AUTISM : CURRENT ISSUES 45
These summaries begin with further evidence about brain structure anomalies among young children diagnosed with autism.
Reference is then made to the apparent significance of paternal age as a factor in the probability of autism among children.
The concept of absent or deficient “inner speech” is discussed as a means of explaining certain characteristics of autism.
The frequently observed pattern of food faddisms among children with autism is described as a potentially dangerous issue in its own right.
The final sections refer, respectively, to the applicability of cognitive behavioural therapy to children and young people with autism, and to the experience of grandparents within families of a child with autism.
M.J.Connor September 2006
The paper exploring the possible aetiological or correlational significance of the volumes of gray and white matter in the brain (Friedman et al 2006) begins with an acknowledgement that there is no clear and consistent evidence by which definitively to set out the cause or causes of autism.
Nevertheless, it is held that there are converging sets of data and opinions, based upon neuro-imaging as well as post-mortem studies, that early and atypical developments within the structure of the brain are implicated.
The brief review set out by these authors suggests that cerebral volume is not enlarged at birth among children subsequently diagnosed with autism, but increased brain size is noted during the third and fourth years of life. This accelerated or over-growth ceases in later childhood with various permutations of anomalies observable in the gray and white matter, brain lobes, and nuclei.
The two most replicated findings relevant to cases of autism are small and densely packed cells in the medial temporal lobe (hippocampus), and reduced numbers of cells in the cerebellum. There may be other cellular abnormalities in a number of regions, consistent with the observed variations in the type and severity of symptoms.
In their own study, Friedman et al began with the hypothesis that gray matter chemicals are selectively altered in autism and ASD; and they applied regression techniques to data relating to a sample of 3 to 4 year old children with ASD, and control samples of children showing developmental delay and those showing typical development.
45 children (38 boys and 7 girls) were compared with 12 children (5 boys and 7 girls) with developmental delay and 10 children (8 boys and 2 girls) with no known developmental deficits.
The results from the analysis of imaging data showed that there appears to be a distinct pattern of gray matter chemical abnormalities among those 3 and 4 year old children with ASD compared to the age matched children with developmental delay and normal development.
The ASD group were found to have decreased gray matter notably with regard to the extent of choline- or creatine- containing substances. This pattern was distinct from that observed in the children with developmental delay, and was held to be indicative of decreased cellularity or density as an ASD-specific anomaly.
However, the ASD sample and the developmental delay sample were comparable in terms of the pattern/volume of white matter …. some decrease in the concentration of cells or volume …. suggesting some shared aetiological features between children with ASD and children with developmental delay.
The authors discussed their findings in terms of the converging evidence for an early and specific abnormality in gray matter within the clinical course of autism and ASD, but it was acknowledged that it cannot be determined whether the autistic characteristics relate to gray matter density per se or to connectivity through decreased dendritic branching.
In a separate paper published a month later (Dager et al 2006), the same team of authors restated their finding of this anomaly with regard to gray matter in the developing brains of young children with autism. They note that the apparent significance of the delayed growth of gray matter challenges that school of thought which has regarded accelerated brain growth as characteristic of autism.
There may be some similarities between children with autism/ASD and children with developmental delay in neuronal growth and maturation, but the significance of these gray matter anomalies lies in the indication of developmental processes specific to autism.
The authors further concluded that there may be as yet unrecognised abnormal processes impacting upon brain neurochemistry or cell density and volume of which the gray matter anomaly is an outcome. They argue that ongoing studies need to take account of even small differences in the chronological age of participants, and the level of severity of the autistic symptoms, given their likely significance for variation in (neurological) growth processes and the (rapid) changes in the associations among factors according to developmental stage and chronological age.
Paternal Age and Autistic Risk
According to research recently completed by Reichenberg et al (2006), the risk of having a child with autism increases in direct association with the age of the father.
