A few weeks back I had the pleasure of an email conversation with Dr Gary Mesibov on the topic of one of his recent papers titled: 'Evidence-based practices and autism'. Some with an interest in autism will know Dr Mesibov is the current Director of Division TEACCH at the University of North Carolina at Chapel Hill.
Although brief, my main reason for contacting Dr Mesibov was related to his views on the use of evidence-based practices guiding good autism practice. Readers may know that this is a topic particularly relevant to the UK following the announcement that NICE are formulating guidelines on best autism practice for children/young people and adults.
Dr Mesibov's recent paper on evidence-based practice (EBD) is an intriguing look at the history, formulation and current guidance on EBD in Psychology and Education fields and how it may/may not relate to autism spectrum conditions. Some of the EBD guidance included in Dr Mesibov's paper, from the very mysteriously titled 'Division 12' group (an off-shoot of the American Psychological Association), can be found here (see Tables 1 and 2).
Without wishing to plagiarise Dr Mesibov's work, the main elements of his writings, as I interpret them (which may be a bias in itself), are: (a) much of the guidance on EBD whilst interesting, has not been applied specifically to autism; (b) that which has been applied, suggests that very few, if any, interventions for autism make the grade - see the recent post on evidence lacking for autism interventions; (c) one of the main reasons why autism research does so badly is because of the difficulties in ascertaining long-term positive outcome following intervention; (d) the large heterogeneity in autism does little to improve the situation; (e) the use of the randomised-controlled trial (RCT) methodology, whilst useful for looking at the manipulation of one variable, loses some of its 'applicability' when applied to more comprehensive intervention programmes that contain multiple components, as many of the educational and behavioural interventions for autism might.
I might add that his overall conclusions are not 'anti-EBD'; indeed quite the contrary. He does however suggest a slightly modified EBD regime which covers many of the points raised above.
To many people, I am sure that some of the points Dr Mesibov raises would be considered heresy. The RCT is after all at the top of the evidence tree (if I was to be a nit-picker though, I might argue that it is topped by the meta-analysis or even the meta-analysis of a meta-analysis). But think about it: suppose you want to examine an educational intervention which might have 6 or 7 important parts to it which may need to be delivered slightly differently according to the person they are being targeted at. How do you formulate a good RCT around that? I might also add that others in autism research have also questioned the usefulness of the RCT (this time applied to ABA).
Don't get me wrong. I am a big fan of the RCT; particularly when you have one intervention/drug/analyte and are comparing them between homogeneous groups. Want to look at the effects of an antibiotic on a particular strain of bacteria? The RCT is your man or woman.
The question is whether RCT applied to a heterogeneous, behaviourally-defined condition looking at multi-component educational or behavioural intervention is necessarily the best course of action? I think the US Agency for Healthcare Research and Quality has already made its mind up (see page 11) although nice to see that the art of medicine might also come into intervention decisions as per my previous post.
Thursday, 7 April 2011
Wednesday, 6 April 2011
Don't give me evils..
Another quick post (honestly!). The title of the post will be recognised by most of the UK audience as taken from Little Britain and everyones favourite 'chav' Vicky Pollard.
Anyway, I stumbled across an article in today's Independent online titled: Why a lack of empathy is the root of all evil.
The article discusses a new book from Prof. Simon Baron-Cohen called 'Zero degrees of empathy: a new theory of human cruelty'. Most people connected to autism will have heard about Prof. Baron-Cohen's theories on empathy and autism. The article has attracted some interesting comments.
That's all.
Anyway, I stumbled across an article in today's Independent online titled: Why a lack of empathy is the root of all evil.
The article discusses a new book from Prof. Simon Baron-Cohen called 'Zero degrees of empathy: a new theory of human cruelty'. Most people connected to autism will have heard about Prof. Baron-Cohen's theories on empathy and autism. The article has attracted some interesting comments.
That's all.
Tuesday, 5 April 2011
Prevalence and incidence of autism in Taiwan
Only a quick post this one on what is a gorgeous sunny day outside.
An early first article has appeared on-line at the Journal of Child Neurology titled: Prevalence and incidence of autism spectrum disorders among National Health Insurance enrollees in Taiwan from 1996 to 2005.
It is another look at the numbers of autism spectrum conditions but this time from a country outside of the "Western, industrialised" team. The main findings are that prevalence of autism, as measured by health service use, increased between 1996 and 2005 from 1.79 per 10,000 to 28.72 per 10,000 in Taiwan. More importantly, incidence (often a point of contention in autism) increased from 0.91 to 4.41 per 10,000 per year from 1997 to 2005. The greatest increase in incidence was in the 0-5 year age group (males).
What does it all mean?
Well, first of all it suggests that the numbers of cases of diagnosed autism were rising, and seemingly rising pretty fast in Taiwan over quite a short period of time (less than 10 years). It also suggests that the risk of being diagnosed with an autism spectrum condition was also increasing; again over a comparatively short period of time.
