmental factors that might turn genes on and off, inadvertently cutting off opportunities to understand how some ADHD traits might, in fact, emerge as a function of environmental contexts, whether as a function of chemical environmental agents or of psychosocial factors. (p. A-5)

The field is without a clear pathophysiological marker of ADHD, and differences in function do not necessarily reflect evidence of internal dysfunction. However, as our instruments improve and allow us to define function more specifically via, for example, measures of executive function (see Nigg, 2006), our knowledge is likely to improve. Timimi et al. (2004) assumed that a disorder cannot exist without a specific medical diagnostic test. In response, Barkley (2004) noted that the absence of such tests does not negate the existence of a disorder; applying such a standard would invalidate dozens of well-established psychological and medical disorders.

Issue 4: Diagnostic Questionnaires for ADHD Are Subjective and Impressionistic

Consistent with its atheoretical orientation, the DSM-IV does not specify the methods by which an ADHD diagnosis should be established. Furthermore, the field is without a diagnostic “gold standard,” although professional organizations such as the American Academy of Child and Adolescent Psychiatry (1997) and the American Academy of Pediatrics (2000) provided valuable evidence-based assessment practice guidelines. There is a lack of convergence among different scales/procedures used to establish the diagnosis. Terms such as “talks too much,” “messy work,” “often,” and “very much” are deemed highly impressionistic and subjective. An assumption of objectivity is created by the application of a rating scale. Furthermore, the perceived lack of a highly reliable measure stimulates the development of other unvalidated measures (e.g., continuous performance tests; Carey, 2002).

Although concerns regarding the use of questionnaires are noteworthy, misinformed application of any assessment tool can lead to errors in diagnostic decision making. Inconsistent application of diagnostic criteria and/or the misinformed use of questionnaires or computer-based measures, while unfortunately common, do not invalidate ADHD or other disorders as diagnostic entities. “Best practices” of clinical assessment necessitate viewing questionnaires not as a diagnostic endpoint, but as a tool for gathering observational data from informants in a systematic manner; using available norms (and evaluating the applicability of such norms for an individual); considering context and rater characteristics that might influence the reliability and validity of this information; integrating information from other sources; and, above all, using professional judgment based on contemporary, evidence-based literature. Thus, as Reid and Maag (1994) stated, “a rating scale diagnosis may be no more accurate than a coin flip in some instances.. .they are no substitute for informed professional judgment” (p. 350).

Regarding the commonly observed modest correlation between “objective” measures (e.g., observational measures, measures of activity, neuropsychological measures, rating scales), Barkley (2006) noted that these weak or absent associations may reflect differences in how we define inattention or hyperactivity. These constructs are not unitary. Differences may be explained by source or method variance, along with the fact that measures often are limited in their sampling of behavior.

ISSUE 5: Medication use for ADHD Has Increased, Is Dangerous, and Represents a Conspiracy to Drug Children Indiscriminately and Create a Fictitious Disorder

This cluster of concerns/innuendos stems from the notion that ADHD has fallen victim to a “medicalization of misbehavior”—invoking a medical diagnosis to explain discomfort that is not caused by a disease and the application of a medical intervention to treat it (Barsky & Borus, 1995; Searight & McLaren, 1998). Summarizing primarily Searight and McLaren, Nigg (2006) stated that the professed overreliance on a medical metaphor and overtreatment

[are] likely due to a confluence of societal, economic, and/or policy factors unrelated to this disease. These include popular media attention to ADHD,.. .increased expectations of children, due to competitive demands in school and society; fiscal pressure on school districts that are unable to provide services for growing numbers of children diagnosed with learning problems and ADHD; fiscal pressure on health care systems, including capitated systems that discourage thorough assessment as well as more costly behavioral or psychological treatment for child disorders; and the recent lifting of the taboo against pharmaceutical companies’ marketing their products directly to consumers. (p. 23)

The increase in prevalence rates of ADHD, particularly in the United States, has given support to claims of medicalization. Although the official prevalence estimate is 3 to 7 percent (APA, 2000), this figure varies tremendously depending on numerous methodological, developmental, and administrative (e.g., changes in laws) parameters (Lahey, Miller, Gordon, & Riley, 1999; Taylor, Sandberg, Thorley, & Giles, 1991). A recent comprehensive review of the worldwide prevalence of ADHD refuted previous claims that ADHD was primarily an “American condition” (Faraone, Sergeant, Gillberg, & Biederman, 2003). Rohde et al. (2005) also cast doubt on ADHD’s being a cultural construct (Timimi & Taylor, 2004).

