**5. Comorbidity between dyslexia and ASD**

hyperactivity/impulsivity compared to subjects diagnosed with Asperger's syndrome. How‐ ever, the prevalence of the categorical diagnosis of ADHD did not differ significantly be‐ tween the groups, nor were gender differences apparent. Although the study presents clear evidence of many cases where patients display symptoms of both ADHD and ASD, the clin‐ ical setting may have led to selection bias as patients with complex needs may be more like‐

Because behaviours associated with both conditions lie on a spectrum extending into the normal range, some studies have found a range of frequency and severity of symptoms. In Mulligan et al.'s (2009) study, for example, 75 of children with ADHD had severe autism traits, and over half showed sub-clinical autism symptoms. Kadesjö and colleagues (Kades‐ jö, Gillberg, & Hagberg, 1999), looked at comorbidity of ADHD in Swedish school-age chil‐ dren and found only 1% of children meeting the threshold for ADHD had comorbid Aspergers Syndrome (AS). The estimates of co-morbidity of ADHD symptoms with ASD symptoms vary widely because of differing methods of case ascertainment. An additional problem is that the estimate of the prevalence of ASD itself has increased so much in west‐

Patricia Howlin (2000) reviewed the estimated rates of co-existing psychiatric disorders in subjects with high functioning ASD and found these estimates varied from 9% to 89% - very substantial differences. However it is possible to generalise; thirty years of research have confirmed that attention deficits and hyperactivity are relatively common in children and adults with ASD even if the exact extent of overlap is dependent on methodology and ascer‐

**Figure 2.** The rising prevalence of autism spectrum disorders over 50 years. (Data from 'Autism Speaks' and CDC, USA)

Recent trends have made categorical diagnosis an integral part of everyday clinical and re‐ search practice (Sonuga-Barke & Halperin, 2010). Christopher Gillberg (2010) points out that clinicians have become focused on dichotomous categories of disorder and that clinics have become increasingly specialized and overlook difficulties not within their immediate juris‐

ern countries, making ASD itself a 'moving target' (Figure 2).

tainment (Hofvander et al., 2009, Sturm, Fernell, & Gillberg, 2004).

ly to seek help.

366 Recent Advances in Autism Spectrum Disorders - Volume I

There is only a small literature on the overlap in symptomology between autism spectrum disorders with those of dyslexia. Officially, as for ADHD, ASD is an exclusionary criterion for diagnosis of dyslexia and vice versa, but ASD also shows overlap with dyslexia in both cognitive and behavioural features (Reiersen & Todd, 2008, Simonoff et al., 2008). A propor‐ tion of children share symptoms between dyslexia, ADHD *and* ASD.

The number of children that do share symptoms of ASD and dyslexia is likely to be small (Wright, Conlon, Wright, & Dyck, 2011). The frequency of reading disorder in combination with disorder of written expression (i.e. dyslexia) was around 14% in a sample of adults with Asperger's Syndrome (AS) so according to this result around one in seven individuals with AS will have co-occurring dyslexia (Hofvander et al., 2009). However the proportion of individuals with dyslexia who have co-occuring AS is likely to be low as Asperger's Syn‐ drome is much a rarer condition than dyslexia.

A common problem for children with dyslexia is misinterpretation of spoken language, which can also manifest itself in comprehension. This produces further overlap with prag‐ matic language impairment (PLI) which itself is virtually indistinguishable from communi‐ cation difficulties associated with high functioning autism. Pragmatic language difficulties may involve literal interpretation so 'run on the spot' would have a child looking for a big black spot to run on, for example. Children with PLI will often fail to interpret the core meaning or saliency of events. This causes a penchant for routine and 'sameness' (also seen in autism and Asperger's Syndrome) as PLI children struggle to generalize and take hold of the meaning of novel situations. Obvious and concrete instructions are clearly understood and carried out, whereas simple but non-literal expressions such as jokes, sarcasm and gen‐ eral social chatting are difficult and may be misinterpretated. PLI may therefore impact on the social abilities of the child who has difficulty interpreting jokes. Current thinking is that PLI is not a problem rooted in language skills but one of social communication and informa‐ tion processing. Griffiths (2007) identified difficulties of this type in dyslexic students, showed they were impaired in making inferences from a story and choosing the right punch-line for a joke. This of course can have implications for written language and exami‐ nations under stress, as well as for a range of social interactions.

