**10. Cognitive causes and developmental consequences**

Many environmental factors have been implicated in ASD but the effect of each is poorly established. After the well publicized paper that linked autism to the MMR vaccination, re‐ search has repeatedly refuted a link between the MMR jab and ASD (Rutter, 2005). Deykin and MacMahon (1979) found increased risk due to exposure to, and clinical illness from, common viral illnesses in the first 18 months of life. In this study, mumps, chickenpox, fever of unknown origin, and ear infections were all significantly associated with ASD risk. Epide‐ miological studies have shown there is a higher rate of adverse prenatal and postnatal events in children with ASD than in the general population (Zwaigenbaum et al., 2002). Newschaffer and colleague's (2007) review named associated obstetric conditions that in‐ cluded low birth weight, gestation duration, and caesarean section. It is possible that such an underlying cause partially could explain both autism and the associated conditions (Ko‐ levzon, Gross, & Reichenberg, 2007). There is evidence to suggest adverse prenatal and peri‐ natal events are also associated with ADHD and cognitive development. Some studies have suggested that the risk of autism may be increased with advancing maternal age (Bolton et al., 1997). Paternal age too has frequently (but not always) associated with autism. There are more mutations in the gametes of older men, and this higher rate of mutation in the genetic material from the paternal side may explain the higher levels of neurodevelopmental disa‐ bilities in their offspring. An alternative explanation is that fathers who themselves have au‐ tistic traits are less likely to have children young. Using anticonvulsants during pregnancy also appears to increase the risk of ASD (Moore et al., 2000). These drugs are used to combat epilepsy which is commonly often comorbid with ASD. Parental occupational exposure to chemicals during the preconception period has also been higher in ASD families than con‐

Environmental risk factors have received widespread media coverage within the last few years, perhaps because of the strong degree of public concern (Russell & Kelly, 2011). In most health and disease categories, a secondary function of diagnosis is to group together people who have a common aetiology. However, the specific effects of genetic factors and environmental risk factors that might play a part in abnormal neural development are large‐ ly unresolved. Goodman and Scott (1997) stress that current understanding of aetiology for childhood developmental conditions will probably look ridiculously simplistic or misguid‐ ed in years to come. Despite, or perhaps because of, the uncertainty, there is an underlying concern among people involved with children who are diagnosed with developmental con‐ ditions that environmental influences may be partially to blame for rising incidence. Novel prenatal and perinatal medical practices, changing diet, shifting family structures and child‐ hood social activities have all been the subject of lay theories to explain rising prevalence not just of ASD, but developmental disorders in childhood more generally, including ADHD

A third possibility is that environmental factors alone may be enough to trigger not just au‐ tistic behaviors, but also other maladaptive behaviors such as inattention. Autistic behaviors

trols in some studies (Felicetti, 1981).

370 Recent Advances in Autism Spectrum Disorders - Volume I

and dyslexia (Russell & Kelly, 2011).

**9. The influence of childcare and the child's environment**

The competing psychological theories that have been put forward concerning the psycho‐ logical mechanisms of ASD include weak central coherence theory, deficits in executive function and the extreme male brain theory, all were reviewed by Happé in 1994.

The extreme male brain theory as developed by Baron-Cohen (2002) suggests that autis‐ tic individuals can systematize—that is, they can develop internal rules of operation but are less effective at empathizing and handling events that are unexpected or social. The theory was developed from the earlier 'theory of mind' (Baron-Cohen, Leslie, & Frith, 1985). This suggested that autistic people lack the ability to understand other peo‐ ples' mental states, put themselves in another person's place or imagine what they might be thinking or experiencing. This lack of mentalising is discussed by Frith and Happé in their discussion of dyslexia, autism and downstream effects of specific impairments (1998). The 'theory of mind' lines up with the 'mirror neuron theory of autism' (Iacoboni & Dapretto, 2006) which was based on the discovery that the macaque monkey brain contained 'mirror neurons' that fired not only when the animal is in action, but also when it observes others carrying out the same actions.

