Understanding ADHD

Over the years, many have tried to make sense of what ADHD is actually caused by. But sadly, the current clinical view of ADHD is lacking a key component, especially in Europe where ICD-10 is being used, and which is lacking one of the most key ingredients in understanding ADHD: Emotions …

ADHD: UNDERSTANDING THE NEUROANATOMY, THE NEUROPSYCHOLOGY, THE SOCIAL AND EMOTIONAL COMPONENT AND CO-MORBID DISORDERS

by Peter ‘ADDspeaker’ Vang

EXECUTIVE SUMMARY

by Peter ‘ADDspeaker’ Vang

In my everyday life, I run a blog, ADDspeaker and a Facebook Group, for people with Adult ADHD, Parents of Children with ADHD, and people from the scientific community. This community has grown vastly popular and have had an expansive growth, with the last year or so.

As the blog and group are for danish natives, i’ve decided to compile this online document, in english, so as to better serve our worldwide community and try adding knowledge from both scientists, clinicians, scholars and not least, patients.

By having this unique mix of patients and professionals joining in with their own unique experiences and knowledge, we have begun to create and brand-new approach to understanding how to manage ADHD in our everyday life, by translating scientific evidence into practical everyday solutions, as well as giving feedback to the researchers, scientists and clinicians, on our communal understanding of Best Practise in Adult ADHD mangement (including parenting).

Prior to that, I‘ve spent 5 years of full-time research, studying scientific publications on the topic of ADHD. About 3 years ago, I contacted Dr. Russell A. Barkley, Ph.D. and asked for his advice regarding the understanding of ADHD, from a scientific, diagnostic, treatment and life perspective, as I was working on a book on Adult ADHD, and since then we have discussed many areas of his research and his experiences working in the clinical field as well, and then combining that information, to that which I’ve gained through my many interactions with people, who themselves have ADHD and therefore can help me better understand and describe what ADHD is in its core, its symptoms and its translation into real life disabilities, for us all (myself included as an Adult with late diagnosed ADHD) to better cope with understanding and managing everyday life, with this complex mental disorder

Although I‘ve spent many hours writing chapters for this book, I’ve never quite seem to get all the pieces to go together and finalized, since new information is presented, almost daily on the topic of ADHD. With more than 32,000 published papers on ADHD in PubMed alone, and being diagnosed with High-Functioning Autism (HFA) as well, I‘ve got some issues on accepting that I cannot include all the latest facts.

So instead, I’ve decided to make this book, into a dynamic online document instead, so as to always be able to reflect the latest and most current, scientific up-to-date information, to my readers. This document will contain references to scientific and behavioral materials, and is to be seen as an One-Stop-Shop for anyone trying to keep up with the fast-paced developments, occurring in this field, daily.

I hope that you will find this document useful, and please let me know if you find any errors (minor or major) by emailing me at: peter.vang @ addspeaker.net or seek friendship on Facebook to get connected.

Currently this document contains mainly the evidence, that is not so widely available, but which is actually at the core of most of our social and interpersonal problems … Emotions.

You can find my profile page here: https://www.facebook.com/addspeaker/

/Peter ‘ADDspeaker’ Vang

Let‘s get to it, then …


The Current Clinical view of ADHD

A disorder of age-inappropriate behavior in two neuropsychological domains:

Inattention

• Poor persistence toward goals or tasks

• Impaired resistance to responding to distractions

• Deficient task re-engagement following disruptions

• Impaired working memory (remembering so as to do – what is to be done)

Hyperactivity-Impulsivity (Inhibition)

• Impaired verbal and motor inhibition

• Impulsive decision making; cannot wait or defer gratification

• Decreased valuing of future (delayed) consequences over immediate ones

• Excessive task-irrelevant movement and verbal behavior

• Fidgeting, squirming, running, climbing, touching

• Restlessness decreases with age, becoming more internal, subjective by adulthood


Primary Symptoms, Diagnostic Criteria, Subtyping, and Prevalence of ADHD

by Walter Roberts, Richard Milich, and Russell A. Barkley
Excerpt From Attention-Deficit Hyperactivity Disorder, Fourth Edition:
A Handbook for Diagnosis and Treatment, Dr. Russell A. Barkley, PhD.
This material may be protected by copyright.

Attention-deficit/hyperactivity disorder (ADHD) is a common and well-recognized behavior disorder that affects millions of children, adolescents, and adults. A tremendous amount of research has been published on the primary characteristics and symptomatology of children and adults with ADHD.

In this chapter, we briefly summarize this research to provide a concise overview of what is known about ADHD as a clinical construct. It is not our goal to review this sizable body of research critically. Instead, we have attempted to summarize information related to the phenomenology of ADHD that can help clinicians by providing the essence of what is known in this field of research to facilitate the diagnosis, assessment, and treatment of children and adults with ADHD.

The chapter begins with a discussion of the current diagnostic criteria for ADHD because these criteria define the clinical construct of ADHD. For this reason, it is important to understand the rationale behind Diagnostic and Statistical Manual of Mental Disorders (DSM) criteria, as well as some of the limitations of this system.

We then review findings on the primary symptoms of this condition (i.e., inattention, hyperactivity–impulsivity) as they occur in children and adults, as well as sluggish cognitive tempo, a “secondary” symptom cluster that may be either a core component of at least some forms of ADHD or an entirely separate disorder that often overlaps with ADHD. What follows is a discussion of how these primary symptoms can change as a function of situational variables. We conclude the chapter with a discussion of the prevalence of ADHD.

DIAGNOSTIC CRITERIA FOR ADHD

Given the nature of our current classification system of psychopathology, it is necessary to begin our discussion of the nature of ADHD by reviewing the diagnostic criteria of the disorder. Simply put, these criteria define what is and is not ADHD. The current official diagnostic criteria for ADHD are described in the fifth edition of the DSM (DSM-5; American Psychiatric Association, 2013), which is used primarily in the United States.

These criteria are similar to those in DSM-IV (American Psychiatric Association, 1994), although there are small changes that we describe throughout this chapter. Table 2.1 presents the DSM-5 criteria. DSM criteria are similar, although not identical, to the definition of the disorder in the 10th edition of the International Classification of Diseases (ICD-10; World Health Organization, 2008), which is used mainly in Europe.

TABLE 2.1. DSM-5 Diagnostic Criteria for ADHD

A.  Either (1) or (2):

(1)  Inattention:

Six (or more) of the following symptoms have persisted for at least 6 months to a degree that is inconsistent with developmental level and that negatively impacts directly on social and academic/occupational activities:

Note: For older adolescents and adults (age 17 and older), at least five symptoms are required. The symptoms are not solely a manifestation of oppositional behavior, defiance, hostility, or failure to understand task instructions.

(a)  often fails to give close attention to details or makes careless mistakes in schoolwork, at work, or during other activities (e.g., overlooks or misses details, work is inaccurate)

(b)  often has difficulty sustaining attention in tasks or play activities (e.g., has difficulty remaining focused during lectures, conversations, or lengthy reading)

(c)  often does not seem to listen when spoken to directly (e.g., mind seems elsewhere, even in the absence of any obvious distraction)

(d)  often does not follow through on instructions and fails to finish schoolwork, chores, or duties in the workplace (e.g., starts tasks but quickly loses focus and is easily sidetracked)

(e)  often has difficulty organizing tasks and activities (e.g., difficulty managing sequential tasks; difficulty keeping materials and belongings in order; messy, disorganized work; has poor time management; fails to meet deadlines)

(f)  often avoids, dislikes, or is reluctant to engage in tasks that require sustained mental effort (e.g., schoolwork or homework; for older adolescents and adults, preparing reports, completing forms, reviewing lengthy papers)

(g)  often loses things necessary for tasks or activities (e.g., school materials, pencils, books, tools, wallets, keys, paperwork, eyeglasses, mobile telephones)

(h)  is often easily distracted by extraneous stimuli (for older adolescents and adults, may include unrelated thoughts)

(i)  is often forgetful in daily activities (e.g., doing chores, running errands; for older adolescents and adults, returning to class, paying bills, keeping appointments)

(2)  Hyperactivity and impulsivity:

Six (or more) of the following symptoms have persisted for at least 6 months to a degree that is inconsistent with developmental level and that negatively impacts directly on social and academic/occupational activities:

Note: For older adolescents and adults (age 17 and older), at least five symptoms are required. The symptoms are not solely a manifestation of oppositional behavior, defiance, hostility, or failure to understand task instructions.

Hyperactivity

(a)  often fidgets with hands or feet or squirms in seat

(b)  often leaves seat situations where remaining seated is expected (e.g., leaves his or her place in the classroom, in the office or other workplace, or in other situations that require remaining in place)

(c)  often runs about or climbs excessively in situations in which it is inappropriate (Note: In adolescents or adults, may be limited to subjective feelings of restlessness)

(d)  often unable to play or engage in leisure activities quietly

(e)  is often “on the go,” acting as if “driven by a motor” (e.g., is unable or uncomfortable being still for extended time, as in restaurants, meetings, etc.; may be experienced by others as being restless or difficult to keep up with)

(f)  often talks excessively

Impulsivity

(g)  often blurts out answers before questions have been completed (e.g., completes people’s sentences; cannot wait for turn in conversation)

(h)  often has difficulty awaiting turn (e.g., while waiting in line)

(i)  often interrupts or intrudes on others (e.g., butts into conversations, games, or activities; may start using other people’s things without asking or receiving permission; for adolescents and adults, may intrude into or take over what others are doing)

B.  Several hyperactive–impulsive or inattentive symptoms that caused impairment were present prior to age 12 years.

C.  Several impairments from the symptoms are present in two or more settings (e.g., at home, school, or work; with friends or relatives; in other activities).

D.  There is clear evidence that the symptoms interfere with, or reduce, the quality of social, academic, or occupational functioning.

E.  The symptoms do not occur exclusively during the course of schizophrenia or another psychotic disorder and are not better accounted for by another mental disorder (e.g., mood disorder, anxiety disorder, dissociative disorder, or a personality disorder).

Specify whether:

314.01 (F90.2) (ADHDC)Combined Presentation:

If both Criteria A1 (inattention) and A2 (hyperactivity-impulsivity) are met for the past 6 months.

314.00 (F90.0) (ADHDPI) Predominantly Inattentive Presentation:

If Criterion A1 (inattention) is met but Criterion A2 (hyperactivity–impulsivity) is not met for the past 6 months.

314.01 (F90.1) (ADHDPHI) Predominantly HyperactiveImpulsive Presentation:

If Criterion A2 (hyperactivity–impulsivity) is met but Criterion A1 (inattention) is not met for the past 6 months.

Specify if:

In partial remission: When full criteria were met in the past, fewer than the full criteria have been met for the past 6 months, and the symptoms still result in impairment in social, academic, or occupational functioning.

Specify current severity:

Mild: Few, if any, symptoms in excess of those required to make the diagnosis are present, and symptoms result in no more than minor impairment in social or occupational functioning.

Moderate: Symptoms or functional impairment between “mild” and “severe” are present.

Severe: Many symptoms in excess of those required to make the diagnosis, or severe symptoms that are particularly severe, are present, or the symptoms result in marked impairment in social occupational functioning.

