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ADHD symptomatology is best conceptualized as a spectrum: a dimensional

versus unitary approach to diagnosis

Article  in  ADHD Attention Deficit and Hyperactivity Disorders · May 2015

DOI: 10.1007/s12402-015-0171-4 · Source: PubMed

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Title: ADHD symptomatology is best conceptualized as a spectrum: A Dimensional versus

Unitary Approach to Diagnosis

Author: Rebeca Heidbreder

PUBMED ID: 25957598

DOI: http://link.springer.com/article/10.1007/s12402-015-0171-4

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Received date: 2-5-2015

Revised date: 3-9-2015

Accepted date: 4-18-2015

Please cite this article as: Heidbreder, R. (2015). ADHD symptomatology is best conceptualized
as a spectrum: a dimensional versus unitary approach to diagnosis. ADHD Attention Deficit and
Hyperactivity Disorders, 7(4), 249-269.

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 ADHD symptomatology is best conceptualized as a spectrum: A Dimensional versus Unitary
Approach to Diagnosis

Rebeca Heidbreder, Ph.D.

PsychResearchCenter, LLC, Powhatan, Virginia

Correspondence concerning this article should be addressed to Rebeca Heidbreder,

PsychResearchCenter, LLC, Powhatan, Virginia, 3669 Michaux Mill Drive, Powhatan, Virginia
23139.

E-mail: [email protected]
 Abstract

Objective: The aim of this paper is to build a case for the utility of conceptualizing ADHD, not

as a unitary disorder that contains several subtypes, but rather as a marker of impairment in

attention and/or impulsivity that can be used to identify one of several disorders belonging to a

spectrum. Method: The literature will be reviewed to provide an overview of what is known

about ADHD in terms of heterogeneity in symptomatology, neuropsychology, neurobiology, as

well as comorbidity with other diseases and treatment options. The data from these areas of

research will be critically analyzed to support the construct of a spectrum of disorders that can

capture the great variability that exists between individuals with ADHD and can discriminate

between separate disorders that manifest similar symptoms. Results: The symptoms associated

with ADHD can be viewed as dimensional markers that point to a spectrum of related disorders

that have as part of their characteristics impairments of attention and impulsivity. The spectrum

can accommodate symmetrically and asymmetrically comorbid psychiatric disorders associated

with ADHD as well as the wide heterogeneity known to be a part of the ADHD disorder.

Conclusions: Individuals presenting with impairments associated with ADHD should be treated

as having a positive marker for a spectrum disorder that has as part of its characteristics

impairments of attention and/or impulsivity. The identification of impairment in attention and/or

impulsivity should be a starting point for further testing rather than being an endpoint of

diagnosis that results in pharmacological treatment that may or may not be the optimal therapy.

Rather than continuing to attribute a large amount of heterogeneity in symptom presentation as

well as a high degree of symmetric and asymmetric comorbidity to a single disorder, clinical

evaluation should turn to the diagnosis of the type of attentional deficit and/or impulsivity an

individual has in order to colocate the individual’s disorder on a spectrum that captures the
heterogeneity in symptomatology, the symmetrical and asymmetrical comorbidity, as well as

subthreshold presentation and other variants often worked in to the disorder of ADHD. The

spectrum model can accommodate not only the psychophysiological profiles of patients, but is

also consistent with what is known about the functional heterogeneity of the prefrontal cortex as

well as the construct that cognitive processes are supported by overlapping and collaborative

networks.

Keywords: ADHD, heterogeneity, spectrum disorder, diagnosis, prefrontal

cortex, comorbidity, neural circuitry, neural networks, attention, impulsivity, mental health

disorders
Introduction

The centuries long observation that certain children exhibit a behavior pattern that is

characterized by fidgetiness and/or frank hyperactivity, and that often presents along with a lack

of attention or focus as well as impulsivity (Anastopoulos, Barkley, & Shelton, 1994; Barkley &

Peters, 2012; Lange, Reichl, Tucha & Tucha, 2010; Taylor, 2011) has resulted in decades of

research about the disorder now known as Attention Deficit Hyperactivity Disorder (ADHD)

(Diagnostic and Statistical Manual of Mental Disorders 5th ed., American Psychiatric

Association, 2013, (DSM V) ). This disorder has been characterized in terms of types and traits

(Fair, Bathula, Nikolas, & Nigg, 2012; Sonuga-Barke, 2002), age (Feldman & Reiff, 2014;

Volkow & Swanson, 2013; Wolraich, 2006), gender (Arnett, Pennington, Willcutt, DeFries &

Olson, 2014; Skogli, Teicher, Andersen, Hovik, & Øie, 2013, Berry, Shaywitz & Shaywitz,

1985), treatment (Bolea-Alamañac et al., 2014; Cunill, Castells, Tobias, & Capellà, 2014;

Ollendorf, Migliaccio-Walle, Colby, & Pearson, 2013; Evan, Owens, & Bunford, 2014;

Stevenson, et al., 2014), duration (Faraone, 2005; Mattfield, et al., 2014; van Lieshout, Luman,

Buitelaar, Rommelse, & Oosterlaan, 2013), comorbidity with other syndromes (Biederman,

Newcorn & Sprich, 1991; DSM V, 2013; Patel, Patel, & Patel, 2012; Pliska, Carlson, &

Swanson, 1999; Williamson, et al., 2014), as well as differences in neuroanatomical structure

and function (Cao, Shu, Cao, Wang, & He, 2014; Valera, Faraone, Murray, & Seidman, 2007;

for review see Rubia, Alegria, & Brinson, 2014 ). The DSM V (2013) characterizes ADHD as a

single disorder the diagnosis of which can be made more specific in terms of the presence or

absence of inattentiveness or hyperactivity to varying degrees as a function of the fulfillment of

several criteria across different settings. There is growing evidence, however, that ADHD is a

much more heterogeneous disorder than such a diagnosis is able to capture not only in children

and adolescents (Fair et al., 2012; Balázs & Keresztény, 2014; Koziol & Budding, 2012; Sonuga-
Barke, 2001; Williamson et al. 2014), but also, and perhaps to an even greater extent, in adults

(DeQuiros & Kinsbourne, 2001; Kessler et al. 2011). Furthermore, it has even been proposed

that the presentation of inattentiveness as the primary symptom in some individuals that are

given the diagnosis of ADHD may be indicative of a similar, but separate disorder (Barkley,

2001; Barkley, 2013; Carlson, 1986; Diamond, 2005; Hinshaw, 2001; Lee, Burns, Snell, &

McBurnett, 2014; Milich, Balentine, & Lynam, 2001). ADHD is also highly comorbid with

other psychiatric disorders with some estimates as high as 60-70% (MTA Cooperative Group,

1999; Patel, Patel, & Patel, 2012). This comorbidity is bidirectional as well in that not only will

the ADHD diagnosed patient have one or more psychiatric or learning disorders, but those

patients with a primary diagnosis of one of several psychiatric disorders also meet criteria for

ADHD at rates higher than the general population (Biederman et al., 1991; Pliszka, 2014),

further complicating the etiology of ADHD and adding to the great variability in the ADHD

population. Given the increasing rate in the diagnosis of ADHD in children (Visser et al, 2013)

and adults (Kessler, Adler, Barkley et al., 2011) as well as the exponential increase in the

treatment of ADHD with pharmacological agents over the last decade, it is increasingly

becoming more important to refine the characterization of ADHD to allow healthcare workers to

delineate specific dysfunctions and maximize efficacy of treatment.

The aim of this paper is to build a case for the utility of conceptualizing ADHD not as a

unitary disorder that contains several subtypes, but rather as a marker of impairment in attention

and/or impulsivity that can be used to identify one of several disorders belonging to a spectrum.

The present review will provide an overview of what is known about ADHD in terms of

heterogeneity in symptomatology, neuropsychology, neurobiology, as well as comorbidity with

other diseases and treatment options. The data from these areas of research will be critically
scrutinized in order to build a case that the current DSM system used as the gold standard for the

diagnosis of ADHD is insufficient either to capture the great variability that can exist between

individuals in their manifestation of the disorder or to discriminate between separate disorders

that manifest similar symptoms. The review will conclude with the suggestion that the construct

of a spectrum is not only better able to handle individual variability and heterogeneity among the

ADHD population in terms of external manifestations such as symptom presentation,

neuropsychological assessment and comorbidity, but given what is known about the

cytoarchitecture and heterogeneity of the prefrontal cortex (Chudasama, 2011; Heidbreder &

Groenewegen, 2003; Kesner & Churchwell, 2011) as well strong evidence supporting that

different cognitive processes are subserved by different subregions of the prefrontal cortex, such

a model can better explain the overlap in symptoms and strong interrelations ADHD has with

other psychiatric diseases.

Prevalence of ADHD

There are many reviews on the historical evolution of ADHD (Anastopoulos et al., 1994;

Barkley & Peters, 2012; Lange et al. 2010; Matthews, Nigg, & Fair, 2014; Tarver, Daley, &

Sayal, 2014) that reveal a disorder first characterized by a hyperkinetic aspect and then the

inability to focus in the presence of excessive distractibility. Over the last few decades, research

has concentrated more on the attention and impulsivity aspects of the disorder as the

understanding of the neural substrates that govern these aspects of cognition has increased and

pharmacological treatment has become more widespread (Douglas, 1972, 1994, 1999, 2005;

Konrad, Neufang, Hanisch, Fink, & Herpertz-Dahlmann, 2006; Leth-Steensen, King, Elbaz, &

Douglas, 2000; Rubia, et al., 2013; Rubia, Smith, Brammer, Toone, & Taylor, 2005). This is
particularly meaningful given that 1) the hyperkinetic portion of the disorder may diminish with

age (Barkley, 1990, 1997; AACAP, 1997), and 2) the disorder may persist into adulthood when

the obvious hyperactivity has all but disappeared (Volkow & Swanson, 2013; Willoughby,

2003). The fact that the disorder may manifest as a constellation of different symptoms

depending on the individual has contributed to the variability in the estimation of the frequency

of the disorder in the population. Whereas the DSM V (2013) states that the prevalence of

ADHD across cultures is about 5% in children and 2.5% in adults, data from the most recent

National Survey of Children's Health (NSCH) (Visser et al. 2013) indicate that as of 2011, the

prevalence in children 4-17 years of age who had ever received a diagnosis of ADHD by a health

care provider as reported by a parent in the United States is approximately 11% (6.4 million

children). The study also states that this figure represents a 42% increase in parent-reported

history of ADHD diagnosis since 2003. In addition, the national yearly rate at which ADHD has

been diagnosed has increased by 5% since 2003; however, the rate of diagnosis varies

substantially by state, from a low of 5.6% in Nevada to a high of 18.7% in Kentucky. All told

the NSCH reveals that, relative to 2003, in 2011 approximately 2 million more American

children had received a diagnosis of ADHD. When Polanczyk, Willcutt, Salum, Kieling, &

Rohde (2014) conducted a meta-analysis of the data found in 135 studies published from 1985 to

2012 and aimed at investigating the prevalence of ADHD worldwide, the results suggested that

differences in the estimates of prevalence were significantly associated with the diagnostic

criteria, impairment criterion and source of information. The authors concluded that accurate

prevalence rates can only be estimated if standardized diagnostic procedures are implemented in

representative samples of the community. In their study, standardized diagnostic criteria were

defined as those studies that used the diagnostic criteria from The Diagnostic and Statistical
Manual of Mental Disorders 3rd ed., American Psychiatric Association, (1980) (DSM III),

Diagnostic and Statistical Manual of Mental Disorders 3rd ed., text rev. American Psychiatric

Association, (1987), (DSM III-R), Diagnostic and Statistical Manual of Mental Disorders 4th

ed., text rev. American Psychiatric Association, (2000) (DSM IV) and the International

Statistical Classification of Diseases and Related Health Problems. World Health Organization,

(1992) (ICD 10). The authors state that when such an approach is taken, not only does the

variability in ADHD prevalence estimates disappear, but so does the increase over time (1994-

2010) in the number of children who meet the criteria for ADHD. Wolraich et al. (2014) also set

out to disentangle the epidemiology of ADHD using the strict definition provided by the DSM

IV (2000), which as in the DSM V (2013), requires information from multiple informants and

settings to establish the diagnosis. Their results yielded an overall prevalence more in line with

the Visser et al. (2013) study than the Polanczyk et al. (2014). Both Wolraich et al. (2014) and

Visser et al. (2013) also found geographical differences in the prevalence range within the

United States. In contrast Polanczyk et al. (2014) found no prevalence variations as a function of

geographical regions of the world.

Though the net objectives in the Polanczyk et al. (2014) study and the Wolraich et al.

(2014) study were the same, that is, to use the DSM diagnostic criteria to provide an estimate of

the prevalence of ADHD, the prevalence rates found by Wolraich et al. (2014) are more than 1.5

times greater than Polanczyk et al. (2014). This difference could indicate that the suspicion

and/or diagnosis of ADHD remains subjective even when formal diagnostic criteria established

by the DSM are implemented. This subjectivity comes primarily from two sources. First, the

presence or absence of symptoms necessary for diagnosis are provided by parents, teachers and

the patient himself, which are then interpreted and evaluated by a clinician. Second, certain
combinations of symptoms are more likely to prompt clinical intervention and a subsequent

diagnosis. There are data supporting that it is the symptomatology associated with hyperactivity,

behavior disruption and disorganization rather than inattention and even impulsivity that will

prompt consideration for clinical or therapeutic intervention (Diamond, 2005, Feldman & Reiff,

2014; Nigg, Willcutt, Doyle & Sonuga-Barke, 2005; Weiss, Worling, Wasdell, 2003). In

addition, there is also evidence suggesting that girls with ADHD are under identified (Berry,

Shaywitz & Shaywitz, 1985; Bruchmüller, Margraf, & Schneider, 2012). This under

identification may be due to the qualitative differences between the genders in their presentation

of ADHD, which include symptom severity, (Arnett, Pennington, Willcutt, DeFries & Olson,

2014), behavior differences (Gaub & Carlson, 1997) and cognitive differences (Arnett,

MacDonald, Pennington, 2013). The qualitative gender difference may, at least in part, also be

responsible for the significant quantitative gender differences in ADHD (Willcutt, 2012). All of

these factors can ostensibly interact with cultural/individual perceptions of what is or is not

considered symptoms of a behavior disorder. Therefore, the very same factors that would tend to

encourage over diagnosis in some cases make it impossible to account for all of the possible

cases that were not included in the studies because of differences in thresholds for seeking

clinical help for a child with ADHD in other cases. This variability in threshold holds

particularly true with respect to comparisons across geographical regions, and may account for

the difference between the Polanczyk et al. (2014) study which failed to find a significant effect

of geographical region and the variance in prevalence among the different geographic regions

found by Visser et al. (2013) and Wolraich et al. (2014).

Diagnosis

The historical evolution of ADHD since the second edition of the DSM (DSM II)

(Diagnostic and Statistical Manual of Mental Disorders 2nd ed., American Psychiatric

Association 1968) until the current fifth edition (DSM V) has seen ebb and flow in terms of

subtyping in an attempt to capture the heterogeneity in the disorder evident to researchers and

clinicians. As suggested by the work on prevalence (Polanczyk et al. 2014; Visser et al. 2013;

Wolraich et al. 2014) reviewed in the previous section, variability in the identification of ADHD

in a patient occurs not only as a function of differences in methodology, but between clinical

evaluations even when there is adherence to the criteria of the DSM. Typically, the suspicion of

a clinical problem begins when either the parent or the teacher starts to notice, among other

things, that the child cannot sit still, struggles to focus and has behavioral issues, which may also

negatively impact academic performance (Sibley, Altszuler, Morrow, & Merrill, 2014). The

physician who ultimately sees the child may reach a diagnosis of ADHD simply based on the

anecdotal evidence from the parent and/or teacher without actually subjecting the child to a

comprehensive assessment (Sciutto & Eisenberg, 2007). The physician may rely on further

interviews, including with the patient himself, rather than standardized assessment tools and may

or may not adhere to the DSM criteria in order to reach their diagnosis and start the child on

medication (Wasserman et. al 1999). Even many psychologists do not regularly follow

assessment procedures that are consistent with the best practice guidelines, which can result in a

false positive diagnosis and the inception of pharmacological therapy (Handler & DuPaul, 2005).

