Sluggish Cognitive Tempo/Concentration Deficit Disorder
Abstract and Keywords
Sluggish cognitive tempo (SCT), or concentration deficit disorder (CDD), comprises excessive daydreaming, staring, mental fogginess and confusion, drowsiness, lethargy, sluggishness, and hypoactivity, among other symptoms. This article summarizes the findings on CDD/SCT and its relationship to attention deficit hyperactivity disorder (ADHD). The cognitive dysfunction underlying CDD remains to be clarified. But its symptoms comprise a two-dimensional structure that is separate from those in ADHD. CDD is reliably associated with social withdrawal and is more strongly related to internalizing than to externalizing psychopathology, in contrast to ADHD. Both ADHD and CDD are impairing, but ADHD is more so. Little evidence exists on the etiologies of CDD or on response to treatments. More research is needed on all facets of CDD before its status as a new disorder can be confirmed.
Throughout their histories official diagnostic taxonomies for mental disorders, such as the Diagnostic and Statistical Manual for Mental Disorders (DSM; American Psychiatric Association, 2013), have recognized but a single attention disorder, currently termed attention deficit hyperactivity disorder (ADHD). In earlier editions of this manual, subtypes of ADHD were periodically recognized but did not represent different attention disorders. Yet in the most recent edition they are termed “presentations,” reflecting the fact that they represent not so much different types of this attention disorder but merely clinical presentations that can differ in symptom severity across time and development. Even these presentations are recognized as sharing a common attention disturbance but varying in the relative severity of symptoms on a hyperactive-impulsive dimension. The dimension reflecting the attention disorder involves poor sustained attention, instruction following, distractibility, lack of attention to detail, forgetfulness, poor organization, and avoidance of sustained mental effort, among other symptoms, that form a single dimension of cohering inattention problems. In contrast to such official taxonomies, the fields of cognitive, experimental, developmental, and neuropsychology have long recognized the existence of several different and empirically established components of attention (Hale & Lewis, 1979). While one of these components reflected sustained attention, such as is deficient in ADHD, others represented alertness, focus-execute, shift, span of apprehension, and divided attention, among other types of attention (Mirsky, 1996; Posner, 1990). Such components are not incorporated into the DSM diagnostic conceptualization of ADHD. However, their existence implies that other disorders of attention should exist that reflect deficits in these other components besides that of a disorder of sustained attention.
The present article proposes the existence of another disorder of attention and presents the evidence for its existence as a relatively distinct disorder from ADHD yet one that can coexist with it. Since the mid-1980s, this new attention disturbance has been termed sluggish cognitive tempo (SCT). But recently I have been encouraging other clinical researchers to adopt the term concentration deficit disorder (CDD) due to the public perception of SCT as pejorative, derogatory, or frankly offensive (Barkley, 2014b; Saxbe & Barkley, 2014). For that reason, the acronym CDD is used throughout the remainder of this article as being synonymous with SCT. Several others have recommended that attention deficit disorder, or ADD, be used for people who are primarily inattentive using the DSM symptom list, yet have few if any symptoms of hyperactive or impulsive behavior (Diamond, 2005). This term is problematic for three reasons. First, ADD is the older term for ADHD dating back to the third edition of DSM in 1980 (DSM–III; American Psychiatric Association, 1980), and so applying it here fosters confusion as to what is meant by ADD—the old condition or the new one with relatively circumscribed problems with inattention. Second, this approach continues to rely on the DSM symptom list of inattention to identify cases of this new attention disorder when evidence is now abundant that a different set of symptoms is likely to better identify and characterize those having CDD. Third, the term SCT suggests that the underlying neuropsychological disturbance has been established when this is not the case, as is made evident later. Instead, CDD seems to be a reasonable term for this condition because it continues to emphasize that a problem with attention exists but it is one that is separate from ADHD, it is not derogatory, and it does not convey the idea that the underlying specific cognitive processes that is dysfunctional is known.
For a mental disorder to be identified as such, it must represent a “harmful dysfunction,” which is to say that it must be shown to involve functional ineffectiveness in a human mental adaptation (a functional mechanism universal to the species) that results in harm to the individual (increased mortality, morbidity, or significant impairment in major life activities; Wakefield, 1999). As just noted, the exact mental adaptation(s) that is failing in CDD/SCT is not well understood, although the symptom dimensions to be discussed later give some clues as to what it/they might be. This means that, for now, CDD/SCT may not yet fully qualify as a mental disorder until more is known about the defective mental functions involved in it. Also, for a disorder to be considered distinct from other disorders, not only must the mental dysfunction be distinct from other disorders but it should differentiate from other disorders, particularly those closely related to it, in its pattern of symptom coherence (dimensional structure), etiologies, developmental course, demographic, neuropsychological, and social correlates and risks; pattern of comorbidity with other mental (and possible medical) disorders; and treatment response. While a number of these topics have been explored in past research and seem supportive of the distinctiveness of CDD/SCT from other disorders, particularly ADHD, other topics (etiologies) have barely been studied or have not been at all as yet (developmental course). Thus there is much work to be done in clinical research on CDD/SCT that could serve as a career-long research focus for young investigators entering the fields of clinical research in psychology and psychiatry (Barkley, 2014b).
This article draws its content largely from my other recent reviews of the literature on CDD/SCT (Barkley 2014a, 2014b; Saxbe & Barkley, 2014), and my two earlier US surveys of large representative child and adult samples with regard to the symptoms of CDD/SCT and their correlates (Barkley, 2012b, 2013).
