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Provisional chapter1
Co-Occurrence of Developmental Disorders:2
Children Who Share Symptoms of Autism,3
Dyslexia and Attention Deficit Hyperactivity Disorder4
Ginny Russell and Zsuzsa Pavelka5
Additional information is available at the end of the chapter6
http://dx.doi.org/10.5772/541597
1. Introduction8
Children with autism spectrum disorders (ASD) have a higher risk of suffering from several9
other conditions. In this chapter I review the extent to which autistic individuals can also expe‐10
rience a range of other difficulties, but my focus will be on the common neurodevelopmental11
disorders. The most common of these include dyslexia, attention deficit hyperactivity disorder12
(ADHD), dyspraxia, specific language impairment, and dyscalculia. There is considerable13
symptom overlap in particular between ADHD and dyslexia, and like autism both are descri‐14
bed as developmental disorders by psychiatric classification systems (American Psychiatric15
Association, 2000; World Health Organization., 1992). Overlapping conditions are termed ‘co-16
morbidity’ by medical practitioners. Co-morbidity may reflect the greater difficulties experi‐17
enced by children with a combination of deficits. Sometimes it is apparent that many children18
with a developmental disorder could be classified in several ways. Here I will firstly examine19
the research evidence that examines how often symptoms of dyslexia and ADHD occur in the20
population of autistic children, and second, review the various theories that have tried to ex‐21
plain why such co-occurring difficulties are so common.22
‘Comorbidity’, a term used in medical literature to mean a dual diagnosis, or multiple diag‐23
noses, can reflect an inability to supply a single diagnosis that accounts for all symptoms.24
Children with ASD have been shown to have higher rates of epilepsy, with 30% of cases25
have epilepsy comorbid (Danielsson, Gillberg, Billstedt, Gillberg, & Olsson, 2005). Other26
conditions that are commonly co-morbid with ASD include hearing impairment (Kielinen,27
Rantala, Timonen, Linna, & Moilanen, 2004) mental health and behavioural problems (Brad‐28
ley, Summers, Wood, & Bryson, 2004), anxiety, and depression (Evans, Canavera, Kleinpet‐29
© 2012 Russell and Pavelka; licensee InTech. This is an open access article distributed under the terms of the
Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits
unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
er, Maccubbin, & Taga, 2005). It has also been shown that parents of autistic children are1
twice as likely themselves to have suffered from psychiatric illness than parents of non-au‐2
tistic children (Daniels et al., 2008).3
Most of these problems are distinct from those examined in this chapter: the common devel‐4
opmental disorders of childhood which are also found to co-occur with autism, particularly5
ADHD and dyslexia.6
Before reviewing the evidence that suggests many children share difficulties symptomatic of7
these conditions, and the theories of why this may be, I will briefly describe how dyslexia8
and ADHD manifest themselves.9
2. Dyslexia10
Dyslexia is conceptualized by both educational bodies and the psychiatric classification sys‐11
tems as a learning difficulty that primarily affects the skills involved in accurate and fluent12
word reading and spelling. Characteristic features of dyslexia are difficulties in phonological13
awareness, verbal memory and verbal processing speed. Dyslexia is developmental delay in14
literacy and generally slow and inaccurate reading and spelling. The definition of dyslexia has15
changed over time, and such changes have often been based on the research that has identified16
a range of associated difficulties that occur with dyslexia. Estimates of the prevalence of dyslex‐17
ia have been complicated because dyslexia cut-offs are contested (Coltheart & Jackson, 1998)18
and dyslexia manifests itself differently in various languages according to levels of phonic reg‐19
ularity (Miles, 2004). Research over the last 40 years has focused on phonological skills. These20
are the reading and de-coding skills used when breaking down language into its component21
sounds and reassembling the parts in order to read or to spell a word.22
Like autism, dyslexic difficulties are considered to exist in a continuum throughout the general23
population (Fawcett, 2012). There is much interest in the association of cognitive ability with24
changing symptom profiles and diagnosis. The definition of dyslexia is in flux, and has been re‐25
cently redefined by many national bodies, for example in the UK, the British Psychological So‐26
ciety, focusing on literacy learning at the 'word level' without attainment discrepancy:27
Dyslexia is evident when accurate and fluent word reading and/or spelling develops very incompletely or with great28
difficulty (British Psychological Society, 1999)29
This definition implies that the problem is severe and persistent despite appropriate learn‐30
ing opportunities. This UK definition differs from the ICD-10 diagnosis of developmental31
dyslexia or ‘Specific Reading Disorder’, which requires a discrepancy between actual read‐32
ing ability and the reading ability predicted by a child’s IQ. So an intellectual disability,33
(generally considered IQ below 70) can co-occur with the British Psychological Society defi‐34
nition of dyslexia. This new definition includes the so called ‘garden variety’ dyslexic chil‐35
Autism / Book 1
2
dren who have difficulties with reading and spelling as well as other generalized intellectual1
disabilities. The implications of including this group as dyslexic mean that more children2
with an intellectual disability would also be classified as ‘dyslexic’. As ASD includes a large3
group with intellectual disability the extension is likely to increase the number of children4
who may be classified as having both conditions. This is important as the clinical and educa‐5
tion label may determine the interventions a particular child receives.6
In addition to these characteristics, dyslexic children may experience visual and auditory7
processing difficulties, similar to hyper or hypo sensitivity often associated with ASD. Like8
the ‘islets of ability’ seen in many children with ASD, some dyslexic children may also have9
strengths in particular areas, such as design, logic, and creative skills.10
3. ADHD11
ADHD is known as ‘Hyperkinetic Disorder’ in ICD-10; there are three subtypes of ADHD12
according the DSM. In the first, a child will primarily have problems with attention which13
may manifest as an inability to remain ‘on task’ for long periods, lack of response to instruc‐14
tion or distractibility. In the second sub-type, symptoms of hyperactivity and impulsivity15
dominate, which is characterized by wriggling, squirming, being unable to sit still, inter‐16
rupting and finding it difficult to wait. Children may also be climbing in inappropriate sit‐17
uations and always on the move when free to do so. The third sub-type is simply the co-18
existence of both attention problems and hyperactivity, with each behavior occurring19
infrequently alone and symptoms starting before seven years of age.20
According to ICD-10, eventually, assessment instruments should develop to the point where21
it is possible to take a quantitative cut-off score to assess ADHD. Like dyslexia and autism,22
the symptoms are behavioural in nature, and are part of a continuously distributed pattern23