These scenarios seem to indicate that clinical practitioners still view ADHD as a

compartmentalized disorder that presents with a concrete and highly recognizable set of

symptoms (Bruchmüller, Margraf, & Schneider, 2012). This narrowed view on positive clinical
presentation is particularly vexing in the area of what defines a clinically significant academic

problem that is specific to the ADHD patient as compared to the academic problems observed in

the normal age matched population (Sibley, Altszuler, Morrow, & Merrill, 2014). The lack of

objective delineation not only muddies the waters, but can also lead to a failure to identify a child

who actually has a clinical problem. For example, teachers may fail to detect children with

symptoms of inattention because they exhibit no hyperactivity and are often quiet and less likely

to act out in the classroom. These children may appear to be working, but they are often not

paying attention to what they are doing. Conversely, some children who are actually exhibiting

the clinical hyperactivity and impulsivity that are characteristic of some forms of ADHD in the

classroom setting will be considered as merely having disciplinary problems, and rather than

being evaluated for the disorder will simply be subject to punitive practices to correct their

behavior.

In their review, Nigg, Willcutt, Doyle, &Sonuga-Burke (2005) point out that though most

theorists do not believe that individuals with ADHD have a unitary disorder with a “common

pathway to their problems” there is still a need to address empirically the heterogeneity that

everyone accepts as fact. Beyond possible differences in neuropsychological profiles that the

authors were specifically addressing, the heterogeneity among the ADHD population can also be

a function of comorbidity, the manner in which the symptoms that are part of the ADHD criteria

for diagnosis combine and present in any one patient, as well as the “subthreshold” (Balázs, &

Keresztény, 2014) presentation of symptoms that does not lead to a true diagnosis of ADHD, but

can still cause impaired function. Furthermore, data is building in support of the idea that some

patients that receive the diagnosis of ADHD may actually be suffering from a disorder that is
separate, but somehow similar to ADHD (e.g., Diamond, 2005; Hinshaw, 2001; Milich,

Balentine, & Lynam, 2001).

Subtype or Separate disorder?

The DSM V (2013) allows for the specification of ADHD along several dimensions

based on the number of criteria that have been fulfilled in the categories of “Inattention” and

“Hyperactivity and Impulsivity.” As a result, the patient with ADHD can be considered to have

a Combined Presentation (the abbreviation “CT” will be used, which refers to the virtually

identical “Combined Type” presentation from the DSM IV-TR) if sufficient criteria from both

categories have been met, a Predominantly Inattentive presentation (PI) if sufficient criteria are

met only for the “Inattention” category, or a Predominantly hyperactive/impulsive type (HI) if

sufficient criteria are met only for the “Hyperactivity and impulsivity” category. The DSM V

(2013) further suggests specifying the disorder in terms of the severity of presentation (mild,

moderate, and severe). Several studies have investigated the cognitive differences between these

subtypes with varying results (e.g., Baeyens, Roeyers, & Walle, 2006; Bonafina, Newcorn,

McKay, Koda, & Halperin, 2000; Chhabildas, Pennington, Willcutt, 2001; Fair et al., 2012;

Faraone, Biederman, Weber & Russell, 1998; Geurts, Verté, Oosterlaan, Roeyers, & Sergeant,

2005; Lockwood, Marcotte, & Stern, 2001; Nigg, Blaskey, Huang-Pollock, & Rappley, 2002;

Riccio, Homack, Jarratt, & Wolfe, 2006; Song & Hakoda, 2014). However, it has been proposed

that the differences between the CT subtype and the PI subtype are significant enough, that rather

than being two different subtypes of the same disorder, the CT and PI subtypes should be

considered as two distinct disorders (Baeyens, Roeyers, & Walle, 2006; Barkley, 2001;

Diamond, 2005; Hinshaw, 2001; Milich, et al., 2001). Both Milich et al. (2001) and Diamond
(2005) provide detailed reviews of the qualitative differences between the two subtypes, which

make a strong case for positing CT and PI as nearly diametrically opposite conditions. Although

the PI subtype represents about 25%-30% of the ADHD cases seen in the clinic (Faraone et al.,

1998; Weiss, Worling, & Wasdell, 2003), in the community it is the more prevalent subtype

(Carlson & Mann, 2000) by nearly double relative to the CT subtype (Gaub & Carlson, 1997).

The CT subtype has almost exactly the opposite prevalence profile, namely in the clinic the CT

subtype is seen nearly twice as much as the PI subtype (Faraone et al. 1998). Furthermore,

whereas gender differences in prevalence ratios for the CT subtype in the community and in the

clinic are significantly different, the PI subtype has practically the same gender distribution in

both the community and the clinic. This discrepancy suggests that not only are individuals with

the PI subtype receiving clinical care at a lower frequency than the CT subtype, but that the CT

subtype is associated with symptoms that are more readily identifiable as being part of a

disorder. It is likely that the very character attributes that distinguish the CT from the PI

subtypes are what prompt the visit to the clinician for further evaluation. Diamond (2005)

reminds us that while individuals with the CT subtype are hyperactive, fidgety, impulsive,

talkative, disinhibited, disorganized and impatient, the PI subtype is characterized by the

inability to pay close attention to detail, difficulty in planning and remembering to do what is

required, and disorganization. Diamond (2005) also points out that though both the PI and CT

subtypes could have the qualifier “easily distracted” added into their characterization, the

difference between them has to do with the type of distractibility that they experience. Whereas

the individual with CT subtype could become easily distracted by another stimulus that enters his

sphere of awareness, the individual with the PI subtype becomes distracted because she loses

interest in the activity she is engaging in. This difference can be qualified as an external versus
internal mode of distractibility. According to Weiss et al. (2003) an individual suffering from

the constellation of symptoms associated with the CT subtype is also more functionally impaired

than someone suffering from the symptoms associated with the PI subtype. Furthermore, the

individual with the CT subtype has a higher likelihood of not only being medicated, but being

medicated at a higher dose (Barkley, 2001; Diamond, 2005; Milich et al., 2001; Weiss et al.,

2003). In fact, Faraone et al. (1998) report that the CT subtype is associated with a more

clinically severe syndrome than either the PI subtype or the HI subtype. Finally, although both

subtypes appear to respond to treatment with stimulants, the CT subtype has a higher probability

of being rated as improved relative to the PI subtype (Weiss et al. 2003).

Although the data are compelling, there is as yet no absolute consensus regarding the

separation of the PI and CT subtypes into two separate disorders. However, the research that has

set in motion part of this debate has inadvertently opened the metaphorical “Pandora’s Box “,

which has postulated the possibility of splitting the PI subtype itself into two different disorders

of attention (Carlson & Mann, 2002). The idea that “sluggish cognitive tempo” (SCT) could be

indicative of an impairment that is separate from the PI subtype was proposed by Carlson &

Mann (2002) as an extension to the findings from McBurnett, Pfiffner, & Frick (2001). In their

view, it may be possible to distinguish two different disorders in patients who have no symptoms

of hyperactivity and impulsivity, but who manifest problems with attention. Namely, one

disorder is characterized by the Inattentive criteria outlined in the DSM, and the second disorder,

seen only in a subset of PI patients, is characterized by specific traits including hypoactivity,

dreaminess, and forgetfulness. There has been a recent resurgence in the number of

investigations aimed at providing evidence for the validity of qualifying SCT as a separate

disorder (Barkley, 2013; Bauermeister, Barkley, Bauermeister, Martinez, & McBurnett, 2012;
Becker, Marshall, & McBurnett, 2014; Lee, Burns, Snell, & McBurnett, 2014; Saxbe & Barkley,

2014). The utility of these and future investigations is not only in their ability to reach

consensus, but more importantly to increase the understanding in psychopathological problems

of attention. As Becker et al. (2013) point out “SCT may be useful as a transdiagnostic

construct”, which could fit in neatly with the reminder from Barkley (2001) that “attention is

multidimensional such that several distinct disorders of attention are likely to be identified

besides ADHD.”

With respect to the CT and HI subtypes, there is evidence to suggest that these may not

be separate conditions that remain stable over time, but rather subsets of each other. On the one

hand, investigators such as Lahey, Pelham, Loney, Lee, & Willcutt (2005) suggest that HI is a

less severe form of CT, perhaps due to the fact that hyperactivity reduces or disappears with age.

On the other hand, Barkley (2007) suggests that the HI form of ADHD is simply a precursor to

the CT form. Data to support either position only adds greater weight to the proposition that

ADHD may not really be one disorder with dimensional presentations, but rather several

disorders that are tied together by “etiological vicinity”.

Finally, the diagnostic criterion of impulsivity has been used to subcategorize patients

diagnosed with ADHD for at least two decades. However, the question about how to define

impulsivity in particular with respect to psychiatric illness still continues to be debated (for

review see Moeller, Barratt, Dougherty, Schmitz, J. M., & Swann, 2014). The list of

“Hyperactivity/Impulsivity” criteria in the DSM V (2013) fail to capture the hallmark traits of

delayed gratification, rapid and unplanned actions, as well as reduced sensitivity to negative

consequences that have historically been associated with impulsivity. In fact though ADHD is

highly comorbid with Conduct Disorder and Oppositional Disorder (Biederman et al. 1991), the
DSM V (2013) definition of the impulsivity associated with “Disruptive impulse control and

conduct disorders” is very different from the impulsivity associated with ADHD; yet, when

referring to the comorbidity with ADHD the DSM V (2013) says that since ADHD individuals

are impulsive, then it is not unusual that they should show this comorbidity. Although the

paragraph on diagnostic features associated with ADHD does mention the hallmark traits

associated with impulsivity, the examples provided for an impulsive action “darting into the

street without looking” or “taking a job without adequate information” only add to the ambiguity

for several reasons. Whereas it is not difficult to envision an individual who cannot wait his

turn, who is on the go, who runs about and intrudes and interrupts as capable of darting into

traffic or making poor career choices, the individual who fits the profile of the PI subtype can

find themselves engaging in these same actions for reasons that have nothing to do with

impulsivity, but instead everything to do with the quality of the attentional processes these

individuals may have access to. Though Barkley(1997) suggests that the differences in the

attention difficulties between the PI and CT subtypes are related to problems with selective

attention in the former and problems with disinhibition in the latter, it is also possible to look at

both subtypes in terms of opposite ends of an attentional spectrum. Specifically, whereas the PI

subtype may have an “attentional spotlight” that is too narrow, the CT and HI subtypes may have

“attentional spotlights” that are too wide. The analogy of an “attentional spotlight” (Posner &

Petersen, 1989) or the fact that it may be too wide in ADHD is not new (Shalev & Tsal, 2003);

however, the idea that the subtypes may vary as a function of the breadth of the attentional

spotlight is. On the one hand, the wide attentional spotlight of the CT and HI subtypes prevents

those individuals from focusing selectively on any one stimulus for an interval long enough to

make evaluative judgments. In other words they are overwhelmed by stimuli, and as such, no
one stimulus necessarily has more salience than another. In contrast, the narrowness of the PI

subtype spotlight does not give them access to many other competing stimuli that may be

available at any one time and are necessary to form an evaluative judgment. As a result, on the

one hand the person with CT or HI subtype may dart across the street or make a bad decision

because they do not rest their focus long enough among the wide range of stimuli available to

them to avoid making a decision that might have negative consequences. In other words, those

individuals cannot stop moving their spotlight across the wide range of stimuli that are available

to them. On the other hand, the PI subtype may have a stagnant spotlight, such that even when

the appropriate information is available, they do not have the ability to access the information

that would permit a better decision. In other words they are not giving their attention to all that

they can. Nevertheless, in both cases the end result is the same.

In sum, there is an abundance of data indicating that the variety in the symptomatology of

patients seeking clinical help for suspected ADHD exceeds the current nosology for the

delineation of this disorder. Furthermore it would appear that the manner in which patients

present these symptoms do not necessarily fall into clear cut categories that are variations within

only one disorder as proposed by the DSM.

Comorbidity

Beyond the recognized variety in symptomatology of ADHD, the accurate diagnosis of a

patient can be confounded by the presence of one or more comorbid disorders. It is now well

established that 50%-75% of patients diagnosed with ADHD will have at least one comorbid

learning disorder, psychiatric disorder or neurodevelopmental disorder (Barkley, 2005,

Biederman et al. 1991; Jensen, Martin, & Cantwell, 1997; Patel et al., 2012; Pliszka et al. 1999).
In addition, an adult with ADHD throughout his lifetime will have six times the likelihood of

developing another psychiatric disorder (Brown, 2006). The extensive review by Biederman et

al. (1991) tells us that ADHD is comorbid with conduct disorder at a rate of between 30-50%,

with oppositional defiant disorder at a rate of at least 35%, with mood disorders at a rate ranging

from 15-75%, with anxiety disorders at a rate of at least 25%, and with learning disabilities at a

rate between 10-92%. ADHD has also been associated with a greater risk for substance abuse

(Wilens & Morrison, 2011). We also know that comorbidity with ADHD can be asymmetrical,

that is, while the rate of ADHD in certain disorders can exceed that in the general population,

patients with ADHD do not necessarily show those same disorders at a rate higher than in the

normal population (Pliszka, 2014). For example, 60% of Tourette patients will be concurrently

diagnosed with ADHD; nevertheless, people with ADHD are not diagnosed with Tourette’s at a

rate higher than what occurs in the general population (Jummani & Coffey, 2014).

Approximately 40% of those diagnosed with borderline personality disorder will also have

received a diagnosis of ADHD (Ferrer, Andión, Matalí, Valero et al., 2010), but borderline

personality disorder does not occur more frequently in those whose primary diagnosis is ADHD.

Patients with bipolar disorder have comorbid ADHD at a rate of 60-90%, but only 22% of

patients with ADHD as a primary diagnosis will have comorbid bipolar disorder (Wilens,

Biederman, Forkner, et al., 2003). Obsessive Compulsive Disorder is highly comorbid with

ADHD particularly in boys in whom the rate of comorbidity is about 50% (Geller, 2006).

Finally there is even some evidence that the presence of ADHD symptoms may be indicative of

premorbid schizophrenia or even be linked with a “distinct neurodevelopmental progression of

schizophrenia” (Marsh & Williams, 2006).

 Certain patterns of comorbidity are also more strongly correlated with ADHD than others

(Greene, Biederman, Faraone et al., 1996; Jensen, Martin, & Cantwell, 1997; Lynam, 1996). For

example, the relationship between ADHD, conduct disorder and/or oppositional defiant disorder

often makes it difficult to distinguish one from the other (Biederman et al. 1991). Though large

epidemiological studies do not usually provide comorbidity rates in ADHD by subtype, Faraone

et al. (1998) found that it is actually the CT form of ADHD that is associated with the highest

rate of comorbidity with conduct disorder and oppositional defiant disorder. Furthermore, the

difference in the rate of comorbidity between the CT and PI groups for these disorders, the so-

called externalizing disorders, was significant. Though the relationship between internalizing

disorders and the different subtypes is not as well defined (for review see Garner, Mrug,

Hodgens, & Patterson, 2012), children with the PI subtype tend to be more socially isolated and

may be associated with a higher rate of comorbid internalizing disorders, including anxiety and

depression, or at the very least are less prone to externalizing disorders (Diamond, 2005).