The study sample comprised records from more than 132,000 children born in Israel during the 1980s, and the following pattern emerged …
The implications included the applicability of the concept of a “ biological clock ” to men (with no evidence from this study of any link between autism in the child and increased maternal age); and it was speculated that genetic mutations in the sperm of the older men could be responsible for the increased risk of autism among their offspring.
The researchers stressed that their findings related to “classical” autism and that they may not necessarily be applicable to other conditions such as Asperger Syndrome; although the data were suggestive of a general association between increased paternal age and ASD.
There was the further speculation
that the impact of the hypothesised mutations in sperm producing cells, or
discrepancies in gene expression, is upon the developing neurological
structures of the child during the pre-natal or early post-natal life.
Meanwhile, there was the acknowledgement that paternal age may be influenced by socio-cultural mores, and that environmental features may play some part in the development of the anomalies characteristic of autism … but converging evidence has pointed to the major influence of genetic factors (the predominance of nature over nurture) in autism and ASD.
Inner Speech Deficits and Autism
Whitehouse et al (2006) cite Vygotsky’s view that language is the critical mediating force interacting with intellectual and environmental stimuli to promote cognitive growth and allied skill development.
They also review research findings which have highlighted the mediating role of inner speech in aspects of executive control such as planning, and flexibility in response to immediate circumstances, and organisation.
The corollary is that a deficit in the internalisation of language will underlie impairments in cognitive and behavioural performance.
All this is very relevant to autism given its characteristic weaknesses in planning, or shifting perceptions, etc. which are part of executive functioning. However, the authors have found very little existing evidence concerning the role of inner speech (or the effects of deficits therein) in autism.
They cite just one study (Russell et al 1999) who showed that a deliberate interference with the use of inner speech among normally developing children leads to poor performance of tasks requiring executive function skills …. performance comparable to what is typically observed among children with autism.
Accordingly, the present authors completed three experiments by which to investigate the use (or non-use) of inner speech among children with autism.
The first experiment involved tasks dependent upon pictorial information.
Experience has shown that when both printed and pictorial information are available in a verbal recall task, it is the pictures upon which the memory processes are concentrated. A common explanatory view holds that pictorial information is processed in terms not only of the actual visual details but also of the spontaneous verbalisation of the content …. there is a dual coding which increases the efficiency of encoding and storage.
In other words, the superior effect of pictorial information is a matter of using inner speech, and limitations in access to inner speech (as hypothesised to affect individuals with autism) would lead to a reduction in this superiority of pictorial information.
The results of varying the type of information to be recalled showed that the picture-superiority effect applied to normally developing children of primary school age in that they recalled significantly more of the pictures than the words. The children with autism recalled significantly fewer pictures than words, and more words than the control children (albeit not significantly so). Thus, the autistic sample did not show the picture-superiority effect … attributable to the limited or absent inner speech.
The second experiment concerned word length and the probability that more words from a list will be recalled when the words are of shorter rather than longer (spoken) duration. This word length effect is assumed to be a matter of the ease of verbal coding.
Existing evidence indicates that such memory effects will only apply when the pictorial information is translated into inner speech labels.
However, the word length effect when applied to pictorial information is not observed among very young children but only emerges at about 7 or 8 years of age …. significantly after the children have shown this effect with aurally presented words.
The participants in this second task were set to recall 5-item sequences and two conditions were employed. The silent condition specifically asked the children not to apply audible verbal labels to the pictures when they were presented (so that there was no requirement to make some verbal encoding/inner speech); while the label condition encouraged the children overtly to produce the verbal labels (which would evoke some encoding via inner speech).
It was hypothesised that the autistic children would show a lesser or absent word length effect in the silent condition where any labelling would involve inner speech, but would perform comparably to controls in the condition which actively encouraged the overt verbal labelling and was less dependent upon the availability of inner speech.
The findings supported the hypothesis in showing that individuals with autism did not make use of inner speech in the way that normally developing children did.
The authors held, accordingly, that the two experiments thus far provided evidence that deficits in the use of inner speech limit the availability of verbal coding to aid memory tasks among children with autism.
