ADHD and Giftedness
Review of possible origins of similar inattentiveness and hyperactive behaviors
found in ADHD and giftedness as well as methods to differentiate between the
two.
Rutger Katz
3072525
Neuroscience & Cognition
University of Utrecht
Contents
Abstract ................................................................................................................................................... 2
Introduction............................................................................................................................................. 3
Behavior................................................................................................................................................... 4
Behavioral aspects of ADHD ................................................................................................................ 4
Cognitive deficits in ADHD................................................................................................................... 4
Intelligence and giftedness.................................................................................................................. 5
Behavioral aspects of giftedness ......................................................................................................... 6
Overexcitabilities ................................................................................................................................. 7
Underachievement in gifted individuals ......................................................................................... 8
The difficulty of diagnosis: giftedness vs. ADHD ................................................................................. 9
Neural structures ................................................................................................................................... 12
Differences in neural structures related to ADHD ............................................................................ 12
Differences in neural structures related to giftedness...................................................................... 14
Neurobiological distinctions between ADHD and giftedness. .......................................................... 16
Genetic and Environmental Factors ...................................................................................................... 18
Genetic and environmental factors ADHD ........................................................................................ 18
Genetic and environmental factors of intelligence ........................................................................... 19
Linking between findings in ADHD and intelligence genetics ........................................................... 20
Summary and Conclusion ...................................................................................................................... 21
Conclusion ......................................................................................................................................... 22
Literature ............................................................................................................................................... 24
Appendix................................................................................................................................................ 32
Appendix 1......................................................................................................................................... 32
OVEREXCITABILITIES ...................................................................................................................... 32
Appendix 2......................................................................................................................................... 34
Common characteristics of gifted underachievers ....................................................................... 34
Appendix 3......................................................................................................................................... 36
Similarities ADHD giftedness (Maud van Thiel, 2010) ................................................................... 36
1
Abstract
Attention Deficit/Hyperactivity Disorder (ADHD) is associated with hyperactivity, inattention and
impulsivity. A review of the literature seems to indicate that gifted individuals can be at risk of being
misdiagnosed as having ADHD. This study investigated the current literature to determine what types
of behaviors demonstrated in gifted individuals can cause such a misdiagnosis. We look at the
neurobiological origins of ADHD and intelligence in order to identify potential parallels that can cause
similar behavior. Further, because ADHD and intelligence are highly heritable, we will also explore
the literature on genetic and environmental factors that influence their development.
The ADHD-like behaviors that gifted individuals can exhibit are so-called ‘overexcitabilities’ which are
driven by different neurobiological mechanisms. Whereas high intelligence is associated with
increased brain size and a more efficient neural network in healthy subjects, ADHD is associated with
reductions in brain size and deficiencies in the neural networks of executive functions. As of yet,
genetic research has been unsuccessful in identifying strong candidate genes associated with the
development of either intelligence or ADHD. However, increasing evidence points to intelligence
holding phenotypical properties in ADHD as well as a moderating effect in the development of ADHD.
In conclusion, gifted individuals can exhibit behaviors, or overexcitabilities, that may mistakenly be
associated with ADHD. However, the neurobiological mechanisms that are associated with high
intelligence are completely different from those that are associated with ADHD. This suggests that
similarities between the inattentive and hyperactive behaviors associated with giftedness and ADHD
are not due to similar neurobiological mechanisms. The different neurobiological mechanisms,
together with cognitive tasks with discriminative properties, may provide a successful measure to
distinguish ADHD and giftedness, and thus prevent misdiagnosis.
2
Introduction
As defined in 1997: “Intelligence is a very general capability that, among other things,
involves the ability to reason, plan, solve problems, think abstractly, comprehend complex ideas,
learn quickly and learn from experience. It is not merely book learning, a narrow academic skill, or
test-taking smarts. Rather, it reflects a broader and deeper capability for comprehending our
surroundings—‘catching on’, ‘making sense’ of things, or ‘figuring out’ what to do. Intelligence, so
defined, can be measured, and intelligence tests measure it well” [1]. Intelligence test results are
represented by the Intelligence Quotient (IQ), which is normally distributed among the population,
with an average total IQ value of 100. Individuals whose intelligence puts them in the top 2% of the
general population are termed ‘gifted’ and can be identified by high scores on IQ tests (higher than
130) or by excellent performances in school or other areas.
Interestingly, gifted individuals can demonstrate behaviors that can appear similar to
behaviors typically demonstrated by individuals diagnosed with attention-deficit hyperactivity
disorder (ADHD). ADHD is the most common childhood disorder, occurring in 5-10% of school-aged
children and is characterized by behaviors related to inattentiveness, hyperactivity, and/or
impulsivity [2]. In an individual with ADHD these symptoms are considered to be maladaptive and
inconsistent with the individual’s developmental level. ADHD is further characterized by impairments
in multiple academic and social domains. The behaviors displayed by children with ADHD and gifted
children may seem similar, which may lead to potential misdiagnosis of ADHD in gifted individuals
[3].
There seem to be two reasons that complicate the correct recognition of giftedness. First,
there appears to be a lack of awareness of the characteristics of gifted individuals, specifically the
hyperactive and inattentive behaviors that resemble ADHD. Second, there appears to be a
predisposition to view these ‘ADHD-like’ behaviors as behaviors indicative of the presence of ADHD
[4]. This view is valid to a certain extent as there is the possibility that an individual is gifted and has
ADHD. Importantly, the presence of above average intelligence does not preclude the diagnosis of
ADHD [5], [6]. Since IQ is normally distributed among the population diagnosed with ADHD [7], we
can assume that between 0.1 and 0.2% of the general population has an IQ > 130 and ADHD.
However, a child who is perceived as being inattentive may not always have an attention disorder; he
or she may simply not be challenged by the material being presented in the classroom [8], and thus
he or she is at risk for misdiagnosis.
In this review we will investigate the origin of the perceived similarities between hyperactive
and inattentive behavior in gifted individuals and in individuals with ADHD. We will begin by
reviewing the literature on ADHD and giftedness in order to identify similarities in behavior. Then we
will review the literature on the neurobiological origins of ADHD and giftedness in order to determine
what neurobiological processes drive the similarities in behavior. Furthermore, because ADHD and
giftedness are highly heritable [9], [10], we will explore genetic and environmental factors that
influence their development. Finally, we will discuss our findings and provide suggestions for future
studies.
3
Behavior
Behavioral aspects of ADHD
ADHD is a developmental neurological disorder that emerges during childhood and is
characterized by inattentiveness or hyperactivity and impulsivity or a combination of the two [2]. The
disorder is heterogeneous and can present itself in patients through symptoms ranging from small
attention problems or dreaminess up to excessive hyperactive, impulsive and unpredictable
behavior. These symptoms decrease from childhood to adulthood resulting in a full remission (not
meeting formal diagnostic criteria) in approximately 15% of the cases [11] and partial remission with
persistent functional impairment in as many as 50-70% of the cases (Antshel & Barkley, 2009).
Especially inattentive symptoms show strong persistence, whereas hyperactive/impulsive symptoms
mostly decline from childhood to adulthood [13].
There are some marked gender differences in ADHD; boys generally show both inattentive
and hyperactive/impulsive symptoms, whereas girls more often only show inattentiveness [14].
Furthermore, girls show increased motor overflow and impairment in planning, while boys show
greater impairment during conscious, effortful response inhibition. The first choice pharmacological
treatment for ADHD is the psychostimulant Methylphenidate (MPH) which alleviates the disruptive
behavioral symptoms in 70% of patients with ADHD [15], [16]. MPH functions by reducing the
reuptake of dopamine and norepinephrine, thus improving the levels and utility of these
neurotransmitters in the brain. Reports indicate that MPH without a prescription has been used as an
academic performance booster or a recreational drug by college students not diagnosed with ADHD
with percentages varying between 3% and 35% (Arria & Wish, 2006).
Comorbidity with other disorders is very common in patients with ADHD with up to 87%
prevalence both in children [18] and adults (Biederman et al., 2006). Most common comorbid
disorders are mood disorders (40% to 61%), substance related disorders (15% to 70%), and anxiety
disorders (30% to 47%) (Kessler et al., 2006; Miller et al., 2007; Sobanski et al., 2007; Sobanski et al.,
2008; Wilens, 2008). Furthermore, children diagnosed with ADHD have an increased risk for
functional impairments in adulthood including occupational, academic, and financial problems as
well as difficulty in maintaining personal relationships (Antshel & Barkley, 2009).
Cognitive deficits in ADHD
Besides the general symptoms of inattentiveness, hyperactivity and impulsivity, patients with
ADHD are characterized by poor performance on several cognitive tests that indicate deficiencies in
executive functions. Among the executive functions that seem to be affected in ADHD are cognitive
control (Casey et al., 2002), temporal processing (Sonuga-Barke et al., 2010), and working memory
[26] that can be measured by e.g. Go-NoGo- or Stroop tasks, duration discrimination or duration
reproduction tasks, and increases in reaction times or increased variability of reaction times
respectively (table 1). The executive function deficiencies associated with ADHD are suggested to be
dissociable: patients with ADHD do not necessarily have deficiencies on all executive functions.
Zeeuw et al. (2012) found that 80% of the subjects with ADHD only had deficiencies in one
4
component of cognitive control, reward sensitivity or timing, suggesting that there are multiple
pathways that lead to the expression of ADHD. Furthermore, even though most children with ADHD
perform average on formal tests of intelligence, ADHD is associated with reduced intelligence at
group level (Frazier et al., 2004). One explanation is that low intelligence and ADHD have shared
genetic influences [29]. Unfortunately, the reduced intelligence score at group level cannot be fully
explained by attention problems or diminished effort during test performance (Jepsen et al., 2009).
Lower IQ scores of patients with ADHD have been associated with poor treatment response (Van der
Oord et al., 2008) and negatively affect long-term functional outcome [32].
Table 1. Overview of executive function deficits associated with ADHD. Beside each executive
function are possible symptoms that result from a deficiency in that executive function and cognitive
task tests that can indicate deficiencies in that executive function.
