Health and Autism Needs, Rights, Responsibilities and Widening Perspectives



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Health and Autism

Needs, Rights, Responsibilities and Widening Perspectives

24th November 2005
Conference Report

CONTENTS
Introduction Page 3
Programme Page 4
Minister’s Speech Page 5
Presentations Page 8

Workshops Page 12

INTRODUCTION
The National Conference on Health and Autism held in Aviemore on 24th November 2005 aimed to widen the dialogue about health needs in autism in Scotland and to focus on contributing to a broader perspective on how we deliver interventions. In total 190 delegates attended the event including 25 parents and carers of people with ASD.
The Public Health Institute of Scotland (PHIS) report on the needs of those with autism spectrum disorders, commissioned by Scottish Ministers, highlighted the need to disseminate research findings to health and social care professionals so that they could consider and apply these in their own localities where they thought it appropriate to do so. The Scottish Executive hosted this conference as part of the implementation of this recommendation.
In the Deputy Minister for Health and Community Care’s welcome speech, he highlighted the responsibility we all have to address the individual needs and rights of people with autism spectrum disorders in relation to health, education and social care. This conference focussed on health and provided an opportunity for health and social care professionals, parents and carers and people with autism spectrum disorders (ASD) to hear the most up to date perspectives on autism health needs and look at where research needs to focus in the future.
The Executive’s ASD Reference Group formed a small planning group of experts who selected an appropriate programme for the day. Experts in the field of ASD were invited to present current research addressing the health needs of people with ASD. The programme included psycho-social interventions and the development of cognitive behaviour therapy; dietary interventions; pharmacological treatments; genetic counselling; improved assessment and diagnosis and the individualised treatment of medical disorders often associated with autism. The prominent immunologist who was invited to speak had to withdraw at short notice. To address this gap, sources of information on immunology have been included in this report in Annex A. Presentations from Tom Jennings, Moira Dickinson and Jane Hook provided delegates with the important perspective of what it means for people and their families to live with ASD.
The conference placed a strong emphasis on the importance of primary health care professionals in effectively treating the wide range of health needs of people with ASD and identifying and treating the comorbid conditions often associated with ASD. The conference report will be disseminated widely to reach health professionals who were unable to attend the conference.


PROGRAMME
9:30 Chairman’s Introduction and Welcome

Ms Jean MacLellan, Scottish Executive Health Department


9:35 Overview of Policy

Mr Lewis Macdonald, Deputy Minister for Health and Community Care.


9:45 Asperger’s Syndrome – Unrecognised, Understood & Beyond

Tom Jennings


10:00 Carer’s views on meeting health needs

Jane Hook MBE & Moira Dickinson


11:00 Biomedical perspectives on autism spectrum disorder: current knowledge and new perspectives

Professor Chris Gillberg MD, PhD


12:00 Future Research Agenda – what is needed?

Dr Justin Williams



12:30 Lunch
13:30 PARALLEL SESSION A

1. Immunology (workshop withdrawn)

2. Dietary issues

Dave Rex, Child Health Lead Dietician, NHS Highland and Gordon Bell, University of Stirling


3. Mental Health: Imaging the developmental neurobiology of ASD

Dr Stephen Lawrie, University of Edinburgh



The contribution of Neuropyschology to our understanding

and management of ASD

Mr Robert Walley, Consultant Clinical Psychologist, NHS Lothian


4. Psycho-social interventions

Dr Ken Aitken, Clinical Psychologist, GGPHCT (Session A)

Dr Tommy MacKay, Consultant Psychologist and Dr Anne Greig, Psychologist, Argyll and Bute Council (Session B)

5. Genetics and ASD

Dr Birgitta Bernhard, SpR in Clinical Genetics, Western General Hospital

Professor Anthony Monaco, Director and Head of Neuro-genetics Group, The Wellcome Trust Centre for Human Genetics.
6. Medication Issues

Dr Anne Gilchrist, Consultant in Adolescent Psychiatry, NHS Grampian Trust



Craig Melville, Senior Lecturer, University of Glasgow
15:00 PARALLEL SESSION B - Repeated as per Session A