that extends into the population at large.24
The persistence of ADHD symptoms is not so marked as for autism. Around 70 to 50 per‐25
cent of those individuals diagnosed in childhood do not continue to have symptoms into26
adulthood (Elia, Ambrosini, & Rapoport, 1999). There is evidence suggesting to some extent27
symptoms of ADHD are expressed in reaction to home (Mulligan et al. 2011) and other envi‐28
ronmental contexts. Individuals with ADHD also tend to develop coping mechanisms to29
compensate for some or all of their impairments. ADHD is diagnosed more often in boys30
with the reported ratio varying from 2:1 to 4:1 (Dulcan, 1997; Kessler et al., 2005) though31
some studies suggest this may be partially due to referral bias where teachers are more like‐32
ly to refer boys than girls (Sciutto, Nolfi, & Bluhm, 2004). Treatments for ADHD involve a33
combination of medication, usually methyphenidates which are well established in improv‐34
ing symptoms of inattention, and behavioral intervention in education and at home. The is‐35
sue of girls being overlooked on identification is a common thread for research in dyslexia,36
ADHD and autism. Our own results suggest there is some evidence to back up the claim37
that boys with ASD symptoms are given the diagnosis more frequently than girls with38
Co-Occurrence of Developmental Disorders: Children who Share Symptoms of Autism, Dyslexia and Attention Deficit
Hyperactivity Disorder
http://dx.doi.org/10.5772/54159
3
equivalent ASD symptoms (Russell, Steer, & Golding, 2011). This may be because the disor‐1
ders tend to be conceptualized as ‘male’ leading to referral bias.2
Because ASD, Dyslexia and ADHD are all behaviorally defined, so ‘symptoms’ are behaviours.3
All three conditions are conceived as particular behaviours along a spectrum, where traits have4
a continuous distribution and extend into the general (non-disordered) population. An arbitra‐5
ry cut off point determines who is considered to be within the various categories and who is6
not. The clinician giving a diagnosis will be responsible for judging where this cut off may7
come, guided by diagnostic criteria and standards within disciplines as well as perceived im‐8
plications: the benfits versus any possible risks of assigning a diagnosis. This is perhaps best es‐9
tablished for autism: Constantino and Todd (2003) measured autistic traits in a large10
community sample, and found no jump in the threshold of autistic behaviours between ‘nor‐11
mal’ individuals and those with an autism spectrum diagnosis, rather they found a continuous12
distribution. These findings concurred with those in a Scandinavian study (Posserud, Lunder‐13
vold, & Gillberg, 2006). One of our own studies has likewise shown that autistic traits do ex‐14
tend into the ‘subclinical’ population (Figure 1). As with dyslexia and ADHD, there is no a15
sharp line separating severity in those with a diagnosis from less severe traits in those without16
(London, 2007). In both dyslexia, ADHD and the autism spectrum, some children have more17
severe difficulties than others, and the symptoms extend into the population of children (and18
adults) as a whole. For dyslexia, there are many people who may have mild dyslexic difficul‐19
ties but perhaps might not qualify as ‘dyslexic’. For autism spectrum disorders, many people20
without an autism diagnosis do have autistic-type behaviours but the severity and frequency21
of those behavioural symptoms is less severe than in those deemed to qualify for a diagnosis.22
23
Figure 1. The distribution of an ASD composite trait in the general population from Russell et al.(2012)24
Autism / Book 1
4
The imposition of a cut off between normality and abnormality is therefore ‘an arbitrary but1
convenient way of converting a dimension into a category’ as Goodman and Scott (1997, p.2
23) point out.3
4. Evidence of symptom overlap – ASD and ADHD4
Various studies have looked for ADHD or ADHD symptoms in samples of children with5
autism or ASD. Rates of ADHD have ranged from 28% to 78% of these samples (Ronald,6
Edelson, Asherson, & Saudino, 2010). Studies that look at ADHD symptoms have reported7
even higher numbers: for example, Sturm, Fernell, & Gillberg, (2004) looked at a sample of8
around 100 high functioning children with ASD and found 95% had attention problems,9
75% had motor difficulties, 86% had problems with regulation of activity level, and 50% had10
impulsiveness. About three-quarters had symptoms compatible with mild or severe ADHD,11
or had deficits in attention, motor control, and perception, indicating a considerable overlap12
between these disorders and high-functioning ASD in children.13
In an large analysis of nine hundred forty-six twins, Reierson and colleagues (2008) assigned14
DSM-IV ADHD diagnoses, and measured autistic traits using the Social Responsiveness15
Scale. The study showed that there are clinically significant elevations of autistic traits in16
children meeting diagnostic criteria for ADHD. These findings confirm results in earlier17
studies (Clark, Feehan, Tinline, & Vostanis, 1999). Santosh and Mijoovic (2004) which found18
children with ADHD had elevated levels of impairment in all three autistic symptom do‐19
mains, namely social deficits, communication and stereotyped behaviors. Clark et al found20
65-80% of parents of children with ADHD reported difficulties in social interaction (particu‐21
larly in empathy and peer relationships) and in communication (particularly in imagination,22
and maintaining conversation). So the presence of autistic traits in children with ADHD ap‐23
pears common (Ronald et al., 2010).24
In an analysis conducted with Lauren Rodgers at the Peninsula Medical School in the UK25
using data from the Millennium Cohort Study, a cohort of around 19,000 children who were26
all born between 2000 and 2002, we noted 44 children had a dual diagnosis of both ASD and27
ADHD (proportion of total population 0.3%) by age seven. The prevalence of children with28
identified ADHD in the ASD sample was 17%. Conversely, the prevalence of children with29
ASD in the ADHD sample was higher at 27%. Both figures indicate substantial overlap be‐30
tween these conditions.31
Various European research groups have examined co-morbid disorders in adults with diag‐32
nosed ASD. An international team lead by Hofvander studied a group of 122 adults with33
normal IQ from specialist clinics in three European cities, Gothenburg, Paris and Malmö34
(Hofvander et al., 2009). Here the overwhelming majority had symptoms of ASD. Nonverbal35
communication problems were also very common, described in 89% of all their subjects. In36
this study over half the participants, (52%) were diagnosed with co-morbid ADHD. Interest‐37
ingly, participants diagnosed with pervasive developmental disorder. ‘Not Otherwise Speci‐38
fied’ (PDD-NOS) diagnosis had significantly more symptoms of inattention and39
Co-Occurrence of Developmental Disorders: Children who Share Symptoms of Autism, Dyslexia and Attention Deficit
Hyperactivity Disorder
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5
hyperactivity/impulsivity compared to subjects diagnosed with Asperger’s syndrome. How‐1
ever, the prevalence of the categorical diagnosis of ADHD did not differ significantly be‐2
tween the groups, nor were gender differences apparent. Although the study presents clear3
evidence of many cases where patients display symptoms of both ADHD and ASD, the clin‐4