Executive Function
Cognitive control
Temporal processing
Reward processing
Attention/Working
memory
Symptoms
Impulsivity
hyperactivity
Duration discrimination
Anticipatory timing
Duration reproduction
Delay aversion
Susceptibility to addiction
Impulsivity
Inattentiveness
Increased reaction times
Tested by
Go-NoGo, Stroop
Duration discrimination,
duration reproduction
Reward delay
Variability of reaction time on
cognitive tasks
Intelligence and giftedness
There are different types of intelligence (i.e. verbal, spatial, and logical) that are normally
distributed among the population: certain people may have a stronger spatial ability while others
may have stronger logical reasoning. Tests that measure intelligence generally consist of either
complex tasks that involve different aspects of reasoning, or batteries of tasks that require different
kinds of cognitive performance. Different elements of intelligence tasks are correlated and generate
a general factor of intelligence, the g-factor (figure 1; Spearman, 1904), which accounts for a large
amount of variance between tests (around 40%). This g-factor also correlates with low level mental
tasks such as sensory discrimination (between 0.68 and 0.92; Deary et al., 2004), visual processing
(0.36; Sheppard & Vernon, 2008) and reaction times (-0.24; Sheppard & Vernon, 2008). The
predictive value of these intelligence tests for this concept of intelligence and the g-factor is
supported by correlations between test results of different types of tests measuring intelligence [36],
data from brain-imaging [37], and genetic studies [38].
5
Figure 1. A.
Correlations found
between the gfactor, cognitive
aspects, and test
results. B. Effect of
age on the g-factor,
and specific
cognitive aspects
(Salthouse, 2004).
Further, intelligence appears to be predictive of certain factors in our lives as IQ scores
correlate positively with socioeconomic successes in education (0.46), occupation (0.37) and income
(0.21) [39]. A standard deviation advantage in IQ scores in childhood was correlated with a 24%
lower risk of death up to age 69 [40]. Also, a standard deviation disadvantage in intelligence around
the age of 20 has been associated with a 50% greater risk of hospitalization, mood disorder, and
alcohol-related disorders (Gale et al., 2010), as well as personality disorders [42].
Gifted individuals are usually defined as belonging to the top 10% of individuals based on
intellect and until the late 1960’s were classified in the United States by arbitrary IQ scores of over
130 depending on the school. At this time, the United States’ federal definition of a gifted individual
is as follows: "The term gifted and talented student means children and youths who give evidence of
higher performance capability in such areas as intellectual, creative, artistic, or leadership capacity,
or in specific academic fields, and who require services or activities not ordinarily provided by the
schools in order to develop such capabilities fully (P.L. 103–382, Title XIV, p. 388).” However,
arbitrary IQ scores are still used in order to identify gifted individuals today. One exception to the
rule are the so-called savants, who, despite having very low IQ scores (20-40), are extremely gifted in
a specific skill like math or music [43]. The savant syndrome can be found in individuals with serious
mental disabilities, approximately one in ten individuals with autistic disorder, and have exceptional
memories in addition to the skill they are gifted in.
Behavioral aspects of giftedness
In general, most attention in research is geared towards learning- and behavioral problems
that often coincide with average or below average IQ. Children with above average IQ are often
‘forgotten’ as they do not seem to experience the same magnitude of problems that is seen in the
children with below average IQ. Above average IQ does seem to coincide with a very specific set of
behaviors such as overreactions or underachievement that, even though these children seem to be
able to compensate for a very long time, may cause specific learning- and behavioral problems as
well [44–46].
6
Overexcitabilities
The work of the Polish psychiatrist Dabrowski (1902-1980) provides a good framework to
study behavior that is demonstrated by gifted individuals. Dabrowski (1977) concluded that gifted
and talented persons are more inclined than non-gifted individuals to have so-called “overexcitability
traits”. Overexcitabilities (OE) are reactions that might last longer, be expressed more strongly and
occur with greater frequency than average. According to Dabrowski’s clinical observations many
children, adolescents, and even adults continuously overreacted toward internal and external
stimulation. These overreactions can be organized in psychomotor, sensual, intellectual,
imaginational, and emotional dimensions. A compact overview of overexcitabilities is given in table 2
and a more extended list can be found in appendix 1. Dabrowski developed the theory of positive
disintegration (TPD) which states that intense psychoneurotic processes, unlike in mainstream
psychology, critical to accelerated development and the formation of personality. He concluded that
stronger OEs are associated with higher developmental potential [47]. He verified this proposition by
comparing gifted students and students with mental retardation. The former exhibited OEs through
symptoms of nervousness and slight neuroses, whereas the latter did not exhibit these
psychoneurotic traits.
Table 2. An overview of the overexcitability dimensions and exhibited behaviors per dimension [48].
Overexcitability dimension
Psychomotor
Sensual
Intellectual
Imaginational
Exhibited behavior
 Heightened excitability of the neuromuscular system
 Capacity for being active and energetic
 Psychomotor expression of emotional tension (i.e. nervous
habits and compulsive talking)










Emotional






Heightened experience of sensual pleasure or displeasure
Sensual expression & outlets for emotional tension (i.e.
overeating and buying sprees)
Aesthetic pleasures (appreciation of beautiful objects)
Heightened need to gain knowledge
Intensified activity of the mind
Penchant for probing questions and problem solving
Preoccupation with logic and theoretical thinking
Heightened play of the imagination
Rich association of images and impressions (real and
imagined)
Spontaneous imagery as an expression of emotional tension
(i.e. elaborate dreams)
Capacity for living in a world of fantasy
Heightened, intense positive and negative feelings
Somatic expressions (i.e. blushing and sweaty palms)
Strong affective expressions
Capacity for strong attachments and deep relationships
Well differentiated feelings toward self
7
The work of Dabrowski led to the development of several OE questionnaires and the claims
that OEs could be used to identify gifted students. However, the context of Dabrowski’s TPD for OEs
has been ignored in most studies. Chang & Kou (2013) reviewed findings of correlations related to
intelligence with OEs from recent studies. They found that gifted individuals had significantly higher
intellectual, imaginational, sensual and emotional OEs than non-gifted individuals. Furthermore,
these studies also found that the intellectual OE was the most important trait of gifted students,
which is characterized by e.g. a higher need to gain knowledge, or a preoccupation with logics and
theoretical thinking. Moreover, Chang found a 0.299 correlation (P<0.1) between IQ and the
intellectual OE subscale and a correlation of 0.171 (P<0.1) between academic performance and the
intellectual OE. Although the coefficients of the correlations were not high, Chang states that the
statistical values imply that intellectual OE might still be an important factor in identifying giftedness
in students. Amongst gifted individuals OEs also specifically relate to gender and age. Gifted females
showed significantly more sensual and emotional OEs compared to males, whereas gifted men
exhibited more significant psychomotor, intellectual and imaginational OEs [50]. Furthermore, young
gifted individuals showed stronger psychomotor and imaginational OEs than older gifted individuals,
whereas older gifted individuals had more significant intellectual and emotional OEs than their
younger counterparts [48].
Underachievement in gifted individuals
According to literature, between 15% and 50% of gifted individuals relative to their
intellectual and creative potentials are underachieving in their personal, work-related and academic
lives [51]. These numbers might even be underreported as most reports only include individuals that
are identified via IQ scores thus excluding gifted individuals who are identified through other means
(e.g. performance, creative products or recommendation) and unidentified gifted individuals.
Because of the misconception that gifted children are guaranteed high achievements and success,
the issue of underachieving gifted individuals has rarely been addressed in the past [52].
Adding to this, there seems to be a lack of consensus over the definition of when a gifted
individual is underachieving, and even the definition of giftedness itself, further obstructing the
identification of underachieving gifted individuals [51]. To quote Morisano & Shore (2010):
“Underachievement in a broad sense might be reflected in low grades and occasionally in
performance on achievement tests, in low levels of effort on extracurricular tasks or within
interpersonal relationships, in a lack of life goals or general direction, or in avoidance of challenging
or creative projects in and out of school, among other possibilities.” Or more simply put;
underachievement can be defined as a discrepancy between ability and achievement.
Individuals that underachieve relative to their potential, independent of whether they are gifted
or not, share many common characteristics. Chief among these are a lack of motivation, low selfesteem and self- confidence, difficulty focusing attention, disorganization, procrastination, and
avoidance of responsibility [53]. Abelman (2006) found that gifted underachievers specifically
succumb to excessive use of computers, videogames and television to escape from school
responsibilities. After a review of the literature, Reis & McCoach (2002) concluded that there are
three basic reasons for underachievement in gifted students which apply to the majority of cases:
8
1. The underachievement masks more serious physical, cognitive, or emotional issues.
2. The underachievement is due to a mismatch between the student and his or her school
and/or home environment.
3. The underachievement is due to personal characteristics such as low self-motivation, low
self-regulation, or low self-efficacy.
A more extensive list of characteristics of gifted underachievers is given in Appendix 2 (Reis &
McCoach, 2000).
As a consequence, underachievement may even hamper the identification of giftedness
itself. IQ results are used as a predictive value for factors representing success like academic
performance, occupation and income. However, as Duckworth et al. (2011) concluded that IQ tests
measure the result of both intelligence and test motivation. The interaction between intelligence and
test motivation from this study is presented in figure 2. It is concluded that a high IQ score requires
both high test motivation as well as high intelligence, but that a low IQ score could be the result of
either lower intelligence or a lack of motivation. This also applies to the negative influence that
executive function impairments can have on IQ scores, for instance in the presence of ADHD. Brown
(2011) suggests that clinicians assessing IQ scores in an individual that is suspected of
underachievement should also consider ADHD as a possible factor and assess related executive
function impairments as well.
Figure 2. Model showing the
influence of test motivation on
the predictive value of intelligence
(Duckworth et al., 2011). All paths
are significantly different from
zero (P < 0.05).
The difficulty of diagnosis: giftedness vs. ADHD
When one takes a closer look at the OEs as described by Dabrowski (1977), some of these
behaviors can easily be mistaken for ADHD symptoms. Webb and his colleagues (2005) were some of
the first to recognize a systematic problem where gifted students were being misdiagnosed with a
mental illness, with ADHD being diagnosed in the majority of the cases. As shown in table 2 attention
problems, impulsive and hyperactive behaviors look very similar between individuals with ADHD and
giftedness (Webb, 2005). This list has been taken up and further extended by therapists in the
Netherlands (Appendix 3). Misinterpreting behavior related to giftedness as ADHD can lead to a
9
wrongful approach in solving underachievement in students, and worse, starting (pharmacological-)
treatment for a disorder that is not present.
Table 3. The comparison Webb (2005) made that demonstrated similarities in behaviors associated
with ADD/ADHD and behaviors associated with giftedness.