SPEECH BY DEPUTY MINISTER FOR HEALTH AND COMMUNITY CARE, LEWIS MACDONALD
Health and Autism – Needs, Rights, Responsibilities And Widening Perspectives Conference
Although I unfortunately cannot be with you today I would like to welcome all of you to this important conference. As the programme states, it aims to give us all the opportunity to think about needs, rights, and responsibilities.
And whilst we all have responsibilities in making sure we do better for people with autism spectrum disorder, it is primarily their individual needs and rights that we want to address.
So what are the needs of people with ASD? To help us identify what we needed to do nationally, the Executive commissioned the Public Health Institute of Scotland to conduct an ASD Needs Assessment some 4 years ago.
That report identified a lack of services and supports for people with ASD in Scotland. It set out a clear need for people to have quicker access to diagnosis and assessment and to have better information about ASD. Most importantly, people with ASD need an appropriate response from health, education and social care services. Today our focus is on health.
Our work to date has included a number of training initiatives that will ensure primary care and social care staff have a better understanding of autism spectrum disorders.
We have also issued a quality standard for diagnostic services that identify what individuals and families can expect from services. A number of diagnosis training pilots are also underway with a view to broadening the range of professionals who can offer this service. The outcome should be to provide quicker access to diagnosis and to more specialist services when these are needed.
I said that people diagnosed with ASD need a response from services. In the past, particularly for adults, there has been little to meet their needs. The Autism Resource Centre in Glasgow and Number 6 in Edinburgh are both projects that are demonstrating how partnerships can deliver services that give adults with ASD – and their family carers – a better quality of life.
For all of us, our quality of life is dictated by how healthy we are. People with ASD are no different. They too are people who need to visit GPs dentists and general health services for the same things as everyone else. However, it is recognised that some are also more vulnerable to other illnesses.
Having a diagnosis of ASD does not mean that problems with physical or mental health are necessarily part of the condition. These problems need to be addressed and treated where appropriate.
However, I am sure you will get a much clearer message from Tom Jennings, Jane Hook and Moira Dickinson about what having an autism spectrum disorder means to people and their families. They know best what their needs are, and can tell us how we can better meet those needs.

I am well aware that the majority of support for children and adults with ASD comes from family carers. They too have needs and rights that include their own health and well-being. The Needs Assessment described the impact on family members of caring for a child or adult with autism.


Part of the stress experienced by families is caused by a lack of services, support and information.
On the information front, the Executive is funding 2 projects that will provide families with a range of essential information about autism, and direct them to where they can get support. Getting this information at the point of diagnosis will hopefully alleviate some of the stress caused by fear and uncertainty.
The Needs Assessment identified the uncertainties about what interventions work for children and adults. I expect most of you here today will be aware of the draft guideline that is being developed by the SIGN Council.
Looking at assessment, diagnosis and clinical interventions for children and young people with autism spectrum disorders, the SIGN Council and development group are conducting a systematic review of evidence.
The SIGN process necessarily uses strict criteria to categorise levels of research evidence to inform recommendations for clinical practice. These rules apply to all guidelines. There are clearly gaps in research into effective interventions for people with autism. The SIGN Guideline and other work will help identify what research is needed.
I know parents will be confused by information about treatments that are not available in Scotland. I am also well aware that some believe we have a closed mind to practice in other parts of the world.
I cannot advocate interventions where there may still be concerns about potential adverse effects. What I can do is to encourage professionals to have an open mind to developing interventions.
And we in the Scottish Executive can help to ensure that information about developments is as widely available as possible. That is what today is about.
I know some people disagree with our approach to autism. Why are we in the Executive following the recommendations of the Needs Assessment? Why are we working to improve life-long services? Some families will be asking why we are not tackling the cause rather than the effect of autism.
Again, I have to take forward policy that is based on the best available scientific evidence. On that basis we have to do more to provide services and support for people with ASD and their families throughout their lives. That is what many families are asking us for.
I am very grateful to members of our national reference group and related sub groups who have given enormous energy and commitment to our common goal of giving people with ASD a better quality of life.
Our future work will move on from diagnosis and training to making sure policy turns into practice. We want to support families to build their capacity to support their sons and daughters. We want to make sure general and specialist services are able to recognise and meet the needs of people with ASD.
And we want to do this with an open mind. Today we want people to have clearer information about successful and developing interventions that improve the health and wellbeing of children and adults with autism spectrum disorders.
I would also like to acknowledge the contribution of the Cross Party Group on Autism in identifying key issues for today’s programme.
I am delighted that so many people with a wealth of knowledge have come here today to share that with you. I am sure many of our delegates will go away with new perspectives on diet and psycho-social interventions, on mental health, genetics and medication.
Professor Gillberg and Dr Williams will no doubt provide everyone with the most up to date perspective on autism and a clear steer about where our research needs to focus in future.
Thank you all for your contribution and for your participation. I hope we can continue to work together to bring about the changes that individuals and families need.
PRESENTATIONS

Asperger’s Syndrome – Unrecognised, Understood and Beyond

Tom Jennings
Tom Jennings was diagnosed with Asperger’s Syndrome in 2003 at the age of 33. Since then he has been regaining lost abilities after struggling with life for many years. An understanding of Asperger’s has unlocked many of his problems and life is making sense, with great relief.
Tom gave an overview of some of the difficulties he has faced. He shared his feelings and experiences, prior to diagnosis and following diagnosis and recognition of his condition. He explained the feelings of fear, pain, confusion and despair he experienced growing up with Asperger’s and not understanding why he felt the way he did.
The diagnosis he received in 2003 was a big relief. He felt he had been ill for 30 years and was shocked and dumbfounded. He was able to start dealing with the implications of his diagnosis and accessing the help that he needed. Tom is now keen to tell people in education the importance of having understanding and respect for those on the autism spectrum.

