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coolblue

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Everything posted by coolblue

  1. It's a 'tic' - well, the word you want is 'tic' - don't know if the movement is or not. This could be due to a compulsive movement - or it could be a way of regulating balance. Ds's speech therapist advised us to allow ds to move around, rather than sit still, when he was having stories read to him, because the balance system is part of the ear and activating it the part of the brain that processes balance can also activate auditory processing. Don't know whether or not her theory is right, but it certainly dramatically improved his ability to concentrate on what was being read to him. Ds moves up and down (as you say, bouncing), rather than to and fro, but he still rolls his head from side to side when he's tired - has done since he was a baby. My guess is that the best way to deal with it is to channel the movement into something socially acceptable - pacing up and down, for example. cb
  2. Quite right too; but wikipedia can also be more reliable than any encyclopedia because world experts can update it on a daily basis, and it's an excellent place to start looking for original source material. cb
  3. The American Psychiatric Association, who publish DSM, think it, too, and you'd expect them to know. http://www.dsm5.org/ProposedRevisions/Pages/proposedrevision.aspx?rid=97 cb
  4. It does mean that, but some therapies have been shown 'not to work' with autistic people in general, when there is evidence that they do have an effect on some individuals. Since autism can have different causes in different people, we need to be pretty clear about what makes an intervention 'obviously' snake oil. cb
  5. Since we don't know what causes autism, I don't think you can dismiss proposed 'cures' as 'obviously' snake oil. And autism can be a challenge that some families rise to admirably, and can destroy others. Depends on the child, the parent and the family circumstances. cb
  6. I have read some of Barry Carpenter's thoughts on this previously, and I wholeheartedly agree with what he has to say about the SEN system (apart from maybe children with ASDs being 'visual learners') I was aware that the number of children with complex difficulties was on the increase because of improved survival rates at birth (has been for some time). I'm just unclear as to what the differences are that he is talking about. For example he mentions children with foetal alcohol syndrome not having a parietal lobe. Given human nature I find it difficult to believe that foetal alchohol syndrome is anything new, and damage to the parietal lobe can arise due to hydrocephalus and epilepsy and strokes. I suppose I'll have to wait for the report. Thanks for letting us know it's coming out. cb
  7. Are you sure, because the only Barry Carpenter I've been able to find involved in this field has had a career in education? http://www.sst-inet.net/about_us/our_partners/academics/professor_barry_carpenter_-.aspx Do you have a link to this guy? That means we've had 40 years of experience of educating children with complex disabilities. I'll be interested to see what's new about the new generation. Sorry to be sceptical, but I get a bit suspicious when people start talking about brain 'wiring'. cb
  8. I certainly agree that there's a need for a fundamental re-evaluation of diagnostic models and educational models, as the current ones we have are not, and have never been, fit for purpose. I wonder what they will recommend instead. I haven't read the report obviously, but the press coverage looks a bit like the news items about the 'unprecedented' weather we had in the UK in the past winter. Yes, premature babies are surviving better and yes being born pre-term can lead to developmental problems, but I'd be interested to know what journalists think happened in the days before antibiotics and when 'childhood illnesses' were commonplace and left children deaf, blind and brain damaged on a regular basis. cb
  9. Except they are not looking at things like urinary peptides (or anything else for that matter) in individual children, but in potentially heterogeneous groups of children with 'autism'. I've lost count of the number of lines of enquiry that have been abandoned because of inconclusive or contradictory findings - which is what you would expect if your experimental group is heterogeneous. The point about the PKU finding was not that the guy was using that specific technology but that he was systematically testing the urine of two siblings to find out what was causing their problems, not everybody's problems. cb
  10. I agree. As long as researchers aren't looking for one-cause-explains-all. If they are, this line of research will also be prematurely abandoned, like many others. No, I'm talking about differences in signs and symptoms at a low-level of complexity; like eye movements, echolalia, hypermobile joints. Almost all the signs and symptoms in the DSM (pick a disorder, any disorder) are at a high level of complexity. Social interaction, communication, attention, reading, writing; they are each hugely complex sets of behaviour brimming over with variables that you need to control for if you are to find out anything useful. Take something like gluten-casein intolerance. Many parents of children on the autistic spectrum have reported positive changes to their children's behaviour on a GFCF diet. But when you look at the GFCF-autism research, you find that participants have been lumped together on the basis of a diagnosis of autism, that gluten and 20-odd caseins have been lumped together as well and that individual differences in urinary peptide levels are reported but have been ignored. Even though they might be telling us about variations at the molecular level (can't get much less complex than that) they often aren't even included in the data. The individual differences could be key. If kid A can't metabolise casein A, that could have significant implications for his or her (and lots of other kids') functioning. It could result in a developmental pathway that cascades into autistic characteristics. Kid B might not be able to metabolise casein B for completely different reasons, and that could result in another developmental pathway that also cascades into autistic characteristics. The reason I cited PKU was because the cause of the complex 'mental retardation' in a sub-group of children was discovered because one mother noticed that her children's urine smelled musty, and supplied a researcher with urine samples to test. If he had adopted the methodology current in autism research, he would have got samples from a group of children with 'mental retardation' and found that their urine turned different colours when tested with ferric chloride and concluded therefore that ferric chloride was not an effective indicator for mental retardation.