Note:
From American Psychiatric Association (2013). Copyright 2013 by the American Psychiatric Association. Reprinted by permission.

DSM-5 criteria stipulate that people must have had their symptoms of ADHD for at least 6 months, and that these symptoms must occur to a degree that is developmentally deviant. The symptoms producing impairment must have developed by 12 years of age. In DSM-5, the number of symptoms required to meet criteria changes according to the individual’s age. For children age 16 or younger, six or more of the nine items from at least one cluster of symptoms must be endorsed as developmentally inappropriate. For adolescents and adults age 17 or older, five or more symptoms from at least one of the symptom clusters must be endorsed. These symptoms must interfere with the individual’s functioning in two or more settings. The presentation of ADHD to be diagnosed depends on whether criteria are met for inattention, hyperactivity–impulsivity, or both: the predominantly inattentive presentation (ADHD-PI), the predominantly hyperactive–impulsive presentation (ADHD-PHI), or the combined presentation (ADHD-C). Severity specifiers can be used to further specify a person’s diagnosis (i.e., mild, moderate, or severe) based on his or her symptom profile and degree of functional impairment. For example, a child who shows six symptoms in both clusters and experiences minimal functional impairment in few settings might be diagnosed with ADHD-C mild, whereas a child with eight inattentive symptoms and two hyperactive–impulsive symptoms who shows considerable impairment across most settings might be diagnosed with ADHD-PI severe.

Situational Pervasiveness

The requirement that symptoms of ADHD should be present in two or more situations was introduced in DSM-IV and formalized as a diagnostic requirement in DSM-5. Given that ADHD appears to result from neurological dysfunction, it is expected that children with the disorder should show symptoms, and to a lesser extent, impairment, in more than one domain of functioning (e.g., at school and at home). If a person has symptoms only in a single setting, then it is likely that environmental influences in that setting rather than ADHD are eliciting the problematic behavior. As such, this requirement has important implications for correctly diagnosing and treating ADHD, but, unfortunately, the specifics of this criterion are not well developed in DSM-5.

An immediate problem with establishing impairment across settings is that information on each setting is often provided by a different informant(s) (e.g., parents, teachers), so ratings on each setting are typically confounded by the source. The degree of agreement between parents and teachers is modest for most dimensions of behavior; it often ranges between .30 and .50, depending on the behavioral dimension being rated (Achenbach, McConaughy, & Howell, 1987; Mitsis, McKay, Schulz, Newcorn, & Halperin, 2000). This relatively modest correlation between parent and teacher reports of behavior sets a low ceiling for the level of agreement that can be expected between two informants.

Possible causes of such disagreement between sources are numerous and difficult to establish on a case-by-case basis. Discrepancies may in part reflect real differences in the child’s behavior in these different settings, probably as a function of true differences in situational demands. School, after all, is quite different from the home environment in its expectations, tasks, social context, and general demands for public self-regulation, and, as we describe later, these situational differences can have profound effects on the behavior of children with ADHD.

The differences may also reflect the degree of historical knowledge the rater possesses concerning that child; at the beginning of the school year, teachers have far less information about a particular child they are asked to describe than will be the case later in the year. But the disagreements may also reflect differences in the attitudes, experiences, and judgments of different people. Although it is likely that teachers have a larger “normative group” against which to compare a single child’s behavior, parents likely have more behavioral observations of their child on which they can base their ratings.

Indeed, parent and teacher ratings of symptoms predict unique components of functional impairment, suggesting that each source of information provides some valid information about the child’s symptoms (Hart, Lahey, Loeber, & Hanson, 1994). As such, clinicians should interpret these assessment sources as providing information on the child in that particular context and nothing more, rather than as evidence as to whether or not the child really has the disorder. When agreement across parent, teacher, and clinician is a requirement for diagnosis, it severely reduces diagnosis (particularly for the ADHD-PI and ADHD-PHI presentations) within the childhood population (Mitsis et al., 2000).

In summary, the requirement that children show ADHD symptoms across settings ensures that those with behavioral problems secondary to specific environmental factors are not diagnosed with ADHD.

However, there are problems with interrater agreement and situational variability in children’s symptoms that can make establishing impairment across settings challenging.

Clinicians do well to remember that no source of information is entirely infallible. There is also no empirical basis for requiring that reports from multiple informants be used to support a diagnosis of ADHD.

Until more research is done to address this issue, even evidence for a history of symptoms across settings should probably be sufficient to satisfy this criterion, rather than the current implicit requirement of agreement between parents and teachers on the number and severity of symptoms—a requirement not actually stated in DSM-5.

Developmental Considerations

Developmental issues continue to pose significant problems for DSM ADHD criteria. The original DSM-IV field trials tested the use of ADHD criteria on children between ages 4 and 16. It is unclear at this time whether the current symptom set is appropriate for use outside of individuals in this age range.This concern arises from the finding that some symptoms, particularly those in the hyperactive–impulsive cluster, decline in frequency as people age (Hinshaw, Owens, Sami, & Fargeon, 2006; Larsson, Lichtenstein, & Larsson, 2006).

This is problematic because applying symptoms that change in frequency across development may result in changing sensitivity and specificity across age groups. Given the age-dependent decline in hyperactive–impulsive symptoms, young preschool-age children (ages 2–3) may be inappropriately diagnosed as having ADHD (false positives), while a smaller than expected percentage of adults would meet the criteria (false negatives).

This problem has been partially addressed in DSM-5. Instead of requiring six symptoms in either cluster for all age groups, older adolescents and adults are required to endorse five or more symptoms in at least one cluster to receive a diagnosis.

Although this is a step in the right direction toward addressing the age-related reduction in hyperactivity–impulsivity symptoms, more could have been done.

First, it is questionable whether a cutoff score of five items is most appropriate for adults. For instance, Murphy and Barkley (1996) initially found that endorsing four items placed older adults at the upper end of the distribution (i.e., > 93rd percentile). Furthermore, those adults who endorsed four or more symptoms continued to show functional impairment, which suggests that their symptoms continued to interfere with their functioning. These findings were later supported by analyses of both large samples of clinic-referred and community adults and children with ADHD followed to young adulthood (Barkley, Murphy, & Fischer, 2008). Subsequently, this cutoff was replicated using a large population sample representative of U.S. adults (Barkley, 2011a). Thus, the currently prescribed five-item cutoff for adults should probably be four symptoms on either list because the use of five items may continue to underidentify impaired adults. Others have also found this threshold to be valid for diagnosing adults with ADHD (see Barkley et al., 2008, for discussion). What this makes plain is that without some age-related adjustments to the thresholds, individuals can outgrow the DSM criteria without outgrowing their disorder, which is seen as developmentally deviant and impairing.

Second, DSM-5 does not adjust the required number of symptoms for preschool children. Unfortunately, there is little research on diagnostic thresholds in preschoolers, and none was done in support of DSM-5. For this reason it is difficult and potentially problematic to diagnose young children using DSM-5 criteria. As discussed earlier, preschool children show higher rates of hyperactive–impulsive symptoms than do school-age children. This may reflect normal developmental patterns rather than higher rates of ADHD in this age group. Indeed, it is in this age group that children are likely to be diagnosed with ADHD-PHI subtype—or “presentation” in DSM-5 terminology—a subtype of the disorder that often remits before adolescence (Willcutt et al., 2012). This may reflect typical developmental patterns rather than true ADHD in young children.

In addition to the necessity of age-dependent changes in the optimal cutoff score, one also must consider that the items themselves become more or less valid as a function of age. The items used to construct DSM-IV symptom lists were initially based entirely on research on children (Spitzer et al., 1990).

To address the more egregious examples of this problem, DSM-5 now includes parenthetical clarifications of many symptoms to advise clinicians on how the symptoms might be expressed in teens or adults. This is because it is likely that a set of items developed specifically for children is not ideal for measuring the same construct in adolescents or adults.

Problematic with this approach to adjusting item content is that the parenthetical clarifications were not themselves tested in any research projects as such to determine whether they in fact are clarifications of that item (are collinear with it) or actually may represent an additional symptom. These clarifications also have not been tested for their accuracy in discriminating teens or adults with ADHD, so while the intent here was commendable, the inclusion of these untested clarifications may pose problems for both reliability and validity of the item pool for diagnosis.

In a large-scale research project intended to identify the best items for the diagnosis of adult ADHD, Barkley and colleagues (2008) tested 99 new symptoms of ADHD, most of which were derived from either chart reviews of several hundred adults diagnosed with the disorder or rating scales and theories of executive functioning. Eight were from the symptom list for oppositional defiant disorder (ODD).

These items, shown in Table 2.2, are listed in descending order of discriminative accuracy. The final two items on this list, taken from DSM-IV, were retained but contributed just 1% more accuracy to the group discriminations. Further analyses showed that a cutoff of 4 of the first seven items or six of the entire list of nine items would be useful for making a diagnosis of adult ADHD, and better at doing so than the DSM-IV.

Other studies have also shown this reduced item set to be useful in identifying adult ADHD (Vergara-Moraques et al., 2011). Using this same original item set, Biederman and colleagues (Biederman et al., 2008) found that just eight items were as useful at identifying functional impairment in adults with ADHD as the entire item set, some of which overlap with those in Table 2.2.

Later, Fedele, Hartung, Canu, and Wilkowski (2010) studied this same item pool for its utility in predicting impairment in ADHD in a large sample of college students and found that 17 items were sufficient to account for such impairment accurately.

Note that Barkley and colleagues (2008) developed their items from those that best discriminated between adults with ADHD and non-ADHD groups; that is a different undertaking than identifying items best at predicting functional impairment, as these latter two studies attempted to do.

So it is not surprising that the resulting reduced item sets found in these studies are not identical. All of this is to say that better items than those in DSM-5 exist as symptoms for diagnosing adults with ADHD, whether for discriminating them from other conditions or for predicting impairment.

Although this information was shared with the DSM-5 committee developing the criteria for ADHD, no new items were eventually included in the final DSM-5 for use with adults.

TABLE 2.2.

A List of Proposed Diagnostic Criteria for ADHD in Adults

Has six (or more) of the following nine symptoms or four or more of the first seven symptoms that have persisted for at least 6 months to a degree that is maladaptive and inconsistent with developmental level:

1. Often easily distracted by extraneous stimuli.

2. Often make decisions impulsively.

3. Often has difficulty stopping activities or behavior when they should do so.

4. Often starts a project or task without reading or listening to directions carefully.

5. Often shows poor follow through on promises or commitments they may make to others.

6. Often has trouble doing things in their proper order or sequence.

7. Often more likely to drive a motor vehicle much faster than others (excessive speeding). (If person has no driving history, substitute: “Often has difficulty engaging in leisure activities or doing fun things quietly.”)