Schaughency, Hynd, et al. (1987) report that 43% of individuals with ADD without

hyperactivity, the DSM III (1980) subtype that is equivalent to the PI subtype of later editions,

also received diagnoses of either anxiety or depression. Patients that have ADD with

hyperactivity, the DSM III subtype that is equivalent to the CT subtype of later editions, were

diagnosed with these disorders only at a rate of about 10%. Faraone et al. (1998) also noted that

the PI subtype was associated with a higher lifetime rate of major depressive disorder relative to

the other subtypes. The study by Weiss et al (2003) that involved comprehensive and

multidisciplinary evaluations also revealed higher rates of anxiety and depression in the PI

subtype than in the CT subtype. Finally, it may be the case that some of the impairment

associated with ADHD subtypes may be more related to the influence of the comorbid disorder
rather than to the disorder of ADHD itself (Milich et al., 2001). For example, Lockwood et al.

(2001) were able to show significant neuropsychological differences at 80% accuracy between

the CT and PI types of ADHD when effect of presence of comorbidity was controlled.

To summarize, there can be no doubt that the relationship that ADHD has with a variety

of psychiatric disorders is a tangled and intricate one and many questions are left begging. There

is still no clear understanding as to why there is such a high incidence of comorbidity between

ADHD and other psychiatric diseases or how the diagnosis of ADHD can seemingly predispose

an individual to another psychiatric disorder at a future date. One explanation may be that

ADHD and its comorbid psychiatric disorders may share a common neural substrate involving

the prefrontal cortex, which as a result of heterogeneity in its neural circuitry can account for a

range of neurological, cognitive and psychiatric disorders (Chudasama, 2011; Heidbreder &

Groenewegen, 2003; Kesner & Churchwell, 2011). Recent evidence also suggests that there may

be a common neural substrate across multiple mental illnesses (Goodkind, Eickhoff, Oathes,

2015).

Pharmacotherapy and alternative therapy for ADHD

Although not an exhaustive review, the evidence provided so far argues against describing a

patient as simply having ADHD or simply amassing together groups of patients that may have

important differences at the level of symptom presentation, underlying psychiatric disease, and

symptom severity leading to impairment under one disorder. Nevertheless, the prescription of

pharmacotherapy to treat the symptoms of what appears to be ADHD often starts without an in-

depth assessment of the true nature of the disorder in the patient. The finding by Wolraich et al.

(2014) that 5.7% of the children sampled in their study received a diagnosis of ADHD and were
prescribed ADHD medication despite the fact that they did not meet the DSM IV-TR (2000)

criteria for ADHD underscores the willingness to treat pharmacologically a set of symptoms that

look like a disorder, but for which there is no objective evidence of its presence in the patient.

Furthermore, even when a diagnosis is made using the criteria provided by the DSM,

pharmacological treatment efficacy may vary significantly depending on the constellation of

symptoms present in the patient (del Campo, Chamberlain, Sahakian, & Robbins 2011; Feldman

& Reiff, 2014; Hale, Reddy, Semrud-Clikeman et al., 2011). As of 2011, 1 million more

children are taking ADHD medication than in 2003 (Visser et. al., 2013). The very significant

increase in use of ADHD pharmacological therapy is best described in the March 2014 Express

Scripts Lab Report “U.S. MEDICATION TRENDS for ATTENTION DEFICIT HYPERACTIVITY

DISORDER”. This report states that ADHD medication use among Americans has risen 35.5%

from 2008 to 2012. This increase has translated into a spending increase on ADHD medication

of 14.2% in 2012 and represents the greatest increase seen among any traditional drug category.

ADHD medication sales are also forecast to continue to grow to nearly 25% by 2015.

The willingness to prescribe pharmacological therapy, specifically stimulants, for the patient

presenting with ADHD symptoms comes in part from the awareness that this type of treatment

seems to work best at alleviating the core symptoms of ADHD (Faraone & Buitelaar, 2010), may

be equally effective across subtypes (Solanto, Newcorn, Vail, et al. 2009), and affects various

aspects of cognition (Coghill, Seth, Pedroso, et al. 2014) by exerting their effects on the frontal

cortex (Rubia, Alegria, Cubillo, et al. 2014). These findings are not surprising since it is well

known that stimulants exert their effects on the dopaminergic network (for review see Segal &

Kuczenski, 1994; Kuczenski & Segal, 1997), and these effects produce changes in behavior

(Volkow et al., 1998). Given that even a single dose of methylphenidate can enhance cognitive
performance in healthy volunteers, and that there is a dose-dependent and a dose–response

relationship that differs across a variety of cognitive domains (Linssen, Sambeth, Vuurman, &

Riedel, 2014), pharmacotherapy as a global treatment for all patients diagnosed with ADHD

without sensitivity to the array of symptoms and functional deficits in any one individual may be

akin to taking a canon to an anthill. For example, though there may be an initial improvement of

some of the symptoms, pharmacotherapy does not always “normalize” cognition and/or behavior

(e.g., Bédard, Stein, Halperin et al., 2015; Gualtieri & Johnson, 2008; Rapport, Denney, DuPaul,

& Gardner, 1994; Hale et al., 2011; Rubia, Halari, Cubillo et al., 2009), and worse yet can end up

precipitating far more serious symptoms, including psychosis if pharmacotherapy is begun when

the relationship between the impairment due to any detected or undetected comorbid disorder

and that due to the ADHD symptoms is unclear (Schaeffer and Ross, 2002). Furthermore, as

suggested earlier, though the evidence to date indicates that pharmacotherapy seems to eliminate

the core symptoms of ADHD irrespective of subtype, there is evidence that the CT subtype has a

higher probability of being rated as improved relative to the PI subtype (Weiss et al. 2003).

Whether or not the differences in efficacy across the different presentations of ADHD as well as

their associated effects on cognition and behavior are linked with differentiable changes in the

aberration patterns of brain activity, and/or, for example, a related change in catecholamine

availability (del Campo, Chamberlain, Sahakian, & Robbins, 2011; Schmeichel & Berridge,

2013) has yet to be fully clarified. Taken together all of these factors point to the great need for

the refinement and deepening of the diagnostic process in order to identify a clear clinical

presentation that can optimize the clinical outcome.

In parallel to the increased use of pharmacotherapy to treat ADHD, there has also been an

explosion in the search for alternatives to the pharmacological treatment of ADHD (Sonuga-
Barke et al. 2013) even though many of these alternative treatments show no evidence of

efficacy. The development of these alternatives has been fueled by variability in efficacy of

pharmacotherapy (Faraone & Buitelaar, 2010), the desire to avoid the known side effects

(Graham et al. 2011; Bolea-Alamañac et al. 2014; Clemow & Walker, 2014) and the unknown

consequences of long term treatment with pharmacotherapy (Volkow & Thomas, 2003; Vitiello,

2001) or simply by the desire to find a more holistic solution in lieu of the pharmacological one

(Timimi, 2004; Metters, 2013).

One area that has received significant attention is the role of diet in ADHD either as the

etiological basis for its symptoms (Wolraich, Milich, Stumbo, & Schultz, 1985; Wolraich et al.

1994) or as an option for treating the symptoms of the patient (Millichap & Yee, 2012; Nigg,

Lewis, Edinger, & Falk, 2012). Recent reviews and meta-analyses of randomized controlled

studies to investigate the effects of dietary treatments for ADHD (Stevenson et al. 2014; Sonuga-

Barke et al. 2013) concluded that though supplementation with free fatty acid appears to have a

small effect on ADHD-related behaviors, there is no definitive effect of dietary treatment on

these behaviors.

There have also been numerous studies that have looked at the effect of exercise on children

with ADHD. A review by Kamp, Sperlich, & Holmberg (2014) on the effects of exercise on

ADHD-related behaviors in children under 14 years of age concluded that a wide variety of

exercises, if implemented for 1-10 weeks, can have a positive effect on motor skills, social

behavior and strength in this population. However, when Hoza et al. (2014) compared the

effects of physical activity and sedentary activity before the start of school on the behavior of

early elementary school age children at risk for ADHD, they were unable to assert conclusively

that there was a difference between interventions. Though the benefits of exercise for the
treatment of ADHD may still be unclear, there is sufficient pre-clinical as well as clinical data on

non-ADHD populations that show that exercise has a beneficial effect on neurobehavioral

functioning and as such may be a direction worth pursuing (Halperin, Berwid, & O’Neill, 2014).

Psychosocial interventions for children and adolescents with ADHD have a long and

controversial history (see Antshel & Barkley, 2011, for a historical review; Pelham & Fabbiano,

2008). Evans, Owens, & Bunford (2014) conducted a meta-analysis on 122 recent studies that

investigated evidenced-based effects of training intervention and behavior management

treatments. Their results confirm that traditional behavior management therapies have a well-

established efficacy, and that organization training also appears to be effective; however,

improvement in function comes only with the implementation of behavior management

techniques (Feldman & Reiff, 2014). Other training interventions including neurofeedback (for

review see Holtmann, Sonuga-Barke, Cortese, & Brandeis, 2014), cognitive training (for review

see Sonuga-Barke, Brandeis, Holtmann, & Cortese, 2014) and social skills training (for review

see Mikami, Jia, & Na, 2014) show little or no efficacy. There are at least two caveats to these

findings. First, most studies do not look at effects of these alternative therapies by subtype.

Mikami et al. (2014), however, did notice that social skills training seemed to be more effective

for the PI subtype than for the CT subtype. Second, the addition of a behavioral therapy

component to the pharmacological treatment does not appear to confer any advantage to the

resolution of symptoms (Jensen et al., 2001; Sonuga-Barke et al. 2013).

Neural Substrates of ADHD

The rationale behind why the core symptoms of ADHD improve with stimulants comes

from decades of research that has revealed the effect of amphetamines on the dopaminergic
network (for review see Segal & Kuczenski, 1994; Kuczenski & Segal, 1997) and its consequent

effects on behavior (Volkow et al., 1998). The effects of varying levels of dopamine in the brain

have been linked specifically to the frontal cortex in normal subjects as well as in a variety of

neurological and psychiatric disorders (for review see Clark & Noudoost, 2014). In particular,

levels of dopamine in the frontal cortex seem to modulate among other things impulsivity

(Dagher & Robbins, 2009; Volkow, Fowler, Wang, Baler, & Telang, 2009; for review see

Sebastian et al., 2014), motivation (Volkow, Wang, Newcorn, et al., 2011) and inattention (Rosa-

Neto, Lou, Cumming, 2005) all hallmark characteristics of ADHD. As a result there has been a

virtual explosion of studies aimed at uncovering differences in anatomy and function in the

brains of ADHD patients relative to normal cohorts. The scientific impetus to conduct such

studies stems presumably from a need to understand what may be dysfunctional or aberrant in

the brain of the ADHD patient as well as the hope of finding a biomarker that could render a

diagnosis conclusive (for review see Shaw et al., 2013). There are basically four main lines of

research with this aim that have identified functional and anatomical differences in the brains of

ADHD patients relative to age matched normal controls: 1) analysis of brain volume and cortical

thickness, 2) functional MRI (fMRI), 3) diffusion tensor imaging studies (DTI) and 4) most

recently connectomics. The combined results from these studies as well as a plethora of meta-

analyses across such studies suggest that on average children and adolescents with ADHD have

reduced brain volumes (Castellanos et al. 2002; Nakao, Radua, Rubia, & Mataix-Cols, 2011;

Lim et al,. 2014), reduced cortical thickness (McLaughlin et al., 2014; Almeida et al., 2010;

Shaw et al., 2013), show deactivation in function relative to controls predominantly in fronto-

striatal, fronto-parietal and fronto-cerebellar regions (for review see Cubillo, Halari, Giampietro,

Taylor, E., & Rubia, 2011 and Rubia et al. 2014) and appear to have abnormalities in functional
connections (Cao et al., 2014; Tomasi & Volkow, 2012; Sripada, Kessler, & Angstadt, 2014)

primarily between these areas as well as a lag in brain maturation both in terms of structure

(Shaw et al., 2007) and functional architecture (Sripada et al. 2014 ).

The regions of brain that show decreased activation in the ADHD patient as measured by

fMRI have historically been thought to support executive function (EF) given in part to the now

well documented finding that patients who have suffered lesions in these areas perform poorly on

tasks that recruit EF such as, but not limited to the Stroop test, Stop-signal task, or Go/no go task,

(Shallice & Burgess, 1991). By extension, when a patient who does not have an observable

injury of the brain performs poorly on such neuropsychological instruments, the implication is

that there is a correlated dysfunction in the areas of brain that support that task (Miyake et al.,

2000). In other words, the rather circular argument states that objective evidence of injury to

these areas is correlated with poor EF as measured by neuropsychological tests, and poor

performance on those same tests is assumed to be the result of underlying abnormality in those

same brain regions. Neuroimaging studies of ADHD patients that have required the performance

of tasks that measure EF during image acquisition, ostensibly in order to activate the neural

substrates which support task execution, have not reliably and consistently shown a significant

correlation between performance on tasks of EF and the activation of the neural substrates

supporting the task. Namely, some studies were successful in demonstrating a correlation

between poor performance and hypoactivation (Booth et al., 2005; Konrad et al., 2006), but

many have failed to show a correlation between performance on these tasks and deactivation of

brain regions recruited during these tasks (Rubia, et al., 2010; Cubillo et al. 2011; Rubia,

Cubillo, Woolley, Brammer, & Smith 2011; Smith et al., 2006, Congdon et al., 2014; Konrad et

al., 2006; Banich et al., 2009), or even to detect significant differences either in performance on
the measure of EF or in the brain activation patterns (Congdon et al., 2014). Furthermore, data

from resting state fMRI studies suggest that the hypoactivation seen on fMRI is unrelated to the

performance of the task during image acquisition (Tian et al., 2008; Yu-Feng et al., 2007;

Hoekzema et al., 2014; Li et al., 2014).

Although the absence of a corroborative behavioral effect does not make neuroimaging

findings irrelevant, it does beg the question as to which of the potential “cognitive algorithms” is

the subject able and not able to recruit during the performance of the task, and how if at all are

they linked to the ongoing detectable activity in the brain (Mostofsky & Simmonds, 2008; for

commentary see Wilkinson & Halligan, 2004). With respect to ADHD there are at least three

issues that need to be evaluated before it will be possible to answer this question. First, is the

variability in the corroboration between performance and activation in the associated neural

substrates due to the neuropsychological task? Second, given the reviewed evidence for

significant differences between subtypes, is the variability in the corroboration between

performance and activation in the neural substrates a function of the heterogeneity in ADHD?

Third, is the variability in the corroboration between performance and activation in the neural

substrates a function of an incomplete understanding about the interaction between heterogeneity

of cognitive processes and heterogeneity in the architecture of the frontal cortex?

Is the variability in the corroboration between performance and activation in the

associated neural substrates due to the neuropsychological task?

One could argue that the sample size in the studies that failed to show a correlation between

hypoactivation in brain regions and performance was too small (in general <20) to detect

performance differences given that previous studies of purely cognitive or neuropsychological

deficits in ADHD with similar sample sizes also failed to show effects associated with deficits in

EF (Barkley, 1997). However, there is also evidence showing that robustness in EF may not be a

valid or reliable measure for the identification of ADHD patients (Barkley, 2012; for review see

Lange et al., 2014). For example, Wåhlstedt, Thorell, & Bohlin (2009) report that 20%-40% of

children with ADHD do not score in the clinically significant impairment range on a variety of

EF measures. Duff & Sulla (2014) also make the case that although poor performance on an EF

measure may be strongly suggestive of the presence of a clinical disorder, failure to demonstrate

impairment on the measure does not belie the existence of a disorder. In addition, there seems to

be a continuum effect such that there is a significant correlation between level of impairment on

EF measures and negative behavioral symptoms. Furthermore, the use of any one “cold”

cognitive construct such as those used in task-related fMRI studies may or may not be truly

representative of EF functioning (Barkley, 2012). For example, there are data suggesting that

simply the addition of a working memory component, which requires the maintenance of an

attentional set in order to complete the task, increases the probability of detecting differences in

neural substrates that are correlated with the performance of a go/no-go task in normal adults,

(e.g., Mostofsky, Schafer, Abrams et al., 2003; Mostofsky& Simmonds2008), a Color-Word

Stroop test in ADHD patients (Burgess, Depue, Ruzic et al., 2010), and an N-back test of

working memory for spatial position (Bédard, Newcorn, Clerkin et al., 2014).

