This set of summaries begins with information by which further to counter the anxieties surrounding the alleged link between the MMR vaccination and autism.

Next, reference is made to a study of self-reported experiences of comprehensive school pupils but with direct comparison against two control groups, despite which the unique vulnerability of the ASD group is underlined.

A brief review is provided of the work on metabolism, and on brain structure and function, at the Autism Research Unit (Sunderland) and the Autism Research Foundation (Boston, USA) respectively ; and the final section relates to an exploration of imitation skills in autism.



M.J.Connor                                                                                                     July 2003 




Further Evidence against the MMR Hypothesis


In a recent publication (Geier and Geier [2003] writing in International Pediatrics  18   108-113) quoting data from the USA Vaccine Adverse Event Reporting System, reference was made to the apparently heightened rate of diagnosed autism among those children treated with the MMR vaccine (25 million injections, 37 diagnoses) compared to the rate associated with the use of the diptheria, tetanus, and pertussis vaccine (63 million injections, 8 diagnoses). This was taken as vindication for their stance by those campaigners opposed to the use of MMR and who associate MMR with the rising rate of diagnosed autism.


However, recent press releases (May 2003) from Professor A. Breckenridge of the Medicines and Healthcare Products Regulatory Agency have firmly rejected any such implication.  He argues that these crude data cannot be used to determine whether some adverse event or condition can be linked causally to vaccination. 

The data have been misused and the methodology of the study is inadequate for any meaningful conclusions ….. for example, the DTP vaccine is given at various times, starting at 2 months, and the one-off MMR is given at around 12-15 months.  One cannot make valid comparisons in the light of these age imbalances.


It was also pointed out that there is the further issue of bias in respect of the possibility that adverse events were reported because of the considerable publicity about an alleged association between MMR use and a subsequent diagnosis of autism.


Similar concerns have been expressed by the authors of a study completed at Cardiff University.  The authors (Lewis et al 2003) sampled the views of large samples of the public on three separate occasions during 2002, and monitored newspaper and radio coverage of the MMR issue between January and September of that year.


The authors express concern lest media stories about the alleged MMR-autism link left a majority of the public with the incorrect impression that experts in the field are evenly divided on this issue. 

The overwhelming majority of paediatricians, mental health staff, and researchers who have any involvement in this issue are entirely satisfied that the MMR vaccination is safe, but the tendency among reporters to give equal scope to both sides of the argument may have given rise to a belief that there was equal evidence for, and commitment to, each view.  There has, in fact, been no evidence to support the initial linking of the MMR vaccine with autism as set out in the paper by Wakefield (1998).


The authors also pondered whether claims that appear to go against the mainstream view should be subject to closer examination before they are published ; and a survey among their sample of members of the public largely supports such a suggestion.


It is recognised that such claims would be regarded as attractive for publication because of their very controversiality, but the authors still argue that caution is required in such an issue that is of legitimate public interest but which may lead to undesirable outcomes (such as lack of confidence in MMR) if the full picture is not conveyed.



Self Report Data (School Experience and Self Esteem)


The present writer (MJC  2000) interviewed a sample of comprehensive school pupils, diagnosed with Asperger Syndrome or ASD, to tap their experience of the school setting, and was able to highlight particular anxieties about social interaction and the problems associated with the long and unstructured lunch times.


A similar exercise was completed by Connor and Clarbour (2002) but this sampling of pupil views and experiences involved a direct comparison between participants diagnosed with ASD and those with other emotional or behavioural difficulties and a further control group with no identified special needs. 

The hypothesis was that the two special needs’ groups would be clearly differentiable from the control group, but would also differ from each other in terms of experiences or attitudes and in attributions for successes and failures.


According to the self esteem scores produced, the two experimental groups did appear significantly lower in self esteem compared to controls. The EBD group scored low in academic and familial areas, while the ASD group scored very poorly (compared to both other groups) in the area of social self esteem.


Many differences were identified in the self report findings concerned with school experiences.

