POISSANT, Hélène
Metacognitive processes in children with attention deficit and hyperactivity disorder (ADHD]
Hélène Poissant, Ph.D
UQAM, DSÉ, C.P. 8888, Succ. Centre-ville
Montréal, P.Q. Canada, H3C 3P8
tél: 514 987 3000 (ext. 8946)
fax: 514 987 4608
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Abstract
In this paper we look at different kind of evidence: neurobiological, neuropsychological and medical and argue that individuals with ADHD may experience a lack of metacognition. Metacognition relates to the consciousness that individuals have about their own thinking processes and to the ability to have control of those processes (Vygotsky, 1934/1962). As a component of the metacognitive system, metacognitive knowledge may be used in four different ways: (1) a person may know when she/he knows (self-consciousness) or do not know when she/he does not know (secondary ignorance), (2) a person may know what she/he knows, which can help her/him to predict her/his abilities to succeed in a given task and to estimate her/his confidence in the outcome, (3) a person may know what she/he needs to know (Markman, 1977) to fill in her/his lack of information (perception of lack of information) or the inconsistencies in a given information (perception of inconsistencies of information), and finally, (4) a person may know the usefulness of some strategies for dealing with a given task, e.g., self-questioning Brown (1978, 1987). Another more dynamic aspect of metacognition is self-regulation. This relates to experience, feelings, and thoughts that occur during an ongoing cognitive activity (Flavell, 1979). Those experiences give individuals an internal feedback about the efficiency of their mental monitoring. Self-regulation can intervene in a cognitive activity without the person’s awareness. However, in some circumstances, adults, and to a lesser extent children, are able to consciously use rules and strategies to solve a problem. On the other hand, individuals with ADHD show an inability to “stop and think” before acting, regardless of the task or the situation. The three major aspects of ADHD are hyperactivity, impulsiveness, and inattentiveness. Moreover, these features appear early in childhood for most individuals with an onset often before seven years of age and are marked by chronic behaviors lasting at least six months. For reasons that we will expose in this paper, we assume that ADHD children may experience difficulty engaging in a reflexive activity such as metacognition.
Key words (10)
Metacognition, children, attentional deficit and hyperactivity disorder (ADHD), neurobiology, neuropsychology, executive function, frontal lobe
Metacognitive Processes in Children with ADHD
Introduction
Prevalence of the full ADHD syndrome is estimated to be 1% to 3% in the American school-aged population, (American Academy of Child and Adolescent Psychiatry, 1997). Another 5% to 10% of this population have a partial ADHD syndrome or one with other problems or psychiatric disorder (comorbidity), such as oppositional defiant or conduct behavior, along with or separate from anxiety and depression. It is estimated that 20% to 30% of the children have learning disabilities and 30% have delayed motor skill development. Moreover, another 15% to 20% may show transient behavior suggestive of ADHD. Boys are about three times more likely than girls to develop ADHD. Symptoms of ADHD seem to decrease with age but related factors seem to increase with age. This results in a 30% to 50% (or more) of children who still manifest symptoms in adulthood (Barkley, 1990). Often undiagnosed or misdiagnosed, adults with ADHD are often restless, easily distracted, struggle to sustain attention, impulsive and impatient, disorganized, and fail to plan ahead. They also experience problems with stress intolerance often leading to an underachievement in education and vocational positions. This results in low self-esteem and increased frustration. For all these reasons, the topic of ADHD is one of the most widely debated in mental health and child development.
DSM-IV Assessment of Attention Deficit with Hyperactivity Disorder
The fourth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV) (American Psychiatric Association, 1994), describes Attention-Deficit/Hyperactivity Disorder (ADHD) as a disorder that can include a list of nine specific symptoms of inattention and nine symptoms of hyperactivity/impulsivity. ADHD of the inattentive type is defined by an individual showing at least six of the following characteristics: a) fails to give close attention to details or makes careless mistakes, b) difficulty sustaining attention, c) does not appear to listen, d) struggles to follow through on instructions, e) difficulty with organization, f) avoids or dislikes requiring sustained mental effort, g) often loses things necessary for tasks, h) easily distracted, i) forgetful in daily activities. ADHD of the hyperactive/impulsive type is defined by an individual experiencing six of the following characteristics: a) fidgets with hands or feet or squirms in seat, b) difficulty remaining seated, c) runs about or climbs excessively (in adults may be limited to subjective feelings of restlessness), d) difficulty engaging in activities quietly, e) acts as if driven by a motor, f) talks excessively, g) blurts out answers before questions have been completed, h) difficulty waiting in turn taking situations, i) interrupts or intrudes upon others. In adults, ADHD is often linked with different problems: (a) deficient sustained attention (reading, paperwork), (b) poor organization, planning and anticipation, (c) procrastination, (d) impulsive decision making style, (e) difficulty to work independently, and (f) demoralization. Recently, new research in neurobiology and neuropsychology had shift the focus from a behavioral description of ADHD (re: DSM-IV) to a more cognitive perspective.