8. Often has difficulty sustaining attention in tasks or leisure activities.

9. Often has difficulty organizing tasks and activities.

Another issue raised from an inspection of the two clusters or dimensions of items suggests that the items for inattention may have a wider developmental applicability across the school-age ranges of childhood and possibly into adolescence and young adulthood (e.g., “Is often easily distracted”). Those for hyperactivity–impulsivity, in contrast, seem much more applicable to young children and less appropriate or not at all applicable to older teens and adults (e.g., “Often leaves seat in situations when remaining seated is expected”). This hypothesis is supported by the previously discussed findings that people show reductions in hyperactive–impulsive symptoms, but not inattentive symptoms, as they age. In other words, it may be that hyperactivity–impulsivity does not actually decline over time, but that instead DSM criteria become less sensitive to these constructs throughout development.

How, then, can clinicians handle these limitations of the DSM criteria related to developmental changes? Although only limited effort is made in DSM-5 to define “developmental inappropriateness,” the ubiquity of well-normed behavior rating scales for ADHD symptoms argues for the use of such instruments to determine the extent of developmental deviance in a particular case (see Chapter 18 for a discussion of these scales). Although not wholly objective, such instruments do provide a means of quantifying parent and teacher opinions in the case of children, and self-report and other-report of symptoms in the case of adults being evaluated for ADHD (Barkley, 2011a; Conners, Erhardt, & Sparrow, 1999). Moreover, national norms are now available for the parent and teacher versions of these instruments for children (DuPaul et al., 1997; DuPaul, Power, McGoey, Ikeda, & Anastopoulos, 1998), and self and other ratings for adults (Barkley, 2011a). The use of such scales automatically provides a means for establishing deviance relative to both age and gender membership of an individual given that norms are provided separately for males and females by age groups.

With such norms available, we must then specify a recommended threshold that is considered “inappropriate.” It would seem prudent to establish a cutoff score on these scales of at least the 90th percentile, and preferably the 93rd percentile, as the demarcation for clinical significance, given that the 93rd percentile (+1.5 standard deviations above the mean) is a traditionally employed cutoff point for this purpose (DuPaul, Power, McGoey, et al., 1998). This recommendation should be taken not as gospel but instead as a guideline for circumventing some of the limitations of DSM criteria. The age-of-onset criterion in DSM-5 specifies that to be diagnosed with ADHD, a person must have shown evidence of symptoms producing impairment when he or she was 12 years of age or younger. In DSM-IV, this age restriction required evidence of impairment prior to age 7. This criterion was challenged by the results of its own field trial (Applegate et al., 1997), and a subsequent review confirmed that strict application of the DSM-IV age-of-onset requirement resulted in underidentification of people showing impairment (Kieling, Kieling, & Rohde, 2010).

Although people with early-onset ADHD (i.e., prior to age 7) appear to have more severe and persistent conditions, with more problems with reading and school performance generally (McGee, Williams, & Feehan, 1992), those with later onset still demonstrate considerable functional impairment related to their symptoms (Faraone et al., 2006). In the original DSM-IV field trials (Applegate et al., 1997), the age 7 age-of-onset criterion resulted in underidentification of children with ADHD-PI, but it performed reasonably well for children with ADHD-C, perhaps because hyperactivity–impulsivity symptoms can result in disruptive behavior that is more salient than symptoms of inattention to teachers and parents. Overall, that DSM-5 requires symptom onset before age 12 rather than age 7 will likely result in fewer false negatives, although clinicians should be cautious if children present with symptoms of hyperactivity that were not present earlier in their development. Clinicians may also want to view age of onset as a guideline that requires onset of symptoms in childhood or adolescence rather than as an empirically supported demarcation between real and false cases of disorder.

We advise this for two reasons.

First, research shows that at least 7–10% of children and adults meeting all other criteria for ADHD have an onset of symptoms after age 12 (Barkley et al., 2008).

Second, self- and parental recall of childhood onset of these symptoms is quite unreliable among teens and adults, on average occurring 4–5 years later than what was established when they were children with ADHD entering a longitudinal study (Barkley et al., 2008).

Subtyping

First and foremost is the concern that the diagnostic category ADHD-PI contains at least two diagnostic subgroups (Diamond, 2005; Milich, Balentine, & Lynam, 2001).

One group includes children who demonstrate clinically significant symptoms of inattention and subclinical, but still considerable, levels of hyperactivity–impulsivity.

Another group comprises children whose inattentive symptoms are linked to problems with arousal and sluggish cognitive tempo (SCT; McBurnett, Pfiffner, & Frick, 2001).

Although we describe the SCT dimension later in this chapter and it is discussed more thoroughly in Chapter 17, suffice to say that there are a number of qualitative differences between individuals with the SCT subset of ADHD-PI and those with “subthreshold” ADHD-C; emerging research suggests that these groups suffer from qualitatively different disorders (Barkley, 2012c, 2013, 2014).

Another subgroup that meets criteria for ADHD-PI is those people who originally met criteria for ADHD-C but experienced the previously described age-related reduction in hyperactive–impulsive symptoms. These individuals likely suffer from a disorder that is qualitatively distinct disorder from that of persons whose symptoms were always consistent with ADHD-PI but due to partial symptom remission in the hyperactive–impulsive cluster do not meet criteria for ADHD-C. One way to address this issue may be to develop a separate set of criteria for individuals with inattentive symptoms but no hyperactive–impulsive symptoms (Adams, Milich, & Fillmore, 2010). This may improve classification accuracy and reduce heterogeneity among people diagnosed with ADHD-PI. Another problem with the subtyping system is that very little is known about differences among the subtypes in terms of developmental trajectory, associated problems, and treatment response. Most of the research on children and adults with ADHD does not differentiate between the groups, so by default most of the participants show a considerable number of hyperactive–impulsive symptoms.

There are, of course, studies that have specifically recruited an ADHD-PI group for comparison with children with ADHD-C (Nigg, Blaskey, Huang-Pollock, & Rappley, 2002); however, these studies are the exception rather than the rule, and even these studies may have limitation in their findings because the ADHD-PI groups typically include both children with “true” ADHD-PI and those with “subthreshold” ADHD-C. Indeed, studies that have attempted to identify groups of children with “pure” inattentive symptoms often report intriguing differences between the subtypes (Adams, Derefinko, Milich, & Fillmore, 2008; Carr, Henderson, & Nigg, 2010; Fillmore, Milich, & Lorch, 2009). As a counterpoint to our view on the importance of subtypes, several studies have shown that children diagnosed with one subtype of ADHD are very likely to meet criteria for another subtype during a later assessment (Willcutt et al., 2012). This subtype instability calls into question the importance of research on the differences between subtypes of the disorder because if subtypes do not persist, then the differences among them are unlikely to be consequential in the long run.

However, it should be noted that some of this subtype instability may result from small changes in symptom count (e.g., six hyperactive–impulsive symptoms during an initial assessment and five hyperactive–impulsive symptoms at follow-up). As discussed earlier, a way to improve subtype stability may be to develop a separate set of criteria for those with heightened inattentive symptoms and few or no hyperactive–impulsive symptoms. A final issue concerns the validity of the ADHD-PHI subtype. This is by far the most uncommon subtype of this disorder; most children who show symptoms of hyperactivity–impulsivity also meet criteria in the inattentive symptom cluster. Those individuals who only meet criteria in the hyperactive–impulsive symptom cluster are mostly young and show the highest level of diagnostic instability over time (Lahey et al., 2005). One source of this diagnostic instability may be that ADHD-PHI is an earlier developmental stage of ADHD-C.

Indeed, many children originally diagnosed with ADHD-PHI are diagnosed with ADHD-C during follow-up assessment.

Another possible source of this diagnostic instability is that young children diagnosed with ADHD-PHI show symptom remission as they age from early to middle childhood. By far the largest proportion of these children do not meet criteria for ADHD at follow-up (Willcutt et al., 2012), which suggests that the original diagnosis reflected a typical developmental phase or even a time-limited behavior disorder.

SUMMARY

To summarize, children and adults with ADHD-PI are a mixed group. Some of them (perhaps 30–50%) have an SCT form of attention disturbance, which may constitute a qualitatively unique disorder from the attention disturbance in ADHD-C. Others are older children and adults who were once diagnosed as having ADHD-C but have shown a decrease in the number and severity of their symptoms of hyperactivity with age, such that they now fall below the critical number of six such symptoms required for the ADHD-C diagnosis. Although the DSM decision rules would reclassify these individuals as having ADHD-PI, clinicians may wish to continue conceptualizing and treating them as having ADHD-C. Despite these limitations, whether people are diagnosed with ADHD-PI or ADHD-C is not entirely consequential at this time given the dearth of research on subtype differences in treatment response, developmental trajectory, and associated problems.


EMOTIONAL DYSREGULATION IS A CORE COMPONENT OF ADHD

Excerpt From Attention-Deficit Hyperactivity Disorder, Fourth Edition:
A Handbook for Diagnosis and Treatment, Dr. Russell A. Barkley, PhD.
This material may be protected by copyright.

As the previous chapter has nicely documented, for over 40 years, clinical descriptions of the core nature of attention-deficit/hyperactivity disorder (ADHD) have focused exclusively on the two-dimensional structure of the disorder cited in clinical diagnostic criteria (inattention, hyperactivity–impulsivity), such as those in the Diagnostic and Statistical Manual of Mental Disorders (DSM-III, DSM-III-R, DSM-IV, DSM-5; American Psychiatric Association, 1980, 1987, 1994, 2013). As noted in DSM-5, the essential feature of ADHD is a persistent pattern of inattention and/or hyperactivity–impulsivity that is more frequent and severe than is typically observed in individuals at a comparable level of development. Such official descriptions concerning the core nature of the disorder and the related symptom lists focus exclusively on a two-dimensional structure as being the central features of the disorder. Here I argue that this overemphasis on the most observable and objectively measurable features of the disorder has led to the exclusion or a deemphasis of another feature of the disorder that is just as central to its understanding yet considerably more difficult to quantify.

EMOTIONAL IMPULSIVITY (EI)

This largely neglected element is a deficiency in both the effortful (executive or cognitive) inhibition and the top-down self-control of emotions in general and particularly those pertaining to the self-regulation of frustration, impatience, and anger. The most noticeable and initial consequence of this deficiency in people with ADHD is a striking propensity for failure to inhibit emotions, or emotional impulsivity (EI).

EI refers to the quickness or speed with which, and the greater likelihood that an individual will react with primary (particularly negative) emotions in response to events compared to others of the same developmental level or age. It is not the same as emotional intensity, which itself can vary across individuals and is not thought to be a problem in those with ADHD.

The primary emotional reactions of those with ADHD are not so much more intense initially as they are less moderated by conscious, effortful executive self-regulation of those emotions. Others may have felt the same emotionally intense reaction to an event but are less likely to display the primary emotional behavior associated with it before moderating its expression and even generating secondary emotional states to counteract or supplant the initial primary ones. The related component to emotional inhibition is emotional self-regulation, which represents a conscious, “top-down” and effortful (executive) moderation of the initial emotional reaction.

Like Melnick and Hinshaw (2000), I defer to Gottman and Katz (1989) for their helpful definition of emotion regulation as the ability to “(a) inhibit inappropriate behavior related to strong negative or positive emotion, (b) self-soothe any physiological arousal that the strong affect has induced, (c) refocus attention, and (d) organize for coordinated action in the service of an external goal” (p. 373).