The inconsistency in the findings relative to the performance of neuropsychological tests by

patients with ADHD may be related to the idea that the heterogeneity of symptom presentation

does not warrant the assumption that the diagnosis of ADHD should lead to a homogeneous

response pattern across patients during a neuropsychological assessment. An analysis conducted

by Fair et al. (2012) clearly indicates that neuropsychological subtypes can be discerned with
high precision not only in children with ADHD, but also in typically developing control youth.

Furthermore, there appears to be an overlap between the heterogeneity found in children with

ADHD and the variation found in typically developing children. With respect to the deficit in

response inhibition that many studies on ADHD assume for purposes of their experiments, the

Fair et al. (2012) analysis reveals that though valid at the group level, if individual results from

the ADHD group are compared with the normal controls, the differences are significant only in

about 50% of the comparisons. A similar pattern was detected for working memory as well as

temporal information processing. The finding that only about 50% of the comparisons were

significant when looked at individually rather than as a group follows the general trend that the

percentage of children with ADHD who show clinically significant impairment varies within the

ADHD population and also as a function of the task being used to measure EF (Wahlstedt et al.

2009). Beyond just the individual versus group comparisons on neuropsychological tests, a

neuroimaging study of the neural substrates of response inhibition in normal adults indicates that

single subject analysis reveals a pattern of activation associated with inhibitory response that is

different from the pattern of activation produced in group analysis (Mostofsky et al. 2003).

Koziol & Budding (2012) argue that precisely because of the highly heterogeneous

character of ADHD, the subtypes provided by the DSM cannot capture the individual nature of

the disorder at the neuropsychological level, and as such, cannot be used to characterize the

disorder in terms of dysfunction of a specific set of neuroanatomical substrates. Rather, ADHD

may perhaps best be described in terms of a continuum or spectrum (Haslam et al, 2006; for

review see Bell, 2011) a notion that is lent even more support from the observation that there are

individuals with sub-threshold ADHD. Balázs & Keresztény (2014) report a wide range (0.8-

23.1%) in the prevalence of subthreshold ADHD due to the lack of uniformity regarding the
minimum number of symptoms that should be used to define subthreshold ADHD functional

impairment. This is the case despite the fact that the DSM V (2013) includes both an ‘‘Other

Specified Attention-Deficit/Hyperactivity Disorder’’ category as well as an ‘‘Unspecified

Attention-Deficit/Hyperactivity Disorder’’ category meant to be used to identify individuals who

have some of the symptoms characteristic of ADHD that cause clinically significant problems in

academics or the work place.

In addition to the heterogeneity in neuropsychological profiles within the ADHD population,

there exists one other caveat that may be confounding the results on neuropsychological tasks of

EF as well as neuroimaging during task execution. There is evidence suggesting that ADHD

performance on many experimental tasks is subject to attentional inconsistency (Castellanos &

Tannock, 2001; Douglas, 1999; Epstein et al., 2003; Leth-Steensen et al. 2000). This finding is

not surprising given that lapses in attention can be, by definition, part of the ADHD disorder

(DSM V, 2013). What is of much greater interest is how these lapses in attention present. Leth-

Steensen et al. (2000) discovered abnormally slow reaction times in the tails, but not the leading

edges of the distribution of the reaction times. Further analysis revealed that group differences

disappeared when only leading edge reaction times for the ADHD group were compared with

those of the control group. Thus, the attentional lapse may be occurring as a function of duration

of the test, suggesting that the longer the test goes on, the poorer the performance of the subject.

However, and in addition, each individual reaction time is made up of a constellation of several

steps each of which may also be affected by attentional lapses. In other words, within any one

response there is the moment when the subject sees the response, decides what to do with it and

then decides how to respond. Each of these steps could be subject to an attentional lapse,

resulting in not only reaction time differences but variability in the times at which areas of brain
devoted to the execution of the steps are recruited. This is an especially important consideration

when attempting to describe the neural substrates of the disorder. Namely, the differences

measured during the performance of these tasks as well as the associated differences in activation

of brain regions across groups may be the result of a comparison made between different

portions of the sequence of operations required to complete the task. The assumption that any

variability simply averages out particularly when such small sample sizes are used may

inadvertently be washing out the very effect that is being sought.

In sum, variability in the performance on neuropsychological tests of EF across the

ADHD population can be attributable to at least four issues. On the one hand it is still not clear

how or if each of the neuropsychological tests used to measure EF in individuals with ADHD is

actually measuring EF or at the very least what aspects of EF it is measuring. Second, there are

not enough data to know how much of a cognitive load needs to be introduced into a

neuropsychological test in order for performance differences relative to controls to be observed.

Third, experimental designs do not take into account either the variability in performance as a

function of test duration or the variability in performance across the span of the test. Both of

these points are especially relevant when testing performance in subjects who are known to have

variations in attention, focus and impulsivity over a span of time. Finally, there are little data

regarding performance differences on neuropsychological tests as a function of ADHD subtype

or severity of symptomatology. Given the evidence presented thus far in the review, there is not

only sufficient support to warrant such investigations, but more importantly there is no rationale

for assuming that patients in which ADHD symptoms have been observed will all perform in a

homogeneous manner.
Is the variability in the corroboration between performance and activation in the neural

substrates a function of the heterogeneity in ADHD?

A great majority of task dependent neuroimaging studies do not make any distinctions in

terms of symptom presentation or subtype of the ADHD subjects (Booth et al., 2005; Hart,

Radua, Nakao, Mataix-Cols & Rubia, 2013; Konrad et al. 2006; Rubia et al., 2005; Rubia et al.

2010; Simmonds, Pekar & Mostofsky, 2008). As has been discussed earlier in this review, there

is converging evidence suggesting that not only are the differences between the variants of

ADHD important, but in some case the differences are so remarkable that they may warrant

being considered as separate disorders rather than subtypes of ADHD. Therefore, as our

understanding about ADHD continues to grow, the evidence must confirm or deny the rationale

for using ADHD as an umbrella term for the various subtypes and/or using only one subtype in

experimental designs.

The comparison of some of the data that have been collected to elucidate the neural

substrates that support working memory exemplify the need to take into account the

heterogeneity seen in ADHD. When adult patients with ADHD (collapsed across all subtypes)

performed an n-back task during the acquisition of fMRI data, significant differences between

adults with and without ADHD were found in the bilateral prefrontal cortices. However, only

men with ADHD showed less activation in a network of brain regions that was lateralized to

right frontal and subcortical regions and left occipital and cerebellar regions relative to controls.

Adult females with and without ADHD were indistinguishable despite the fact that ADHD

symptomatology in both the females and males was similar (Valera, Brown, Biederman et al.,

2010). Burgess et al. (2010) looked at the brains of adult males and females specifically with CT

subtype ADHD with fMRI while they performed either a working memory digit span or spatial
span task. They found decreased function in the left dorsolateral prefrontal cortex relative to

normal controls; however this study did not look at gender differences. Mills, Bathula, Dias et

al. (2012) found evidence for atypical thalamic connectivity with cortical structures in children

with ADHD (collapsed across subtypes) related to their performance on a task of spatial span

working memory using rs-fcMRI. Massat, Slama, Kavec, Linotte et al. (2012) also studied

children with CT subtype ADHD using fMRI to investigate differences in activation patterns

between that group and normal controls while performing an n-back working memory task, and

their data found no evidence for differences in prefrontal areas between children with CT

subtype ADHD and normal cohorts, but did find decreased activation in inferior parietal cortex,

as well as decreased activity in the striatum and the cerebellum.

When Lockwood et al. (2001) explicitly targeted the identification of differences between

ADHD subtypes with respect to neuropsychological performance, all attempts were made to

minimize methodological limitations including insuring that all participants were medication

free, that clinical diagnosis was accurate, that there was no comorbidity, and that there was equal

representation across genders. Their results indicate that the PI subtype had greater difficulty

selecting previously presented auditory information from prompted material. This finding agrees

with the hypothesis discussed earlier in this review that the PI subtype is associated with a

narrow focus of attention. In other words, one explanation for their findings could be that the

discrimination between previously heard and currently heard material was difficult because the

children stagnated their attention at different times during the previously presented stimuli and as

such some of the information was not encoded into memory. In contrast children with the CT

subtype showed impaired response inhibition and reengagement as well as difficulty carrying out

goal directed activities. This finding also fits with the previously presented hypothesis that the
CT subtype is associated with the inability to stop shifting focus, which in this case resulted in

attending to inappropriate stimuli.

The postulates from the Barkley (1997) model of ADHD that only the CT and HI

subtypes, but not the PI subtype, are associated with EF deficits, have led to several studies

aimed at investigating the validity of this claim. Though several studies did not find differences

in EF across subtypes (e.g., see Duff & Sulla, 2014 for review; Geurts et al. 2005; Riccio et al.

2006; Song & Hakoda, 2014), the failure to find differences may be the result of assuming a

binary response across a homogeneous test. That is to say, the expectation is that the response

from individuals of one subtype will somehow be discrete from the other subtype. What is

lacking in most of these studies, and serendipitously discovered in the Song &Hakoda (2014)

study is that cognitive load, particularly with respect to working memory, may elicit the

difference that is being investigated. In fact, Diamond (2005) suggests that the primary deficit of

the PI subtype is in working memory. Furthermore, in their study on the comparison between

children with low working memory and children with the CT subtype of ADHD, Holmes, Hilton,

Alloway et al. (2014) report that children with a diagnosis of low working memory are almost

indistinguishable to CT subtype children across many assessments, including EF and degree of

inattentive behavior. However, what distinguished the two groups were the externalized

behaviors, namely, the hyperactivity and impulsivity associated with the CT subtype and the

significantly slower response times in the low working memory group. These findings led the

authors to postulate that individuals diagnosed with low working memory may actually be

manifesting the PI subtype of ADHD.

Finally, there are preliminary data that provide some justification for taking into account the

heterogeneity seen in ADHD when designing experiments that measure brain activity. Although
their study did not seek to uncover task-related differences in brain using fMRI, Fair, Nigg, Iyer

et al. (2012) did discover that resting-state functional connectivity MRI (rs-fcMRI) was able to

differentiate between the CT and PI subtypes of ADHD. Another study using DTI uncovered a

network of connections in the right frontal regions that was able to differentiate between the CT

and PI subtypes; specifically there was decreased connectivity in the CT subtype compared with

the PI subtype (Hong, Zalesky, Fornito et al., 2014). Both studies suggest that there could be

neural signatures that are specific to at least two ADHD subtypes. As such, not taking into

consideration the heterogeneity that exists in ADHD and mixing the results of qualitatively

different groups can actually end up cancelling out the differences one is searching for (Barkley

2001).

Taken together, all of these results point to the conclusion that there is no rationale for

using exclusively one subtype in an experimental design; or worse yet, to group together several

subtypes under one umbrella category labeled as ADHD. Additionally, the Lockwood et al.

(2001) study underscores the importance of using heterogeneous attentional measures if the aim

is to assess neuropsychological differences between ADHD subtypes. Failure to do so could

lead to the inaccurate collection of data and the erroneous interpretation of results. Finally, the

data that do exist pertaining to the neural substrates associated with the heterogeneity found in

ADHD actually provide some evidence that symptomatological variants may be supported by

different brain circuits, and as such, could theoretically be considered as related, but separate

disorders.
Is the variability in the corroboration between performance and activation in the neural

substrates a function of an incomplete understanding about the interaction between

heterogeneity of cognitive processes and heterogeneity in the architecture of the frontal

cortex?

The data pointing to impairment of EF in ADHD as well as an observed hypoactivation

of the frontal cortex in patients with ADHD can lead to the assumption that EF is exclusively a

function of the prefrontal cortex. However, paraphrasing from both Dimond (1980) and Barkley

(2012), the functions of the frontal lobe are as varied as it is large, and the dimensionality of EF

is as broad as it is deep. Therefore, perhaps a better way to conceive of the prefrontal cortex is as

a way station to different functions given its various interconnections with cortical and

subcortical regions (Cubillo et al., 2011; Stuss & Benson, 1986), particularly since there is strong

evidence supporting that different cognitive processes are subserved by different subregions of

the prefrontal cortex (Chudsama, 2011; Heidbreder & Groenewegen, 2003; Kesner &

Churchwell, 2011). In a meta-analysis of lesion and functional neuroimaging studies that

investigated the role of the frontal lobes and EF, Alvarez & Emory (2006) concluded that the

participation of the frontal lobes in EF is linked to the sensitivity of the different tests used to

measure EF, each of which might be recruiting different cognitive processes. Their findings

support the idea that EF is “fractionable” (Lopez-Vergara & Colder, 2013; Miyake et al. 2000).

However, as the review by Donohoe & Robertson (2003) points out, though there is evidence for

the discrete neuroanatomical separation of the different “fractions” of EF, there remains overlap

between the different executive measures because they are correlated with each other and are

causally related to each other. Furthermore in their review on working memory and EF,

Carpenter, Just, & Reichle (2000) provide converging evidence for a system in which rather than
there being an association between each fraction of EF and a single cortical area, each cortical

region has more than one function, and the functions of each of the regions may overlap each

other. The authors suggest further that each task may prompt a different combination of several

brain regions depending on the requirements of the task. Since this “nondiscreteness of

specialization” proposed by Carpenter et al. (2000) is probably a reality of cortical organization

in general, it can also serve as a point of departure for a novel way of conceptualizing ADHD.

Do ADHD symptoms point to a spectrum instead of a disorder?

If the DSM is correct, then there are more than 70 million children and more than 60

million adults worldwide that have ADHD. These estimates have been made despite the fact that

as Brown (2006) so succinctly puts “There is no one test that can determine whether a given

individual meets DSM diagnostic criteria for ADHD. This is a diagnosis that depends on the

judgment of a skilled clinician who knows what ADHD looks like and can use data from

multiple aspects of the individual’s daily life over protracted periods of time to differentiate it

from other possible causes of impairment.” What is so interesting about Brown’s statement is

that on the one hand he acknowledges that there is no single test to determine if someone has

ADHD, but at the same time suggests that skilled clinicians nevertheless somehow “know” what

ADHD looks like. Brown’s comment is actually corroborated by what the team of scientists

from Johns Hopkins who won the “The ADHD-200 Global Competition”

(http://fcon_1000.projects.nitrc.org/indi/adhd200/) discovered. They were able to demonstrate

that there was a much greater probability of correctly discriminating between typically

developing children and children with ADHD than there was for correctly identifying children

with a true positive diagnosis of ADHD. Interestingly, the Johns Hopkins team was also able to
discern the subtypes of ADHD with high accuracy. This pattern of discrimination indicates that

the individual who receives a diagnosis of ADHD is different from a normal individual, yet the

diagnosis of ADHD is not associated with a signature that either renders the diagnosis

unequivocable or is sufficiently unique that variations in presentation are not easily

distinguishable. The primary aim of the present review was to elucidate whether or not there is

something unique to “know” about ADHD such that every one of those hundreds of millions of

individuals could somehow fit under the same single disorder; or rather, if there was some way

to take what is known about ADHD and use it as a diagnostic tool for a spectrum of disorders

that as Asperger (1979) said are “…at once so alike, but so different…” and yet the

“…differences are so great…”

The data on the prevalence, diagnosis, heterogeneity and comorbidity of ADHD

described in this review all point to the struggle at trying to fit a wide variety of clinical

presentations into the diagnostic criteria for a single disorder that usually leads to a debate about

what should and should not be included. Though the observation of certain behavioral traits as

indicated by the DSM V (2013) is undeniably necessary to identify individuals at risk, the

diagnostic process is limited by the assumed need to fit a wide variety of symptoms under one

rubric in part because of the limitation of therapeutic avenues, but more importantly because of

the urgency to bring relief to an individual whose ability to engage in the everyday functions of

life can be severely compromised. One way out of the conundrum of having to use a single

diagnosis for so many clinical presentations is to think of ADHD as a “psychophysiological

modality” that can be expressed across a spectrum that can accommodate the wide heterogeneity

observed in ADHD. Earlier in this review, the idea of varying widths of attentional spotlights

was introduced as a way in which to describe the differences in attention and hence impulsivity
exhibited by the PI and CT subtypes of ADHD. Specifically, whereas the PI subtype was

described as having a narrow spotlight of attention, the CT and HI subtypes were described as

having wide spotlights of attention. The width of the spotlight dictated the degree to which an

individual had access to information as well as the ability the individual had to focus on

information. As a result of a narrow spotlight of attention, the patient with PI subtype fails to

detect certain external stimuli because they are outside of his attentional focus. The extended

spotlight width of the CT subtype creates a stimulus overload by allowing too many external

stimuli to flood the attentional space, making it difficult for the patient to focus on any one of the

myriad of external stimuli to which these patients have access. Each subtype can also be

associated with an observed or perceived impulsivity. The PI subtype may appear impulsive

only because decisions made were based strictly on information that the patient could access. On

the other hand, the impulsivity of the CT subtype could be the result of an inability to focus on

the necessary bits of information to which the patient has access. In other words, the difference

between the two can be summarized as “not having access“ versus “not knowing what to select.”