Regarding medication usage, prescription rates have increased dramatically in recent years (Cooper, 2002; Feussner, 2002) and there is clear regional variability in treatment rates (Cox, Motheral, Henderson, & Mager, 2003). Barkley (2004) noted several legitimate reasons for the rise in medication use, including “increasing evidence for the safety and effectiveness of some medications. The increased recognition that girls, teens, and adults can also have the disorder, changes in special education regulations, and the rise of public awareness about the disorder” (p. 68).

The safety and effectiveness of pharmacotherapy for ADHD, a long-standing practice, is well documented (Connor, 2006; Greenhill, 2002), although certainly not uniformly accepted or without need for further study (Carey, 2002; Diller, 1998; Rowland, Umbach, O’Callaghan, Miller, & Dunnick, 2002). Risk of substance abuse appears not to be due to ADHD per se, but rather to associations between conduct disorder and ADHD (Klein, 2002). In fact, stimulant treatment for ADHD actually reduces the risk of later substance-use disorders (see Connor, 2006). Equating the rise of medication use to “de facto evidence of something scandalous or reprehensible taking place in our professions” (Barkley, 2004, p. 68) breeds use of innuendos, faulty logic, and skewed interpretation of clinical case studies and research findings. The multiple domains of impairment necessitate the development of additional treatment strategies, although one cannot discount the immense gains afforded by behavioral, psychosocial, and special education interventions.

Summary

We have presented an overview of historical and contemporary issues pertaining to the developmental disorder currently known as ADHD. In this context, we employed several criteria to articulate both the validity of ADHD and future directions needed to clarify some key elements of this disorder. These criteria allow empirically minded, informed professionals to recognize ADHD as a “real” disorder, one with clear associated functional impairments and negative sequelae affecting a sizeable percentage of children and adults alike. Those people who see ADHD as a myth may be motivated by comparable levels of moral belief and theoretical fortitude, although often misdirected. Many also cast innuendos, misconstrued interpretations of the literature, and unsupported claims about society and professions gone awry. However, scientific findings are open to public scrutiny that allows for objectivity, replication, and self-correction to occur. It is through these mechanisms that claims such as the nonexistence of depression in children, “refrigerator parents” being responsible for autism, and the “myth” of ADHD have been addressed. Future research agendas offer exciting opportunities to advance our knowledge about the heterogeneity of ADHD, identify the mechanisms that underlie core symptoms of ADHD, and improve our ability to treat ADHD even more effectively.

References:

Achenbach, T. M., & Edelbrock, C. (1983). Manual for the child behavior checklist and revised child behavior profile. Burlington: University of Vermont.
Achenbach, T. M., McConaughy, S. H., & Howell, C. T. (1987). Child/adolescent behavioral and emotional problems: Implications of cross-informant correlations for situational specificity. Psychological Bulletin, 101, 213-232.
American Academy of Child and Adolescent Psychiatry, Workgroup on Quality Issues. (1997). Practice parameters for the assessment and treatment of children, adolescents, and adults with attention-deficit/hyperactivity disorder. Journal of the American Academy of Child and Adolescent Psychiatry, 36, 85S-121S.
American Academy of Pediatrics. (2000). Clinical practice guidelines: Diagnosis and evaluation of the child with attention-deficit/hyperactivity disorder. Pediatrics, 105, 1158-1170.
American Psychiatric Association. (1968). Diagnostic and statistical manual of mental disorders (2nd ed.). Washington, DC: Author.
American Psychiatric Association. (1980). Diagnostic and statistical manual of mental disorders (3rd ed.). Washington, DC: Author.
American Psychiatric Association. (1987). Diagnostic and statistical manual of mental disorders (3rd ed., Rev. ed.). Washington, DC: Author.
American Psychiatric Association. (2000). Diagnostic and statistical manual of mental disorders (4th ed., Rev. ed.). Washington, DC: Author.
Antshel, K. M., Phillips, M. H., Gordon, M., Barkley, R. A., & Faraone, S. V. (2006). Is ADHD a valid disorder in children with intellectual delays? Clinical Psychology Review, 26, 555-572.
Bandura, A. (1969). Principles of behavior modification. New York: Holt, Rinehart & Winston.
Barkley, R. A. (2002). ADHD—Long-term course, adult outcome, and comorbid disorders. In P. S. Jensen & J. R. Cooper (Eds.), Attention deficit hyperactivity disorder: State of the science, best practices (pp. 4-1-4-12). Kingston, NJ: Civic Research Institute.
Barkley, R. A. (2006). Attention-deficit hyperactivity disorder: A handbook for diagnosis and treatment (3rd ed.). New York: Guilford.
Barkley, R. A., & 20 Coendorsers. (2004). Critique or misrepresentation? A reply to Timimi et al. [2004]. Clinical Child and Family Psychology Review, 7, 65-69.
Barkley, R. A., Cook, E. H., Jr., Diamond, A., Zametkin, A., Thapar, A., Teeter, A., et al. (2002). International consensus statement on ADHD. Clinical Child and Family Psychology
Review, 5, 89-111. Barkley, R. A., Fischer, M., Smallish, L., & Fletcher, K. (2002). The persistence of attention-deficit/hyperactivity disorder into young adulthood as a function of reporting source and definition of disorder. Journal of Abnormal Psychology, 111, 279-289.
Barsky, A. J., & Borus, J. F. (1995). Somatization and medicalization in the era of managed care. Journal of the American Medical Association, 274, 1931-1934.
Carey, W. B. (2002). Is ADHD a valid disorder? In P. S. Jensen & J. R. Cooper (Eds.), Attention deficit hyperactivity disorder: State of the science, best practices (pp. 3-1-3-19). Kingston, NJ: Civic Research Institute.
Carlson, C., & Mann, M. (2002). Sluggish cognitive tempo predicts a different pattern of impairment in the attention deficit hyperactivity disorder, predominantly inattentive type. Journal of Clinical Child and Adolescent Psychology, 31, 123-129.
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, 486-502.
Conners, C. K., & Jensen, P. S. (2002). Is ADHD a real disorder? In P. S. Jensen & J. R. Cooper (Eds.), Attention deficit hyperactivity disorder: State of the science, best practices (pp. P1-1-P1-3). Kingston, NJ: Civic Research Institute.
Connor, D. F. (2006). Stimulants. In R. A. Barkley (Ed.), Attention-deficit hyperactivity disorder: A handbook for diagnosis and treatment (3rd ed., pp. 608-647). New York: Guilford Press.
Cooper, J. R. (2002). Availability of stimulant medications— nature and extent of abuse and associated harm. In P. S. Jensen & J. R. Cooper (Eds.), Attention deficit hyperactivity disorder: State of the science, best practices (pp. 21-1-21-18). Kingston, NJ: Civic Research Institute.
Cox, E. R., Motheral, B. R., Henderson, R. R., & Mager, D. (2003). Geographic variations in the prevalence of stimulant medication use among children 5 to 14 years old: Results from a commercially insured U.S. sample. Pediatrics, 111, 237-243.