Behaviors associated with ADD/ADHD
Poorly sustained attention in almost all situations
Diminished persistence on tasks not having
immediate consequences
Impulsivity, poor ability to delay gratification
Impaired adherence to commands to regulate or
inhibit behavior in social contexts
More active, restless than normal children
Difficulty adhering to rules and regulations
Behaviors Associated with Giftedness
Poor attention, boredom, daydreaming in
specific situations
Low tolerance for persistence on tasks that seem
irrelevant
Judgment lags behind intellect
Intensity may lead to power struggles with
authorities
High activity level; may need less sleep
Questions rules, customs, and traditions
On the other hand giftedness can also compensate for executive function impairments that
are associated with ADHD. In order to be diagnosed as ADHD, according to DSM IV ADHD associated
symptoms should be present before the age of 7 [2]. However, many gifted ADHD students reported
that they were able to live up to high expectations in elementary school. It was not until secondary
school where ADHD impairments became an obstacle when students must keep track and prioritize
between homework assignments from different teachers [57]. In these individuals the ADHD-like
symptoms are most likely mistakenly attributed to their giftedness, which obscured the presence of
ADHD. Besides potentially obscuring ADHD, giftedness can also obscure the presence of other
disorders, such as learning disabilities (i.e. dyslexia or dyscalculia) as Webb (2005) and Reis &
McCoach (2002) mentioned. Reis & McCoach (2002) formulated a list (table 4) of characteristics
gifted students with a LD may possess that hamper identification as gifted, and formulate
characteristics associated with giftedness.
Table 4. Characteristics of gifted students with learning disabilities (Reis & McCoach, 2002)
Characteristics that hamper identification as
gifted
•Frustration with inability to master certain
academic skill
•Learned helplessness
•General lack of motivation
•Disruptive classroom behavior
•Perfectionism
•Super sensitivity
•Failure to complete assignments
•Lack of organizational skills
•Demonstration of poor listening and
concentration skills
•Deficiency in tasks emphasizing memory and
perceptual abilities
•Low self-esteem
Characteristics associated with giftedness
•Advanced vocabulary use
•Exceptional analytic abilities
•High levels of creativity
•Advanced problem solving skills
•Ability to think of divergent ideas and solutions
•Specific aptitude (artistic, musical, or
mechanical)
•Wide variety of interests
•Good memory
•Task commitment
•Spatial abilities
10
•Unrealistic self-expectations
•Absence of social skills with some peers
It seems that both ADHD and intelligence are heterogeneous on a behavioral level. There is
great variation in executive function deficits and behaviors associated with ADHD as well as a
variation in expressions of OEs that are associated with giftedness across different dimensions and
talents (i.e. math, music, problem solving) associated with giftedness. Because of the similarities
between disruptive behaviors associated with ADHD and OEs expressed in to giftedness, on first sight
it seems difficult to accurately attribute disruptive behaviors to either ADHD or giftedness based
solely on behavioral observations. Furthermore, giftedness can obscure mental illnesses or learning
disorders or even be obscured itself as a result of underachievement. In the next chapter we review
the neurobiological literature on ADHD and giftedness to see whether it possible to differentiate
between the two on a neurobiological level and find possible causes for similarities in inattentive and
hyperactive behaviors.
11
Neural structures
ADHD is characterized by impulsivity, hyperactivity and inattention, which are behaviors that
could also be exhibited by gifted children, as theorized above. In this section we review findings on
neural features associated with ADHD, giftedness, and compare these in order to determine if there
are any neural correlates that could explain the observed similarities in behavior between the two.
Differences in neural structures related to ADHD
Brain development in ADHD is characterized by a delay in cortical maturation. Compared to
the cortical thickness of typically developing children, children with ADHD show a delay in cortical
thickness maturation (measured from 5 years of age onwards) and a thinner cortex overall [58].
Furthermore, there are global overall reductions (3-4%) in all four major lobes of white and gray
matter in children with ADHD compared to age- and gender-matched controls [59]. These reductions
are primarily localized in the prefrontal cortex (PFC) which accounts for 48% of the total reductions in
gray matter. The corpus callosum, cerebellum and basal ganglia are also affected by reductions in
gray and white matter. Studies investigating the basal ganglia have produced contradictory results
however, with some studies showing reductions in gray matter while others showing increases in
gray matter [59].
Besides the reductions in brain size, studies have also found significant differences in the
neural networks that are linked to symptoms of ADHD. Wang et al. (2009) demonstrated that, in the
context of small-world network typology, the topologies of the neural networks in individuals with
ADHD are altered compared to typically developing controls. The study showed that ADHD brains
have a tendency towards decreased global efficiency of the brain networks overall. Furthermore,
nodal efficiency (average shortest path lengths between nodes) in children with ADHD was
negatively affected at several regions of prefrontal, temporal, and occipital cortices. Cubillo et al.
(2012) tied together several studies that found abnormalities in specific neural networks associated
with ADHD and formulated a theory on how ADHD originates from executive function network
deficiencies. Zelazo and Muller (2002)(2002) the distinction between “Cool” and “Hot” executive
function networks that have specific functions but also interact with each other. The Cool executive
function networks mediate motor response, interference inhibition, cognitive flexibility, temporal
foresight, selective and sustained attention, working memory, motor and timing processes. The Hot
executive function networks mediate temporal discounting, reward processing and reward
anticipation. The Cool executive function networks include the lateral inferior/dorsolateral and
dorsomedial fronto-striatal, fronto-parietal and fronto- cerebellar neural networks, while the Hot
executive function networks include the lateral orbitofrontal and ventromedial networks. A
schematic representation of these networks is shown in figure 3. The network theory is further
supported by the alleviating effect MPH has on the executive function deficits that are associated
with ADHD. MPH functions by both the up-regulation of dysfunctional fronto-striato-thalamocerebellar and parieto-temporal attention networks and the down-regulation of hyper-sensitive
orbitofrontal activation for reward processing [62].
12
Figure 3. Schematic representation of the MRI evidence for structural and functional brain
abnormalities in children and adults with ADHD in overlapping neural networks that
mediate “cool” cognitive-abstract and “hot” reward-associated executive and cognitive
functions. IFG = inferior frontal gyrus; OFC = orbitofrontal cortex; DLPFC = dorsolateral
prefrontal cortex; vmOFC = ventromedial orbitofrontal cortex; d/vACC = dorsal/ventral ACC
cortex; SMA = Supplementary Motor Area. (Cubillo et al. 2012)
It must be mentioned that the majority of the studies has not excluded ADHD patients who
show comorbidities with conduct disorder and antisocial personality disorder. These antisocial
behaviors are also associated with abnormalities in the same neural networks that show
abnormalities in ADHD [63]. Furthermore imaging studies are based on group statistics on relatively
small numbers. And that due to the effects of long-term medication on normalization of basal ganglia
the current literature shows a more lenient deficit picture from what would be observed in untreated
patients (Nakao et al., 2011).
In the previous chapter we found that executive function deficits (cognitive control, reward
sensitivity and timing) associated with ADHD were dissociable, indicating heterogeneity in executive
function deficits and subgroups in the ADHD population (De Zeeuw et al., 2012). However, there is a
lack of studies comparing neural network deficiencies between subgroups of ADHD patients [14].
Although it has been strongly suggested that the heterogeneity found in the neuropsychological
impairments associated with ADHD coincides with heterogeneity in executive function networks,
there is no conclusive evidence thereof at this time [14]. However, we can conclude that ADHD is
related to a disrupted and delayed development of cortical thickness maturation. This coincides with
13
a thinner cortex overall and abnormalities in the hot and cold executive function networks that are
theoretically the cause of the behavioral symptoms and executive function deficits associated with
the disease. Use of MPH normalizes the fronto-striato-thalamo-cerebellar and parieto-temporal
attention networks, and orbitofrontal reward networks [62], which alleviates disruptive behaviors in
70% of patients with ADHD.
Differences in neural structures related to giftedness
Research into the neurobiology of giftedness is much less extensive compared to the
literature on the neurobiology of ADHD. The main findings are that there is a correlation between
brain size and general intelligence of between 0.35 and 0.4 in healthy individuals [65]. Shaw et al.
(2006) showed that the development of cortical thickness varies across different levels of
intelligence. Cortical thickness normally increases after birth and starts to decrease around the age of
6 until it stabilizes around the age of 20. Shaw et al. (2006) found that the cortex of children with a
high intelligence was still thickening until the age of 12, after which the cortex thins (even more
strongly compared to children with average intelligence) until it stabilizes around the age of 20. This
resulted in children with high intelligence scores to have a lower cortical thickness compared to
children with lower intelligence scores around the age of 7. However, cortical thickness was higher in
the prefrontal and temporal lobes compared to children with lower intelligence scores around the
age of 12 and then again average around the age of 19. Karama et al. (2009)(2009) found positive
correlations of 0.15 to 0.32 between general intelligence and cortical thickness distributed through
frontal, parietal, temporal and occipital brain regions. They suggested that the association between
cortical thickness and cognitive ability is weaker at younger ages, which could explain how children
with a thinner cortex around the age of 6 could have a higher intelligence then those with a thicker
cortex. Furthermore, the size of specific brain regions (Brodmanns areas 22, 40, 44 and 45) were
found to be correlated to OE traits [49]. Besides differences in size and cortical thickness, brains of
individuals with higher intelligence also seem to process information more efficient, that is, use
fewer resources during relatively easy cognitive tasks [67]. In addition, during very complex tasks,
more intelligent brains recruit more cortical resources in order to solve a problem.
The identification of what the contribution of specific brain features contribute to
intelligence has been complicated by the finding that correlations differ between certain brain
features and intelligence in different groups of similar intelligence. Though first discovered in studies
comparing brain features between the sexes (Haier et al, 2005), it became apparent that two
individuals could achieve identical intelligence scores through the use of different brain structures, as
a result from different training, or using different cognitive strategies [69]. Furthermore, people
seem to be able to compensate for cognitive deficits or overcome cognitive challenges by recruiting
brain areas previously only indirectly correlated to intelligence, especially frontal and corresponding
contralateral areas (Van den Heuvel et al., 2009). Even though certain brain features seem more
likely to directly contribute to intelligence than others, there is considerable heterogeneity [71].
However, this might also be related to individual differences in strategies when solving cognitive
tasks [72].