An alternative psychological theory for autism is provided by Frith whose 'weak central co‐ herence' theory (Frith, 2003; Happé & Frith, 2006) describes the ability to place information in a context in order to give it meaning. Most people pull together numerous stimuli to form a coherent picture of the world, allowing them to see the 'bigger picture'. In central coher‐ ence theory, the failure to appreciate the whole accounts for the piecemeal way in which people with ASD acquire knowledge. People with ASD may also show relative strengths in some areas, known as 'islets of ability'; and this accounts for savant skills. Related to central coherence is the theory that autistic behaviours are due to interference in executive function (Hill, 2004). Executive functions coordinate the flow of information processing in the brain and are the mechanisms of transferring attention from one thing to another flexibly and easily. They allow people to plan strategically, solve problems and set objectives. Their ab‐ sence means autistic people show an inability to plan and attain overarching goals. This manifests as easily distractible behaviour and reliance on routines. Such psychological theo‐ ries of ASD are useful models but have also been subject to criticism. Bailey and Parr (2003) describe such theories of psychological mechanisms as 'narrow cognitive conceptualisa‐ tions' (p. 27), because they cannot accommodate the presence of sub-clinical autistic traits in the general population.

In a similar way, it is possible to theorize that each domain of behavioural impairment in the triad for autism might lead to another. In a review of evidence for single genetic or cognitive causes for autism, Happé, Ronald, and Plomin (2006) note that twin studies suggest combi‐ nations of largely non-overlapping genes act on each area of impairment. Their own study found only modest correlations between the three domains of behavioural traits in the triad (namely deficits in social skills and communication and stereotyped behaviour or restricted interests). In the general population, correlations ranged from 0.1- 0.4 for the relationship of each domain to the other. This evidence shows that the three types of autistic traits may be clustered or linked or co-inherited, but with a weak association. These low correlations could be attributed to developmental pathways factors as well as genetic links. Such residu‐ al downstream developmental effects are easy to conceptualise. If a young boy is very aso‐ cial for example, then his communication skills will not be practised with peers, so he is unlikely to develop as quickly in measures of communication as a more sociable child. The weak correlation between repetitive behaviours is harder to explain. Speculation is possible: repetitive behaviours have been shown to have both self-stimulatory as well as calming functions (Turner, 1999). Repetitive behaviours can therefore be interpreted as responses to unwanted stimuli, e.g. social stimuli with which autistic people have difficulty. Williams (1994) has given a first person account of use of repetitive behaviours to ameliorate the stress of social situations. Conversely, the need for stimulatory repetitive behaviours, con‐ centrating on drawing lines or circles for example, may interfere with social opportunities. Weak associations do not confirm or deny genetic co-inheritance. Developmental pathways

Co-Occurrence of Developmental Disorders: Children Who Share Symptoms of Autism, Dyslexia and Attention Deficit

Hyperactivity Disorder

373

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

where one type of behaviour leads to another may also provide a partial explanation.

This they call the 'pervasive developmental environment'.

so it may that processing speed underlies the link (Bental & Tirosh, 2007).

In a different but related developmental scenario, Cheslack-Postava and Jordan –Young (2012) suggest that a child's upbringing is highly gendered, and proposed a gendered em‐ bodiment model for autism. They cite numerous studies illustrating that the nature of pa‐ renting in particular depends on the gender of the child. This they use to describe a gendered theory of development of autism, although the model could also explain the large predominance of boys with other developmental disorders. Cooper (2001) suggests boys are socialized to encourage competition and activity thus a conflict between passivity required at western schools and masculine identity is generated. Some behaviours associated with ADHD when used excessively in school environments, climbing trees for example, are en‐ couraged more often in boys than girls. Cheslack-Postava and Jordan –Young suggest such gendered social processes interact with biology to promote certain 'disordered' behaviours.

As well as downstream developmental models, some theorists have suggested one cognitive deficit may underlie several symptomatic behaviours. Although the cognitive/psychological theories of dyslexia and autism seem quite distinct, some research does suggest children with both ADHD and dyslexic difficulties show a distinctive deficit in rapid naming speed,

A second example is provided by executive function which is impaired in both autism and ADHD (Willcutt et al, 2005). According to some models, an underlying impairment in execu‐ tive function prevents children from coordinating information processing in the brain, and

