Diagnosis of autismBMJ 2003; 327 doi: https://doi.org/10.1136/bmj.327.7413.488 (Published 28 August 2003) Cite this as: BMJ 2003;327:488
All rapid responses
Statistics have proved that many with autism also suffer from epilepsy, which is abnormal formation of synapses. However, there is no effective treatment for this problem. We can only relieve the symptom by medication.
In Taiwan, many parents don't want their children to go to special needs school for fear that their children would be labeled as abnormal children. They will send their children to normal elementary schools to receive education. It may cause lots of problems if the teachers or classmates are not willing to help them, or don't know how to do. Therefore, the following is a method created by an elementary school teacher who succeeded in dealing with this problem.
1. Former preparation
Many other students may not have the experience to get along with people with autism and epilepsy, so it is really significant to have the whole class to learn about the situation of this "unique" person. Doctors or special education teachers should be in the class to clarify the situation of autism and epilepsy to other students, making sure that everyone is prepared to face the problem that may happen.
2. The steps to take when epilepsy occurs
First, tell the other students that epilepsy has occurred and let everyone stay quietly, and look at the clock for five minutes instead of staring at the patient.
Meanwhile, the teacher walks to the patient and lets him lie on the side, then put the coat on him for fear that he would get cold if incontinence happened?
Then, one of the assigned students should call the health center, another one should call the patient’s mother.
While waiting, the teacher should stay quietly besides the patient and use tissues to clear the patient’s mouth. Hold him lightly if twitch happens. After the twitch, call his name lightly to make sure he is still awake.
When the health center’s teacher comes, tell the condition and onset time to her and decide whether to go to hospital or not.
3. After the emergency, it is really important to praise other students that they did a good job. This may spur children into being willing to help others later.
Epileptic fits are not lethal if appropriate steps are undertaken. However, many people don’t know how simple it is to help a person with epilepsy and autism. If we have the opportunity to teach elementary school students to face this problem, it might encourage them to willingly help others.
Competing interests: No competing interests
My Daughter was diagnosed with ASD at the age of 2 yrs and 6 Months.
She had no eye contact , flapped her arms , stood swaying in front of the
TV watching Barney and Sesame Street. You could go up behind her and make
a loud clapping noise and she would not acknowledge it, you couldn't
startle her. After the devasting diagnosis, I started researching
everything I could to help her recover and she has had almost every
therapy in some form or another and now at the age of 13, she craves
relationships with her peers and wants to be like any other teenager!
The therapies she has had over the last 10 years include: Music Therapy,
Hanen Program (A commication program developed in Canada for Parents,
delivered by qualified Speech & Language Therapists), Vitamin Therapy,
DMG (Dimithilglycine) (A Nutrient found in rice, but available in more
adequate amounts from health stores in disolvable tablet form),Omega oils,
Ambrotose ( A Glyconutrient, which the a well known Scientist Magazine
recently wrote a report stating glyconutrients have been proven to aid
cell to cell communication! This is 10 years after I ordered it from the
States and gave it to my daughter! It is now available in the UK),
Homeopathy (from my GP who is an expert in this field, luckily for me and
my daughter!)The homeopathy has helped to detoxify her from the harmful
effects of mercury and aluminium found in vaccines, Sensory Integration
Therapy, Eurythmy Therapy, Art Therapy, to name but a few. I didn't do the
LOVAAS Options or Sunrise programs but used some of the ideas behind these
therapies in every day situations as and when they arose during the
day.She has never swam with the Dolphins either.
I DID stop my daughter hand flapping and other self stimming behaviours,
as I believe as did her Sensory Integration Therapist and her GP, that
while a child is hand flapping or doing any other form of self stimming,
they are not able to be aware whats in the world around them and fall
deeper and deeper in to their own solitairy world! She is now a very
communicative, sociable, teenager who wants to do and achieve the same as
her peers around her. She still has autism but she is now learning how to
live with it and enjoy life and what it has to offer, she is still
learning (and so am I!) but I truely believe if we had not intervened at
an early age she would not be the sociable, communicative young lady she
is today! She loves dancing and has won competitions for it, going in to a
dance hall full of children and adults, with music blaring and dances a
full routine, and can wait and listen for her number to be called out for
recalls!! When she was 4 the main stream school she attended for her first
two years (BIG MISTAKE!) couldn't get her in the assembly hall, without
her putting her hands over her ears and screaming!
She still attends a special centre for young people with ASD and has a lot
more to learn and understand about the world and the concepts and dangers
in it, but she loves life and wants to do everything other teenage girls
of her age want to do! And now she has the coping stategies and people
with the expertise around her, to help her do that!
But as another parent has commented on here, these interventions and
therapies are not readily available, as a parent you are not told about
them, for fear you are given "false hope" and it takes alot of energy to
research and find the therapists to do them, not to mention the cost!