The fact that increasing incidence was noted for the younger age group (0-5 years) is important because it means that risk of autism diagnosis was greatest for this younger age group. This might have some implication for suggestions about increasing numbers being partially due to diagnosis in later childhood or adulthood (I stress 'might').
The authors of the Taiwan study also mention higher incidence in urban areas which could also be of some interest (whether due to geographic service provision or a role for some environmental factors).
The down-side to the data: well it was based on a database of service use, which might suggest that it misses cases where such services are not used (or not reported to be used); hence representing an under-estimation of cases (I don't know enough about the Taiwanese healthcare system to comment further).
It also looks like they did not go out and confirm the accuracy of the diagnosis, rather reliant on assessments for autism being accurately completed (although other papers from Taiwan suggest diagnostic provisions should not be under-estimated). I talked about diagnosis and diagnostic stability previously.
As the years push on and we spend longer with our current ICD and DSM diagnostic manual versions - nearly 20 years with each manual, it should mean that we start to get a clearer picture on prevalence and incidence worldwide without interference from things like changing diagnostic criteria.
If, as appears to be the trend, prevalence and incidence of autism is increasing worldwide, serious questions need to be asked about the possible factors governing such a change in numbers and perhaps more importantly, the provisions in place / to be put in place to ensure adequate services for all those diagnosed, particularly in these times of austerity.
An early first article has appeared on-line at the Journal of Child Neurology titled: Prevalence and incidence of autism spectrum disorders among National Health Insurance enrollees in Taiwan from 1996 to 2005.
It is another look at the numbers of autism spectrum conditions but this time from a country outside of the "Western, industrialised" team. The main findings are that prevalence of autism, as measured by health service use, increased between 1996 and 2005 from 1.79 per 10,000 to 28.72 per 10,000 in Taiwan. More importantly, incidence (often a point of contention in autism) increased from 0.91 to 4.41 per 10,000 per year from 1997 to 2005. The greatest increase in incidence was in the 0-5 year age group (males).
What does it all mean?
Well, first of all it suggests that the numbers of cases of diagnosed autism were rising, and seemingly rising pretty fast in Taiwan over quite a short period of time (less than 10 years). It also suggests that the risk of being diagnosed with an autism spectrum condition was also increasing; again over a comparatively short period of time.
The fact that increasing incidence was noted for the younger age group (0-5 years) is important because it means that risk of autism diagnosis was greatest for this younger age group. This might have some implication for suggestions about increasing numbers being partially due to diagnosis in later childhood or adulthood (I stress 'might').
The authors of the Taiwan study also mention higher incidence in urban areas which could also be of some interest (whether due to geographic service provision or a role for some environmental factors).
The down-side to the data: well it was based on a database of service use, which might suggest that it misses cases where such services are not used (or not reported to be used); hence representing an under-estimation of cases (I don't know enough about the Taiwanese healthcare system to comment further).
It also looks like they did not go out and confirm the accuracy of the diagnosis, rather reliant on assessments for autism being accurately completed (although other papers from Taiwan suggest diagnostic provisions should not be under-estimated). I talked about diagnosis and diagnostic stability previously.
As the years push on and we spend longer with our current ICD and DSM diagnostic manual versions - nearly 20 years with each manual, it should mean that we start to get a clearer picture on prevalence and incidence worldwide without interference from things like changing diagnostic criteria.
If, as appears to be the trend, prevalence and incidence of autism is increasing worldwide, serious questions need to be asked about the possible factors governing such a change in numbers and perhaps more importantly, the provisions in place / to be put in place to ensure adequate services for all those diagnosed, particularly in these times of austerity.
The strange case of ICD code F84.8
We all make mistakes. I do however consider myself to be quite a consientious person; checking and re-checking various things in my life (I am one of those people who has to make sure that the gas cooker is turned off every evening before bed, even though I have no history of ever leaving it on).
I did however make a recent mistake on a reply post I made over at autism.about.com run by Lisa Jo Rudy on the topic of 'Atypical autism or PDD-NOS'. The discussion thread was all about labels and diagnoses; to which I posted, what I thought was an interesting point; a reply which mentioned the ICD-10 criteria for autism spectrum conditions which contained a typo. I was corrected, I might add, by someone with sharper eyes than I.
Getting back to my post: I mentioned those peculiar codes of the ICD-10 autism criteria: F84.8 Other Pervasive Developmental Disorder and F84.9 Pervasive Developmental Disorder, unspecified. It has always been a little bit of a mystery to me as to why ICD-10 contains both these two codings. Maybe I should back up a little and show readers what codings are available in ICD-10 pertient to pervasive developmental disorders:
Then our mystery F84.8 and F84.9.
