DEVELOPMENTAL NEUROPSYCHOLOGY, 35(5), 475–493

Copyright © 2010 Taylor & Francis Group, LLC

ISSN: 8756-5641 print / 1532-6942 online
DOI: 10.1080/875656412010494748

Comorbidity of ADHD and Dyslexia

Eva Germanò and Antonella Gagliano

Division of Child Neurology and Psychiatry
Pediatric Department of Policlinico G. Martino, University of Messina
Gazzi-Messina, Italy

Paolo Curatolo
Pediatric Neurology Unit, Tor Vergata, Department of Neuroscience
University of Rome, Roma, Italy

Comorbidity of attention deficit hyperactivity disorder (ADHD) and reading disorder (RD) is fre-
quent. Comorbid subjects show a neuropsychological profile characterized by failure of various cog-
nitive functions with an additive-effect that can determine more severe functional deficits. Comorbid
RD may be a marker for a group of children with ADHD with more severe cognitive deficits, and a
worse neuropsychological, academic, and behavioral outcome. The article focuses on the link be-
tween RD and ADHD from an epidemiological, genetic, neurofunctional, neuropsychological, and
therapeutic perspective and summarizes the characteristics of the comorbid phenotype.

Reading disability (RD) and attention deficit hyperactivity disorder (ADHD) are two of the most
common disorders diagnosed in childhood and each of them occurs in approximately 5% of the
population (Diagnostic and Statistical Manual of Mental Disorders–Text Revision; American
Psychiatric Association, 2000). Over 80% of children with ADHD and 60% of children with RD
meet the criteria for at least one additional diagnosis (Willcutt & Pennington, 2000a, 2000b). RD,
commonly referred to as dyslexia, is defined as an unexpected, specific, and persistent failure to
acquire efficient reading skills despite conventional instruction, adequate intelligence, and socio-
cultural opportunity (APA, 2000). ADHD is one of the most prevalent developmental disorders,
characterized by excessive activity, short attention span, and impulsivity (APA, 2000). Recent ad-
vances from neuroimaging and molecular genetics have improved our understanding of the
neurobiology of ADHD (Curatolo, Paloscia, D’Agati, Moavero, & Pasini, 2008).
ADHD is a highly comorbid condition (Gillberg et al., 2004; Banaschewski, Neale, Rothen-
berger, & Roessner, 2007). Psychiatric comorbidities include oppositional defiant disorder, con-
duct disorder, anxiety, and depression (Jensen et al., 2001). Other types of comorbidities reported
are RD, developmental coordination disorder, and language disorder (Gilger, Pennington, &
DeFries, 1992; Cohen et al., 2000). Among psychiatric disorders, ADHD is the most frequently
associated with dyslexia (Kronenberger & Dunn, 2003). Attention and learning problems usually

Correspondence should be addressed to Antonella Gagliano, M.D., Division of Child Neurology and Psychiatry, Pedi-
atric Department of Policlinico G. Martino, University of Messina, Via Consolare Valeria, 98125 Gazzi-Messina, Italy.
E-mail: antonella.gagliano@unime.it
476 GERMANÒ, GAGLIANO, CURATOLO

are considered inter-related and on a continuum (Mayes, Calhoun & Crowell, 2000). Between the
two disorders there is a bidirectional relationship since the comorbidity is very high if one exam-
ines children with dyslexia for ADHD (Willcutt & Pennington, 2000a) or children with ADHD
for dyslexia (Sanson, Prior & Smart, 1996). Reading difficulties appears to be strongly related
with the predominantly inattentive type of ADHD rather than hyperactivity or impulsivity
(Willcutt & Pennington, 2000b). Furthermore, in ADHD subjects a disability in written expres-
sion seems more common (Mayes & Calhoun, 2007). Based on Mayes and coll. evidences, chil-
dren with reading, math, or spelling deficits plus ADHD have more severe learning and attention
problems than children with only one of the two conditions. Some studies have suggested that
comorbid RD may be a marker for a group of children with ADHD with more severe cognitive
deficits; these children are more impaired on both executive and nonexecutive functions (Purvis
& Tannock, 2000; Seidman, Biederman, Monuteaux, Coyle, & Faraone, 2001; Willcutt et al.,
2001; Willcutt, Doyle, Nigg, Faraone & Pennington, 2005a).
ADHD females may be less vulnerable to the executive deficits displayed by boys (Seidman et
al., 1997), although further studies missed to detect a gender difference on intentional and execu-
tive functions (Rucklidge & Tannock, 2002). According to other studies, RD was significantly as-
sociated with inattention in both girls and boys, but with hyperactivity/impulsivity (H/I) only in
boys (Willcutt & Pennington, 2000a). Furthermore, the hyperactive and impulsive behaviors ex-
hibited by boys with RD may be more disruptive than the inattentive behaviors exhibited by girls,
and may therefore be a more frequent cause for clinical referrals. According to these authors, this
condition could partially explain the discrepancy between the gender ratio in referred RD children
(approximately 4 boys to 1 girl)
Children with comorbid problems have more secondary problems, such as low self-esteem, be-
havioral problems, and dropping out of school, and a worse outcome compared with children diag-
nosed with only ADHD or RD (Willcutt et al., 2001). Moreover, individuals with comorbid RD and
ADHD are at higher risk of other disruptive disorders (Willcutt & Pennington, 2000b). There was
some evidence consistent with the possibility that RD might have effects on behavioral outcome of
comorbid children; RD might contribute to the persistence of features of conduct disorder in chil-
dren with comorbid problems (Chadwick, Taylor, Taylor, Heptinstall, & Danckaerts, 1999). There-
fore, early identification and intervention are important to improve the outcome of affected subjects.
In this review we focused on the link between RD and ADHD from an epidemiological, ge-
netic, neurofunctional, neuropsychological, and therapeutic perspective and summarized the
characteristics of the comorbid phenotype.

EPIDEMIOLOGICAL FINDINGS

The comorbidity of ADHD and RD is found in both clinical and community samples (Gilger et al.,
1992). These disorders co-occur more often than would be expected on the basis of chance, indi-
cating that this comorbidity is not a consequence of selection bias. Although the extent of the
overlap has inevitably varied from study to study depending on the definition of reading disability
and the criteria used in identifying hyperactivity, the association between them is not really in
doubt. In samples of subjects with ADHD, the rate of RD is between 18–45% (August &
Garfinkel, 1990; Dykman & Ackerman, 1991; Mayes et al., 2000; Semrud-Clickeman et al., 992;
Loo et al., 2004; Wisniewska, Baranowska, & Wendorff, 2007), whereas in samples of RD chil-
 ADHD AND DYSLEXIA 477

dren, 18–42% also meet criteria for ADHD (Gayan et al., 2005; Gilger et al., 1992; Willcutt &
Pennington, 2000b). Table 1 summarizes epidemiological data concerning this association. The
wide variability of overlapping percentage is most likely due to different reasons. First, children
with ADHD are assessed with different clinical instruments, and recruited using different diag-
nostic criteria (DSM or International Classification of Disease-Tenth Revision [ICD-10]). Fur-
thermore, the definition of RD varied from study to study and the most conventional and widely
used indicator of RD (discrepancy between IQ and achievement test scores) is not always used in
the determination of RD. Moreover, the prevalence of dyslexia varies across different cultures de-
pending on the complexity of the orthographic rules.

GENETIC FINDINGS

Several family and twin studies have demonstrated that both RD and ADHD are heritable
(Dell’homme, Kim, Loo, Yang, & Smalley, 2007; Friedman, Chhabildas, Budhiraja, Willcutt, &
Pennington, 2003; Gayan & Olson, 2001; Willcutt, Pennington & DeFries, 2000c). Heritability
estimates of ADHD are generally in the range of 70–80% (Faraone et al., 2005); the mean
heritability for ADHD was shown to be 77% (Biederman, 2005). Similarly high estimates of
heritability have been found for RD (40–60%) (Gayan & Olson, 1999; Ziegler et al., 2005).
Targeted linkage and association analyses and genome scans, carried out independently for RD
and ADHD, have identified potential susceptibility loci that may increase the risk of being af-
fected with a disorder. To date, linkage analyses in families with dyslexia have identified nine
chromosome regions—dyslexia susceptibility 1 (DYX1), dyslexia susceptibility 9 (DYX
9)—listed by the HUGO Gene Nomenclature Committee in which the presence of susceptibility
genes is suspected. Furthermore, linkage findings in dyslexia are relatively consistent across stud-
ies in comparison to findings for other neuropsychiatric disorders. This is particularly true for
chromosome regions 6p21–p22 (DYX2), 15q21(DYX1), and 1p34–p36 (DYX8) (Chapman et
al., 2004; Cope et al., 2005; Grigorenko et al., 2001, 2003).
Six independent genome-wide ADHD linkage scans have been conducted. Several novel
genomic regions might harbor ADHD susceptibility genes, with the most prominent findings on

TABLE 1
Epidemiological Data

Author Cases RD in ADHD ADHD in RD

August & Garfinkel, 1990 115 boys ADHD 39%

Dykman & Ackerman, 1991 182 ADHD 45%
Semrud-Clikeman et al., 1992 60 ADHD 38%
Ginger et al., 1992 140 RD 39%
Willcutt & Pennington, 2000 209 RD 42% in males
18% in females
Mayes et al., 2000 86 ADHD 26%
Loo et al., 2004 407 ADHD 18-23%
Gayan et al., 2005 505 RD 36%
Wisniewska et al., 2007 28 ADHD 18%

ADHD = attention deficit hyperactivity disorder; RD = reading disorder.