ical setting may have led to selection bias as patients with complex needs may be more like‐5
ly to seek help.6
Because behaviours associated with both conditions lie on a spectrum extending into the7
normal range, some studies have found a range of frequency and severity of symptoms. In8
Mulligan et al.’s (2009) study, for example, 75 of children with ADHD had severe autism9
traits, and over half showed sub-clinical autism symptoms. Kadesjö and colleagues (Kades‐10
jö, Gillberg, & Hagberg, 1999), however, looked at comorbidity of ADHD in Swedish school-11
age children and found only 1% of children meeting the threshold for ADHD had comorbid12
Aspergers Syndrome (AS). The estimates of co-morbidity of ADHD symptoms with ASD13
symptoms vary widely because of differing methods of case ascertainment. An additional14
problem is that the estimate of the prevalence of ASD itself has increased so much in west‐15
ern countries, making ASD itself a ‘moving target’ (Figure 2).16
Patricia Howlin (2000) reviewed the estimated rates of co-existing psychiatric disorders in17
subjects with high functioning ASD and found these estimates varied from 9% to 89% - very18
substantial differences. However it is possible to generalise; thirty years of research have19
confirmed that attention deficits and hyperactivity are relatively common in children and20
adults with ASD even if the exact extent of overlap is dependent on methodology and ascer‐21
tainment (Hofvander et al., 2009, Sturm, Fernell, & Gillberg, 2004).22
23
Figure 2. The rising prevalence of autism spectrum disorders over 50 years. (Data from ‘Autism Speaks’ and CDC, USA)24
Recent trends have made categorical diagnosis an integral part of everyday clinical and re‐25
search practice (Sonuga-Barke & Halperin, 2010). Christopher Gillberg (2010) points out that26
clinicians have become focused on dichotomous categories of disorder and that clinics have27
become increasingly specialized and overlook difficulties not within their immediate juris‐28
Autism / Book 1
6
diction. Gillberg has argued that co-existence of disorders is the rule rather than the excep‐1
tion in child psychiatry and developmental medicine. He has coined the acronym ESSENCE2
(referring to Early Symptomatic Syndromes Eliciting3
Neurodevelopmental Clinical Examinations). This describes cases where a combination of4
symptoms including inattention, hyperactivity, social and reading difficulties are observed.5
Major problems in at least one ESSENCE domain before age 5 years often signal major prob‐6
lems in the same or overlapping domains years later.7
To summarize, although ADHD and ASD are separate and recognizable, there is good evi‐8
dence that these conditions co-occur, constituting an amalgam of problems.9
5. Comorbidity between dyslexia and ASD10
There is only a small literature on the overlap in symptomology between autism spectrum11
disorders with those of dyslexia. Officially, as for ADHD, ASD is an exclusionary criterion12
for diagnosis of dyslexia and vice versa, and ASD also shows overlap with dyslexia in both13
cognitive and behavioural features (Reiersen & Todd, 2008, Simonoff et al., 2008). A propor‐14
tion of children share symptoms between dyslexia, ADHD and ASD.15
The proportion of children that do share symptoms of ASD and dyslexia is likely to be small16
(Wright, Conlon, Wright, & Dyck, 2011). The frequency of reading disorder in combination17
with disorder of written expression (i.e. dyslexia) was around 14% in a sample of adults18
with Asperger’s Syndrome (AS) so according to this result around one in seven individuals19
with AS will have co-occurring dyslexia (Hofvander et al., 2009). However the proportion of20
individuals with dyslexia who have co-occuring AS is likely to be low as Asperger’s Syn‐21
drome is much a rarer condition than dyslexia.22
A common problem for children with dyslexia is misinterpretation of spoken language,23
which can also manifest itself in comprehension. This produces further overlap with prag‐24
matic language impairment (PLI) which itself is virtually indistinguishable from communi‐25
cation difficulties associated with high functioning autism. Pragmatic language difficulties26
may involve literal interpretation so ‘run on the spot’ would have a child looking for a big27
black spot to run on, for example. Children with PLI will often fail to interpret the core28
meaning or saliency of events. This causes a penchant for routine and 'sameness' (also seen29
in autism and Asperger's Syndrome) as PLI children struggle to generalize and take hold of30
the meaning of novel situations. Obvious and concrete instructions are clearly understood31
and carried out, whereas simple but non-literal expressions such as jokes, sarcasm and gen‐32
eral social chatting are difficult and may be misinterpretated. PLI may therefore impact on33
the social abilities of the child who has difficulty interpreting jokes. Current thinking is that34
PLI is not a problem rooted in language skills but one of social communication and informa‐35
tion processing. Griffiths (2007) identified difficulties of this type in dyslexic students,36
showed they were impaired in making inferences from a story and choosing the right37
punch-line for a joke. This of course can have implications for written language and exami‐38
nations under stress, as well as for a range of social interactions.39
Co-Occurrence of Developmental Disorders: Children who Share Symptoms of Autism, Dyslexia and Attention Deficit
Hyperactivity Disorder
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7
It is not just that ASD is co-morbid with dyslexia and ADHD. Other studies have noted high1
comorbidity with other developmental disorders. Dyspraxia and dyscalculia and conditions2
with shared symptoms such as specific language impairment are frequently comorbid with3
autism. Also dyslexia and ADHD themselves co-occur: Willcutt and colleagues (Willcutt,4
Doyle, Nigg, Faraone, & Pennington, 2005) showed that 40% of a sample of twins with ei‐5
ther dyslexia or ADHD was co-morbid for the other disorder. Reading difficulties were6
measured with both rating scale and an objective task in a study by Cheung et al. (2012) and7
correlations were observed among ADHD, reading difficulties and IQ. Over half, (53%-72%)8
of the overlapping familial influences between ADHD and reading difficulties were not9
shared with IQ. In a school based study Kadesjö and colleagues found 40% of children with10
ADHD showed reading problems and 29% writing problems (2005). Again, looking at the11
picture built up in the literature, there is good evidence to suggest that some children do12
suffer from symptoms of both dyslexia and ASD, although this is not so well established,13
and does not occur so frequently as co-morbidity between ADHD and ASD.14
6. Reasons for co-occurrence of ASD with other developmental disorders15
Several theories have been put forward to explain the shared symptoms of the various de‐16
velopmental conditions – in other words why specific learning and language and social dis‐17
orders are not specific. It is likely that all the explanations below play a part in co-18
occurrence; the causality of co-morbidity is most probably due to a complex web of19
interacting factors.20
7. Genetic explanations21
One of the most persuasive explanations is that a genetic predisposition may lead to abnor‐22
mal neurological development, which in turn may manifest in various different aberrant be‐23
haviors and developmental delays. As autism, ADHD and dyslexia and other24