F84.9 PDD unspecified has a description saying that it is a residual category for PDD where there is either inadequate information or contradictory findings regarding diagnosis. F84.8 has no description at all. No description but present - the strange case of F84.8.
If we assume that F84.1 (atypical autism) is equivalent to PDD-NOS (or Autism Spectrum Disorder in the UK) and F84.9 is a catch-all for autism or PDD-NOS where some issue/s are present which do not make diagnosis as clear-cut, we are still left questioning what fits into F84.8.
Looking at the research where F84.8 is mentioned I'm afraid I am none the wiser. This paper, published in BMC Pediatrics on the early detection of autism spectrum conditions in the UK makes reference to the coding. The authors imply that F84.1 is correctly used to determine atypical autism but then go on to say that semantic pragmatic language disorder is also covered under either F84.1 or F84.8 or F84.9. This paper also makes reference to the F84.8 and F84.9 codings but again I don't see the distinction.
I assume that, at the time of the ICD-10 planning, there was some logic as to how these codings would be used. Was F84.8 the 'overspill of the overspill' coding?
To quote from Sir Arthur's greatest invention: "when you have eliminated the impossible, whatever remains, however improbable must be the truth".
I did however make a recent mistake on a reply post I made over at autism.about.com run by Lisa Jo Rudy on the topic of 'Atypical autism or PDD-NOS'. The discussion thread was all about labels and diagnoses; to which I posted, what I thought was an interesting point; a reply which mentioned the ICD-10 criteria for autism spectrum conditions which contained a typo. I was corrected, I might add, by someone with sharper eyes than I.
Getting back to my post: I mentioned those peculiar codes of the ICD-10 autism criteria: F84.8 Other Pervasive Developmental Disorder and F84.9 Pervasive Developmental Disorder, unspecified. It has always been a little bit of a mystery to me as to why ICD-10 contains both these two codings. Maybe I should back up a little and show readers what codings are available in ICD-10 pertient to pervasive developmental disorders:
- F84.0 = childhood autism.
- F84.1 = atypical autism (including some sub-categories for areas of atypicaility).
- F84.2 = Rett syndrome.
- F84.3 = other childhood disintegrative disorder.
- F84.4 = overactive disorder(?).
- F84.5 = Asperger syndrome.
Then our mystery F84.8 and F84.9.
F84.9 PDD unspecified has a description saying that it is a residual category for PDD where there is either inadequate information or contradictory findings regarding diagnosis. F84.8 has no description at all. No description but present - the strange case of F84.8.
If we assume that F84.1 (atypical autism) is equivalent to PDD-NOS (or Autism Spectrum Disorder in the UK) and F84.9 is a catch-all for autism or PDD-NOS where some issue/s are present which do not make diagnosis as clear-cut, we are still left questioning what fits into F84.8.
Looking at the research where F84.8 is mentioned I'm afraid I am none the wiser. This paper, published in BMC Pediatrics on the early detection of autism spectrum conditions in the UK makes reference to the coding. The authors imply that F84.1 is correctly used to determine atypical autism but then go on to say that semantic pragmatic language disorder is also covered under either F84.1 or F84.8 or F84.9. This paper also makes reference to the F84.8 and F84.9 codings but again I don't see the distinction.
I assume that, at the time of the ICD-10 planning, there was some logic as to how these codings would be used. Was F84.8 the 'overspill of the overspill' coding?
To quote from Sir Arthur's greatest invention: "when you have eliminated the impossible, whatever remains, however improbable must be the truth".
Monday, 4 April 2011
Evidence lacking for most autism treatments
There has been some media interest in a series of reviews published in the American Academy of Pediatrics journal 'Pediatrics' on the effects of various medication strategies and behavioural therapies being used with autism spectrum conditions. A link to the relevant abstracts can be found here, here and here. Some viewers may know that this is the same journal that published various guidelines on gastrointestinal issues related to autism a little while back that I touched upon in a previous blog entry.
I initially had mixed feelings about the conclusions drawn from these reviews and the subsequent press coverage. The underlying message seemed to be that for most 'treatment options' there was no convincing evidence that they "actually help kids get better" (their quote not mine) at least in the long-term; although accepting short-term gains for some. Mixed feelings because of how this represents the current state of management and intervention options for (children with) autism - i.e. how little we actually know despite literally millions of pounds, dollars, Euro etc of research money being spent on R&D.
I was however heartened by the call for further research into these areas and also the suggestion that 'best' and 'non-responders' to intervention should be a focus, going back to the notion of autism and n=1. Breaking down what was actually included as part of these reviews, the authors looked at various pharmacotherapies being used in autism as well as various behavioural therapies. Their conclusions were that whilst some interventions seemed to show often quite pronounced positive effects for individuals, very little is known about the factors governing response and the characteristics pertinent to a positive response in the longer term.