DEFICIENT EMOTIONAL SELF-REGULATION (DESR)

Its opposite is referred to here as deficient emotional self-regulation (DESR). Notice that the definition incorporates emotional inhibition as the first step in emotional self-regulation, which is consistent with the view to be taken here and that of my theory of executive functioning in ADHD (Barkley, 1997a, 1997c, 2012b). Yet it will prove helpful in the following discussion to identify them separately as EI and DESR, with the understanding that the former is the initial step contained within the latter.

That is because one cannot self-soothe or otherwise moderate one’s initial emotional reactions to events if he or she has not first inhibited the impulsive expression of those initial reactions. EI therefore interferes with subsequent efforts to engage in emotional self-regulation. It is also helpful to separate them because most of the available research in ADHD and emotions seems to be directed at documenting the first (EI) more than the second (DESR).

EI-DESR

This chapter examines the importance of EI–DESR in understanding the nature of ADHD. It also seeks to explain why the explicit recognition of EI–DESR as a central feature of the disorder may prove useful in broadening our understanding of the emotional and social maladjustment evident in cases of the disorder.

Apart from providing a more accurate clinical portrayal of the disorder for both greater professional and public understanding, this argument stresses that formally acknowledging the place of EI–DESR has a sound basis in:

(1) the history of ADHD

(2) the neuropsychological nature of the disorder

(3) the neuroanatomy of ADHD

(4) the empirical research on the symptoms of EI–DESR in ADHD

(5) the linkage of ADHD with oppositional defiant disorder (ODD), among other comorbidities

(6) the concurrent and later impairments often seen in ADHD, especially in the domains of social functioning.

Others have also argued that emotional dysregulation is an important component of ADHD based on lines of evidence other than those I summarize here (Martel, 2009; Skirrow, McLoughlin, Kuntsi, & Asherson, 2009).

As I discuss below, it is especially this impulsive aspect of ADHD that provides a strong link between ADHD and EI–DESR through the disruption of emotional inhibition, item (a) in the definition of DESR, as noted earlier.

As Martel (2009) reasoned, the hyperactive–impulsive (HI) dimension of ADHD is associated with a breakdown in the emotionality component (EI) whereas inattention is associated with a breakdown in the regulatory side (DESR).

Martel further argued that breakdowns in regulatory control of emotion are a specific signature of ADHD, whereas increased negative emotionality may be nonspecific and shared across the disruptive disorders (ADHD, ODD, and conduct disorder [CD]) accounting for their comorbidity—a point with which I agree, as will be shown later.


THE IMPORTANCE OF EI–DESR IN THE NEUROPSYCHOLOGY OF ADHD

Excerpt From Attention-Deficit Hyperactivity Disorder, Fourth Edition:
A Handbook for Diagnosis and Treatment, Dr. Russell A. Barkley, PhD.
This material may be protected by copyright
.

The past 16 years have witnessed a renewed interest in the difficulties with emotion regulation in ADHD among theorists grappling with model building. I have previously attempted to set forth a more comprehensive neuropsychological theory of ADHD (Barkley, 1997a, 1997c, 2012a, 2012c) that went beyond those at the time that stipulated the central feature of ADHD to be a problem with behavioral inhibition (Quay, 1987, 1997) or of an energetic pool of motivation or arousal (Sergeant, 1988; van der Meere & Sergeant, 1988).

Five executive functions (EFs) were identified in my initial theory that could be implicated in ADHD: behavioral inhibition, nonverbal working memory (chiefly visual imagery and private audition), verbal working memory (primarily private self-speech), the self-regulation of emotion–motivation–arousal (using these working memory systems), and reconstitution (generating multiple response options through a process of mental play [analysis and synthesis]). To this I have more recently added self-awareness (Barkley, 2012c).

These executive functions provide for human “self-regulation,” defined as (1) any action one directs at oneself (2) in order to change subsequent behavior (3) so as to alter a distant or delayed consequence and thereby maximize those consequences. Each EF, in fact, was argued to constitute a specific form of self-control or self-directed activities (e.g., self-directed attention, self-restraint, self-imaging, self-speech, self-emoting, and self-play).

All functioned in concert for the overarching purpose of guiding behavior across time delays toward future goals that served to maximize delayed rather than immediate consequences. The executive deficits associated with ADHD led to a seventh nonexecutive deficit in the control of motor behavior via the EFs that disrupted its coordination, temporal sequencing, and hierarchical structure during goal-directed activities.

This EF-based theory of ADHD reinserted EI–DESR into a central theoretical position in understanding the nature of the disorder. It viewed emotional inhibition and the subsequent self-regulation of emotion as being one among the five (now six; Barkley, 2012a, 2012c) major EFs and argued that ADHD involved a disruption in it. In essence, this EF operated in conjunction with that of behavioral inhibition chiefly to accomplish four purposes very similar to the components of the earlier definition of emotional regulation by Gottman and Katz (1989). First, the inhibitory function served to delay (inhibit) the initial prepotent or dominant responses to an event, including their emotional tone and other emotional behavior, so that both the motor response and related emotional behavior were deferred.

This set the stage for the second purpose of this EF, which was the modification of the initial emotional state to make it more congruent with and supportive of the individual’s long-term goals. In part, this involved the use of the working memory systems (self-directed visual imagery and self-speech) to assist with self-soothing of emotional arousal and to create hindsight.

The latter allowed the individual to consider consciously what had previously been experienced in similar situations and so guide the construction of the eventual response to the event informed by such prior information. This retrospective function of the working memory systems led to foresight or the prospective function. That function was the construction of an expectation about the situation and a consideration of potential future consequences that would arise for responding in various ways.

This led to a conscious anticipation of that hypothetical future, and the selection and construction of a preparatory set of responses of what to do and when that would be more consistent with the longer-term welfare (goals) of the individual. In using the working memory systems in this way, the individual automatically has the additional capacity to delay the prepotent emotional response to that same event and use visual imagery and private speech to create alternative, competing secondary emotional states to it.

This is because covert visual imagery and covert self-speech, among other forms of covert self-directed behavior, produce not only private images and verbalizations but also the private emotional charges associated with them (Damasio, 1994, 1995; Fuster, 1997). Such use of private action to countermand or counterbalance the initial emotional charge of external events contributes to self-soothing of emotional arousal and the formation of more socially appropriate emotional responses.

They also contribute to the development of emotional self-control (Kopp, 1982). In short, the individual possesses not only a means to consider and construct alternative motor responses to an event that will better maximize future consequences but also a capacity to construct alternative emotional responses joined to those behavioral actions that serve to achieve the same ends.

To summarize, this theory predicts two interrelated emotional problems for those with ADHD: one inhibitory and the other self-regulatory. The first problem is likely to be far more related to the HI symptom dimension and less so to the inattention dimension, whereas the second may be more related to the inattention dimension given its close connection to working memory systems and the manipulation of their content. Those with ADHD will be as impulsive with their primary emotions as they are with their motor or behavioral responses because they are essentially a single unitary event: Action and emotion are united in the response.

And the person with ADHD will not be able to generate the countervailing secondary emotion needed to quell the primary one provoked by the event or to self-soothe primary emotional arousal to moderate the expression of his or her emotions so that he or she is more socially acceptable, much less to provide the emotional support needed for the alternative goal-directed behavior. This is the self-regulatory aspect of the executive system that is contingent on the inhibitory action and is also viewed as deficient in ADHD.

According to this theory, to the extent that an individual with ADHD displays a deficiency in behavioral inhibition or impulsiveness, he or she will automatically display an equivalent degree of deficiency in emotional inhibition or emotional impulsiveness. From this perspective, emotional impulsiveness, or EI, and the associated subsequent deficiency in the self-regulation of emotions, are just as much a part of ADHD as behavioral impulsiveness, and the associated problems with behavioral self-regulation. Still (1902) had reached the same conclusion for similar reasons.

But there are two other purposes to the EF of emotional inhibition/self-regulation. To understand them we must first dissect the concept of emotion. Emotions are motivational states. They can be regarded as arising from a two-dimensional process (Gray, 1994; Lang, 1995): One dimension is motivational and comprises approach–avoidance valences concerning any analysis of our actions and their attendant consequences (reinforcement–punishment); the other, a dimension of arousal that is orthogonal to the motivational one, contributes to the degree of activation, force, or intensity of the motivational state. Largely unappreciated to date by many researchers in the field of ADHD is that this view of emotion would lead to the prediction of both motivational and arousal problems inherent in those with ADHD. If one’s emotional responses to events are as impulsive as his or her behavioral ones, then so will be his or her motivational and arousal responses.

Given that these features of emotion form a unity (emotion–motivation–arousal), the more impulsively one’s emotions are directly elicited by environmental events, the more one’s motivation and arousal will be determined by and dependent on those events. As argued in this theory, the more one is able to manage, moderate, and manipulate one’s emotional states via self-regulation in the service of their future goals, the more one automatically is capable of manipulating one’s own motivational and arousal states to achieve those same ends.

This is because the latter states (motivation and arousal) are the basis for the former one (emotion). ADHD must therefore involve a deficit in self-motivation and the self-regulation of arousal in support of future, goal-directed behavior as surely as it involves a deficit in the regulation of emotion for this self-same end.

It is the capacity to self-motivate that serves to bridge gaps across delays and longer periods of time in the absence of consequences and therefore motivates delayed gratification and future-directed behavior (Fuster, 1997; Mischel et al., 1989). The evidence for such motivational deficits in ADHD is long-standing (Glow & Glow, 1979) and substantial (Luman, Oosterlaan, & Sergeant, 2005), and is supported below in the neuroanatomical network(s) underlying ADHD, especially the role of the anterior cingulate cortex in governing the amygdala specifically and the limbic system more generally. But the existence of and theoretical basis for this emotional–motivational component of ADHD goes largely unnoticed in current diagnostic conceptualizations of the disorder.

My theory of ADHD is not the only one that posits that difficulties with emotion regulation are likely to arise in ADHD. More recently, Nigg and Casey (2005) suggested that three distinguishable neural networks are to be found in the neuroanatomical regions implicated in ADHD, and that these cortical–subcortical loops or networks account for both the cognitive and affective response regulation problems seen in ADHD.

Nigg and Casey posit that disruption of the frontal–limbic pathway would give rise to difficulties with emotion regulation in ADHD, while the frontal–striatal (working memory and response selection) and frontal–cerebellar pathways (temporal organizing and timing of behavior) would be associated with the more cognitive deficits of knowing the “what” and “when,” respectively, of preparing for and responding to events in various situations.

They argued that affect regulation, motivation, and emotionally reactive responding are important in ADHD, and that dysfunction in the frontal–limbic–amygdala circuit probably accounts for it. A short time later, Sagvolden, Johansen, Aase, and Russell (2005) published their dopaminergic theory of ADHD, which predicted difficulties with impulsive emotion and low frustration tolerance as a consequence of hypodopaminergic activation in at least one of the three dopamine networks in this model (the mesolimbic pathway).

