AUTISM : CURRENT ISSUES 23

These notes begin with a summary of work which explores a hypothesis linking the aetiology of autism to an impairment in the interaction of neural networks and a failure to integrate information from different neural locations.

There follows a description of the possible ways in which autism can be differentiated from mental retardation by the end of the first year.

The importance for positive mental health of parental self-efficacy in managing autistic behaviours in their children is discussed.

The final section highlights some current tentative thoughts on possible causal factors.

 

The Temporal Binding Deficit Hypothesis

The paper by Brock et al (2002) concerned with actual cognitive and neurological mechanisms underlying autism (or, at least, the core symptom of weak central coherence) is introduced by a reference to the triad of impairments in social interaction, communication, and behavioural flexibility, and to the perceptual anomalies that may differentiate autism from general learning difficulty.

Frith (1989) is quoted as suggesting that many of these perceptual, or attentional, anomalies in autism could be explained in terms of a difficulty in integrating different pieces of information or putting them into context, and of a bias towards local rather than global processing. This concept of " weak central coherence " has, however, been criticised on the grounds that it is largely descriptive rather than explanatory and the mechanics of the condition are not addressed.

Brock et al hypothesise that weak central coherence results from a failure to integrate information from different specific networks in the brain and that this impairment will become increasingly evident as the developing brain becomes more specialised. It is their proposition that the deficit in central coherence is associated with impairments of temporal binding between local networks, and that this inefficient temporal binding could be significant in the behavioural inflexibility and the social or communicatory aspects of autism.

" Central Coherence " is defined as .. The everyday tendency to process incoming information in its context ; pulling information together for higher level meaning often at the expense of memory for detail (Happe 1999). Individuals with autism, however, frequently show an emphasis upon details which are remembered at the expense of the wider picture.

Accordingly, such individuals will perform well on tasks which require processing of constituent parts of objects or scenes but poorly when it is necessary to process the whole thing. For example, there will be good performance in seeking to identify a hidden shape within a larger picture, or in completing a block design task. Children with autism draw faces bit by bit rather than beginning with the overall shape, and savant artists with autism draw pictures detail by detail instead of starting with the general framework.

Further, individuals with autism can process the meaning of single words but may have difficulty in coping with a sentence containing a homophone ( such as " In her dress there was a large tear " or " In her eye there was a large tear "). There is an inability to scan the whole sentence for its meaning in order correctly to read the ambiguous word.

It is the contention of Brock et al that findings of this kind may be explicable in terms of impaired neural integration.

They go on to describe how information processing in the mature brain occurs in separate specialised functional areas, but these areas do not work in isolation. Instead, the completion of any activity is associated with the simultaneous activation of various cortical areas and success is a function on the effective integration of neural output from the separate areas. Autistic symptoms may reflect some failure within the processes underlying this neural integration.

So, the hypothesis has it that while typical brain development involves the emergence of functionally specialised but integrated areas, brain development in autism involves the emergence of functionally specialist areas which become increasingly isolated from each other over time. As a result, there will be impairment in those cognitive skills requiring the integrated action of a number of areas while skills relying on relatively localised neural activity will be unimpaired.

In low-functioning individuals, the impairment will be pervasive and involve an almost total lack of integration, but in higher-functioning individuals there may be adequate integration between at least proximal brain areas such that perceptual processing will be more efficient.

This begs the question of the nature of the process by which different brain areas do interact and this has become known as the " binding problem ".

Two hypotheses exist, one referring to combination coding and the other to temporal binding (and it is the latter which the current authors favour in seeking to understand autistic symptoms).

To illustrate the two hypotheses, the example is given of a simple neural network involved in processing an array which contains either a triangle or a square in the upper or lower half so that the shape and its position may be processed by the firing of two neurons. However, this simple processing could not cope with a situation where both shapes are presented simultaneously.

The combination coding solution involves an additional four neurons that each respond to one of the four possible combinations of shape and position (and there is evidence . eg Hubel and Weisel 1977 . that combination coding does occur in early visual processing). However, it is held by various researchers that combination coding cannot provide a complete solution to the integration issues given, for example, the impossibility of having sufficient capacity to code for every possible combination of features in a (complex) visual array.

The temporal binding solution has it that combinations of features can be represented by the synchronous firing of neurons responding to the different dimensions of a stimulus. In the example, the appropriate neurons for triangle and top would be active simultaneously but fire at a different time than the neurons linked to square and bottom.

The current position according to a number of authors (eg Singer 1999) is that combination coding may provide a partial solution to integration but that temporal binding is required whenever the cognitive demand is beyond a matter of familiar and well learned material and involves perceiving and representing novel stimuli.

