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Abnormal Brain Structure & Autism

Alan Challoner MA (Phil) MChS

Introduction
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
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Autism.docx
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Abnormal Brain Structure & Autism

Alan Challoner MA (Phil.) MChS

In an earlier study, Courchesne et al, in reinforcing the view that autism involves abnormal
regulation of brain growth during early life, show that there is an unusual developmental
neuro-anatomic phenotype characterised by hyperplasia of cerebellar white matter,
neocortical grey matter, and cerebral white matter at the youngest ages with slowed
growth thereafter; slowed growth in the cerebellar hemispheres; and a smaller vermis at all
ages examined.3
They hypothesised the genetic factors most likely underlie this growth abnormality, and
suggest that future genetic research might usefully explore linkage between autism and
genes that are known to alter white matter development. One example of such a gene is
p27, which regulates proliferation of glial and neural cells and affects myelin formation by
oligodendrocytes. Loss of the p27 gene may lead to additional glial and neuronal cell
divisions before withdrawal from cell proliferation cycles. In mice with this gene knocked
out, there was a 250% increase in glial fibrillary acid proteinstaining glia cells in the
cerebellum and a 30% increase in numbers of neurons in CA1 of the hippocampus.4
Another important aetiology is excitotoxicity, an involvement that may allow the brain to
discard useless connections or reduce poorly functioning neurons. If neurons are stimulated
by toxins, lack of oxygen or are affected by genetic programmes, they release glutamate.
This process may be involved in stroke, Alzheimers disease, and other neuro-degenerative
conditions, possibly including schizophrenia.

Courchesne, E.; Karns, C.M.; Davis, H.R.; Ziccardi, R.; Carper, R.A.; Tigue, Z.D.; Chisum, H.J.;

Moses, P.; Pierce, K.; Lord, C.; Lincoln, A.J.; Pizzo, S.; Schreibman, L.; Haas, R.H.; Akshoomoff,
N.A.; & Courchesne, R.Y. Unusual brain growth patterns in early life in patients with autistic
disorder An MRI study.

Neurology 2001;57:245254.
4 Casaccia-Bonnefil P, Tikoo R, Kiyokawa H, Friedrich J, Chao M, Koff A. Oligodendrocite precurser
differentiation is perturbed in the absence of the cyclin-dependent kinase inhibitor p27kip1. Genes Dev
1997;11:23352346..

Gordon WP. Neurotoxic theory of autism. In: Naruse H, Ornitz EM, eds. Neurobiology of infantile autism:
proceedings of the International Symposium on Neurobiology of Infantile Autism, Tokyo, 1011 November
1990: satellite meeting of thejoint convention of the 5th International Child Neurology Congress and the 3rd
Asian and Oceanian Congress of Child Neurology.New York: Elsevier Science, 1992:373376
5

Cox A, Charman T, Baron-Cohen S, et al. Autism spectrum disorders at 20 and 42 months of age: stability
of clinical and ADI-R diagnosis. J Child Psychol Psychiatry 1999;5:719732.
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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. A postnatal period of extreme maldevelopment of these two major brain
structures will almost certainly be manifest in aberrant behavioural expression, and it is
during this early period (typically 12 to 24 months) that parents most often first express
concern about their childs development. 6 During this developmental period, the human
brain undergoes rapid synaptogenesis, expansion of dendritic and axon arbors, and

Alternatively, one pathology could trigger the second; although it is unclear how Purkinje
neuron loss could trigger excessive axonal or glial/myelin growth in cerebellar white matter,
excessive proliferation of excitatory axonal projections might be speculated to lead to
pathologic excitotoxicity and Purkinje death. Excitotoxicity as a patho-physiologic factor in
autism has previously been proposed.5

Abnormal Brain Structure & Autism

Alan Challoner MA (Phil.) MChS

selection of which neuronal elements to keep or eliminate. 7 8 9 10 In the normally