It is not just that ASD is co-morbid with dyslexia and ADHD. Other studies have noted high comorbidity with other developmental disorders. Dyspraxia and dyscalculia and conditions with shared symptoms such as specific language impairment are frequently comorbid with autism. Also dyslexia and ADHD themselves co-occur Willcutt and colleagues (Willcutt, Doyle, Nigg, Faraone, & Pennington, 2005) showed that 40% of a sample of twins with ei‐ ther dyslexia or ADHD was co-morbid for the other disorder. Reading difficulties were measured with both rating scale and an objective task in a study by Cheung et al. (2012) and correlations were observed among ADHD, reading difficulties and IQ. Over half, (53%-72%) of the overlapping familial influences between ADHD and reading difficulties were not shared with IQ. In a school based study Kadesjö and colleagues found 40% of children with ADHD showed reading problems and 29% writing problems (2005).

volved in neural development, but exact mutations within the candidate genes have yet to be identified (Freitag, 2007). Furthermore, different individuals may have mutations in dif‐ ferent sets of genes and most of the discovered gene variations are likely to have a low pene‐ trance, thus not all carriers will develop the disorder. There may be interactions among mutations in several genes, e.g. between regulatory genes and coding regions, or between the environment and mutated genes, altering their expression. The effect of a mutation or deletion can depend on processes relating to gene expression and regulation as well as the

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http://dx.doi.org/10.5772/54159

The advent of genomics and the emphasis placed on this has led to much research to identi‐ fy genetic predispositions to ASD. The field of psychiatry as a whole has been 'geneticised' according to some social theorists. This refers to the potential reclassification of psychiatric conditions in the light of findings from molecular biology. For example, a particular sub-cat‐ egory of DSM-IV schizophrenia has been linked to a substitution of a single base in the se‐ quence of DNA of a particular gene localised to a precise place on a particular chromosome, leading to a substitution of one amino-acid for another in an enzyme involved in neuro‐ transmission. Hedgecoe (2001) provides a discussion of the geneticisation of schizophrenia. The debate as to whether the old psychiatric systems of classification should be overhauled in the light of new genomic knowledge which illuminates genetic aetiologies is ongoing

A second theory is that an environmental insult or a stressful event in the life of the fetus or in a young child's life, may trigger a genetic predisposition to be expressed. Thus this consti‐ tutes a gene- environmental interaction theory. An example might be the high testosterone levels in the womb that have been observed in some studies. Baron-Cohen's Cambridge group, for example, has carried out work that has suggested high levels of fetal testosterone may be linked to the development of autistic traits (Ingudomnukul, Baron-Cohen, Wheel‐ wright, & Knickmeyer, 2007). According to the gene-environment explanation, the elevated testosterone might lead to the differential expression of genes controlling the neurological development of the child. Another example that has been quite widely publicized concerns Omega 3 fatty acids. These have been implicated by Richardson (2006), who has argued that attention-deficit/hyperactivity disorder, dyslexia, developmental coordination disorder (dyspraxia) and conditions on the autism spectrum may all share common origins triggered by problems with phospholipid (fatty acid) metabolism. However this is just one genetic / environmental explanation for co-occurrence that vies with several others, and the available

In the majority of cases, the gene-environment hypothesis seems highly plausible. It may be that autism and co-occurring developmental conditions may all be caused by a genet‐ ic predisposition which is triggered by an early environmental influence (Trottier, Srivas‐

subsequent effects on the expression of other genes.

(Ericson & Doyle, 2003).

**8. Gene-environment interactions**

evidence is subject to interpretation.

tava, & Walker, 1999).

Overall, the literature suggests, there is good evidence to suggest that some children do suf‐ fer from symptoms of both dyslexia and ASD, although this is not so well established, and does not occur so frequently as co-morbidity between ADHD and ASD.