Carer’s Views on Meeting Health Needs
Jane Hook MBE
Jane is the mother of Rachel, now 19, who has autism. After a traumatic experience in fighting for diagnosis and support, she felt compelled to fight and help other families gain diagnosis and assessment, appropriate education and family support.
Jane addressed the difficulties experienced by children and adults with ASD in accessing mainstream health services. She described the problems she faces when taking her daughter to the dentist to illustrate the need for professionals to be trained adequately to treat people with ASD.
Jane highlighted the importance of professionals in primary care providing effective and appropriate care to the range of health needs of people with autism spectrum disorders.
Moira Dickinson
Moira has two daughters, Sarah age 20 who was diagnosed at 3 1/2 with high functioning autism and Joanna aged 14. Moira explained that having to fight for Sarah to get her needs met has had an impact on all the family. They really saw progress in addressing Sarah’s needs when she started a unit specifically for high function autism/ Aspergers at a High School.
Moira talked about a Communication Passport Sarah carries, which outlines her skills and also describes some of the communication problems people may experience in dealing with Sarah.
Moira described her daughter Sarah’s experience at a further education college, where she was supported with a class teacher and speech therapist before starting a 2 year course, but she had been unable to complete the second year due to too much change and unsupported activities. Moira’s talk focussed on the need for support in colleges and special courses aimed at people with ASD. She also highlighted the need for support for siblings of people with ASD.
Moira explained that there is help out there to support people with autism and their families but many are still unable to access it. We now need to focus on making support accessible.

Bio-medical perspectives on autism spectrum disorder: current knowledge and new perspectives

Christopher Gillberg MD PhD

Professor of Child and Adolescent Psychiatry.
Professor Gillberg is one of the leading international researchers on autism spectrum disorders and other neuropsychiatric disorders with early childhood onset. Professor Gillberg is also a clinician with more than 30 years of experience in psychiatry and child neurology.
Key Messages
Autism is a behavioural syndrome comprising restricted two-way social interaction, restricted verbal and non-verbal communication and restricted imagination/behavioural repertoire. It comes in several different clinical variants including autistic disorder and Asperger’s syndrome, and with or without major comorbidities (mental retardation, epilepsy, chromosomal, and other medical disorders). Reference is now often made to autism spectrum disorders, a term covering both the classic Kanner syndrome of autism and the variants described by Asperger and Heller plus a number of other autistic-like conditions. A number of behavioural problems commonly occur in autism. These include attention deficits, hyperactivity, obsessions and compulsions, depression, anxiety, tics and violent behaviours.
Autism is one of the most strongly genetic conditions in child neurology/psychiatry. However, it can also be primarily associated with major brain damage caused by a number of well-established medical conditions, such as PKU, rubella embryopathy, herpes encephalitis, tuberous sclerosis and a number of chromosomal disorders, including the fragile X syndrome.
Autism spectrum disorders occur in more that 0.5% of the general population of children, whereas the classic condition that Kanner described is probably at a rate of 0.1-0.2%. There is no good evidence that the prevalence of autism has actually increased, but the diagnostic boundaries have been broadened and awareness has increased dramatically over the past twenty years, leading to more cases being detected and correctly diagnosed.
Educational and behavioural interventions can lead to lasting improvements. Medical therapies can sometimes be helpful. Genetic and clinical research as well as basic neurobiological studies will help throw considerably more light on the various syndromes in the autism spectrum during the next five to ten years. At the present stage of our knowledge, autism spectrum disorders usually lead to life-long disability to one degree or another even though variability in terms of outcome is very considerable.

Future Research Agenda – What is Needed?

Dr Justin Williams

Senior Lecturer and Hon. Consultant in Child Psychiatry, University of Aberdeen and Royal Aberdeen Children’s Hospital
Key Messages
We have now reached a stage where Autism is a well-defined condition, awareness is high and excellent diagnostic methods are available. Now we need to develop effective psychological and biological treatments. Even though autism is inherited many environmental factors may affect the outcome. For example the treatment of comorbid conditions which may have very severe consequences in themselves, therapeutic interventions or the social environment. Comorbidity is common and not an exception and all challenging behaviour should not be assumed to be simply arising from untreatable autism. Better assessment and treatment of comorbidity is required.
The issue of brain growth rates was considered. Brain images of people with autism show the grey matter in the brain is increased and white matter decreased. This would indicate there is poor long-range connectivity and greater local connectivity. Psychological processes dependent on long range activity include imitation and joint attention. Impairments in white and grey matter development affect these functions developing. Impaired connectivity between frontal and dorsal systems may lead to poor joint attentions, rigid inflexible behaviour and frontal immaturity.
A number of potential targets for research to improve therapies were outlined including: white and grey matter development; attentional regulation and the development of motor skills in autism; mechanisms of anxiety; and interventions that promote imitation and joint attention skills.

WORKSHOPS
Workshop 1. Immunology
This workshop was withdrawn as the speaker was unable to attend. A list of peer reviewed publications on immunology and autism can be found in Annex A.

Workshop 2. Dietary Issues
Diet and ASD – How Do They Affect Each Other?