developmental conditions are all highly heritable, so they all have a large genetic compo‐25
nent, the theory seems plausible. The same genetic anomaly may lead to several disorders or26
psychiatric conditions. In other words one genotype may lead to several (related) pheno‐27
types. This is known as ‘pleiotropy’. Researchers have suggested that co-occurrence of au‐28
tism and ADHD (and other developmental disorders) may reflect such common genetic29
causes (Reierson et al, 2008). In this model, the origins of both sets of difficulties are due to30
common genetic anomalies that predispose children to delayed or atypical neurological de‐31
velopment. Certainly, specific genetic anomalies have been associated with a range of psy‐32
chopathologies in adulthood. However, the genetic picture is complex and exact pathways33
are not established. It is estimated there are more than a thousand gene variations which34
could disrupt brain development enough to result in social delays (Sanders et al., 2012).35
Such a genetic predisposition is almost certainly complex and multi factorial. So far, over36
100 candidate genes have been associated with ASD, most of which encode proteins in‐37
Autism / Book 1
8
volved in neural development, but exact mutations within the candidate genes have yet to1
be identified (Freitag, 2007). Furthermore, different individuals may have mutations in dif‐2
ferent sets of genes and most of the discovered gene variations are likely to have a low pene‐3
trance, thus not all carriers will develop the disorder. There may be interactions among4
mutations in several genes, e.g. between regulatory genes and coding regions, or between5
the environment and mutated genes, altering their expression. The effect of a mutation or6
deletion can depend on processes relating to gene expression and regulation as well as the7
subsequent effects on the expression of other genes.8
The advent of genomics and the emphasis placed on this has led to much research to identi‐9
fy genetic predispositions to ASD. The field of psychiatry as a whole has been ‘geneticised’10
according to some social theorists. This refers to the potential reclassification of psychiatric11
conditions in the light of findings from molecular biology. For example, a particular sub-cat‐12
egory of DSM-IV schizophrenia has been linked to a substitution of a single base in the se‐13
quence of DNA of a particular gene localised to a precise place on a particular chromosome,14
leading to a substitution of one amino-acid for another in an enzyme involved in neuro‐15
transmission. The increase in research on genetic predisposing factors has lead to a partial16
‘geneticisation’ of many psychiatric conditions. Hedgecoe (2001) provides a discussion of17
the geneticisation of schizophrenia. The debate as to whether the old psychiatric systems of18
classification should be overhauled in the light of new genomic knowledge which illumi‐19
nates genetic aetiologies is ongoing (Ericson & Doyle, 2003).20
8. Gene-environment interactions21
A second theory is that an environmental insult or a stressful event in the life of the fetus or22
in a young child’s life, may trigger a genetic predisposition to be expressed. Thus this consti‐23
tutes a gene- environmental interaction theory. An example might be the high testosterone24
levels in the womb that have been observed in some studies. Baron-Cohen’s Cambridge25
group, for example, has carried out work that has suggested high levels of fetal testosterone26
may be linked to the development of autistic traits ((Ingudomnukul, Baron-Cohen, Wheel‐27
wright, & Knickmeyer, 2007). According to the gene-environment explanation, the elevated28
testosterone might lead to the differential expression of genes controlling the neurological29
development of the child. Another example that has been quite widely publicized concerns30
Omega 3 fatty acids. These have been implicated by Richardson (2006), who has argued that31
attention-deficit/hyperactivity disorder, dyslexia, developmental coordination disorder32
(dyspraxia) and conditions on the autism spectrum may all share common origins triggered33
by problems with phospholipid (fatty acid) metabolism. However this is just one genetic /34
environmental explanation for co-occurrence that vies with several others, and the available35
evidence is subject to interpretation.36
In the majority of cases, the gene-environment hypothesis seems highly plausible. It may37
be that autism and co-occurring developmental conditions may all be caused by a genet‐38
ic predisposition which is triggered by an early environmental influence (Trottier, Srivas‐39
tava, & Walker, 1999).40
Co-Occurrence of Developmental Disorders: Children who Share Symptoms of Autism, Dyslexia and Attention Deficit
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Many environmental factors have been implicated in ASD but the effect of each is poorly1
established. After the well publicized paper that linked autism to the MMR vaccination, re‐2
search has repeatedly refuted a link between the MMR jab and ASD (Rutter, 2005). Deykin3
and MacMahon (1979) found increased risk due to exposure to, and clinical illness from,4
common viral illnesses in the first 18 months of life. In this study, mumps, chickenpox, fever5
of unknown origin, and ear infections were all significantly associated with ASD risk. Epide‐6
miological studies have shown there is a higher rate of adverse prenatal and postnatal7
events in children with ASD than in the general population (Zwaigenbaum et al., 2002).8
Newschaffer and colleague’s (2007) review named associated obstetric conditions that in‐9
cluded low birth weight, gestation duration, and caesarean section. It is possible that such10
an underlying cause partially could explain both autism and the associated conditions (Ko‐11
levzon, Gross, & Reichenberg, 2007). There is evidence to suggest adverse prenatal and peri‐12
natal events are also associated with ADHD and cognitive development. Some studies have13
suggested that the risk of autism may be increased with advancing maternal age (Bolton et14
al., 1997). Paternal age too has frequently (but not always) associated with autism. There are15
more mutations in the gametes of older men, and this higher rate of mutation in the genetic16
material from the paternal side may explain the higher levels of neurodevelopmental disa‐17
bilities in their offspring. An alternative explanation is that fathers who themselves have au‐18
tistic traits are less likely to have children young. Using anticonvulsants during pregnancy19
also appears to increase the risk of ASD (Moore et al., 2000). These drugs are used to combat20
epilepsy which is commonly often comorbid with ASD. Parental occupational exposure to21
chemicals during the preconception period has also been higher in ASD families than con‐22
trols in some studies (Felicetti, 1981).23
Environmental risk factors have received widespread media coverage within the last few24
years, perhaps because of the strong degree of public concern (Russell & Kelly, 2011). In25
most health and disease categories, a secondary function of diagnosis is to group together26
people who have a common aetiology. However, the specific effects of genetic factors and27
environmental risk factors that might play a part in abnormal neural development are large‐28
ly unresolved. Goodman and Scott (1997) stress that current understanding of aetiology for29
childhood developmental conditions will probably look ridiculously simplistic or misguid‐30