Barkley (1997) suggests that problems with selective attention are associated with the PI subtype

and inhibition was the problem with the CT subtype. The suggestion here is that both inhibition

and selective attention are a problem for the CT subtype. That is, though the patient with the CT

subtype may not be able to inhibit competing responses, they also cannot select the appropriate

responses for evaluation. On the other hand, although the patient with PI subtype may have a

deficit of selective attention, it is unclear whether or not the selection of what to attend to is

under his voluntary control. As such, the CT and PI subtypes can be considered to lie on a

spectrum that varies as a function of attention and impulsivity.

 A spectrum of attention and impulsivity could also accommodate the extremely high

symmetrical and asymmetrical comorbidity linked with ADHD since so many of these comorbid

disorders also show impairment in attention and/or impulsivity as part of their own clinical

profiles. Although it is neither the intention nor the scope of this review to map out entirely what

such a spectrum of disorders could look like, three separate psychiatric disorders that have been

associated with ADHD (schizophrenia, obsessive compulsive disorder (OCD) and conduct

disorder) will be used to illustrate how they could be colocalized on the spectrum.

Schizophrenia is associated with a vast number of symptoms, including delusions,

hallucinations, flat affect, and inappropriate emotional expression that originate from completely

within the schizophrenic patient rather than as a reaction to external stimuli. As a result, the

schizophrenic can be viewed as having an extremely narrow attentional focus inasmuch as the

patient is focused almost exclusively on internally generated stimuli, leaving little breadth of

attention to dedicate to the external world. The schizophrenic patient also shows no impulsivity

to the extent that he can be considered even risk aversive (Reddy, Lee, Davis, 2014). Thus,

schizophrenia would be colocalized on the part of the spectrum that is associated with the most

narrow attentional focus and the lowest degree of impulsivity, giving it a greater “etiological

vicinity” to the PI subtype than the CT subtype.

Conversely, the CT subtype and conduct disorder could be seen as having a very

proximal “etiological vicinity” and would be extremely close in terms of their colocalization on

the proposed spectrum. Both disorders are characterized by high levels of impulsivity and both

have an overly wide attentional spotlight, making it difficult for patients with either disorder to

focus on the appropriate stimuli that would lead to good decision making. Though their very

high symmetrical comorbidity and similarity in characteristics invite the tendency to want to
consider them as a single disorder (Biederman et al. 1991), there are sufficient fine differences,

for example in the exhibition of defiance, that would separate these disorders on the spectrum.

OCD would be colocalized somewhere between the PI subtype and schizophrenia and the

CT subtype and conduct disorder. The patient with OCD is characterized by the presence of

obsessions and/or compulsions with some patients showing relatively more impulsivity than

others (Kashyap, Fontenelle, Miguel, 2012). OCD patients are also classified according to the

degree of insight they have related to the nature of their disorder. The OCD patient who shows

the greatest impulsivity also has the poorest insight where poor insight is defined by the patient’s

belief that his OCD compulsions are warranted and true (Kashyap et al., 2012). Poor insight is

thus considered a form of delusion, and since delusion is the result of internally generated beliefs

the attentional spotlight would be narrowed. However, because the internally generated beliefs

are about external stimuli, and not an imagined construct as in schizophrenia, the attentional

spotlight would not be as narrow as in schizophrenia. Thus, this type of OCD would be

colocalized partly in the direction of the part of the spectrum associated with some impulsivity

and partly in the direction of a narrowing width of attentional spotlight. Conversely, some OCD

patients have low impulsivity and high insight. This type of OCD would be colocalized in the

direction of that part of the spectrum associated with little or no impulsivity and in the direction

of a growing width of attentional spotlight. Thus, the spectrum approach to identifying disordes

of attention and impulsivity avoid many pitfalls. IT is a system that permits less subjectivity and

more objectivity because now the focus is on the quality of the defect rater than on using the

presence of the defect to position the disorder under one category or a subset of the same

category. It is not inconceivable that sucha s sytem could lead to customizable treatment even as

medicine moves towards individual gene based treatment approaches.

 The concept of looking at a group of psychiatric disorders as interrelated because they

share a common psychophysiological modality that comprises varying degrees of two major

cognitive functions in this case, attention and impulsivity, is plausible not only as part of

psychological theory, but also as part of what we know about the function of the brain. The

neurological construct supporting this idea would be similar to the one Carpenter et al. (2000)

write about, that is, of a “cognitive process that spans multiple cortical sites with closely

collaborative and overlapping functions”. Data about the symmetric and asymmetric

comorbidity associated with ADHD as well as the heterogeneity that has been observed within

the disorder implicate the prefrontal cortex (PFC) as a major site for the dysfunction. There is an

abundance of evidence indicating that the PFC is a heterogeneous structure that is divisible not

only in terms of its cytoarchitectonics, (Heidbreder & Groenewegen, 2003), but also on the basis

of differences in connectivity patterns with structures such as the amygdala, the temporal cortex,

the parietal cortex, thalamic nuclei, hippocampus, dorsal and ventral striatum, hypothalamus, and

midbrain, as well as with one another (Chudsama, 2011). Furthermore, the manipulation of the

different regions of the PFC produce distinct and dissociable cognitive deficits including

impaired attention, poor working memory, dysregulated affect, abnormal decision-making,

impulsivity, inflexibility, and profound disinhibition (Kesner & Churchwell, 2011). Therefore, it

is not difficult to envision a neural circuit governing attention and impulsivity that allocates

dynamically to a vast number of other neural circuits that underlie any number of disorders. The

contribution of this “attentional/impulsivity neural circuit” to the network of neural circuits

associated with a particular disorder allow for that disorder to be collocated along the spectrum

defined by the “attentional/impulsivity neural circuit”. Finally, such a spectrum is not limited to

clinically disordered states, but can also capture the heterogeneity in the “attentional/impulsivity”
dimension seen in the general population that may affect behavior, but does not necessarily cause

impairment.

The benefit of characterizing comorbid disorders and interrelated impairments as varying

along one dimension that spans a spectrum and using it as a starting point for diagnosis and

treatment has several advantages. For example, in the case of ADHD, diagnosis is the result of a

convergence of opinions (teachers, parents, clinicians, and multiple settings) that confirm that a

child is impaired from the point of view of attention and/or from the point of view of

hyperactivity/impulsivity. In other words, the endpoint of the diagnosis is the confirmation of

impairment in those domains. In contrast, that convergence of opinions could become the

starting point if we accept that the presence of those symptoms could point to any one of the

disorders that make up part of the spectrum. The physician, therefore, will be prompted to start a

deeper clinical investigation rather than simply halted after observing that a patient has a

particular constellation of symptoms. Thus, the impairment in attention/

hyperactivity/impulsivity will itself not be the disorder, but rather the marker for any of several

disorders that are interrelated. This type of diagnostic also allows for greater flexibility in the

identification of individuals who do not naturally come to mind when we think of the disorder

ADHD, for example, patients who show an SCT profile or subthreshold patients. Additionally,

if clinicians use the attention/hyperactivity/impulsivity marker as the start of their diagnosis, the

diagnostic tools that will be used to refine their opinion about the patient could not only reduce

the total number of patients treated pharmacologically, but also reduce the number of individuals

who engage in the feigning and malingering to obtain a prescription for ADHD medication, a

problem which is currently on the rise (Quinn, 2003; Tucha, Fuermaier, Koerts, Groen, &

Thome, 2014).
 In order to develop better and more varied treatment options for people who have

impairments in the “attention/impulsivity” dimension, data sets generated with much greater

scrutiny reliability and validity must be constructed. Data are lacking in the ability to

discriminate among the heterogeneity in what today is known as ADHD. Few data have been

collected under conditions that elucidate, for example, within subject differences across

neuropsychological tests, or between subtype differences on the same neuropsychological test.

There remains an urgent need to create experimental designs that carefully control for the

different presentations of attention/impulsivity/hyperactivity, including as a function of age and

gender. As the pieces of the puzzle come together not only will we be able to increase our

understanding about how impairments in attention and impulsivity can present, but we will also

elucidate how the different cognitive processes may be distributed across the neural networks

that make up the heterogeneity of the prefrontal cortex. Data already exist that point to

similarities in the underlying neural pathology associated with some psychiatric diseases and

patients presenting with ADHD (e.g., for review see Banaschewski, Hollis, Oosterlaan et al.,

2005; Rubia et al. 2010); however, there is also evidence for shared neural substrates across

diverse psychopathologies (Goodkin et al., 2015). Further clarification related to the neural

networks that support the different disorders that lie across the spectrum will lead to both the

prescription of the appropriate treatments that are available today as well as the dentification of

new treatments that target specific populations of neurotransmitters associated with the neural

networks.

In summary, precisely because the symptoms of inattention and impulsivity are not

unique to ADHD and there is an exceedingly high and unexplained symmetrical and

asymmetrical comorbidity of many psychiatric diseases with ADHD, it is reasonable to stop

considering ADHD as a single disorder. Rather, future investigations should use what is known

about ADHD to develop further the idea that individuals who show the symptoms typical of

ADHD may be pointing to a different more specific disorder that is part of a larger spectrum.
References

Almeida, L. G., Ricardo-Garcell, J., Prado, H., Barajas, L., Fernández-Bouzas, A., Ávila, D., &

Martínez, R. B. (2010). Reduced right frontal cortical thickness in children, adolescents

and adults with ADHD and its correlation to clinical variables: a cross-sectional

study. Journal of psychiatric research, 44(16), 1214-1223.

Alvarez, J. A., & Emory, E. (2006). Executive function and the frontal lobes: a meta-analytic

review. Neuropsychology review, 16(1), 17-42.

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.-revised). Washington, DC: Author.

American Psychiatric Association. (1994). Diagnostic and statistical manual of mental disorders

(4th ed.). Washington, DC: Author.

American Psychiatric Association. (2000). Diagnostic And Statistical Manual Of Mental

Disorders DSM-IV- TR Fourth Edition (Text Revision) Author: American Psychiatr.

American Psychiatric Association. (2013). The Diagnostic and Statistical Manual of Mental

Disorders: DSM 5. bookpointUS.

Anastopoulos, A., Barkley, R., & Shelton, T. (1994). The history and diagnosis of attention

deficit/hyperactivity disorder. Therapeutic care and education, 3, 96-96.

Antshel, K. M., & Barkley, R. (2011). Overview and historical background of attention deficit

hyperactivity disorder. In S. W. Evans & B. Hoza (Eds.), Treating attention-

deficit=hyperactivity disorder: Assessment and intervention in developmental context

(pp. 1–1 to1–30). New York, NY: Civic Research Institute.

Arnett, A. B., MacDonald, B., & Pennington, B. F. (2013). Cognitive and behavioral indicators

of ADHD symptoms prior to school age. Journal of Child Psychology and

Psychiatry, 54(12), 1284-1294.

Arnett, A. B., Pennington, B. F., Willcutt, E. G., DeFries, J. C., & Olson, R. K. (2014). Sex

differences in ADHD symptom severity. Journal of Child Psychology and Psychiatry.

Baeyens, D., Roeyers, H., & Walle, J. V. (2006). Subtypes of attention-deficit/hyperactivity

disorder (ADHD): distinct or related disorders across measurement levels?. Child

Psychiatry and Human Development, 36(4), 403-417.

Bagot, K. S., & Kaminer, Y. (2014). Efficacy of stimulants for cognitive enhancement in non‐

attention deficit hyperactivity disorder youth: a systematic review. Addiction, 109(4),

547-557.
Balázs, J., & Keresztény, Á. (2014). Subthreshold attention deficit hyperactivity in children and

adolescents: a systematic review. European child & adolescent psychiatry, 1-16.

Banaschewski, T., Hollis, C., Oosterlaan, J., Roeyers, H., & Rubia, K. W. E. 2005. Towards an

understanding of unique and shared pathways in the psychopathophysiology of

AD/HD. Developmental Science, 8, 132-140.

Banich, M. T., Burgess, G. C., Depue, B. E., Ruzic, L., Bidwell, L., Hitt-Laustsen, S., Du, Y.P.,

& Willcutt, E. G. (2009). The neural basis of sustained and transient attentional control in

young adults with ADHD. Neuropsychologia, 47(14), 3095-3104.

Barkley, R. A. (1997). Behavioral inhibition, sustained attention, and executive functions:

constructing a unifying theory of ADHD. Psychological bulletin, 121(1), 65.

Barkley, R. A. (2001). The inattentive type of ADHD as a distinct disorder: What remains to be

done. Clinical Psychology: Science and Practice, 8(4), 489-493.

Barkley, R. A. (2005). Attention-deficit hyperactivity disorder: A handbook for diagnosis and

treatment (Vol. 1). Guilford Press.

Barkley, R. A. (2007). What may be in store for DSM-V. ADHD Report, 15, 1-7.

Barkley, R. A. (2012). Executive functions: What they are, how they work, and why they evolved.

Guilford Press.
Barkley, R. A. (2013). Distinguishing sluggish cognitive tempo from ADHD in children and

adolescents: executive functioning, impairment, and comorbidity. Journal of Clinical

Child and Adolescent Psychology.

Barkley, R., & Peters, H. (2012) The Earliest Reference to ADHD in the Medical Literature?
Melchior Adam Weikard's Description in 1775 of "Attention Deficit" (Mangel der

Aufmerksamkeit, Attentio Volubilis). Journal of Attention Disorders, 16(8), 623-630.

Barkley, R. A. (2013). Distinguishing sluggish cognitive tempo from ADHD in children and

adolescents: executive functioning, impairment, and comorbidity.Journal of Clinical

Child & Adolescent Psychology, 42(2), 161-173.

Bauermeister, J. J., Barkley, R. A., Bauermeister, J. A., Martinez, J. V., & McBurnett, K. (2012).

Validity of the sluggish cognitive tempo, inattention, and hyperactivity symptom

dimensions: neuropsychological and psychosocial correlates. Journal of Abnormal Child

Psychology, 40, 683–697.

Becker, S. P., Marshall, S. A., & McBurnett, K. (2014). Sluggish cognitive tempo in abnormal

child psychology: An historical overview and introduction to the Special Section. Journal

of abnormal child psychology, 42(1), 1-6.

Bédard, A. C. V., Newcorn, J. H., Clerkin, S. M., Krone, B., Fan, J., Halperin, J. M., & Schulz,

K. P. (2014). Reduced Prefrontal Efficiency for Visuospatial Working Memory in

Attention-Deficit/Hyperactivity Disorder. Journal of the American Academy of Child &

Adolescent Psychiatry, 53(9), 1020-1030.

Bédard, A. C. V., Stein, M. A., Halperin, J. M., Krone, B., Rajwan, E., & Newcorn, J. H. (2015).