The ASD group showed more signs of isolation from the rest of their age group than did either the EBD or control groups, reporting fewer close friends and social encounters, and a preference for some individual activity by which to occupy break times.  This group also differed from the other participants in expressing a preference for scientific and practical subjects, and a dislike of games or PE and any subject involving a high level of verbal interchange.

However, both the ASD and EBD groups were more likely than controls to want to change something about themselves, with further implications for a fragile self image.


Further analysis supported the view (as set out by Bless and Amrein 1992) that a simple focus upon scholastic work would not reveal the underlying difficulties and anxieties experienced by the students with ASD.  Inclusion may, in many or most cases, enhance scholastic opportunities, but the social and emotional difficulties may be considerable but unrecognised … with implications for ensuring both staff and peer awareness of the nature of autistic spectrum disadvantages and idiosyncracies, and for a whole school approach to ensure consistency of expectations and routines.


The issue of the long lunch time was raised in that the majority of EBD students and control students used this time to interact with a wide range of peers, but only 1 student (of 28) in the ASD group reported the same opportunity, with the others describing their wandering around on their own or spending the time working on one of the school computers.


From the interviews, there was either direct or implicit support for the probability, as set out by Jordan (1998), that the deficiency in Theory of Mind will underlie ongoing social problems. 

The example was given of a lack of awareness about the ideal or comfortable space between self and others, and of either experiencing or causing stress by invading the private space of fellow students.  It was suggested that the ASD students will be happier in those classrooms where there is a very clear structure and a “formal” atmosphere rather than one in which movement around the class or shared working are permitted or encouraged …. unless the students with ASD are more carefully prepared or supported in such settings.

This further highlighted the problems that the ASD group would experience if there were different standards among staff concerning the kind of behaviour or level of noise tolerated in a given class such that the concept of whole school approaches is underlined as a means of ensuring that these students do recognise what is expected in any lesson.


The final points concerned the variation in abilities, scholastic and social, among all students including the ASD sample, with implications for recognising individual strengths and weaknesses when planning school placement and arrangements within any school ….. there is a need to avoid the “ one size fits all” view of inclusion.


There was also reference to the general downward slide in self esteem among all students between what is observed early in Year 7 and what is observed in Year 8 and perhaps beyond.

It may be the case for many students that self esteem recovers as they become attuned to the new routines and gradually gain more senior status with the passage of time, but the ASD students may less readily regain positive self esteem unless the transition to the comprehensive school is planned and managed with care and with much opportunity for induction sessions and ensuring that the students are aware in advance of even the most basic arrangements and routines that they will be encountering.


In other words, the vulnerability of students with ASD in the mainstream comprehensive is not simply a matter of the presence of special needs of an emotional or behavioural type, but reflects a particular vulnerability differentiable from the EBD difficulties experienced by other students who are not diagnosed with ASD. 


(On a related issue, it would be of relevance to quote the comment of a parent of a boy of secondary school age with an autistic spectrum disorder in response to hearing about the present writer’s difficulty in identifying a viably large sample of ASD students despite all the evidence for significant numbers of such individuals. 

This parent held that his son could be described as a boy with quite severe difficulties, and these are well recognised among those who have a need to know, but who does not have a “formal” diagnosis of autism within his records.

It is reported that the family have not sought a formal diagnosis because of the fear lest it would have an extremely negative impact upon him.  The boy recognises his “oddness” and “difference” and knows about Asperger Syndrome, but a diagnosis would be something too tangible to be able to dismiss and would depress him still further than is the current case.

Here is, therefore, a further and possibly common complication in respect of clarifying data on the [known] prevalence of ASD). 



The Metabolic Hypothesis of Autism


This next section is acknowledged not to be very recent, but does provide a brief overview of the kind of work being pursued at the Autism Research Unit at the University of Sunderland.