The Symptoms of Concentration Deficit Disorder (Sluggish Cognitive Tempo)
Because CDD is not included in any official taxonomy of mental disorders, there are no standardized criteria for its identification. But clinical investigators have conducted numerous studies on proposed symptom lists to identify those that are most coherent with each other and distinct from other dimensions of psychological problems, the results of which can serve as the basis for constructing a standardized set of criteria for this condition (Barkley, 2012b, 2013; Carlson & Mann 2002; Garner, Marceaux, Mrug, Patterson, & Hodgens, 2010; McBurnett, Pfiffner, & Frick, 2001; Penny, Waschbusch, Klein, Corkum, & Eskes, 2009; Todd, Rasmussen, Wood, Levy, & Hay, 2004). While more than 26 items were identified as being potentially associated with CDD from a survey of experts (see Penny et al., 2009), those symptoms that are most commonly linked to the disorder and form distinct sets of symptoms in factor analysis are (a) daydreaming; (b) trouble staying awake/alert; (c) mentally foggy/easily confused; (d) stares a lot; (e) spacey, mind is elsewhere, or seems to be in a world of their own; (f) lethargic or appears tired; (g) underactive; (h) slow-moving/sluggish; (i) does not process questions or explanations accurately; (j) drowsy/sleepy appearance; (k) apathetic/withdrawn; (l) lost in thoughts; (m) slow to complete tasks; and (n) unmotivated or lacks initiative/effort fades. The last two symptoms and related items, however, are as likely to be associated with ADHD as with CDD/SCT in children or adolescents, and thus are not very distinctive of SCT. They would not be suggested for further study as a means of distinguishing these two attention disorders (Barkley, 2013; Burns, Servera, Bernad, Carrillo, & Cardo, 2013; Lee, Burns, Snell, & McBurnett, 2014). But the remaining twelve, among others (Penny et al., 2009), appear to be highly useful for making such distinctions.
When these 12 symptoms or highly related ones are analyzed in large samples of children, they have been found to form at least one, and usually two, dimensions that are distinct from those for ADHD (or from other dimensions of psychopathology). One factor comprises a Sleepy/Sluggish/Underactive dimension that seems motoric or behavioral in substance while the other factor forms a Daydreaming/Slow symptom dimension that may represent a cognitive dysfunction (Barkley, 2013; Burns et al., 2013; Jacobson et al., 2012; McBurnett et al., 2001; Penny et al., 2009; Todd et al., 2004). Some studies using additional items have sometimes found a third factor that comprises items related to low motivation, effort, initiative, or persistence. As noted previously, such items are as or more related to the inattentive symptom dimension of ADHD than to these other two CDD symptom dimensions and thus are not distinctive of SCT or sufficiently differentiate it (Barkley, 2013). It seems that just as ADHD comprises both a cognitive (inattention [IN]) and motoric (hyperactive-impulsive [HI]) factor structure, so too does CDD.
These cognitive and motoric factors have been found using different types of assessment methods, particularly parent and teacher ratings (Barkley, 2013; Bauermeister, Barkley, Bauermeister, Martinez, & McBurnett, 2012; Becker, Luebbe, Fite, Stoppelbein, & Greening, 2014; Burns et al., 2013; Garner et al., 2010; Hartman, Willcutt, Rhee, & Pennington, 2004; Jacobson et al., 2012; Lee et al., 2014; McBurnett et al., 2014; Penny et al., 2009; Willcutt et al., 2014). But they have also been evident in direct observations of behavior taken in school (McConaughy, Ivanova, Antshel, Eiraldi, & Dumenci, 2009), as well as those taken in clinics (McConaughy, Ivanova, Antshel, & Eiraldi, 2009). A distinct factor of CDD symptoms from those of ADHD has also been noted in the first study of adult self-ratings in a representative sample of US adults (Barkley, 2012b) in which CDD items were included in an adult ADHD rating scale (Barkley, 2011a).
The relationship of CDD symptoms to those of ADHD are moderately correlated, mainly between the cognitive Daydreaming factor and the IN dimension of ADHD. Yet the factors remain distinct from each other in all studies of this issue to date. Even with samples selected for the ADHD Inattentive type (now presentation), children elevated in the CDD symptoms differ in a number of respects from those who are low in that symptom dimension (Capdevila-Brophy et al., 2014; Marshall, Evans, Eiraldi, Becker, & Power, 2014), although there has been one exception (Harrington & Waldman, 2010). The totality of evidence here implies that CDD and ADHD IN symptoms are not identifying the same attention problem. Despite this moderate correlation between CDD inattention and ADHD IN symptoms, the CDD set is substantially less correlated with either of the ADHD symptom dimensions than the two CDD symptom dimensions are to each other. Just as the two symptom dimensions of ADHD more closely cohere to each other than to those of CDD, the CDD dimensions are more coherent with each other than they are to ADHD dimensions (Barkley, 2012b, 2013; Penney et al., 2009). All this is consistent with the idea that CDD is distinct from ADHD even if it may be associated with it to some extent.