Differential impact of methylphenidate and atomoxetine on sustained attention in youth

with attention‐deficit/hyperactivity disorder.Journal of Child Psychology and

Psychiatry, 56(1), 40-48.

Bell, E. C., Willson, M. C., Wilman, A. H., Dave, S., & Silverstone, P. H. (2006). Males and

females differ in brain activation during cognitive tasks.Neuroimage, 30(2), 529-538.

Berry, C. A., Shaywitz, S. E., & Shaywitz, B. A. (1985). Girls with attention deficit disorder: a

silent minority? A report on behavioral and cognitive characteristics. Pediatrics, 76(5),

801-809.

Biederman, J., Newcorn, J., & Sprich, S. (1991). Comorbidity of attention deficit hyperactivity

disorder. American journal of psychiatry, 148(5), 564-577.

Bolea-Alamañac, B., Nutt, D. J., Adamou, M., Asherson, P., Bazire, S., Coghill, D., Heal, D.,

Müller, U., Nash, J., Santosh, P., Sayag, K., Sonuga-Barke, E., & Young, S. J. (2014).

Evidence-based guidelines for the pharmacological management of attention deficit

hyperactivity disorder: Update on recommendations from the British Association for

Psychopharmacology. Journal of Psychopharmacology, 28(3), 179-203.

Bonafina, M. A., Newcorn, J. H., McKay, K. E., Koda, V. H., & Halperin, J. M. (2000). ADHD

and Reading Disabilities A Cluster Analytic Approach for Distinguishing

Subgroups. Journal of Learning Disabilities, 33(3), 297-307.

Booth, J. R., Burman, D. D., Meyer, J. R., Lei, Z., Trommer, B. L., Davenport, N. D., Li, W.,

Parrish, T.B., Gitleman, D.R., & Marsel Mesulam, M. (2005). Larger deficits in brain

networks for response inhibition than for visual selective attention in attention deficit

hyperactivity disorder (ADHD). Journal of Child Psychology and Psychiatry, 46(1), 94-

111.

Brown, T. E. (2006). Executive functions and attention deficit hyperactivity disorder:

Implications of two conflicting views. International Journal of Disability, Development

and Education, 53(1), 35-46.

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.

Burgess, G. C., Depue, B. E., Ruzic, L., Willcutt, E. G., Du, Y. P., & Banich, M. T. (2010).

Attentional control activation relates to working memory in attention-

deficit/hyperactivity disorder. Biological psychiatry, 67(7), 632-640.

child psychology, 29(6), 529-540.

Cao, M., Shu, N., Cao, Q., Wang, Y., & He, Y. (2014). Imaging Functional and Structural Brain

Connectomics in Attention-Deficit/Hyperactivity Disorder. Molecular neurobiology, 1-

13.

Carlson, C. L. (1986). Attention deficit disorder with and without hyperactivity: A review of

preliminary experimental evidence. In B. B. Lahey & A. E. Kazdin (Eds.), Advances in

 clinical child psychology (Vol. 9, pp. 153–175). New York, NY: Plenum.

Carlson, C. L., & Mann, M. (2000). Attention-deficit/hyperactivity disorder, predominately

inattentive subtype. Child and Adolescent Psychiatric Clinics of North America.

Carlson, C. L., & 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(1), 123-129.

Carpenter, P. A., Just, M. A., & Reichle, E. D. (2000). Working memory and executive function:

evidence from neuroimaging. Current opinion in neurobiology, 10(2), 195-199.

Castellanos, F. X., Lee, P. P., Sharp, W., Jeffries, N. O., Greenstein, D. K., Clasen, L. S.,

Blumenthal, J.D., James, R. S., Ebens, C.L., Walter, J.M., Zijdenbos, A., Evans, A.C.,

Giedd, J.N., & Rapoport, J. L. (2002). Developmental trajectories of brain volume

abnormalities in children and adolescents with attention-deficit/hyperactivity

disorder. Jama, 288(14), 1740-1748.

Castellanos, F. X., & Proal, E. (2012). Large-scale brain systems in ADHD: beyond the

prefrontal–striatal model. Trends in cognitive sciences, 16(1), 17-26.

Castellanos, F. X., & Tannock, R. (2002). Neuroscience of attention-deficit/hyperactivity

disorder: the search for endophenotypes. Nature Reviews Neuroscience, 3(8), 617-628.

Chhabildas, N., Pennington, B. F., & Willcutt, E. G. (2001). A comparison of the

 neuropsychological profiles of the DSM-IV subtypes of ADHD. Journal of abnormal

child psychology, 29(6), 529-540.

Chudasama, Y. (2011). Animal models of prefrontal-executive function.Behavioral

neuroscience, 125(3), 327.

Clark, K. L., & Noudoost, B. (2014). The role of prefrontal catecholamines in attention and

working memory. Frontiers in neural circuits, 8.

Clemow, D. B., & Walker, D. J. (2014). The potential for misuse and abuse of medications in

ADHD: a review. Postgraduate medicine, 126(5), 64-81.

Coghill, D. R., Seth, S., Pedroso, S., Usala, T., Currie, J., & Gagliano, A. (2014). Effects of

methylphenidate on cognitive functions in children and adolescents with attention-

deficit/hyperactivity disorder: evidence from a systematic review and a meta-

analysis. Biological psychiatry, 76(8), 603-615.

Congdon, E., Altshuler, L. L., Mumford, J. A., Karlsgodt, K. H., Sabb, F. W., Ventura, J.,

McGough, J.J., London, E.D., Cannon, T.D., Bilder, R.M., & Poldrack, R. A. (2014).

Neural activation during response inhibition in adult attention-deficit/hyperactivity

disorder: Preliminary findings on the effects of medication and symptom

severity. Psychiatry Research: Neuroimaging, 222(1), 17-28.

Cubillo, A., Halari, R., Giampietro, V., Taylor, E., & Rubia, K. (2011). Fronto-striatal

underactivation during interference inhibition and attention allocation in grown up

 children with attention deficit/hyperactivity disorder and persistent symptoms. Psychiatry

Research: Neuroimaging, 193(1), 17-27.

Cunill, R., Castells, X., Tobias, A., & Capellà, D. (2015). Pharmacological treatment of attention

deficit hyperactivity disorder with co-morbid drug dependence. Journal of

Psychopharmacology, 29(1), 15-23.

Dagher, A., & Robbins, T. W. (2009). Personality, addiction, dopamine: insights from

Parkinson's disease. Neuron, 61(4), 502-510.

De Luca, C. R., & Leventer, R. J. (2008). Developmental trajectories of executive functions

across the lifespan. Executive functions and the frontal lobes: A lifespan perspective, 3,

21.

del Campo, N., Chamberlain, S. R., Sahakian, B. J., & Robbins, T. W. (2011). The roles of

dopamine and noradrenaline in the pathophysiology and treatment of attention-

deficit/hyperactivity disorder. Biological psychiatry, 69(12), e145-e157.

Diamond, A. (2005). Attention-deficit disorder (attention-deficit/hyperactivity disorder without

hyperactivity): A neurobiologically and behaviorally distinct disorder from attention-

deficit/hyperactivity disorder (with hyperactivity).Development and

psychopathology, 17(03), 807-825.

Donohoe, G., & Robertson, I. H. (2003). Can specific deficits in executive functioning explain

the negative symptoms of schizophrenia? A review.Neurocase, 9(2), 97-108.

Douglas, V. I. (1972). Stop, look and listen: the problem of sustained attention and impulse

control in hyperactive and normal children. Canadian Journal of Behavioural

Science/Revue canadienne des sciences du comportement, 4(4), 259.

Douglas, V. I. (1999). Cognitive control processes in attention deficit/hyperactivity disorder.

In Handbook of disruptive behavior disorders (pp. 105-138). Springer US.

Douglas, V. I. (2005). Cognitive Deficits in Children with Attention Deficit Hyperactivity

Disorder: A Long-Term Follow-Up. Canadian Psychology/Psychologie

canadienne, 46(1), 23.

Duff, C. T., & Sulla, E. M. (2014). Measuring Executive Function in the Differential Diagnosis

of Attention-Deficit/Hyperactivity Disorder: Does It Really Tell Us Anything?. Applied

Neuropsychology: Child, (ahead-of-print), 1-9.

Dulcan, M. (1997). Practice parameters for the assessment and treatment of children,

adolescents, and adults with attention-deficit/hyperactivity disorder. American Academy

of Child and Adolescent Psychiatry. Journal of the American Academy of Child and

Adolescent Psychiatry, 36(10 Suppl), 85S-121S.

Epstein, J. N., Erkanli, A., Conners, C. K., Klaric, J., Costello, J. E., & Angold, A. (2003).

Relations between continuous performance test performance measures and ADHD

behaviors. Journal of abnormal child psychology, 31(5), 543-554.

Epstein, J. N., Keith Conners, C., Hervey, A. S., Tonev, S. T., Eugene Arnold, L., Abikoff, H.
 B., Elliott, G., Greenhill, L.L., Hechtman, L., Hoagwood, K., Hinshaw, S.P., Hoza, B.,

Jensen, P.S., March, J.S., Newcorn, J.H., Pelham, W.E., Severe, J.B., Swanson, J.M.,

Wells, K., Vitiello, B., & Wigal, T. (2006). Assessing medication effects in the MTA

study using neuropsychological outcomes. Journal of Child Psychology and

Psychiatry, 47(5), 446-456.

Evans, S., Owens, J., & Bunford, N. (2014). Evidence-Based Psychosocial Treatments for

Children and Adolescents with Attention-Deficit/Hyperactivity Disorder. Journal of

Clinical Child & Adolescent Psychology, 43(4), 1-25

Faraone, S. (2005). The scientific foundation for understanding attention-deficit/hyperactivity

disorder as a valid psychiatric disorder. European Child & Adolescent Psychiatry, 14, 1-

10.

Faraone, S. V., Biederman, J., Weber, W., & Russell, R. L. (1998). Psychiatric,

neuropsychological, and psychosocial features of DSM-IV subtypes of attention-

deficit/hyperactivity disorder: results from a clinically referred sample. Journal of the

American Academy of Child & Adolescent Psychiatry, 37(2), 185-193.

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(4), 353-364.

Fair, D., Bathula, D., Nikolas, M., & Nigg, J. (2012). Distinct neuropsychological subgroups in

typically developing youth inform heterogeneity in children with ADHD. Proceedings of

 the National Academy of Sciences, 109(17), 6769-6774.

Fair, D. A., Nigg, J. T., Iyer, S., Bathula, D., Mills, K. L., Dosenbach, N. U., Schlaggar, B.L.,

Mennes, M., Gutman, D., Bangaru, S., Buitelaar, J.K., Dickstein, D.P., Di Martino, A.,

Kennedy, D.N., Kelly, C., Luna, B., Schweitzer, J.B., Velanova, K.,Wang, Y.F.,

Mostofsky, F., Castellanos, F.X., & Milham, M. P. (2012). Distinct neural

signatures detected for ADHD subtypes after controlling for micro-movements in

resting state functional connectivity MRI data. Frontiers in systems

neuroscience, 6.

Feldman, H. M., & Reiff, M. I. (2014). Attention Deficit–Hyperactivity Disorder in Children and

Adolescents. New England Journal of Medicine, 370(9), 838-846.

Ferrer, M., Andión, Ó., Matalí, J., Valero, S., Navarro, J. A., Ramos-Quiroga, J. A., Torrubia, R.,

& Casas, M. (2010). Comorbid attention-deficit/hyperactivity disorder in borderline

patients defines an impulsive subtype of borderline personality disorder. Journal of

personality disorders, 24(6), 812-822.

Garner, A. A., Mrug, S., Hodgens, B., & Patterson, C. (2012). Do symptoms of sluggish

cognitive tempo in children with ADHD symptoms represent comorbid internalizing

difficulties?. Journal of attention disorders, 1087054711431456.

Gaub, M., & Carlson, C. L. (1997). Gender differences in ADHD: a meta-analysis and critical

review. Journal of the American Academy of Child & Adolescent Psychiatry, 36(8),

1036-1045.
Geller, D. A. (2006). Obsessive-compulsive and spectrum disorders in children and

adolescents. Psychiatric Clinics of North America, 29(2), 353-370.

Geurts, H. M., Verté, S., Oosterlaan, J., Roeyers, H., & Sergeant, J. A. (2005). ADHD subtypes:

do they differ in their executive functioning profile?. Archives of Clinical

Neuropsychology, 20(4), 457-477.

Gevins, A., & Smith, M. E. (2000). Neurophysiological measures of working memory and

individual differences in cognitive ability and cognitive style.Cerebral Cortex, 10(9),

829-839.

Goodkind M., Eickhoff S.B., Oathes D.J., Jiang, Y., Chang, A., Jones-Hagata, L.B., Ortega,
B.N., Zaiko, Y.V., Roach, E.L., Korgaonkar, M.S., Grieve, S.M., Galatzer-Levy, I., Fox,
P.T., Etkin, A. Identification of a Common Neurobiological Substrate for Mental
Illness. JAMA Psychiatry. Published online February 04, 2015.

Graham, J., Banaschewski, T., Buitelaar, J., Coghill, D., Danckaerts, M., Dittmann, R. W.,

Döpfner, M., Hamilton, R., Hollis, C., Holtmann, M., Hulpke-Wette, M., Lecendreux,

M., Rosenthal, E., Rothenberger, A., Santosh, P., Sergeant, J., Simonoff, E., Sonuga-

Barke, E., Wong, I.C.K., Zuddas, A., Steinhausen, H.C., & Taylor, E. (2011). European

guidelines on managing adverse effects of medication for ADHD. European child &

adolescent psychiatry, 20(1), 17-37.

Greene, R. W., Biederman, J., Faraone, S. V., Ouellette, C. A.,Penn, C., & Griffin, S. (1996).

Toward a new psychometric definition of social disability in children with Attention-

Deficit Hyperactivity Disorder. Journal of the American Academy of Child and

 Adolescent Psychiatry, 35, 571–578.

Gualtieri, C. T., & Johnson, L. G. (2008). Medications do not necessarily normalize cognition in

ADHD patients. Journal of attention disorders, 11(4), 459-469.

Haslam, N., Williams, B., Prior, M., Haslam, R., Graetz, B., & Sawyer, M. (2006). The

latent structure of attention-deficit/hyperactivity disorder: A taxometric

analysis. Australian and New Zealand Journal of Psychiatry, 40(8), 639-647.

Hale, J. B., Reddy, L. A., Semrud-Clikeman, M., Hain, L. A., Whitaker, J., Morley, J.,

Lawrence, K., Smith, A. & Jones, N. (2011). Executive impairment determines ADHD

medication response: implications for academic achievement. Journal of Learning

Disabilities, 44(2), 196-212.

Halperin, J. M., Berwid, O. G., & O’Neill, S. (2014). Healthy Body, Healthy Mind?: The

Effectiveness of Physical Activity to Treat ADHD in Children. Child and adolescent

psychiatric clinics of North America, 23(4), 899-936.

Handler, M. W., & DuPaul, G. J. (2005). Assessment of ADHD: Differences across psychology

specialty areas. Journal of attention disorders, 9(2), 402-412.

Hart, H., Radua, J., Nakao, T., Mataix-Cols, D., & Rubia, K. (2013). Meta-analysis of functional

magnetic resonance imaging studies of inhibition and attention in attention-

deficit/hyperactivity disorder: exploring task-specific, stimulant medication, and age

effects. JAMA psychiatry, 70(2), 185-198.

Heidbreder, C. A., & Groenewegen, H. J. (2003). The medial prefrontal cortex in the rat:

evidence for a dorso-ventral distinction based upon functional and anatomical

characteristics. Neuroscience & Biobehavioral Reviews, 27(6), 555-579.

Hinshaw, S. P. (2001). Is the inattentive type of ADHD a separate disorder?.Clinical

Psychology: Science and Practice, 8(4), 498-501.

