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Alan Challoner MA (Phil) MChS
Researchers no longer consider autism to be a rare disorder. At one time, only two to four
children per 10,000 were considered autistic, but with milder cases factored in, one in 500
children is now considered to be autistic to some degree. However it is not infrequent that
the subtle signs of the milder cases are being missed by physicians and other early
childhood workers, according to the report published in the December 2002 issue of the
Journal of Autism and Developmental Disorders.
Autism also brings about abnormalities in the brain (other than those, which cause it) by
interfering with normal development, both cognitive and emotional.
We should also be very careful about the ways in which we treat children with autism.
Behavioural characteristics often are part of their coping strategy. Their brain has adapted
to the damage it has received, and their behaviour reflects the reparation and tolerance
of what has happened to them. It is wrong that their behaviour should be stylised as
pathological and treated with psychotropic drugs.
Aetiology of autism spectrum disorders
Professor Peter Szatmari in his Editorial1, misses important aetiology of autism spectrum
disorders. Although he includes a brief note on environmental risk factors, he omits toxic
considerations. He goes on to write that the MMR vaccine is not an environmental risk
factor, but omits any reference to the DPT (whole cell) vaccine. It is now accepted that
constituents of the whole cell DPT vaccine can pass the blood/brain barrier. If they do so,
they then can cause sporadic damage to the brain. Abnormal brain structure has been
put forward by researchers looking for a cause for autism. These have involved the
amygdala, the hippocampus, the cerebellum and the caudate nucleus.
Eric Courchesne et al have shown that neo-cerebellar damage impairs the ability to rapidly
and accurately change attentional maps during shifts of attention between auditory and
visual information as well as between perceptual domains within the visual modality.
During recent studies they have attempted to reveal the underlying causes of autism using
a variety of techniques. Particular emphasis was placed on techniques that have been
used by a number of different laboratories, including structural magnetic resonance
imaging and post-mortem studies of neuro-anatomy. Neuro-biological and
neuropsychological data from individuals across a wide age range were examined from a
neuro-developmental perspective. From these recent advances they have developed a
growth dysregulation hypothesis of autism. 2
Szatmari, P. The causes of autism spectrum disorders. Editorial, BMJ 2003;326:173-174
Akshoomoff N, Pierce K, Courchesne E. The neurobiological basis of autism from a developmental
perspective. Dev Psychopathol 2002 Summer 14:613-34
C:\Users\Alan\Documents\WorkFiles\Research Work\TREATISE Papers\Abnormal Brain Structure &
. although it is unclear how Purkinje neuron loss could trigger excessive axonal or glial/myelin growth in cerebellar white matter. Autism spectrum disorders at 20 and 42 months of age: stability of clinical and ADI-R diagnosis. Davis. there was a 250% increase in glial fibrillary acid protein–staining glia cells in the cerebellum and a 30% increase in numbers of neurons in CA1 of the hippocampus.. Koff A. Loss of the p27 gene may lead to additional glial and neuronal cell divisions before withdrawal from cell proliferation cycles. J Child Psychol Psychiatry 1999.. Tokyo. A postnatal period of extreme maldevelopment of these two major brain structures will almost certainly be manifest in aberrant behavioural expression. L. Lincoln. If neurons are stimulated by toxins. they release glutamate. 6 Page The coexistence of both cerebral and cerebellar maldevelopment may explain why the impairments in higher cognitive functions in autism are pervasive and persistent across the life span. show that there is an unusual developmental neuro-anatomic phenotype characterised by hyperplasia of cerebellar white matter.. Unusual brain growth patterns in early life in patients with autistic disorder An MRI study. Friedrich J. an involvement that may allow the brain to discard useless connections or reduce poorly functioning neurons. Ornitz EM..J... Gordon WP.New York: Elsevier Science. H. and cerebral white matter at the youngest ages with slowed growth thereafter. K. Schreibman. Pizzo. 6 During this developmental period. excessive proliferation of excitatory axonal projections might be speculated to lead to pathologic excitotoxicity and Purkinje death. Tikoo R. Z. expansion of dendritic and axon arbors.3 They hypothesised the genetic factors most likely underlie this growth abnormality. A. C. the human brain undergoes rapid synaptogenesis. This process may be involved in stroke..R... Ziccardi. lack of oxygen or are affected by genetic programmes. Charman T. R. Baron-Cohen S.. Tigue. Lord. et al.5:719–732.4 Another important aetiology is excitotoxicity.H.A.57:245–254. P. Chao M.11:2335–2346. one pathology could trigger the second. E. Karns. Chisum. Carper. C. Kiyokawa H.D. Oligodendrocite precurser differentiation is perturbed in the absence of the cyclin-dependent kinase inhibitor p27kip1..A. N.Y. possibly including schizophrenia. Haas. Excitotoxicity as a patho-physiologic factor in autism has previously been proposed. 