In their review, Whiteley et al (1998) describe the ongoing liaison with, and data gathering, from a sample of nearly 400 parents and carers of children with autism or pervasive developmental disorders in their testing of the metabolic theory. Such a theory is held  potentially to be able to account for differences in levels of functioning, and to accommodate research data from a range of disciplines thus integrating external and intrinsic factors.


In their presentation of outcomes so far, the authors describe how various factors apparently associated with autism and pervasive disorders can be clustered in 4 categories.

Firstly, with regard to peri- and early post-natal conditions, a significant percentage (27+%) of parents indicated the presence of at least 1 adverse factor.  The most frequently cited factors were ….. the tangling of the umbilical cord around the infant’s neck, signs of foetal distress, or anoxia and the child becoming blue.

A small percentage (2+%) were born at least 3 weeeks pre-term, and similar small percentages were said to have had an aided delivery involving a forceps or suction delivery, or to have had a caesarean birth.


Secondly, gastrointestinal problems are held to affect individuals relatively commonly, so that, for example, 5 children had diagnoses of gastroenteritis at some point, 3 had experienced stenosis (a narrowing of the passage from stomach to small intestine), and a small percentage of the sample of children had experienced other problems such as dysfunctional gut syndrome, colitis, etc..


Thirdly, there appears to have been something of a cluster of viral infections among this target sample with a diagnosis of chicken pox as the most common (n=16). 8 of the children were said to have contracted chicken pox before symptom onset and ASD diagnosis.  19 other individuals were reported to have experienced “mystery” viral infections which were not identified but 11 cases preceded the onset of symptoms. A further small number of children experienced other viral conditions such as 4 with viral meningitis, 4 with measles, 3 with pertussis, 2 with pneumonia, 2 with rubella, 2 with herpes, and 1 with scarlet fever.


Fourthly, 4 children were identified with chromosomal anomalies such as deletion ; and other cases included on of Batten’s Disease, 2 with anaemia, and 1 with malformation of head and skeletal system.


The authors discuss these findings in terms of supporting existing research evidence pointing towards the increased incidence of adverse prenatal conditions among children later identified with ASD, and of the comorbidity and possible significance of a range of viral or bacterial or genetic conditions.

It is acknowledged that present evidence still cannot offer direct support for the relationship between certain adverse factors or disease states and the autistic condition, although the data were held to be consistent with the view of autism as a metabolic disorder.


The authors go on to mention the possible significance of gastrointestinal disorders in increasing intestinal permeability, and the relative frequency with which conditions such as coeliac disease or Crohn’s disease are found in the families of children with autism was taken as a possible pointer towards some genetic predisposition towards a combination of gastrointestinal disease and autism.

However, they recognise that caution must be used in interpreting these findings, especially as they were taken from parent-completed survey data rather than from full medical histories, but they still argue that the number and range of factors arising form this kind of study would give the metabolic theory a basis.


(The present writer – MJC – acknowledges his inexperience and lack of knowledge of this specialist and medically-oriented field, but would still speculate whether the numbers are too small to allow for aetiological claims, and whether there is the risk of confounding correlation or comorbidity with causation. 

Further, there are no control and comparison data, and it would be interesting to know what is the likely incidence of the kinds of conditions or adverse factors observed among a number of similar-sized samples of children who show normal development [or, at least, who are not later diagnosed with ASD or pervasive developmental disorder].

However, it might be legitimate further to ponder whether autism can be viewed as some unitary condition or whether children diagnosed with this condition represent a range of aetiological routes and a range of types and levels of symptoms, as implicit within the concept of an autistic spectrum.)






Nervous System Research       


The comments above on the part of the present writer could equally apply to this brief introduction to the work of the Autism Research Foundation, a consortium of researchers from a number of American hospitals and universities.


The description of the ongoing research emphasises the lack of evidence for, and the discrediting of, the old hypothesis linking autism to a failure on the part of parents to respond to the child’s attention-seeking or affiliation-seeking behaviours.  It is argued, instead, that the exact cause (or causes) of autism cannot yet be identified and methods of intervention and treatment may still be seen a varied and experimental with inconsistent outcomes. 