This pathway is similar to the frontal–limbic pathway in the Nigg and Casey model, and is said to produce much the same emotional consequences in ADHD. This frontal–limbic pathway has more recently been identified as that mediating the “hot” or emotional–impulsive, hyperactive, and motivational features of ADHD (and EF) as distinguished from the “cool” pathways (frontal–striatal, frontal–cerebellar) believed to mediate the attention, disorganization, working memory, and timing problems in ADHD (Castellanos, Sonuga-Barke, Milham, & Tannock, 2006).

The central dogma on the nature of ADHD prevailing at the moment, and captured in DSM descriptions and criteria (see Chapter 2), does not acknowledge such deficits in emotion regulation as an inherent part of ADHD. It views problems with emotional control as merely associated features. But there are not only good historical grounds for correcting this abandonment of EI–DESR in the nature of ADHD, as shown earlier, but as the previous discussion attests, there are also good theoretical reasons for doing so.


THE IMPORTANCE OF EI–DESR IN THE NEUROANATOMY OF ADHD

Excerpt From Attention-Deficit Hyperactivity Disorder, Fourth Edition:
A Handbook for Diagnosis and Treatment, Dr. Russell A. Barkley, PhD.
This material may be protected by copyright.

Regardless of, or apart from, theoretical predictions about the role of EI–DESR in the central nature of ADHD, the growing body of evidence on the neuroanatomical networks that underlie the disorder provides further justification for the inclusion of EI–DESR as a core feature of this disorder.

The networks believed to give rise to the inattentive, hyperactive, and impulsive behavior of those with ADHD, reflecting their deficient self-regulation, are also the networks that govern the inhibition of reactive emotion and the subsequent cognitive, effortful, top-down, or executive control of emotion. Specifically, these are the lateral prefrontal cortex (LPFC) and the anterior cingulate cortex (ACC). It is not my purpose in this chapter to give a detailed and critical review of the results of neuroimaging studies of ADHD

Suffice to say here, detailed reviews and meta-analyses of the research appear to support the conclusion that at least five brain regions are involved in ADHD (Bush, Valera, & Seidman, 2005; Cortese et al., 2012; Hart, Radua, Nakao, Mataix-Cols, & Rubia, 2013; Hutchinson, Mathias, & Banich, 2008; Mackie et al., 2007; Paloyelis, Mehta, Kuntsi, & Asherson, 2007; Valera, Faraone, Murray, & Seidman, 2007): (1) the LPFC, (2) the ACC, (3) the basal ganglia (and particularly the caudate of the striatum), (4) the splenium of the corpus callosum, and (5) the cerebellum (especially the vermis). Where asymmetries are found in these regions, evidence suggests greater involvement of the right hemisphere than left in the disorder (Valera et al., 2007).

Noteworthy is that differences in the size and functioning of these regions have been found in the unaffected first-degree relatives of people with ADHD, which suggests that they may be part of a familial endophenotype for the disorder. The deficits found in relatives often fall intermediate between affected people with ADHD and control groups (Mulder et al., 2008).

Several of these affected brain regions are also found to distinguish among people with ADHD, those with CD (Rubia et al., 2009), and those with bipolar disorder (Biederman, Makris, et al., 2008). Also of importance is that the size and level of activity within these regions are correlated with the degree of ADHD symptoms (Casey et al., 1997).

Studies of the cognitive or conscious regulation of emotion have implicated the LPFC, medial PFC, and ACC, along with its connections to the amygdala (and limbic system more generally) in this executive function (Ochsner & Gross, 2005). Of interest to this analysis is that the little research that exists has found that the generation of emotion from an aversive external stimulus was largely driven by activation in the amygdala in a bottom-up fashion of brain activation.

In contrast the conscious and volitional generation of an emotion to a mentally represented event held in mind (working memory) revealed a more top-down activation of the LPFC, the medial PFC, the ACC, then the amygdala. Except for the amygdala, the remaining brain regions have also been implicated in ADHD, as noted earlier.

From this vantage point, studies indicate that the neuroanatomical network involved in conscious emotional self-regulation in normal brain functioning would be disturbed in those with ADHD given the association of ADHD with deviations in most of the same regions involved in that network. This disturbance would constitute a top-down problem in the conscious regulation of emotions and not a bottom-up problem of an overactive amygdala–limbic system.

In essence, ADHD creates a state in which the normal emotion-generating properties of the limbic system and particularly the anger-, frustration-, and aggression-generating properties of the amygdala are inadequately regulated by higher cortical regions and intermediate structures (nucleus acumbens, etc.). These higher level regions provide for self-control and take over the emotions in the service of longer-term goal-directed, hierarchically organized, and socially acceptable behavior.

One key to understanding how EI–DESR may arise in ADHD is the ACC. As reviews have noted, this brain region traditionally has been associated with the limbic system, and it is likely through the ACC, in part, that a top-down cortical (conscious or volitional) regulation of the emotional system (limbic system) is achieved (Bush, Luu, & Posner, 2000). Such a top-down hierarchical regulation of conscious, complex, goal-directed behavior has been attributed to a caudal-to-rostral, anterior-to-posterior organization of the PFC (Badre, 2008).

This makes clear why the smaller size and functional deficits in the PFC in ADHD would give rise to a breakdown in self-regulation and in the hierarchical organization of goal-directed actions. Concerning the specific thesis of this chapter, these reviews suggest that it may be via the connections to the ACC that this top-down control by the PFC is exercised over emotional behavior and its support of goal-directed actions (Etkin, Egner, Peraza, Kandel, & Hirsch, 2006; Ochsner & Gross, 2005).

The ACC can be subdivided into two regions, dorsal (upper) and rostral–ventral (lower), that may distinguish between the cognitive–executive activities and the emotion regulation activities of the ACC, respectively (Bush et al., 2000). Neuroimaging studies of ADHD have not made much of an effort to distinguish between these two functional zones of the ACC. But a few studies suggest that both zones of the ACC are involved in ADHD (Bush et al., 2000; Krauel et al., 2007). This helps to explain partially both the difficulties with behavioral and emotional self-regulation associated with this disorder.

As some reviews have noted, it is also likely that it is through the ACC that drive and motivation have an influence over motor functioning (Paus, 2001). This would be consistent with the theoretical positions staked out earlier that ADHD, which seems to arise in part from deficits in the ACC, would involve impaired drive and motivation along with those of EI–DESR.

For the time being, the reliable finding of ACC involvement in ADHD, in addition to that of the LPFC, suggests that this may be one of the neuroanatomical bases for anticipating that EI–DESR would be as much of a core deficit associated with ADHD as would the other EFs regulated by this network.

This hypothesis of problematic top-down management of the amygdala–limbic system by the executive brain (PFC) in ADHD gained recent support in findings of dysfunctional connectivity in amygdala–LPFC networks in ADHD that were directly associated with the degree of emotional lability (Hulvershorn et al., 2014).


EVIDENCE FOR EI–DESR IN ADHD

Excerpt From Attention-Deficit Hyperactivity Disorder, Fourth Edition:
A Handbook for Diagnosis and Treatment, Dr. Russell A. Barkley, PhD.
This material may be protected by copyright
.

So far, it has been shown that there are sound historical, theoretical (neuropsychological), and neuroanatomical reasons for believing that EI–DESR should be a central deficit in ADHD. But is it? What is the evidence for such emotion regulation problems apart from the clinical observations of historically significant figures, the theoretical propositions, or the neuroanatomical findings in the field of ADHD? The growing body of evidence that has begun to accumulate on this topic suggests that ADHD is associated with emotional dysregulation.

Until the past few years, very few studies bothered to focus on this issue. And, of course, this seems to be due in part to difficulties involved in the measurement of emotional behavior relative to the more easily assessed motor and attention behaviors involved in the disorder, as noted earlier. It may also be yet another indication that removing these emotional aspects of the disorder from clinical diagnostic criteria beginning with DSM-II and relegating them to the status of associated features in DSM-III onward may have led to relatively less interest among researchers in their involvement in ADHD.


THE IMPORTANCE OF EI–DESR SYMPTOMS IN UNDERSTANDING COMORBIDITY WITH ODD

Excerpt From Attention-Deficit Hyperactivity Disorder, Fourth Edition:
A Handbook for Diagnosis and Treatment, Dr. Russell A. Barkley, PhD.
This material may be protected by copyright.

ODD is characterized in DSM-5 as “a frequent and persistent pattern of angry/irritable mood, argumentative/defiant behavior, or vindictiveness . . . ” (American Psychiatric Association, 2013, p. 463). It comprises a set of eight symptoms, at least three of which reflect negative affect (loses temper, touchy or easily annoyed, angry and resentful), while four reflect social conflict with others (argues with adults, defies or refuses to comply, deliberately annoys others, blames others for his or her own mistakes). The final symptom likely relates to both an affective and a social component of the disorder (acts spiteful or vindictive) and may be more related to CD.

ODD has a point prevalence of 1.4% of girls and 3.2% of boys in children ages 5–16 years, with 36% of girls and 43% of boys with ODD having another disorder (Maughan, Rowe, Messer, Goodman, & Meltzer, 2004). Lifetime prevalence of ODD is 10.2%, with over 92% of such cases having another comorbid disorder (Nock, Kazdin, Hiripi, & Kessler, 2007). The most common comorbidity is ADHD or impulse control disorders (Maughan et al., 2004; Nock et al., 2007; Speltz, McClellan, DeKlyen, & Jones, 1999).

The inverse is also true. ODD is the most common comorbid psychiatric disorder seen in conjunction with ADHD, occurring on average in 65% of cases and in as many as 84% of clinic-referred cases in childhood (see Chapter 5). It is possible that this may even be an underestimate given that such studies may not distinguish among ADHD subtypes. It is ADHD-C with which ODD is likely to have a far greater affiliation than with ADHD-PI or SCT/CDD (Milich et al., 2001; see also Chapter 17).

ODD is 11 times more likely to coexist with ADHD than to occur at its base rate in the general population even in epidemiological samples (Angold, Costello, & Erkanli, 1999). ODD has also been found to be a common comorbidity in children with ADHD followed to adulthood (50% of those with persistent ADHD) and in clinic-referred adults with ADHD (Barkley et al., 2008), occurring in up to 35–53% of these adult cases according to self-reported information. This source of information may lead to underestimates of disorder among patients with ADHD (Barkley et al., 2008).

It is certainly possible that ADHD is one of several causes or contributing factors to the risk for ODD. Suggestive evidence for such a causal or contributory relationship comes from several lines of research findings.

First, the severity of ADHD is certainly significantly and substantially correlated with the risk for and severity of ODD, with correlations between the two dimensions rising to as high as .91 in teenagers (Barkley, Guevremont, Anastopoulos, DuPaul, & Shelton, 1993) and ranging from .68 to .86 in younger children (Burns & Walsh, 2002; Gadow & Nolan, 2002; Harvey, Friedman-Weieneth, Goldstein, & Sherman, 2007).

Using data from my various studies, I analyzed available data for this review and found correlations between ADHD and ODD symptoms to be .72 in our study of kindergarten children with high levels of disruptive behavior and a control group (Shelton et al., 1998), .71 in self-reports of retrospective childhood symptoms in our follow-up study of hyperactive children to age 21 (Fischer, Barkley, Smallish, & Fletcher, 2002), .70 in the employer ratings of those participants’ current symptoms at work, and .77 in participants’ own ratings of those same symptoms in the workplace. All of these results show a robust relationship between the severity of symptoms of these two disorders.