Hoekzema, E., Carmona, S., Ramos‐Quiroga, J. A., Richarte Fernández, V., Bosch, R., Soliva, J.

C., Rovira, M., Bulbena, A., Tobeña, A., Casas, M., & Vilarroya, O. (2014). An

independent components and functional connectivity analysis of resting state fMRI data

points to neural network dysregulation in adult ADHD. Human brain mapping, 35(4),

1261-1272.

Holmes, J., Hilton, K. A., Place, M., Alloway, T. P., Elliott, J. G., & Gathercole, S. E. (2014).

Children with low working memory and children with ADHD: same or

different?. Frontiers in human neuroscience, 8.

Holtmann, M., Sonuga-Barke, E., Cortese, S., & Brandeis, D. (2014). Neurofeedback for ADHD:

a review of current evidence. Child and adolescent psychiatric clinics of North

America, 23(4), 789-806.

Hong, S. B., Zalesky, A., Fornito, A., Park, S., Yang, Y. H., Park, M. H., Song, I.C., Sohn, C.H.,

Shin, M.S., Kim, B.N., Cho, S.C., Han, D.H., Cheong, J.H. & Kim, J. W. (2014).

Connectomic disturbances in attention-deficit/hyperactivity disorder: A whole-brain

tractography analysis. Biological psychiatry, 76(8), 656-663.

Hoza, B., Smith, A. L., Shoulberg, E. K., Linnea, K. S., Dorsch, T. E., Blazo, J. A., Alerding,

C.L., & McCabe, G. P. (2014). A Randomized Trial Examining the Effects of Aerobic

Physical Activity on Attention-Deficit/Hyperactivity Disorder Symptoms in Young

Children. Journal of abnormal child psychology, 1-13.

Jensen, P. S., Hinshaw, S. P., Kraemer, H. C., Lenora, N., Newcorn, J. H., Abikoff, H. B.,

March, J.S., Arnold, L.E., Cantwell, D.P., Conners, C.K., Elliott, G.R., Greenhill, L.L.,

Hechtman, L., Hoza, B., Pelham, W.E., Severe, J.B., Swanson, J.M., Wells, K.C., Wigal,

T., & Vitiello, B. (2001). ADHD comorbidity findings from the MTA study: comparing

comorbid subgroups. Journal of the American Academy of Child & Adolescent

Psychiatry, 40(2), 147-158.

Jensen, P. S., Hinshaw, S. P., Swanson, J. M., Greenhill, L. L., Conners, C. K., Arnold, L. E.,

Abikoff, H.B ., Elliott, G., Hechtman, L., Hoza, B., March, J.S., Newcorn, J., Severe,

J.B., Vitiello, B., Wells, K., & Wigal, T. (2001). Findings from the NIMH Multimodal

Treatment Study of ADHD (MTA): implications and applications for primary care

providers. Journal of Developmental & Behavioral Pediatrics, 22(1), 60-73.

Jensen, P. S., Martin, D., & Cantwell, D. P. (1997). Comorbidity in ADHD: implications for

research, practice, and DSM-V. Journal of the American Academy of Child & Adolescent

Psychiatry, 36(8), 1065-1079.

Jummani, R., & Coffey, B. J. (2014). ADHD and tic disorders. Attention-Deficit Hyperactivity

Disorder in Adults and Children, 343.

Kamp, C. F., Sperlich, B., & Holmberg, H. C. (2014). Exercise reduces the symptoms of

attention‐deficit/hyperactivity disorder and improves social behaviour, motor skills,

strength and neuropsychological parameters. Acta Paediatrica.

Kashyap, H., Fontenelle, L. F., Miguel, E. C., Ferrão, Y. A., Torres, A. R., Shavitt, R. G.,

Ferreira-Garcia, R., do Rosario, M. & Yücel, M. (2012). ‘Impulsive compulsivity’in

obsessive-compulsive disorder: A phenotypic marker of patients with poor clinical

outcome. Journal of psychiatric research, 46(9), 1146-1152.

Kesner, R. P., & Churchwell, J. C. (2011). An analysis of rat prefrontal cortex in mediating

executive function. Neurobiology of learning and memory, 96(3), 417-431.

Kessler, R., Adler, L., Barkley, R., Biederman, J., Conners, C. K., Greenhill, L. L., & Spencer, T.

(2011). The prevalence and correlates of adult ADHD. ADHD in Adults:

Characterization, Diagnosis, and Treatment, 9.

Ko, J. H., & Strafella, A. P. (2012). Dopaminergic Neurotransmission in the Human Brain New

Lessons from Perturbation and Imaging. The Neuroscientist, 18(2), 149-168.

Konrad, K., Neufang, S., Hanisch, C., Fink, G. R., & Herpertz-Dahlmann, B. (2006).

Dysfunctional attentional networks in children with attention deficit/hyperactivity

disorder: evidence from an event-related functional magnetic resonance imaging

study. Biological psychiatry, 59(7), 643-651.

Koyuncu, A., Ertekin, E., Yüksel, Ç., Ertekin, B. A., Çelebi, F., Binbay, Z., & Tükel, R. (2014).

Predominantly Inattentive Type of ADHD Is Associated With Social Anxiety

Disorder. Journal of attention disorders, 1087054714533193.

Koziol, L. F., & Budding, D. (2012). Requiem for a diagnosis: attention-deficit hyperactivity

disorder. Applied Neuropsychology: Child, 1(1), 2-5.

Kuczenski, R., & Segal, D. S. (1997). Effects of methylphenidate on extracellular dopamine,

serotonin, and norepinephrine: comparison with amphetamine. Journal of

neurochemistry, 68(5), 2032- 2037.

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., Schaughency, E. A., Hynd, G. W., Carlson, C. L., & Nieves, N. (1987). Attention

deficit disorder with and without hyperactivity: Comparison of behavioral characteristics

of clinic-referred children. Journal of the American Academy of Child & Adolescent

Psychiatry, 26(5), 718-723.

Lange, K., Reichl, S., Lange, K., Tucha, L., & Tucha, O. (2010). The history of attention deficit

hyperactivity disorder. ADHD Attention Deficit and Hyperactivity Disorders, 2(4), 241-

255.

Lee, S., Burns, G. L., Snell, J., & McBurnett, K. (2014). Validity of the sluggish cognitive tempo
 symptom dimension in children: Sluggish cognitive tempo and ADHD-inattention as

distinct symptom dimensions. Journal of abnormal child psychology, 42(1), 7-19.

Lensing, M. B., Zeiner, P., Sandvik, L., & Opjordsmoen, S. (2013). Adults with ADHD: use and

misuse of stimulant medication as reported by patients and their primary care

physicians. ADHD Attention Deficit and Hyperactivity Disorders, 5(4), 369-376.

Leth-Steensen, C., King Elbaz, Z., & Douglas, V. I. (2000). Mean response times, variability,

and skew in the responding of ADHD children: a response time distributional

approach. Acta psychologica, 104(2), 167-190.

Lezak, M. D. (Ed.). (2004). Neuropsychological assessment. Oxford university press.

Li, F., He, N., Li, Y., Chen, L., Huang, X., Lui, S., Guo, L., Kemp, G.J., & Gong, Q. (2014).

Intrinsic Brain Abnormalities in Attention Deficit Hyperactivity Disorder: A Resting-

State Functional MR Imaging Study. Radiology.

Lim, L., Chantiluke, K., Cubillo, A. I., Smith, A. B., Simmons, A., Mehta, M. A., & Rubia, K.

(2014). Disorder-specific grey matter deficits in attention deficit hyperactivity disorder

relative to autism spectrum disorder. Psychological medicine, 1-12.

Linssen, A. M. W., Sambeth, A., Vuurman, E. F. P. M., & Riedel, W. J. (2014). Cognitive

effects of methylphenidate in healthy volunteers: a review of single dose

studies. International Journal of Neuropsychopharmacology, 17(6), 961-977.

Lockwood, K. A., Marcotte, A. C., & Stern, C. (2001). Differentiation of attention-

deficit/hyperactivity disorder subtypes: application of a neuropsychological model of

attention. Journal of Clinical and Experimental Neuropsychology, 23(3), 317-330.

Lopez-Vergara, H. I., & Colder, C. R. (2013). An Examination of the Specificity of Motivation

and Executive Functioning in ADHD Symptom-Clusters in Adolescence. Journal of

pediatric psychology, 38(10), 1081-1090.

Lynam, D. R. (1996). The early identification of chronic offenders: Who is the fledgling

psychopath? Psychological Bulletin,120, 209–234.

Marsh, P. J., & Williams, L. M. (2006). ADHD and schizophrenia phenomenology: visual

scanpaths to emotional faces as a potential psychophysiological marker?. Neuroscience &

Biobehavioral Reviews, 30(5), 651-665.

Massat, I., Slama, H., Kavec, M., Linotte, S., Mary, A., Baleriaux, D., Metens, T., Mendlewicz,

J. & Peigneux, P. (2012). Working memory-related functional brain patterns in never

medicated children with ADHD. PloS one, 7(11), e49392.

Mattfeld, A. T., Gabrieli, J. D., Biederman, J., Spencer, T., Brown, A., Kotte, A., Kagan, E., &

Whitfield-Gabrieli, S. (2014). Brain differences between persistent and remitted attention

deficit hyperactivity disorder. Brain, awu137.

Matthews, M., Nigg, J.T., & Fair, D.A. (2014). Attention Deficit Hyperactivity Disorder.

Current Topics in Behavioral Neuroscicence,. 2014 ; 16: 235–266

McBurnett, K., Pfiffner, L. J., & Frick, P. J. (2001). Symptom properties as a function of ADHD

type: An argument for continued study of sluggish cognitive tempo. Journal of abnormal

child psychology, 29(3), 207-213.

McLaughlin, K. A., Sheridan, M. A., Winter, W., Fox, N. A., Zeanah, C. H., & Nelson, C. A.

(2014). Widespread reductions in cortical thickness following severe early-life

deprivation: a neurodevelopmental pathway to attention-deficit/hyperactivity

disorder. Biological psychiatry, 76(8), 629-638

Metters, S. ADHD–Where can we turn for help?

Mikami, A. Y., Jia, M., & Na, J. J. (2014). Social Skills Training. Child and adolescent

psychiatric clinics of North America, 23(4), 775-788.

Milich, R., Balentine, A. C., & Lynam, D. R. (2001). ADHD combined type and ADHD

predominantly inattentive type are distinct and unrelated disorders.Clinical psychology:

science and practice, 8(4), 463-488.

Millichap, J. G., & Yee, M. M. (2012). The diet factor in attention-deficit/hyperactivity

disorder. Pediatrics, 129(2), 330-337.

Mills, K. L., Bathula, D., Dias, T. G. C., Iyer, S. P., Fenesy, M. C., Musser, E. D., Stevens, C.A.,

Thurlow, B.L., Carpenter, S.D., Nagel, B.J., Nigg, J.T.. & Fair, D. A. (2012). Altered

cortico-striatal–thalamic connectivity in relation to spatial working memory capacity in

 children with ADHD. Frontiers in psychiatry, 3.

Milner, B. (1963). Effects of different brain lesions on card sorting: The role of the frontal

lobes. Archives of Neurology, 9(1), 90-00.

Miyake, A., Friedman, N. P., Emerson, M. J., Witzki, A. H., Howerter, A., & Wager, T. D.

(2000). The unity and diversity of executive functions and their contributions to complex

“frontal lobe” tasks: A latent variable analysis.Cognitive psychology, 41(1), 49-100.

Moeller, F. G., Barratt, E. S., Dougherty, D. M., Schmitz, J. M., & Swann, A. C. (2014).

Psychiatric aspects of impulsivity.

Mostofsky, S. H., Schafer, J. G., Abrams, M. T., Goldberg, M. C., Flower, A. A., Boyce, A.,

Courtney, S.M., Calhoun, V.D., Kraut, M.A., Denckla, M.B., & Pekar, J. J. (2003). fMRI

evidence that the neural basis of response inhibition is task-dependent. Cognitive Brain

Research, 17(2), 419-430.

Mostofsky, S., & Simmonds, D. (2008). Response inhibition and response selection: two sides of

the same coin. Cognitive Neuroscience, Journal of, 20(5), 751-761.

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.

Nakao, T., Radua, C., Rubia, K., & Mataix-Cols, D. (2011). Gray matter volume abnormalities in

ADHD and the effects of stimulant medication: voxel-based meta-analysis. Am J

 Psychiatry, 168(11), 1154-63.

Nigg, J. T., Willcutt, E. G., Doyle, A. E., & Sonuga-Barke, E. J. (2005). Causal heterogeneity in

attention-deficit/hyperactivity disorder: do we need neuropsychologically impaired

subtypes?. Biological psychiatry, 57(11), 1224-1230.

Nigg, J. T., Blaskey, L. G., Huang-Pollock, C. L., & Rappley, M. D. (2002). Neuropsychological

executive functions and DSM-IV ADHD subtypes. Journal of the American Academy of

Child & Adolescent Psychiatry, 41(1), 59-66.

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.

Ogundele, M. O., Ayyash, H. F., & Banerjee, S. (2011). Role of computerised continuous

performance task tests in ADHD. Progress in Neurology and Psychiatry, 15(3), 8-13.

Ollendorf, D. A., Migliaccio-Walle, K., Colby, J. A., & Pearson, S. D. (2013). Management

options for children with attention-deficit/hyperactivity disorder: a regional perspective

on value. Journal of comparative effectiveness research,2(3), 261-271.

Patel, N., Patel, M., & Patel, H. (2012). ADHD and Comorbid Conditions. Attention Deficit

Hyperactivity Disorder/Book, 1, 978-9.

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.

Pliszka, S. R., Carlson, C. L., & Swanson, J. M. (1999). ADHD With Comorbid Disorders:

Clinical Assessment and Management. Guilford Press, 72 Spring Street, NY, NY 10012.

Pliszka, S. R. (2014). Conceptual issues in understanding comorbidity in ADHD. Attention-

Deficit Hyperactivity Disorder in Adults and Children, 63.

Polanczyk, G. V., Willcutt, E. G., Salum, G. A., Kieling, C., & Rohde, L. A. (2014). ADHD

prevalence estimates across three decades: an updated systematic review and meta-

regression analysis. International journal of epidemiology, 43(2), 434-442.

Posner, M. I., & Petersen, S. E. (1989). The attention system of the human brain (No. TR-89-1).

WASHINGTON UNIV ST LOUIS MO DEPT OF NEUROLOGY.

Quinn, C. A. (2003). Detection of malingering in assessment of adult ADHD.Archives of

Clinical Neuropsychology, 18(4), 379-395.

Rabiner, D. L. (2013). Stimulant prescription cautions: addressing misuse, diversion and

malingering. Current psychiatry reports, 15(7), 1-8.

Rapport, M. D., Denney, C., DuPaul, G. J., & Gardner, M. J. (1994). Attention deficit disorder

and methylphenidate: normalization rates, clinical effectiveness, and response prediction

in 76 children. Journal of the American Academy of Child & Adolescent

 Psychiatry, 33(6), 882-893.

Reddy, L.F., Lee, J., Davis, M.C., Altshuler, L., Glahn, D.C., Milowitz, D.J. & Green, M.F.

(2014). Impulsivity and risk taking in bipolar disorder and schizophrenia.

Neuropsychopharmacology, 39(2), 456-63.

Riccio, C. A., Homack, S., Jarratt, K. P., & Wolfe, M. E. (2006). Differences in academic and

executive function domains among children with ADHD predominantly inattentive and

combined types. Archives of Clinical Neuropsychology, 21(7), 657-667

Rosa-Neto, P., Lou, H. C., Cumming, P., Pryds, O., Karrebaek, H., Lunding, J., & Gjedde, A.

2005). Methylphenidate-evoked changes in striatal dopamine correlate with inattention

and impulsivity in adolescents with attention deficit hyperactivity

disorder. Neuroimage, 25(3), 868-876

Rubia, K., Alegria, A. A., Cubillo, A. I., Smith, A. B., Brammer, M. J., & Radua, J. (2014).