Dave Rex, Child Health Lead Dietician, NHS Highland
Key Messages
Most children with ASD have diets that are particularly (self) restricted which can affect behaviour due to a variety of reasons which may include blood sugar fluctuations, lack of iron and zinc, and lack of vitamins. There may well be sub-groups within the ASD population with shared biochemical and physiological problems, who would be more likely to respond to a particular dietary intervention. Dieticians need to develop a supporting role, helping to navigate families safely through the considerable “trial and error” of diet therapy in ASD. Scientific evidence may be weak, but there is little conclusive evidence against these interventions either. The best known and least controversial interventions were covered by the workshop.
Gluten and Casein Free Diets There is insufficient evidence for this to become the standard treatment for all people with ASD. However, there is enough evidence to warrant a supervised trial in some cases. Casein free trials take 6 weeks, and gluten free trials take 6 months before conclusions can be drawn. If no benefits are seen, the substance should be re-introduced. Both diets can be difficult to follow, particularly for people with ASD as so many of them are already highly selective in their food choices. Appropriate dietary supervision helps to ensure that important nutrients are replaced with other food sources or supplements. There is evidence however that the nutrition status of children with ASD on GF / CF diets is no worse than those children with ASD who are not on the diet.
Fish oil supplements are widely used by families affected by ASD. Anecdotal accounts of positive impact are common place. There is also a published case study describing the positive impact of fish oil on a patient with ASD. However, there have been no placebo controlled studies using fish oil supplements for ASD. Some fairly well designed studies do suggest a positive effect in other neuro-developmental disorders and mood disorders. Because fish oil takes time to build up in the fatty tissue it is sensible to give any trial a while to take effect. If no improvements are seen after 3 months (the length of most research trials), it should be stopped. EPA in fish oil may be more important than DHA.
Table Summarising Diet Therapy in ASD


Intervention

Difficulty


Evidence of Efficacy

Negative impact on nutrition

Comments

Fish oil supplements

Low

Low

None

Moderate evidence for typically co-morbid conditions.

Gluten and casein free diet

High

Moderate

Possible

Consider impact on magnesium, calcium, protein and fibre intake

Removal of “excitotoxin” food additives

Low

Low

None

ASD specific evidence is lacking, but it is easy to do.

Moderate vitamin / mineral supplement

Low

Moderate

None

Useful for selective eaters. May help parents and carers relax at mealtimes.


Phenol / amine restriction

Moderate

Low

Possible

Fruit & veg have positive antioxidant role which may be particularly important in ASD



Essential Fatty Acid (Efa) Deficiency in Autism and Related Neurodevelopmental Disorders

Gordon Bell, Nutrition Group, Institute of Aquaculture, University of Stirling.
Key Messages
Fatty acid deficiency may cause autoimmune problems, GI/urinary problems, sleep problems, mood disorders, behavioural problems and perceptual and cognitive difficulties. There is evidence that EPA and GLA supplementation may help improve the general health, sleep pattern, cognitive skills, concentration and sociability of children with ASD However some parents have also reported improved cognitive skills but increased hyperactivity and behavioural problems following increased fish oil intake. This can sometimes be reversed by pre-loading with GLA or increasing GLA intake while maintaining the EPA dose.
More research is needed on diet therapy and ASD. Dr Bell has received funding from the Chief Scientist’s office for a 2 year study of “Blood fatty acid and phospholipase A2 as indicators of abnormal phospholipid metabolism in autism: The potential for intervention using fatty acid supplements”.

Workshop 3. Mental Health
Imaging the Developmental neurobiology of ASD

Dr Stephen Lawrie

Reader in Psychiatry, University of Edinburgh
Brain imaging in ASD can screen for structural brain lesions (sMRI) and diagnose epilepsy (EEG). With ongoing research and a refined understanding it also has the potential to aid in the identification of risk genes and their phenotypic expression. Imaging (and/or genetics) could also aid in early diagnosis, prognostic and treatment planning, and even in developing new treatments.
There are key problems in conducting reliable and valid brain imaging studies of ASD including the impossibility of finding an appropriate control group and capturing the developmental path. The key findings concerning brain structure (including from systematic reviews and meta-analyses) can be influenced by the choice of different control groups.
Structural and functional imaging studies in ASD have begun to identify consistent global and regional brain differences compared to healthy controls. These can be linked to early genetic effects and (social and motor) aspects of the typical features of ASD.

The Contribution of Neuropsychology to our Understanding and Clinical Management of Autistic Spectrum Disorders

Mr Robert Walley

Consultant Clinical Psychologist, Primary Care Division – NHS Lothian
Mr Walley was unable to present at the conference. The following is the synopsis he provided beforehand.
The presentation will include a brief introduction to the study of neuropsychology. It will then review the major psychological theories/models that have been helpful in our understanding of autistic spectrum disorders and discuss their general utility in relation to clinical management. The neuropsychological aspects of these theories will then be discussed with particular reference to the “ Theory of Mind “ and Executive Dysfunction models. The presentation will conclude by discussing how our improved understanding of the neuropsychology of autistic spectrum disorders may help in its management.
Workshop 4: Psycho-social Interventions