ed in years to come. Despite, or perhaps because of, the uncertainty, there is an underlying31
concern among people involved with children who are diagnosed with developmental con‐32
ditions that environmental influences may be partially to blame for rising incidence. Novel33
prenatal and perinatal medical practices, changing diet, shifting family structures and child‐34
hood social activities have all been the subject of lay theories to explain rising prevalence not35
just of ASD, but developmental disorders in childhood more generally, including ADHD36
and dyslexia (Russell & Kelly, 2011).37
9. The influence of childcare and the child’s environment38
A third possibility is that environmental factors alone may be enough to trigger not just au‐39
tistic behaviors, but also other maladaptive behaviors such as inattention. Autistic behaviors40
Autism / Book 1
10
were observed in a study of abandoned Romanian children, conducted by Sir Michael Rut‐1
ter and colleagues (1999). As well as cases with known genetic causes, in some cases, under‐2
lying social factors may predispose autistic symptoms. In this study, Rutter and colleagues3
noted a very high instance of autism (6%) in the Romanian baby cohort, which they put4
down to poor early care. These children exhibited typical symptoms of autism at four years5
old, but unlike cases of autism without maltreatment, symptoms by age 6 were much mild‐6
er. This case is an illustration of how children who share severe autistic symptoms at young7
ages may have differing developmental trajectories. In this study, the symptoms of autism8
may have been triggered primarily by the early neglect, rather than by a genetic predisposi‐9
tion, for if a genetic predisposition was involved it would effect 6% or more of the babies, a10
very high proportion.11
It is not just aetiological environmental factors that seem to lead to increased risks of dis‐12
playing autistic behaviours. Aetiological causes can be distinguished from proximate deter‐13
minates which occur at the same time as symptoms, for example, social situations or14
fluorescent lights may exacerbate the expression of ASD symptoms. There are also those in‐15
fluences in the environment that are sometimes referred to in psychiatry as maintenance fac‐16
tors, including stigmatisation and labelling. Although their influence in perpetuating ASD17
and other developmental disorders is unclear, an influence in maintaining symptomatic be‐18
haviours of autism and co-morbid conditions can not be discounted. Biological causes and19
behavioural outcomes are mediated by experiential and environmental factors.20
10. Cognitive causes and developmental consequences21
The competing psychological theories that have been put forward concerning the psycho‐22
logical mechanisms of ASD include weak central coherence theory, deficits in executive23
function and the extreme male brain theory, all were reviewed by Happé in 1994.24
The extreme male brain theory as developed by Baron-Cohen (2002) suggests that autis‐25
tic individuals can systematize—that is, they can develop internal rules of operation—26
but are less effective at empathizing and handling events that are unexpected or social.27
The theory was developed from the earlier ‘theory of mind’ (Baron-Cohen, Leslie, &28
Frith, 1985). This suggested that autistic people lack the ability to understand other peo‐29
ples’ mental states, put themselves in another person’s place or imagine what they might30
be thinking or experiencing. This lack of mentalising is discussed by Frith and Happé in31
their discussion of dyslexia, autism and downstream effects of specific impairments32
(1998). The ‘theory of mind’ lines up with the ‘mirror neuron theory of autism’ (Iacoboni33
& Dapretto, 2006) which was based on the discovery that the macaque monkey brain34
contained ‘mirror neurons’ that fired not only when the animal is in action, but also35
when it observes others carrying out the same actions.36
An alternative psychological theory for autism is provided by Frith whose ‘weak central co‐37
herence’ theory (Frith, 2003; Happé & Frith, 2006) describes the ability to place information38
in a context in order to give it meaning. Most people pull together numerous stimuli to form39
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a coherent picture of the world, allowing them to see the ‘bigger picture’. In central coher‐1
ence theory, the failure to appreciate the whole accounts for the piecemeal way in which2
people with ASD acquire knowledge. People with ASD may also show relative strengths in3
some areas, known as ‘islets of ability’; and this accounts for savant skills. Related to central4
coherence is the theory that autistic behaviours are due to interference in executive function5
(Hill, 2004). Executive functions coordinate the flow of information processing in the brain6
and are the mechanisms of transferring attention from one thing to another flexibly and7
easily. They allow people to plan strategically, solve problems and set objectives. Their ab‐8
sence means autistic people show an inability to plan and attain overarching goals. This9
manifests as easily distractible behaviour and reliance on routines. Such psychological theo‐10
ries of ASD are useful models but have also been subject to criticism. Bailey and Parr (2003)11
describe such theories of psychological mechanisms as ‘narrow cognitive conceptualisa‐12
tions’ (p. 27), because they cannot accommodate the presence of sub-clinical autistic traits in13
the general population.14
These theories seem very distinct from some psychological theories that explain dyslexic15
type and attention and hyperactive difficulties. Although, deficits in executive function have16
been suggested as causal for ADHD, as they affect both cognitive and motivational systems17
(Willcutt et al., 2005). Frith and Happé (1998) focusing on dyslexia and autism, argue that18
psychological mechanisms could act as ‘gateways’ to impairment in other domains. These19
downstream developmental effects have not yet been fully considered, they suggest. Al‐20
though they focus on autism and dyslexia, ADHD and other developmental disorders could21
easily be included in their model. As they point out, both dyslexia and autism have genetic22
origins, an anatomical basis and extremely variable behavioral manifestations. Their idea is23
that in addition to the genetic and anatomical origins, an additional developmental pathway24
may contribute to later difficulties. They argue that specific impairments seen in dyslexia or25
autism (such as dyslexic phonological or autistic mentalising difficulties) may have a ‘gate‐26
keeping’ function and subsequently lead to difficulties in other areas. Thus impairments in27
domain-specific functions may have wide ranging developmental effects.28
The idea put simply is that during development, one behavior exacerbates problems in oth‐29
er domains. It is perhaps easier to understand given a few concrete examples. Frith and30
Happé suggest that the core autistic difficulty of social engagement may lead to missed op‐31
portunities for learning, including learning vocabulary. This may effect language acquisition32
and in turn the development of language based skills evident in dyslexia. An easier pathway33
to understand might be via gatekeeping function of inattention. If a child is inattentive (a34
core symptom of ADHD) then the likelihood is they may struggle to focus on learning to35