14
The parieto-frontal integration theory of intelligence (P-FIT) currently provides the best
available theory as to where intelligence is localized in the brain [73]. According to the P-FIT theory,
information is captured in the extrastriate cortex (BAs 18-19) and fusiform gyrus (BA 37), which
contribute to the recognition, imagery and elaboration of visual input, and Wernicke’s area (BA 22),
which does the same for syntactic auditory input. This information is then processed in the
supramarginal (BA 40), superior parietal (BA 7), and angular (BA 39) gyri of the parietal lobe, where
structural symbolism, abstraction and elaboration of the information takes place. These parietal
regions then interact with the frontal cortex (especially BAs 6, 9, 10, 45, 46 and 47) in order to form a
working memory network so that different responses can be formed. These responses can then be
engaged or inhibited in the anterior cingulate cortex (BA 32) in order to produce the best response
while inhibiting the alternatives. In turn, these interactions between brain regions are dependent on
the functioning of the white matter fibers that connect them, such as the arcuate fasciculus. For
most of these brain regions, the left hemisphere is more important for the performance of the
cognitive tasks than the right hemisphere. A schematic representation of the P-FIT is given in figure 4
[74].
Figure 4. The loci of intelligence
differences according to the P-FIT
theory. The figure shows Brodmann
Areas (BAs) involved in intelligence,
as well as BAs shown in green
indicate predominantly lefthemispheric correlations and BAs
shown in pink indicate
predominantly right-hemispheric
correlations with intelligence. The
arcuate fasciculus (shown in yellow)
is candidate for a white matter tract
that connects the involved brain
regions. (Deary, Penke, & Johnson,
2010)
The growing consensus that intelligence does not reside in a single brain region, but rather is
the result of different brain regions working together, implies that the transfer of information by
white matter between different brain areas becomes an important factor in intelligence as well. And
indeed, using diffusion tensor imaging (DTI), measuring water diffusion parameters of white matter
which indicates their integrity, white matter integrity has been found to correlate 0.37 with
intelligence tests for young individuals (11 years old) and between 0.36 and 0.56 for older individuals
(83 years old) [75]. A lesion study showed that the integrity of long association fibers such as the
arcuate and uncinate fasciluli contributes the most to processing speed [76]. Furthermore,
correlations were found by Li et al. (2009) that higher intelligence is correlated with shorter
15
characteristic path lengths and a higher global efficiency of the networks, which may indicate that
more efficient parallel information transfer results in a higher intelligence.
In short, we found that high intelligence is generally correlated with a larger brain, increased
network efficiency, and a different path of cortical thickness maturation resulting in a thicker cortex.
Although we know that certain brain areas contribute to intelligence, individuals can use their brain
differently for similar performance on intelligence tests. Furthermore, we do not know exactly how
the altered brain developmental path leads to increased intelligence.
Neurobiological distinctions between ADHD and giftedness.
The previous sections in this chapter indicate that individuals with ADHD as well as
individuals with above average intelligence show a different path of cortical development when
compared to typically developing controls. Individuals with ADHD show a delayed cortical thickness
maturation while individuals with high intelligence start with thinner cortices around the age of 7,
have thicker cortices around the age of 12 and end up with cortices of average thickness around the
age of 19 (Shaw 2006). This coincides with the observation of smaller brain size for individuals with
ADHD and larger brain sizes for individuals with high intelligence which could suggest a causal
connection between the cortical thickness maturation and brain size later on. Furthermore, while the
brains of highly intelligent individuals show increased network and processing efficiency, the brains
of individuals with ADHD show decreased network efficiency (in the executive function hot and cold
networks that were discussed earlier). This suggests that the similarity in behavior that has been
observed in ADHD and giftedness has a different neurobiological basis. However, as ADHD and
giftedness are heterogeneous and can occur in the same individual, discovering direct interactions
between the two could be complicated. Unfortunately, there are few MRI studies focusing on the
interaction between ADHD and variations of intelligence. In part, this is due to the opinion that
intelligence should not be a covariate in cognitive studies of neurodevelopmental disorders [78].
They state are that, IQ does not meet the requirements of a covariate because it measures aptitude
and potential rather than achievement and performance. Furthermore, they suggest that using IQ as
a matching variable or covariate produces overcorrected, anomalous, and counterintuitive findings
about neurocognitive function.
One MRI study on the interaction between intelligence and ADHD found that the delay of
cortical development commonly associated with ADHD is most markedly present in individuals with
low intelligence scores (De Zeeuw et al., 2012). Individuals with ADHD and high intelligence scores
showed a pattern of cortical development similar to healthy individuals with high intelligence.
However, there were global reductions in brain volume that remain stable during development
resulting in an overall thinner cortex across all ages (figure 5). This suggests that variations in
intelligence are associated with specific brain development trajectories in ADHD and, as the authors
state. These findings, together with other findings of genetic overlap between IQ and ADHD [80], add
support that intelligence should be taken as a covariate in studies of neurodevelopmental disorders.
16
Figure 5. Hypothetical
model of differences in
cortical thickness and
cerebral gray matter volume
in children with ADHD and
low (A, B and C) or high IQ
(D, E, F). (De Zeeuw et al.,
2012)
In short, we can conclude that the neurobiological mechanisms associated with ADHD are
different from those associated with high intelligence. This suggests that the inattentive and
hyperactive behaviors in ADHD and giftedness are caused by different neural features. Although we
do not know if and how features of intelligence interact with the features of ADHD and vice-versa at
a functional level, we do find an interaction between the two at a developmental stage. In the next
section we will review findings from genetic studies. These findings could provide a clue as to what
factors influence how ADHD and differences in intelligence can develop.
17
Genetic and Environmental Factors
Both intelligence [10] and ADHD [9] are known to be highly heritable, with heritability
estimates between 70-80% for both. However, intelligence and ADHD also show substantial
heterogeneity which might complicate the identification of genes that contribute to those high
heritability estimates. In this section we will explore the most important findings in these fields as
well as the effect of intelligence on the development of ADHD.
Genetic and environmental factors ADHD
Recent studies have produced a large number of candidate genes that show significant
associations with ADHD. However, a lot of these findings were not replicated or did not withstand
meta-analysis [81].
The most robust findings were for the DRD4, DRD5, DAT4 and COMT genes (table 2). DRD4
and DRD5 are both dopamine receptor genes, DAT4 is a dopamine transport gene and COMT
catalyzes the degradation of dopamine. The DRD4, DRD5 and DAT4 genes were found to be directly
associated with ADHD, while it is suggested that COMT is associated with comorbid antisocial
behavior in ADHD [82]. Mill et al. (2006) showed through replicated findings that polymorphisms in
the DRD4 and DAT1 genes were associated with variation in intellectual functioning among children
diagnosed with ADHD, apart from the severity of their symptoms. Furthermore, evidence from
longitudinal studies suggested that these polymorphisms indicated a greater risk for a poor adult
prognosis in children diagnosed with ADHD. However, as the odds ratios (OR) in table 2 demonstrate,
it must be noted that the genetic risks implicated in ADHD tend to have small effect sizes or be rare
and often also increase the risk of many other types of psychopathology unrelated to ADHD [84].
Table 5. Candidate genes
associated with ADHD. OR
indicates the effect size of
each gene polymorphism on
the development of ADHD
(Thapar, Cooper, Eyre, &
Langley, 2012).
18
The heritability estimates of 75% implicate that environmental factors also play a role in the
development of ADHD. A large number of environmental factors, such as prenatal risks or birth
compilations, have been studied (table 6; Thapar, Cooper, Eyre, & Langley, 2012). However, the
evidence provided by these studies, and thus the effect of these risk factors, remains equivocal due
to study limitations or a lack or reproduction [82]. The only exceptions are the associations of fetal
alcohol syndrome and premature and/or low birth weight children and ADHD. However, it is not
known if prematurity and/or low birth weight are risk markers of ADHD or merely causal.
Furthermore, some of these environmental factors might be modified by genetic influences and vice
versa (gene-environment interaction). For example, the use of maternal alcohol consumption during
pregnancy might hold a stronger risk for children with a dopamine transporter susceptibility gene
[85]. All in all, there are few robust findings of genes which strongly contribute to the development
of ADHD. Furthermore, although environmental factors seem to be associated with ADHD, their
influence on the development of the disorder remains mostly unknown.
Table 6.
Environmental risks
for the development
of ADHD (Thapar,
Cooper, Eyre, &
Langley, 2012).
Genetic and environmental factors of intelligence
Though it is still unknown why, the heritability of intelligence (as measured through the g
factor) increases with age, while environmental (shared and unique) effects decrease with age [86].
At early childhood heritability accounts for 23% of the variance in the g-factor, whereas shared
environment accounts for 74% of the variance. However, in middle childhood it is heritability
accounts for 62% and shared environment accounts for 33% of the variability. Furthermore,
environmental factors might moderate heritability of intelligence. Lower socioeconomic status was
correlated with increased shared economic factors of 58% and decreased genetic factors 10%
compared to high socioeconomic status with 15% and 71% respectively [87]. It should also be noted
that parents pass both their genes for intelligence as well as the associated socioeconomic status to
their offspring which could lead to a gene-environment interaction accounting for more variance in
intelligence.
Although the research on genes related to intelligence has been extensive, as of yet, no
individual genetic variants are found to be directly related to intelligence [88]. The only association
currently found is that older people with the e4 allele of the gene for apolipoprotein E (APOE) tend to
19
have lower cognitive ability [89]. One theory on the genetic basis of intelligence is that small effects
of many genes contribute to the additive genetic influence on intelligence. This theory is supported
by the study of Davies et al. (2011) that showed that a substantial proportion (40 to 50%) of variation
in cognitive ability is associated with common SNPs. This could explain why the heritability of
intelligence is so high, why intelligence is heterogeneous, and so few genes have been found that
contribute directly to (aspects of) intelligence.
Linking between findings in ADHD and intelligence genetics
It appears that there are still no good candidate genes with a large enough effect size that
explain the variability in either intelligence or ADHD despite their high genetic heritability. However,
Rommelse et al. (2008) found that affected and non-affected siblings of children with ADHD were all
impaired in the same executive functions as well as verbal IQ compared to the children diagnosed
with ADHD. This suggests that intelligence and deficiencies in specific executive functions have
endophenotypic properties in ADHD. Twin studies have also shown that the relationship between
ADHD and a lower intelligence is almost entirely explained by shared genetic factors [80].