If parents were told about all the possible things they could try and be
allowed to make an informed choice and have the services available to try,
maybe more autistic children would stand a better chance of reaching their
My work is not done, there is still more to learn and stages of her life
to help her through.......
SHE STILL HAS AUTISM BUT AUTISM DOESN'T HAVE HER!
Competing interests: No competing interests
The diagnosis of autism may be relatively straightforward as far
autistic symptoms are concerned, while the clinician may be in difficulty
when trying to ascertain the cognitive level of the affected individual.
This is particularly true when assessing non-verbal individuals. As
reviewed by Rapin and Dunn , language deficits in autism span from mild
difficulties in lexicon and prosody to verbal agnosia and a complete
absence of verbal productions. In this article we describe the atypical
case of an adolescent with autism who shows a complete absence of spoken
language and a rich and articulate inner language.
D. V. was born in 1989, by caesarian section delivery for failure to
progress, which followed a physiological full-term pregnancy. He was in
good health after birth and looked very much like an average baby during
the first twelve months of life. His mother started noticing something
wrong in his behaviour when he was 24 months old: he would not gaze at her
eyes as before, he appeared detached from his environment, and showed a
sad expression. His language then regressed, from an ability to produce a
few contextually meaningful words to a total absence of spoken language.
At the age of 3, he was clearly disabled in his interactions with peers,
although he seemed to long for their proximity. He very frequently
indulged in stereotyped behaviours, like rocking, spinning himself and
various objects, swallowing in a repeated and purposeless way and laughing
or crying without an apparent reason. D. V.’s behavioural picture
satisfied DSM III-R’s  criteria for autism.
As prescribed by the italian law, D. V. was mainstreamed throughout
his school years, and since the age of 4 he had been assigned a special
teacher (F. S.) for most of his school hours. During the years of primary
school he was assigned another special teacher for the school hours, while
he was assisted at home by his own relatives and by F. S. for 18 hours a
week. F. S. very soon started a program of parent-training, and she also
engaged D. V. in outdoor activities aimed at improving his ability to
relate to other persons.
D. V. was clumsy and very delayed in his ability to draw, but he promptly
directed his gaze toward a detail in the environment under a verbal
request by his home teacher. During the school years he frequently
approached his peers, but he could not play interactively with them.
We felt unable to formally assess his cognitive level, but we were almost
convinced that he had mental retardation.
D. V. needed strong prompts by his home teacher when he started to
write isolated words at the age of 8, and he refused to transfer those
achievements to the classroom. Apart from verbal reassurances, prompting
consisted in his home teacher pointing with her index finger to the left
of the paper where D. V. was requested to write, without any direct
contact with him, and without any verbal or physical suggestion. If that
prompt was interrupted, then he would stop writing and close his exercise
Under the constant tutoring of his caregivers, D. V.’s writing abilities
showed gradual improvements until the age of 14, when he unexpectedly
became able to autonomously write not only words and simple phrases but
also his own ideas, introspections and remembrances, still under the same
kind of prompting.
We present here a few excerpts, literally translated from D. V.’s
manuscripts in Italian, his only language. In the first manuscript he
gives an account of his relationship with his brother: “Dear C., … even if
we live under the same roof we do not know each other you are young so I
introduce myself I am D. your big brother who looked constantly absent but
on the contrary was watching you as you were growing up … I was born
normal as every other child but it is not clear to me what happened only
that I could not speak with anybody I always envied you because everybody
took care of the small newborn. Nobody ever thought that D. could have
desires and dreams as you do, the problem is that I did not know how to
say it … I know that I will be never considered as a normal person but
Alessandra has made me feel special and she has made me feel like to be as
you are. I love you do not give up your attempts to know me”. In another
manuscript, D. V. addressed his father: “Dear dad, I have realized that I
never dedicated a letter to you … I miss you when you are at work, and you
stay out all day. I do not know how much you have accepted me I do not
know how often you have felt ashamed to keep me near you… I wish I had
what other children have got go out with the family for a walk go to a
party play with you and have a bike to go out with you and you can teach
me how to use it”.
D. V. wrote about his disability, affirming that he was very ill, but
not stupid. He explained that he could accept to write down his ideas only
when “sincerely friendly people” paid full attention to him; “other people
must deserve me”, he stated.
Assessment after 14 years of age.
The diagnosis of autism was confirmed by two different child
psychiatrists (S. L. and C. D.), according to DSM IV criteria, and we also
tested D. V. with the WISC-R , italian version, to verify his I. Q. He
correctly gave written answers to questions such as: “what do rage and joy
have in common?” (a: “they are feelings”), “what is the importance of
having senators and deputies” (a: “to steer Italy and to govern it
democratically”). His verbal IQ was 112, performance 55, full scale 83.