  11. In whom is there not a single structure involved? In whom are there characteristics at the microscopic and neurochemical level? In all people with autistic traits? In some? I understand that. The reason I referred to Fragile X and PKU in the first place is that neither causal factor was discovered by looking at signs and symptoms at a high level of complexity, such as 'autism' or 'mental retardation' and trying to find out what low-level genetic mutations or metabolic variations people with those signs and symptoms had in common. Both were discovered by looking at low-level differences. Referring to environmental factors or genetic susceptibility isn't an explanation of anything. I'm not suggesting it is. All I'm saying is you can't rule out environmental factors until they have been definitively ruled out. Well, quite. How can you develop a testable hypothesis from something as complex as 'autism'? cb
  12. Sorry, misread your question. I thought the pathway in the full version was full of pitfalls; it assumes that a subjective diagnosis can have a degree of 'certainty'; it relies on the co-operation of different agencies, and on the involvement of other services - when people in other services are often sceptical about the very existence of autism.
  13. I agree it overlooks the reality of the situation in several ways, not just the one you've mentioned. I'm sceptical about the value of a diagnosis per se. I think it would be much more useful just to cut to the chase and draw up an individual profile for the child (the second stage they recommend).
  14. How has this assumption been arrived at? What grounds are there for making it? Assuming that everybody diagnosed with autism has a brain 'abnormality' (which I think it's fairly safe to assume because it's the brain that deals with social interaction, communication and the regulation of behaviour) that brain abnormality can have one or more of three primary origins: the neural substrate - the way the structure of the brain initially developed; the brain physiology; and the quality of information going into the brain. The information is ultimately sensory information - either from internal or external sources - and if it's impaired, because of abnormalities with sense organs for example, that impairment will affect the structure and function of the parts of the brain that process it (or don't process it, depending). In spite of the fact that many people diagnosed with autism have sensory processing abnormalities, it's always assumed that those abnormalities arise in the brain, rather than outside it. I don't think that's a safe assumption to make either. We can't rule anything out until it's been ruled out. And the reason we can't fully explain pathogenesis is because, IMO, everyone is after the holy grail of the cause of autism in general, rather than what is causing autism in individuals. Somebody finds an abnormal corpus callosum and looks at more corpora callosa (if that's the correct plural) and finds the others are all normal - so abnormalities of the corpus callosum are assumed not to cause autism. Then somebody discovers an abnormal cerebellum, and then that other cerebella are either normal or abnormal in different ways, so autism can't be caused by cerebellar abnormalities. Environmental factors are going to impact at every step of the pathway from genome to phenome.
  15. It's not just the parents, baddad. In the draft NICE guidance on diagnosis of autism spectrum disorders - all 250 pages of it - they talk about the certainty of a diagnosis. This is a subjective matching against some rather vague criteria they are talking about. They even have some complex stats relating to its reliability. cb
  16. Different areas use different pathways for diagnosis. Ring up and ask them about how they use their database. cb
  17. Why Fragile X - is it because of the nature of the signs and symptoms it results in? Why could it not be causative of autism? I get the impression that you are assuming that autistic characteristics have a common cause at some level - brain structure or function perhaps - a 'fan in - fan out' model. Am I right? That's one possibility. However, there are other possibilities. I don't think it's safe to assume that autistic characteristics emerge from a gene-brain structure/function-autistic characteristics pathway. Genetic and environmental factors could cause problems with the input of sensory information - a pathway that could lead to brain abnormalities via development and a pathway that is widely ignored in autism research. Agreed. And that is largely because we are assuming that all people with autism have a shared physical difference at some point in the genome-phenome pathway. Given the wide phenotype I don't think that's a safe assumption. You can categorise signs and symptoms at different levels of complexity. 'Respiratory disorder' - a diagnosis at a high level of complexity - is fine for some purposes - hospital admin or a press release for a celebrity. However, you would want to get to a lower level of complexity in order to treat the disorder. A GP might make a diagnosis by exclusion of a viral infection, for example. That's more specific than 'respiratory disorder', but it doesn't tell you what virus is involved. Most of the time you wouldn't need to know. If it's important - there's a serious viral infection going round and you need to know about cases - then you could go to a lower level of complexity and identify the strain of virus. You would make a distinction between groups according to specific symptoms only as a provisional measure until you had figured out the cause of the symptoms. It could be that they all have the same cause - or that the causes are different. I have no problem with 'autism' as a label indicating the type of behaviours involved. However, a diagnosis at this level of complexity is no use whatsoever when it comes to supporting an individual - you would need to know precisely what that person had difficulty with and what their health issues were. Nor is it any use for research purposes - if you are investigating specific low-level traits like lack of eye contact or echolalia. In such cases you would want to look for sub-groups within the autism diagnosis. Going back to PKU - it wasn't the 'mental retardation' outcome of PKU that led to the discovery of its cause - it was the musty smell of the children's urine that led to urine samples being investigated. If all children with 'mental retardation' had been investigated as a group, PKU would still be undiscovered, I suspect.