1992:373–376 5 Cox A. H. Alzheimer’s disease. Neurotoxic theory of autism.. Courchesne et al. Neurobiology of infantile autism: proceedings of the International Symposium on Neurobiology of Infantile Autism.. neocortical grey matter.) MChS In an earlier study. and a smaller vermis at all ages examined. 3 Courchesne. & Courchesne. and 2 Alternatively.5 . Genes Dev 1997. and other neuro-degenerative conditions. In mice with this gene knocked out. and suggest that future genetic research might usefully explore linkage between autism and genes that are known to alter white matter development. In: Naruse H. eds. One example of such a gene is p27. Neurology 2001.. R. Akshoomoff. R. which regulates proliferation of glial and neural cells and affects myelin formation by oligodendrocytes. 4 Casaccia-Bonnefil P. in reinforcing the view that autism involves abnormal regulation of brain growth during early life. Moses.. 10–11 November 1990: satellite meeting of thejoint convention of the 5th International Child Neurology Congress and the 3rd Asian and Oceanian Congress of Child Neurology. S.M.J.Abnormal Brain Structure & Autism Alan Challoner MA (Phil. and it is during this early period (typically 12 to 24 months) that parents most often first express concern about their child’s development. R. slowed growth in the cerebellar hemispheres. Pierce.
Sherman JC. growth. . Grether JK. Courchesne E. Acta Anat 1961. including tests of source memory and executive functions (e. 14 Desmond JE. vasoactive intestinal peptide..275:1940–1943. 12 Courchesne E. For instance. Ann Neurol 2001. Sejnowski TJ. Chisum H.6:697–722. 387:167–178. I. 8 Huttenlocher PR. Maturation of the middle frontal gyrus. Ginier BL. and working memory). Structural organization of the human cerebral cortex. 11 12 In the autistic brain. Neuropeptides and neurotrophins in neonatal blood of children with autism or mental retardation. 6:388– 399. Cereb Cortex 1994. J Cogn Neurosci 1994. The cerebellar cognitive affective syndrome.18:3563–3573. as a member of a research panel convened by the American Academy of Neurology. Buxton RB. functions. 16 17 So. Behav Brain Sci 1998.” In addition. 9 Quartz SR. et al. Brain 1998. the cerebellum and certain cerebral regions may perform analogous. or semantic association. cerebellar cortex is activated by tasks that commonly activate frontal cortex. shifting attention. Fiez JA. such as tasks involving working memory. 11 Quartz SR. Neural activity-dependent brain changes in development: implications for psychopathology. 13 14 15 Adults with cerebellar lesions show impaired performance on similar frontal lobe tasks.17:9675–9685. van Groenigen WB. and it was hypothesised that abnormal elevations may result in unusual regional growth abnormalities (e. most children should be pointing as a nonverbal communication gesture and babbling. 18 These brain growth factors play roles in neural proliferation. Croen LA. Mason CA. Regional differences in synaptogenesis in human cerebral cortex. J Neurosci 1998. The neural basis of cognitive development: a constructivist manifesto. Videen TO. attention. Eric Courchesne et al (idem). 7 8 9 10 In the normally developing brain.20: 537–596. Granule neuron regulation of Purkinje cell development: striking a balance between neurotrophin and glutamate signaling. 19 Morrison ME. further hypothesise that in autism there is a relationship between abnormally elevated brain growth factors at birth and the abnormal brain growth patterns described above. but. J Comp Neurol 1997. Townsend J. in the normal brain. cognitive planning. in early life the autistic brain exhibits premature “growth without guidance. The neural basis of cognitive development: a constructivist manifesto. neurotrophin-4. 18 Nelson KB. Lobular patterns of cerebellar activation in verbal working memory and finger-tapping tasks as revealed by functional MRI. 17 Schmahmann JD. Dev Psychopathol 1994. et al. Glover GH. Dev Psychopathol 1994. the presence of both cerebral and cerebellar defects from the earliest stages of cognitive development would likely result in severe and persistent functional deficits. Behav Brain Sci 1998.20: 537–596. J Neurosci 1997. calcitonin-related gene peptide) have been found in neonatal blood spots of individuals who later developed autism and mental retardation. Townsend J. Abnormally elevated brain neurotrophins and neuropeptides (brain-derived neurotrophic factor. Intramodality shifting attention in children with damage to the cerebellum.g. differentiation. overgrowth in the cerebrum due to excessive sparing of neurons and stimulation of growth of neural elements. Chisum H. Science 1997. paradoxically..47:72–111.Abnormal Brain Structure & Autism Alan Challoner MA (Phil.6:697–722. 