Others have also found that the severity of ADHD is predictive of the severity of later anger and verbal aggression in adolescence among children diagnosed with ADHD (Harty et al., 2009). And it is the persistence of ADHD from childhood to adolescence that explains these difficulties with anger and verbal aggression in adolescence (Harty et al., 2009).

Second, the prevalence of ODD alone is most common in the preschool age group and becomes relatively less common by school age and onward, occurring in just 1–3% of children after age 5 (Maughan et al., 2004; Bauermeister, 1992; Lavigne et al., 2001). After this age, approximately half or more cases of ODD are comorbid with ADHD. ADHD is therefore associated with the persistence of ODD over development, which may further imply a causal connection between the two disorders.

Third, some longitudinal research using preschool children shows that initial ADHD symptoms, particularly the HI dimension, are predictive of higher ODD scores 1 and 2 years later, whereas initial ODD scores were not predictive of later HI or inattention symptoms (Burns & Walsh, 2002). These findings hold even after statistically accounting for the ability of each symptom dimension to predict itself over time.

As those authors noted, this suggests that the HI dimension of ADHD influences the development of ODD behavior in some way. This is consistent with substantial research showing that impulsivity or response inhibition, not hyperactivity, is linked to risk for and severity of conduct problems or externalizing behavior generally, both concurrently and longitudinally into adolescence (Berlin & Bohlin, 2002; Olson, Schilling, & Bates, 1999).

Any initial link of hyperactivity to conduct problems seems to be accounted for by its association with poor inhibition (Berlin & Bohlin, 2002). Other follow-up research with this age group suggests that early-onset ODD is predictive of both later ODD and later ODD with ADHD, but that its stability over development when occurring alone was quite low, with approximately half of all cases remitting every 1–2 years (from 24% in preschool to 5% at 5-year follow-up; Lavigne et al., 2001).

Speltz and colleagues (1999) found that early-onset ODD predicted later risk for ADHD as well. With development, ODD shows an increasing affiliation with ADHD, and especially persistent ADHD (Lavigne et al., 2001). And when ODD occurs with ADHD, it is significantly persistent over the next 4- to 10-year period (August, Realmuto, Joyce, & Hektner, 1999; Biederman, Petty, Dolan, et al., 2008; Speltz et al., 1999).

Fourth, studies of preschool children with hyperactivity (HYP) alone, ODD alone, and both disorders find that only the HYP groups are associated with greater pre- and perinatal risk factors and with a family history of both ADHD and ODD, whereas ODD alone is not (Harvey et al., 2007). Noteworthy as well is that children with HYP alone still had relatives with higher rates of ODD, whereas children with ODD alone did not.

Further study of these preschool groups showed that both the children with HYP and HYP/ODD had greater levels of parental ADHD symptoms, maternal Axis I psychiatric disorders, negative life events, paternal Axis II psychiatric disorders, marital status, couple conflict, or the use of low intensity couples’ conflict tactics (Goldstein, Harvey, Freidman-Weieneth, Pierce, et al., 2007). (Only ODD was not further studied in this subsequent research because it was not found initially to be assosciated with biogenetic risk factors.)

Yet these two groups did differ in the degree of maternal Axis II psychopathology, paternal Axis I psychopathology, and the use of more severe couple conflict tactics. This suggests that genetic and biological contributors to disorder are chiefly linked with ADHD (HYP) whether it occurs with or without ODD, and not with ODD alone.

It further suggests that there exists a genetic predisposition to ADHD that also seems to create a risk factor for ODD in relatives. It further implies that social-environmental factors may be more responsible for preschool ODD when it occurs alone than is the case with ADHD or ADHD with ODD.

Obviously this suggests that ADHD is not the only contributor or cause of ODD, especially in the preschool age group in which ADHD can exist alone (Bauermeister, 1992; Gadow & Nolan, 2002).

But it does suggest that when ODD exists alone, it is not an especially developmentally persistent disorder unless it is linked to ADHD. It also intimates that the nature of ODD when it occurs alone in the preschool age group may have more to do with both the behavioral or social conflict component of the disorder and its greater situation specificity toward parents than its EI component, as the more detailed investigation on the nature of ODD by Hoffenaar and Hoeksma (2002) suggests.

And that social component of ODD alone may explain why it is associated with disrupted parenting and family stress both concurrently (Cunningham & Boyle, 2002) and over development (Burke, Pardini, & Loeber, 2008), whereas ADHD alone shows no such reciprocal effects of parent–child interactions over development (Burke et al., 2008).

All this could explain the very low level of concurrent validity (interjudge agreement and discrimination on observational measures) of ODD only relative to ADHD and especially their combination, which has substantially greater concurrent validity (Harvey et al., 2007).

Research on ODD rarely separates these two components (emotional, social conflict) out for an examination of their development, correlates, stability, and contributors/causes.

The behavioral–social component of ODD may be more likely to arise from disrupted parenting and family stressors, along with associated mismanagement of the gambits of preschool children’s sporadically defiant behavior (Barkley, 1997c; Burke et al., 2008; Cunningham & Boyle, 2002; Lahey & Waldman, 2003; Moffitt, 1993; Patterson, DeGarmo, & Knutson, 2000).

The emotional component of ODD may involve an underlying neuropsychological deficit in emotional impulsiveness and perhaps to a lesser extent its deficient self-regulation, as is argued here and by others (Martel, 2009) to be the case in ADHD.

In my opinion, it is the underappreciated EI–DESR symptoms of ADHD that are most likely to explain this high level of comorbidity of ADHD with ODD as categories of disorders and their strong relationship when assessed dimensionally.

This is evident in the fact that the three symptoms reflecting negative emotion in the ODD symptom list are very similar to those believed to comprise EI noted earlier (low frustration tolerance, quickness to anger, impatience, and emotional excitability).

As shown earlier, these EI symptoms and related problems with DESR are more common in children with ADHD. Research on the construct of oppositionality using a larger range of items identifies two large trait factors as more likely representing this construct or disorder, along with a set of situation-specific factors (parents, other authorities, peers) (Hoffenaar & Hoeksma, 2002). As noted earlier, these two trait factors are emotional and behavioral (social conflict). DSM-5 now reflects this dichotomy of the ODD symptoms.

Others have also argued for viewing ODD as having two components (emotional and social behavioral; Burke, Loeber, & Pardini, 2009). They seem most likely to represent the components of negative affectivity and social behavioral conflict discussed earlier for DSM-5 symptoms.

Supporting this distinction between these components are recent findings that the emotional symptoms of ODD are more predictive of later internalizing disorders, and particularly depression, whereas social conflict symptoms are more related to the developmental risk for CD (Burke, 2009).

Given that three of the symptoms of ODD appear to involve EI–DESR, children with ADHD-C could be considered to be virtually borderline or subthreshold cases of ODD as a consequence.

Their low frustration tolerance, impatience, and quickness to anger set them up for patterns of reactive verbal aggression during provocative encounters with parents and peers, perhaps explaining why reactively aggressive children often show significantly higher rates of ADHD symptoms than do proactively aggressive children or control groups (Vitaro, Brendgen, & Tremblay, 2002).

Indeed, as Martel and Nigg (2006) found, it is the temperamental trait of negative affectivity associated with ADHD in children that is most closely linked to their risk for ODD.

As Ambrosini, Bennett, and Elia (2013) also observed, children with ADHD who also manifest irritable mood are those most likely to be at risk for ODD and mood disorders, and such irritable mood is closely linked to having ADHD-C.

Children with ADHD would therefore require the development of just one or two additional symptoms from the social interaction conflict component before crossing the requisite diagnostic threshold of four symptoms for ODD.

Indeed, given that verbal aggression has been shown to be part of the greater anger evident in ADHD (Harty et al., 2009), a fourth symptom of ODD may already exist in those with ADHD (stubbornness, defiance, refusal to obey).

Further supporting this view that it is the negative emotionality dimension of ADHD that links it to ODD, genetic studies using twins indicate that a substantial portion of the additive genetic, nonadditive genetic, and nonshared environmental contributions to ADHD, ODD, and CD are in fact shared with negative emotionality (Singh & Waldman, 2010).

This rise in the occurrence and severity of the social-interactional component of ODD in children with ADHD and its persistence over time may have as much to do with the severity of ADHD and parenting stress, parental psychopathology, its relationship to disrupted parenting, and severity of parent conflict as with biogenetic contributors associated with ADHD and the EI–DESR component of ODD (August et al., 1999; Burke et al., 2008; Goldstein, Harvey, & Friedman-Weieneth, 2007; Goldstein, Harvey, Friedman-Weieneth, et al., 2007; Johnston & Mash, 2001).

It may well be that this rise in the social conflict component of ODD further accounts for its developmental linkage to concurrent and later CD, and the reason that ADHD is often seen as a precursor to CD.

The link between ADHD and CD appears to be largely mediated by the development of ODD in that developmental pathway (Angold et al., 1999; Biederman, Petty, Dolan, et al., 2008; Biederman, Petty, Monuteaux, et al., 2008; van Lier, van der Ende, Koot, & Verhulst, 2007; Rowe, Maughan, Pickles, Costello, & Angold, 2002; Whittinger, Langley, Fowler, Thomas, & Thapar, 2007), at least in males, and between ADHD and major depression–anxiety in both males and females with ADHD and ODD (Biederman, Petty, Dolan, et al., 2008; Biederman, Petty, Monuteaux, et al., 2008; van Lier et al., 2007; Rowe et al., 2002).

The causal or at least contributory link of ADHD to ODD is also evident in the earlier findings that it is largely the poor inhibition symptoms (impulsivity) of ADHD that show the strongest link to risk for ODD specifically and its reflection in the more general ratings of conduct problems (Martel & Nigg, 2006).

Symptoms of EI–DESR have been repeatedly shown to be an inherent part of the impulsive dimension of ADHD (see earlier discussion) and therefore may easily provide the explanatory link of this dimension to ODD symptoms. In fact, some factor-analytic studies of both ADHD and ODD symptoms reveal that the impulsive symptoms in ADHD also gross-load substantially onto the factor representing ODD nearly as much as they do on the HI factor of ADHD (Burns, Boe, Walsh, Sommers-Flanagan, & Teegarden, 2001).

Intervention studies likewise show that improvements in ADHD symptoms are closely associated with improvements in ODD symptoms (Biederman et al., 2007; MTA Cooperative Group, 1999).

These findings are consistent with the hypothesis presented here that some ODD symptoms are a consequence of ADHD itself and especially its EI–DESR component. Thus, reducing ADHD symptoms using medications should result in nearly comparable reductions in symptoms of ODD.

The available evidence can at least be taken to suggest that the high comorbidity between ADHD and ODD is most likely driven in large part by the EI–DESR component of ADHD as part of the larger impulsivity dimension of ADHD.

This problem with emotional impulsiveness and poor self-regulation of elicited emotions is especially problematic for negative affectivity, and specifically for low frustration tolerance, quickness to anger, emotional excitability or reactivity, and hostility or reactive aggression.