However, the authors argue that, with gradual clinical advances, it has become evident that autism is a disorder of the developing nervous system and is likely to be of prenatal onset.


Members of the research team have focused upon systematic studies of the structure and functioning of the brains of individuals with autism, and have identified two major features.

Firstly, reference is made to the interference with the normal development and functioning of the limbic system which is significant for the regulation of cognitive and learning processes.  Secondly, the cerebellum and related areas have been shown to be affected in that the component nerve cells in the case of children with autism are unusually small or even deficient in number when such cells in normally developing individuals are quite large.


The implication is for some active and pathological process occurring in the early stages of development, although the precise significance of these changes in the cerebellum and related areas is not clear ; hence the plan to extend the studies into systematic and quantitative analysis of the cerebellar, cortical, limbic, and brainstem regions and to correlate the data which emerge with data from magnetic resonance imaging which will provide a picture of brain activation. 

The combined pictures of microscopic anomalies can then be matched to detailed behavioural and symptom profiles of the individuals concerned in order further to explore the details of the specific brain regions most affected in autism. 

One particular hypothesis to explore is that of malfunctioning neurotransmitter systems in the brain stem and limbic system.



Imitation in Young Children with Autism


The research of Rogers et al (2003) begins with the observation that imitation of the actions of other people is an emergent skill in newborns and it elaborates rapidly and considerably over the first two years.  One view of imitation is of a “ fixed action pattern ” rather than as intentional behaviour, but a stronger and more current view is of imitation as effortful and voluntary.


Imitation appears to serve several functions including the establishment of an initial sense of connectedness with others and a form of communication.  A later function, beginning at around 6 months of age, is that of providing the child with some information about other people’s actions or intentions and is a precursor to an expansion of social learning and interaction. 

Findings from magnetic resonance imaging suggest that at least two brain regions are involved in the imitation processes …. Broca’s area in the left frontal cortex (with a possible role in establishing meaning), and an area in the right parietal cortex (with a possible role in coding kinaesthetic aspects).


However, difficulty with imitation of other people’s movements appears to be particularly relevant in autism.

The lack of social and emotional reciprocity (or mirroring) in autism is described as particularly striking and, in fact, appears to be unique to autism.


It is further suggested by Rogers and Pennington (1991) that an imitation deficit may be fundamental to the general social deficits involved in autism ; and ongoing questions concern whether problems with timing and coordination of imitated movements may disrupt the dyadic experiences ; or whether there is a lack of adequate feedback and “self-messages” for the person who is being mirrored (or, actually, not being mirrored adequately) by the other and autistic individual.


One hypothesis concerning the imitation deficit involves dyspraxia and an inability to plan and execute new or complex movements in the absence of other motor symptoms.  Alternatively, the deficit has been considered to be a possible matter of impairments in shared attention. 

Further, there is ongoing debate whether imitation is a unitary skill or whether there is a disassociation between imitating actions on objects and imitating body or facial actions, and evidence exists (Stone et al 1999) that imitations of some functional action upon objects are less impaired in autism than imitation of body actions without objects. Imitation of oral-facial movements is most severely limited.

This may reflect the differentiability of the two types of imitation, with the imitation of functional behaviours a matter of instrumental learning while facial imitation is much more associated with interpersonal skills and communication.


The present study by Rogers et al (op.cit) set out to explore the hypotheses that imitation deficits are more pervasive among children with autism that control or clinical control children (ie  children with disorders such as Down Syndrome, fragile X, or general developmental delay of mixed aetiology) ; and that the greatest deficits are found with oral-facial imitation and imitation of actions upon objects are least impaired.

There was also the question whether a relationship exists between the levels of motor function or social responsiveness and imitation capacity.