Research finds as well that the CDD symptom sets are much less related to the HI symptom dimension than they do are to that of ADHD IN symptoms (Barkley, 2012a, 2012b; Burns et al., 2013; Hartman et al., 2004; Garner et al., 2010; Jacobson et al., 2012; Penny et al., 2009; Wahlstedt & Bohlin, 2010). More telling of a distinctiveness of CDD is that its relationship to the HI symptoms becomes negative when analyses control for the relationship of ADHD IN with CDD (Lee et al., 2014; Penny et al., 2009). This is evidence that CDD symptoms are only partially coupled to ADHD IN symptoms yet are distinct from both ADHD symptom lists as much as are other symptoms dimensions of child and adult psychopathology to each other.
As for the prevalence of CDD, when cast in the form of a disorder, only two surveys have been done using representative US samples of children (Barkley, 2013) and adults (Barkley, 2012b). In these studies, a symptom of CDD was considered significant or clinically present if it occurred often or more frequently, consistent with DSM symptom frequency guidelines (American Psychiatric Association, 2013). A threshold for the number of symptoms was then selected that met or surpassed the 93rd percentile for the respective population samples (3+ out of 12 for children, 5+ out of 9 for adults) so as to reflect developmental inappropriateness of symptom severity, again consistent with DSM guidelines. Likewise, cases also had to have significant impairment in one or more major life activities (i.e., home, school, work, etc.). When these criteria were applied, approximately 5% of the participants in each survey could be classified as having CDD.
A Brief History of Concentration Deficit Disorder (Sluggish Cognitive Tempo)
Having explained the nature of the symptom structure of CDD, it is now valuable to consider the history of clinical research into this condition. Probably the first clinical description of a CDD-like attention problem can be found in the medical textbook of Alexander Crichton (1798/1976; see Palmer & Finger, 2001). He mentioned two attention disorders, one of which resembles that of ADHD (distractible, lack of persistence, etc.). The second one involved individuals with “low power” of attention or arousal. He described such cases as prone to staring or frequent daydreaming and to otherwise seeming sluggish and erratic in accurately processing information. Crichton further explained that this condition could be linked to debility or torpor of the body that results in these cases being retiring, unsocial, and having few friendships or attachments of any kind. He reported that the friendships such people had were seldom of an enduring nature. Crichton further argued that the faculty of attention could be so weakened as to leave an individual insensible to external objects or to impressions that ordinarily would awaken typical responses and social feelings. As we will see later, this description shares some characteristics with what has been discovered to date about CDD. However, it is reasonable to say that Crichton’s description could also apply to cases of autistic spectrum disorders, schizoid or schizotypal personality disorders, or even some aspects of psychopathy.
Modern research on CDD, however, starts in the 1980s resulting directly from the creation of two subtypes of ADHD in DSM–III (American Psychiatric Association, 1980)—attention deficit disorder with (ADD+H) and without (ADD–H) hyperactivity. This distinction was based mainly on anecdotes of clinician members of the committee who saw cases involving inattention only in their clinical practice yet who had little if any evidence of hyperactivity or impulsivity that characterized ADD+H (I was a member of that committee). At first, the DSM–III mistakenly placed impulsiveness in with the inattentive symptoms, creating this dichotomy on the basis of hyperactivity alone. However, later research found that the impulsive symptoms were so highly correlated with hyperactivity as to form a single factor or dimension (Carlson, 1986; Lahey, Schaughency, Strauss, & Frame, 1984; Milich, Ballentine, & Lynam, 2001) making it quite difficult to find cases that were inattentive and impulsive but not hyperactivity. The mistake was quickly corrected by researchers wishing to study these two subtypes of ADD who sorted them into cases of inattention that were high or low in the severity of their HI symptom dimension. The first few papers making such comparisons found only a few differences between them, mainly in a greater occurrence of learning disabilities and lack of motivation (Maurer & Stewart, 1980), less risk for conduct problems and peer unpopularity, and a greater likelihood of social shyness and withdrawal in the –H subset (Pelham, Atkins, & Murphy, 1981; Lahey et al., 1984) but few significant differences in performance of neuropsychological tests (Carlson, Lahey, & Neeper, 1986). In contrast, other studies found just minor differences between these +H and –H subtypes (King & Young, 1982).
It appears that the term SCT was first used by Ben Lahey and colleagues in that 1984 paper and again in 1985 (Lahey, Schaughency, Frame, & Strauss, 1985) to describe the greater frequency of symptoms of drowsiness, sluggishness, and daydreaming in the ADD–H group (Carlson, personal communication, November 20, 2013), although Neeper, a graduate student of Caryn Carlson’s, also subsequently used it to label a factor consisting of these and other CDD that was distinct from that for ADD+H (Carlson, 1986). In the Lahey et al. (1985) study, the authors went further to argue that the cases high in CDD symptoms formed a different type of attention disorder from ADD+H rather than being a subtype of a shared disorder of ADD. Despite the mixed pattern of results across studies, early (Carlson, 1986) and later reviewers reached the same conclusion that enough differences were emerging to suggests that those having ADD–H, especially that subset characterized by CDD symptoms, may have a distinct attention disorder from ADHD (Milich et al., 2001).