The only performance sub-test he coped with efficiently was picture
completion. When D.V. was 15, his score at the CARS  was in the range
of severe autism (40.5), and his mean developmental age at the Vineland
Adaptive Behavior Scales , Italian version was 3 years, 6 months. So,
considering his performances under neither help nor prompt, he was very
D.V. now shows average levels of learning through written assessments,
after concluding the third year of a professional school and he has been
well accepted and helped by his schoolmates.
His writing style is peculiar: D.V. moves almost mechanically from the
left to the right side of the paper, producing a simplified and
stereotyped kind of block letters.
The case of D. V. has added to our understanding of autism. The full-
blown autistic picture that D. V. presented, together with a complete
absence of language and low performance abilities were all misleading
signs for us. Although we underestimated D. V.’s real potential, years of
mainstreaming and home teaching seem to have been helpful in his case. We
doubt that this boy would have been able to assimilate the same elements
of knowledge and concepts had he been involved in an individualized
teaching in a class for children with mental retardation. To our
knowledge, there have not been reports of similar cases in the literature,
although some high - functioning persons with autism have referred of
being more able to express themselves through their writings than during
direct verbal interaction . This case indicates that in severe cases of
autism, complex reasoning is possible, and that the deficit of
coordination between brain organizations may be limited to systems which
mediate the translation of thoughts to spoken words and phrases and to
sectors controlling non-verbal aspects of cognitive functioning. Although
speculative, our inference is that if autism is a dysfunction of
interneurons [7, 8], then the brain (cortical and possibly subcortical)
distribution of that dysfunction may produce different clinical profiles
in different individuals, unexpectedly sparing networks of complex
processing in sporadic cases.
We are grateful to D. V.’s parents and to him, for giving his written
assent to the publication of this manuscript.
1. Rapin I, Dunn M. Update on the language disorders of individuals
on the autistic spectrum. Brain Development, 2003, 25:166-72.
2. American Psychiatric Association. Diagnostic and statistical
manual of mental disorders (3rd ed. revised). 1987, Washington, DC:
3. Wechsler D. Manual for the Weschsler Intellingence Scale for
Children, New York: Psychological Corporation, 1949 (Italian edition, O.
4. Schopler EC, Reichler RJ, & Renner B. The Childhood Autism
Rating Scale (CARS), Los Angeles, CA: Western Psychological Services,
5. Sparrow S, Balla D & Cicchetti D. Vineland Adaptive Behavior
Scales. American Guidance Service, Circle Pines, MN, 1984. (Italian
edition, O. S., Florence).
6. Williams D. Autism, an inside-out approach, Jessica Kingsley
Publishers, London, 1996.
7. Petropoulos H, Friedman SD, Shaw DWW, Artru AA, Dawson G, Dager
SR. Gray matter abnormalities in autism spectrum disorder revealed by T2
relaxation. Neurology 2006;67:632–636.
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revealed by T2 relaxation. (letter) Neurology. 2007;68(15):1237; authors
Competing interests: No competing interests
The case of SM, a women with a selective bilateral damage to the
amygdala and to a small portion of adjacent enthorinal cortex ,
suggests that the amygdala has a role in guiding visual attention to
sensible cues in human faces. SM fails to direct her gaze toward the eyes
region of faces, when she explores facial expressions, but her recognition
of fear in faces is similar to controls when she is actively prompted to
explore that region.
It would be oversimplistic to directly associate the gazing behavior of SM
with the deficit in visual fixation shown by persons with autism, as it
would be simplistic to ascribe the whole of the autistic symptomatology to
a frontal dysfunction. SM shows an array of social impairments but she is
not autistic, and frontal patients are not autistic either, although they
may fail in executive tasks, by definition, or in mindreading tasks.
The point I would like to rise here is related to the guiding role of the
amygdala in selective attention.
Attention has been defined as “an enhancement of activity in the
attended set of pathways relative to the unattended set’’ . Recent
studies have shown that higher neural centers can influence lower centers
when the latter are processing either external, or internal data. Bar 
proposed that feedback signals from the prefrontal cortex to lower visual
pathways have a role in the rapid recognition of percepts. Mechelli et al
 found that the prefrontal cortex activates category-selective zones of
the extrastriate cortex during visual imagery. Ishai et al  have
demonstrated that the brain areas that are activated during tasks of
visual imagery and rehearsal of famous faces are the same which are
activated during the real perception of the same targets, albeit in a less
It is plausible that both the limbic system and the prefrontal cortex
send signals to visual pathways at various levels in order to make
priorities among perceptive data, creating contrasts between contextually
significant and less relevant perceptive elements. Our subjective and
adaptive mirroring of the environment is probably actively shaped by top-
down processes, or feedbacks  realizing a parallel system of
interconnections between neural structures.