478 GERMANÒ, GAGLIANO, CURATOLO

chromosomes 5p and 17p being detected in several studies (Arcos-Burgos et al., 2004; Asherson
et al., 2008; Bakker et al., 2003; Faraone et al., 2007; Fisher et al., 2002a, 2002b; Ogdie et al.,
2003).
There is some overlap between linkage regions suggested by genome-wide linkage analyses of
RD and ADHD, which might be explained by pleiotropy for these disorders. These regions in-
clude 1p36, 2q22–35, 3p12–q13, 4q12–13, 6p21–22, 6q12–14, 13q22–33, and 15q15–21 (see Ta-
ble 2). However, some regions, positively associated to ADHD or dyslexia, are also associated to
other developmental disorder, such as autism. As some studies suggest, the chromosome regions
6q, 2q, 3p, and 15q are likely to contain risk genes for autism (Duvall et al., 2007; Muhle,
Trentacoste, & Rapin, 2004). These pattern of results reduce the specificity of overlap between
linkage regions described for RD and ADHD. Furthermore, it is important to underline that link-
age of both disorders to the same chromosomal region do not automatically implies that the same
gene is involved. Some studies do not support a common genetic basis between ADHD and dys-
lexia. Marino et al. (2003) tested within-family association and linkage disequilibrium between
four genetic markers at DRD4, DRD3, DRD2, and DAT loci, and dyslexia, in a sample of 130 Ital-
ian dyslexic children, 16.9% of whom had comorbid ADHD. No evidence of either association or
linkage disequilibrium was found in the total sample or in the comorbid subgroup. Hsiung,
Kaplan, Petryshen, Lu, and Field (2004) investigated DRD4 as a candidate gene for dyslexia by
testing for linkage and association with 14 markers at and around the DRD4 locus on chromosome
11p15.5. However, linkage disequilibrium analysis showed no significant evidence for associa-
tion between dyslexia and DRD4 or HRAS. In particular, dyslexic subjects showed no significant
increase of the DRD4 7-repeat allele associated with ADHD.
The bivariate heritability between RD and ADHD is more pronounced for the inattentive
symptoms of ADHD than the hyperactive/impulsive ones (Willcutt et al., 2003). The 1p36 region
may harbor a pleiotropic quantitative trait locus affecting both inattention and dyslexia (Zhou et
al., 2008).
Bivariate twin analyses suggest that comorbidity between RD and ADHD may be largely due
to common genetic influences (Light, Pennington, Gilger, & DeFries, 1995; Stevenson et al.,
1993; Willcutt & Pennington, 2000b). The ADRA2A gene (Stevenson, Pennington, Gilger,
DeFries, & Gillis, 2005) or chromosomal regions (6p21.3; Willcutt et al., 2002) may play a role in
susceptibility for both the conditions.

TABLE 2
Overview of Risk Loci Shared by RD and ADHD Identified in Linkage Studies

Chromosome RD ADHD

1p36 DYX8 (de Kovel et al., 2007) Zhou et al., 2008

2q22-35 Rasking et al., 2005 Romanos et al., 2008
3p12-q13 DYX5 (Nopola-Hemmi et al., 2001) Bakker et al., 2003
4q12-13 Fisher et al., 2002 Arcos-Burgos et al., 2004
6p21-22 DYX2 (Grigorenko et al., 2003) Willcutt et al., 2002
6q 12-14 DYX4 (Petryshen et al., 2001) Ogdie et al., 2003
13q22-33 Fisher et al., 2002a; Igo et al., 2006 Bakker et al., 2003
15q15-21 DYX1 (Chapman et al., 2004) Bakker et al., 2003

Approximately LOD scores >1. ADHD = attention deficit hyperactivity disorder; RD = reading disorder.
 ADHD AND DYSLEXIA 479

Some studies with genome-wide investigations have been conducted which aimed at identify-
ing chromosomal loci with pleiotropic effects on dyslexia and ADHD. In the Colorado sample,
families with dyslexia having ADHD problems showed evidence for linkages in chromosome re-
gions 14q32, 13q32, and at 20q11 (Gayan et al., 2005).
In families with ADHD, evidence for linkage is shown for reading ability in regions 10q32, 16p12,
and 17q22 (Loo et al., 2004). These loci may have pleiotropic effects on both RD and ADHD. Therefore,
supposedly distinct diagnoses such as RD and ADHD may be due in part to pleiotropic nes that entail
risk for more than one disorder (Willcutt, Pennington, Olson, & Defries, 2007). Thus, pleiotropic
genes may be the rule, rather than the exception, in the aetiology of complex characters. Nevertheless,
multiple endophenotypes have to interact to determine the finally observed abnormal phenotype.

NEUROIMAGING FINDINGS

Many abnormalities in different brain regions have been reported in ADHD, including smaller total
brain volumes and reduced volumes in the right frontal lobe, right caudate nucleus, cerebellar hemi-
spheres, and cerebellar vermis (Castellanos et al., 2002; Mackie et al., 2007; Valera, Faraone,
Murray, & Seidman, 2007). Functional imaging studies by Single Photon Emission Computed To-
mography (SPECT) and positron emission tomography (PET) uncovered anomalies in the frontal
lobes and in the basal ganglia of individuals with ADHD (Ernst, 2003). Functional magnetic reso-
nance imaging (fMRI) studies show decreased functioning of dorsolateral prefrontal cortex and
dorsal anterior midcingulated cortex on tasks requiring inhibitory control (Bush et al., 2008;
Rubia et al., 1999; Tamm, Menon, Ringel, & Reiss, 2004; Zang et al., 2005) and hypoactivation in
the right inferior prefrontal cortex and in the precuneus and posterior cingulated cortex on inhibi-
tory-tasks (Rubia, Smith, Brammer, Toone, & Taylor, 2005). Other recent studies show reduced
activation of temporal lobes, basal ganglia, and parietal lobe (Rubia, Smith, Brammer, & Taylor,
2007; Silk et al., 2005; Smith, Taylor, Brammer, Toone, & Rubia, 2006; Vance et al., 2007).
There is substantial evidence of brain abnormalities in dyslexia too (Shaywitz et al., 1998).
Structural imaging findings include reduced volumes in the inferior frontal gyrus (pars triangularis),
in the right anterior cerebellar lobe (Eckert et al., 2003) and in the temporal lobes (Vinckenbosk,
Robichon, & Eliez, 2005), less gray matter volume in the left and right fusiform gyrus, in the bilat-
eral anterior cerebellum and in the right supramarginal gyrus (Kronbichler et al., 2008).
fMRI studies, examining phonological processing in dyslexic adults and children, have consis-
tently found a disruption of 2 left hemisphere posterior brain systems, 1 parietal-temporal
(Shaywitz et al., 2002; Temple et al., 2001), the other occipital-temporal, with compensatory en-
gagement of anterior systems around the inferior frontal gyrus (Hoeft et al., 2007) and a posterior
(right occipital-temporal) system (for review, see Temple, 2002 and Shaywitz, 2006).
Shared biological processes may underlie reading and ADHD. A common neural mechanism
might be a variation in cerebral lateralization, particularly related to language processing. Support
for such a mechanism is evident from brain-imaging studies of dyslexic and ADHD individuals, in
whom reversed asymmetry of hemisphere structures such as planum temporale, caudate nucleus,
and frontal lobes have been observed (Foster, Hynd, Morgan, & Hugdahl, 2002; Pueyo et al., 2000).
Lower cerebellar volume has been found in ADHD (Castellanos et al., 2002); lower cerebellar
volume in anterior lobe (Eckert et al., 2003) and less gray matter volume have been found in the
cerebellum in dyslexia (Kronbichler et al., 2008).
480 GERMANÒ, GAGLIANO, CURATOLO

Recent studies have found dysfunctions in temporal regions in ADHD individuals (Smith et al.,
2006; Rubia et al., 2007) and, in particular, reduced activation in temporal lobe regions (Shafritz et
al., 2004); differences of activation in the same areas are associated with neural deficits in dyslexia
(Temple et al., 2001; Shaywitz et al., 2002; Kronbichler et al., 2006; Hoeft et al., 2007).
Striatal dysfunctions have been often observed in both ADHD and RD (Shafritz et al., 2004). A
great number of studies have examined the neuroanatomic and neurofunctional variables in
ADHD and in dyslexic subjects (Table 3). However, to date there are no detailed neuroimaging
studies of the comorbid phenotype. It could be possible to find different and specific neurological
pattern in subjects with both disorders, instead of a summation of the two disorders. It is well
known that disorders like ADHD and RD are the result of a dysfunction in neural networks, not in
localized structures. Thus, future researches using Magnetic Resonance Spectroscopy (MRS) and
fMRI are needed to elucidate the underlying neural circuits of the comorbid phenotype.

NEUROPSYCHOLOGICAL FINDINGS

ADHD Phenotype
Individuals with ADHD present difficulties on a variety of neurocognitive measures: problem
solving, planning orienting, alerting, cognitive flexibility, sustained attention, response inhibi-
tion, and visual working memory (WM) (Voeller, 2004).
Based on similarities between ADHD symptoms and the behavioral sequelae of frontal lobe in-
juries, several authors have proposed that ADHD is attributable to a deficit in executive functions

TABLE 3
Functional/Structural Neuroimaging Alterations Shared in RD and ADHD

Neuroimaging Alterations RD ADHD

Lower cerebellar volume
Dysfunctions in temporal regions
Striatal dysfunction
Asymmetry of hemisphere
structures
Eckert et al., 2003; Kronbichler et
al., 2008
Temple et al., 2001; Shaywitz et al.,
2002; Kronbichler et al., 2006;
Hoeft et al., 2007
Shafritz et al., 2004
Planum temporale:
Dalby et al., 1998; Eckert and
Leonard, 2000; Foster et al., 2000
Lobar asymmetries:
Zadina et al., 2006
Berquin et al., 1998; Mostofsky et al.,
1998; Castellanos et al., 2002; Hill et
al., 2003; Mackie et al., 2007
Smith et al., 2006; Rubia et al., 2007;
Shafritz et al., 2004
Shafritz et al., 2004; Rubia et al., 2007
Caudate nucleus:
Hynd et al., 1993; Pueyo et al., 2000;
Schrimsher et al., 2002; Pineda et al.,
2002; Uhlíkova et al., 2007
Putamen nucleus:
Wellington et al., 2006
Globus pallidus:
Uhkikova et al., 2007
Prefrontal cortical convolution:
Li et al., 2007
Frontal lobe:
Pueyo et al., 2000

ADHD = attention deficit hyperactivity disorder; RD = reading disorder.