Crystal, D. S., Ostrander, R., Chen, R. S., & August, G. J. (2001). Multimethod assessment of psychopathology among DSM-IV subtypes of children with attention-deficit/hyperactivity disorder: Self-, parent, and teacher reports. Journal of Abnormal Child Psychology, 29, 189-205.
Diller, L. H. (1998). Running on Ritalin: A physician reflects on children, society, and performance in a pill. New York: Bantam Books.
Douglas, V. E. (1983). Attention and cognitive problems. In M. Rutter (Ed.), Developmental neuropsychiatry (pp. 280-329). New York: Guilford Press.
S. V. (2005). The scientific foundation for understanding attention-deficit/hyperactivity disorder as a valid psychiatric disorder. European Child and Adolescent Psychiatry, 14, 1-10.
Faraone, S. V., & Doyle, A. E. (2001). The nature and heritability of attention-deficit/hyperactivity disorder. Child and Adolescent Psychiatric Clinics of North America, 10,299-316.
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-disorder/hyperactivity disorder. Biological Psychiatry, 57, 1313-1323.
Faraone, S. V., Sergeant, J., Gillberg, C., & Biederman, J. (2003). The worldwide prevalence of ADHD: Is it an American condition? World Psychiatry, 2, 104-113.
Feussner, G. (2002). Diversion, trafficking, and abuse of methylphenidate. In P. S. Jensen & J. R. Cooper (Eds.), Attention deficit hyperactivity disorder: State of the science, best practices (pp. 20-1-20-20). Kingston, NJ: Civic Research Institute.
Greenhill, L. L. (2002). Stimulant medication treatment of children with attention-deficit hyperactivity disorder. In P. S. Jensen & J. R. Cooper (Eds.), Attention deficit hyperactivity disorder: State of the science, best practices (pp. 9-1-9-27). Kingston, NJ: Civic Research Institute.
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.
Hinshaw, S. P. (2002). Is ADHD an impairing condition in childhood and adolescence? In P. S. Jensen & J. R. Cooper (Eds.), Attention deficit hyperactivity disorder: State of the science, best practices (pp. 5-1-5-21). Kingston, NJ: Civic Research Institute.
Hudziak, J. J., Heath, A. C., Madden, P. F., Reich, W., Bucholz, K. K., Slutske, W., et al. (1998). Latent class factor analysis of DSM-IV ADHD: A twin study of female adolescents. Journal of the American Academy of Child and Adolescent Psychiatry, 37, 848-857.
Hudziak, J. J., Wadsworth, M. E., Heath, A. C., & Achenbach,T. M. (1999). Latent class analysis of child behavior checklist attention problems. Journal of the American Academy of Child and Adolescent Psychiatry, 38, 985-991.
Jensen, P. S., & Cooper, J. R. (2002). Attention deficit hyperactivity disorder: State of the science, best practices. Kingston, NJ: Civic Research Institute.
Kamphaus, R. W., & Campbell, J. M. (2006). Psychodiagnostic assessment of children: Dimensional and categorical approaches. Hoboken, NJ: Wiley & Sons.
Klein, R. G. (2002). Alcohol, stimulants, nicotine, and otherdrugs in ADHD. In P. S. Jensen & J. R. Cooper (Eds.), Attention deficit hyperactivity disorder: State of the science, best practices (pp. 16-1-16-17). Kingston, NJ: Civic Research Institute.
Lahey, B. B., Applegate, B., McBurnett, K., Biederman, J., Greenhill, L., Hynd, G. W., et al. (1994). DSM-IV Field Trials for attention deficit hyperactivity disorder in children and adolescents. American Journal of Psychiatry, 151, 1673-1685.
Lahey, B. B., Miller, T. L., Gordon, R. A., & Riley, A. W. (1999). Developmental epidemiology of the disruptive behavior disorders. In H. C. Quay & A. E. Hogan (Eds.), Handbook of disruptive behavior disorders (pp. 23-48). New York: Kluwer Academic/Plenum Press.
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.
Lahey, B. B., & Willcutt, E. G. (2002). Validity of the diagnosis and dimensions of attention deficit hyperactivity disorder. In P. S. Jensen & J. R. Cooper (Eds.), Attention deficit hyper-activity disorder: State of the science, best practices (pp. 1-1-1-23).
Kingston, NJ: Civic Research Institute. Levy, F., & Hay, D. (2001). Attention, genes, and ADHD. Philadelphia: Brunner-Routledge.
Levy, F., Hay, D. A., McStephen, M., Wood, C., & Waldman, I. (1997). Attention-deficit hyperactivity disorder: A category or a continuum? Genetic analysis of a large-scale twin study.