Ken Aitken

Clinical Psychologist, GGPHCT
Tommy MacKay & Dr Anne Greig

Consultant Psychologist, Psychology Consultancy Services and National Centre for Autism Studies, University of Strathclyde
A wide range of psycho-social interventions have been used with autism spectrum disorders. These include very diverse approaches such as applied behavioural analysis (ABA), Option and social interaction training.
This workshop provided an overview of this field and of the status of a variety of interventions in terms of their evidence base. The presenters talked about aspects of their own current work and interests in this area, including the developing field of cognitive behaviour therapy (CBT) and its application to autism.
Ken Aitken reported on the regional variations in reported prevalence of ASD in Scotland. He also outlined the features that he recommended should lead to early investigations for ASD including: no babbling by 12 months; no pointing or other gesturing by 12 months; no single words by 16 months; no 2-word spontaneous phrases (not echolalic) by 24 months; or any loss of any language or social skills at any age. He detailed the history of psychosocial interventions with ASD and focused on commonalities across clinical subgroups of ASD.
A number of limitations were discussed in giving general statements about treatment approaches which are effective with ASD. Firstly there is a wide span of cognitive and verbal abilities in those with ASD - it is important to ensure that the published literature in on use of the technique with a comparable population. Also there are difficulties in ensuring “treatment fidelity” - there are now a number of studies on the differences found between early intervention programmes, comparing parent and professionally led interventions.


Workshop 5: Genetics and ASD

Dr Birgitta Bernhard

Specialist Registrar Clinical Genetics

South East of Scotland Clinical Genetics Services, Western General Hospital
Identifiable syndromes and chromosome abnormalities account for a small percentage of ASDs. It should not be assumed that an apparent lack of dysmorphism prevents the need for molecular and cytogenetic testing. Shared symptoms may result from the disruption of gene or protein systems that may also be disrupted in the complex genetic syndrome of ASD. Genetic counselling remains challenging given the complexity of the phenotype and the underlying aetiology. The presentation reviewed current approaches and discussed the role of the clinical geneticist.

Professor Tony Monaco

Director and Head of Neuro-genetics Group

The Wellcome Trust Centre for Human Genetics
Rapid progress has been made in the molecular understanding of single gene disorders during the last 15 years. A new challenge in human genetics is to unravel the genetics of more complex, polygenic diseases, which are relatively frequent in the population. Using resources provided by the human genome project and advances in genotyping technology and statistical genetics, research groups at the Wellcome Trust Centre for Human genetics are searching for susceptibility genes underlying polygenic disorders.
Professor Monaco explained his laboratory have initiated genetic studies of complex neurodevelopmental disorders of childhood, including autism. As part of the International Molecular Genetic Study of Autism Consortium (IMGSAC), his team have completed a full genome scan for susceptibility genes in autism and found strong evidence for linkage to chromosomes 2q, 7q and 16p1-4. These chromosome regions implicated by family studies in autism have been replicated in independent families. The regions containing the susceptibility gene(s) are being further investigated by family based association studies. Candidate genes in the critical region are tested for etiologic mutations or variants that are potentially involved in susceptibility to autism. Recently, using a high density screen of single nucleotide polymorphisms on chromosome 7q and 2q, we have identified strong SNP associations with autism which now require replication in independent cohorts. Our goal is for a molecular understanding of the neurodevelopmental pathways involved in autism, which should enable better diagnosis and potential treatments.
Professor Monaco gave a summary of molecular genetics research into ASD - several groups have carried out genome screens for linkage to autistic spectrum disorder and there is encouraging convergent evidence for linkage in some regions. Many candidate screening and association studies have been carried out, but no etiological variants have been so far conclusively identified in the majority of families with autism. Several positive risk haplotypes have been identified on chromosome 7q and 2q that need to be replicated.

Workshop 6. Medication Issues

Dr Anne Gilchrist

Consultant in Adolescent Psychiatry, NHS Grampian Trust
Dr Craig Melville

Senior Lecturer, University of Glasgow
Estimates of the proportion of individuals with autism spectrum disorders receiving psychotropic medication vary from 20% to over 70%, depending on the sample of individuals studied. Use of medication has implications for individuals, their families, and for professionals in a wide range of agencies, including educational and social care as well as health services.
Medication may be prescribed for several reasons, including treatment of a diagnosed condition, such as depression; attempted treatment of the core features of autism spectrum disorders; or for the management of problem behaviours, such as aggression. This workshop explored the principles, evidence base and practical use of psychotropic medication when working with individuals of any age with autism spectrum disorders.
ANNEX A

BASIC PEER REVIEWED PUBLICATIONS ON IMMUNOLOGY AND AUTISM


Connolly AM, Chez M, Streif EM, Keeling RM, Golumbek PT, Kwon JM, Riviello JJ, Robinson RG, Neuman RJ & Deuel RM.

Brain-Derived Neurotrophic Factor and Auto antibodies to Neural Antigens in Sera of Children with Autistic Spectrum Disorders, Landau-Kleffner Syndrome, and Epilepsy.

Biol Psychiatry. 2005 Sep 19; [Epub ahead of print]

PMID: 16181614
Laurence JA & Fatemi SH.

Glial fibrillary acidic protein is elevated in superior frontal, parietal and cerebellar cortices of autistic subjects.

Cerebellum. 2005;4(3):206-10.

PMID: 16147953


Zimmerman AW, Jyonouchi H, Comi AM, Connors SL, Milstien S, Varsou A & Heyes MP.

Cerebrospinal fluid and serum markers of inflammation in autism.