Top-down processes are seemingly involved in imagery, working memory
and attention. While visual pathways are the most studied system as far as
feedbacks are concerned, it is reasonable to assume that an analogous
modulation of brain functions takes place in other cortical (and possibly
Our everyday experience provides useful hints, in this regard. While
we are able to perceive two or more different voices at the same time,
only one of these voices can be fully processed for comprehension.
Consider now the following situation: I am listening to an cognitively
interesting news bulletin when a second, familiar voice enters my
perceptive field. If the voice has a neutral content, most of the times I
will be able to automatically keep that voice in a unattended position in
my cognitive apparatus. But if the voice has an affective meaning for me,
it will probably displace the first attended track (the news) and gain its
way upward the hierarchy of neural computation. I will process that voice
in order to understand the messages it conveys and what is the most
appropriate action to take in response. I may still try to refocus on the
news, and be successful in that task, but only if the affective resonance
of the second voice is not particularly strong. I presume that in order to
gain prominence, the added voice has been recognized by my limbic system,
while my struggling to keep on listening to the news might be the
consequence of an activation of the prefrontal cortex. There is a
variability of responses, of course, and I suspect that, on the average,
men would be more prone to be captured by news (or football, according to
preferences) and women would be more ready to respond to the voice of a
close relative. Moreover, attention to football could be directed by
signals from the limbic system in men.
Frith [quoted by Hill and Frith, 7] has hypothesized that the pruning
of top-down synapses is delayed in autism, leading in some cases to an
enlarged brain, an executive dysfunction and a perceptual overload.
Brock et al , have recently proposed the “Temporal binding model
of autism”: they maintain that in autism there is an impairment in the
synchronization between distant brain organizations, that this could be at
the basis of a “weak central coherence” and that it could explain many of
the cognitive symptoms of autism.
A basic endophenotype of autism might be a reduction in the amplitude of
synchronously elicitable mental function with relative preservation of
discrete processing .
I would extend Brock et al’s line of reasoning, and speculate that
the whole system of top-down modulations might be a dysfunctional system
in at least some cases of autism. As a consequence, the underconnectivity
between brain areas which has been recently detected in autistic
individuals  might be a modulatory underconnectivity, a failure of
meta-connectivity. In physiological conditions, the information coming
from sensory organs and from the activation of processing areas in the
absence of external stimuli (id est imagery, speculative activities and
maybe dreaming) would be coordinated by a well functioning top-down
modulatory system. In severe autism, on the other hand, all sensory data
would have equal opportunity, or on the contrary a reduced opportunity to
be processed by distributed and potentially dedicated, but inconsistently
activated brain circuitries.
A failure in the synchronization of task-oriented neural webs might
easily explain the social deficits of persons with autism, as a reduced
power of computation of incoming complex stimuli would render other
peoples’ actions, intentions and ambiguous behaviors impossible to decode
with the necessary speed. Given the complexity of social relationships,
individuals with autism would prefer isolation to the frustrating
experience of interpersonal unfitness.
Spratling  has reviewed the role of apical dendrites in the
regulation of the response of pyramidal neurons to “feedforward” signals,
id est signals coming from the periphery of the nervous system and
ascending toward higher levels of neural computation. His model gives a
logical account of the more active role in perception, speculation and
action planning that human brain has been deemed as endowed with by many
researchers in recent years. I suggest that a role of apical dendrites and
related synapses should be considered when studying the basic dysfunction
of autism. An in-built, distributed system of modulation of brain
functions, with important nodes of activity in the limbic system, in the
prefrontal and parietal cortex and possibly in the cerebellum might be
dysfunctional in this disorder. Fatemi et al  have found a reduction
of Reelin, a glycoprotein responsible for the normal layering of brain in
superior frontal and cerebellar cortices of brains of persons with autism.
Mukaetova-Ladinska et al.  detected a reduction of MAP2 protein
associated with cytoarchitectonic changes in the dorsolateral prefrontal
cortex of individuals with autism. If a link between these
neurobiological, genetic, imaging and behavioral findings will be
confirmed, then new light may be shed on some pathogenic ways of autism
and useful elements might be added to treatment guidelines. If the deficit
in autism is one of undersynchronization and underorganization of
cognitive functions, then addressing to the globality of the child and her
hidden assets in a nearly spontaneous setting and in a period in which her
brain is very plastic should have more chance of success than
systematically drill on discrete areas of competence.
1. Adolphs R, Gosselin F, Buchanan TW, Tranel D, Schyns P, Damasio
AR. A mechanism for impaired fear recognition after amygdala damage.
2. LaBerge, D. Attentional Processing. 1995; Harvard Univ. Press,
3. Bar M. A cortical mechanism for triggering top-down facilitation
in visual object recognition. J Cogn Neurosci. 2003;15:600-9. Review.