Thus, ADHD strongly predisposes children toward the emotional component of ODD requiring that they simply need to develop just one symptom from the behavioral social conflict component of ODD to become fully diagnosable as having ODD.

It seems likely that this evolution of ADHD with subthreshold emotional ODD to full ODD with the additional social conflict component may be associated with or a consequence of the family environment (specifically, disrupted parenting and related parental psychopathology, family stressors, and more severe marital conflict tactics). The point here is that this link would be far less obvious if the role of EI–DESR as a core element of ADHD were not made explicit.

This pathway by which ADHD contributes to risk for ODD through the former’s EI–DESR component not only helps us better to understand the comorbidity of ADHD with ODD across development, but it also suggests one pathway through which EI–DESR then contributes to the risk for depression and anxiety later in adolescence.

As noted earlier, research indicates that it is the emotional dysregulation component of ODD that is associated with those downstream developmental risks, and that component is largely a function of the coexistence of ADHD with ODD. As Martel (2009) also noted, the EI component of ADHD is part of a general liability for all three externalizing disorders. As I argue here, it may also be an indirect pathway for later risks for other emotion-related comorbidities evident in ADHD.


THE IMPORTANCE OF EI–DESR IN IMPAIRMENTS OF ADHD

Excerpt From Attention-Deficit Hyperactivity Disorder, Fourth Edition:
A Handbook for Diagnosis and Treatment, Dr. Russell A. Barkley, PhD.
This material may be protected by copyright.

So far, I have argued in this chapter that EI-DESR is a core feature of ADHD, and that this creates a significant overlap with the negative emotional component of ODD, thus predisposing those with ADHD to a high risk for developing ODD, among other disorders.

This emotional feature of ADHD, however, and its link to ODD, may also provide a clearer understanding of some of the social impairments that are likely to arise in conjunction with ADHD. My purpose here is not to review the extensive literature on social impairment in ADHD but simply to suggest that one contributor to it is likely to be the EI–DESR component of ADHD.

Within the family, the impulsive emotions and their poor self-regulation of children with ADHD would be expected to increase parental controlling responses and parental expressed emotion as part of the reciprocity involved in parent-child interactions (Danforth, Barkley, & Stokes, 1991; Johnston & Mash, 2001; Mash & Johnston, 1990).

As discussed earlier, these interactions, if not dealt with constructively by parents, may foster children’s transition from just having the EI–DESR and associated emotional component of ADHD to the behavioral or social conflict component and therefore the likelihood of receiving a formal diagnosis of ODD.

Certainly, the excessive activity, poor sustained attention, and verbal and motor impulsiveness in ADHD would by themselves be expected to result in increased controlling responses from parents, as they clearly seem to do, with a commensurate diminution in such responses when the child is treated with stimulants (Danforth et al., 1991). Longitudinal studies likewise are in keeping with a greater effect of child ADHD on parental behavior than of parental behavior on child ADHD (Burke et al., 2008; Lifford, Harold, & Thapar, 2008).

The evidence is substantial that ADHD in children is associated with significantly elevated reports of parenting stress and family conflict, poorer parenting practices, greater parental commands and punishment, vacillation between lax and harsh punishment, and a reduced sense of parenting competence (Fischer, 1990; Johnston & Mash, 2001; Mash & Johnston, 1990).

Observational studies of parent–child interactions find that increased levels of parental commands and instructions, reduced parental responsiveness to child-initiated interactions, greater parental negativity, and greater levels of parental rejection and coercion yield poorer child compliance (Johnston & Mash, 2001).

While these findings for ratings and observations are often more severe in families having children with both ADHD and ODD (or conduct problems), they are higher in families with children who have ADHD only than in control groups. This illustrates the point that ADHD alone is sufficient to increase parent–child conflict and stress.

It is quite possible that the degree of child EI–DESR is one contributor to such conflicts, along with the more traditional dyad of ADHD symptoms, and that ADHD medication management that results in changes in the EI–DESR component contributes to improved parent–child interactions.

Suggestive evidence of this is found in the further increases in parent–child conflict and parenting stress that are often found when ODD symptoms are also elevated (Barkley et al., 2008; Johnston & Mash, 2001).

The effect of ADHD medications on parent–child interactions is largely to reduce both the child’s negative behavior and noncompliance, and it is these changes that result in reduced parental controlling behavior and negativity toward the child (Danforth et al., 1991; Johnston & Mash, 2001).

Although far less studied, the same appears to be true of the teacher–child interactions of children with ADHD and the effects of medication treatment (Whalen, Henker, & Dotemoto, 1980).

It is not unreasonable to assume that the EI–DESR component of ADHD contributes partially to children’s interaction problems with adult authorities and that it is the resulting changes in this component by ADHD medications that partially result in improvements in these interactions.

Also supportive of the argument made here are findings that children with ADHD-C have higher levels of family conflict and parenting stress than do children with ADHD-PI (Lewis, 1992; Paternite, Loney, & Roberts, 1996).

Since the EI-DESR element of ADHD has been shown to be most closely linked to the HI symptom dimension and this is more severe in children with ADHD-C than in those with ADHD-PI, this would imply that such EI–DESR problems may be a contributor to these problems with family functioning.

Unfortunately, studies of both ADHD and its comorbidity with ODD and their impact on parenting and parent–child relations have not usually singled out the EI–DESR component of ADHD for its contribution to these problems, so its specific role in these family conflicts remains conjectural at the moment.

It may remain so if the EI–DESR component of ADHD is not made more explicit, so as to encourage greater care in future research to examine it relative to the other well-known symptom dyads of ADHD.

The majority of children with ADHD are likely to experience peer rejection (52-80%; Hoza, 2007).

They are often rated as scoring lower in terms of peer social preferences, higher in their negative impact on peer relations, and they are less well liked and more likely to have fewer close friends.

These problems are not simply a function of comorbidity with other disorders; they appear to arise from ADHD specifically (Hoza et al., 2005; Nijmeijer et al., 2008). And they do not appear to result from overall lower rates of positive behavior exhibited by children with ADHD because these rates are often close to those found in control children. It is the higher rates of negative interactions they initiate that distinguish between ADHD and control groups (Abikoff et al., 2004; Whalen & Henker, 1985).

As noted by Whalen and Henker (1992), the emotional dysregulation seen in children with ADHD is a major contributor to disrupting the smoothness, reciprocity, and cooperative activities involved in peer relationships.

Recent evidence suggests that peer relationship problems in children with ADHD are best predicted specifically by their difficulties with following rules, their reduced helping behavior, their whining, and their inattention (Mrug, Hoza, Pelham, Gnagy, & Greiner, 2007).

Other studies have also found both the level of child impulsiveness and verbal and physical anger and aggression to be important predictors of peer interaction problems and rejection (Buhrmester, Camparo, Christensen, Gonzalez, & Hinshaw, 1992; Melnick & Hinshaw, 2000; Hinshaw, 2003).

Such findings support Whalen and Henker’s (1992) conclusions about the source of peer relationship problems in children with ADHD and specifically imply that EI–DESR is at least one of the contributing factors to peer relationship difficulties associated with ADHD.

This is also the case for typically developing children. Negative emotionality is a major predictor of peer likability (Dougherty, 2006; Schultz, Izard, Stapleton, Buckingham-Howes, & Bear, 2009).

As with parent–child and teacher–child interactions, the effects of ADHD medications are largely to reduce such negative emotions, thereby resulting in improved peer relations, often with little or no added benefits to be gained from adding social skills training (Abikoff et al., 2004; Cunningham, Siegel, & Offord, 1985; MTA Cooperative Group, 1999).

But as with studies of parent–child relations, the link here between EI–DESR and peer relationships problems in ADHD needs more study, but it is likely to be proven correct given the evidence that in typical children negative emotionality is a major predictor of social status (Dougherty, 2006).

Other domains of functional impairment, particularly in adults, may also be related at least in part to the degree of EI–DESR present in cases of ADHD. Skirrow and Asherson (2013) found that emotional lability in adults with ADHD is a significant predictor of impairment in daily life independent of the other two ADHD symptom dimensions. Later research by Surman and colleagues (2013) found similar results, and that EI–DESR predicted lower quality of life and social adjustment.

My colleagues and I also examined predictors of being fired or dismissed from employment and those of poor work performance as rated by supervisors in adults with ADHD. We found that the degree of ADHD symptoms significantly predicted the latter work performance problems, but level of emotional impulsiveness was predictive of occupational impairment generally and the percentage of jobs from which the adult had been fired specifically (Barkley & Fischer, 2010; Barkley & Murphy, 2010). Others have also found emotional problems to be a major pathway from ADHD to impaired occupational outcomes (Gjervan, Hjemdal, & Nordahl, in press).

Just as symptoms of EI–DESR may impair the peer and cohabiting relationships of adults with ADHD, they may also interfere with their cohabiting/marital relationships. There are only a few studies of the dating and marital relations of teens and adults with ADHD, but they indicate greater levels of conflict and dissatisfaction relative to control samples (Barkley et al., 2008).

It seems quite likely that problems with EI–DESR may be one factor in such relationship strife, as might persistent ODD that is related to it. This was indeed found to be the case in subsequent analyses of these two large databases of adults with ADHD and children growing up with ADHD followed as adults (Barkley & Fischer, 2010; Barkley & Murphy, 2010). Surman and colleagues (2013) later replicated these findings in their large study of adults with ADHD.

Parenting may also be adversely affected by the problems with EI–DESR in adults with ADHD. Studies of parents with ADHD have revealed higher levels of family conflict more generally and lower levels of cohesion (Biederman, Faraone, & Monuteaux, 2002).

Research using more specific measures of parenting find greater negative parenting, higher ratings of expressed negative emotion, and lower levels of positive parenting in mothers with high levels of ADHD symptoms (Chronis-Toscano et al., 2008; Psychogiou, Daley, Thompson, & Sonuga-Barke, 2008) and more negative, critical, overreactive, and authoritarian parenting in fathers with higher symptom levels of ADHD (Arnold, O’Leary, & Edwards, 1997).

Adult self-reports of EI symptoms on the Conners Adult ADHD Rating Scale were found to be significantly associated with the findings for both negative and positive parenting (Chronis-Tuscano et al., 2008), supporting the argument here that EI–DESR is one factor contributing to the parenting problems of adults with ADHD.

While one factor in such disrupted parenting is certainly the fact that 40–60% of the children of adults with ADHD have the same disorder, as well as ODD, or at least more symptoms of both than do control groups (Barkley et al., 2008), problematic parenting remains evident even after controlling for related disorders in the children (Murray & Johnston, 2006), suggesting that EI–DESR may be one contributor to impaired parenting in adults with ADHD.

It is certainly a predictor of both parenting stress among adults with ADHD and the degree of oppositionality in their offspring (Barkley & Murphy, 2010) and siblings (Sobanski et al., 2010; Surman et al., 2011).

Research on the driving of people with ADHD indicates not only numerous deficits and adverse outcomes in this domain of major life activity (Barkley & Cox, 2007) but also has specifically noted elevated rates of driving anger, hostility, and aggression (road rage) among both adults with ADHD and college students showing elevated rates of ADHD (Richards et al., 2006). Road rage is a major contributor to risk for traffic citations and car crashes (see Richards et al., 2006) above and beyond factors such as driver inattention.