 ADHD AND DYSLEXIA 481

(EF) (Barkley, 1997). Barkley proposed the Inhibition model, a comprehensive theory that recog-
nizes in deficient inhibitory control the core deficit of ADHD that secondarily disrupts other EF
processes (Barkley, 1997; Shanahan, Pennington, & Willcutt, 2008), particularly response inhibi-
tion, vigilance, WM, and planning (Willcutt et al., 2005a). Empirical evidence suggests multiple
deficits of WM, with a greater impairment of spatial central executive WM rather than verbal cen-
tral executive WM (Martinussen, Hayden, Hogg-Johnson, & Tannock, 2005). However, EF
weaknesses are neither necessary, nor sufficient to explain all cases of ADHD since not all sub-
jects with ADHD show neuropsychological deficits (Willcutt et al., 2005a ).
An alternative model presents ADHD as resulting from impaired signalling of delayed rewards
arising from disturbance in motivational processes (Sonuga-Barke, 1994). Other patterns of impair-
ment in non-inhibitory domains such as state regulation (Cognitive-energetic model, Sergeant,
2005; Sergeant et al., 1999) and temporal processing (Castellanos & Tannock, 2002) were found.
Neuropsychological findings emphasize particular components of a unified self-regulatory
system, which emerges from the infant to toddler years, consolidates from the preschool to early
childhood years, and continues to mature through adolescence. The self-regulatory abilities of the
child depend on the mutual interplay of: strength of the affective response to incentive; state regu-
lation; ability to redirect attention or suppress responses to regulate affect and behavior (executive
functions); emerging language abilities (Nigg, 2005).
These evidences provide the idea of neuropsychologically heterogeneous nature of the disor-
der (Nigg, 2006; Sonuga-Barke, 2005; Willcutt et al., 2005b), and support the likelihood that mul-
tiple neurodevelopmental pathways underpin this disorder, highlighting the need for theoretical
models of ADHD to combine motivational and cognitive elements.

RD Phenotype

Several theories have been proposed for the cause of dyslexia.

The dominant phonological deficit explanation suggests that dyslexia is a language-based dis-
order characterised by difficulties in single-word decoding (Orton, 1995) and phonological pro-
cessing (Snowling, 2000) that prevents learning of letter and phoneme associations. According to
this theory, affected individuals have specific difficulties in perceiving and segmenting pho-
nemes, leading to difficulties in establishing a connection between phonemes and graphemes
(Ramus et al., 2003). However, the purely phonological theory of dyslexia cannot account for
low-level visual, sensory, and motor coordination deficits reported in many subjects.
The magnocellular deficit theory accounts for disturbances in visual processing (Eden, Van-
Meter, Rumsey, & Zeffiro, 1996); this theory proposes that in a proportion of individuals with
dyslexia, the perception of visual, rapid moving stimuli and stimuli of low spatial frequency and
low contrast is impaired. This hypothesis in its dominant version assumes degraded visual input
due to poor binocular fixation as the cause of the reading difficulties. This deficit is associated, at
the central nervous system level, with impaired sensitivity of cells within the retinocortical
magnocellular pathway (Stein, 2001).
The automaticity/cerebellar deficit hypothesis suggests that the automatization of cognitive
processes and motor control in the cerebellum is disturbed in individuals with dyslexia (Nicolson,
Fawcett, & Dean, 2001). The role of the cerebellum in the pathogenesis of dyslexia stems from the
conceptualization of dyslexia as a learning disorder, in which failure to acquire and automatize
reading and writing skills might be the most prominent symptom. (Fawcett & Nicholson, 1999).
482 GERMANÒ, GAGLIANO, CURATOLO

Comorbid Phenotype and Hypotheses to Explain Comorbidity

Several clinical researches and theoretical accounts have been proposed in the past to understand
the neuropsychological correlates of comorbid phenotypes and to explain comorbidity between
ADHD and RD. For each competing hypothesis, a different neuropsychological profile of the
comorbid phenotype, related to RD-only and the ADHD-only phenotypes, has been described.
A first hypothesis suggested that RD may cause the symptoms of ADHD as a consequence of
frustrations elicited by difficulties with reading (Pisecco, Baker, Silva, & Brooke, 1996). Accord-
ing to this hypothesis, comorbid phenotype exhibits the neuropsychological deficits of RD only
and the behavioral characteristics of both disorders, since the RD genotype, under particular envi-
ronmental conditions, mimics the ADHD phenotype (Phenocopy hypothesis; Pennington, Grois-
ser & Welsh, 1993). Consequently, it was assumed that comorbid subjects had the same
neuropsychological weakness exhibited by subjects with the first disorder only. Further studies
did not support this hypothesis (Nigg, Hinshaw, Carte, & Treuting, 1998; Rucklidge & Tannock,
2002; Willcutt et al., 2001) and it became increasingly clear that comorbid RD and ADHD chil-
dren exhibited the combination of the deficits in the RD-only and ADHD-only subjects group.
Another interesting hypothesis explaining comorbidity was proposed: the Cross-assortment
hypothesis (Faraone, Biederman, Lehman, & Keenan, 1993). It suggested that ADHD and RD are
transmitted independently in families and that their co-occurrence may be due to non-random
mating. According to this theory, spouses of those with ADHD had significantly higher rates of
RD than spouses of those without ADHD. In keeping with this model, the cognitive profile of
comorbid phenotype seemed consistent with the additive combination of the deficits of the
RD-only and the ADHD-only phenotypes. But following studies suggested that cross-assortment
hypothesis is not likely to provide a sufficient explanation for the larger part of comorbid cases
(Doyle, Faraone, DuPrue, & Biederman, 2001; Friedman et al., 2003) and that further studies are
needed to fully understand the neuropsychological correlates of RD-ADHD comorbidity. In their
first studies, Pennington and colleagues postulated a significant double dissociation between RD
and ADHD (Pennington et al., 1993). With the aim of examining phonological and executive abil-
ities, they used a full 2 × 2 (RD × ADHD) design and found data confirming the double dissocia-
tion model. According to this model, RD and ADHD were linked with two opposite patterns of
impairment in two different cognitive domains. Furthermore, a growing amount of evidence
seemed to confirm that comorbid RD and ADHD subjects showed the additive combination of the
deficit associated with each single disorder (Pisecco, Baker, Silva & Broke, 2001; Swanson,
Mink, & Bocian, 1999; Willcutt et al., 2001). Hence, the double dissociation hypothesis between
RD and ADHD explained that ADHD-only subjects appeared impaired on executive abilities, but
not on phonological abilities; RD-only subjects exhibited phonological processing deficits, but
not executive functions deficits (Marzocchi et al., 2008; Purvis & Tannock, 1997; Willcutt et al.,
2001) and comorbid subjects showed a sum of the previous deficits (Willcutt et al., 2001). Conse-
quently, three independent phenotypes were described: a phoneme awareness/verbal working
memory deficit for the RD only phenotype, an executive/inhibition deficit for the ADHD only
phenotype; an additive combination for comorbid phenotype, arising from a coexistence of core
neuropsychological deficits of both disorders. As predicted by this model, a single neuro-
psychological deficit is the cause of each disorder: a phonological deficit sustains dyslexia and an
inhibition deficit explains ADHD (Pennington et al., 1993). Moreover many studies reported
slower rapid automized naming (RAN) performances in RD and in comorbid phenotype, but not
 ADHD AND DYSLEXIA 483

in ADHD only phenotype (Felton, Wood, Brown, Campbell, & Harter, 1987; Raberger &
Wimmer, 2003; Semrud-Clickeman, Guy, & Griffin, 2000), also in studies carried out in non-al-
phabetic language communities (Chan, Hung, Liu, & Lee, 2008). These findings seem to recog-
nize RAN impairment as a specific deficit for dyslexic children, supporting double dissociation
hypothesis.
More recently, various studies provided an increasing amount of evidence for more cognitive
deficits underlying ADHD and RD, questioning a complete dissociation of the core deficits of two
disorders. In fact, executive function deficits have been demonstrated in children with dyslexia
(Purvis & Tannock, 2000; Rucklidge & Tannock, 2002; Willcutt et al., 2001) and subtle deficits in
verbal storage and verbal central executive domains were found in ADHD subjects (Martinussen
& Tannock, 2006). In addition, dyslexic subjects show a high cognitive impulsivity probably re-
lated with a frontal functions impairment (Donfrancesco, Mugnaini, & Dell’Uomo, 2005). Fur-
ther studies reported a higher cognitive impulsivity level in comorbid phenotype than in subjects
with ADHD only, characterizing impulsivity as a common factor in both ADHD and RD (Purvis
& Tannock, 2000).
In parallel, throughout genetic studies, it became progressively clear that some of the etiologi-
cal factors are shared in ADHD and RD and that it is possible to found genetic overlaps between
these two disorders (Gayan et al., 2005; Loo et al., 2004). Given that RD and ADHD present
shared genetic risk factors, it is highly probable that they have shared cognitive risk factors as
well.
The cognitive subtype hypothesis (Rucklidge & Tannock, 2002) predicts that the neuro-
psychological deficits of the comorbid group are different from the simple additive combination
of the deficits associated with RD-only and the ADHD-only groups since there is a significant in-
teraction between RD and ADHD on at least some of the neurocognitive weaknesses. So, individ-
uals with RD and ADHD generally seem to have slower naming speed, specifically concerning
naming letters and digits tasks in RD (Wolf & Bowers, 1999) and for objects and colors tasks in
ADHD (Ghelani, Sidhu, Unesh, & Tannock, 2004; Tannock, Martinussen, & Frijters, 2000).
Neuropsychological background of co-occurring dyslexia and ADHD can be understood as the
co-existence of phonological short-term memory deficits and central executive deficits (Tiffin-
Richards, Hasselhorn, Woerner, Rothenberger, & Banaschewski, 2008), sustaining an incomplete
dissociation of executive and linguistic functions in dyslexia and ADHD.
Moreover, it was observed that the comorbid group may differ from the simple additive combi-
nation of the deficits associated with RD and ADHD in consequence of specific additional cogni-
tive weakness, such as rapid naming and reaction times, forming an unique cognitive subtype
more clinically impaired (specific subtype hypothesis, Rucklidge & Tannock, 2002). In concor-
dance with this model a unique deficit in RAN tasks and more severe impairment on verbal work-
ing memory (WM), in comparison to pure phenotypes, were described in the comorbid phenotype
(Bental & Tirosh, 2007). Latest findings seem to recognize WM and RAN impairment as possible
specific deficits for comorbid children. Another important impairment described in comorbid
phenotype is the processing speed deficit that appears to be related to both RD and ADHD
(Shanahan et al., 2006; Willcutt et al., 2005b). It seems a shared cognitive risk factor that could ex-
plain the comorbidity of ADHD and RD, and which could represent the most promising candidate
as a neuropsychological endophenotype (Willcutt et al., 2005b).
Altogether, a set of hypotheses has been based on a deterministic etiological cognitive model
for RD and ADHD, focused on a single cognitive cause (Single cognitive deficit model, Penning-
484 GERMANÒ, GAGLIANO, CURATOLO