developing brain, shaping of neural architecture and connectivity is theorised to be
significantly influenced or directed by functional neural activity driven by learning and
experience. 11 12 In the autistic brain, however, the researchers speculated that growth
and elaboration of neural architecture and connectivity occurs prematurely and without
being guided by functional experiences and adaptive learning; that is, in early life the
autistic brain exhibits premature growth without guidance.
In addition, the cerebellum and certain cerebral regions may perform analogous, possibly
complementary, functions. For instance, in the normal brain, cerebellar cortex is activated
by tasks that commonly activate frontal cortex, such as tasks involving working memory,
attention, or semantic association. 13 14 15 Adults with cerebellar lesions show impaired
performance on similar frontal lobe tasks, including tests of source memory and executive
functions (e.g., shifting attention, cognitive planning, and working memory). 16 17 So, the
presence of both cerebral and cerebellar defects from the earliest stages of cognitive
development would likely result in severe and persistent functional deficits.
Abnormally elevated brain neurotrophins and neuropeptides (brain-derived neurotrophic
factor, neurotrophin-4, vasoactive intestinal peptide, calcitonin-related gene peptide)
have been found in neonatal blood spots of individuals who later developed autism and
mental retardation. 18 These brain growth factors play roles in neural proliferation,
migration, differentiation, growth, and circuit organisation, and it was hypothesised that
abnormal elevations may result in unusual regional growth abnormalities (e.g., overgrowth
in the cerebrum due to excessive sparing of neurons and stimulation of growth of neural
elements, but, paradoxically, loss of Purkinje cells in the cerebellum 19). Eric Courchesne et
al (idem), 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.

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Pauline Filipek has said, as a member of a research panel convened by the American
Academy of Neurology, "By 12 months of age, most children should be pointing as a nonverbal communication gesture and babbling. By 16 months of age they should have in

7Schade JP, van Groenigen WB. Structural organization of the human cerebral cortex. I. Maturation of the
middle frontal gyrus. Acta Anat 1961;47:72111.
8 Huttenlocher PR, Dabholkar AS. Regional differences in synaptogenesis in human cerebral cortex. J Comp
Neurol 1997; 387:167178.
9 Quartz SR, Sejnowski TJ. The neural basis of cognitive development: a constructivist manifesto. Behav Brain
Sci 1998;20: 537596.
10 Courchesne E, Chisum H, Townsend J. Neural activity-dependent brain changes in development:
implications for psychopathology. Dev Psychopathol 1994;6:697722.
11 Quartz SR, Sejnowski TJ. The neural basis of cognitive development: a constructivist manifesto. Behav Brain
Sci 1998;20: 537596.
12 Courchesne E, Chisum H, Townsend J. Neural activitydependent brain changes in development:
implications for psychopathology. Dev Psychopathol 1994;6:697722.
13 Allen G, Buxton RB, Wong EC, Courchesne E. Attentional activation of the cerebellum independent of
motor involvement. Science 1997;275:19401943.
14 Desmond JE, Gabrieli JD, Wagner AD, Ginier BL, Glover GH. Lobular patterns of cerebellar activation in
verbal working memory and finger-tapping tasks as revealed by functional MRI. J Neurosci 1997;17:96759685.
15 Raichle ME, Fiez JA, Videen TO, et al. Practice-related changes in human brain functional anatomy during
nonmotor learning. Cereb Cortex 1994; 4:826.
16 Akshoomoff NA. Intramodality shifting attention in children with damage to the cerebellum. J Cogn Neurosci
1994; 6:388 399.
17 Schmahmann JD, Sherman JC. The cerebellar cognitive affective syndrome. Brain 1998; 121:561579.
18 Nelson KB, Grether JK, Croen LA, et al. Neuropeptides and neurotrophins in neonatal blood of children
with autism or mental retardation. Ann Neurol 2001;49:597606.
19 Morrison ME, Mason CA. Granule neuron regulation of Purkinje cell development: striking a balance
between neurotrophin and glutamate signaling. J Neurosci 1998;18:35633573.

Abnormal Brain Structure & Autism

Alan Challoner MA (Phil.) MChS

their vocabulary words other than mummy and daddy, and by 24 months of age, they
should be using phrases." 20
Goldberg has told us that,
In the past, autism was considered a "psychiatric" disorder. We now know that autism is a
"medical condition," not a mental disorder. 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, in
medicine).
Even though children with classic autism might be helped medically as our knowledge of
the brains physiology expands, for now it might be helpful to separate children afflicted
with autistic syndrome from those with classic autism. As children with autistic syndrome
increasingly become categorised as a "medical" problem, 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.
Increased frontal perfusion may be related to "hyperfrontality" disorder, and cerebellar
hypoperfusion to motility impairment. Temporal lobe hypoperfusion and other areas of
dysfunction remain in spite of multiple various therapies used by these children. We are
looking at anatomical markings, defining autism / PDD dysfunction, correlating to models
proposed by behavioural neurologists.
Past focus for autistic children has been on trainability, co-operation, and behaviour, NOT
on improving the cognitive processing. A shift to the idea of "rehabilitation" is already in
motion; a full review of techniques and goals is urgently needed.
Based on NeuroSPECT findings, implications are that medications or efforts to "calm" the
brain and child down, may further shut down the areas in which we want to improve blood
flow and function and down regulated blood flow. 21
There are also indications that particular parts of the brain can be shown to be damaged in
the autistic person. Studies in animals have recorded symptoms typical of autism in young
animals with amygdala lesions. Amygdala dysfunction has also been implicated in human
disorders ranging from social anxiety to depression and to autism.
Another study also suggests that brain damage may bring with it autistic syndrome. More
than one area of the brain is responsible for autistic behaviour in children with tuberous
sclerosis and brain lesions, according to an article published in the October 9, 2001 issue of
Neurology, the scientific journal of the American Academy of Neurology.