With regard to autism, Brock et al argue that the symptom of weak central processing results from some impairment in temporal binding so that the individuals affected are obliged to rely upon combination coding. It is the impairment of temporal binding between local neural networks that underlie the deficits observed in autism even if integrative mechanisms within local networks may be unaffected or even enhanced.

The impairment may be seen as "hypocoupling" whereby local networks do not become temporally connected with each other so that bits of information are processed separately.

Weak central coherence is the observable or cognitive manifestation of hypocoupling which, itself, may reflect some neurotransmitter imbalance or an absence of longer range connections in the cortex, so that there is emerging a link between structural or neurochemical abnormalities and the cognitive impairments characteristic of autism.

This view is supported by evidence from EEG studies which show that, in children between 2 and 4 years of age, there are cycles of EEG coherence between cortical areas which are held to reflect an increase in synapse strength or numbers followed by synapse pruning, and it is likely that children with autism would show some idiosyncratic variation or disturbance in these cycles.

There has also been a long term view (see, for example, McLelland 2000) that autism is a matter of diffuse abnormalities of brain organisation. Certain brain areas have either too many or too few processing units ; or there is excessive inhibitory feedback between neuronal groupings.

Such views predict that individuals with autism will tend to treat similar stimuli as if they are quite different thus explaining both the impaired generalisation of learning and the enhanced discrimination skills observed in autism.

In any event, the temporal binding deficit can also explain the reduced ability to make use of context in language processing. Individual words are processed out of context so that sentences containing homophones, for example, are not interpreted correctly even if the meaning of the individual words is unimpaired because this skill involves local activity and well-established associations between semantic and phonological representations.

Similarly, behavioural inflexibility or difficulty in shifting attention may be a matter of some lack of the modulating influence of frontal networks on other areas of the brain. It is suggested that a reduction in binding between frontal and posterior networks could reduce executive control and lead to the observed symptoms.

It is also noted that social and communicatory weaknesses (or absent theory of mind) are a function of an inability to integrate multiple sources of social information, or a residue from earlier failure to establish joint attention which itself may be a function of the binding/integration weaknesses.

Brock et al conclude that temporal binding is a significant issue although they acknowledge that this concept cannot provide a complete account of all the autistic deficits. For example, impairments in affective relationships occur in the absence of other autistic-type symptoms and may be explicable in terms of quite different underlying deficits. This view is also consistent with ongoing genetic studies which suggest that autism is related to the convergence of several interacting genes.

The conclusion is that the temporal binding deficit may encompass much converging evidence and is a helpful working hypothesis for examining links between brain organisation and observable behaviour, but it is indeed a working hypothesis and likely to undergo modifications as more knowledge accrues.

Differentiating Autism from Mental Retardation in 1 Year Old Infants

It is now commonly accepted that early intervention in autism is very important in increasing the probability of positive long term prognosis in many individuals. This implies the desirability of early identification of autism, but it is noted by Osterling et al (2002) that a confident diagnosis may not be made until the child is between 3 and 4 years of age.

However, it has been recognised for a long time (see, for example, Ornitz et al 1977)

that parents can recognise anomalous signs and symptoms indicative of autism very early in their children's lives, with many parents suspecting a problem before the children have reached their first birthday and most parents expressing concern to a pediatrician by the time the children have attained 18 months.

So, there is a discrepancy between the ages at which symptoms are detectable and at which diagnosis is made and intervention begun.

A complication is that early development in autism is frequently characterised by a delay or absence of typical behaviours, and autistic symptoms may be confounded with those of general learning disability. It is important, therefore, to recognise the ways in which children with autism and children with mental retardation differ in the types of early impairments shown.

The children with mental retardation are likely to show impairmants across a number of areas including communication, social, and motor skills, with a global delay matching the level of retardation. The children with autism (without mental retardation) would be more likely to show significant delays in social skill development such as eye contact, social communication, and shared attention.

Dahlgren and Gillberg (1989) compared parental reports of behaviours in the first 2 years of children later diagnosed with autism or mental retardation, and described how the children with autism had been seen as unusual in their social behaviour, play, and perceptual sensitivities ; and, compared to the children with mental retardation, had shown poor attention, unresponsiveness to their name, a tendency frequently to mouth objects, and an aversion to touch.

A further complicating variable is the age of onset of autistic symptoms in that, while most children demonstrate symptoms in early infancy, there is a significant minority

(around 20 %) who display largely normal development for anything between 18 and 36 months before there is a loss of social and communication skills and an onset of perseverative behaviours.

Osterling et al note that, because diagnosis may come relatively late, there is a lack of studies involving behaviours in the earliest months or years of children with autism.

Reference is made to an earlier study (Osterling and Dawson 1994) where home video tapes of infants later diagnosed with autism were compared with tapes of children diagnosed with pervasive developmental disorder and of children who showed normal development.