ton et al., 1993). Comorbid phenotype does not exhibit a specific weakness on any functions that
are not impaired in at least one of the other two groups (Willcutt et al., 2005b). This raises the is-
sue that each disorder may result from a different combination of cognitive deficits, some shared
and some not shared. Thus far, different pathways may lead up to the comorbid ADHD + RD
phenotype.
However, most of the findings, taken together, lead to reject the simple cognitive deficit model
of ADHD and RD and to conclude that the overlap of more factors produce comorbidity (Penning-
ton, 2006). Finding a shared cognitive risk factor between two comorbid disorders is consistent
with multiple deficit hypothesis of both disorders (Shanahan et al., 2006). The aetiology of com-
plex behavioral disorders involves the interaction of multiple risk and protective factors, which
can be either genetic or environmental (Multiple deficit model, Pennington, 2006; Sonuga-Barke,
2005).
The development of behavioral symptoms that define these disorders is based on the balance
between risk and protective factors. Thus the relation between RD and ADHD might be attribut-
able to common etiological influences that increase susceptibility to both disorders (Common eti-
ology model, Willcutt et al., 2003; Willcutt et al., 2005b; Willcutt et al., 2007).
Table 4 summarizes the neuropsychological correlates and the models or hypothesis for RD +
ADHD comorbidity.

TREATMENT OPTIONS

Effective intervention programs for dyslexia provide children with systematic instruction in criti-
cal components of reading: phonemic awareness, phonics, fluency, vocabulary, and comprehen-
sion strategies (Shaywitz, Gruen, & Shaywitz, 2007). Proper treatment plans are necessary to
guide parents and to offer adequate coping strategies (Lagae, 2008). An essential component of
the management of dyslexia in students in secondary school incorporates the provision of extra
time and assistive technology aids (Shaywitz et al., 2007). Evidence-based treatments for ADHD
include a combination of pharmacological and behavioral interventions. The use of a multimodal
treatment is currently considered the most appropriate approach (Kaiser, Hoza, & Hurt, 2008). A
broad set of interventions including behavioral therapy and parent training, school consultation,
and academic interventions are recommended (Wolraich et al., 2005). In children with ADHD
and RD comorbid condition treatment approaches must address both disorders. They need a com-
plete psychoeducational treatment program (cognitive–behavioral training and phonological pro-
grams) that may be useful for reducing behavioral and reading problems.
Identification and treatment of any comorbid psychiatric issues and involvement of the family
in the treatment processes are an important part of intervention. An early treatment can remediate,
and may prevent, reading difficulties in primary school-aged children since it can change the tra-
jectory in terms of language, reading skills, and self-esteem (Sundheim & Voeller, 2004).
Multiple studies have shown short-term effects of Methylphenidate (MPH) on the core
symptoms of ADHD, cognitive laboratory tasks and academic performance in children with
ADHD (Spencer et al., 1996; Wilens & Spencer., 2000). MPH improves reading performance in
children with ADHD and comorbid dyslexia (Bental & Tirosh, 2008; Keulers et al., 2007;
Shafritz et al., 2004). These data support a possible influence of MPH on cognitive attention
functions related to reading skills in the comorbid group. Several explanations for the effects of
 ADHD AND DYSLEXIA 485

TABLE 4
Neuropsychological Correlates and Models for RD + ADHD Comorbidity

Authors Comorbid Phenotype Models and Hypothesis

Pennington et al., 1993
Faraone et al., 1993
Purvis & Tannock, 1997;
Willcutt et al., 2001
Rucklidge & Tannock, 2002
Willcutt et al., 2005; Shanahan
et al., 2006
Bental & Tirosh, 2007
Tiffin-Richards et al., 2008
Felton et al., 1987; Semrud-
Clikeman et al., 2000;
Raberger & Wimmer, 2003;
Chan et al., 2008
Comorbid group had the symptoms of ADHD, Phenocopy hypothesis
but not the underlying executive deficit
The cognitive profile of comorbid phenotype is Cross Assortment hypothesis
consistent with the additive combination of
the deficits of the RD-only and the
ADHD-only phenotypes
ADHD subjects are impaired on executive Double dissociation hypothesis
abilities, but not on phonological abilities; RD
subjects exhibit phonological processing
deficits, but not executive functions deficits;
comorbid phenotype arises from an additive
combination of all previous
neuropsychological deficits
Comorbid group was slower with rapid naming Specific subtype hypothesis
and had slower reaction times. It is a specific
subtype, more clinically impaired
Processing speed deficit is a shared cognitive Multiple deficit model/Common
deficit aetiology hypothesis
Comorbid group shows a more severe Specific subtype hypothesis
impairment in verbal WM and a unique deficit
in rapid naming
Working memory is a shared cognitive deficit; Multiple deficit model/Common
phonological short-term memory deficits and aetiology hypothesis
central executive deficits coexist
Slower performances in rapid automatized Double dissociation hypothesis
naming tasks (RAN) in RD and in comorbid
phenotype but not in ADHD only phenotype

ADHD = attention deficit hyperactivity disorder; RD = reading disorder; WM = working memory.

MPH on academic learning have been proposed: improved ability to selectively attend to rele-
vant stimuli (Balthazor, Wagner, & Pelham, 1991) and better efficiency of specific and/or gen-
eral cognitive processes (Keulers et al., 2007). fMRI findings (Shafritz et al., 2004) demonstrate
neural dysfunction and neural effects of MPH in adolescents with ADHD or RD during the per-
formance of attention tasks. MPH increase striatal activation for both ADHD and RD adoles-
cents (Shafritz et al., 2004).
Recent evidence from randomised controlled trials show cognitive effects of polyunsaturated
fatty acids in children with ADHD. The main improvement reported in ADHD sample was in the
ability to switch and control attention (Sinn, Bryan, & Wilson, 2008). There is little evidence of
efficacy on comorbid phenotype: a reduction of ADHD-related symptoms was described in chil-
dren with specific learning difficulties using highly unsaturated fatty acids (HUFA) supple-
mentation (Richardson & Puri, 2002). A constitutional inefficiency in the conversion of essential
fatty acid precursor to unsaturated fatty acids has been proposed as a factor not only in ADHD
(Stevens et al., 1995) but also in dyslexia and dyspraxia (Stordy, 2000). In these conditions with a
486 GERMANÒ, GAGLIANO, CURATOLO

biological basis, phospholipids metabolism looks like a promising paradigm and could help to ac-
count for many features that are common not only to these conditions.

FUTURE DIRECTION

The overall pattern of research suggests that ADHD and RD are both related to weakness on most
neurocognitive domains. As noted previously, comorbid children show a phenotype with more se-
vere cognitive deficits and worse neuropsychological, academic, and behavioral outcomes, com-
pared with children diagnosed with only ADHD or RD. Thus, when a patient receives a diagnosis
of ADHD, it is very important to complete the assessment with academic tests in order to identify
a potential specific learning disability.
Both behavioral and molecular genetic studies support a partly shared genetic etiology be-
tween ADHD and RD and draw the comorbid phenotype as the result of the overlap of risk factors
producing a high rate of co-occurrence of these disorders. It seems that the ADHD/RD children
have difficulty with different aspects of information processing, memory functions, and cognitive
speed. Future research should address to delineate clearly the neuropsychological profile of
comorbid phenotype, drawing strengths and weaknesses of a unique adverse developmental con-
dition.
Recent evidence from an event-related potential study (Dhar, Been, Minderaa, & Althaus,
2008) supported the concept that comorbid subjects differ from ADHD in information processing
characteristics although comorbid subjects are very close to RD in some event-related measures.
Measures of task-related neurophysiological and behavioral variables should help to clarify rela-
tionships between brain activity and differences in cognitive and behavioral characteristics of
comorbid phenotype.
Research should also address molecular genetic analyses of this group of patients in order to fa-
cilitate the identification of genes for RD, ADHD, and their comorbidity. It has been hypothesized
that genetic and environmental factors relate to psychiatric disorders, such as ADHD, through the
effect of intermediating, vulnerability traits called endophenotypes. The purpose in determining
causality and characteristics of comorbid phenotypes would be to establish whether their behav-
ioral profiles are genetically related to more stable phenotypes with a clear genetic connection
(endophenotype).
Finally, it has also been hypothesized that some male-based neurodevelopmental disorders are
associated with high maternal intrauterine testosterone concentrations (Beech & Beauvois, 2006;
James, 2008); future studies could investigate the possible influences of excessive androgen expo-
sure in early brain development impairing aspects of RD and ADHD.