But these early distinctions were not sufficient for the revised third edition of DSM (DSM–III–R; American Psychiatric Association, 1987) to retain the +H and –H distinctions in ADD. Instead, the disorder became the single entity now termed ADHD; the ADD–H group was retitled as “Undifferentiated” ADHD and placed in the appendix with a call for further research into its nature. Research would continue to explore differences between these +H and –H subtypes of ADD for a few years thereafter (Barkley, DuPaul, & McMurray, 1990) and continue to document greater CDD symptoms in the ADD–H group. One study also suggested that the –H group may have less of a positive response and a different dose–response profile to the stimulant medication methylphenidate than did the +H group (Barkley, DuPaul, & McMurray, 1991). By 1994, these +H and –H subtypes returned as the ADHD Combined type (C) versus ADHD Predominantly Inattentive (I) type in the fourth edition of the DSM (DSM–IV; American Psychiatric Association, 1994). This distinction once again resulted in numerous studies comparing the C- and I-types for another two decades. Reviewers at the time (Wheeler & Carlson, 1994) and later (Milich et al., 2001) concluded that the various differences found earlier between ADD+H and –H could be extended to the newly created I-type versus C-type children in DSM–IV. Milich and colleagues went so far as to argue that the symptoms of SCT should be used to directly select for children having this second attention disorder rather than continue to identify them indirectly using high ADHD IN symptoms but low HI symptoms. Indeed, as many as 30% to 63% of cases of the I-type have high levels of CDD (Carlson & Mann, 2002; Garner et al., 2010; McBurnett et al., 2001).
In the past decade, an increasing number of studies have done just that. One of the first papers to separate out children having CDD/SCT symptoms from within the I-type was Carlson and Mann (2002). Both groups had similar levels of learning problems and inattention. But CDD/SCT children had less externalizing symptoms and higher levels of unhappiness, anxiety/depression, withdrawn behavior, and social dysfunction. Many subsequent studies have found this way of identifying cases of CDD to be more likely to reveal differences from ADHD cases than was the earlier +H and –H subtyping in ADD (Barkley, 2012b, 2013; McBurnett et al., 2001; Garner et al., 2010; Penny et al., 2009; Skirbekk, Hansen, Oerbeck, & Kristensen, 2011).
In summation, the construct of CDD/SCT grew out of efforts to identify differences between subtypes of ADD and subsequently ADHD children. While differences between those subtypes proved mixed and unconvincing of any substantial or qualitative differences, research focusing specifically on children having CDD/SCT proved more promising. Evidence of this can be seen in the numerous studies on CDD/SCT in a special issue of the Journal of Abnormal Child Psychology (2014, vol. 42, no. 1).
Demographic Differences Between Concentration Deficit Disorder and Attention Deficit Hyperactivity Disorder
As noted earlier, one source of evidence as to whether or not these two attention disorders are distinct from each other is in their patterns of relationships to various demographic factors, such as age, sex, education, social class, and so on. Just a few studies have examined such associations. They found that CDD was not related to child age, gender, or minority status (Barkley, 2012b, 2013; Garner et al., 2010; Jacobson et al., 2012). In contrast, symptoms of ADHD often decrease across with age during childhood into young adulthood (Barkley, 2012b, 2013; Barkley, Murphy, & Fischer, 2008). In the study of children, I (Barkley, 2013) found that those having a research diagnosis of CDD were older than those with ADHD, implying a somewhat later age of onset for the condition when it is cast as a categorical disorder. Also, research routinely finds that ADHD symptoms occur more often in boys than girls during childhood and adolescence but come close to equalizing in adulthood (Barkley, 2012b, 2013; Barkley et al., 2008; Burns et al., 2013). This is not the case for CDD/SCT, where males have only slightly more symptoms than females in childhood in some but not all studies and no evident sex differences by adulthood (Barkley, 2012b, 2013; Burns et al., 2013). This lack of association of CDD symptoms with age and only slightly, if at all, with sex was also evident in the recent study by Lee et al. (2014) on teacher ratings; on parent ratings only a very small difference was evident for these demographic factors.
Differences among ethnic groups in CDD symptoms have not been evident in just the few studies examining this issue (Barkley, 2012b, 2013; Garner et al., 2010; Jacobson et al., 2012). For ADHD symptoms there seems to be slight but statistically significant elevations among Hispanic-Latino children than other ethnic groups.
I surveyed a representative US sample of children (Barkley, 2013) and observed that children meeting a research diagnosis of CDD came from families with lower parental education, lower annual household income, and a greater likelihood of a parent being out of work due to disability. Likewise, in my survey of a representative sample of US adults (Barkley, 2012b) those classified as CDD also had less education and less annual income. For cases in which CDD was comorbid with ADHD (Barkley, 2012b), those adults were more likely to be unmarried and to be out of work on disability compared to adults with ADHD alone. While far more research on these demographic correlates is needed, the existing patterns suggest that CDD is not differentially associated with age or sex differences as is ADHD and might be more strongly associated with psychosocial adversity or stressors than is ADHD.
Are There Neuropsychological Differences Between Concentration Deficit Disorder and Attention Deficit Hyperactivity Disorder?
The research literature on neuropsychological deficits linked to ADHD is extensive and involves as many as 500 studies (Frazier, Demaree, & Youngstrom, 2004; Hervey, Epstein, & Curry, 2004; Willcutt, Doyle, Nigg, Faraone, & Pennington, 2005). By contrast, only a few studies have been done with CDD. One such study found that CDD was associated with problems with early information processing or selective attention that is not typical of ADHD (Huang-Pollack, Nigg, & Carr, 2005). If this study could be replicated, then this would be an important cognitive (attention) difference distinguishing the attention deficits in CDD versus ADHD. Slower motor speed was associated with CDD in some studies (Adams, Milich, & Fillmore, 2010; Garner et al., 2010) in keeping with its sluggish symptoms, but another study (Bauermeister et al., 2012) was not able to replicate this difference between CDD and ADHD cases. Only a single study has examined spatial memory performance in CDD, and it found greater variability that was not evident in the ADHD cases (Skirbekk et al., 2011) even after controlling for any overlap of CDD with ADHD IN symptoms. Just two studies employed tests of executive functioning (EF) in studying CDD. Unlike ADHD, where deficits in inhibition and nonverbal working memory are well documented (Willcutt et al., 2005), CDD was only weakly associated with EF deficits, if at all (Bauermeister et al., 2012; Wahlsted & Bohlin, 2010).