These theories seem very distinct from some psychological theories that explain dyslexic type and attention and hyperactive difficulties. The exception to this is that, deficits in exec‐ utive function have been suggested as causal for ADHD, as they affect both cognitive and motivational systems (Willcutt et al., 2005). Frith and Happé (1998) focusing on dyslexia and autism, argue that psychological mechanisms could act as 'gateways' to impairment in other domains. These downstream developmental effects have not yet been fully considered, they suggest. Although they focus on autism and dyslexia, ADHD and other developmental dis‐ orders could easily be included in their model. As they point out, both dyslexia and autism have genetic origins, an anatomical basis and extremely variable behavioral manifestations. Their idea is that in addition to the genetic and anatomical origins, an additional develop‐ mental pathway may contribute to later difficulties. They argue that specific impairments seen in dyslexia or autism (such as dyslexic phonological or autistic mentalising difficulties) may have a 'gatekeeping' function and subsequently lead to difficulties in other areas. Thus impairments in domain-specific functions may have wide ranging developmental effects.

The idea put simply is that during development, one behavior exacerbates problems in oth‐ er domains. It is perhaps easier to understand given a few concrete examples. Frith and Happé suggest that the core autistic difficulty of social engagement may lead to missed op‐ portunities for learning, including learning vocabulary. This may effect language acquisition and in turn the development of language based skills evident in dyslexia. An easier pathway to understand might be via gatekeeping function of inattention. If a child is inattentive (a core symptom of ADHD) then the likelihood is they may struggle to focus on learning to read. Hence difficulties symptomatic of dyslexia may be expected. Conversely perhaps read‐ ing difficulties are primary, in which case inattention might come from frustration and in‐ ability to deal with task demands. This direction of causality seems likely in the sub-group of ADHD children whose problems only appear at school, and who are more likely than other groups to show reading problems according to Taylor (2011). Furthermore, an inatten‐ tive child may find it difficult to socialize normally, and may have difficulties following in‐ struction. This may lead to the impairment in social skills symptomatic of autism.

a coherent picture of the world, allowing them to see the 'bigger picture'. In central coher‐ ence theory, the failure to appreciate the whole accounts for the piecemeal way in which people with ASD acquire knowledge. People with ASD may also show relative strengths in some areas, known as 'islets of ability'; and this accounts for savant skills. Related to central coherence is the theory that autistic behaviours are due to interference in executive function (Hill, 2004). Executive functions coordinate the flow of information processing in the brain and are the mechanisms of transferring attention from one thing to another flexibly and easily. They allow people to plan strategically, solve problems and set objectives. Their ab‐ sence means autistic people show an inability to plan and attain overarching goals. This manifests as easily distractible behaviour and reliance on routines. Such psychological theo‐ ries of ASD are useful models but have also been subject to criticism. Bailey and Parr (2003) describe such theories of psychological mechanisms as 'narrow cognitive conceptualisa‐ tions' (p. 27), because they cannot accommodate the presence of sub-clinical autistic traits in

These theories seem very distinct from some psychological theories that explain dyslexic type and attention and hyperactive difficulties. The exception to this is that, deficits in exec‐ utive function have been suggested as causal for ADHD, as they affect both cognitive and motivational systems (Willcutt et al., 2005). Frith and Happé (1998) focusing on dyslexia and autism, argue that psychological mechanisms could act as 'gateways' to impairment in other domains. These downstream developmental effects have not yet been fully considered, they suggest. Although they focus on autism and dyslexia, ADHD and other developmental dis‐ orders could easily be included in their model. As they point out, both dyslexia and autism have genetic origins, an anatomical basis and extremely variable behavioral manifestations. Their idea is that in addition to the genetic and anatomical origins, an additional develop‐ mental pathway may contribute to later difficulties. They argue that specific impairments seen in dyslexia or autism (such as dyslexic phonological or autistic mentalising difficulties) may have a 'gatekeeping' function and subsequently lead to difficulties in other areas. Thus impairments in domain-specific functions may have wide ranging developmental effects.

The idea put simply is that during development, one behavior exacerbates problems in oth‐ er domains. It is perhaps easier to understand given a few concrete examples. Frith and Happé suggest that the core autistic difficulty of social engagement may lead to missed op‐ portunities for learning, including learning vocabulary. This may effect language acquisition and in turn the development of language based skills evident in dyslexia. An easier pathway to understand might be via gatekeeping function of inattention. If a child is inattentive (a core symptom of ADHD) then the likelihood is they may struggle to focus on learning to read. Hence difficulties symptomatic of dyslexia may be expected. Conversely perhaps read‐ ing difficulties are primary, in which case inattention might come from frustration and in‐ ability to deal with task demands. This direction of causality seems likely in the sub-group of ADHD children whose problems only appear at school, and who are more likely than other groups to show reading problems according to Taylor (2011). Furthermore, an inatten‐ tive child may find it difficult to socialize normally, and may have difficulties following in‐

struction. This may lead to the impairment in social skills symptomatic of autism.

the general population.