The third experiment involved a task-switching format where the children had to alternate between two simple operations … addition sums and subtraction sums.
The hypothesis was that, however simple the tasks themselves, the constant switching increases the pressure upon cognitive resources of which a significant element is inner speech; and that performance would vary according to whether the children are allowed to verbalise and evoke inner speech to remind them of the need to alternate, or are asked to avoid so-doing.
Therefore, children with autism and normally developing children would be differentiable in terms of changes in performance on the switching task as a result of their differential access to inner speech, with the normally developing group showing the greater difference according to the availability of inner speech.
The results showed that the blocking of inner speech did not have an impact on the performance of the children with autism, supporting the view that these children do not use inner speech, anyway, to complete such tasks.
The overall conclusion restated the view that children with autism have limitations in their use of inner speech … although it is not clear whether it is a matter of a lack of any such facility, a failure to utilise this facility, or a developmental delay in the acquisition of the facility.
What matters is the likelihood that problems in internalising language among children with autism will inhibit the development of further linguistic skills with implications for general communicative and social skills.
Effects of (Severe) Food Faddism
It is noted by Uyanik et al (2006) that eating disorders are common among children with autism, and it is their view that such disorders can introduce a potentially serious complication for the management of the children and for their general health.
They describe the case of an 8-year old boy who was referred to their clinic because of a progressive visual impairment which first appeared as a loss of night vision and which evolved into an inability to open his eyes. Verbal communication had been markedly limited, and seizures were evident from the age of 3 years. Self injurious and aggressive behaviours had developed along with characteristically autistic symptoms of repetitive behaviours such as spinning objects and hand flapping.
Investigations revealed that, for the previous 4 years, the boy had eaten nothing but fried potatoes and had drunk nothing but water, and he was diagnosed with a vitamin A deficiency as a result of malnutrition.
Dietary treatment including multivitamin supplementation was instigated, and, within a month, there were signs of corneal improvement and of some positive papillary light reflexes.
In their discussion, the authors highlighted the risk of nutritional deficiencies and their complications which, in the case of some children with autism, arise as a result of a refusal to eat anything but items from a very limited set of foods.
It is their view that children with autism who have severely restricted diets will show an enhanced prevalence of essential amino acid deficiencies which may bring about negative impacts for the developing brain (presumably in the production or functioning of neural transmitters).
The implication is for early intervention to include assessments of dietary habits in order, where necessary, to intervene before the risk of sensory and physical impairments is realised.
Asperger Syndrome and Cognitive Behaviour Therapy (CBT)
The investigation by Greig and Mackay (2005) addressed the question whether CBT could be adapted to manage the social, emotional, and behavioural needs of a 12 year old boy diagnosed with Asperger syndrome.
An associated question concerned the desirability of a continuing role for educational psychologists in offering direct therapeutic intervention along with supporting other professionals in pursuing individual casework.
In any event, the increase in the number of children and young people who are diagnosed with Asperger syndrome indicates that this is an area where it is important for educational psychologists to maintain a high and up to date level of knowledge in order to offer effective support and advice.
Children and young people with Asperger syndrome are seen by these authors as presenting a particular challenge in that their generally good abilities are appropriate for access to mainstream school opportunities, but the expectations upon them alongside the subtle but real difficulties in communication or in social interactional style place them at risk for (secondary) emotional disorders …. and evidence is cited for the enhanced risk of depression or anxiety or anger among adolescents with this syndrome.
In considering the use of CBT with cases of Asperger syndrome, Greig and Mackay describe how it has become established as an effective technique for managing a variety of mental health issues such as depression or anxiety.
However, hitherto there has existed a relatively common belief that CBT might not be effective with the Asperger population because of their weaknesses in abstract or flexible thinking; but the present authors cite the emerging view that work with children and young people with Asperger syndrome can be valuable if it is adapted to match the individual’s level of cognitive development and style.