REFERENCES

American Psychiatric Association. (2000). Diagnostic and statistical manual of mental disorders, 4th edition (DSM-IV
text revision). Washington, DC: American Psychiatric Association.
Arcos-Burgos, M., Castellanos, F. X., Pineda, D., Lopera, F., Palacio, J. D., Palacio, L. G., et al. (2004). Attention-defi-
cit/hyperactivity disorder in a population isolate: Linkage to loci at 4q13.2, 5q33.3, 11q22, and 17p11. American Jour-
nal of Human Genetics, 75, 998–1014.
 ADHD AND DYSLEXIA 487

Asherson, P., Zhou, K., Anney, R. J., Franke, B., Buitelaar, J., Ebstein, R., et al. (2008). A high density SNP linkage scan
with 142 combined subtype ADHD sib pairs identifies linkage regions on chromosomes 9 and 16. Molecular Psychia-
try, 13, 514–521.
August, G. J., & Garfinkel, B. D. (1990). Comorbidity of ADHD and reading disability among clinic-referred children.
Journal of Abnormal Child Psychology, 18, 29–45.
Bakker, S. C., van der Meulen, E. M., Buitelaar, J. K., Sandkuijl, L. A., Pauls, D. L., Monsuur, A. J., et al. (2003). A
whole-genome scan in 164 Dutch sib pairs with attention-deficit/hyperactivity disorder: Suggestive evidence for link-
age on chromosomes 7p and 15q. American Journal of Human Genetics, 72, 1251–1260.
Balthazor, M. J., Wagner, R. K., Pelham, W. E. (1991). The specificity of the effects of stimulant medication on classroom
learning-related measures of cognitive processing for attention deficit disorder children. Journal of Abnormal Child
Psychology, 19, 35–52.
Banaschewski, T., Neale, B. M., Rothenberger, A., & Roessner, V. (2007). Comorbidity of tic disorders & ADHD—Con-
ceptual and methodological considerations. European Child and Adolescent Psychiatry, 16, I/5–I/14.
Barkley, R. A. (1997). Behavioral inhibition, sustained attention, and executive function: Constructing a unified theory of
ADHD. Psychological Bulletin, 121, 65–94.
Beech, J. R., Beauvois, M. W. (2006). Early experience of sex hormones as a predictor of reading, phonology, and auditory
perception. Brain and Language, 96, 49–58.
Bental, B., & Tirosh, E. (2007). The relationship between attention, executive functions and reading domain abilities in at-
tention deficit hyperactivity disorder and reading disorder: A comparative study. Journal of Child Psychology and Psy-
chiatry, 48, 455–463.
Bental, B., & Tirosh, E. (2008). The effects of methylphenidate on word decoding accuracy in boys with attention-defi-
cit/hyperactivity disorder. Journal of Clinical Psychopharmacology, 28, 89–92.
Biederman, J. (2005). Attention-deficit/hyperactivity disorder: A selective overview. Biological Psychiatry, 57, 1215–
1220.
Bush, G., Spencer, T. J., Holmes, J., Shin, L. M., Valera, E. M., Seidman, L. J., Makris, N., Surman, C., Aleardi, M., Mick,
E., & Biederman, J. (2008). Functional magnetic resonance imaging of methylphenidate and placebo in attention-defi-
cit/hyperactivity disorder during the multi-source interference task. Archives of General Psychiatry, 65, 102–114.
Castellanos, F. X., Lee, P. P., Sharp, W., Jeffries, N. O., Greenstein, D. K., Clasen, L. S., et al. (2002). Developmental tra-
jectories of brain volume abnormalities in children and adolescents with attention-deficit/hyperactivity disorder. Jour-
nal of the American Medical Association, 288, 1740–1748.
Castellanos, F. X., & Tannock, R. (2002). Neuroscience of attention-deficit/hyperactivity disorder: The search for
endophenotypes. Nature Reviews Neuroscience, 3, 617–628.
Chadwick, O., Taylor, E., Taylor, A., Heptinstall, E., & Danckaerts, M. (1999). Hyperactivity and reading disability: A
longitudinal study of the nature of the association. Journal of Child Psychology and Psychiatry, 40, 1039–1050.
Chan, W. S. R., Hung, S. F., Liu, S. N., & Lee, C. K. K. (2008). Cognitive profiling in Chinese developmental dyslexia
with attention deficits hyperactivity disorder. Reading and Writing, 21, 661–674.
Chapman, N. H., Igo, R. P., Thomson, J. B., Matsushita, M., Brkanac, Z., Holzman, T., et al. (2004). Linkage analyses of
four regions previously implicated in dyslexia: Confirmation of a locus on chromosome 15q. American Journal of Med-
ical Genetics. Part B, Neuropsychiatric genetics, 131, 67–75.
Cohen, N. J., Vallance, D. D., Barwick, M., Im, N., Menna, R., Horodezky, N. B., et al. (2000). The interface between
ADHD and language impairment: An examination of language, achievement, and cognitive processing. Journal of
Child Psychology and Psychiatry, 41, 353–62.
Cope, N., Harold, D., Hill, G., Moskvina, V., Stevenson, J., Holmans, P., et al. (2005). Strong evidence that KIAA0319 on
chromosome 6p is a susceptibility gene for developmental dyslexia. American Journal of Human Genetics, 76,
581–591.
Curatolo, P., Paloscia, C., D’Agati, E., Moavero, R., & Pasini, A. (2008). The neurobiology of attention deficit/ hyperac-
tivity disorder. European Journal of Paediatric Neurology, Jul 19 (Epub ahead of print).
Dalby, M. A., Elbro, C., & Stødkilde-Jørgensen, H. (1998). Temporal lobe asymmetry and dyslexia: An in vivo study us-
ing MRI. Brain and Language, 62, 51–69.
de Kovel, C., Franke, B., Hol, F. A., Lebrec, J., Maassen, B., Brunner, H., et al. (2007). Confirmation of dyslexia suscepti-
bility loci on chromosomes 1p and 2p, but not 6p in a Dutch sib-pair collection. American Journal of Medical Genetics.
Part B, Neuropsychiatric Genetics (published online ahead of print September 20).
Del’homme, M., Kim, T. S., Loo, S. K., Yang, M. H., & Smalley, S. L. (2007). Familiar association and frequency of
learning disabilities in ADHD sibling pair families. Journal of Abnormal Child Psychology, 35, 55–62.
488 GERMANÒ, GAGLIANO, CURATOLO

Dhar, M., Been, P. H., Minderaa, R. B., & Althaus, M. (2008). Distinct information processing characteristics in Dyslexia
and ADHD during a covert orienting task: An event-related potential study. Clinical Neurophysiology, 119(9),
2011–2025.
Donfrancesco, R., Mugnaini, D., & Dell’Uomo, A. (2005). Cognitive impulsivity in specific learning disabilities. Euro-
pean Child & Adolescence Psychiatry, 14, 270–275.
Doyle, A. E., Faraone, S. V., DuPrue, E. P., & Biederman, J. (2001). Separating attention deficit hyperactivity disorder and
learning disabilities in girls: A familial risk analysis. American Journal of Psychiatry, 158, 1666–1672.
Duvall, J. A., Lu, A., Cantor, R. M., Todd, R. D., Constantino, J. N., Geschwind, D. H. (2007). A quantitative trait locus
analysis of social responsiveness in multiplex autism families. American Journal of Psychiatry, 164, 656–662.
Dykman, R. A., & Ackerman, P. T. (1991). Attention deficit disorder and specifc reading disability: Separate but often
overlapping disorders. Journal of Learning Disabilities, 2, 96–103.
Eckert, M. A., & Leonard, C. M. (2000). Structural imaging in dyslexia: The planum temporale. Mental Retardation and
Developmental Disabilities Research Reviews, 6, 198–206.
Eckert, M. A., Leonard, C. M., Richards, T. L., Aylward, E. H., Thomson, J., & Berninger, V. W. (2003). Anatomical cor-
relates of dyslexia: Frontal and cerebellar findings. Brain, 126, 482–494.
Eden, G. F., VanMeter, J. W., Rumsey, J. M., & Zeffiro T. A. (1996). The visual deficit theory of developmental dyslexia.
Neuroimage, 4, S108–117.
Ernst, M., Kimes, A. S., London, E. D., Matochik, J. A., Eldreth, D., Tata, S., et al. (2003). Neural substrates of decision
making in adults with attention deficit hyperactivity disorder. American Journal of Psychiatry, 160, 1061–1070.
Faraone, S. V., Biederman, J., Lehman, B. K., & Keenan, K. (1993). Evidence for the independent familial transmission of
attention deficit hyperactivity disorder and learning disabilities: Results from a family genetic study. American Journal
of Psychiatry, 150, 891–895.
Faraone, S. V., Perlis, R., Doyle, A. E., Smoller, J. W., Goralnick, J. J., Holmgren, M. A., et al. (2005). Molecular genetics
of attention deficit hyperactivity disorder. Biological Psychiatry, 57, 1313–1323.
Faraone, S. V., Doyle, A. E., Lasky-Su, J., Sklar, P. B., D’Angelo, E., Gonzalez-Heydrich, J., et al. (2007). Linkage analy-
sis of attention deficit hyperactivity disorder. American Journal of Medical Genetics. Part B, Neuropsychiatric Genet-
ics (published online ahead of print December 14).
Fawcett, A. J., & Nicolson, R. I. (1999). Performance of dyslexic children on cerebellar and cognitive tests. Journal of Mo-
tor Behavior, 31, 68–78.
Felton, R. H., Wood, F. B., Brown, I. S., Campbell, S. K., & Harter, M. R. (1987). Separate verbal memory and naming
deficits in attention deficit disorder and reading disability. Brain and Language, 31, 171–184.
Fisher, S. E., Francks, C., Marlow, A. J., MacPhie, I. L., Newbury, D. F., Cardon, L. R., et al. (2002a). Independent ge-
nome-wide scans identify a chromosome 18 quantitative- trait locus influencing dyslexia. Nature Genetics, 30, 86–91.
Fisher, S. E., Francks, C., McCracken, J. T., McGough, J. J., Marlow, A. J., MacPhie, I. L., et al. (2002b). A genomewide
scan for loci involved in attention-deficit/hyperactivity disorder. American Journal of Human Genetics, 70, 1183–1196.
Foster, L. M., Hynd, G., Morgan, A. E., & Hugdahl, K. (2002). Planum temporale asymmetry and ear advantage in
dichotic listening in developmental dyslexia and ADHD. Journal of International Neuropsychological Society, 8,
22–36.
Friedman, M. C., Chhabildas, N., Budhiraja, N., Willcutt, E. G., & Pennington, B. F. (2003). Etiology of the comorbidity
between RD and ADHD: Exploration of the non-random mating hypothesis. American Journal of Medical Genetics.
Part B, Neuropsychiatric Genetics, 120, 109–115.
Gayan, J., & Olson, R. K. (1999). Reading disability: Evidence for a genetic etiology. European Child and Adolescent
Psychiatry, 8, S52–S55.
Gayan, J., & Olson, R. K. (2001). Genetic and environmental influences on orthographic and phonological skills in chil-
dren with reading disabilities. Developmental Neuropsychology, 20, 483–507.
Gayán, J., Willcutt, E. G., Fisher, S. E., Francks, C., Cardon, L. R., Olson, R. K., et al. (2005). Bivariate linkage scan for
reading disability and attention-deficit/hyperactivity disorder localizes pleiotropic loci. Journal of Child Psychology
and Psychiatry, 46, 1045–1056.
Ghelani, K., Sidhu, R., Unesh, J., & Tannock, R. (2004). Adolescent with reading disabilities and attention-deficit hyper-
activity disorder. Dyslexia, 10, 364–384.
Gilger, J. W., Pennington, B. F., & DeFries, J. C. (1992). A twin study of the etiology of comorbidity: ADHD and dyslexia.
Journal of the American Academy of Child & Adolescent Psychiatry, 31, 343–348.
Gillberg, C., Gillberg, I. C., Rasmussin, P., Kadesjo, B., Soderstrom, H., Rastam, M., et al. (2004). Co-existing disorders
in ADHD—Implications for diagnosis and intervention. European Child and Adolescent Psychiatry, 13, 80–92.
 ADHD AND DYSLEXIA 489