  18. The three behavioural domains that make up 'autism' are all highly complex. That means that there are many potential routes to their disruption. Sometimes a single gene can express itself in many different functions. Sometimes the expression of many genes converges on a single process. Depending on the processes a gene is involved in, it's possible for one gene to cause autism (as in PKU or Fragile X) or for several genes to cause it. The problem is with the concept of 'autism'. Yes, some people do meet the criteria for autism, but that doesn't mean they have 'a' condition which we happen to call autism. What they have is outcomes of their gene expression or physiology that result in disruption to certain aspects of their behaviour. A diagnosis of 'autism' is akin to a diagnosis of 'respiratory disorder'. There's no doubt that patients with respiratory disorders could all have a cough, difficulty breathing and fluid on their lungs. It doesn't mean they all have the same thing wrong with their breathing apparatus. 'Respiratory disorder' is a useful label for some purposes, but no self-respecting medic would stop there when trying to find out what was causing a patient's health problems.
  19. The recent NICE guideline http://guidance.nice.org.uk/CG/Wave15/78/Consultation/Latest says that 60 medical conditions are associated with autism. Gillberg & Coleman in " The Biology of the Autistic Syndromes" (1992) list dozens of such associated conditions documented as co-occurring with a diagnosis of autism. I know 'associated with' doesn't mean 'causing', but since the conditions include abnormalities in all but three chromosomes and a bunch of viral infections you do wonder. What concerns me is why possible links between known medical conditions and autism are no longer the focus of attention, as Baddad points out. cb
  20. I think there are real problems in trying to define autism in its 'strictest and purest sense'. Autism is a construct invented by a psychiatrist (Eugen Bleuler) to describe the self-absorbed characteristics seen in schizophrenia, and later applied to two groups of children by Kanner and Asperger. In Asperger's cases the children were very similar to each other in their behaviour; in Kanner's cases they were very varied. The reason both of them thought that the children's difficulty with social skills was a core issue was because both Kanner and Asperger were using a psychodynamic model of human behaviour, in which social interaction was a central feature. Kanner saw the children's difficulties in feeding as infants as part and parcel of their social interaction. Nowadays any language difficulty experienced by a child that had previously had such difficulty suckling that they had to be tube-fed would not be attributed to a problem with social interaction (I hope!), but to a physical problem, possibly with the facial nerves or muscles. The physical characteristics that accompany the behavioural features of autism are essentially overlooked because autistic spectrum disorders/conditions are defined in behavioural terms and classified as 'mental' disorders. This is not a satisfactory state of affairs in my view. cb
  21. Me too. Autism is a description of certain aspects of behaviour. The same genetic disorder could underlie both the autism and the learning difficulties in some people. I think the method of classification is at fault AND our understanding is at fault if we assume that a descriptive term for aspects of behaviour is necessarily a symptom of a distinct, single condition. I was stunned to find IQ still being used as a measure of anything - the sub-tests are useful, but the overall score is more or less meaningless.
  22. Hi kelly Making errors with pronouns is common in autistic spectrum disorders. So is repeating the same phrase over and over. So is not answering questions or changing the subject or talking about things you've never experienced (the frogs in someone else's pond). And visual and auditory processing difficulties. He was in a new environment with someone he didn't know and quite likely experiencing sensory overload. I'm glad they are getting on with the assessment. It sounds as if they got quite a lot of responses from your boy, so will be able to form a clear picture of his areas of difficulty. If it's any consolation he sounds exactly like my son at the same age, who is now a quirky 12 year-old with a lot of issues to cope with but great company and bright and entertaining with a dry sense of humour. This was a kid who said nothing at all some days when he was little and never showed much interest in anything except books. Actually, he's still not interested in much apart from books. Hope it all goes well next week. cb
  23. Hi Cait A diagnosis of an ASD is an *exclusion* diagnosis. That means it's a label applied to the child's symptoms after conditions known to cause autistic characteristics have been ruled out. It isn't a diagnosis in the same way that, say Down syndrome or Fragile X is a diagnosis, it's a label that says 'this child has these kind of symptoms but we don't know what causes them'. Before my son was diagnosed with ASD his paediatrician gave him a battery of blood tests to rule out other conditions - which is what should happen, because there are at least 60 known conditions associated with ASD-type symptoms. It's important to rule these out, because if a child has a known genetic or metabolic disorder, then doctors will be aware of other health issues associated with them, and will be able to offer appropriate advice, support and treatment. cb
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