372 Recent Advances in Autism Spectrum Disorders - Volume I

In a similar way, it is possible to theorize that each domain of behavioural impairment in the triad for autism might lead to another. In a review of evidence for single genetic or cognitive causes for autism, Happé, Ronald, and Plomin (2006) note that twin studies suggest combi‐ nations of largely non-overlapping genes act on each area of impairment. Their own study found only modest correlations between the three domains of behavioural traits in the triad (namely deficits in social skills and communication and stereotyped behaviour or restricted interests). In the general population, correlations ranged from 0.1- 0.4 for the relationship of each domain to the other. This evidence shows that the three types of autistic traits may be clustered or linked or co-inherited, but with a weak association. These low correlations could be attributed to developmental pathways factors as well as genetic links. Such residu‐ al downstream developmental effects are easy to conceptualise. If a young boy is very aso‐ cial for example, then his communication skills will not be practised with peers, so he is unlikely to develop as quickly in measures of communication as a more sociable child. The weak correlation between repetitive behaviours is harder to explain. Speculation is possible: repetitive behaviours have been shown to have both self-stimulatory as well as calming functions (Turner, 1999). Repetitive behaviours can therefore be interpreted as responses to unwanted stimuli, e.g. social stimuli with which autistic people have difficulty. Williams (1994) has given a first person account of use of repetitive behaviours to ameliorate the stress of social situations. Conversely, the need for stimulatory repetitive behaviours, con‐ centrating on drawing lines or circles for example, may interfere with social opportunities. Weak associations do not confirm or deny genetic co-inheritance. Developmental pathways where one type of behaviour leads to another may also provide a partial explanation.

In a different but related developmental scenario, Cheslack-Postava and Jordan –Young (2012) suggest that a child's upbringing is highly gendered, and proposed a gendered em‐ bodiment model for autism. They cite numerous studies illustrating that the nature of pa‐ renting in particular depends on the gender of the child. This they use to describe a gendered theory of development of autism, although the model could also explain the large predominance of boys with other developmental disorders. Cooper (2001) suggests boys are socialized to encourage competition and activity thus a conflict between passivity required at western schools and masculine identity is generated. Some behaviours associated with ADHD when used excessively in school environments, climbing trees for example, are en‐ couraged more often in boys than girls. Cheslack-Postava and Jordan –Young suggest such gendered social processes interact with biology to promote certain 'disordered' behaviours. This they call the 'pervasive developmental environment'.

As well as downstream developmental models, some theorists have suggested one cognitive deficit may underlie several symptomatic behaviours. Although the cognitive/psychological theories of dyslexia and autism seem quite distinct, some research does suggest children with both ADHD and dyslexic difficulties show a distinctive deficit in rapid naming speed, so it may that processing speed underlies the link (Bental & Tirosh, 2007).

A second example is provided by executive function which is impaired in both autism and ADHD (Willcutt et al, 2005). According to some models, an underlying impairment in execu‐ tive function prevents children from coordinating information processing in the brain, and prevents the transfer attention from one thing to another. It is easy to understand how this ab‐ sence may translate into symptoms of either autism, due to inability to plan with strategic over‐ arching vision, and hence reliance on routines, or as inattention and distractibility symptomatic of ADHD. Executive functions are neuropsychological processes needed to sus‐ tain problem-solving toward a goal. Executive functions allow a resolution of conflict when two responses are simultaneously called for by stimuli. In the laboratory, the Stroop task is an example. The conflicting combination of a word like *red* written in green ink creates conflict when the task is to say the color of the ink (green), due to the overlearned reading response that automatically elicits the response based on the meaning of the word (red). Executive function allows for the inhibition of the overlearned response and the execution of a response that is more appropriate given the context. Research has confirmed the involvement of deficits in ex‐ ecutive functions that are essential for effective self-regulation in people with ADHD. The mental processes most often listed as being part of the notion of executive function are quite di‐ verse so there is no standardized definition. They include: inhibition, resistance to distraction, self-awareness, working memory, emotional self-control, and even self-motivation. Bramham and colleagues (2009) found that both adults with ASD and ADHD had impaired executive function, although they did have distinctive profiles. Nyden and colleagues found that chil‐ dren with Asperger's Syndrome and dyslexia did not differ in tests of executive function: they could not establish any test of executive function that captured the differences in these disor‐ ders (1999).