121:561–579. Neural activitydependent brain changes in development: implications for psychopathology. and circuit organisation. Wagner AD. "By 12 months of age. 16 Akshoomoff NA. migration.) MChS selection of which neuronal elements to keep or eliminate. Gabrieli JD. Sejnowski TJ. the researchers speculated that growth and elaboration of neural architecture and connectivity occurs prematurely and without being guided by functional experiences and adaptive learning. 15 Raichle ME. Wong EC. Attentional activation of the cerebellum independent of motor involvement. 4:8–26. Practice-related changes in human brain functional anatomy during nonmotor learning. however. Dabholkar AS. 10 Courchesne E. that is. loss of Purkinje cells in the cerebellum 19). possibly complementary. 13 Allen G. shaping of neural architecture and connectivity is theorised to be significantly influenced or directed by functional neural activity driven by learning and experience. By 16 months of age they should have in 7Schade JP.g.49:597–606. Page 3 Pauline Filipek has said.
Frontal and Temporal Lobe Dysfunction in autism and Other Related Disorders: ADHD and OCD. they should be using phrases. 2001 issue of Neurology. Alasbimn Journa1(4): July 1999. As children with autistic syndrome increasingly become categorised as a "medical" problem. More than one area of the brain is responsible for autistic behaviour in children with tuberous sclerosis and brain lesions." 4 In a study of 26 children with tuberous sclerosis complex (TSC). autism results from a complex combination of events in different parts of the brain. and behaviour. Temporal lobe hypoperfusion and other areas of dysfunction remain in spite of multiple various therapies used by these children. may further shut down the areas in which we want to improve blood flow and function and down regulated blood flow. Increased frontal perfusion may be related to "hyperfrontality" disorder. Chugani. Michigan.htm . correlating to models proposed by behavioural neurologists.” 21 There are also indications that particular parts of the brain can be shown to be damaged in the autistic person.) MChS their vocabulary words other than ‘mummy’ and ‘daddy’. for now it might be helpful to separate children afflicted with autistic syndrome from those with classic autism. NOT on improving the cognitive processing. Amygdala dysfunction has also been implicated in human disorders ranging from social anxiety to depression and to autism. Detroit.cl/revistas/4/goldberg. separating them from the many negative connotations and hopelessness associated with "classic" autism could be advantageous to promoting research and funding to help these children. http://www.alasbimnjournal. 20 21 Filipek. a researcher at the PET Center at Children's Hospital of Michigan. according to an article published in the October 9. and cerebellar hypoperfusion to motility impairment. co-operation. Perhaps one of the reasons no one has come up with an answer for autism is the way we have thought of it (or rather did not think of it. defining autism / PDD dysfunction. Page Researchers used MRI and PET exams to study how brain lesions resulted in common behaviours of autism including difficulties in social interaction and communication. We now know that autism is a "medical condition. Journal of Autism and Developmental Disorders (1999. a genetic disorder that causes benign lesions or tumours to form in many different organs. "We wanted to know if where the tuber was located or what it was 'doing' in the brain could predict behaviours of autism. Another study also suggests that brain damage may bring with it autistic syndrome." not a mental disorder.Abnormal Brain Structure & Autism Alan Challoner MA (Phil. a full review of techniques and goals is urgently needed. "We found that in these children. including the brain where the lesions are called "tubers.” Autism is a common occurrence in children with TSC. and by 24 months of age. Even though children with classic autism might be helped medically as our knowledge of the brain’s physiology expands. the scientific journal of the American Academy of Neurology." said Diane C. We are looking at anatomical markings." 20 Goldberg has told us that. Past focus for autistic children has been on trainability. Based on NeuroSPECT findings. Studies in animals have recorded symptoms typical of autism in young animals with amygdala lesions. rather than from one single source. “In the past. PhD. M. autism was considered a "psychiatric" disorder. and narrow and repetitive stereotyped behaviour. 29:437-482) Goldberg. A shift to the idea of "rehabilitation" is already in motion. implications are that medications or efforts to "calm" the brain and child down. Pauline. in medicine).