Grigorenko, E. L., Wood, F. B., Meyer, M. S., Pauls, J. E., Hart L. A., & Pauls, D. L. (2001). Linkage studies suggest a pos-
sible locus for developmental dyslexia on chromosome 1p. American Journal of Medical Genetics, 105, 120–129.
Grigorenko, E. L., Wood, F. B., Golovyan, L., Meyer, M., Romano, C., & Pauls, D. (2003). Continuing the search for dys-
lexia genes on 6p. American Journal of Medical Genetics. Part B, Neuropsychiatric Genetics, 118, 89–98.
Hoeft, F., Meyler, A., Hemandez, A., Juel, C., Taylor-Hill, H., Martindale, J. L., et al. (2007). Functional and mor-
phometric brain dissociation between dyslexia and reading ability. Proceedings of the National Academy of Sciences of
the United States of America, 104, 4234–4239.
Hsiung, G-Y. R., Kaplan, B. J., Petryshen, T. L., Lu, S., & Field, L. L. (2004). A dyslexia susceptibility locus (DYX7)
linked to dopamine D4 receptor (DRD4) region on chromosome 11p15.5. American Journal of Medical Genetic. Part
B, Neuropsychiatric Genetics, 125B, 112–119.
Hynd, G. W., Hern, K. L., Novey, E. S., Eliopulos, D., Marshall, R., Gonzalez, J. J., et al. (1993). Attention deficit-hyper-
activity disorder and asymmetry of the caudate nucleus. Journal of Child Neurology, 8, 339–347.
Igo, R. P. Jr., Chapman, N. H., Berninger, V. W., Matsushita, M., Brkanac, Z., Rothstein, J. H., et al. (2006). Genomewide
scan for real-word reading subphenotypes of dyslexia: Novel chromosome 13 locus and genetic complexity. American
Journal of Medical Genetics. Part B, Neuropsychiatric Genetics, 141B, 15–27.
James, W. H. (2008). Further evidence that some male-based neurodevelopmental disorders are associated with high
intrauterine testosterone concentrations. Developmental Medicine and Child Neurology, 50, 15–18.
Jensen, P. S., Hinshaw, S. P., Kraemer, H. C., Lenora, N., Newcorn, J. H., Abikoff, H. B., et al. (2001). ADHD
comorbidity findings from the MTA study: Comparing comorbid subgroups. Journal of the American Academy of Child
& Adolescent Psychiatry, 40, 147–158.
Kaiser, N. M., Hoza, B., & Hurt, E. A. (2008). Multimodal treatment for childhood attention-deficit/hyperactivity disor-
der. Expert Review of Neurotherapeutics, 8, 1573–1583.
Keulers, E. H., Hendriksen, J. G., Feron, F. J., Wassenberg, R., Wuisman-Frerker, M. G., Jolles, J., et al. (2007).
Methylphenidate improves reading performance in children with attention deficit hyperactivity disorder and comorbid
dyslexia: An unblinded clinical trial. European Journal of Paediatric Neurology, 11, 21–28.
Kronbichler, M., Hutzler, F., Staffen, W., Mair, A., Ladurner, G., & Wimmer, H. (2006). Evidence for a dysfunction of left
posterior reading areas in German Dyslexic readers. Neuropsychologia, 44, 1822–1832.
Kronbichler, M., Wimmer, H., Staffen, W., Hutzler, F., Mair, A., & Ladurner, G. (2008). Developmental dyslexia: Gray
matter abnormalities in the occipitotemporal cortex. Human Brain Mapping, 29, 613–625.
Kronenberger, W. G., & Dunn, D. W. (2003). Learning disorders. Neurologic Clinics, 1, 941–952.
Lagae, L. (2008). Learning disabilities: Definitions, epidemiology, diagnosis, and intervention strategies. Pediatric
Clinics of North America, 55, 1259–1268.
Li, X., Jiang, J., Zhu, W., Yu, C., Sui, M., Wang, Y., et al. (2007). Asymmetry of prefrontal cortical convolution complex-
ity in males with attention-deficit/hyperactivity disorder using fractal information dimension. Brain & Development,
29, 649–655.
Light, J. C., Pennington, B. F., Gilger, J. W., & DeFries, J. C. (1995). Reading disability and hyperactivity disorder: Evi-
dence for a common genetic etiology. Developmental Neuropsychology, 11, 323–335.
Loo, S. K., Fisher, S. E., Francks, C., Ogdie, M. N., MacPhie, I. L., Yang, M., et al. (2004). Genome-wide scan of reading
ability in affected sibling pairs with attention-deficit/hyperactivity disorder: Unique and shared genetic effects. Molecu-
lar Psychiatry, 9, 485–493.
Mackie, S., Shaw, P., Lenroot, R., Pierson, R., Greenstein, D. K., Nugent, T. F. 3rd, et al. (2007). Cerebellar development
and clinical outcome in attention deficit hyperactivity disorder. American Journal of Psychiatry, 164, 647–655.
Marino, C., Giorda, R., Vanzin, L., Molteni, M., Lorusso, M. L., Nobile, M., et al. (2003). No evidence for association and
linkage disequilibrium between dyslexia and markers of four dopamine-related genes. European Child & Adolescent
Psychiatry, 12, 198–202.
Martinussen, R., Hayden, J., Hogg-Johnson, S., & Tannock, R. (2005). A meta-analysis of working memory impairments
in children with attention-deficit/hyperactivity disorder. Journal American Academy Child Adolescents Psychiatry, 44,
377–384.
Martinussen, R., & Tannock, R. (2006). Working memory impairments in children with attention-deficit hyperactivity
disorder with and without comorbid language learning disorders. Journal of Clinical and Experimental Neuro-
psychology, 28, 1073–1094.
Marzocchi, G. M., Oosterlaan, J., Zuddas, A., Cavolina, P., Geurts, H., Redigolo, D., et al. (2008). Contrasting deficits on
executive functions between ADHD and reading disabled children. Journal of Child Psychology and Psychiatry, 49,
543–552.
490 GERMANÒ, GAGLIANO, CURATOLO