Pediatr Neurol. 2005 Sep;33(3):195-201.

PMID: 16139734


Sperner-Unterweger B.

Immunological aetiology of major psychiatric disorders: evidence and therapeutic implications.

Drugs. 2005; 65(11):1493-520. Review.

PMID: 16033289


Levy SE & Hyman SL.

Novel treatments for autistic spectrum disorders.

Ment Retard Dev Disabil Res Rev. 2005; 11(2):131-42. Review.

PMID: 15977319


Bazar KA, Yun AJ, Lee PY, Daniel SM & Doux JD.

Obesity and ADHD may represent different manifestations of a common environmental over sampling syndrome: a model for revealing mechanistic overlap among cognitive, metabolic, and inflammatory disorders.

Med Hypotheses. 2005 May 16; [Epub ahead of print]

PMID: 15905045


Splawski I, Timothy KW, Decher N, Kumar P, Sachse FB, Beggs AH, Sanguinetti MC & Keating MT.

Severe arrhythmia disorder caused by cardiac L-type calcium channel mutations.

Proc Natl Acad Sci U S A. 2005 Jun 7;102(23):8089-96; discussion 8086-8. Epub 2005 Apr 29.

PMID: 15863612


Libbey JE, Sweeten TL, McMahon WM & Fujinami RS.

Autistic disorder and viral infections.

J Neurovirol. 2005 Feb; 11(1):1-10. Review.

PMID: 15804954


Jyonouchi H, Geng L, Ruby A & Zimmerman-Bier B.

Dysregulated innate immune responses in young children with autism spectrum disorders: their relationship to gastrointestinal symptoms and dietary intervention.

Neuropsychobiology. 2005; 51(2):77-85.

PMID: 15741748


Croen LA, Grether JK, Yoshida CK, Odouli R & Van de Water J.

Maternal autoimmune diseases, asthma and allergies, and childhood autism spectrum disorders: a case-control study.

Arch Pediatr Adolesc Med. 2005 Feb; 159(2):151-7.

PMID: 15699309


Ashwood P, Anthony A, Torrente F & Wakefield AJ.

Spontaneous mucosal lymphocyte cytokine profiles in children with autism and gastrointestinal symptoms: mucosal immune activation and reduced counter regulatory interleukin-10.

J Clin Immunol. 2004 Nov; 24(6):664-73.

PMID: 15622451


Kennedy RC, Byers VS & Marchalonis JJ.

Measles virus infection and vaccination: potential role in chronic illness and associated adverse events.

Crit Rev Immunol. 2004; 24(2):129-56. Review.

PMID: 15581394


Trajkovski V, Ajdinski L & Spiroski M.

Plasma concentration of immunoglobulin classes and subclasses in children with autism in the Republic of Macedonia: retrospective study.

Croat Med J. 2004 Dec;45(6):746-9.

PMID: 15578810


Ashwood P & Van de Water J.

Is autism an autoimmune disease?

Autoimmun Rev. 2004 Nov; 3(7-8):557-62. Review.

PMID: 15546805


Vargas DL, Nascimbene C, Krishnan C, Zimmerman AW & Pardo CA.

Neuroglial activation and neuroinflammation in the brain of patients with autism.

Ann Neurol. 2005 Jan;57(1):67-81. Erratum in: Ann Neurol. 2005 Feb;57(2):304.

PMID: 15546155


Vojdani A, O'Bryan T, Green JA, Mccandless J, Woeller KN, Vojdani E, Nourian AA & Cooper EL.

Immune response to dietary proteins, gliadin and cerebellar peptides in children with autism.

Nutr Neurosci. 2004 Jun; 7(3):151-61.

PMID: 15526989


Yun AJ, Bazar KA & Lee PY.

Pineal attrition, loss of cognitive plasticity, and onset of puberty during the teen years: is it a modern maladaptation exposed by evolutionary displacement?

Med Hypotheses. 2004; 63(6):939-50.

PMID: 15504560


Splawski I, Timothy KW, Sharpe LM, Decher N, Kumar P, Bloise R, Napolitano C, Schwartz PJ, Joseph RM, Condouris K, Tager-Flusberg H, Priori SG, Sanguinetti MC & Keating MT.

Ca (V) 1.2 calcium channel dysfunction causes a multisystem disorder including arrhythmia and autism.

Cell. 2004 Oct 1; 119(1):19-31.

PMID: 15454078


Ashwood P &Van de Water J.

A review of autism and the immune response.

Clin Dev Immunol. 2004 Jun; 11(2):165-74. Review. No abstract available.

PMID: 15330453


Silva SC, Correia C, Fesel C, Barreto M, Coutinho AM, Marques C, Miguel TS, Ataide A, Bento C, Borges L, Oliveira G & Vicente AM.

Autoantibody repertoires to brain tissue in autism nuclear families.

J Neuroimmunol. 2004 Jul; 152(1-2):176-82.

PMID: 15223250


Hornig M, Chian D & Lipkin WI.

Neurotoxic effects of postnatal thimerosal are mouse strain dependent.

Mol Psychiatry. 2004 Sep; 9(9):833-45.