Echelard D. the part of the brain responsible for co-ordination. Simon. These suggest that impairment in face recognition may turn out to be one of the earliest indicators of abnormal brain development in autism. Baron-Cohen’s work in autism has added support to this idea. 23 Stone. Neurology 2002 Jul 23. amygdala enlargement was in excess of increased cerebral volume. This idea of the "social brain" was first written about in the 1980s by Lesley Brothers at the University of California. for example. 10 p2677. Brain structural abnormalities in young children with autism spectrum disorder. Acquired theory of mind impairments in individuals with bilateral amygdala lesions.22 Baron-Cohen suggests that there are particular parts of the brain that play a role in social understanding. such as their beliefs. Donald.W. Maravilla KR. Valerie Stone has also contributed to this research. 1999.] Understanding Other Minds Perspectives from Developmental Cognitive Neuroscience Second Edition. Munson J. Vol. S. 22 Reported in European Journal of Neuroscience.) MChS Defects in the cerebellum. and don't know whether another monkey is being friendly. Helen & Cohen. Autistic children's problems with social behaviour may result from their difficulty making inferences about others' mental states. its social behaviour changes. If a monkey has a lesion in the amygdala.. V. licking and mating attempts. Certain kinds of neurological patients also show specific deficits in social functioning. Calder. or not. Artru AA. Shaw DW. The monkeys no longer know where they fit in the social group." she said. Friedman SD. but this increase was proportional to overall increases in cerebral volume. Since all of the children in the study reacted 5 Geraldine Dawson reported particular findings in April 2001 at the annual meeting of the Society for Research in Child Development in Minneapolis. A. J. [Eds. Baron-Cohen.24 Children with the developmental disorder of autism suffer from a deficit in theory of mind. OUP. Tager-Flusberg. This inborn interest in faces is the start of social development. In research by Sparkes et al. Keane. A. and the result was the development of some of the traits typical of autism. 24 Sparks BF. (in press). Baron-Cohen. Cerebellar volume for the ASD group was increased in comparison with a TD group..23 One of those parts is the amygdala. Her research involved looking for parallels between the social deficits (particularly theory of mind deficits) exhibited by individuals with autism and patients with frontal lobe or amygdala damage. Neuropsychologia.E. Giedd JN. have been induced in guinea pigs. Measurements of amygdalae and hippocampi in this group of young children with ASD revealed enlargement bilaterally that was proportional to overall increases in total cerebral volume. . In a subgroup of children with ASD with strictly defined autism. knowledge and desires — is a central cognitive faculty underlying our ability to engage in social interaction. She has written that the ability to infer others' mental states. Dager SR.Abnormal Brain Structure & Autism Alan Challoner MA (Phil. "This new study tells us something very fundamental about abnormalities in autism. Dawson G. Aylward EH. Los Angeles.25 children with autism spectrum disorder (ASD) were found to have significantly increased cerebral volumes compared with typically developing (TD) and developmentally delayed (DD) children. They were much less inclined to interact with their fellow animals. It may be an important clue to actual brain circuits that are not functioning properly.C. they did far less sniffing. & Young.59(2):184-92 25 Page "We know that even new-born babies are drawn to face-like stimuli. and showed a reluctance to explore or respond to their surroundings.. There were similar findings of cerebral enlargement for both girls and boys with ASD.