Furthermore, the genetic factors affecting intelligence are disparate from those influencing other
cognitive endophenotypes in ADHD [92], [93]. This suggests that there are separate pathways from
genes to behavior for intelligence and specific executive function deficiency endophenotypes that
are related to ADHD. However, how the genetic and environmental factors affect the development of
the brain is still unknown. The theory of many genes of small effects underlying the additive genetic
influences on intelligence seems to hold true for both intelligence and ADHD. This could in any case
explain the heterogeneity in ADHD behaviors, the lack of strong genetic associations, and the
suggested endophenotypic properties of intelligence and cognitive control in ADHD.
In conclusion, although both ADHD and intelligence are highly heritable, only few genes have
been reported that strongly contribute to the expression of either ADHD or intelligence. Further,
there are environmental factors can modify the expression of genes and indirectly influence the
development of ADHD and intelligence. However, how genes contribute to the development of
ADHD and intelligence is still not well understood.
20
Summary and Conclusion
With this review we set out to investigate the origin of the perceived similarities between
overexcitabilities in gifted individuals and inattentive and hyperactive/impulsive behaviors expressed
by individuals with ADHD.
We found that gifted individuals often exhibit behaviors called overexcitabilities which could
be mistaken for ADHD related behavior. More specific: gifted children can exhibit behaviors like high
activity levels, poor attention due to boredom and a tendency to question rules that do not seem
logical, while children with ADHD may appear to be restless, have difficulty sustaining attention and
break rules by accident through impulsive actions (Webb, 2005). These behaviors can lead to
underachievement in school in gifted students as well as students diagnosed with ADHD. As it is
possible for gifted individuals to have ADHD (ref) or a learning disability, the identification of
giftedness or a psychiatric disorder such as ADHD can be difficult based on the observation of
expressed behavior in their home-, or school environment, or academic results alone. However, on a
cognitive level, children with ADHD show deficiencies in certain executive function tasks that are
specific to ADHD. At the same time IQ tests are still the primary tool to identify giftedness, although
an important factor in test outcome is test motivation as well as the possibility of the presence of
talents not tested by IQ tests (i.e. music and creativity). It appears that on a cognitive level there are
ways to discriminate between giftedness and ADHD. Although MPH can be a successful prescription
drug to treat ADHD, it does not seem suitable as a test to distinguish between giftedness and ADHD.
MPH only works for 70% of individuals with ADHD and the dosage has to be adjusted per individual.
Furthermore, its usage as an academic performance and concentration booster in students not
diagnosed with ADHD suggests that it could reduce inattentiveness in gifted individuals and
individuals diagnosed with ADHD in an equal manner.
We looked into the neurobiology of intelligence and ADHD to discover if the two show
neurobiological similarities that could explain exhibited inattentive and hyperactive behavior. In
general, we found that ADHD is associated with neural network deficiencies and thinner cortices,
whereas giftedness is associated with higher neural network efficiency and larger brains. However,
we also found that there is heterogeneity in neural features associated with ADHD, which might
cause the heterogeneity in executive function deficits and disruptive behaviors. This heterogeneity is
also found in neural activity, neural features, and cognitive strategies, which on one hand can lead to
similar performance on intelligence tests, but on the other hand could lead to the heterogeneity
found in intelligence. An interesting finding is that both ADHD and high intelligence are associated
with different cortical thickness pathways and the stabilizing effect of a high intelligence on cortical
thickness maturation in children with ADHD [79]. This suggests that there might be an interaction
between intelligence and ADHD. However, more research is necessary in order to elucidate the
nature of this interaction. Because gifted individuals with ADHD can still suffer from executive
function deficiencies in the same range as individuals with ADHD of average intelligence, increased
network efficiency associated with higher intelligence probably does not compensate for the
executive function network deficiencies that are associated with ADHD (Antshel et al., 2010). This
would suggest that network efficiency deficits due to ADHD are caused by changes in different white
matter attributes in comparison to the white matter attributes result in increased network efficiency
21
in the brains gifted individuals. In short, it appears that inattentive and hyperactive behaviors
associated with high intelligence and ADHD are driven by different neurobiological properties.
Furthermore, even though both are heterogeneous on a neurobiological level, there are certain
markers, i.e. adult cortical thickness and neural network efficiency/deficiencies, which could be used
to differentiate between high intelligence and ADHD.
Finally, both ADHD and intelligence are highly heritable. However, few genes have been
identified that strongly contribute to the expression of either ADHD or intelligence. Furthermore, it
seems that there are certain risk-genes mediated by environmental influences that contribute to the
development of ADHD or interfere with the potential of a high intelligence in a child. Within the
population of individuals with ADHD there appear to be certain endophenotypes based on
intelligence and/or deficiencies in specific EFs. Also, the genetic factors that are associated with a low
intelligence are different from those that are associated with executive function endophenotypes.
This is further supported by the difference in cortical thickness maturation between children
diagnosed with ADHD of high intelligence and low intelligence [79]. The theory that many genes of
small effects underlie the additive genetic influences on intelligence can explain the high heritability
of intelligence, the heterogeneity and the lack of identifying strongly contributing genes. That same
theory could also apply to the genetic influences on the development of ADHD, which is also still
unknown due to a lack in discoveries of strongly contributing genes to ADHD. This theory could also
explain the different endophenotypes of ADHD.
From this review we can conclude that gifted children can exhibit behaviors that could be
mistaken for ADHD. However, these behaviors are motivated through different neural mechanisms.
Through the use of cognitive tasks e.g. the Stroop or Go/NoGo task, that tap into executive function
deficits that are specific to ADHD, even in gifted children ADHD can be accurately diagnosed.
Furthermore, the typical delayed cortical thickness maturation found in children diagnosed with
ADHD seems to be normalized if the children’s IQ is high warrants further study. The genes driving
the development of intelligence as well as ADHD are still not well understood. The theory that many
genes of small effects underlie the additive genetic influence in intelligence could also apply to the
genetic influence in the development of ADHD. We suggest further research in the possibility of this
theory also applying to genetic influence in the development of ADHD and other neuropsychological
disorders.
Conclusion
Gifted individuals can exhibit behaviors called overexcitabilities that may be perceived as
behaviors normally associated with ADHD. Based solely on behavior and academic achievements it is
difficult to make a correct diagnosis. However, cognitive tasks detecting the executive function
deficits associated with ADHD can be used for accurate diagnosis of ADHD. These seemingly similar
behaviors are most likely driven by different neurobiological mechanisms. Whereas high intelligence
is associated with increased brain size and a more efficient neural network, ADHD is associated with
reductions in brain size and deficiencies in the neural networks of executive functions. There does
seem to be a normalizing effect of high intelligence in the normally delayed cortical thickness
maturation associated with ADHD, but more research is needed to study this effect. As of yet, genetic
22
research has been unsuccessful in identifying strong candidate genes associated with the
development of either intelligence or ADHD. The theory of many genes of small effects underlying
the additive genetic influence in intelligence could be applicable to the genetic influence in the
development of ADHD. In any case, further research is needed to solve the problem of potential
misdiagnosis in children with ADHD and/or high intelligence.
23
Literature
[1]
L. S. Gottfredson, “Mainstream science on intelligence: An editorial with 52 signatories,
history, and bibliography,” Intelligence, vol. 24, no. 1, pp. 13–23, Jan. 1997.
[2]
American Psychiatric Association, Diagnostic and Statistical Manual of Mental Disorders (4th
ed.). Washington DC: American Psychiatric Publishing, 1994.
[3]
J. T. Webb, Misdiagnosis and Dual Diagnoses of Gifted Children and Adults: ADHD, Bipolar,
OCD, Asperger’s, Depression and other disorders. Great Potential PressInc, 2005.
[4]
A. N. Rinn and M. J. Reynolds, “Overexcitabilities and ADHD in the Gifted: An Examination,”
Roeper Review, vol. 34, no. 1, pp. 38–45, Jan. 2012.
[5]
K. M. Antshel, S. V Faraone, K. Stallone, A. Nave, F. a Kaufmann, A. Doyle, R. Fried, L. Seidman,
and J. Biederman, “Is attention deficit hyperactivity disorder a valid diagnosis in the presence
of high IQ? Results from the MGH Longitudinal Family Studies of ADHD.,” Journal of child
psychology and psychiatry, and allied disciplines, vol. 48, no. 7, pp. 687–94, Jul. 2007.
[6]
M. L. Cordeiro, A. C. Farias, A. Cunha, C. R. Benko, L. G. Farias, M. T. Costa, L. F. Martins, and J.
T. McCracken, “Co-Occurrence of ADHD and high IQ: a case series empirical study.,” Journal of
attention disorders, vol. 15, no. 6, pp. 485–90, Aug. 2011.
[7]
B. Kaplan and S. Crawford, “The IQs of children with ADHD are normally distributed,” Journal
of Learning …, 2000.
[8]
D. N. Hartnett, J. M. Nelson, and A. N. Rinn, “Gifted or ADHD ? The Possibilities of
Misdiagnosis,” 2004.
[9]
S. V Faraone and J. Biederman, “What is the prevalence of adult ADHD? Results of a
population screen of 966 adults.,” Journal of attention disorders, vol. 9, no. 2, pp. 384–91,
Nov. 2005.
[10]
I. J. Deary, W. Johnson, and L. M. Houlihan, “Genetic foundations of human intelligence.,”
Human genetics, vol. 126, no. 1, pp. 215–32, Jul. 2009.
[11]
S. V Faraone, J. Biederman, and E. Mick, “The age-dependent decline of attention deficit
hyperactivity disorder: a meta-analysis of follow-up studies.,” Psychological medicine, vol. 36,
no. 2, pp. 159–65, Feb. 2006.
[12]
K. M. Antshel and R. Barkley, “Developmental and behavioral disorders grown up: attention
deficit hyperactivity disorder,” Journal of Developmental & Behavioral …, vol. 30, no. 1, pp.
81–90, 2009.
[13]
J. Biederman, E. Mick, and S. V Faraone, “Age-dependent decline of symptoms of attention
deficit hyperactivity disorder: impact of remission definition and symptom type.,” The
American journal of psychiatry, vol. 157, no. 5, pp. 816–8, May 2000.
24
[14]
A. Cubillo, R. Halari, A. Smith, E. Taylor, and K. Rubia, “A review of fronto-striatal and frontocortical brain abnormalities in children and adults with Attention Deficit Hyperactivity
Disorder (ADHD) and new evidence for dysfunction in adults with ADHD during motivation
and attention.,” Cortex; a journal devoted to the study of the nervous system and behavior,
vol. 48, no. 2, pp. 194–215, Feb. 2012.
[15]
A. F. T. Arnsten, “Stimulants: Therapeutic actions in ADHD.,” Neuropsychopharmacology :
official publication of the American College of Neuropsychopharmacology, vol. 31, no. 11, pp.