EF tests are not significantly correlated with rating scales of EF in daily life (Toplak, West, & Stanovich, 2013), and therefore the latter need to be studied separately in evaluating the relationship of CDD to EF in daily life. Four studies to date have done so. In the large surveys of US representative samples of both children and adults (Barkley, 2012b, 2013), I found that CDD was largely not a disorder of EF in view of only very weak relationships evident between the CDD symptom dimension and four of the five EF deficit dimensions (< 1% shared variance) when statistically controlling for any association of CDD with ADHD symptoms. There was a small contribution of CDD to the Planning and Problem-Solving EF dimension (< 5%) after statistically controlling for ADHD symptom overlap with CDD symptoms. In contrast, the ADHD IN dimension accounted for a majority of variance across most EF dimensions; the ADHD HI dimension explained a far smaller share of the variance, being mainly linked to the EF dimensions of Self-Restraint (inhibition) and Emotional Self-Regulation. Becker and Langberg (2014) likewise noted that CDD made a small contribution to variance on the Metacognitive factor of the Behavior Rating Inventory of Executive Functioning; again, ADHD IN contributed far more variance to that factor. Jimenez, Ballabriga, Martin, Arrufat, and Giacobo (2013) similarly noted a small contribution of CDD symptoms to this same EF dimension of the Behavior Rating Inventory of Executive Functioning, even after controlling for ADHD inattention. And, similar to my own findings noted previously, Langberg, Becker, and Dvorsky (2014) found that CDD symptoms were linked to a small but significant degree to parent-reported organizational problems in their children but not for teacher ratings of such difficulties. It seems evident across all of these studies utilizing EF rating scales that CDD has no significant association with EF inhibitory problems, whereas those problems are substantial in ADHD. CDD does have a minor relationship to organizational (metacognitive) EF deficits in daily life, but this is in sharp contrast to the far greater and pervasive deficits across all EF dimensions found in studies of ADHD (Barkley, 2012b, 2013). This pattern implies that the cognitive problems underlying CDD are not like those involved in ADHD, which is important for establishing that CDD is not a subtype of ADHD but a distinct disorder from it and involving different neuropsychological mechanisms.
Patterns of Comorbidity in Concentration Deficit Disorder and Attention Deficit Hyperactivity Disorder
One of the most reliable findings across many studies of CDD is that it is more strongly linked to internalizing symptoms generally and anxiety/depression specifically than are ADHD symptoms, while the latter are more strongly associated with externalizing psychopathology, such as defiance and conduct problems, than is CDD (Bauermeister et al., 2012; Becker & Langberg, 2013; Becker, Luebbe, et al., 2014; Capdevila-Brophy et al., 2014; Carlson & Mann, 2002; Garner et al., 2010; Hartman et al., 2004; Penny et al., 2009). This link of CDD with internalizing symptoms is evident even after statistically controlling for the contribution of ADHD symptoms to those internalizing symptoms (Bauermeister et al., 2012; Becker & Langberg, 2014; Becker, Langberg, Luebbe, Dvorsky, & Flannery, 2014; Burns et al., 2013; Lee et al., 2014; Penny et al., 2009; Willcutt et al., 2014). Yet when CDD symptoms are statistically controlled, the ADHD IN dimension is far less linked to internalizing symptoms, if at all (Lee et al., 2014; Penny et al., 2009). The linkage of CDD to depression remains even after controlling for parental internalizing dimensions (Becker, Langberg, et al., 2014; Becker, Luebbe, et al., 2014).
The opposite pattern emerges when studying the relationship of these two attention disorders to externalizing symptoms. ADHD is reliability associated with a higher risk for externalizing symptoms generally, and oppositional defiant disorder (ODD) and conduct disorder specifically. For instance, ODD is 11 times more likely to occur in cases of ADHD than it does in the general population (Angold, Costello, & Erkanli, 1999). However, CDD has no relationship to ODD symptoms or risk for that disorder (Barkley, 2013; Burns et al., 2013; Lee et al., 2014; Penny et al., 2009). In fact, if the overlap of ADHD with CDD is removed statistically, the relationship of CDD with ODD symptoms may even be significantly negative (Penny et al., 2009). From these findings it is reasonable to assume that CDD would have little or no associations with conduct disorder, substance use disorders, or adult antisocial personality disorder, all of which are linked to varying degrees with ODD. Other evidence for this lack of or even negative association of CDD with externalizing problems is evident in a study using direct observations of disciplinary actions (i.e., time-outs) received on an inpatient unit (Becker, Luebbe, et al., 2014). Disruptive or aggressive behavior leads to disciplinary actions that are positively linked to the HI symptoms of ADHD, but they are negatively associated with CDD symptom severity.