Mayes, S. D., Calhoun, S. L. & Crowell, E. W. (2000). Learning disabilities and ADHD: Overlapping spectrum disorder.
Journal of Learning Disabilities, 33, 417–424.
Mayes, S. D., & Calhoun, S. L. (2007). Learning attention, writing, and processing speed in typical children and children
with ADHD, autism, anxiety, depression, and oppositional- defiant disorder. Child Neuropsychology, 13, 469–493.
Muhle, R., Trentacoste, S. V., & Rapin, I. (2004). The genetic of autism. Pediatrics, 113, e472–486.
Nicolson, R. I., Fawcett, A. J., & Dean, P. (2001). Developmental dyslexia: The cerebellar deficit hypothesis. Trends in
Neurosciences, 24, 508–511.
Nigg, J. T., Hinshaw, S. P., Carte, E., & Treuting, J. (1998). Neuropsychological correlates of childhood attention-defi-
cit/hyperactivity disorders: Explainable by comorbid disruptive behavior or reading problems? Journal of Abnormal
Psychology, 107, 468–480.
Nigg, J. T. (2005). Neuropsychologic theory and findings in ADHD: The state of the field and salient challenges for the
coming decade. Biological Psychiatry, 57, 1424–1435.
Nigg, J. T. (2006). What causes ADHD? Understanding what goes wrong and why. New York: Guilford Press.
Nopola-Hemmi, J., Myllyluoma, B., Haltia, T., Taipale, M., Ollikainen, V., Ahonen, T., et al. (2001). A dominant gene for
developmental dyslexia on chromosome 3. Journal of Medical Genetics, 38, 658–664.
Ogdie, M. N., Macphie, I. L., Minassian, S. L., Yang, M., Fisher, S. E., Francks, C., et al. (2003). A genomewide scan for
attention-deficit/hyperactivity disorder in an extended sample: Suggestive linkage on 17p11. American Journal of Hu-
man Genetics, 72, 1268–1279.
Orton Society. (1995). Definition of dyslexia: Report from committee of members. Perspectives, 21, 16–17.
Pennington, B. F., Grossier, D., & Welsh, M. C. (1993). Contrasting deficits in attention deficit hyperactivity disorder ver-
sus reading disability. Developmental Psychology, 29, 511–523.
Pennington, B. F. (2006). From single to multiple deficit models of developmental disorders. Cognition, 101, 385–413.
Pineda, D. A., Restrepo, M. A., Sarmiento, R. J., Gutierrez, J. E., Vargas, S. A., Quiroz, Y. T., et al. (2002). Statistical anal-
yses of structural magnetic resonance imaging of the head of the caudate nucleus in Colombian children with atten-
tion-deficit hyperactivity disorder. Journal of Child Neurology, 17, 97–105.
Pisecco, S., Baker, D. B., Silva, P. A., & Brooke, M. (1996). Behavioral distinctions in children with reading disabilities
and/or ADHD. Journal of the American Academy of Child and Adolescent psychiatry, 35, 1477–1484.
Pisecco, S., Baker, D. B., Silva, P. A., & Brooke, M. (2001). Boys with reading disabilities and/or ADHD: Distinctions in
early childhood. Journal of Learning Disabilities, 34, 98–106.
Pueyo, R., Maneru, C., Vendrell, P., Mataro, M., Estevez Gonzales, A., Garcia-Sanchez, C., et al. (2000). Attention deficit
hyperactivity disorder. Cerebral asymmetry observed on magnetic resonance. Revista de Neurología, 30, 920–925.
Purvis, K. L., & Tannock, R. (1997). Language abilities in children with attention deficit hyperactivity disorder, reading
disabilities, and normal controls. Journal of Abnormal Child Psychology, 25, 133–144.
Purvis, K. L., & Tannock, R. (2000). Phonological processing, not inhibitory control, differentiates ADHD and reading
disability. Journal of the American Academy of Child & Adolescent Psychiatry, 39, 485–494.
Raberger, T., & Wimmer, H. (2003). On the automaticity/cerebellar hypothesis of dyslexia: Balancing and continuos rapid
naming in dyslexic and ADHD. Neuropsychologia, 41, 1493–1497.
Ramus, F., Rosen, S., Dakin, S. C., Day, B. L., Castellote, J. M., White, S., et al. (2003) Theories of developmental dys-
lexia: Insights from a multiple case study of dyslexic adults. Brain, 126, 841–865.
Raskind, W. H., Igo, R. P., Chapman, N. H., Berninger, V. W., Thomson, J. B., Matsushita, M., et al. (2005). A genome
scan in multigenerational families with dyslexia: Identification of a novel locus on chromosome 2q that contributes to
phonological decoding efficiency. Molecular Psychiatry, 10, 699–711.
Richardson, A. J., & Puri B. K. (2002). A randomized double-blind, placebo-controlled study of the effects of sup-
plementation with highly unsaturated fatty acids on ADHD-related symptoms in children with specific learning diffi-
culties. Progress in Neuro-Psychopharmacology and Biological Psychiatry, 26, 233–239.
Romanos, M., Freitag, C., Jacob, C., Craig, D. W., Dempfle, A., Nguyen, T. T., et al. (2008). Genome-wide linkage analy-
sis of ADHD using high-density SNP arrays: Novel loci at 5q13.1 and 14q12. Molecular Psychiatry, Feb 26 (Epub
ahead of print).
Rubia, K., Overmeyer, S., Taylor, E., Brammer, M., Williams, S. C., Simmons, A., et al. (1999). Hypofrontality in atten-
tion deficit hyperactivity disorder during higher-order motor control: A study with fnctional MRI. American Journal of
Psychiatry, 156, 891–896.
Rubia, K., Smith, A. B., Brammer, M. J., Toone, B., & Taylor, E. (2005). Abnormal brain activation during inhibi-
tion and error detection in medication- naive adolescents with ADHD. American Journal of Psychiatry, 162,
1067–1075.
 ADHD AND DYSLEXIA 491

Rubia, K., Smith, A. B., Brammer, M. J., & Taylor, E. (2007). Temporal lobe dysfunction in medication-naïve boys with
attention-deficit/hyperactivity disorder during attention allocation and its relation to response variability. Biological
Psychiatry, 62, 999–1006.
Rucklidge, J. J., & Tannock, R. (2002). Neuropsychological profiles of adolescents with ADHD: Effects of reading diffi-
culties and gender. Journal of Child Psychology and Psychiatry, 23, 988–1003.
Sanson, A., Prior, M., & Smart, D. (1996). Reading disabilities with and without behaviour problems at 7-8 years: Predic-
tion from longitudinal data from infancy to 6 years. Journal of Child Psychology and Psychiatry, 37, 529–541.
Schrimsher, G. W., Billingsley, R. L., Jackson, E. F., & Moore, B. D. 3rd. (2002). Caudate nucleus volume asymmetry
predicts attention-deficit hyperactivity disorder (ADHD) symptomatology in children. Journal of Child Neurology, 17,
877–884.
Seidman, L. J., Biederman, J., Monuteaux, M. C., Coyle, A. E., & Faraone, S. V. (2001). Learning disabilities and execu-
tive dysfunction in boys with attention-deficit/hyperactivity disorder. Neuropsychology, 15, 544–556.
Seidman, L. J., Biederman, J., Faraone, S. V, Weber, W., Mennin, D., & Jones, J. (1997). A pilot study of neuro-
psychological functions in girls with ADHD. Journal of the American Academy of Child and Adolescent Psychiatry, 35,
355–373.
Semrud-Clickeman, M., Biederman, J., Sprich-Buckminster, S., Lehman, B. K., Faraone, S. V., & Norman, D. (1992).
Comorbidity between ADHD and learning disability: A review and report in a clinically referred sample. Journal of the
American Academy of Child & Adolescent Psychiatry, 31, 439–448.
Semrud-Clickeman, M., Guy, K., & Griffin, J. D. (2000). Rapid naming deficits in children and adolescents with reading
disabilities and attention deficits hyperactivity disorder. Brain and Language, 74, 70–83.
Sergeant, J. A., Oosterlaan, J., & Meere van der, J. J. (1999). Information processing and energetic factors in attention-def-
icit/hyperactivity disorder. In H. C. Quay & A. Hogan (Ed.), Handbook of disruptive behaviour disorders (pp. 75–104).
New York: Plenum Press.
Sergeant, J. A. (2005). Modelling ADHD: A critical appraisal of the cognitive-energetic model. Biological Psychiatry, 57,
1248–1253.
Shafritz, K. M., Marchione, K., Gore, J. C., Shaywitz, S. E., & Shaywitz, B. A. (2004). The effect of methylphenidate on
neural systems of attention in ADHD. American Journal of Psychiatry, 161, 1990–1997.
Shanahan, M. A., Pennington, B. F., Yerys, B. E., Scott, A., Boada, R., Willcutt, E. G., et al. (2006). Processing speed defi-
cits in attention deficit/hyperactivity disorder and reading disability. Journal of Abnormal Child Psychology, 34,
585–602.
Shanahan, M. A., Pennington, B. F., & Willcutt, E. W. (2008). Do motivational incentives reduce the inhibition deficit in
ADHD? Developmental Neuropsychology, 33, 137–159.
Shaywitz, B. A., Lyon, G. R., Shaywitz, S. E. (2006). The role of functional magnetic resonance in understanding reading
and dyslexia. Developmental Neuropsychology, 30, 613–632.
Shaywitz, B. A., Shaywitz, S. E., Pugh, K. R., Mencl, W. E., Fulbright, R. K., Skudlarski, P., et al. (2002). Disruption of
posterior brain systems for reading in children with developmental dyslexia. Biological Psychiatry, 52, 101–110.
Shaywitz, S. E., Gruen, J. R., & Shaywitz, B. A. (2007). Management of dyslexia, its rationale, and underlying
neurobiology. Pediatric Clinics of North America, 54, 609–623.
Shaywitz, S. E., Shaywitz, B. A., Pugh, K. R., Fulbright, R. K., Constable, R. T., Mencl, W. E., et al. (1998). Functional
disruption in the organization of the brain for reading in dyslexia. Proceedings of the National Academy of Sciences of
the United States of America, 95, 2636–2641.
Silk, T., Vance, A., Rinehart, N., Egan, G., O’Boyle, M., Bradshaw, J. L., et al. (2005). Fronto-parietal activation in atten-
tion-deficit hyperactivity disorder, combined type: Functional magnetic resonance imaging study. British Journal of
Psychiatry, 187, 282–283.
Sinn, N., Bryan, J., & Wilson, C. (2008). Cognitive effects of polyunsaturated fatty acids in children with attention deficit hyper-
activity disorder symptoms: A randomised controlled trial. Prostaglandins Leukotrienes Essent Fatty Acids, 78, 311–326.
Smith, A. B., Taylor, E., Brammer, M., Toone, B., & Rubia, K. (2006). Task-specific hypoactivation in prefrontal and
temporoparietal brain regions during motor inhibition and task switching in medication-naive children and adolescents
with attention deficit hyperactivity disorder. American Journal of Psychiatry, 163, 1044–1051.
Snowling, M. (2000). Dyslexia (2nd ed.). Oxford: Blackwell.
Sonuga-Barke, E. J. S. (1994). On dysfunction and function in psychological theories of childhood disorders. Journal of
Child Psychology and Psychiatry, 35, 801–815.
Sonuga-Barke, E. J. (2005). Causal models of attention-deficit /hyperactivity disorder: From common simple deficits to
multiple developmental pathways. Biological Psychiatry, 57, 1231–1238.
492 GERMANÒ, GAGLIANO, CURATOLO