2376–83, Nov. 2006.
[16]
T. E. Wilens, “Effects of methylphenidate on the catecholaminergic system in attentiondeficit/hyperactivity disorder.,” Journal of clinical psychopharmacology, vol. 28, no. 3 Suppl 2,
pp. S46–53, Jun. 2008.
[17]
A. Arria and E. Wish, “Nonmedical use of prescription stimulants among students,” Pediatric
annals, vol. 35, no. 8, pp. 565–571, 2006.
[18]
G. L. Blackman, R. Ostrander, and K. C. Herman, “Children with ADHD and depression: a
multisource, multimethod assessment of clinical, social, and academic functioning.,” Journal
of attention disorders, vol. 8, no. 4, pp. 195–207, May 2005.
[19]
J. Biederman, M. C. Monuteaux, E. Mick, T. Spencer, T. E. Wilens, J. M. Silva, L. E. Snyder, and
S. V Faraone, “Young adult outcome of attention deficit hyperactivity disorder: a controlled
10-year follow-up study.,” Psychological medicine, vol. 36, no. 2, pp. 167–79, Feb. 2006.
[20]
R. C. Kessler, L. Adler, R. Barkley, J. Biederman, C. K. Conners, O. Demler, S. V Faraone, L. L.
Greenhill, M. J. Howes, K. Secnik, T. Spencer, T. B. Ustun, E. E. Walters, and A. M. Zaslavsky,
“The prevalence and correlates of adult ADHD in the United States: results from the National
Comorbidity Survey Replication.,” The American journal of psychiatry, vol. 163, no. 4, pp. 716–
23, Apr. 2006.
[21]
T. W. Miller, J. T. Nigg, and S. V. Faraone, “Axis I and II comorbidity in adults with ADHD.,”
Journal of abnormal psychology, vol. 116, no. 3, p. 519, 2007.
[22]
E. Sobanski, D. Brüggemann, B. Alm, S. Kern, M. Deschner, T. Schubert, A. Philipsen, and M.
Rietschel, “Psychiatric comorbidity and functional impairment in a clinically referred sample of
adults with attention-deficit/hyperactivity disorder (ADHD).,” European archives of psychiatry
and clinical neuroscience, vol. 257, no. 7, pp. 371–7, Oct. 2007.
[23]
E. Sobanski, M. Schredl, N. Kettler, and B. Alm, “Sleep in adults with attention deficit
hyperactivity disorder (ADHD) before and during treatment with methylphenidate: a
controlled polysomnographic study.,” Sleep, vol. 31, no. 3, pp. 375–81, Mar. 2008.
[24]
B. J. Casey, N. Tottenham, and J. Fossella, “Clinical, imaging, lesion, and genetic approaches
toward a model of cognitive control.,” Developmental psychobiology, vol. 40, no. 3, pp. 237–
54, Apr. 2002.
[25]
E. Sonuga-Barke, P. Bitsakou, and M. Thompson, “Beyond the Dual Pathway Model: Evidence
for the Dissociation of Timing, Inhibitory, and Delay-Related Impairments in Attention25
Deficit/Hyperactivity Disorder,” Journal of the American Academy of Child & Adolescent
Psychiatry, vol. 49, no. 4, pp. 345–355, Apr. 2010.
[26]
L. J. Kasper, R. M. Alderson, and K. L. Hudec, “Moderators of working memory deficits in
children with attention-deficit/hyperactivity disorder (ADHD): a meta-analytic review.,”
Clinical psychology review, vol. 32, no. 7, pp. 605–17, Nov. 2012.
[27]
P. de Zeeuw, J. Weusten, S. van Dijk, J. van Belle, and S. Durston, “Deficits in cognitive control,
timing and reward sensitivity appear to be dissociable in ADHD.,” PloS one, vol. 7, no. 12, p.
e51416, Jan. 2012.
[28]
T. W. Frazier, H. a Demaree, and E. a Youngstrom, “Meta-analysis of intellectual and
neuropsychological test performance in attention-deficit/hyperactivity disorder.,”
Neuropsychology, vol. 18, no. 3, pp. 543–55, Jul. 2004.
[29]
J. Kuntsi, T. C. Eley, a Taylor, C. Hughes, P. Asherson, a Caspi, and T. E. Moffitt, “Co-occurrence
of ADHD and low IQ has genetic origins.,” American journal of medical genetics. Part B,
Neuropsychiatric genetics : the official publication of the International Society of Psychiatric
Genetics, vol. 124B, no. 1, pp. 41–7, Jan. 2004.
[30]
J. R. M. Jepsen, B. Fagerlund, and E. L. Mortensen, “Do attention deficits influence IQ
assessment in children and adolescents with ADHD?,” Journal of attention disorders, vol. 12,
no. 6, pp. 551–62, May 2009.
[31]
S. van der Oord, P. J. M. Prins, J. Oosterlaan, and P. M. G. Emmelkamp, “Treatment of
attention deficit hyperactivity disorder in children. Predictors of treatment outcome.,”
European child & adolescent psychiatry, vol. 17, no. 2, pp. 73–81, Mar. 2008.
[32]
J. M. Swanson, S. P. Hinshaw, L. E. Arnold, R. D. Gibbons, S. Marcus, K. Hur, P. S. Jensen, B.
Vitiello, H. B. Abikoff, L. L. Greenhill, L. Hechtman, W. E. Pelham, K. C. Wells, C. K. Conners, J.
S. March, G. R. Elliott, J. N. Epstein, K. Hoagwood, B. Hoza, B. S. G. Molina, J. H. Newcorn, J. B.
Severe, and T. Wigal, “Secondary evaluations of MTA 36-month outcomes: propensity score
and growth mixture model analyses.,” Journal of the American Academy of Child and
Adolescent Psychiatry, vol. 46, no. 8, pp. 1003–14, Aug. 2007.
[33]
C. Spearman, “‘ General Intelligence,’ Objectively Determined and Measured,” The American
Journal of Psychology, vol. 15, no. 2, pp. 201–292, 1904.
[34]
I. J. Deary, P. J. Bell, A. J. Bell, M. L. Campbell, and N. D. Fazal, “Sensory discrimination and
intelligence: testing Spearman’s other hypothesis.,” The American journal of psychology, vol.
117, no. 1, pp. 1–18, Jan. 2004.
[35]
L. D. Sheppard and P. a. Vernon, “Intelligence and speed of information-processing: A review
of 50 years of research,” Personality and Individual Differences, vol. 44, no. 3, pp. 535–551,
Feb. 2008.
[36]
W. Johnson, J. te Nijenhuis, and T. J. Bouchard, “Still just 1 g: Consistent results from five test
batteries,” Intelligence, vol. 36, no. 1, pp. 81–95, Jan. 2008.
26
[37]
M. McDaniel, “Big-brained people are smarter: A meta-analysis of the relationship between in
vivo brain volume and intelligence,” Intelligence, vol. 33, no. 4, pp. 337–346, Jul. 2005.
[38]
F. V Rijsdijk, P. A. Vernon, and D. I. Boomsma, “Application of hierarchical genetic models to
Raven and WAIS subtests: a Dutch twin study.,” Behavior genetics, vol. 32, no. 3, pp. 199–210,
May 2002.
[39]
T. Strenze, “Intelligence and socioeconomic success: A meta-analytic review of longitudinal
research,” Intelligence, vol. 35, no. 5, pp. 401–426, Sep. 2007.
[40]
C. M. Calvin, I. J. Deary, C. Fenton, B. A. Roberts, G. Der, N. Leckenby, and G. D. Batty,
“Intelligence in youth and all-cause-mortality: systematic review with meta-analysis.,”
International journal of epidemiology, vol. 40, no. 3, pp. 626–44, Jun. 2011.
[41]
C. R. Gale, G. D. Batty, P. Tynelius, I. J. Deary, and F. Rasmussen, “Intelligence in early
adulthood and subsequent hospitalization for mental disorders.,” Epidemiology (Cambridge,
Mass.), vol. 21, no. 1, pp. 70–7, Jan. 2010.
[42]
P. Moran and B. Klinteberg, “Brief report: childhood intelligence predicts hospitalization with
personality disorder in adulthood: evidence from a population-based study in Sweden,”
Journal of personality …, vol. 23, no. 5, pp. 535–540, 2009.
[43]
D. a Treffert, “The savant syndrome: an extraordinary condition. A synopsis: past, present,
future.,” Philosophical transactions of the Royal Society of London. Series B, Biological
sciences, vol. 364, no. 1522, pp. 1351–7, May 2009.
[44]
M. Neihart, “The impact of giftedness on psychological well•being: What does the empirical
literature say?,” Roeper Review, vol. 22, no. 1, pp. 10–17, 1999.
[45]
S. M. Reis and D. B. McCoach, “The Underachievement of Gifted Students: What Do We Know
and Where Do We Go?,” Gifted Child Quarterly, vol. 44, no. 3, pp. 152–170, Jul. 2000.
[46]
J. Grobman, “Underachievement in exceptionally gifted adolescents and young adults: A
psychiatrist’s view,” Prufrock Journal, vol. XVII, no. 4, pp. 199–210, 2006.
[47]
K. Dabrowski and M. M. Piechowski, Theory of levels of emotional development. Oceanside,
NY: Dabor Science, 1977.
[48]
M. M. Piechowski and N. Colangole, “Development potential of the gifted,” Gifted Child
Quarterly, vol. 28, no. 2, pp. 80–88, 1984.
[49]
H.-J. Chang and C.-C. Kuo, “Overexcitabilities: Empirical studies and application,” Learning and
Individual Differences, vol. 23, pp. 53–63, Feb. 2013.
[50]
K. Sandal-Miller, “A comparison of Darbowski’s concept of overexcitabilities with measures of
verbal and mathematical aptitude among academically precocious adolescents.,” University of
Denver, 1988.
[51]
D. Morisano and B. M. Shore, “Can Personal Goal Setting Tap the Potential of the Gifted
Underachiever?,” Roeper Review, vol. 32, no. 4, pp. 249–258, Sep. 2010.
27
[52]
V. Vlahovic-Stetic, V. V. Vidovic, and L. Arambasic, “Motivational Characteristics in
Mathematical Achievement: a study of gifted high‐achieving, gifted underachieving and non‐
gifted pupils,” High Ability Studies, vol. 10, no. 1, pp. 37–49, Jun. 1999.