PMID: 15184908


Vojdani A, Bazargan M, Vojdani E, Samadi J, Nourian AA, Eghbalieh N & Cooper EL.

Heat shock protein and gliadin peptide promote development of peptidase antibodies in children with autism and patients with autoimmune disease.

Clin Diagn Lab Immunol. 2004 May; 11(3):515-24.

PMID: 15138176


Sweeten TL, Posey DJ, Shankar S & McDougle CJ.

High nitric oxide production in autistic disorder: a possible role for interferon-gamma.

Biol Psychiatry. 2004 Feb 15; 55(4):434-7.

PMID: 14960298


Vojdani A, Pangborn JB, Vojdani E & Cooper EL.

Infections, toxic chemicals and dietary peptides binding to lymphocyte receptors and tissue enzymes are major instigators of autoimmunity in autism.

Int J Immunopathol Pharmacol. 2003 Sep-Dec; 16(3):189-99.

PMID: 14611720


Sweeten TL, Bowyer SL, Posey DJ, Halberstadt GM & McDougle CJ.

Increased prevalence of familial autoimmunity in probands with pervasive developmental disorders.

Paediatrics. 2003 Nov; 112(5):e420.

PMID: 14595086


Kurup RK & Kurup PA.

A hypothalamic digoxin-mediated model for autism.

Int J Neurosci. 2003 Nov; 113(11):1537-59.

PMID: 14585753


Ferrante P, Saresella M, Guerini FR, Marzorati M, Musetti MC & Cazzullo AG.

Significant association of HLA A2-DR11 with CD4 naive decrease in autistic children.

Biomed Pharmacother. 2003 Oct;57(8):372-4.

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Lipkin WI & Hornig M.

Microbiology and immunology of autism spectrum disorders.

Novartis Found Symp. 2003; 251:129-43; discussion 144-8, 281-97.

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Torres AR.

Is fever suppression involved in the etiology of autism and neurodevelopmental disorders?

BMC Pediatr. 2003 Sep 2; 3:9. Epub 2003 Sep 2. Review.

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Oh HM, Oh JM, Choi SC, Kim SW, Han WC, Kim TH, Park DS & Jun CD.

An efficient method for the rapid establishment of Epstein-Barr virus immortalization of human B lymphocytes.

Cell Prolif. 2003 Aug; 36(4):191-7.

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Sweeten TL, Posey DJ & McDougle CJ.

High blood monocyte counts and neopterin levels in children with autistic disorder.

Am J Psychiatry. 2003 Sep; 160(9):1691-3.

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DeFelice ML, Ruchelli ED, Markowitz JE, Strogatz M, Reddy KP, Kadivar K, Mulberg AE & Brown KA.

Intestinal cytokines in children with pervasive developmental disorders.

Am J Gastroenterol. 2003 Aug; 98(8):1777-82.

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Padhye U.

Excess dietary iron is the root cause for increase in childhood autism and allergies.

Med Hypotheses. 2003 Aug; 61(2):220-2. Review.

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Singh VK & Jensen RL.

Elevated levels of measles antibodies in children with autism.

Pediatr Neurol. 2003 Apr; 28(4):292-4.

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Lee DA, Lopez-Alberola R & Bhattacharjee M.

Childhood autism: a circuit syndrome?

Neurologist. 2003 Mar; 9(2):99-109. Review.

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Mari M, Castiello U, Marks D, Marraffa C & Prior M.

The reach-to-grasp movement in children with autism spectrum disorder.

Philos Trans R Soc Lond B Biol Sci. 2003 Feb 28; 358(1430):393-403. Review.

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Zoroglu SS, Yurekli M, Meram I, Sogut S, Tutkun H, Yetkin O, Sivasli E, Savas HA, Yanik M, Herken H & Akyol O.

Pathophysiological role of nitric oxide and adrenomedullin in autism.

Cell Biochem Funct. 2003 Mar; 21(1):55-60.

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Shi L, Fatemi SH, Sidwell RW & Patterson PH.

Maternal influenza infection causes marked behavioural and pharmacological changes in the offspring.

J Neurosci. 2003 Jan 1; 23(1):297-302.

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Kidd PM.

Autism, an extreme challenge to integrative medicine. Part 2: medical management.

Altern Med Rev. 2002 Dec; 7(6):472-99. Review.

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Increased serum albumin, gamma globulin, immunoglobulin IgG, and IgG2 and IgG4 in autism.

Psychol Med. 2002 Nov; 32(8):1457-63.

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Jyonouchi H, Sun S & Itokazu N.

Innate immunity associated with inflammatory responses and cytokine production against common dietary proteins in patients with autism spectrum disorder.

Neuropsychobiology. 2002; 46(2):76-84.

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Wank R.

Schizophrenia and other mental disorders require long-term adoptive immunotherapy.

Med Hypotheses. 2002 Aug; 59(2):154-8.

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Krause I, He XS, Gershwin ME & Shoenfeld Y.

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J Autism Dev Disord. 2002 Aug; 32(4):337-45. Review.

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Kidd PM.

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Altern Med Rev. 2002 Aug; 7(4):292-316. Review.

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Vojdani A, Campbell AW, Anyanwu E, Kashanian A, Bock K & Vojdani E.