This implies that problems with EI–DESR may make a specific contribution to the driving problems of adults with ADHD, above and beyond just their problems with attention.

Subsequent research indeed has found this to be the case, with EI making unique contributions to crash risk (Barkley & Fischer, 2010; Surman et al., 2013) and to driving while intoxicated, above and beyond contributions made by traditional ADHD symptoms.

Likewise, a few studies have found a link between EI–DESR in adults with ADHD and their higher risk for arrest rates (Barkley & Fischer, 2010; Barkley & Murphy, 2010; Surman et al., 2013).

Important to note, once again, is that these contributions are over and above those made by the traditional ADHD symptom dimensions in predicting these adverse outcomes.

Although all this evidence is suggestive of a link between EI–DESR problems inherent in ADHD and these various areas of impairment, such a link has not been established directly.

This is largely because the EI–DESR aspects of ADHD have not been considered to be a central component of ADHD and are therefore not likely to be evaluated directly in research in these and other areas of impairment arising from the disorder.

So long as a central role of emotional dysregulation is unacknowledged or at least underappreciated as being a part of ADHD, as Harty and colleagues (2009) suggested, its importance in research on impairment may remain understudied.


CONCLUSIONS AND CLINICAL IMPLICATIONS

Excerpt From Attention-Deficit Hyperactivity Disorder, Fourth Edition:
A Handbook for Diagnosis and Treatment, Dr. Russell A. Barkley, PhD.
This material may be protected by copyright.

In this chapter I have argued that EI–DESR is a core feature of ADHD that deserves to be represented in its own right both in conceptualizations of the disorder, as it is in current theories, and in diagnostic criteria for the disorder, as it has not been since DSM-II. A similar stance has been taken by other reviewers as well (Corbisiero, Stieglitz, Retz, & Roster, 2013; Martel, 2009; Skirrow et al., 2009).

This argument is based on the historical record over its initial 175-year history, until the 1960s and 1970s, which considered problems with emotion regulation to be part of the disorder.

At that time, this component of the disorder was split off from its conceptualization and relegated to the status of an associated feature, if mentioned at all.

However, current theories of the disorder have resurrected its place in the nature of ADHD itself and in doing so is supported by findings on the neuroanatomical basis of ADHD and the association of that neural network with EI–DESR.

This EI–DESR element of ADHD is probably a specific consequence of the neurodevelopmental abnormalities evident in the frontal–limbic pathway (dorsolateral PFC and ACC) of the brain and particularly the top-down governing (cognitive–effortful) influence of these structures (via the ACC) over the amygdala specifically and the limbic system more generally(emotional brain).

As shown here, there is a growing body of evidence that both children and adults with ADHD actually do have significant EI symptoms. Problems with DESR also seem evident but have been far less studied in research on ADHD.

Acknowledging the place of EI–DESR in ADHD also contributes to our understanding of the high comorbidity of ADHD and ODD, and the social impairments associated with the disorder.

Having ADHD-C virtually creates a borderline case of ODD in children because these EI symptoms constitute at least three to four of the eight symptoms on the diagnostic symptom list for ODD (DSM-5).

I have attempted to clarify that EI–DESR is not just an associated feature of ADHD or a mere function of comorbidity, that it is inherent in the disorder itself.

Making its presence explicit in our conceptualizations of ADHD and its diagnostic criteria can serve to better illustrate just why ADHD shows such a high rate of comorbidity with ODD and with reactive aggression.

ADHD is surely not the sole or exclusive cause of ODD, but it does strongly predispose those with the disorder to at least the three to four emotion-based symptoms of ODD (its emotional component).

When combined with disrupted parenting and other social and situational factors, it is but a small step (one symptom) to developing the behavioral or social conflict component of ODD, and thereby crossing the diagnostic threshold into clinically diagnosable ODD.

Research on the family, teacher, and peer relations of individuals with ADHD suggests that the EI–DESR aspects of ADHD are major contributors to the problems experienced in these relationships.

Therefore, as noted in Chapter 23 on social skills training, one major component of such intervention must target the emotional dysregulation that so often drives the social rejection of these children and adults, in addition to more traditional social behaviors such as sharing, cooperation, taking turns, and so forth.

Adding EI–DESR back into ADHD also helps one to understand the impact ADHD medications may have on this domain. If ADHD includes this EI component, then medical treatments that succeed in reducing ADHD symptoms should likely impact the emotional ones as well.

Research on the medications for ADHD has long suggested just that; the reduction of ADHD symptoms by medications is also associated with a reduction in associated ODD symptoms; the two reductions are highly correlated with each other.

This, as I have argued, likely occurs through the impact of medications on the “hot” EI–DESR executive network component of ADHD. But the different ADHD medication types may well achieve this effect on EI–DESR via different routes.

The foregoing neuroimaging research implies that stimulants may act on emotion largely by dampening or even suppressing limbic system activity, an effect that does not seem to occur with the nonstimulants.

Hence, high dosing with stimulants could lead to emotional blunting or constriction of normal affect. In contrast, nonstimulants such as atomoxetine may work by activating anterior cingulate and frontal executive networks, thus facilitating the executive management of emotions generated via the limbic system rather than suppressing them. Guanfacine XR (extended release) (INTUNIV) and related drugs may achieve their emotion-regulating properties through finer tuning of the alpha2 receptors in the frontal cortex and therefore achieve clearer neuronal signaling that results in executive control over emotional states.

All this is admittedly speculative, based on a very limited set of findings on the differences in effects of ADHD medications evident in functional neuroimaging studies.

But for now it may help clinicians better understand the differing impacts of ADHD medication types on emotion regulation.

Future revisions to the diagnostic criteria for ADHD (i.e., DSM-6) would do well to list explicitly at least the EI symptoms evident in ADHD, most likely on the impulsivity dimension, in order to underscore the importance of this aspect of ADHD beyond just the inattention and HI symptoms now showcased in these criteria.

Along with reducing the overemphasis on hyperactivity and verbal impulsiveness on this symptom dimension and explicitly adding impulsive behavior and decision making to it, the inclusion of symptoms of EI–DESR would serve to represent better our current conceptualization of the disorder. This would also encourage investigators to study this aspect of ADHD explicitly in their research on comorbidity, impairments, and treatment response.

Regardless of what the next DSM may include, clinicians need to be cognizant of the EI–DESR symptoms inherent in ADHD and evaluate them as much as they evaluate the traditional ADHD symptoms during their initial assessment of a patient for ADHD.

Doing so can provide not only a clearer and more comprehensive account of the patient’s current status but also a richer understanding of the basis for many of the impairments the patient may be experiencing that are partly or largely a consequence of this emotional component of ADHD.

That ADHD includes such a component likewise needs to be explained by clinicians to their patients with ADHD and their families, so that they, too, gain such a better, more complete understanding of the condition and why patients may emote as they do.

Interventions need to target this component of ADHD in addition to the ongoing efforts to develop both psychosocial and medical interventions that focus on the traditional symptom complex of ADHD and its related “cold” cognitive executive deficits, and how best to help family members cope with and assist the patient with ADHD in the effective management of their emotional dysregulation.

Yet none of this is to suggest that all of the emotional difficulties seen in a patient with ADHD can be written off to the emotional dysregulation component championed in this chapter.

As subsequent chapters make plain, ADHD is certainly associated with an elevated risk for various mood and anxiety disorders.

How, then, are we to distinguish which affective disturbances belong to ADHD and which require the search for a comorbid affective disorder to account for them? There is little direct research on the issue, but the findings to date suggest some tentative clinical guidelines for such differential diagnosis.

First, consider that the emotional disturbances in ADHD are just that—emotions, and not moods. Emotions are of short duration, are provoked, and often are situation-specific to the setting of the provocation.

They are also largely rational, which is to say understandable, to others given that typical people would have had the same subjective reaction to the provocation.

But the difference is that the typical person would have acted to suppress the voluntary aspects of the emotion over which they have some volitional control rather than express it publicly.

They would then have engaged in the self-regulatory steps to down-regulate or otherwise alter the emotion to make it more compatible with the situation, others, and the person’s longer-term goals and welfare.

Recovery from such a provoked change in emotional state can be relatively quick compared to a change in mood, though perhaps not as easily as is seen in typical people given that those with ADHD have more difficulties down-regulating strong emotions using executive self-control.

In contrast, a mood is just that—a long-duration change in emotional state that is often cross-situational and may arise without provocation or from trivial events that would often not have led others to react in this fashion. It can be described as capricious, as well as extreme.

Consequently, it is not rational in the sense that other people would have the same emotional state under these circumstances over such an extended period of time and across settings.

Admittedly, the dividing line between an emotion and a mood is not as crisp as is portrayed here.

But the previous guidelines seem sensible at this time to guide clinicians in sorting out what affective symptoms of a patient with ADHD belong to that disorder and its EI–DESR problems, and what symptoms are likely to be attributable to a comorbid disorder.

In summary, it is time to return EI–DESR to its rightful place in the core or central components of ADHD.


KEY CLINICAL POINTS

Excerpt From Attention-Deficit Hyperactivity Disorder, Fourth Edition:
A Handbook for Diagnosis and Treatment, Dr. Russell A. Barkley, PhD.
This material may be protected by copyright.

⁃ During the first 170 years of its medical history, ADHD and its precursor disorders were believed to involve deficits in emotional inhibition and self-regulation, along with the core problems with attention and HI behavior.

⁃ Beginning in the 1960s, especially with DSM-II, the symptoms of EI and DESR were divorced from the core deficits of ADHD, and treated as merely associated problems that may arise in some cases.

⁃ Compelling evidence now argues for the return of EI–DESR to the status of a core component of ADHD in its conceptualization and DSM diagnostic criteria. The argument is based on six lines of reasoning and evidence:

• EI–DESR has a long history of being a central feature of ADHD in its clinical conceptualization.

• Current neuropsychological theories of ADHD consider EI–DESR to be just such a central component.

• The neuroanatomical findings associated with ADHD would have to give rise to commensurate symptoms of EI–DESR.

• Ample evidence now exists that children and adults with ADHD are highly likely to manifest EI–DESR (low frustration tolerance, impatience, quickness to anger, and being easily excited to emotional reactions more generally).

• Returning EI-DESR to a central place in ADHD would more clearly show the basis for its high comorbidity with ODD and probably several related disorders.

• Promoting EI–DESR back to the status of a core component would also clarify one basis for the frequent social interaction problems and impairments in several other domains of major life activities (work, driving, marriage/cohabiting, and parenting) seen in ADHD.

⁃ Understanding the role of EI–DESR in ADHD would assist with differential diagnosis and reduce misdiagnosing emotional problems in ADHD as entirely arising from comorbidity.

⁃ ADHD medications appear to reduce the EI–DESR component of ADHD as much as they do traditional ADHD symptom dimensions, yet they may do so through different neural mechanisms and networks.

⁃ Psychosocial interventions for ADHD should include programs targeted at helping patients with EI–DESR specifically rather than just traditional ADHD symptom dimensions.

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