4. Mechelli A, Price CJ, Friston KJ, Ishai A. Where bottom-up meets
top-down: neuronal interactions during perception and imagery. Cereb
5. Ishai A, Haxby JV, Ungerleider LG. Visual imagery of famous faces:
effects of memory and attention revealed by fMRI. Neuroimage. 2002;17:1729
6. Engel AK, Fries P, Singer W. Dynamic predictions: oscillations and
synchrony in top-down processing. Nat Rev Neurosci. 2001;2:704-16. Review.
7. Hill EL, Frith U. Understanding autism: insights from mind and
brain. Philos Trans R Soc Lond B Biol Sci. 2003;358:281-9. Review.
8. Brock J, Brown CC, Boucher J, Rippon G. The temporal binding
deficit hypothesis of autism. Dev Psychopathol. 2002;14:209-24.
9. Loddo, S.“ Autism: multiple genes acting on a distributed neural
target?” Canadian Journal of Psychiatry. 2004;49: 219-220. Letter.
10. Just MA, Cherkassky VL, Keller TA, Minshew NJ. Cortical
activation and synchronization during sentence comprehension in high-
functioning autism: evidence of underconnectivity. Brain 2004;127:1811-21.
11. Spratling MW. Cortical region interactions and the functional
role of apical dendrites. Behavioral and Cognitive Neuroscience Reviews.
12. Fatemi SH, Snow AV, Stary JM, Araghi-Niknam M, Reutiman TJ, Lee
S, Brooks AI, Pearce DA. Reelin signaling is impaired in autism. Biol
13. Mukaetova-Ladinska EB, Arnold H, Jaros E, Perry R, Perry E.
Depletion of MAP2 expression and laminar cytoarchitectonic changes in
dorsolateral prefrontal cortex in adult autistic individuals. Neuropathol
Appl Neurobiol. 2004;30:615-23.
Competing interests: No competing interests
Limits of the underconnectivity theory of autism
A reader of this E-forum has sent me a comment, in which he relates
the underconnectivity theory of autism with what I have suggested in my
previous rapid responses about the pathogenesis of the disorder. This
colleague refers to the newly emerging concept that local
hyperconnectivity coupled with distant underconnectivity of brain
organizations could be the basis of autistic symptomatology.
I have been reading a few interesting articles in support of the
underconnectivity theory of autism [see for example references 1 and 2,
although the points of view of the two research groups do not coincide
completely]. Very briefly, this theory entails that brain computational
centers work in a less synchronized way in autism, especially when higher
- order integrative functions are at stake. Dynamic imaging studies have
been conducted which support this theory, and I have been taking these
results as a confirmation of what clinicians have been inferring until now
from the observation of the behavior of persons with autism, id est the
presence of a deficit in the multiple parallel processing of receptive and
executive data .
However, there are some aspects of normal brain functioning and of
autism which the underconnectivity theory seems unable to explain. I will
quote some of them.
1) How in individuals without autism (hence with a diffusely good
neural connectivity) are computational centers involved in the processing
of a specific perceptive and/or motor and/or speculative task included in
the synchronous web of active processing while unnecessary centers are
2) How are previously excluded neural areas flexibly reintroduced in
that web when the individual is coping with a new task, a task which is
completely different and requires the contribution of different areas?
Think about shifting from observing an event which happens in one
particular site, to listening to a dialogue taking place elsewhere, to
speculating on the two perceptions while filtering out the data which are
still coming from both of them.
3) How can normally developing children so rapidly and precisely
change their operational targets, in strict connection with the requests
of the environmental and/or as the result of their free choice, while
children with autism show variable levels of impairment in this ability?
In autism, variations in the control of attentional shifts and probably of
thought processes seem to range from a virtual absence of control to less
readily detectable impairments. Nonetheless, it is reasonable to assume
that a certain ability to modify patterns of neural arousal, with a shift
in the distribution of neural connectivity is possible even in individuals
with autism, and especially in high functioning individuals, albeit much
4) How can the underconnectivity theory account for the frequent
phenomenon of altered sensitivity in autism? Normal individuals are able
to regulate the intensity of all but the most strong and abrupt variations
in their perceptions of the environment, and even some physical pain can
be less disturbing when the average individual is involved in an absorbing
intellectual, emotional, or physical task.
It becomes then necessary to think about connectivity not as a stable
quality of neural organizations, but as a phenomenon subject to goal -
I think that, to explain normal brain functioning and the autistic
dysfunction, we must draw the underconnectivity theory nearer to the weak
central coherence theory. We must presume that a smooth and rapid change
in the distribution of neural connectivity in normality is driven by the
active intervention of a modulatory circuit. My opinion is that it is
precisely this circuit that is out of order in autism. Two consequences
would derive from this impairment: a reduction in the extension of the
online web of synchronous neural arousal, wherein higher order
computational centers will be less represented, and a slower ability of
the same web to reconfigure itself following the continuously changing
requests stemming from the environment or from the willing self. In fact
this ability to synchronize, connect, activate, filter out and exclude
neural organizations could be the main factor of our physiological ability
to perceive ourselves with a distinct sense of personal continuity and
identity and a sense of independent choice.