Neurobiological Evidence
The etiology of ADHD is controversial because both biologic and social factors have been postulated. Experts have investigated the causes of ADHD and link it either to genetic (Biederman et al., 1992) or environmental causes (Cadoret and Stewart, 1991; Chandola, Robling, Peters, Melville-Thomas, & McGuffin, 1992). Heredity is an important predictor, since about 25 % of the fathers and 17 to 25% of the mothers of ADHD children have this condition (American Academy of Child and Adolescent Psychiatry, 1997). For example, Faraone, Biederman, and Milberger (1994)’s family-genetic study showed that ADHD aggregates in nuclear families and that second-degree relatives of ADHD probands were at increased risk for ADHD compared to second-degree relatives of normal control probands. A study of Faraone, Biederman, Keenan, and Tsuang (1991) indicates that the relatives of girls with ADHD had a higher risk of also being affected by this condition. Morevoer, there is 75 to 91% chance that a twin (identical or nonidentical) has it (Levy, Hay, McStephen, Wood, & Waldman,1997) and 13 to 35% chance that another child in the family has ADHD (Gross-Tsur, Shalev, & Amir, 1991). Other research based on genetic mechanism indicates that the dopamine pathways in the brain, which link the basal ganglia and frontal cortex, appear to play an important role in ADHD (Hechtman, 1994).
Among the diverse biological hypotheses regarding the etiology of ADHD, the hypothesis of frontal dysfunction remains strong. The influence of frontal systems on attention, particularly the elements of higher mental control postulated as prefrontal functions, are illustrated through the presentation of a number of syndromes of abnormal mental awareness associated with prefrontal minimal brain damage (Benson, 1991). For example, Ross, Hommer, Breiger, Varley, and Radant’s (1994) study indicates that children with ADHD showed, relative to normal controls, deficits on inhibiting response during a delay period (800-msec). This difficulty to inhibit response in ADHD may be associated with pathology located outside the dorsolateral prefrontal cortex.
Research based on brain imaging indicates that areas in the prefrontal lobe, basal ganglia, and striatum are reduced by about 10 percent in size and activity. These areas are thought to be involved in response, attention, and sensitivity to reward. Zametkin, Nordahl, Gross, King, Semple et al. (1990), using a positron emission tomography scanner (PET scan) observed important differences between people who have ADHD and those who do not. In adults with ADHD, the brain areas that control attention used less glucose, which indicates less activity. Another study, conducted by Shue and Douglas (1992), indicates that ADHD children differed significantly from controls on tasks involving motor control and problem solving skills known to be sensitive to frontal lobe dysfunction.
Klorman (1991) using cognitive event-related potentials (ERP) procedure found that children with ADHD make more errors and react more slowly than controls in tests of sustained attention. Coincident with their poor performance, children with ADHD have smaller late positive components of the ERP. Frank, Seiden, and Napolitano (1994), used this technology to discover that children with learning disabilities (LD) with or without ADHD both have smaller P3 wave amplitude compared to normal children when all groups have to perform an auditory task (two-tone discrimination). Frank et al. (1994) concluded that the smaller P3 amplitude in children with LD-ADHD reflects cognitive and processing difficulties, which frequently coexist with ADHD in these children but that are not specifically related to an attention deficit. Robaey, Cansino, Dugas, and Renault (1995), correlated ERP measurements with scores on the Wechler Intelligence Scale for Children Third Edition (WISC-III) and on a Piagetian battery (Cognitive Development Scale for Children) in normal and ADHD children. Amplitudes and latencies of a fronto-central P250 and of the parieto-occipital N250, P350 and P500 were measured concurrently in four categorization tasks derived from the tests. Their results indicated that in hyperactive children there is a negative correlation between P250 amplitude and the children’s verbalize test scores. In addition, latency-based correlations found in normals were lacking in children with ADHD. They concluded that intelligence forms may not refer to the same use of the same processes in ADHD and normals.