Antibodies to neuron-specific antigens in children with autism: possible cross-reaction with encephalitogenic proteins from milk, Chlamydia pneumoniae and Streptococcus group A.

J Neuroimmunol. 2002 Aug;129(1-2):168-77. Erratum in: J Neuroimmunol 2002 Sep;130(1-2):248.

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Wakefield AJ.

Enterocolitis, autism and measles virus.

Mol Psychiatry. 2002; 7 Suppl 2:S44-6. Review. No abstract available.

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Wakefield AJ, Puleston JM, Montgomery SM, Anthony A, O'Leary JJ & Murch SH.

Review article: the concept of entero-colonic encephalopathy, autism and opioid receptor ligands.

Aliment Pharmacol Ther. 2002 Apr; 16(4):663-74. Review.

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Korvatska E, Van de Water J, Anders TF & Gershwin ME.

Genetic and immunologic considerations in autism.

Neurobiol Dis. 2002 Mar; 9(2):107-25. Review. Erratum in: Neurobiol Dis 2002 Jun; 10(1):69.

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Maternal infection: window on neuroimmune interactions in foetal brain development and mental illness.

Curr Opin Neurobiol. 2002 Feb; 12(1):115-8.

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Combination vaccines: defining and addressing current safety concerns.

Clin Infect Dis. 2001 Dec 15; 33 Suppl 4:S312-8. Review.

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Ment Retard Dev Disabil Res Rev. 2001; 7(3):200-10. Review.

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No association between the 4g/5G polymorphism of the plasminogen activator inhibitor-1 gene promoter and autistic disorder.

Psychiatr Genet. 2001 Jun; 11(2):99-103.

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Front Biosci. 2001 Aug 1; 6:D936-43. Review.

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Application of genomeceuticals to the molecular and immunological aspects of autism.

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Bornavirus tropism and targeted pathogenesis: virus-host interactions in a neurodevelopmental model.

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Curr Top Microbiol Immunol. 2001; 253:157-77.

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Malek-Ahmadi P.

Cytokines and etiopathogenesis of pervasive developmental disorders.

Med Hypotheses. 2001 Mar; 56(3):321-4.

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Binstock T.

Intra-monocyte pathogens delineate autism subgroups.

Med Hypotheses. 2001 Apr; 56(4):523-31.

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Bernard S, Enayati A, Redwood L, Roger H & Binstock T.

Autism: a novel form of mercury poisoning.

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Eur Psychiatry. 2001 Feb; 16(1):3-10. Review.

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Adenosine deaminase alleles and autistic disorder: case-control and family-based association studies.

Am J Med Genet. 2000 Dec 4;96(6):784-90.

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Immunological treatments for autism.

J Autism Dev Disord. 2000 Oct; 30(5):475-9.

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Is autism a G-alpha protein defect reversible with natural vitamin A?

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The ratio of 2nd to 4th digit length: a new predictor of disease predisposition?

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An infection-based model of neurodevelopmental damage.

Proc Natl Acad Sci U S A. 1999 Oct 12; 96(21):12102-7.

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Peripheral lymphocyte subsets and other immune aspects in Rett syndrome.

Pediatr Neurol. 1999 Sep; 21(3):619-21.

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Familial clustering of autoimmune disorders and evaluation of medical risk factors in autism.

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Serum autoantibodies to brain in Landau-Kleffner variant, autism, and other neurologic disorders.

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Autism: xenobiotic influences.

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Ann Ist Super Sanita. 1996; 32(3):351-9.

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Psychiatr Enfant. 1995; 38(2):495-527. French.

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DR-positive T cells in autism: association with decreased plasma levels of the complement C4B protein.

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Evaluating the empirical support for the Geschwind-Behan-Galaburda model of cerebral lateralization.

Brain Cogn. 1994 Nov; 26(2):103-67.

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Human parvovirus B19 antibodies in infantile autism.

J Child Neurol. 1994 Jan; 9(1):104-5. No abstract available.

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[Psychoneuroimmunology]

Z Kinder Jugendpsychiatr. 1993 Jun; 21(2):71-2. German. No abstract available.

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Changes of soluble interleukin-2, interleukin-2 receptor, T8 antigen, and interleukin-1 in the serum of autistic children.

Clin Immunol Immunopathol. 1991 Dec; 61(3):448-55. Erratum in: Clin Immunol Immunopathol 1992 Jun; 63(3):292.

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Francesetti G, Gecele M & Meluzzi A.

[Psycho immunology. II. The neuroendocrine system and the immune system in autism and schizophrenia]

Minerva Psichiatr. 1991 Apr-Jun; 32(2):75-82. Review. Italian.

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Root-Bernstein RS & Westall FC.

Serotonin binding sites. II. Muramyl dipeptide binds to serotonin binding sites on myelin basic protein, LHRH, and MSH-ACTH 4-10.

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CD4+ helper T cell depression in autism.

Immunol Lett. 1990 Sep; 25(4):341-5.

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Immunol Invest. 1990 Jun; 19(3):245-51.

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Is autism associated with anomalous dominance?

J Autism Dev Disord. 1988 Dec; 18(4):539-51. Review.

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