[53]
R. Abelman, “Fighting the war on indecency: Mediating TV, internet, and videogame usage
among achieving and underachieving gifted children,” Roeper Review, vol. 29, no. 2, pp. 100–
112, 2006.
[54]
S. M. Reis and D. B. McCoach, “Underachievement in Gifted and Talented Students With
Special Needs,” Exceptionality, vol. 10, no. 2, pp. 113–125, Jun. 2002.
[55]
A. L. Duckworth, P. D. Quinn, D. R. Lynam, R. Loeber, and M. Stouthamer-Loeber, “Role of test
motivation in intelligence testing.,” Proceedings of the National Academy of Sciences of the
United States of America, vol. 108, no. 19, pp. 7716–20, May 2011.
[56]
T. E. Brown, “Executive function impairments in high IQ children and adolescents with ADHD,”
Open Journal of Psychiatry, vol. 01, no. 02, pp. 56–65, 2011.
[57]
J. M. Langberg, J. N. Epstein, M. Altaye, B. S. G. Molina, L. E. Arnold, and B. Vitiello, “The
transition to middle school is associated with changes in the developmental trajectory of
ADHD symptomatology in young adolescents with ADHD.,” Journal of clinical child and
adolescent psychology : the official journal for the Society of Clinical Child and Adolescent
Psychology, American Psychological Association, Division 53, vol. 37, no. 3, pp. 651–63, Jul.
2008.
[58]
P. Shaw, D. Greenstein, J. Lerch, L. Clasen, R. Lenroot, N. Gogtay, a Evans, J. Rapoport, and J.
Giedd, “Intellectual ability and cortical development in children and adolescents.,” Nature,
vol. 440, no. 7084, pp. 676–9, Mar. 2006.
[59]
A. L. Krain and F. X. Castellanos, “Brain development and ADHD.,” Clinical psychology review,
vol. 26, no. 4, pp. 433–44, Aug. 2006.
[60]
L. Wang, C. Zhu, Y. He, Y. Zang, Q. Cao, H. Zhang, Q. Zhong, and Y. Wang, “Altered small-world
brain functional networks in children with attention-deficit/hyperactivity disorder.,” Human
brain mapping, vol. 30, no. 2, pp. 638–49, Feb. 2009.
[61]
P. D. Zelazo and U. Müller, Executive function in typical and atypical development. Blackwell
Publishing, 2002.
[62]
K. Rubia, R. Halari, A. Cubillo, A.-M. Mohammad, M. Brammer, and E. Taylor,
“Methylphenidate normalises activation and functional connectivity deficits in attention and
motivation networks in medication-naïve children with ADHD during a rewarded continuous
performance task.,” Neuropharmacology, vol. 57, no. 7–8, pp. 640–52, Dec. 2009.
[63]
K. Rubia, A. Cubillo, A. B. Smith, J. Woolley, I. Heyman, and M. J. Brammer, “Disorder-specific
dysfunction in right inferior prefrontal cortex during two inhibition tasks in boys with
attention-deficit hyperactivity disorder compared to boys with obsessive-compulsive
disorder.,” Human brain mapping, vol. 31, no. 2, pp. 287–99, Feb. 2010.
28
[64]
T. Nakao, J. Radua, K. Rubia, and D. Mataix-Cols, “Gray matter volume abnormalities in ADHD:
voxel-based meta-analysis exploring the effects of age and stimulant medication.,” The
American journal of psychiatry, vol. 168, no. 11, pp. 1154–63, Nov. 2011.
[65]
I. J. Deary, “Intelligence.,” Annual review of psychology, vol. 63, pp. 453–82, Jan. 2012.
[66]
S. Karama, Y. Ad-Dab’bagh, and R. Haier, “Positive association between cognitive ability and
cortical thickness in a representative US sample of healthy 6 to 18 year-olds,” Intelligence, vol.
37, no. 2, pp. 145–155, 2009.
[67]
R. J. Haier, B. V. Siegel, K. H. Nuechterlein, E. Hazlett, J. C. Wu, J. Paek, H. L. Browning, and M.
S. Buchsbaum, “Cortical glucose metabolic rate correlates of abstract reasoning and attention
studied with positron emission tomography,” Intelligence, vol. 12, no. 2, pp. 199–217, Apr.
1988.
[68]
R. J. Haier, R. E. Jung, R. a Yeo, K. Head, and M. T. Alkire, “The neuroanatomy of general
intelligence: sex matters.,” NeuroImage, vol. 25, no. 1, pp. 320–7, Mar. 2005.
[69]
A. C. Neubauer and A. Fink, “Intelligence and neural efficiency.,” Neuroscience and
biobehavioral reviews, vol. 33, no. 7, pp. 1004–23, Jul. 2009.
[70]
M. P. van den Heuvel, C. J. Stam, R. S. Kahn, and H. E. Hulshoff Pol, “Efficiency of functional
brain networks and intellectual performance.,” The Journal of neuroscience : the official
journal of the Society for Neuroscience, vol. 29, no. 23, pp. 7619–24, Jun. 2009.
[71]
R. J. Haier, R. Colom, D. H. Schroeder, C. a. Condon, C. Tang, E. Eaves, and K. Head, “Gray
matter and intelligence factors: Is there a neuro-g?,” Intelligence, vol. 37, no. 2, pp. 136–144,
Mar. 2009.
[72]
A. C. Neubauer and A. Fink, “Intelligence and neural efficiency: Measures of brain activation
versus measures of functional connectivity in the brain,” Intelligence, vol. 37, no. 2, pp. 223–
229, Mar. 2009.
[73]
R. E. Jung and R. J. Haier, “The Parieto-Frontal Integration Theory (P-FIT) of intelligence:
converging neuroimaging evidence.,” The Behavioral and brain sciences, vol. 30, no. 2, pp.
135–54; discussion 154–87, May 2007.
[74]
I. J. Deary, L. Penke, and W. Johnson, “The neuroscience of human intelligence differences.,”
Nature reviews. Neuroscience, vol. 11, no. 3, pp. 201–11, Mar. 2010.
[75]
I. J. Deary, F. M. Spinath, and T. C. Bates, “Genetics of intelligence.,” European journal of
human genetics, vol. 14, no. 6, pp. 690–700, Jun. 2006.
[76]
A. Turken, S. Whitfield-Gabrieli, R. Bammer, J. V Baldo, N. F. Dronkers, and J. D. E. Gabrieli,
“Cognitive processing speed and the structure of white matter pathways: convergent
evidence from normal variation and lesion studies.,” NeuroImage, vol. 42, no. 2, pp. 1032–44,
Aug. 2008.
[77]
Y. Li, Y. Liu, J. Li, W. Qin, K. Li, C. Yu, and T. Jiang, “Brain anatomical network and intelligence.,”
PLoS computational biology, vol. 5, no. 5, p. e1000395, May 2009.
29
[78]
M. Dennis, D. Francis, P. Cirino, R. Schachar, M. Barnes, and J. Fletcher, “Why IQ is not a
covariate in cognitive studies of neurodevelopmental disorders,” Journal of the International
Neuropsychological Society, vol. 15, no. 3, pp. 331–343, 2009.
[79]
P. de Zeeuw, H. G. Schnack, J. van Belle, J. Weusten, S. van Dijk, M. Langen, R. M. Brouwer, H.
van Engeland, and S. Durston, “Differential brain development with low and high IQ in
attention-deficit/hyperactivity disorder.,” PloS one, vol. 7, no. 4, p. e35770, Jan. 2012.
[80]
T. J. C. Polderman, M. F. Gosso, D. Posthuma, T. C. E. M. Van Beijsterveldt, P. Heutink, F. C.
Verhulst, and D. I. Boomsma, “A longitudinal twin study on IQ, executive functioning, and
attention problems during childhood and early adolescence,” Acta neurol. belg, vol. 106, pp.
191–207, 2006.
[81]
I. R. Gizer, C. Ficks, and I. D. Waldman, “Candidate gene studies of ADHD: a meta-analytic
review.,” Human genetics, vol. 126, no. 1, pp. 51–90, Jul. 2009.
[82]
A. Thapar, M. Cooper, R. Jefferies, and E. Stergiakouli, “What causes attention deficit
hyperactivity disorder?,” Archives of disease in childhood, vol. 97, no. 3, pp. 260–5, Mar. 2012.
[83]
J. Mill, A. Caspi, B. S. Williams, I. Craig, A. Taylor, M. Polo-Tomas, C. W. Berridge, R. Poulton,
and T. E. Moffitt, “Prediction of heterogeneity in intelligence and adult prognosis by genetic
polymorphisms in the dopamine system among children with attention-deficit/hyperactivity
disorder,” Archives of general psychiatry, vol. 63, no. 4, pp. 462–9, Apr. 2006.
[84]
A. Thapar, M. Cooper, O. Eyre, and K. Langley, “Practitioner Review: What have we learnt
about the causes of ADHD?,” Journal of child psychology and psychiatry, and allied disciplines,
vol. 1, pp. 3–16, Sep. 2012.
[85]
K. Brookes, X. Xu, W. Chen, K. Zhou, B. Neale, N. Lowe, R. Anney, R. Aneey, B. Franke, M. Gill,
R. Ebstein, J. Buitelaar, P. Sham, D. Campbell, J. Knight, P. Andreou, M. Altink, R. Arnold, F.
Boer, C. Buschgens, L. Butler, H. Christiansen, L. Feldman, K. Fleischman, E. Fliers, R. HoweForbes, A. Goldfarb, A. Heise, I. Gabriëls, I. Korn-Lubetzki, L. Johansson, R. Marco, S. Medad, R.
Minderaa, F. Mulas, U. Müller, A. Mulligan, K. Rabin, N. Rommelse, V. Sethna, J. Sorohan, H.
Uebel, L. Psychogiou, A. Weeks, R. Barrett, I. Craig, T. Banaschewski, E. Sonuga-Barke, J.
Eisenberg, J. Kuntsi, I. Manor, P. McGuffin, A. Miranda, R. D. Oades, R. Plomin, H. Roeyers, A.
Rothenberger, J. Sergeant, H.-C. Steinhausen, E. Taylor, M. Thompson, S. V Faraone, and P.
Asherson, “The analysis of 51 genes in DSM-IV combined type attention deficit hyperactivity
disorder: association signals in DRD4, DAT1 and 16 other genes.,” Molecular psychiatry, vol.
11, no. 10, pp. 934–53, Oct. 2006.