It was demonstrated that the autistic sample and the normally developing sample could be differentiated by the end of their first year. The significant differences were in the areas of social behaviour (looking at faces, seeking contact), joint attention, and certain autistic behaviours such as failing to orient, self stimulation, and covering ears. How often a child looked at the face of another person was a major pointer towards classifying the children.

The goal of the present study by Osterling et al (opp. cit) was to identify differences in the early development of children later diagnosed with autism or with mental retardation (and to replicate the 1994 study in observing how social and joint attentional behaviours could assist in differentiating the two groups).

The children included a group with autism some of whom also experienced mental retardation, a group with mental retardation, and a group of normally developing children. The autistic sample were subdivided into an early onset group (symptoms observable by 12 months, and a later onset group (symptoms only observable after the first year). The children were between the ages of 3 and 10 at the time of the study, and parents were asked to supply videotapes of their children made during the early years.

The tapes were analysed according to a pre-determined behavioural code which focused upon social, gaze, motor, affective, communicative, and joint attention behaviours.

The results showed that infants with late onset of autism demonstrated a different pattern of behaviours than the other infants with autism, namely a higher level of orienting to name or looking at other people or sharing attention.

Infants with autism and infants with both autism and mental retardation showed significantly less orienting to name or looking at others than infants with mental retardation only. The autistic group as a whole showed less shared attention or looking at other people, and significantly more repetitive behaviours, than the other groups.

The authors concluded that, by 12 months, children with autism can be distinguished from children with mental retardation and from those developing normally. Social behaviours appeared most significant, along with the probability of a high-level of repetitive motor actions.

On the other hand, it is acknowledged that infants with mental retardation also used gesture or engaged in shared attention less frequently, and showed repetitive motor actions more frequently, than normally developing children. In other words, at 1 year there can still be some confounding of general developmental delay and autism.

There was a replication of the earlier study in that it was confirmed how differences in early attention to language and social stimuli characterised infants with autism, but the present study differed from the earlier one in detecting differences in the amount of repetitive motor actions between groups.

The authors also stressed that, if early social and prelinguistic behaviours like looking at people and orienting to name appear disturbed in young children with autism, whereas such behaviours appear to be intact among infants of 1 year who are later diagnosed with mental retardation, then impairments in looking at others and in orienting to name should be particularly useful as initial markers of autism.

It is recommended, therefore, that screening for autism in very young children should include attention to the child's ability to observe and respond to the social world. Social attention and social responsiveness appear to be important areas on which to base early identification, although it is acknowledged that accuracy of assessment may require specific probes in a clinic setting rather than attempting to monitor behaviours in everyday settings.

Behaviour Problems in Autism and Parental Efficacy

Hastings and Brown (2002) point out that among the most significant stressors for parents and carers is the extent of behavioural difficulty shown by children with developmental disabilities.

However, self-efficacy (defined by Bandura [1989] in terms of perceptions of one's own skills) is seen as an important factor when it comes to facing this kind of stress, with higher levels of self efficacy associated with psychological well-being or reduced distress.

It is further argued, according to the adaptation theory of Taylor (1983), that individuals develop coping strategies that serve to enhance feelings of efficacy and positive self-concept when faced with traumatic events .... a " positive spin " is placed upon on the strategies and upon the situation which in itself facilitates willingness to continue to cope.

Hastings and Brown note some danger here and refer to the dynamic relationship between the child's behaviour and the parents' reactions with the possible implication that parents may act in a way which manages the behaviour difficulty or the stress in the short term but which increases the probability of their continuation in the longer term.

Therefore, their study set out to explore the role of self-efficacy in the relationship between behaviours observed in the child with autism and parental strategies and feelings of well-being with the hypothesis that self-efficacy will act as a mediator.

They worked with a sample of mothers and fathers of children with autism attending specialist schools and with a mean age of 12+. The Developmental Behaviour Checklist was completed by teaching staff to rate the extent of the children's behaviour difficulties ; and parents completed a checklist by which to produce an estimate of self-efficacy with regard to the behaviour difficulties or of their feelings of anxiety/depression.

The data confirmed the high level of potential mental health problems among the parents of children with autism, but also suggested that mothers and fathers may be affected differently by their child's needs and behaviour.

Fathers with high self-efficacy were less anxious than fathers with low self-efficacy when the child had a high level of behaviour problems ; when the child showed a low level of behaviour problems, the paternal self-efficacy had no effect on their anxiety. In other words, feelings of self-efficacy acted as a protective factor for fathers countering the risk of raised anxiety when the child displayed significant behaviour problems.

Mothers with higher levels of self-efficacy were consistently less anxious and more positive, although maternal feelings of self-efficacy were strongly reated to the level of the child's behaviour problems.