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Researchers used MRI and PET exams to study how brain lesions resulted in common
behaviours of autism including difficulties in social interaction and communication, and
narrow and repetitive stereotyped behaviour. "We wanted to know if where the tuber was
located or what it was 'doing' in the brain could predict behaviours of autism," said Diane
C. Chugani, PhD, a researcher at the PET Center at Children's Hospital of Michigan, Detroit,
Michigan. "We found that in these children, autism results from a complex combination of
events in different parts of the brain, rather than from one single source."

In a study of 26 children with tuberous sclerosis complex (TSC), a genetic disorder that
causes benign lesions or tumours to form in many different organs, including the brain
where the lesions are called "tubers. Autism is a common occurrence in children with TSC.

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Filipek, Pauline. Journal of Autism and Developmental Disorders (1999; 29:437-482)

Goldberg, M. Frontal and Temporal Lobe Dysfunction in autism and Other Related Disorders: ADHD and
OCD. Alasbimn Journa1(4): July 1999. http://www.alasbimnjournal.cl/revistas/4/goldberg.htm

Abnormal Brain Structure & Autism

Alan Challoner MA (Phil.) MChS

Defects in the cerebellum, the part of the brain responsible for co-ordination, have been
induced in guinea pigs, and the result was the development of some of the traits typical of
autism. They were much less inclined to interact with their fellow animals, they did far less
sniffing, licking and mating attempts, and showed a reluctance to explore or respond to
their surroundings.22
Baron-Cohen suggests that there are particular parts of the brain that play a role in social
understanding.23 One of those parts is the amygdala. If a monkey has a lesion in the
amygdala, for example, its social behaviour changes. The monkeys no longer know where
they fit in the social group, and don't know whether another monkey is being friendly, or
not. This idea of the "social brain" was first written about in the 1980s by Lesley Brothers at
the University of California, Los Angeles. Baron-Cohens work in autism has added support
to this idea.
Valerie Stone has also contributed to this research. She has written that the ability to infer
others' mental states, such as their beliefs, knowledge and desires is a central cognitive
faculty underlying our ability to engage in social interaction.24 Children with the
developmental disorder of autism suffer from a deficit in theory of mind. Autistic children's
problems with social behaviour may result from their difficulty making inferences about
others' mental states. Certain kinds of neurological patients also show specific deficits in
social functioning. 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.
In research by Sparkes et al,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. Cerebellar volume for the ASD group was
increased in comparison with a TD group, but this increase was proportional to overall
increases in cerebral volume.
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. There were similar findings of cerebral enlargement for both girls and boys with
ASD. In a subgroup of children with ASD with strictly defined autism, amygdala
enlargement was in excess of increased cerebral volume.

22

Reported in European Journal of Neuroscience, Vol. 10 p2677.

Baron-Cohen, Simon; Tager-Flusberg, Helen & Cohen, Donald. [Eds.] Understanding Other Minds Perspectives from Developmental Cognitive Neuroscience Second Edition. OUP, 1999.

23

Stone, V.E., Baron-Cohen, S., Calder, A.C., Keane, J. & Young, A.W. (in press). Acquired theory of mind
impairments in individuals with bilateral amygdala lesions. Neuropsychologia.
24

Sparks BF, Friedman SD, Shaw DW, Aylward EH, Echelard D, Artru AA, Maravilla KR, Giedd JN,
Munson J, Dawson G, Dager SR. Brain structural abnormalities in young children with autism spectrum
disorder. Neurology 2002 Jul 23;59(2):184-92

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"We know that even new-born babies are drawn to face-like stimuli. This inborn interest in
faces is the start of social development," she said. "This new study tells us something very
fundamental about abnormalities in autism. It may be an important clue to actual brain
circuits that are not functioning properly. Since all of the children in the study reacted

Geraldine Dawson reported particular findings in April 2001 at the annual meeting of the
Society for Research in Child Development in Minneapolis. These suggest that impairment
in face recognition may turn out to be one of the earliest indicators of abnormal brain
development in autism.