Spencer, T., Biederman, J., Wilens, T., Harding, M., O’Donnell, D., & Griffin, S. (1996). Pharmacotherapy of ADHD
across the life circle. Journal of the American Academy of Child & Adolescent Psychiatry, 35, 409–432.
Stein, J. (2001). The sensory basis of reading problems. Developmental Neuropsychology, 20, 509–534.
Stevens, L. J., Zentall, S. S., Deck, J. L., Abate, M. L., Watkins, B. A., Lipp, S. R., et al. (1995). Essential fatty acid metab-
olism in boys with attention-deficit hyperactivity disorder. American Journal of Clinical Nutrition, 62, 761–768.
Stevenson, J., Pennington, B. F., Gilger, J. W., DeFries, J. C., & Gillis, J. J. (1993). Hyperactivity and spelling disability:
Testing for shared genetic aetiology. Journal of Child Psychology and Psychiatry, 34, 1137–1152.
Stevenson, J., Langley, K., Pay, H., Payton, A., Worthington, J., Ollier, W., et al. (2005). Attention deficit hyperactivity
disorder with reading disabilities: Preliminary genetic findings on the involvement of the ADRA2A gene. Journal of
Child Psychology and Psychiatry, 46, 1081–1088.
Stordy, B. J. (2000). Dark adaptation, motor skills, docosahexaenoic acid, and dyslexia. American Journal of Clinical Nu-
trition, 71, 323S–326S.
Sundheim, S. T., & Voeller, K. K. (2004). Psychiatric implications of language disorders and learning disabilities: Risks
and management. Journal of Child Neurology, 19, 814–826.
Swanson, H. L., Mink, J., & Bocian, K. M. (1999). Cognitive processing deficits in poor readers with symptoms of reading
disabilities and ADHD: More a like than different? Journal of Educational Psychology, 91, 321–333.
Tamm, L., Menon, V., Ringel, J., & Reiss, A. L. (2004). Event-related fMRI evidence of frontotemporal involvement in
aberrant response inhibition and task switching in attention-deficit/hyperactivity disorder. Journal of the American
Academy of Child & Adolescent Psychiatry, 43, 1430–1440.
Tannock, R., Martinussen, R., & Frijters, J. (2000). Naming sped performance and stimulant effects indicate effortful, se-
mantic processing deficit in attention deficit/hyperactivity disorder. Journal of the American Academy of Child and Ad-
olescent Psychiatry, 28, 237–252.
Temple, E., Poldrack, R. A., Salidis, J., Deutsch, G. K., Tallal, P., Merzenich, M. M., et al. (2001). Disrupted neural re-
sponses to phonological and orthographic processing in dyslexic children: An fMRI study. Neuroreport, 12,
299–307.
Temple, E. (2002). Brain mechanisms in normal and dyslexic readers. Current Opinion in Neurobiology, 12, 178–183.
Tiffin-Richards, M. C., Hasselhorn, M., Woerner, W., Rothenberger, A., & Banaschewski, T. (2008). Phonological
short-term memory and central executive processing in attention-deficit/hyperactivity disorder with/without dys-
lexia—Evidence of cognitive overlap. Journal of Neural Transmission, 115, 227–234.
Uhlíkova, P., Paclt, I., Vaneckova, M., Morcinek, T., Seidel, Z., Krasensky, J., et al. (2007). Asymmetry of basal ganglia in
children with attention deficit hyperactivity disorder. Neuroendocrinology Letters, 28, 604–609.
Valera, E. M., Faraone, S. V., Murray, K. E., & Seidman, L. J. (2007). Meta-analysis of structural imaging findings in at-
tention-deficit/hyperactivity disorder. Biological Psychiatry, 61, 1361–1369.
Vance, A., Silk, T. J., Casey, M., Rinehart, N. J., Bradshaw, J. L., Bellgrove, M. A., et al. (2007). Right parietal dysfunc-
tion in children with attention deficit hyperactivity disorder, combined type: A functional MRI study. Molecular Psy-
chiatry, 12, 826–832.
Vinckenbosch, E., Robichon, F., & Eliez, S. (2005). Gray matter alteration in dyslexia: Converging evidence from volu-
metric and voxel-by-voxel MRI analyses. Neuropsychologia, 43, 324–331
Voeller, K. K. S. (2004). Attention-deficit hyperactivity disorder (ADHD). Journal of Child Neurology, 19, 798–814.
Wellington, T. M., Semrud-Clikeman, M., Gregory, A. L., Murphy, J. M., & Lancaster, J. L. (2006). Magnetic resonance
imaging volumetric analysis of the putamen in children with ADHD: Combined type versus control. Journal of Atten-
tion Disorders, 10, 171–180.
Wilens, T. E., & Spencer, T. J. (2000). The stimulants revisited. Child and Adolescent Psychiatric Clinics of North Amer-
ica, 9, 573–603.
Willcutt, E. G., & Pennington, B. F. (2000a). Comorbidity of reading disability and attention-deficit/hyperactivity disor-
der: Differences by gender and subtype. Journal of Learning Disabilities, 33, 179–191.
Willcutt, E. G., & Pennington, B. F. (2000b). Psychiatric comorbidity in children and adolescent with reading disability.
Journal of Child Psychology and Psychiatry, 41, 1039–1048.
Willcutt, E. G., Pennington, B. F., & DeFries, J. C. (2000c). A twin study of comorbidity between attention-deficit/hyper-
activity disorder and reading disability. American Journal of Medical Genetics (Neuropsychiatrics Genetics), 96,
293–301.
Willcutt, E. G., Pennington, B. F., Boada, R., Ogline, J. S., Tunick, R. A., Chhabildas, N. A., et al. (2001). A comparison of
the cognitive deficits in reading disability and attention-deficit/hyperactivity disorder. Journal of Abnormal Psychol-
ogy, 110, 157–172.
 ADHD AND DYSLEXIA 493

Willcutt, E. G., Pennington, B. F., Smith, S. D., Cardon, L. R., Gayán, J., Knopik, V. S., et al. (2002). Quantitative trait lo-
cus for reading disability on chromosome 6p is pleiotropic for attention-deficit/hyperactivity disorder. American Jour-
nal of Medical Genetics, 114, 260–268.
Willcutt, E. G., DeFries, J. C., Pennington, B. F., Olson, R. K., Smith, S. D., & Cardon, L. R. (2003). Genetic etiology of
comorbid reading difficulties and ADHD. In R. Plomin, J. C. DeFries, P. McGuffin, & I. Craig (Ed.), Behavioural ge-
netics in a postgenomic era (pp. 227–246). Washington, DC: American Psychological Association.
Willcutt, E. G, Doyle, A. E., Nigg, J. T., Faraone S. V., & Pennington, B. F. (2005a). Validity of the executive function the-
ory of attention-deficit/hyperactivity disorder: A meta-analytic review. Biology Psychiatry, 57, 1336–1346.
Willcutt, E. G., Pennington, B. F., Olson, R. K., Chhabildas, N., & Hulslander, J. (2005b). Neuropsychological analyses of
comorbidity between reading disability and attention deficit hyperactivity disorder: In search of the common deficit.
Developmental Neuropsychology, 27, 35–78.
Willcutt, E. G., Pennington, B. F., Olson, R. K., & Defries, J. C. (2007). Understanding comorbidity: A twin study of read-
ing disability and attention-deficit/hyperactivity disorder. American Journal of Medical Genetics. Part B, Neuropsychi-
atric Genetics, 144B, 709–714.
Wisniewska, B., Baranowska, W., & Wendorff, J. (2007). The assessment of comorbid disorders in ADHD children and
adolescents. Advanced Medical Science, 52, 215–217.
Wolf, M., & Browers, P. G. (1999). The double-deficit hypothesis for the developmental dyslexia. Journal of Educational
Psychology, 91, 415–438.
Zadina, J. N., Corey, D. M., Casbergue, R. M., Lemen, L. C., Rouse, J. C., Knaus, T. A., et al. (2006). Lobar asymmetries
in subtypes of dyslexic and control subjects. Journal of Child Neurology, 21, 922–931.
Zang, Y. F., Jin, Z., Weng, X. C., Zhang, L., Zeng, Y. W., Yang, L., et al. (2005). Functional MRI in attention-deficit hy-
peractivity disorder: Evidence for hypofrontality. Brain & Development, 27, 544–550.
Zhou, K., Asherson, P., Sham, P., Franke, B., Anney, R. J., Buitelaar, J., et al. (2008). Linkage to Chromosome 1p36 for at-
tention-deficit/hyperactivity disorder traits in school and home settings. Biological Psychiatry, Apr 23 (Epub ahead of
print).
Ziegler, A., Konig, I. R., Deimel, W., Plume, E., Nothen, M. M., Propping, P., et al. (2005). Developmental dyslexia—Re-
currence risk estimates from a German bi-center study using the single proband sib pair design. Human Heredity, 59,
136–143.
Copyright of Developmental Neuropsychology is the property of Taylor & Francis Ltd and its content may not
be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written
permission. However, users may print, download, or email articles for individual use.