**Author details**

**12. Conclusion**

378 Recent Advances in Autism Spectrum Disorders - Volume I

categories do not exist in real life.

predicting ongoing child development.

Two conclusions can be drawn. First, co-morbidities between developmental disorders are common, and second, the causes of these overlapping difficulties are likely to be complex, multifactorial and interacting. Firstly, the high overlap between symptoms of different de‐ velopmental disorders has been identified in a number of studies and there is an interna‐ tional consensus on this overlap. Studies from Canada, the UK, USA and Scandinavia all show how hard it is provide an unequivocal diagnosis, leading to the quote from Kaplan and her colleagues (2001) *in developmental disorders co-morbidity is the rule, not the exception.* This was informed by the group's work studying a population-based sample of 179 children receiving special support in Calgary: If the children met the dyslexia criteria, there was a 51.6% chance of having another disorder. If the children met the ADHD criteria there was an 80.4% chance of having another disorder. They criticize the term 'comorbidity', as it implies unsubstantiated presumption of independent aetiologies. The authors argue that discrete

Secondly, in considering the reasons for co-morbidities, a complex bio-psycho-social model is required that leads to symptoms that may result in diagnosis. The nature of the diagnosis itself may depend on social context as well as an individual child's behaviour. A hint of this complexity is achieved in Figure 3, which is a schematic diagram of various potential causal pathways. It is plausible that the same underlying genetic or neurological mechanisms may underlie co-occurrence of dyslexia, ADHD and ASD. The reverse pathways are not at first so obvious. But recent advances in systems biology have shown that the environment of the cell affects gene expression and protein synthesis at molecular levels. Thus environmental influences can alter 'core' biology: for example Mack and Mack (1992) describe how tweak‐ ing rats' whiskers changes gene expression in the sensory cortex. In systems theory, genetic influences are conceptualised more like a set of piano keys on which notes may be played or not played, played slowly or quickly, and there is enormous variation in the music pro‐ duced even with the same basic set of keys. So the cellular environment can affect genetic expression. A simplified model underlying much behaviour genetics research envisages a direct linear relationship between individual genes and behaviours. The reality is likely to be far more complex with gene networks and multiple environmental factors impacting brain development and function, which in turn will influence behaviour (Hamer, 2002). Kar‐ miloff-Smith (2007) emphasizes how learning and experience effects gene expression in hu‐ mans. Such scholars demonstrate that the social can affect the biological as well as the more intuitive path of genetic origin leading to neurological development leading to aberrant be‐ haviour. Diagnosis itself may influence behaviour too, through differential treatment and in‐ terventions. Thus the pervasive developmental environment is composed of many related factors, environmental stresses, and genetic predispositions, and the social contexts all of which may interact to produce developmental outcomes that themselves may contribute to

Snowling (2012) suggests a new dimensional classification of disorder, where deficits in dif‐ ferent components of learning are seen as additive, impacting on the potential for remedia‐ Ginny Russell1 and Zsuzsa Pavelka2

1 University of Exeter Medical School, ESRC Centre for Genomics in Society, UK

2 University of Milan, Italy

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**Chapter 18**

**Pre-Existing Differences in**

Jenny Fairthorne, Amanda Langridge,

Additional information is available at the end of the chapter

the *FMR1* gene confirming a diagnosis of Fragile X syndrome. [15]

Jenny Bourke and Helen Leonard

http://dx.doi.org/10.5772/54488

**1. Introduction**

**Mothers of Children with Autism Spectrum**

**Disorder and/or Intellectual Disability: A Review**

The autism spectrum disorders (ASD) represent a group of severe and chronic neuro-devel‐ opmental disorders often simply referred to as autism. [1] Using the criteria provided by the *Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition*, ASD are diagnosed by impairments within the three strands of DSM-4: *social interaction, communication* and *repetitive behaviours or interests*. [2] The aetiology of autism is complex. [3] Research has implicated a strong genetic basis [4-7] involving multiple genes [5, 7, 8] and possible gene-environment interactions. [9-13] Advances in chromosomal microarray analysis and gene sequencing technologies have improved diagnoses and suggest that aetiologies of ASD will continue to be uncovered. [9] In addition, a child presenting with autistic symptoms may be found to have a certain genetic mutation which accounts for their true underlying biological diagnosis. For example, a diagnosis of Rett syndrome would be confirmed when a girl with ASD and intellectual disability was found to have a mutation of the *MECP2* gene on the X-chromosome. [14] Children with ASD and intellectual disability have been found to have an expansion of

Autism and intellectual disability commonly coexist with 30-80% of persons with ASD reported as also having ID. [16, 17] Currently, the relationship between ASD and comorbid ID is poorly understood. [18] However, it is known that phenotypically, persons with these disorders can be grouped into the three categories of ASD without ID, ASD with ID and ID only. [18] Intellectual disability (ID) is characterized by an intelligence quotient (IQ) of less than 70 which is associated with limitations in at least two areas of adaptive skill and which

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