temptations (problem-solving), and may have even used words of encouragement toward yourself to enhance the like‐

Co-Occurrence of Developmental Disorders: Children Who Share Symptoms of Autism, Dyslexia and Attention Deficit

Hyperactivity Disorder

375

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

Barkley explains that these and other mental activities are usually included in the under‐ standing of human self-regulation, and it is difficulties in these areas (which are processes in executive function) that may lead to ADHD. Children with ADHD are distractible and selfregulation, the ability to override incoming stimuli, to see the bigger picture and lack the ability to see the consequences of their future actions. Children with ASD have difficulties transferring attention from one thing to another because they also lack overview (and impli‐

Gooch, Snowling and Hulme (2011) note that deficits in time perception (the ability to judge the length of time intervals) have been found in children with both dyslexia and ADHD. These researchers found children with comorbid dyslexia and attention problems performed poorly on measures of executive function as well as on phonological tasks. However, their results were interpreted as the effect of independent underlying cognitive causes. Although deficits in duration discrimination were associated with both dyslexia and attention prob‐ lems, they concluded the results supported the claim that the two disorders are products of

Developmental models explain comorbidity of developmental disorders by shared cognitive deficits, either as 'gateways' as in Frith and Happés (1998) model, where one difficulty leads to another later in life, or as underlying shared deficits, for example impaired executive function causing both autism and ADHD. The alternative model suggests that cognitive dif‐ ficulties associated with each disorder are distinct, but multiple cognitive deficits arise from similar genetic/environmental origins. All these theories have some empirical support.

different cognitive defects originating from shared genes with pleiotropic effects.

**11. Diagnostic substitution and the influence of society and culture**

When symptoms of two or more conditions are shared, whatever the psychological mecha‐ nisms (whether or not there are shared underlying cognitive deficits, and /or genetic and neurological differences) then the area of functioning that is highlighted as a problem may depend on which tests are administered. In our recent research we followed a six year old child who was assessed by three educational psychologists and one multidisciplinary team, each blind to the findings of the others. One concluded that the child had dyspraxia, two that the child had dyslexic difficulties, and a third that borderline AS was likely. We inter‐ preted these differences in the use of diagnostic labels as dependent on settings that varied during assessments, and assessment methods that exposed different types of behaviour (Russell, Norwich, & Gwernan-Jones, 2012). This work suggests that which diagnosis is as‐ signed depends to some extent on social and cultural factors as well as actual symptoms. If a child has symptoms of several disorders, then one context or test may draw out symptoms associated with one disorder, whereas another setting may expose symptoms of another.

lihood that you would follow your plan (self-motivation).

cations of their actions in the future).

Russell Barkley (2012) conceptualizes executive control as the methods of self-regulation. He writes entertainingly on how a person might use executive functions to resist the temptation to buy a tempting pastry from a shop:

…avert your eyes from the counter, walk to a different section of the shop away from the tempting goodies, engage yourself in mental conversation about why you need to not buy those products, and even visualize an image of the new slenderer version of yourself you expect to achieve in the near future. All of these are self-directed actions you are using to try and alter the likelihood of giving into temptation and therefore increase your chances of meeting your goal of weight loss this month. This situation calls upon a number of distinct yet interacting mental abilities to successfully negotiate the situation. You have to be aware that a dilemma has arisen when you walked into the shop (self-aware‐ ness), you have to restrain your urge to order the pastry to go with the coffee you have ordered (inhibition), you redirected your attention away from the tempting objects (executive attention or attentional management), you spoke to yourself using your mind's voice (verbal self-instruction or working memory), and you visualized an image of your goal and what you would look like when you successfully attain it (nonverbal working memory, or visual imagery). You may also have found yourself thinking about various other ways you could have coped effectively with these Co-Occurrence of Developmental Disorders: Children Who Share Symptoms of Autism, Dyslexia and Attention Deficit Hyperactivity Disorder http://dx.doi.org/10.5772/54159 375

temptations (problem-solving), and may have even used words of encouragement toward yourself to enhance the like‐

lihood that you would follow your plan (self-motivation).