Journal of the American Academy of Child and Adolescent Psychiatry, 36, 737-744.
Mash, E. J., & Wolfe, D. A. (2005). Abnormal child psychology (3rd ed.). Belmont, CA: Wadsworth.
McBurnett, K., Pfiffner, L. J., & Frick, P. J. (2001). Symptom properties as a function of ADHD type: An argument for the continued study of sluggish cognitive tempo. Journal of Abnormal Child Psychology, 29, 207-213.
Milberger, S., Biederman, J., Faraone, S. V., Murphy, J., & Tsuang, M. T. (1995). Attention deficit hyperactivity dis-order and comorbid disorders: Issues of overlapping symptoms. American Journal of Psychiatry, 152, 1793-1799.
Milich, R., Balentine, A., & Lynam, D. (2001). ADHD combined type and ADHD predominantly inattentive type are distinct and unrelated disorders. Clinical Psychology: Science and Practice, 8, 463-488.
MTA Cooperative Group. (1999). A 14-month randomized clinical trial of treatment strategies for attention-deficit/ hyperactivity disorder. Archives of General Psychiatry, 56, 1073-1086.
National Institutes of Health Consensus Development Conference Statement. (2000).Diagnosis and treatment of attention-deficit/ hyperactivity disorder (ADHD). Journal of the American Academy of Child and Adolescent Psychiatry, 39, 182-188.
Nigg, J. T. (2005). Neuropsychologic theory and findings in attention-deficit/hyperactivity disorder: The state of the field and salient challenges for the coming decade. Biological Psychiatry, 57, 1424-1435.
Nigg, J. T. (2006). What causes ADHD? Understanding what goes wrong and why. New York: Guilford Press.
Nigg, J. T., Blaskey, L. B., Huang-Pollock, C., & Rappley, M. D. (2002). Neuropsychological executive functions and ADHD DSM-IV subtypes. Journal of the American Academy of Child and Adolescent Psychiatry, 41, 59-66.
Pelham, 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, 449-476.
Reid, R., & Maag, J. W. (1994). How many fidgets in a pretty much: A critique of behavior rating scales for identifying students with ADHD. Journal of School Psychology, 32, 339-354.
Robins, E., & Guze, S. B. (1970). Establishment of diagnostic validity in psychiatric illness: Its application to schizophrenia. American Journal of Psychiatry, 126, 983-987.
Rohde, L. A., Szobot, C., Polanczyk, G., Schmitz, M., Martins, S., & Tramontina, S. (2005). Attention-deficit/hyperactivity disorder in a diverse culture: Do research and clinical findings support the notion of a cultural construct for the disorder? Biological Psychiatry, 57, 1436-1441.
Rowland, A. S., Umbach, D. M., O’Callaghan, J. P., Miller, D. B., & Dunnick, J. K. (2002). Public health and toxicological issues concerning stimulant treatment for ADHD. In P. S. Jensen & J. R. Cooper (Eds.), Attention deficit hyperactivity disorder: State of the science, best practices (pp. 10-1-1016). Kingston, NJ: Civic Research Institute.
Searight, H. R., & McLaren, A. L. (1998). Attention-deficit hyperactivity disorder: The medicalization of misbehavior. Journal of Clinical Psychology in Medical Settings, 5, 467-495.
Seidman, L. J., Valera, E. M., & Makris, N. (2005). Structural brain imaging of attention-deficit/hyperactivity disorder. Biological Psychiatry, 57, 1263-1272.
Sroufe, L. A. (1997). Psychopathology as an outcome of development. Developmental Psychopathology, 9, 251-268.
Taylor, E., Sandberg, S., Thorley, G., & Giles, S. (1991). The epidemiology of childhood hyperactivity. London: Oxford University Press.
Timimi, S., & 33 Coendorsers. (2004). A critique of the International Consensus Statement on ADHD [Barkley et al., 2002]. Clinical Child and Family Psychology Review, 7, 59-63.
Timimi, S., & Taylor, E. (2004). ADHD is best understood as a cultural construct: In debate. British Journal of Psychiatry, 184, 8-9.
Wakefield, J. C. (1992). The concept of mental disorder: On the boundary between biological facts and social values. American Psychologist, 47, 373-388.
J. C. (1999). Evolutionary versus prototype analyses of the concept of disorder. Journal of Abnormal Psychology, 108, 374-399.
Willcutt, E. G., Doyle, A. E., Nigg, J. T., Faraone, S. V., & Pennington, B. F. (2005). Validity of the executive function theory of attention-deficit/hyperactivity disorder: A meta-analytic review. Biological Psychiatry, 57, 1336-1346.