A deficit in the coordination of neural functions in autism could act as
the “bottleneck”  that narrows the passage from lower-complexity brain
activities (e.g. the reproduction of visual images by primary cortical
areas in the occipital lobe) to higher-complexity brain activities (the
transformation of those images into more meaningful abstractions by the
fusiform gyrus and related circuitries).
It is possible that mechanisms for distinguishing internally
generated data from data coming from the five senses are included in the
functions of this modulatory circuit. This would explain the genesis of
the hallucinations of individuals with schizophrenia, and of the
hallucinations supposed to be present also in persons with autism. The two
pathologies would differ because in autism this putative dismodulation
would start very early in life, probably under the overburdening effects
of a rapid increase in the maturation of brain organizations and of their
hard-wired connections to the whole brain apparatus, while in
schizophrenia a breakdown of central integration would take place during
the final phases of enlargement of the computational potential of the
human brain, when the last cortical areas become part of the whole
Neurobiological findings such as macrocrania, an increase of white and
gray matter and the minicolumnar changes in the cortex  might be
explained by a reduction in the physiological, pre-programmed neuronal
death, which could be related to the underfunctioning of this integrative
and maybe onthogenesis – regulating circuit.
This meta-circuit might be extensively distributed in the brain, and
linked with the prefrontal cortex, where plans for actions are constantly
produced and adaptively modified; with the temporal lobes, where previous
and actual aversive situations are detected); with the cerebellum, which
might actually configure the web of arousal depending on signals coming
from the other nodes of the system; and with the thalamus, where the
monitoring and regulation of sensory inputs might take place.
1. Just MA, Cherkassky VL, Keller TA, Minshew NJ. Cortical activation
and synchronization during sentence comprehension in high-functioning
autism: evidence of underconnectivity. Brain 2004; 127: 1811-21.
2. Belmonte MK, Allen G, Beckel-Mitchener A, Boulanger LM, Carper RA,
Webb SJ. Autism and abnormal development of brain connectivity. J
Neurosci. 2004; 24: 9228-31.
3. Loddo, S. An attempt to define the core dysfunction of autism.
Autism, (2004); 8, 335-336.
4. Castelli F, Frith C, Happe F, Frith U. Autism, Asperger syndrome
and brain mechanisms for the attribution of mental states to animated
shapes. Brain. 2002. 125:1839-49
5. Casanova MF, Buxhoeveden DP, Switala AE, Roy E Minicolumnar
pathology in autism. Neurology 2002 58:428–432
Competing interests: No competing interests
There seems very little enthusiasm for the professionals to connect
autism to brain damage. I have previously shown how they are related. If
brain damage has some connection with individuals who have autism or show
aspects of the condition, then should they be prescribing psychotropic
drugs as suggested by Dr P V Finn Cosgrove? Clinical trials of these drugs
have not included children or those with brain damage.
My daughter was placed on psychotropic drugs at the age of ten years.
This was because the psychiatrists who ‘control’ those with ‘learning
disabilities’, could not see beyond the ends of their noses. They had no
conception what it was like to be brain-damaged at five months of age; or
of what the neurological consequences might have been. Nor did they stop
to wonder for a moment what the effect of these drugs might be on one
whose neurological functioning was abnormal.
I sometimes wonder what it is really like to be the person who is my
daughter. In a world that has robbed her of many of the connections that
we expect to have in place, she has to find some solid ground on which she
can walk with certainty. She is unable to create this for herself and
relies entirely on others for her safety, security and peace of mind. Yet,
constantly, the ground is dug out from under her feet and she finds
herself falling, she grabs at anything that might keep her upright and
doing so may well pull other things down. Then she has to say sorry for
things that she can’t help, without knowing how not to have them happen
The fear of rejection or abandonment is around every corner, yet she
is not able to determine how to prevent it. Sleep for her might be a haven
of peace, the only place in the day where she does not have to worry about
what people think or how they might react. But even this haven, this
single place that we all believe to be a right, is taken from her by the
forces of medication. She finds her day to be at a divergence from that of
others, a bizarre collection of hours that have no connection.
She seeks release in things that are soothing and repetitive and this
then becomes a circle of entrapment, a rotating disc, the movement of
which, at first enjoyable, becomes a sinister whirligig from which there
is no escape except by someone who recognises her plight and changes the
path. Everyday she must wonder what she has to do to get things right and
every day she finds there is no answer. Pleasures are peripheral and
always at someone else’s whim or design. She can never plan for tomorrow
because tomorrow is as far off for her as next year or next century. All
she has are her memories of the past and so many of them have been bad
She makes constant demands upon all of those around her, demands that
do not originate from selfishness but as a result of her brain damage;
from the denial of an ability to do things for herself, to be autonomous.