Effects of stimulants on brain function in attention-deficit/hyperactivity disorder: a

systematic review and meta-analysis. Biological psychiatry, 76(8), 616-628.

Rubia, K., Alegria, A., & Brinson, H. (2014). Imaging the ADHD brain: disorder-specificity,

medication effects and clinical translation. Expert review of neurotherapeutics, (0), 1-20.

Rubia, K., Cubillo, A., Smith, A. B., Woolley, J., Heyman, I., & Brammer, M. J. (2010).

Disorder‐specific dysfunction in right inferior prefrontal cortex during two inhibition

tasks in boys with attention‐deficit hyperactivity disorder compared to boys with

obsessive–compulsive disorder. Human brain mapping, 31(2), 287-299.

Rubia, K., Cubillo, A., Woolley, J., Brammer, M. J., & Smith, A. (2011). Disorder‐specific

dysfunctions in patients with attention‐deficit/hyperactivity disorder compared to patients

with obsessive‐compulsive disorder during interference inhibition and attention

allocation. Human brain mapping, 32(4), 601-611.

Rubia, K., Halari, R., Cubillo, A., Mohammad, A. M., Brammer, M., & Taylor, E. (2009).

Methylphenidate normalises activation and functional connectivity deficits in attention

and motivation networks in medication-naive children with ADHD during a rewarded

continuous performance task. Neuropharmacology,57(7), 640-652.

Rubia, K., Smith, A. B., Brammer, M. J., Toone, B., & Taylor, E. (2005). Abnormal brain

activation during inhibition and error detection in medication-naive adolescents with

ADHD. American Journal of Psychiatry, 162(6), 1067-1075.

Ruscio, A. M., Stein, D. J., Chiu, W. T., & Kessler, R. C. (2010). The epidemiology of

obsessive-compulsive disorder in the National Comorbidity Survey

Replication. Molecular psychiatry, 15(1), 53-63.

Saxbe, C., & Barkley, R. A. (2014). The second attention disorder? Sluggish cognitive tempo vs.

attention-deficit/hyperactivity disorder: update for clinicians. Journal of Psychiatric

Practice®, 20(1), 38-49.

Schaeffer, J. L., & Ross, R. G. (2002). Childhood-onset schizophrenia: premorbid and prodromal

diagnostic and treatment histories. Journal of the American Academy of Child &
 Adolescent Psychiatry, 41(5), 538-545.

Shalev, L., & Tsal, Y. (2003). The wide attentional window a major deficit of children with

attention difficulties. Journal of Learning Disabilities, 36(6), 517-527.

Schmeichel, B. E., & Berridge, C. W. (2013). Neurocircuitry underlying the preferential

sensitivity of prefrontal catecholamines to low-dose

psychostimulants. Neuropsychopharmacology, 38(6), 1078-1084.

Schmitz, M., Ludwig, H., & Rohde, L. A. (2010). Do hyperactive symptoms matter in ADHD-I

restricted phenotype?. Journal of Clinical Child & Adolescent Psychology, 39(6), 741-

748.

Sciutto, M. J., & Eisenberg, M. (2007). Evaluating the evidence for and against the

overdiagnosis of ADHD. Journal of Attention Disorders, 11(2), 106-113.

Sebastian, A., Jung, P., Krause-Utz, A., Lieb, K., Schmahl, C., & Tüscher, O. (2014). Frontal

dysfunctions of impulse control–a systematic review in borderline personality disorder

and attention-deficit/hyperactivity disorder. Frontiers in human neuroscience, 8.

Segal, D. S., & Kuczenski, R. (1994). Behavioral pharmacology of amphetamine. Amphetamine

and its analogs: Psychopharmacology, toxicology and abuse. San Diego, Academic

Press, Inc., 115-150.

Shallice, T., & Burgess, P. (1991). Higher-order cognitive impairments and frontal lobe lesions

in man. Frontal lobe function and dysfunction, 125-138.

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(8), 599-606.

Shaw, P., Eckstrand, K., Sharp, W., Blumenthal, J., Lerch, J. P., Greenstein, D., Clasen, L.,

Evans, A., Giedd, J., & Rapoport, J. L. (2007). Attention-deficit/hyperactivity disorder is

characterized by a delay in cortical maturation. Proceedings of the National Academy of

Sciences, 104(49), 19649-19654.

Sibley, M. H., Altszuler, A. R., Morrow, A. S., & Merrill, B. M. (2014). Mapping the academic

problem behaviors of adolescents with ADHD. School Psychology Quarterly, 29(4), 422.

Simmonds, D. J., Pekar, J. J., & Mostofsky, S. H. (2008). Meta-analysis of Go/No-go tasks

demonstrating that fMRI activation associated with response inhibition is task-

dependent. Neuropsychologia, 46(1), 224-232.

Skogli, E. W., Teicher, M. H., Andersen, P. N., Hovik, K. T., & Øie, M. (2013). ADHD in girls

and boys–gender differences in co-existing symptoms and executive function

measures. BMC psychiatry, 13(1), 298.

Smith, A., Taylor, E., Brammer, M., Toone, B., & Rubia, K. (2006). Task-specific

hypoactivation in prefrontal and temporoparietal brain regions during motor inhibition

and task switching in medication-naive children and adolescents with attention deficit

hyperactivity disorder. American Journal of Psychiatry, 163(6), 1044-1051.

Solanto, M., Newcorn, J., Vail, L., Gilbert, S., Ivanov, I., & Lara, R. (2009). Stimulant drug

response in the predominantly inattentive and combined subtypes of attention-

deficit/hyperactivity disorder. Journal of child and adolescent

psychopharmacology, 19(6), 663-671

Song, Y., & Hakoda, Y. (2014). Executive and Non-Executive Functions in Attention Deficit

Hyperactivity Disorder of the Inattentive Type (ADHD-I): A Cognitive Profile. Journal

of Behavioral and Brain Science, 2014.

Sonuga-Barke, E. J. (2002). Psychological heterogeneity in AD/HD—a dual pathway model of

behaviour and cognition. Behavioural brain research, 130(1), 29-36.

Sonuga-Barke, E. J., Brandeis, D., Cortese, S., Daley, D., Ferrin, M., Holtmann, M., Stevenson,

J., Danckaerts, M., van der Oord, S., Döpfner, M., Dittmann, R.W., Simonoff, E.,

Zuddas, A., Banaschewski, T., Buitelaar, J., Coghill, D., Hollis, C., Konofal, E.,

Lecendreux, M., Wong, I.C.K., & Sergeant, J. (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

Sonuga-Barke, E., Brandeis, D., Holtmann, M., & Cortese, S. (2014). Computer-based Cognitive

Training for ADHD: A Review of Current Evidence. Child and adolescent psychiatric

clinics of North America, 23(4), 807-824.

Sripada, C. S., Kessler, D., & Angstadt, M. (2014). Lag in maturation of the brain’s intrinsic
 functional architecture in attention-deficit/hyperactivity disorder. Proceedings of the

National Academy of Sciences, 111(39), 14259-14264.

Stevenson, J., Buitelaar, J., Cortese, S., Ferrin, M., Konofal, E., Lecendreux, M., Simonoff, E.,

Wong, C.K. & Sonuga‐Barke, E. (2014). Research Review: The role of diet in the

treatment of attention‐ deficit/hyperactivity disorder–an appraisal of the evidence on

efficacy and recommendations on the design of future studies. Journal of Child

Psychology and Psychiatry, 55(5), 416-427.

Stuss, D. T., & Benson, D. F. (1986). The Frontal Lobes (Raven, New York).StussThe Frontal

Lobes1986

Stuss, D. T., Floden, D., Alexander, M. P., Levine, B., & Katz, D. (2001). Stroop performance in

focal lesion patients: dissociation of processes and frontal lobe lesion

location. Neuropsychologia, 39(8), 771-786.

Takeda, T., Ambrosini, P. J., & Elia, J. (2012). What can ADHD without comorbidity teach us

about comorbidity?. Research in developmental disabilities, 33(2), 419-425.

Tarver, J., Daley, D., & Sayal, K. (2014). Attention‐deficit hyperactivity disorder (ADHD): an

updated review of the essential facts. Child: care, health and development.

Taylor, E. (2011). Antecedents of ADHD: A historical account of diagnostic concepts. ADHD

Attention Deficit and Hyperactivity Disorders, 3(2), 69-75.

Tian, L., Jiang, T., Liang, M., Zang, Y., He, Y., Sui, M., & Wang, Y. (2008). Enhanced resting-

state brain activities in ADHD patients: a fMRI study. Brain and Development, 30(5),

342-348.

Timimi, S. (2004). Developing Nontoxic Approaches to Helping Children Who Could Be

Diagnosed With ADHD and Their Families: Reflections of a United Kingdom

Clinician. Ethical Human Sciences and Services, 6(1), 41-52.

Tomasi, D., & Volkow, N. D. (2012). Abnormal functional connectivity in children with

attention-deficit/hyperactivity disorder. Biological psychiatry,71(5), 443-450.

Tucha, L., Fuermaier, A. B., Koerts, J., Groen, Y., & Thome, J. (2014). Detection of feigned

attention deficit hyperactivity disorder. Journal of Neural Transmission, 1-12.

Valera, E. M., Brown, A., Biederman, J., Faraone, S. V., Makris, N., Monuteaux, M. C.,

Whitfield-Gabrielli, S., Vitulano, M., Schiller, M.. & Seidman, L. J (2010). Sex

differences in the functional neuroanatomy of working memory in adults with

ADHD. The American Journal of Psychiatry, 167(1), 86–94.

Valera, E. M., Faraone, S. V., Murray, K. E., & Seidman, L. J. (2007). Meta-analysis of

structural imaging findings in attention-deficit/hyperactivity disorder. Biological

psychiatry, 61(12), 1361-1369.

Vande Voort, J. L., He, J. P., Jameson, N. D., & Merikangas, K. R. (2014). Impact of the DSM-5

Attention-Deficit/Hyperactivity Disorder (ADHD) Age of Onset Criterion in the US

 Adolescent Population. Journal of the American Academy of Child & Adolescent

Psychiatry.

van Lieshout, M., Luman, M., Buitelaar, J., Rommelse, N. N. J., & Oosterlaan, J. (2013). Does

neurocognitive functioning predict future or persistence of ADHD? A systematic

review. Clinical psychology review, 33(4), 539-560.

Visser, S. N., Danielson, M. L., Bitsko, R. H., Holbrook, J. R., Kogan, M. D., Ghandour, R. M.,

Perous, R, & Blumberg, S. J. (2014). Trends in the parent-report of health care provider-

diagnosed and medicated attention-deficit/hyperactivity disorder: United States, 2003–

2011. Journal of the American Academy of Child & Adolescent Psychiatry, 53(1), 34-46.

Vitiello, B. (2001). Long-term effects of stimulant medications on the brain: possible relevance

to the treatment of attention deficit hyperactivity disorder. Journal of Child and

Adolescent Psychopharmacology, 11(1), 25-34.

Volkow, N. D., Fowler, J. S., Wang, G. J., Baler, R., & Telang, F. (2009). Imaging dopamine's

role in drug abuse and addiction. Neuropharmacology, 56, 3-8.

Volkow, N. D., & Insel, T. R. (2003). What are the long-term effects of methylphenidate

treatment?. Biological psychiatry, 54(12), 1307-1309.

Volkow, N. D., & Swanson, J. M. (2013). Adult Attention Deficit–Hyperactivity Disorder. New

England Journal of Medicine, 369(20), 1935-1944.

Volkow, N. D., Wang, G. J., Fowler, J. S., Gatley, S. J., Logan, J., Ding, Y. S., Hitzemann, R.,

& Pappas, N. (1998). Dopamine transporter occupancies in the human brain induced by

therapeutic doses of oral methylphenidate. American Journal of Psychiatry, 155(10),

1325-1331.

Volkow, N. D., Wang, G. J., Newcorn, J. H., Kollins, S. H., Wigal, T. L., Telang, F., Fowler,

J.S., Goldstein, R.Z., Klein, N., Logan, J.,Wong, C., & Swanson, J. M. (2011).

Motivation deficit in ADHD is associated with dysfunction of the dopamine reward

pathway. Molecular psychiatry, 16(11), 1147-1154.

Wåhlstedt, C., Thorell, L. B., & Bohlin, G. (2009). Heterogeneity in ADHD: neuropsychological

pathways, comorbidity and symptom domains. Journal of abnormal child

psychology, 37(4), 551-564.

Wasserman, R. C., Kelleher, K. J., Bocian, A., Baker, A., Childs, G. E., Indacochea, F., Stulp,

C., & Gardner, W. P. (1999). Identification of attentional and hyperactivity problems in

primary care: a report from pediatric research in office settings and the ambulatory

sentinel practice network. Pediatrics, 103(3), e38-e38.

Weiss, M., Worling, D., & Wasdell, M. (2003). A chart review study of the inattentive and

combined types of ADHD. Journal of Attention Disorders, 7(1), 1-9.

Wilens, T. E., Biederman, J., Forkner, P., Ditterline, J., Morris, M., Moore, H., Galdo, M.,

Spencer, T.J., & Wozniak, J. (2003). Patterns of comorbidity and dysfunction in

clinically referred preschool and school-age children with bipolar disorder. Journal of
 child and adolescent psychopharmacology, 13(4), 495-505.

Wilens, T. E., & Morrison, N. R. (2011). The intersection of attention-deficit/hyperactivity

disorder and substance abuse. Current opinion in psychiatry, 24(4), 280.

Willcutt, E. G. (2012). The prevalence of DSM-IV attention-deficit/hyperactivity disorder: a

meta-analytic review. Neurotherapeutics, 9(3), 490-499.

Wilkinson, D., & Halligan, P. (2004). The relevance of behavioural measures for functional-

imaging studies of cognition. Nature Reviews Neuroscience, 5(1), 67-73.

Williamson, K. D., Combs, H. L., Berry, D. T., Harp, J. P., Mason, L. H., & Edmundson, M.

(2014). Discriminating Among ADHD Alone, ADHD With a Comorbid Psychological

Disorder, and Feigned ADHD in a College Sample. The Clinical

neuropsychologist, 28(7), 1182-1196.

Willoughby, M. T. (2003). Developmental course of ADHD symptomatology during the

transition from childhood to adolescence: a review with recommendations. Journal of

Child Psychology and Psychiatry, 44(1), 88-106.

Wolraich, M., Milich, R., Stumbo, P., & Schultz, F. (1985). Effects of sucrose ingestion on the

behavior of hyperactive boys. The Journal of pediatrics,106(4), 675-682.

Wolraich, M. L., Lindgren, S. D., Stumbo, P. J., Stegink, L. D., Appelbaum, M. I., & Kiritsy, M.

C. (1994). Effects of diets high in sucrose or aspartame on the behavior and cognitive
 performance of children. New England Journal of Medicine, 330(5), 301-307.

Wolraich, M. L. (2006). Attention-deficit/hyperactivity disorder: Can it be recognized and

treated in children younger than 5 years?. Infants & Young Children, 19(2), 86-93.

Wolraich, M.L., McKeown, R.E., Visser, S.N., Bard, D., Cuffe, S., Neas, B., Geryk, L.L.,

Doffing, M., Bottsi, M., Abramowitz, A.J., Beck, L. Holbrook, J.R., Danielson, M.

(2014). The Prevalence of ADHD: Its Diagnosis and Treatment in Four School Districts

Across Two States. Journal of Attention Disorders, 18 (7), 563-575.

Yu-Feng, Z., Yong, H., Chao-Zhe, Z., Qing-Jiu, C., Man-Qiu, S., Meng, L., Li-Xia, T., Tian-Zi,

J., & Yu-Feng, W. (2007). Altered baseline brain activity in children with ADHD

revealed by resting-state functional MRI. Brain and Development, 29(2), 83-91.

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