Abnormal Brain Structure & Autism

Alan Challoner MA (Phil.) MChS

similarly to toys and only the children with autism had problems with face recognition, it tells
us autism is not a global problem. Rather, it indicates an abnormality in those brain circuits
responsible for social function. It highlights that autism is a disorder of the social brain.
Dawson said the idea that face recognition may be hard-wired, or something people are
born with, is controversial.
Withdrawing from social interaction and communication is a hallmark of autism, and
researchers have identified structural differences in the brains of autism patients that might
explain the behaviour.26
Using computerised imaging, researchers have observed mini-columnar abnormalities in
the frontal and temporal lobes of autistic patients. 27 The study by scientists at the Medical
College of Georgia, the University of South Carolina, and the Downtown VA Medical
Center in Augusta, Georgia, is reported in Neurology, the scientific journal of the American
Academy of Neurology.
A mini-column is a basic organisational unit of brain cells and connective wiring allows an
individual to take in information, process it, and respond. Thus, any changes in size, shape
or location of the mini-column will have an effect on the processing capacity of the brain.
For the study, scientists examined the brain tissue of nine autistic patients and nine controls
using five measures: columnar width, peripheral neuropil space, mean inter-neuronal
distance, compactness, and grey level index.
According to study author, Manuel F. Casanova, MD, a neurologist and neuro-pathologist
at the Downtown VA Medical Center in Augusta, Georgia, the examinations revealed that
the cell mini-columns of autistic patients are significantly smaller, but there are many more
of them.
Casanova reports that evolution of the brain has kept mini-column size essentially constant
while increasing total cortical surface area, which in larger brains has resulted in more
columns per brain and thus more processing units and increased complexity.
This would be consistent with an existing theory that autistic individuals suffer a chronic state
of over-arousal, and portray abnormal behaviours to diminish the arousal. The lack of
lateral inhibitors, contained in the cortex, would affect an individual's ability to discriminate
between competing sensory information, (Casanova, idem). 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.

Casanova MF, Buxhoeveden DP, Switala AE, Roy E. Minicolumnar pathology in autism. Neurology 2002
Feb 12; 58(3): 428-32.

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The frontal lobe of the brain is involved with reasoning, planning, parts of speech and movement, emotions
and problem-solving. The temporal lobe is involved with perception and recognition of sound and memory.

Sparks BF, Friedman SD, Shaw DW, Aylward EH, Echelard D, Artru AA, Maravilla KR, Giedd JN,
Munson J, Dawson G, Dager SR. Brain structural abnormalities in young children with autism spectrum
disorder. Neurology 2002 Jul 23; 59(2): 184-92.

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Volumes of the cerebrum, cerebellum, amygdala, and hippocampus were measured from
three-dimensional coronal MR images acquired from 45 children with ASD, 26 TD children,

As mentioned above, Sparks et al 28 explored the specific gross neuro-anatomic substrates


of this brain developmental disorder. They examined brain morphometric features in a
large sample of carefully diagnosed 3- 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.

Abnormal Brain Structure & Autism

Alan Challoner MA (Phil.) MChS

and 14 DD children. The volumes were analysed with respect to age, sex, volume of the
cerebrum, and clinical status.
Children with ASD were found to have significantly increased cerebral volumes compared
with TD and DD children. Cerebellar volume for the ASD group was increased in
comparison with the TD group, but this increase was proportional to overall increases in
cerebral volume. The DD group had smaller cerebellar volumes compared with both of the
other groups. 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. There were similar findings of cerebral enlargement for
both girls and boys with ASD. For sub-region analyses, structural abnormalities were
observed primarily in boys, although this may reflect low statistical power issues because of
the small sample (seven girls with ASD) studied.
Among the ASD group, structural findings were independent of non-verbal IQ. In a
subgroup of children with ASD with strictly defined autism, amygdala enlargement was in
excess of increased cerebral volume.
The authors believe that these structural findings suggest abnormal brain developmental
processes early in the clinical course of autism. Research currently is underway to better
elucidate mechanisms underlying these structural abnormalities and their longitudinal
progression.