[86]
O. Davis, C. Haworth, and R. Plomin, “Dramatic Increase in Heritability of Cognitive
Development from Early to Middle Childhood An 8-Year Longitudinal Study of 8,700 Pairs of
Twins,” Psychological Science, vol. 20, no. 10, pp. 1301–1309, 2009.
[87]
E. Turkheimer and A. Haley, “Socioeconomic status modifies heritability of IQ in young
children,” Psychological …, vol. 14, no. 6, pp. 623–628, 2003.
[88]
A. Payton, “The impact of genetic research on our understanding of normal cognitive ageing:
1995 to 2009.,” Neuropsychology review, vol. 19, no. 4, pp. 451–77, Dec. 2009.
30
[89]
N. M. Wisdom, J. L. Callahan, and K. a Hawkins, “The effects of apolipoprotein E on nonimpaired cognitive functioning: a meta-analysis.,” Neurobiology of aging, vol. 32, no. 1, pp.
63–74, Jan. 2011.
[90]
G. Davies, A. Tenesa, A. Payton, and J. Yang, “Genome-wide association studies establish that
human intelligence is highly heritable and polygenic,” Molecular …, vol. 16, no. 10, pp. 996–
1005, 2011.
[91]
N. N. J. Rommelse, M. E. Altink, J. Oosterlaan, C. J. M. Buschgens, J. Buitelaar, and J. a
Sergeant, “Support for an independent familial segregation of executive and intelligence
endophenotypes in ADHD families.,” Psychological medicine, vol. 38, no. 11, pp. 1595–606,
Nov. 2008.
[92]
A. Wood and F. Rijsdijk, “The relationship between ADHD and key cognitive phenotypes is not
mediated by shared familial effects with IQ,” Psychological …, vol. 41, no. 4, pp. 861–871,
2011.
[93]
A. Wood, “Separation of genetic influences on attention deficit hyperactivity disorder
symptoms and reaction time performance from those on IQ,” Psychological …, vol. 40, no. 6,
pp. 1027–1037, 2010.
[94]
K. M. Antshel, S. V Faraone, K. Maglione, A. E. Doyle, R. Fried, L. J. Seidman, and J. Biederman,
“Executive functioning in high-IQ adults with ADHD.,” Psychological medicine, vol. 40, no. 11,
pp. 1909–18, Nov. 2010.
[95]
F. Falk, M. Piechowski, and S. Lind, “Criteria for rating the intensity of overexcitabilities,”
University of Akron, 1994.
31
Appendix
Appendix 1
OVEREXCITABILITIES (Adapted from Falk, Piechowski, & Lind, 1994)
Psychomotor




Heightened excitability of the neuromuscular system
Capacity for being active and energetic; Love of movement for its own sake
Organic surplus of energy [Rapid speech; marked excitation; intense physical activity; need
for action]
Psychomotor expression of emotional tension [Compulsive talking and chattering; impulsive
actions; acting out; nervous habits (tics, nail biting); drive; workaholicism; organizing;
competitiveness]
Sensual




Heightened experience of sensual pleasure or displeasure [Seeing; smelling; tasting;
touching; hearing]
Intense sexuality
Sensual expression & outlets for emotional tension [Overeating; buying sprees; seeking the
limelight]
Aesthetic pleasures [Appreciation of beautiful objects, words, music, form, color, balance]
Intellectual





Heightened need to seek understanding and truth, to gain knowledge, analyze and
synthesize
Intensified activity of the mind [Curiosity; concentration; capacity for sustained intellectual
effort; avid reading; keen observation; detailed planning; detailed visual recall]
Penchant for probing questions; problem solving [Search for truth, understanding; tenacity in
problem solving]
Preoccupation with logic and theoretical thinking [Love of theory and analysis; thinking about
thinking; non-judgmental introspection; moral thinking; conceptual and intuitive integration;
independence of thought (sometimes criticism)]
Development of new concepts
32
Imaginational




Heightened play of the imagination
Rich association of images and impressions (real and imagined) [Frequent use of image and
metaphor; facility for invention and fantasy; detailed visualization; poetic and dramatic
perception; animistic thinking; magical thinking]
Spontaneous imagery as an expression of emotional tension [Animistic imagery; mixing truth
and fiction; elaborate dreams; illusions]
Capacity for living in a world of fantasy [predilection for fairy and magic tales; creation of
private worlds, imaginary companions; dramatization]
Emotional





Heightened, intense positive and negative feelings [Extremes of emotion; complex emotions
and feelings; identification with others' feelings; high degree of differentiation of
interpersonal feeling; awareness of range and intensity of feelings]
Somatic expressions [tense stomach; sinking heart; blushing; flushing, pounding heart,
sweaty palms]
Strong affective expressions [Inhibition (timidity, shyness); ecstasy, euphoria, pride; strong
affective memory; feelings of unreality, fears and anxieties; feelings of guilt; concern with
death; depressive and suicidal moods]
Capacity for strong attachments and deep relationships [strong emotional ties and
attachments to persons, living things, places; compassion, responsiveness to others;
empathy; sensitivity in relationships; difficulty adjusting to new environments; loneliness;
conflicts with others over depth of relationship; intense desire to offer love]
Well differentiated feelings toward self [Awareness of one’s real self; inner dialogue and selfjudgment]
33
Appendix 2
Common characteristics of gifted underachievers [45]
Personality characteristics









Low self-esteem, low self-concept, low self-efficacy.
Alienated or withdrawn; distrustful, or pessimistic.
Anxious, impulsive, inattentive, hyperactive, or distractible; may exhibit ADD or ADHD
symptoms.
Aggressive, hostile, resentful, or touchy.
Depressed.
Passive-aggressive trait disturbance.
More socially than academically oriented. May be extroverted. May be easygoing,
considerate, and/or unassuming.
Dependent, less resilient than high achievers.
Socially immature.
Internal Mediators






Fear of failure; gifted underachievers may avoid competition or challenging situations to
protect their self-image or their ability.
Fear of success.
Attribute successes or failures to outside forces; exhibit an external locus of control, attribute
successes to luck and failures to lack of ability; externalize conflict and problems.
Negative attitude toward school.
Antisocial or rebellious.
Self-critical or perfectionistic; feeling guilty about not living up to the expectations of others.
Differential Thinking Skills/ Styles



Perform less well on tasks that require detail-oriented or convergent thinking skills than their
achieving counterparts.
Score lower on sequential tasks such as repeating digits, repeating sentences, coding,
computation, and spelling.
Lack insight and critical ability.
34
Maladaptive Strategies




Lack goal-directed behavior; fail to set realistic goals for themselves.
Poor coping skills; develop coping mechanisms that successfully reduce short-term stress,
but inhibit long-term success.
Possess poor self-regulation strategies; low tolerance for frustration; lack perseverance; lack
self-control.
Use defense mechanisms.
Positive Attributes



Intense outside interests, commitment to self-selected work.
Creative.
Demonstrate honesty and integrity in rejecting unchallenging coursework.
35
Appendix 3
Similarities ADHD giftedness (Maud van Thiel, 2010)
ADHD
HOGE INTELLIGENTIE
Aandachtstekort
geen aandacht voor details; maakt achteloze
fouten
er valt geen reden voor te ontdekken,
onverklaarbaar
sommige vormen van hoge intelligentie zijn juist
niet gericht op precisie, maar veel meer op de
grote lijn
moeite met vasthouden van aandacht
in nagenoeg alles situaties, dus ook in situaties die
in principe de belangstelling genieten
in specifieke situaties, desinteresse bij thema's die
te simpel of reeds bekend zijn, gaan dan
dagdromen
luistert niet wanneer aangesproken
ten gevolge van ongedifferentieerde chaos in hoofd omdat ze met interessantere dingen bezig zijn, op
een consistente manier diep in gedachten
verzonken
volgt instructies niet op
omdat ze vergeten worden; problemen met
aanpassing aan regels en voorschriften in het
algemeen
omdat ze niet zinnig geacht worden; alleen
aanpassing aan regels die begrepen en
geaccepteerd worden actief regels: gewoonten en
tradities aan de kaak te stellen, intens willen weten
waarom
kan taken en activiteiten niet organiseren
terwijl ze dit wel willen, kunnen het overzicht niet
krijgen
alleen wanneer ze het niet willen, als ze de
ordening niet nodig of zinloos vinden
gering doorzettingsvermogen
geen doorzettingsvermogen bij taken die niet
onmiddellijk negatieve sancties tot gevolg hebben
geen doorzettingsvermogen bij taken die niet
relevant lijken
raakt dingen kwijt, vergeetachtig
ten gevolge van chaos
omdat ze (op een consistente manier) met andere
dingen bezig zijn
36
snel afgeleid
dwaalt zonder reden af, op zoek naar afleiders
afgeleid door sensitieve prikkels (geuren, geluiden,
bewegingen)
Hyperactiviteit
wriemelen en wiebelen, staat steeds op en gaat
lopen, wanneer dat niet de bedoeling is, ongepast
rennen en klimmen
rusteloos zonder doel, 'op drift geslagen',
'springveer' die afloopt; in veel situaties
gevolg van desinteresse; proberen verveling te
bestrijden en concentratie te bevorderen door
zichzelf anderszins te prikkelen (kauwgom kauwen
verhoogt concentratie); in bepaalde situaties
onuitputtelijk energiek
zonder doel, telkens van doel veranderend
niet rusten voordat doel bereikt is, doel
vasthouden, gevolg van intensiteit en
nieuwsgierigheid
Impusliviteit
voortijdig antwoord geven
gokken, klok en klepel, er vaak naast zitten
meestal goed zitten, precies weten waar het om
gaat
kan niet op beurt wachten
vertoont in nagenoeg alle situaties een ongericht
gebrek aan geduld, algemene geringe
frustratietolerantie
ongeduldig door inhoudelijk enthousiasme en uit
nieuwsgierigheid
verstoren van spel of andermans bezigheden
zonder doel en zonder begrip van of belangstelling
voor datgene waarmee de anderen bezig zijn
uit inhoudelijk ongeduld, omdat ze sneller verder
willen; goed begrip van waar de anderen mee
bezig zijn of waar het om gaat, wat het doel is
ongepaste vragen stellen
gering vermogen om iets uit te stellen zonder
aangegeven/aanwijsbare reden
met aanwijsbare reden: de intellectuele
nieuwsgierigheid wint het van het sociaal
oordeelsvermogen
37