read. Hence difficulties symptomatic of dyslexia may be expected. Conversely perhaps read‐36
ing difficulties are primary, in which case inattention might come from frustration and in‐37
ability to deal with task demands. This direction of causality seems likely in the sub-group38
of ADHD children whose problems only appear at school, and who are more likely than39
other groups to show reading problems according to Taylor (2011). Furthermore, an inatten‐40
tive child may find it difficult to socialize normally, and may have difficulties following in‐41
struction. This may lead to the impairment in social skills symptomatic of autism.42
Autism / Book 1
12
In a similar way, it is possible to theorize that each domain of behavioural impairment in the1
triad for autism might lead to another. In a review of evidence for single genetic or cognitive2
causes for autism, Happé, Ronald, and Plomin (2006) note that twin studies suggest combi‐3
nations of largely non-overlapping genes act on each area of impairment. Their own study4
found only modest correlations between the three domains of behavioural traits in the triad5
(namely deficits in social skills and communication and stereotyped behaviour or restricted6
interests). In the general population, correlations ranged from 0.1- 0.4 for the relationship of7
each domain to the other. This evidence shows that the three types of autistic traits may be8
clustered or linked or co-inherited, but with a weak association. These low correlations9
could be attributed to developmental pathways factors as well as genetic links. Such residu‐10
al downstream developmental effects are easy to conceptualise. If a young boy is very aso‐11
cial for example, then his communication skills will not be practised with peers, so he is12
unlikely to develop as quickly in measures of communication as a more sociable child. The13
weak correlation between repetitive behaviours is harder to explain. Speculation is possible:14
repetitive behaviours have been shown to have both self-stimulatory as well as calming15
functions (Turner, 1999). Repetitive behaviours can therefore be interpreted as responses to16
unwanted stimuli, e.g. social stimuli with which autistic people have difficulty. Williams17
(1994) has given a first person account of use of repetitive behaviours to ameliorate the18
stress of social situations. Conversely, the need for stimulatory repetitive behaviours, con‐19
centrating on drawing lines or circles for example, may interfere with social opportunities.20
Weak associations do not confirm or deny genetic co-inheritance. Developmental pathways21
where one type of behaviour leads to another may also provide a partial explanation.22
In a different but related developmental scenario, Cheslack-Postava and Jordan –Young23
(2012) suggest that a child’s upbringing is highly gendered, and proposed a gendered em‐24
bodiment model for autism. They cite numerous studies illustrating that the nature of pa‐25
renting in particular depends on the gender of the child. This they use to describe a26
gendered theory of development of autism, although the model could also explain the large27
predominance of boys with other developmental disorders. Cooper (2001) suggests boys are28
socialized to encourage competition and activity thus a conflict between passivity required29
at western schools and masculine identity is generated. Some behaviours associated with30
ADHD when used excessively in school environments, climbing trees for example, are en‐31
couraged more often in boys than girls. Cheslack-Postava and Jordan –Young suggest such32
gendered social processes interact with biology to promote certain ‘disordered’ behaviours.33
This they call the ‘pervasive developmental environment’.34
As well as downstream developmental models, some theorists have suggested one cognitive35
deficit may underlie several symptomatic behaviours. Although the cognitive/psychological36
theories of dyslexia and autism seem quite distinct, some research does suggest children37
with both ADHD and dyslexic difficulties show a distinctive deficit in rapid naming speed,38
so it may that processing speed underlies the link (Bental & Tirosh, 2007).39
A second example is provided by executive function which is impaired in both autism and40
ADHD (Willcutt et al, 2005). An underlying impairment in executive function prevents chil‐41
dren from coordinating information processing in the brain, and prevents the transfer atten‐42
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tion from one thing to another. It is easy to understand how this absence may translate into1
symptoms of either autism, due to inability to plan with strategic overarching vision, and2
hence reliance on routines, or as inattention and distractibility symptomatic of ADHD. Execu‐3
tive functions are neuropsychological processes needed to sustain problem-solving toward a4
goal. Executive functions allow a resolution of conflict when two responses are simultaneously5
called for by stimuli. In the laboratory, the Stroop task is an example. The conflicting combina‐6
tion of a word like red written in green ink creates conflict when the task is to say the color of the7
ink (green), due to the overlearned reading response that automatically elicits the response8
based on the meaning of the word (red). Executive function allows for the inhibition of the9
overlearned response and the execution of a response that is more appropriate given the con‐10
text. Research has confirmed the involvement of deficits in executive functions that are essen‐11
tial for effective self-regulation in people with ADHD. The mental processes most often listed12
as being part of the notion of executive function are quite diverse so there is no standardized13
definition. They include: inhibition, resistance to distraction, self-awareness, working memo‐14
ry, emotional self-control, and even self-motivation. Bramham and colleagues (2009) found15
that both adults with ASD and ADHD had impaired executive function, although they did16
have distinctive profiles. Nyden and colleagues found that children with Asperger’s Syn‐17
drome and dyslexia did not differ in tests of executive function: they could not establish any18
test of executive function that captured the differences in these disorders (1999).19
Russell Barkley (2012) conceptualizes executive control as the methods of self-regulation. He20
writes entertainingly on how a person might use executive functions to resist the temptation21
to buy a tempting pastry from a shop:22
…avert your eyes from the counter, walk to a different section of the shop away from the tempting goodies, engage23
yourself in mental conversation about why you need to not buy those products, and even visualize an image of the24
new slenderer version of yourself you expect to achieve in the near future. All of these are self-directed actions you are25
using to try and alter the likelihood of giving into temptation and therefore increase your chances of meeting your goal26
of weight loss this month. This situation calls upon a number of distinct yet interacting mental abilities to successfully27
negotiate the situation. You have to be aware that a dilemma has arisen when you walked into the shop (self-aware‐28
ness), you have to restrain your urge to order the pastry to go with the coffee you have ordered (inhibition), you re-29
directed your attention away from the tempting objects (executive attention or attentional management), you spoke to30