prevents the transfer attention from one thing to another. It is easy to understand how this ab‐ sence may translate into symptoms of either autism, due to inability to plan with strategic over‐ arching vision, and hence reliance on routines, or as inattention and distractibility symptomatic of ADHD. Executive functions are neuropsychological processes needed to sus‐ tain problem-solving toward a goal. Executive functions allow a resolution of conflict when two responses are simultaneously called for by stimuli. In the laboratory, the Stroop task is an example. The conflicting combination of a word like *red* written in green ink creates conflict when the task is to say the color of the ink (green), due to the overlearned reading response that automatically elicits the response based on the meaning of the word (red). Executive function allows for the inhibition of the overlearned response and the execution of a response that is more appropriate given the context. Research has confirmed the involvement of deficits in ex‐ ecutive functions that are essential for effective self-regulation in people with ADHD. The mental processes most often listed as being part of the notion of executive function are quite di‐ verse so there is no standardized definition. They include: inhibition, resistance to distraction, self-awareness, working memory, emotional self-control, and even self-motivation. Bramham and colleagues (2009) found that both adults with ASD and ADHD had impaired executive function, although they did have distinctive profiles. Nyden and colleagues found that chil‐ dren with Asperger's Syndrome and dyslexia did not differ in tests of executive function: they could not establish any test of executive function that captured the differences in these disor‐

Russell Barkley (2012) conceptualizes executive control as the methods of self-regulation. He writes entertainingly on how a person might use executive functions to resist the temptation

…avert your eyes from the counter, walk to a different section of the shop away from the tempting goodies, engage yourself in mental conversation about why you need to not buy those products, and even visualize an image of the new slenderer version of yourself you expect to achieve in the near future. All of these are self-directed actions you are using to try and alter the likelihood of giving into temptation and therefore increase your chances of meeting your goal of weight loss this month. This situation calls upon a number of distinct yet interacting mental abilities to successfully negotiate the situation. You have to be aware that a dilemma has arisen when you walked into the shop (self-aware‐ ness), you have to restrain your urge to order the pastry to go with the coffee you have ordered (inhibition), you redirected your attention away from the tempting objects (executive attention or attentional management), you spoke to yourself using your mind's voice (verbal self-instruction or working memory), and you visualized an image of your goal and what you would look like when you successfully attain it (nonverbal working memory, or visual imagery). You may also have found yourself thinking about various other ways you could have coped effectively with these

ders (1999).

to buy a tempting pastry from a shop:

374 Recent Advances in Autism Spectrum Disorders - Volume I

Barkley explains that these and other mental activities are usually included in the under‐ standing of human self-regulation, and it is difficulties in these areas (which are processes in executive function) that may lead to ADHD. Children with ADHD are distractible and selfregulation, the ability to override incoming stimuli, to see the bigger picture and lack the ability to see the consequences of their future actions. Children with ASD have difficulties transferring attention from one thing to another because they also lack overview (and impli‐ cations of their actions in the future).

Gooch, Snowling and Hulme (2011) note that deficits in time perception (the ability to judge the length of time intervals) have been found in children with both dyslexia and ADHD. These researchers found children with comorbid dyslexia and attention problems performed poorly on measures of executive function as well as on phonological tasks. However, their results were interpreted as the effect of independent underlying cognitive causes. Although deficits in duration discrimination were associated with both dyslexia and attention prob‐ lems, they concluded the results supported the claim that the two disorders are products of different cognitive defects originating from shared genes with pleiotropic effects.

Developmental models explain comorbidity of developmental disorders by shared cognitive deficits, either as 'gateways' as in Frith and Happés (1998) model, where one difficulty leads to another later in life, or as underlying shared deficits, for example impaired executive function causing both autism and ADHD. The alternative model suggests that cognitive dif‐ ficulties associated with each disorder are distinct, but multiple cognitive deficits arise from similar genetic/environmental origins. All these theories have some empirical support.