In having to rely so much upon others she becomes an instrument for them
on which to practice. They are not judges, as she is, whether they get
things right. So, right or wrong she has to submit to interpretations of
her desires and live with whatever results.
Father of a daughter who has brain damage and autism
Competing interests: No competing interests
First of all I wish you were right about the "Autism Lobby" being
powerful. In 2003, in the US alone, the pharmaceutical companies spent
more than $400 Million on lobbying congress and they had a ratio of 1.2
paid lobbyer per congressman. Parents of autistic kid cannot afford that
kind of lobbying because: a) they are busy recovering their kids with
expansive treatments that are not covered by medical insurance, b) they
are busy reading scientific articles about autism since most doctors dont
read them and c) an autistic kid take more of your time at home to
confort, heal and direct. Basically, most parents like me are exhausted,
and lack sleep.
I strongly disagree with you about early diagnosis and treatment. It
can make a difference between an autistic kid that will recover and have a
full life and one that will never recover and spent his whole life in an
From my experience as a parent of an autistic kid, I wish that I knew
that my kid was autistic at 13 months instead of 18 months. After the MMR
and 4 other vaccinations, my son regressed. He stoped talking, had a hard
time sleeping at night, stopped smiling and going to the door when I was
entering home. He just stayed in a corner and played with the same toy.
That difference of six month would have made me 1) stop the regular
vaccinations at 18 months which made him worse, 2) started reading and
understanding autism early, 3) started the gluten-free casein-free diet
early enough to make him sleep through the night and be ready to learn
during the day and most importanly 4) started the ABA (Applied Behavior
Threapy) at 13 months instead of 20 months. The difference in the recovery
is huge. He would have been recovered by 3 years old if I had started
therapy by 13 months. Now, it will take until five or six years before he
will be fully recovered.
My kid (20 months at that time)started ABA therapy at the same time
than a four-year old kid. After just two months, my kid started already
taking again as compared to the four-year old kid. Go to any respectable
ABA therapy center and ask around. It takes much longer to rehab kids who
start late than kids who start early. You can teach a kid how to learn,
ask , interact much easily if the kid is young enough.
Early diagnosis and intervention (Diet and ABA, no drugs) is up to
now the only thing that can make a difference in the life of an autistic
Parent of an autistic kid
Competing interests: No competing interests
Dr P V Finn Cosgrove writes that:
“What matters as regards the Diagnosis of Autism is that research
into Autism can only take place, and research can only advance the
treatment of this disorder, if and only if it is AUTISM which is being
studied and not Autistic Spectrum Disorders.”
As I have pointed out before, there is a difference between autism of
genetic origin (classical autism) and autistic spectrum disorder, or
whatever other notation is used to encompass the disability caused by
brain damage to the centres in the brain that then bring about some of the
symptoms of autism.
Another concern is the idea that autism of whichever sort needs to be
‘treated’ at all. I cannot understand how the basic condition is
treatable. Co-morbidities that arise may well require treatment, but in my
view the original condition is untreatable. Has anyone ever been able to
‘treat’ autism successfully?
Father of daughter with brain-damage-induced autism
Competing interests: No competing interests
A mother of a person with autism affirms in her communication to this
Journal "I often tried to tell my son's teachers that language is a second
language to him". Parents very often offer us useful insights on mental
functioning in the autistic spectrum disorders (ASD). Language, similarly
to other higher order abilities, is rarely if ever fully automated to the
level of a spontaneous ability in ASD. When listening to these children
and adolescents we perceive a lack of global control on fluid and prosodic
utterances. Many persons with ASD speak through an effortful process which
is probably run in a piece - meal "analytical" way every time the
individual tries to communicate. Seemingly in order to a simplify the task
of speaking, even some high-functioning individuals with AD concentrate on
partial elements of language, are slow in finding contextually appropriate
words, use a simple syntax and tend to exclude prosody. The production of
syntactically more elaborated, ready - made phrases, often derived from
the repetitive listening of videocassettes does not signal the acquisition
of a flexible, goal-calibrated grammar. Some individuals with ASD and an
average or above-average verbal I.Q. develop an intriguing expertise in
building up and verbally transmitting their knowledge about their
preferred topics, but the rich lexicon they show is usually confined to
these topics, while the pragmatic aspects of their language and their
social exchanges are usually impaired.
The process of "learning" entails the acquisition of new data and a
transformation on them. Both declarative and procedural knowledge require
an elaboration of the neurally processable material before proceeding to
storage. In the case of declarative knowledge, for example, an upward
movement toward the formation of categories brings about a clearer, more
reasoned view of our environment. Analogously, an integration of simple
procedures into more complex schemata of action allows us to be more
efficient every time we rehearse and apply those procedures. We appreciate
this in every field, from driving to diagnosing, to socially relating.