The basic principle underlying the operation of CBT is that what matters is not some actual event or circumstance but the personal interpretation of, and the implication drawn from, that event or circumstance. The individual may take a disproportionately negative view, for example, and the perceptions, and the accompanying thoughts and feelings, can be resistant to change.
The role of the therapist is to explore the pattern of thinking and to demonstrate how the individual perception can have a generally negative impact upon mood, behaviour, or even physical functioning.
The argument in favour of CBT continues by noting how CBT has been used with cases of anxiety and depression, and it is held that the rigid and negative perceptions of individuals with Asperger syndrome have something in common with these “traditional” beneficiaries of CBT in terms, for example, of polarised thinking or fatalistic feelings, or inaccurate attributions about the actions of other people.
What matters for the Asperger population is ensuring that the approach is modified to take account of the characteristic weaknesses such as a limited Theory of Mind or poor executive functioning (planning, reflecting on experience, etc.).
Meanwhile, the time that may be needed to process ideas and suggested strategies, and the preference for a clear and predictable structure to interaction, are well reconcilable with the nature of CBT with its regular sessions and routines.
The single case study described by Greig and Mackay was that of a boy in his first year of secondary schooling, and who showed good ability and satisfactory existing achievement. Nevertheless, there was a perceived gap between actual and potential achievement attributable to his Asperger style and his specific problems in class such as short attention/concentration span limited self organisation, and attention seeking behaviour.
Peer relationships, self esteem, and reactions to changes in routine, were reported to be further areas of difficulty.
The particular pattern of the CBT in this case involved the establishment of some imaginary characters who would act as a prompt for thinking more flexibly about issues and for considering alternative (more positive) interpretations of events.
They would also be called upon to offer advice about tasks or situations found challenging and assist in finding solutions and in regulating thoughts and beliefs.
Ij this particular case, the boy was able to create a range of characters, depicted as occupying different sections of his brain, and available to help with a range of issues.
“Chatterbox”, for example, was available to help the boy to recognise when to stop talking, when to allow someone else to talk without interruption, and how to show interest. “Gaffa” was available to help with interactions and to describe ways of initiating and maintaining social contacts.
A chief character had the responsibility always to be on the look out for potential problems and conflicts, and to flash up warning lights in the boy’s head indicating when he should stop, when he should think, and when he could safely take some action.
“Aspie” was an unhelpful character likely to blow things out of proportion or to try to act without thinking, and “Aspie Hunter “ had the task of identifying when Aspie was showing signs of bringing about these negative actions and of intervening to prevent them.
The evaluation indicated a significant shift for the better between the baseline measures of anxiety, anger/stress, and depression, and the follow-up measures completed after the total of 15 sessions spread over the latter part of the Summer term of year 7 and early part of the Autumn term of Year 8.
The initial measures had been indicative of significant problems, whereas the follow up measures indicated that emotional status was within normal limits for the age group. Anger responses remained relatively high, but still within the average range.
Improvement in social competence, while less marked, was still observable; and the teachers reported an observably improved adjustment to the school setting and demands.
The authors concluded by reinforcing the view that CBT has a place in the range of supportive interventions available to children and young people with Asperger syndrome, that this population will continue to be significant in respect of demands upon the support services, and that therapeutic intervention of this kind may well both suit the particular skills of the educational psychologists and match the perceived significance of individual casework in the views of school staff about the use of educational psychologists’ time.
Grandparents and ASD
It is established that the care and management of a child with ASD can put considerable pressure upon parents, and they may well experience a need for enhanced support.
Margetts et al (2006) note that a significant source of support lies within members of the extended family, notably including the grandparents, but that little literature exists about the experiences and perceptions of the grandparents of a child with ASD.
This is in contrast to the considerable body of information concerning the role of grandparents in respect of children with a physical disability or a learning difficulty. Existing studies have indicated the perceived importance of the grandparents
(particularly maternal grandparents) in offering emotional support to the parents of children with physical disabilities; and in contributing to the well-being of mothers who are caring for a child with learning difficulties.