In addition, an important area of ADHD research includes investigations of the brain structures. For example, Hynd, Hern, Novey, Eliopulos, Marshall, et al. (1993), employed magnetic resonance imaging (MRI) to investigate the patterns of morphology of the caudate nucleus in normal and ADHD children. Their results indicate that 72.7% of normal children evidenced a left-larger-than-right pattern of asymmetry, whereas 63.6% of the ADHD children had the reverse pattern of asymmetry. This asymmetry was most notable in boys with ADHD. These results may account for the asymmetries observed in neurotransmitter systems implicated in ADHD. Using the same technology, Semrud-Clikeman, Filipek, Biederman, Steingard, Kennedy, et al. (1994), demonstrated that right-handed male subjects with ADHD have significantly smaller posterior corpus callosum regions than the control group. Moreover, these areas may be related to sustained attention deficits, which in turn impact on the development of more advanced level of attention such as self-regulation. Brain asymmetries and developmental changes in specific anatomical structures linked to ADHD are, however, still controversial topics.
Neuropsychological evidence
Now many psychologists speak of ADHD in terms of an “outlier in the spectrum of human neurological variation” rather than merely as a disorder. The symptoms related to ADHD may appear at one time or another in all individuals, but are more persistent or severe in people with ADHD (Barkley, 1990). Such manifestation of the symptoms was sufficient ground for Barkley (1997,1998) to challenge the DSM-IV primary characteristics associated with ADHD: inattention or inconsistent attention, hyperactivity and impulsiveness. ADHD would have more to do with a lost of interest than with a deficit to concentrate. Barkley points to persistence of effort and impulse control rather than in default in the filtering system of attention. For ADHD children, the urge to act is not controlled or inhibited, so that we may consider the child as hyper-responsive rather than hyperactive. By the age of about four, normal children start to develop self-control along with an internalized language while ADHD children seem to fail to do so and have difficulty to provide a delayed answer (see the above study of Ross, Hommer, Breiger, Varley, and Radant, 1994).
Barkley’s neuropsychological theory predicts that children with ADHD will have a poorer working memory than their normal peers. To be able to hold in memory an information, for even a very short period of time, enables the individual to analyze and reflect about this information. The inability to reflect and therefore to wait prevents the child from behaving in a proper way. For the same reason, children with ADHD will find it difficult to hold back their emotions and seem to feel them more intensively than average people. Such difficulties also lead to a lack of objectivity and consequently make goal-directed behavior less likely. Barkley’s theory also predicts that an important part in self-control and reflection, i.e., the internalized language, is impaired in children with ADHD. The ability to hold a thought enables humans to organize information and to elaborate new relations among this information that lead to a deeper understanding. The inability to do so gives the impression that children with ADHD have difficulty to explain things and do not get to the point but rather around the point. According to Barkley (1997), the disorder in response inhibition and executive function associated with ADHD have among consequences an impairment in self-regulation, an impairment in behavior organization toward the future (or planning), and an impairment in social effectiveness.
A meta-analysis conducted by Barkley, Grodzinsky, and DuPaul (1992) reviewing 22 neuropsychological studies of frontal lobe functions in children with ADHD, predominantly hyperactive or predominantly inattentive, indicates that tests of response inhibition reliably distinguished ADHD children from normal children. Their meta-analysis also suggests that both ADHD groups made more omission errors on a Continuous Performance Test and performed more poorly on the word and interference portions of the Stroop Test compared to normals. Both types of ADHD shared similar deficits on some frontal lobe tests while difficulties related to perceptual-motor speed and processing were found only in children with ADHD predominantly inattentive. Thus, these executive function tests may be helpful in the diagnosis of ADHD children and in the comparison with normals.