It is hypothesised that the differences between the mothers and fathers may be related to the extent of direct day to day involvement with the child. It may be that the extent of involvement in the care of the child is more predictive of paternal stress in that fathers may not be greatly involved when the child presents low levels of difficulty ; but when the behaviour problems are greater, it becomes necessary and important for the fathers to be more involved.

The authors acknowledge that the findings should be treated with caution because the sample of participants was relatively small (26 mothers and 20 fathers) and may not have been representative of all parents of children with autism (since the bias was towards parents in the higher part of the spectrum in terms of level of education, and since many of the children attended specialist and weekly-boarding schools).


Nevertheless, they concluded that self-efficacy can be viewed as a compensatory factor for mothers of children with autism in terms of the impact upon their anxiety or depression ; and as a protective factor for fathers of children with autism since it appears to operate only under conditions of high risk.

The implication is that interventions, administered by the parents, which serve to ameliorate observed problems in the children will also increase the feelings of self- sufficiency and self-efficacy in the parents thus proving beneficial directly and indirectly for the mental health of both mothers and fathers, although the effects are a little less predictable for mothers than for fathers according to the outcomes of this study.

Possible Aetiological Factors

Work in progress at the Cambridge Autism Research Centre (Baron-Cohen et al, and reported in the press by McKie and Gould 2002) has raised the possibility that high amounts of testosterone in the pre-natal environment could be linked to autism.

It has been found that this hormone is linked to children's abilities to communicate and empathise with others, and it is planned to carry out a wider scale study of this possible link between testosterone levels and autism (or failure to develop social skills).

Baron-Cohen is quoted as referring to the spectrum concept of autism, and to the possible role of testosterone in determining an individual's level of social skill.

It is noted that identifying testosterone as significant for the aetiology of social disabilities and autism would explain why boys tend to be poorer at socialising than girls and why many more boys than girls are diagnosed with autism.

Using measures of testosterone in samples of amniotic fluid, it has been found that some boy babies may have low levels of testosterone (less than the average for girls), while some girl babies may have a level equal to the average for boys.

In respect of later behaviours, it was found that an infant's ability to maintain eye contact with a parent was correlated with testosterone level. Further, elevated testosterone was correlated with the smallest vocabulary at a given age, while a low level was correlated with the greatest vocabulary knowledge.

It is also noted that this hormone has a stimulating effect upon the development of the right side of the brain and it is speculated that this may be associated with a corresponding inhibition of development of the left side which is responsible for the majority of language and social skills.

The research team acknowledge that testosterone is unlikely to be identified as the cause of autism, but it may play a part in a complex interaction with other factors

(with the implication that autism is a condition with a number of causal routes).

Meanwhile, evidence has been found for the possibility that a regressive type of autism may have an autoimmune basis either directly or indirectly from some autoimmune intestinal disorder.

Torrente et al [and summarised by Barclay] (2002) report findings of a novel form of enteropathy in children with autism characterised by an anomalous pattern of intestinal cell development. The children in question had been observed to make apparently normal early development, but to have shown a marked regression in the second year, with a possible link with immunologic abnormalities and unpredicted bowel pathology.

However, the authors acknowledge that these findings may be of limited relevance for children with autism generally, but they do note how some children with regressive autism respond to enteric therapy.

Reference is made to the possibility of a genetic condition affecting several systems, with autoimmune mechanisms a further avenue for ongoing research, (increasing the validity, one might think, of the multi-causal and non-unitary view of autism).

Finally, while an increased rate of minor birth and pregnancy complications appears to accompany familial factors associated with autism, it is held that such complications are not a risk factor for autism generally (or sporadic cases without the familial factors).

Zwaigenbaum et al (2002) hold that pregnancy and birth complications are not a direct cause of autism. They may play a role but should not be overestimated in the aetiology of autism ; instead it is suggested that the child at risk for autism may show developmental anomalies pre-natally which underlie the higher risk of complications.

* * * * * *

M.J.Connor June 2002

REFERENCES

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Brock J., Brown C., Boucher J., and Rippon G. 2002 The temporal binding deficit of autism. Development and Psychopathology 14 209-224

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Frith U. 1989 Autism : Explaining the Enigma. Oxford : Blackwell

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McKie R. and Gold K. 2002 Testosterone levels may cause autism. The Observer 19th. May : News, Page 7

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Osterling J., Dawson G., and Munson J. 2002 Early recognition of 1-year old infants with ASD versus mental retardation. Development and Psychopathology 14 239-251

Singer W. 1999 Binding by Neural Synchrony. Cambridge, Mass.: MIT Press

Taylor S. 1983 Adjustment to threatening events. American Psychologist 38 1161-1173

Zwaigenbaum L. et al 2002 Minor birth complications and the development of autism. Journal of the American Academy of Child and Adolescent Psychiatry 41 572-579

 

This article is reproduced by kind permission of the author.

© Mike Connor 2002.

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