My own survey of US children collected information on professional diagnoses of 17 different learning, developmental, and psychiatric disorders as reported by parents concerning the past professional diagnoses their children had received (Barkley, 2013). It revealed that both CDD and ADHD were associated with elevated rates for 11 of the 17 disorders. However, CDD was not associated with higher rates of reading or math disorders, hearing impairment, oppositional defiant, anxiety, or bipolar disorder diagnoses than in the control cases, whereas ADHD was linked to higher rates for all of these disorders except hearing impairments. But the CDD group had a higher rate of depression than either the controls or those with ADHD. In sum, CDD is reliably and more strongly associated with internalizing symptoms and related disorders than is ADHD while ADHD is more strongly related to the externalizing disorders than is CDD. Such evidence reflects a double dissociation between CDD and ADHD that supports distinguishing these two attention disorders from each other.
The Nature of Impairments in Concentration Deficit Disorder Versus Attention Deficit Hyperactivity Disorder
Symptoms refer to the cognitive and behavioral expressions of a mental disorder while impairment refers to the adverse consequences that accrue to individuals as a result of their symptoms that render them functionally ineffective in various domains of major life activities, such as academic, social, and occupational functioning, among others (Barkley, 2011b, 2012a). Here I examine what little is known about impairments associated with CDD.
Studies of CDD have shown it to be reliably linked to social problems generally and social withdrawal specifically (Becker & Langberg, 2013; Becker, Luebbe, et al., 2014; Burns et al., 2013; Capdevila-Brophy et al., 2014; Garner et al., 2010; Marshall et al., 2014; Willcutt et al., 2014). This is true also when cases of ADHD Inattentive presentation are sorted into those high and low in CDD symptoms (Capdevila-Brophy et al., 2014), arguing that it is CDD symptoms specifically that are linked to this pattern of social passivity, withdrawal, shyness, and even anxiety. Such findings may be even more apparent in teacher than in parent ratings (Bauermeister et al., 2012; Becker & Langberg, 2013), perhaps owing to the greater opportunity of teachers to witness peer interactions.
The most detailed study of the specific social behavior problems linked to CDD was conducted by Mikami, Huang-Pollack, Pfiffner, McBurnett, and Hangai (2007). They employed detailed observations of children interacting using a simulated chat room, comparing ADHD and control children while examining the contribution of their level of CDD symptoms to their social conduct. In their analyses, the authors statistically controlled for ADHD type, IQ, reading ability, and typing skill. Results showed that CDD independently contributed to fewer total responses in the chat room, less perception of subtle social cues, less memory for the conversation, and a smaller proportion of hostile responses. While these findings agree with the more general findings discussed earlier that CDD is linked to greater socially withdrawn, it also suggests a role of CDD in the attention to and an encoding of social cues that may partially explain impairment in critical social processing and behavior that are of a different sort than seen ADHD (social intrusion, aggression, bossiness, excessive speech, etc.). The negative relationship of CDD to aggressive behavior is likewise consistent with studies using parent and teacher ratings of behavior (discussed later).
It is important to emphasize here that the association of CDD to social impairment survives the statistically controlling of severity of ADHD symptoms, as well as those of ODD, conduct disorder, generalized anxiety disorder, major depressive disorder, and even IQ (see studies in special issue on CDD, Journal of Abnormal Child Psychology, 2014; also Burns et al., 2013). It also survives statistical controlling for demographic factors. This illustrates the point that CDD makes a distinct contribution to social impairment apart from any that may be due to the IN dimension of ADHD; their contributions are independent or additive, not redundant (Burns et al., 2013; Willcutt et al., 2014).
Academic Performance and Achievement
Even though CDD is far less associated with disruptive and aggressive social behavior and more with social withdrawal, it appears to contribute unique problems to academic performance and possibly math specifically. In a study of Puerto Rican children, Bauermeister et al. (2012) noted that CDD and ADHD IN were each significantly and independently associated with lower academic achievement scores on testing after controlling for the other set of symptoms; HI symptoms did not manifest this connection. This study also observed that severity of CDD uniquely contributed to low math performance even after controlling for the overlap of CDD with ADHD IN symptoms. Burns et al. (2013) reported a similar relationship between CDD and ratings of academic impairment even after controlling for ADHD IN symptoms. But this relationship is not evident across all studies of CDD and may be related to the types of measures employed. At least three studies (Becker & Langberg, 2013; Langberg Becker, & Dvorsky, 2014; Watabe, Owens, Evans, & Brandt, 2014) did not find an association of CDD with academic achievement tests after controlling for IQ and ADHD symptoms or found it to be rather weak. Therefore, CDD seems to be related to problems in teacher- or parent-rated academic performance even if it is not reliably associated with poor scores on specific achievement tests.
Parent and self-ratings of impairment in 15 domains of impairment were studied in my surveys of representative US samples of adults and children, respectively (Barkley, 2012b, 2013) using newly developed impairment rating scales (Barkley, 2011b, 2012a). Groups were created for CDD only, those with ADHD only, and those with both conditions; the remainder became the control group. In the study of children (Barkley, 2013), I noted that CDD was linked to more severe impairments in all domains relative to the community control group. But the CDD group reported more difficulties in the Community-Leisure domains relative to the Home-School (work) domains. The ADHD cases were also more impaired across all domains than the control group, but they had their greatest difficulties in the Home-School domains related to work. Compared to CDD, ADHD produced a pattern of more pervasive impairment (across more domains), placing the ADHD cases in the bottom 7% of the population in at least twice as many of the 15 domains as was the case for the CDD group. When the relative contributions of symptom dimensions were studied for their respective contributions to impairment, the ADHD IN symptom dimension contributed markedly more variance to impairment in the Home-School domains than did the ADHD HI dimension or the CDD dimensions. The HI dimension contributed more variance to Community-Leisure impairments than to the Home-School domains. I found that CDD symptoms also did so but to a far lesser extent. Consistent with other research discussed earlier, these results show that CDD is less impairing than ADHD in work-related settings at home and school, although both are more impairing compared to the control group. Moreover, both ADHD and CDD symptoms contributed uniquely to impairment after controlling for the other symptom dimensions, although ADHD IN symptoms accounted for a greater proportion of variance in each summary score.