yourself using your mind’s voice (verbal self-instruction or working memory), and you visualized an image of your31
goal and what you would look like when you successfully attain it (nonverbal working memory, or visual imagery).32
You may also have found yourself thinking about various other ways you could have coped effectively with these33
temptations (problem-solving), and may have even used words of encouragement toward yourself to enhance the like‐34
lihood that you would follow your plan (self-motivation).35
Autism / Book 1
14
Barkley explains that these and other mental activities are usually included in the under‐1
standing of human self-regulation, and it is difficulties in these areas (which are processes in2
executive function) that may lead to ADHD. Children with ADHD are distractible and lack3
self-regulation, the ability to override incoming stimuli, to see the bigger picture and lack4
the ability to see the consequences of their future actions. Children with ASD have difficul‐5
ties transferring attention from one thing to another because they also lack overview (and6
implications of their actions in the future).7
Gooch, Snowling and Hulme (2011) note that deficits in time perception (the ability to judge8
the length of time intervals) have been found in children with both dyslexia and ADHD.9
These researchers found children with comorbid dyslexia and attention problems performed10
poorly on measures of executive function as well as on phonological tasks. However, their11
results were interpreted as the effect of independent underlying cognitive causes. Although12
deficits in duration discrimination were associated with both dyslexia and attention prob‐13
lems, they concluded the results supported the claim that the two disorders are products of14
different cognitive defects originating from shared genes with pleiotropic effects.15
Developmental models explain comorbidity of developmental disorders by shared cognitive16
deficits, either as ‘gateways’ as in Frith and Happés (1998) model, where one difficulty leads17
to another later in life, or as underlying shared deficits, for example impaired executive18
function causing both autism and ADHD. The alternative model suggests that cognitive dif‐19
ficulties associated with each disorder are distinct, but multiple cognitive deficits arise from20
similar genetic/environmental origins. All these theories have some empirical support.21
11. Diagnostic substitution and the influence of society and culture22
When symptoms of two or more conditions are shared, whatever the psychological mecha‐23
nisms (whether or not there are shared underlying cognitive deficits, and /or genetic and24
neurological differences) then the area of functioning that is highlighted as a problem may25
depend on which tests are administered. In our recent research we followed a six year old26
child who was assessed by three educational psychologists and one multidisciplinary team,27
each blind to the findings of the others. One concluded that the child had dyspraxia, two28
that the child had dyslexic difficulties, and a third that borderline AS was likely. We inter‐29
preted these differences in the use of diagnostic labels as dependent on settings that varied30
during assessments, and assessment methods that exposed different types of behaviour31
(Russell, Norwich, & Gwernan-Jones, 2012). This work suggests that which diagnosis is as‐32
signed depends to some extent on social and cultural factors as well as actual symptoms. If a33
child has symptoms of several disorders, then one context or test may draw out symptoms34
associated with one disorder, whereas another setting may expose symptoms of another.35
Thus for co-occurring symptoms it is difficult to differentiate between disorders, the likeli‐36
hood that a co-morbid disorder will be missed is increased. This emphasizes the need for37
assessment in multiple settings and reassessment over time.38
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One of the most compelling cross cultural descriptions of how autism is regarded across1
various cultures was the book Unstrange Minds. Written by the anthropologist Roy Grinker2
(2008), Grinker explains how the category of ASD is contingent on the culture through3
which it is expressed- the condition is associated with differing levels of stigma in different4
cultures. In the US, several studies have also shown that clinicians may diagnose ASD when5
resources are targeted at the diagnosis, whereas previously, under other circumstances, they6
may have diagnosed another category of childhood disorder. Paul Shattuck has written7
about the extent to which increases in the administrative prevalence of autism have been as‐8
sociated with corresponding decreases in the use of other diagnostic categories, mental re‐9
tardation and learning disabilities (2006). This process of ‘diagnostic substitution’ he argues,10
may partially explain the rise in prevalence in autism in the US.11
Our own work suggests that since the 1980s, the recorded prevalence of both ASD and12
ADHD in the UK has increased dramatically. We examined data from both the Millennium13
Cohort Study, (the large cohort of around 19,000 children who have been followed from14
their birth through to seven years old and beyond), and another cohort, called the British15
Cohort Study, where children were born thirty years previously. Both cohorts were repre‐16
sentative of the UK as a whole, and medical reports of both ASD and ADHD were given17
when children were age seven for in 2007-9 and ten in 1980. The results from 2007 contrast‐18
ed with the 1980 sample at age 10. Only 11 children in the 1970 British Cohort Study were19
reported as having ADHD in their medical exam, giving an estimated prevalence of 0.083%.20
The autism diagnosis was rarely used with just 3 children assigned the label; 0.023% of chil‐21
dren. A number of other child psychiatric diagnoses were available and many of these were22
diagnosed during the medical exams. Details of these alternative labels are given in Table 1.23
1980 Diagnosis (ICD 9 codes) N of children Percentage of total examined %
Autism (299.0/1/8/9) 3 0.023
ADHD (314.00/01, 314.9) 11 0.083
Disturbance in emotions (313) 7 0.053
Delays in development: Reading
(315.0) 13 0.098
Delays in learning & development
(315.2/8/9/5) 81 0.614
Delays in language
(315.3)
62
(1 autism co-morbid) 0.462
Impulse control (312.3/9) 1 0.007
Mild mental retardation
(317)
34
(1 ADHD co-morbid) 0.258
Other specified delays in
development (318)
22
(1 ADHD co-morbid) 0.166
Unspecified delays in development
(319)
25
(1 ADHD co-morbid) 0.379
Total 259 1.961
Table 1. Named conditions using ICD-9 categories for 10 year old children in 1980 (n=13201).24
Autism / Book 116
Among the 14,043 children in the 2007 cohort, 209 (1.49%) were reported to have ASD, and1
180 (1.28%) were reported having been given an ADHD diagnosis by a clinician. There was2
disproportional stratification in the Millennium Cohort, meaning that all analyses were3
weighted to account for the clustering and over-inclusion of participants from disadvantag‐4
ed areas. After weighting, 1.7 % of children were reported as having an ASD (95% CI,5
1.4-1.99). 1.3% of these were boys, and 0.25% girls, giving boy girl ratio of approx 5:1 for6
ASD. Surprisingly, the figure for ADHD was lower. After weighting, 1.4% of the population7
were reported as having ADHD (95% CI, 1.2-1.7). Of these, 2.3% were boys and 0.25% girls,8
giving a gender ratio of approximately of 1 girl to every 4 boys with ADHD.9