Their own survey elicited opinions from a sample of 6 grandparents (3 maternal grandmothers, 2 paternal grandmothers, and 1 paternal grandfather) via interviews which sought views on the following topics ….
Various categories of response emerged, but three major themes were identified.
Firstly, the parental bond referred to the way in which the grandparents’ concern for their own adult child as well as the grandchild involved a high level of care, with some blurring of the distinction between child and grandchild in respect of the recipient of that care. The clear implication was for concern not just for the grandchild with ASD but for the well being of the child’s parent(s), and anxiety over the pressure put upon the relationship between the mother and father.
Further elements involved memory for milestones along with some enhanced attention to, or spoiling of the child, with ASD as a kind of compensation for the difficulties which the child him or herself would not understand.
The identification with the child’s mother or father was seen as reflective of the early and protective bonding between mother and infant.
Secondly, striving for answers involved some dilemma about how to be supportive without undermining or belittling the parental role. There was also the anxiety about wanting to be supportive while lacking knowledge about the nature and implications of ASD.
One practical role was that of acting as an advocate and pressing for support for the family from social services or other agencies.
Also within this theme was the matter of attributing blame …. such as the (alleged) effects of MMR, or any issue other than genetic inheritance.
Thirdly, keeping intact included seeking a balance between worrying for all the rest of the family and handing back responsibility to the parents. There was also uncertainty about how to deal with a situation where siblings of the child with ASD receive limited attention (and sometimes inappropriately generous material rewards as compensation for this situation).
It was commonly found that, as grandparents felt that issues had resolved themselves and that the family situation was stable, some other concern or stressor would arise … such as the approach of the time when the child is to start school or to move to a different school.
The authors’ summary and conclusion recognise the small size of the sample but they offer the recommendation that, given the apparent significance of the grandparents’ role and the associated anxieties, grandparents should be regarded as potentially major sources of support to parents at the very difficult time of the identification of ASD in the child.
This would involve their not only supplying information to assessing teams but also being the recipients of information about ASD and the implications for the child.
Further, their advocacy role would usefully be recognised and reinforced via inclusion in the support and advice available from services already involved.
In practical terms, it is recommended that assessment and advisory teams routinely ask parents if they would like to be accompanied to consultations by the grandparents, and that the grandparents themselves can be given access to advice and guidance in order that they can determine how best they can support their own son or daughter, plus partner, as well as the grandchild.
* * * * * *
M.J.Connor September 2006
Friedman S., Shaw D., Artru A., Dawson G., Petropoulos H., and Dager S. 2006 Gray and white matter brain chemistry in young children with autism. Archives of General Psychiatry 63 786-794
Dager S., Friedman S., Shaw D., Artru A., Dawson G., and Petropoulos H. 2006
Structural brain abnormality in autistic children. Summary available in Medscape Medical News. Original article in Neurology 67 632-636
Greig A. and Mackay T. 2005 Asperger syndrome and cognitive behaviour therapy. Educational and Child Psychology 22(4) 4-15
Margetts J., Le Couteur A., and Croom S. 2006 Families in a state of flux : The experience of grandparents in autistic spectrum disorder. Child : Care, Health, and Development 32(5) 565-574
Reichenberg A., Gross R., Weiser M. et al 2006 Advancing paternal age and autism. Archives of General Psychiatry 63 1026-1032
Russell J., Jarrold C., and Hood B. 1999 Two intact executive capacities in children with autism. Journal of Autism and Developmental Disorders 29 103-112
Uyanik O., Dogangun B., Kayaalp L., Korkmaz B., and Dervent A. 2006 Food faddism causing vision loss in an autistic child. Child : Care, Health, and Development 32(5) 601-602
Whitehouse A., Mayberry M., and Durkin K. 2006 Inner speech impairments in autism. Journal of Child Psychology and Psychiatry 47(8) 857-865
© Mike Connor 2006.
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