The study of US adults (Barkley, 2012b) employed a rating scale of 15 domains of impairment different from the scale used in the children’s survey. Once again, I found that both the CDD-only and ADHD-only groups self-reported more impairment than did the control adults. But, unlike in the children’s survey, the adults with CDD were as impaired as the adults with ADHD in overall rated mean impairment. Yet, just as in the children’s survey, ADHD resulted in more pervasive impairment (across more domains) than did CDD. The results of both studies showed that the impact of the two disorders was additive. That is to say that when CDD occurred with ADHD, the severity of impairments across the domains was significantly greater than for either disorder alone.
More recently, two studies by Combs and colleagues examined the impact of CDD on several specific domains of impairment in large adult community samples (Combs, Canu, Broman, & Nieman, 2013; Combs, Canu, Broman-Fulks, Rocheleau, & Nieman, 2012). In one study (Combs et al., 2013), results showed that symptoms of both CDD and ADHD contributed unique variance to negative quality of life ratings after controlling for the other set of symptoms. These distinct contributions of each disorder remained even after controlling for anxiety, depression, and some demographic factors. The second study (Combs et al., 2012) found mainly the same results on ratings of self-reported stress in adults. Taken together, the limited research on impairment to date shows that CDD makes a distinct contribution of impairments in various domains of functioning both in children and adults that is separate from but additive with those impairments linked to ADHD. This distinct impact of CDD is also independent of comorbidity with other disorders and demographic factors, once again supporting the view that CDD is a distinct disorder from ADHD even if it may overlap with ADHD symptoms.
What Are the Causes of Concentration Deficit Disorder?
Very little is known about the causes of CDD. In the area of genetic contributions to CDD, there seems to be just one study (Moruzzi, Rijsdijk, & Battaglia, 2014). It found that variance in the symptoms of CDD were largely due to genetic influences, having a heritability only slightly less than that seen in ADHD. Interestingly, results showed that nearly half of this genetic contribution to CDD was shared with that of ADHD. But half of the genetic influence was not shared with ADHD, implying that there may be some distinct genetic influences on CDD apart from those contributing to ADHD. Also of interest was the observation that there was a somewhat greater contribution of unshared or unique environmental factors to CDD than was the case for ADHD. In both disorders, the shared environmental factors made little, if any, significant contribution.
There was a significant relationship of CDD symptoms to prenatal alcohol exposure noted in one study (Graham et al., 2013). Another reported that higher CDD symptoms seemed to be a treatment-emergent side effect in cases of pediatric acute lymphoblastic leukemia (Reeves et al., 2007). A neuro-imaging study of CDD symptoms is now underway (Schweitzer, personal communication, May 2014) and may hopefully shed more light on possible neurological factors related to CDD. Apart from the three studies mentioned here, no other research on etiology could be located for this review.
That said, the findings for demographic factors might imply that CDD may be a correlate if not a consequence of various social adversities, as CDD was linked even more to parent disability status than was ADHD. If CDD is like ADHD one can expect it to have multiple etiologies.
Can Concentration Deficit Disorder Coexist with Attention Deficit Hyperactivity Disorder?
If CDD is a distinct disorder from ADHD, there is no reason why the former could not show some pattern of overlap with the latter given that comorbidity is commonplace in mental disorders. Unfortunately, much of the early research on CDD selected cases from among children referred to clinics for concerns about ADHD or studied the CDD symptom dimension in cases meeting criteria for ADHD. Such a method of recruitment can automatically make it seem as if CDD is a subtype of ADHD and precludes any study of their overlap. More recent studies have used general population or clinical samples to address this issue, allowing for the opportunity for CDD to be seen independently of ADHD, if such is the case in reality. For instance, in my survey of US children (Barkley, 2013), I found that 59% of the children qualifying for a research diagnosis of CDD met research criteria for having ADHD. But only 39% of the children qualifying for ADHD of any type also qualified for CDD. These findings agree with prior studies of children (Garner et al., 2010; Hartman et al., 2004). Similarly, in my survey of US adults (Barkley, 2012b) in which 5.8% met criteria for CDD, 54% had ADHD but nearly half did not. In addition, approximately half of individuals qualifying for ADHD of any type (46%) also qualified for CDD. I interpreted this pattern as one of comorbidity between two relatively distinct but related or partially coupled disorders. A similar pattern exists between anxiety and depression, for example.