On the other hand, methylphenidate (MPH) a psychostimulant of the central nervous system is well recognized to improve ADHD symptomatology. There are several advantages from its intake. MPH benefits in children include increase of their compliance to maternal commands (Barkley, 1988), increase in persistence to tasks (Carlson, Pelham, Milich, & Hoza, 1993) an element that we may associate with metacognition (see Metacognitive Functioning section), improvement of their working memory (Tannock, Ickowicz, & Schachar, 1995), improvement of their social behavior with peers and adults as well as academic performance (Klein, 1993), and improvement on the Go-no go test indicating a decrease in the tendency of children with ADHD to make impulsive commission errors (Trommer, Hoeppner, & Zecker, 1991). In addition, there is evidence that implicates the actions of MPH on the frontal lobe region (Kuczenski, Segal, Leith, & Applegate, 1987; Yasushi, 1987). The drug acts as a dopamine agonist and as such increases the level of available dopamine in the system. Dopaminergic neurons are found in areas such as frontal lobe and limbic system, that are involved in the control of problematic behaviors of children (e.g., motor control, impulsiveness). Furthermore, MPH demonstrated significant effects on tests sensitive to frontal lobe dysfunction such as spatial working memory and planning (Elliot, Sahakian, Matthews, Bannerjea, Rimmer, et al., 1997).
Metacognitive functioning and dysfunctioning
According to Brown (1978, 1987), metacognitive knowledge is used in four different ways: (1) individuals may «know when» they know («self-consciousness») or do «not know when» they do not know («secondary ignorance»), (2) individuals may «know what» they know, which can help them to predict their abilities to succeed in a given task and to estimate their confidence in the outcome, (3) individuals may «know what they need » to know (Markman, 1977) to fill in their lack of information («perception of lack of information») or the inconsistencies in a given information («perception of inconsistencies of information»), and finally, (4) individuals «may know the usefulness of strategies» for dealing with a given task. See figure 1 and 2 for an expansion of Brown’s «self-consciousness» and «secondary ignorance» concepts.
Contrary to normal metacognitive functioning, metacognitive dysfunctioning involves a problem in the experience or feeling of conscious awareness of one’s own cognitive performance (Shimamura, 1994). Disruptions of metacognition, characterized by cognition without awareness, can take many clinical forms such as memory without awareness (Jacoby & Witherspoon, 1982). The lack of awareness reported in some clinical cases suggests that many cognitive functions may operate without conscious control. This also suggests that cognitive functions have a componential aspect, that is neural circuits operating in parallel with other metacognitive functions (Shimamura, 1994). Thus different metacognitive impairments may involve different neural circuits depending on the type of cognitive functions that is disrupted. This hypothesis seems to be confirmed in some neurological pathologies. For example, it was found that in organic amnesia patients certain aspects of new learning capacity (during a perceptual-motor skill task and a mirror-reading skill task) are preserved even though the patients did not have an awareness of their capacity or did not have a conscious recollection of having engaged in the task before. This phenomena resembles, although in a reverse way, the “know when” component of metacognition (see Brown, 1978), but here patients do not know when they know (a special case of secondary ignorance). For Shimamura (1994), these findings suggest that certain parts of memory capacity, namely its conscious recollection component may be distinct of its unconscious automatic component. See figure 2 for a reinterpretation of Brown’s secondary ignorance concept in the light of the knowing without awareness phenomenon.
The involvement of frontal lobe in feeling-of-knowing and metacognition seems to be confirmed by other studies. For example, Janowsky, Shimamura, and Squire, (1989) found that patients with frontal lesions were impaired in the ability to judge what they had learned. Other clinical observations (in Korsakoff’s patients) indicate an impairment in their feeling-of-knowing accuracy in addition to deficits in encoding, attention and memory for temporal order. According to Shimamura (1994), one possible explanation implies that frontal lobe damage mediates disorders of metamemory (knowledge of one’s memory capabilities and of strategies that can help memory). Deficits in metamemory expressed by failed judgments and decision making is consistent with other disorders related with frontal lobe dysfunctioning. Patients with frontal lobe lesions do not experiment impairment in perception and memory but rather an impairment in the evaluation or integration of these cognitive functions. Thus the metacognitive impairment related to frontal lesions may be due to a failure to make appropriate judgments based on perceptual and semantic knowledge (Shimamura, 1994).