One interpretation of the historical shift is that diagnostic substitution has occurred: children10
with similar symptoms in 1980 may have been more likely to receive generalised labels of11
‘delays in learning & development’ than ASD or ADHD. So changing diagnostic practice,12
cultural factors and context may do much to explain both co-morbidity and rising preva‐13
lence. The steep rise in children assigned these diagnoses cannot be totally explained by the14
substitution mechanism- twice as many children were given either ASD or ADHD diagno‐15
ses in 2009 as the total number diagnosed with any type of developmental disorder in 1980.16
Context also has a big part to play in the identification of difficulties, in terms of what is con‐17
sidered to be ‘disordered’. Social constructionists have also pointed out that the conceptuali‐18
zation of difficulties associated with both dyslexia and ASD as ‘disorders’ is itself a product19
of social and cultural standards, and of course the definition of each disorder has changed20
over time. This has prompted calls for the term autism spectrum ‘conditions’ to replace au‐21
tism spectrum ‘disorders’ (2009). Our own analysis of the Millennium Cohort has shown a22
strong association between ADHD and poverty, reflecting findings from US studies which23
have also found differing levels of ADHD amongst various ethnic groups- Hispanic children24
were more likely to be identified with ADHD in a study by Akinbami et al. (2011). It is un‐25
clear whether this is entirely due to greater awareness and access to health care in some26
groups, differential reporting about the same level of difficulties between ethnic groups or27
whether children in different groups have truly varying symptom levels (Boyle et al., 2011).28
A study by Cuccaro et al. (1996) showed the nature of diagnosis of developmental disorders29
varied according to the socio-economic status of the child’s family; autism was more likely30
to be identified in children of higher income families, although no biases of SES were found31
for identification with ADHD. Cooper (2001) points out that the behaviour symptomatic of32
ADHD becomes problematic where high value is placed on ability to remain sedentary and33
sustain attention on tasks, in other words, in schools. Hulme and Snowling (2009) describe34
how differences of this nature must therefore be thought of as both biological and as a prod‐35
uct of the social and environmental world.36
12. Conclusion37
Two conclusions can be drawn. First, co-morbidities between developmental disorders are38
common, and second, the causes of these overlapping difficulties are likely to be complex,39
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multifactorial and interacting. Firstly, the high overlap between symptoms of different de‐1
velopmental disorders has been identified in a number of studies and there is an interna‐2
tional consensus on this overlap. Studies from Canada, the UK, USA and Scandinavia all3
show how hard it is provide an unequivocal diagnosis, leading to the quote from Kaplan4
and her colleagues (2001) in developmental disorders co-morbidity is the rule, not the exception.5
This was informed by the group’s work studying a population-based sample of 179 children6
receiving special support in Calgary: If the children met the dyslexia criteria, there was a7
51.6% chance of having another disorder. If the children met the ADHD criteria there was an8
80.4% chance of having another disorder. They criticize the term ‘comorbidity’, as it implies9
unsubstantiated presumption of independent aetiologies. The authors argue that discrete10
categories do not exist in real life.11
Secondly, in considering the reasons for co-morbidities, a complex bio-psycho-social model12
is required that leads to symptoms that may result in diagnosis. The nature of the diagnosis13
itself may depend on social context as well as an individual child’s behaviour. A hint of this14
complexity is achieved in Figure 3, which is a schematic diagram of various potential causal15
pathways. It is plausible that the same underlying genetic or neurological mechanisms may16
underlie co-occurrence of dyslexia, ADHD and ASD. The reverse pathways are not at first so17
obvious. But recent advances in systems biology have shown that the environment of the18
cell affects gene expression and protein synthesis at molecular levels. Thus environmental19
influences can alter ‘core’ biology: for example Mack and Mack (1992) describe how tweak‐20
ing rats’ whiskers changes gene expression in the sensory cortex. In systems theory, genetic21
influences are conceptualised more like a set of piano keys on which notes may be played or22
not played, played slowly or quickly, and there is enormous variation in the music pro‐23
duced even with the same basic set of keys. So the cellular environment can affect genetic24
expression. A simplified model underlying much behaviour genetics research envisages a25
direct linear relationship between individual genes and behaviours. The reality is likely to26
be far more complex with gene networks and multiple environmental factors impacting27
brain development and function, which in turn will influence behaviour (Hamer, 2002). Kar‐28
miloff-Smith (2007) emphasizes how learning and experience effects gene expression in hu‐29
mans. Such scholars demonstrate that the social can affect the biological as well as the more30
intuitive path of genetic origin leading to neurological development leading to aberrant be‐31
haviour. Diagnosis itself may influence behaviour too, through differential treatment and in‐32
terventions. Thus the pervasive developmental environment is composed of many related33
factors, environmental stresses, and genetic predispositions, and the social contexts all of34
which may interact to produce developmental outcomes that themselves may contribute to35
predicting ongoing child development.36
Snowling (2012) suggests a new dimensional classification of disorder, where deficits in dif‐37
ferent components of learning are seen as additive, impacting on the potential for remedia‐38
tion, rather than classing children into dichotomous ‘disorder’ categories. Taylor (2011)39
notes that for many children, it is better to think of changes in cognitive style, learning and40
motivation rather than symptoms. Both conclude that it is important to examine children for41
evidence of co-occurring disorders, and not simply continue to examine the areas which we42
Autism / Book 1
18
expect to be impaired according to categorization. The practical application of assessing chil‐1
dren for a range of difficulties is that children will be best helped not by any all encompass‐2
ing diagnosis, but by individual analysis of their strengths and weaknesses. Future research3
may be wise to focus on the individual profiles of children across a broad range of areas,4
looking at the unique strengths, as well as the weaknesses of the individual children, so that5
parents and educators may adapt their support accordingly, regardless of the diagnostic la‐6
bel a child receives.7
8
Figure 3. Schematic of interacting causal mechanisms for co-morbidity.9
Author details10
Ginny Russell and Zsuzsa Pavelka11
Child Health Group, Peninsula College of Medicine and Dentistry, ESRC Centre for Genom‐12
ics in Society, University of Exeter, UK13
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Hyperactivity Disorder
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