In the case of ASD, these processes of categorization and
automatization are probably hampered. It is also possible that the smooth
access to procedural and declarative neural reservoirs, where incoming
data are supposed to inform dedicated circuitries, is less efficient in
persons with autism. This could explain motor clumsiness (especially for
complex movements), difficulties in language, and, at least partially,
lack of spontaneity in interpersonal relationships, as social scripts must
themselves be automated through expertise, rehearsed and adapted online,
while acting. So, it may be the case that persons with ASD are capable
only of a partial transformation of inputs, especially of the more complex
ones, and have to adjust to the use of alternative procedures when
remembering, thinking and acting. Some high functioning persons with
autism speak of their ability to rehearse entire sequences of scenes they
observed, like playing a videotape in their minds, while they are unable
to comment or even mentally elaborate upon the same sequences in reality
and in real time.
Recent studies by Keysar et al.  and by Epsley et al.  suggest
that normal adults use their "Theory of Mind" abilities as an option, and
not as a permanently installed ability. An economic principle seems to
dictate the use of the lowest level of mental energies and the fewest
neural modules for a particular task: only a part of all our mental
faculties are used when we are manipulating perceptual, speculative and
motor data. Selective attention may be but one aspect of this regulating
principle, either in the form of focusing on a specific group of elements
in our attentional field and/or considering only the surface of them.It
may be the case that while persons without autism process information
similarly to the person with autism in certain circumstances, making a
sectorial and isolated use of brain circuits, an easy reversibility of
this kind of processing is what distinguishes normal functioning from
functioning in ASD.
So we use echolalia to keep in a stand-by position a phrase we heard after
our brain had already started processing another important mental task.
Once the latter task is accomplished, we are free to examine the meaning
of that phrase. We happen to apply our mindreading abilities and recognize
the necessity of taking into consideration our interlocutor perspective, a
few seconds after detecting that we have made an egocentric error in
judgment. In this latter case, additional neural circuits are activated in
order to reach a broader view and a deeper understanding of a particular
(social) situation. In a sense, this dynamic progression toward a wider
computing power, which is detectable even in normal adults, reflects
onthogenesis (the progressive maturation and enlargement of available
neural circuits during the development of the child, particularly along
the cerebello-prefrontal axis) and phylogenesis (the increasing
complexities of nervous systems, from lower species to humans).
We eumetrically avoid painful feelings, thoughts and insights, when
we make use of so-called psychic defenses. A basic role of the cerebellum
in the regulation of mental processes has been advocated recently [3, for
a review]. While a dysfunction of the cerebellum as a part of a wider
integrative system  could explain the above mentioned autistic deficits
in transforming experiential data into higher-order data and in accessing
them with rapidity and precision, a well functioning integrative system,
under the aversive influence of structures like the amygdala in the
temporal lobe could explain the unconscious barrage to uncomfortable
Temple Grandin, an introspective high-functioning person with autism,
affirms : "In my mind there is no subconscious. Images are constantly
passing through the computer screen of my imagination".
1. Keysar B, Lin S, Barr DJ. Limits on theory of mind use in adults.
Cognition, 2003, 89:25-41.
2. Epley N, Morewedge CK, Keysar B. Perspective Taking in Children and
Adults: Equivalent Egocentrism but Differential Correction. In press.
3. Habas C. The cerebellum: from motor coordination to cognitive function.
Rev Neurol (Paris), 2001, 157:1471-97.
4. Loddo, S. "The causes of autism and schizophrenia" Rapid response to
Szatmari: "The causes of autistic spectrum disorders" Electronic British
Medical Journal, 2003, http://bmj.com/cgi/eletters/326/7382/173#33854.
5. Grandin, T. Genius May Be an Abnormality: Educating Students with
Asperger's Syndrome, or High Functioning. Autism.
Competing interests: No competing interests
Dr. Silvio has a deep understanding of autism. I often tried to tell
my son's teachers that language is a second language to him. He has always
seeked input visually and through music, which do not ask for
integration.The visuo-spatial aspect is true, also. At four years old, my
son tested as a ten year old..., but was borderline MR in most other
aspects.His IQ now at age 10 is about 120.
I would not hestitate to say that autism is a way of being as opposed
to a disability. To those able to adapt to this world, ie, those having
fewer autistic traits, often... can enjoy "success" in a neurotypical way,
often exceeding their peers.
I also have a nephew who never had a label. He is in the ninth grade
with "A+" grades typically. He used to obsess on vaccuum cleaners, line up
his toys, and has always appeared to be morbidly shy. I think he will be
Parent of ASD child
Competing interests: No competing interests