The participants involved groups of children with autism, Down Syndrome, developmental delay, and typically developing children.   All the children in the clinical groups were between the ages of 21 and 50 months ; and the control group comprised children between 18 and 24 months. The groups were matched for non-verbal IQ and fine motor skills, but the control children were not only younger but had higher verbal IQs.


The results replicated the reported earlier findings and supported the view of robust differences in the imitation performance of very young children with autism  compared to other children …. including those with other disabilities.

The autistic group were indeed particularly poor in respect of oral-facial actions , but, while performance on manual actions was poorer than that of controls, it was not significantly so.


Further analysis of the children’s measured abilities and developmental rates suggested two possible scenarios …. firstly, that the imitation deficit  impacts negatively on the child’s capacity to develop skills possibly as a result of problems in learning from natural opportunities ; or, secondly, that a deficit in imitation is associated with poorer cognitive functioning in general …. but further studies will be needed to explore these issues.


For the autistic group, an important finding was that imitation abilities were strongly associated with joint attention abilities and with the severity of autistic symptoms. In other words, the imitation weaknesses appear to be a core part of the primary symptom set associated with early autism.


There was no support for the hypothesis linking some general motor planning or action deficit with the imitation weaknesses since the autistic sample performed as well as other participants on standardised measures of fine and gross motor skills.

In other words, some mechanism other than a generalised dyspraxia underlies the problems with motor imitation in autism …. although it is just possible that some specific oral-motor impairment could have a disruptive impact on imitation generally.

Social responsiveness correlated significantly with imitation performance albeit not accounting for further variance in observed performance in the lab setting.

It was speculated that the scaffolding afforded for imitation provided by the experimental procedures may have led to some overestimation of imitation performance among the autistic children and that, in a day to day setting, children with autism can be differentiated all the more sharply from other children in terms of imitation.


This led to the speculation that the difference between performances in the two settings may be a matter of the lack of social rewards or lack of social attention evoked towards others, and a lack of attention shifting, in the natural setting.


The authors concluded that difficulties with imitation appear to be a fundamental part  of autism, with implications for the importance of pursuing research about means of enhancing imitation skills and the impact upon other aspects of functioning.   A greater understanding here may well lead to a greater understanding of the “ social core ” of autism.


                                  *          *          *          *          *          *          *


M.J.Connor                                                                                                     July 2003





Bless G. and Amrein C.  1992   The integration of pupils with learning difficulties.  European Journal of Special Needs Education  7  11-19


Connor M.  2000   Asperger syndrome and the self-reports of comprehensive school students.   Educational Psychology in Practice  16(3)  285-296


Connor T. and Clarbour J.  2002   A comparison of self esteem scores and attributions for success and failure among secondary school students with autistic spectrum disorder, peers with other emotional and behavioural difficulties, and normally functioning controls.  Unpublished thesis completed as part of the requirements for the B.Sc Psychology degree, University of York


Jordan R.  1998   Autistic Spectrum Disorders.   London : Fulton Publishers


Lewis J. et al  2003   Media coverage misled Britons on the MMR-autism link.  Study published by the Economic and Social Research Council ….. summarised in Medscape News (Reuters Health Information)


Rogers S., Hepburn S., Stackhouse T., and Wehner E.  2003   Imitation performance in toddlers with autism and those with other developmental disorders.   Journal of Child Psychology and Psychiatry  44(5)  763-781


Rogers S. and Pennington B.  1991   A theoretical approach to the deficits in infantile autism.   Development and Psychopathology  3  137-162


Stone W.,  Lee E., Ashford L., et al  1999   Can autism be diagnosed accurately in children under three years ?   Journal of Child Psychology and Psychiatry  40  219-226


Whiteley P., Rodgers J., and Shattock P.  1998   A review of records at the Autism Research Unit : birth, gastrointestinal, and viral factors supporting a metabolic hypothesis of autistic spectrum disorders.   Paper presented  at the Durham Conference (NAS)

This article is reproduced by kind permission of the author.

© Mike Connor 2003.

Back to NAS Surrey Branch Welcome Page