emotions and problem-solving. contained in the cortex. planning. researchers have observed mini-columnar abnormalities in the frontal and temporal lobes of autistic patients. (Casanova. amygdala. 59(2): 184-92. Researchers do not yet know whether the difference in the number and size of the mini-columns is attributable to a gene mutation or some other factor. the University of South Carolina. and grey level index. They examined brain morphometric features in a large sample of carefully diagnosed 3. Withdrawing from social interaction and communication is a hallmark of autism. Echelard D. Sparks et al 28 explored the specific gross neuro-anatomic substrates of this brain developmental disorder. Artru AA. 58(3): 428-32. Dawson G. The lack of lateral inhibitors.to 4-year-old children with autism spectrum disorder (ASD) compared with age-matched control groups of typically developing (TD) children and developmentally delayed (DD) children. Dager SR. and respond. and hippocampus were measured from three-dimensional coronal MR images acquired from 45 children with ASD.) MChS similarly to toys and only the children with autism had problems with face recognition. the scientific journal of the American Academy of Neurology. is reported in Neurology. any changes in size. process it. MD.26 Using computerised imaging. but there are many more of them. Manuel F. A mini-column is a basic organisational unit of brain cells and connective wiring allows an individual to take in information. Brain structural abnormalities in young children with autism spectrum disorder. Buxhoeveden DP. parts of speech and movement. For the study. Aylward EH. the examinations revealed that the cell mini-columns of autistic patients are significantly smaller. Minicolumnar pathology in autism.” Dawson said the idea that face recognition may be hard-wired. and the Downtown VA Medical Center in Augusta. . Roy E. Maravilla KR. 6 As mentioned above. Thus. and researchers have identified structural differences in the brains of autism patients that might explain the behaviour. Rather. Friedman SD. 26 27 The frontal lobe of the brain is involved with reasoning. Casanova reports that evolution of the brain has kept mini-column size essentially constant while increasing total cortical surface area. would affect an individual's ability to discriminate between competing sensory information. This would be consistent with an existing theory that autistic individuals suffer a chronic state of over-arousal. or something people are born with. cerebellum. The temporal lobe is involved with perception and recognition of sound and memory. Georgia. 27 The study by scientists at the Medical College of Georgia. Giedd JN. According to study author. it indicates an abnormality in those brain circuits responsible for social function. Georgia. compactness.Abnormal Brain Structure & Autism Alan Challoner MA (Phil. a neurologist and neuro-pathologist at the Downtown VA Medical Center in Augusta. mean inter-neuronal distance. shape or location of the mini-column will have an effect on the processing capacity of the brain. Casanova MF. Munson J. 28 Page Volumes of the cerebrum. which in larger brains has resulted in more columns per brain and thus more processing units and increased complexity. Switala AE. It highlights that autism is a disorder of the social brain. it tells us autism is not a global problem. is controversial. Neurology 2002 Feb 12. and portray abnormal behaviours to diminish the arousal. Neurology 2002 Jul 23. Shaw DW. 26 TD children. peripheral neuropil space. Sparks BF. scientists examined the brain tissue of nine autistic patients and nine controls using five measures: columnar width. idem). Casanova.
BMJ Classified. . there seems to be a situation where the psychiatrist is unable to understand the person or the person’s condition. amygdala enlargement was in excess of increased cerebral volume. 29 29 Middleton. sex.) MChS and 14 DD children. In a subgroup of children with ASD with strictly defined autism. 7 Due to the problems associated with early brain damage. When the person seems to respond favourably to some aspects of this treatment.Abnormal Brain Structure & Autism Alan Challoner MA (Phil. For sub-region analyses. pp2-3. the transition to community care has not loosened the hold which psychiatrists have on this group of people. believe that there will always remain a specific role for clinicians within the field of ‘learning disability’ (whatever the cause). Cerebellar volume for the ASD group was increased in comparison with the TD group. However it can only be a lack of common sense that allows psychiatrists to conflate psychoses and brain damage. despite general recruitment problems in psychiatry bears reference to this. and clinical status. structural findings were independent of non-verbal IQ. A lack of professional development and understanding. Autism and its Treatment Psychiatrists and their predecessors. ‘will do’ as a clinical entity. Research currently is underway to better elucidate mechanisms underlying these structural abnormalities and their longitudinal progression. but for him it reinforces his view that the image he has created. but this increase was proportional to overall increases in cerebral volume. and the lack of neuropsychological knowledge. The DD group had smaller cerebellar volumes compared with both of the other groups. Psychiatry of learning disability. Most psychiatric faculty members. Page In order to justify his interventions. Measurements of amygdalae and hippocampi in this group of young children with ASD revealed enlargement bilaterally that was proportional to overall increases in total cerebral volume. 13 May 2000. General executive and administrative laziness brought this about and little has been done to make any adequate change. picked up those who were developmentally and intellectually disabled and they have been running with them ever since. structural abnormalities were observed primarily in boys. however. There were similar findings of cerebral enlargement for both girls and boys with ASD. volume of the cerebrum. This has existed in some guise since the asylums and workhouses of the early 1800s. Ken. The volumes were analysed with respect to age. Isla & Courtenay. The fact that about 77% of UK consultant posts and 74% of specialist registrar national training numbers are filled. Among the ASD group. Children with ASD were found to have significantly increased cerebral volumes compared with TD and DD children. the psychiatrist has to create the person the image of what he is able to understand and to treat. although this may reflect low statistical power issues because of the small sample (seven girls with ASD) studied. the psychiatrist does not attribute this to his good fortune. Although many fewer of these subjects are now in hospital. The authors believe that these structural findings suggest abnormal brain developmental processes early in the clinical course of autism. However it is often the case that the psychiatrist is the only available professional who can attend the person concerned. in the middle ages. together with only a fairly recent burgeoning of brain science may have aided this débâcle.