Musings on the Mental Dysfunction in Concentration Deficit Disorder
As I noted elsewhere (Barkley, 2014a, 2014b), CDD resembles a dysfunction in the focus/execute component of attention in Mirsky’s (1996) model. Perhaps CDD is a form of hypersomnia or arousal disorder as its symptoms do include items such as sleepiness, low arousal or energy, or drowsiness (Penny et al., 2009). However, a recent study in college students showed that while both CDD and ADHD symptom dimensions were significantly associated with daytime sleepiness, items related to sleepiness formed a distinct factor from those of CDD and ADHD in a factor analysis (Langberg, Becker, Dvorsky, & Luebbe, 2014). This linkage of CDD to sleepiness remained even after controlling for ADHD, anxiety, and depression symptoms (Langberg, Becker, Dvorsky, et al., 2014), so its relationship is unique and not driven by any overlap with the latter disorders.
A fascinating possibility is that CDD might represent pathological mind-wandering (Adams et al., 2010). Mind-wandering is commonplace and seems to arise when a primary task that is being performed makes few demands on effortful processing or thinking. This allows the contemplative or problem-solving capacity of the EF system to focus on more salient personal concerns (a secondary task; Smallwood & Schooler, 2006). When poorly regulated, however, mind-wandering can lead to making numerous errors in the primary task with which it is interfering. This has been seen in adverse effects on EF task performance (Smallwood & Schooler, 2006) and could result from reduced meta-awareness or self-monitoring of pursuit of the goal, diminished working memory capacity available for pursing the external goals, and so on. Excessive mind-wandering has also been found to negatively affect academic performance (Smallwood, Fishman, & Schooler, 2007). This hypothesis about CDD as excessive mind-wandering seems worthy of future investigation.
The Lack of Treatment Research on Concentration Deficit Disorder
To date, just two studies have been done on treatments for SCT, both involving children. One study examined atomoxetine, a nonstimulant ADHD medication, for its effects on CDD symptoms specifically (Wietecha et al., 2013). The groups involved had ADHD, a reading disorder, or both conditions. Results showed that this norepinephrine reuptake inhibitor was effective at reducing CDD symptoms even after statistically controlling for the overlap of CDD with ADHD symptoms. The improvement in CDD symptoms was also apparent in the group with dyslexia only.
What other medications might work? Early studies on stimulants (methylphenidate) for treating ADHD I-type cases did not find them to be particularly effective (Milich et al., 2001). For instance, in my own study of ADHD I-type versus ADHD C-type cases of children, we found a modest positive response to methylphenidate, but this mainly occurred at low doses. Also, only 20% of the I-type cases remained on this medication after a double-blind, placebo-controlled trial whereas the vast majority of C-type children stayed on the medication after the trial (Barkley et al., 1991). No stimulant medication studies have been done specifically on cases chosen for having CDD. It is interesting to speculate that in view of the relationship of CDD with anxiety and depression, SSRIs might be a type of medication to investigate further for CDD. As noted previously, CDD has a relationship with daytime sleepiness, making the study of antinarcoleptics, such as modafinil, worthy of consideration.
One study of behavior modification for CDD symptoms employed traditional home and school contingency management methods that targeted the specific symptoms of CDD (Pfiffner et al., 2007). Significant benefits were evident from the intervention. Cognitive behavioral therapy has not been shown to be useful for childhood ADHD (Abikoff, 1987), but it has proven useful for cases of anxiety and/or depression. It deserves to be studied as a possible intervention for CDD in view of the relationship of CDD to these disorders, as noted previously. Certainly if CDD continues to show patterns of findings supporting its distinctiveness from ADHD, then treatments for ADHD cannot be automatically assumed to work for CDD, nor can those treatments that have failed for ADHD be thus ruled out for CDD.
Conclusions and Future Directions
Studies to date have shown that CDD has a distinct pattern of symptom dimensions that are not simply extensions of the symptom dimensions of ADHD but are quasi-independent from them. This provides indirect evidence that the attention disorder likely to underlie CDD is probably not the same as that found in ADHD. While there exists a moderate relationship between CDD symptoms and those of ADHD IN, there is little association of CDD with ADHD HI symptoms. There is a reliable and greater association of CDD symptoms with internalizing symptom dimensions but a far weaker relationship to externalizing psychopathology than is true for ADHD; that relationship may even be a negative one once the overlap of ADHD and CDD are statistically controlled. Also, a reliable set of findings shows that CDD is more strongly linked to social withdrawal and possibly peer neglect than is ADHD, which is much more strongly related to disruptive social behavior, aggression and disciplinary reactions, and peer rejection. CDD creates some risk for poor academic performance even independently of its association with ADHD IN symptoms, though to a lesser degree in children than does ADHD. CDD may be more specifically related to deficits in math performance, although the latter finding is not especially reliable at this time and worthy of further research. Both CDD and ADHD result in greater impairment in various domains of major life activities using impairment rating scales, but the pattern is such that ADHD is more severely and pervasively impairing than is CDD. Yet each disorder makes unique contributions to impairment, and their comorbidity results in significantly greater impairment than is evident for either disorder alone. The few studies of population samples indicate some comorbidity between ADHD and CDD/SCT with approximately half of those having one condition also having the other. Yet the disorders can also exist alone. The evidence to date does not unequivocally support CDD as a new mental disorder as yet. But the findings so far are suggestive of such an eventual distinctiveness. Future research needs to focus on replicating prior studies concerning symptom composition and structure, neurocognitive deficits, and domains of impairment. More important, research needs to address the dearth of evidence concerning etiologies, development and life course, and differential response to various treatments if the concept of CDD as a new attention disorder is to be confirmed. Certainly, CDD offers great promise for young clinical investigators seeking an area of research specialization to which they can make significant and likely career-long contributions.
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