Autism and its Treatment


Psychiatrists and their predecessors, in the middle ages, picked up those who were
developmentally and intellectually disabled and they have been running with them ever
since.
General executive and administrative laziness brought this about and little has been done
to make any adequate change. Although many fewer of these subjects are now in
hospital, the transition to community care has not loosened the hold which psychiatrists
have on this group of people.
A lack of professional development and understanding, together with only a fairly recent
burgeoning of brain science may have aided this dbcle. However it can only be a lack
of common sense that allows psychiatrists to conflate psychoses and brain damage.

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In order to justify his interventions, the psychiatrist has to create the person the image of
what he is able to understand and to treat. When the person seems to respond favourably
to some aspects of this treatment, the psychiatrist does not attribute this to his good fortune,
but for him it reinforces his view that the image he has created, will do as a clinical entity.

Due to the problems associated with early brain damage, and the lack of neuropsychological knowledge, there seems to be a situation where the psychiatrist is unable to
understand the person or the persons condition. However it is often the case that the
psychiatrist is the only available professional who can attend the person concerned. Most
psychiatric faculty members, however, believe that there will always remain a specific role
for clinicians within the field of learning disability (whatever the cause). This has existed in
some guise since the asylums and workhouses of the early 1800s. The fact that about 77%
of UK consultant posts and 74% of specialist registrar national training numbers are filled,
despite general recruitment problems in psychiatry bears reference to this. 29

29

Middleton, Isla & Courtenay, Ken. Psychiatry of learning disability. BMJ Classified; pp2-3, 13 May 2000.

Abnormal Brain Structure & Autism

Alan Challoner MA (Phil.) MChS

When the person does not respond favourably, the psychiatrist views this outcome as an
indication of the intractability of the condition he has created.
The past decade has seen a dramatic increase in the use of medications in children and
adolescents with psychiatric disorders. Despite a lack of clear scientific evidence for their
efficacy and long-term safety, at least to date, psychotropic medications have been used
quite widely in children and adolescents. 30
Researchers discussed these issues in a series of presentations at the APA meeting in 2000,
reporting on novel antipsychotics and anti-seizure medications, as well as medication use in
incarcerated youth.
Antipsychotics are often used in this co-morbid population, yet few studies are looking for
efficacy and safety. In a study presented by Dr. Hussain, 31 of Prince Albert, Canada, 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.
The researchers compared the consensus diagnosis, which used all the information from
medical records and structured diagnostic interviews, to the discharge diagnoses of the
independent clinician. Overall, there was least agreement for the diagnosis of bipolar
disorder, where the clinician was over-diagnosing bipolarity. The study showed the
increased rate of diagnosis of bipolar disorder by clinicians when the best estimate
diagnosis by researchers refuted it.
Another point to be aware of is that "brain-damaged" children may be much more sensitive
to side effects of drugs than normal children. Drugs normally used to help anxiety or sleep
sometimes have the opposite effect in susceptible children. This is not to say that they must
never be used, merely that it may be a matter of trial and error to find something that suits
the child. It may be that some children with brain damage are more susceptible to food
additives or colourings as well, although this has not been proved.

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Medications may be useful for symptoms which interfere with participation in educational
interventions or are a source of impairment or distress to the individual. These medications
are not specific to autism and do not treat core aspects of the disorder, and their potential
side effects should be carefully considered. The neuroleptics, selective serotonin re-uptake
inhibitors, tricyclic antidepressants, lithium and mood stabilisers, and anxiolytics have been
used in these patients with only varying degrees of success.

As with the use of any psychopharmacological agent, care should be taken in the
selection and administration of medications. 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. Since individuals with autism/PDD are often non-verbal, reliance typically is
made on reports and observation of specific behaviours. This can be an advantage in
many ways in helping to document the efficacy of the selected medication. However, it is
important not to lose sight of the overall goal of facilitating the child's adjustment and
engagement with educational intervention. For example, sedation might be
misinterpreted as a positive therapeutic response. Issues of informed consent should be
carefully considered, particularly as many agents have yet to be approved for use in
children; close follow-up is required.

30 Weller, Elizabeth B. Issues in Child and Adolescent Psychopharmacology. American Psychiatric Association
153rd Annual Meeting. Day 3 - May 16, 2000.

Hussain MZ. Novel antipsychotic in ADHD with conduct disorder. Program and abstracts from the 153rd
Annual American Psychiatric Association Meeting, May 13-18, 2000; Chicago, Illinois. Abstract 35.

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Abnormal Brain Structure & Autism

Alan Challoner MA (Phil.) MChS

Dietary and other alternative treatments are not clearly established as being efficacious.
Families should be helped to make informed decisions about their use of alternative
treatments. Treatments that pose some risk to the child and family should be actively
discouraged.

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26 January 2013