It may be that some children with brain damage are more susceptible to food additives or colourings as well. Antipsychotics are often used in this co-morbid population. and their potential side effects should be carefully considered. Drugs normally used to help anxiety or sleep sometimes have the opposite effect in susceptible children. reporting on novel antipsychotics and anti-seizure medications. 31 . May 13-18. Novel antipsychotic in ADHD with conduct disorder. and anxiolytics have been used in these patients with only varying degrees of success. 50 children aged 6 to 14 (74% being male) with co-morbid diagnosis of ADHD and conduct disorder who had not responded to stimulants alone were randomly assigned to risperidone or olanzapine augmentation. Despite a lack of clear scientific evidence for their efficacy and long-term safety. These medications are not specific to autism and do not treat core aspects of the disorder. 2000. merely that it may be a matter of trial and error to find something that suits the child.May 16. 8 As with the use of any psychopharmacological agent. This is not to say that they must never be used. However. The past decade has seen a dramatic increase in the use of medications in children and adolescents with psychiatric disorders. particularly as many agents have yet to be approved for use in children. yet few studies are looking for efficacy and safety. Another point to be aware of is that "brain-damaged" children may be much more sensitive to side effects of drugs than normal children. it is important not to lose sight of the overall goal of facilitating the child's adjustment and engagement with educational intervention. 31 of Prince Albert. Page Medications may be useful for symptoms which interfere with participation in educational interventions or are a source of impairment or distress to the individual. This can be an advantage in many ways in helping to document the efficacy of the selected medication. selective serotonin re-uptake inhibitors. tricyclic antidepressants.Abnormal Brain Structure & Autism Alan Challoner MA (Phil. Hussain. In a study presented by Dr. care should be taken in the selection and administration of medications. Day 3 . Overall. Elizabeth B. Since individuals with autism/PDD are often non-verbal. Illinois. reliance typically is made on reports and observation of specific behaviours. Issues in Child and Adolescent Psychopharmacology. close follow-up is required. at least to date. although this has not been proved. Hussain MZ. The researchers compared the consensus diagnosis. Program and abstracts from the 153rd Annual American Psychiatric Association Meeting. For example. there was least agreement for the diagnosis of bipolar disorder. lithium and mood stabilisers. The profile of side effects and risk as well as potential benefits will of course vary depending on the agent used and the target symptoms. as well as medication use in incarcerated youth. The neuroleptics. Canada. American Psychiatric Association 153rd Annual Meeting. where the clinician was over-diagnosing bipolarity.) MChS When the person does not respond favourably. Chicago. 30 Weller. psychotropic medications have been used quite widely in children and adolescents. the psychiatrist views this outcome as an indication of the intractability of the condition he has ‘created’. 2000. Issues of informed consent should be carefully considered. which used all the information from medical records and structured diagnostic interviews. Abstract 35. sedation might be misinterpreted as a positive therapeutic response. to the discharge diagnoses of the independent clinician. The study showed the increased rate of diagnosis of bipolar disorder by clinicians when the best estimate diagnosis by researchers refuted it. 30 Researchers discussed these issues in a series of presentations at the APA meeting in 2000.
Abnormal Brain Structure & Autism Alan Challoner MA (Phil. Treatments that pose some risk to the child and family should be actively discouraged. Page 9 26 January 2013 . Families should be helped to make informed decisions about their use of alternative treatments.) MChS Dietary and other alternative treatments are not clearly established as being efficacious.
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