Medications used to tackle challenging and repetitive behaviours specific to autism did receive a general thumbs up. Important however was the highlighting of 'side-effects' of said medications; particularly dyskinesia and weight gain following use of drugs like risperidone and aripriprazole. Unfortunately also, the anti-depressant medications didn't fare well; following on from the recent meta-analysis of SSRI use for autism shown here detailing limited effectiveness.
The one area of review that did provide the most convincing findings was related to a lack of general efficacy for the gastrointestinal hormone secretin for autism and a strange call to research it no more - strange because for about 5-6 years it hasn't; or not at least under large-scale controlled-trial conditions. What more is there to say? Well not much really.
I'd like to think that if there are lessons to be learned from these reviews they are these: (1) autism is not autism but autisms - focusing on sub-groups, and more importantly looking at best- and non-responder characteristics to various interventions, is probably the best way forward; (2) 'short-term' gains are important - but longer study periods or follow-up studies are required to see how these gains translate into long-term outcome - how we measure 'outcome' is another matter; (3) co-morbidity is something that perhaps has been given too little attention in autism intervention research - is intervention affecting core symptoms or impacting on peripheral symptoms? Does it make any difference anyway?
All of this is perhaps more fodder for the upcoming NICE review of autism coming to a station near you soon (at least in the UK).
I initially had mixed feelings about the conclusions drawn from these reviews and the subsequent press coverage. The underlying message seemed to be that for most 'treatment options' there was no convincing evidence that they "actually help kids get better" (their quote not mine) at least in the long-term; although accepting short-term gains for some. Mixed feelings because of how this represents the current state of management and intervention options for (children with) autism - i.e. how little we actually know despite literally millions of pounds, dollars, Euro etc of research money being spent on R&D.
I was however heartened by the call for further research into these areas and also the suggestion that 'best' and 'non-responders' to intervention should be a focus, going back to the notion of autism and n=1. Breaking down what was actually included as part of these reviews, the authors looked at various pharmacotherapies being used in autism as well as various behavioural therapies. Their conclusions were that whilst some interventions seemed to show often quite pronounced positive effects for individuals, very little is known about the factors governing response and the characteristics pertinent to a positive response in the longer term.
Medications used to tackle challenging and repetitive behaviours specific to autism did receive a general thumbs up. Important however was the highlighting of 'side-effects' of said medications; particularly dyskinesia and weight gain following use of drugs like risperidone and aripriprazole. Unfortunately also, the anti-depressant medications didn't fare well; following on from the recent meta-analysis of SSRI use for autism shown here detailing limited effectiveness.
The one area of review that did provide the most convincing findings was related to a lack of general efficacy for the gastrointestinal hormone secretin for autism and a strange call to research it no more - strange because for about 5-6 years it hasn't; or not at least under large-scale controlled-trial conditions. What more is there to say? Well not much really.
I'd like to think that if there are lessons to be learned from these reviews they are these: (1) autism is not autism but autisms - focusing on sub-groups, and more importantly looking at best- and non-responder characteristics to various interventions, is probably the best way forward; (2) 'short-term' gains are important - but longer study periods or follow-up studies are required to see how these gains translate into long-term outcome - how we measure 'outcome' is another matter; (3) co-morbidity is something that perhaps has been given too little attention in autism intervention research - is intervention affecting core symptoms or impacting on peripheral symptoms? Does it make any difference anyway?
All of this is perhaps more fodder for the upcoming NICE review of autism coming to a station near you soon (at least in the UK).
All hail the gut bacteria
'Flash, ah-ahh'. Flash Gordon. You remember him, and that fantastic film in 1980 with the soundtrack by Queen. Max von Sydow played Ming the Merciless who ruled Mongo with a iron fist. 'All hail Ming, Ruler of the Universe' was the chant from his (dis)loyal subjects. Well, Ming might well have been Ruler of the Cosmos, but us humans may very well bow down to another Ruler - or should I say a couple of trillion Rulers - our endogenous gut bacteria.
Despite my previous posts examining a possible relationship between some cases of autism spectrum conditions and 'abnormal' gut bacteria, this post is a little different. Different because it is not looking at gut bacteria in relation to autism per se, but rather some wider research.
Before I start, I want to acknowledge a few sources of information including Emily Deans over at Evolutionary Psychiatry, Maff at the Environmental Illness Resource and the Neurophilosophy blog (I don't want any charges of plagiarism levelled against me).
My attention was turned to two papers published recently on a possible bi-directional relationship between gut bacteria and behaviour in mice. By bi-directional, I mean that gut bacteria could influence behaviour and behaviour could influence gut bacteria. OK I hear you cry, fine if you are a mouse - and you would be absolutely right. But remember that mice are used to build a variety of different models of human functioning including that related to autism (see special edition of the Autism Research journal on mouse models).
Both the papers highlighted have generated quite a bit of discussion on their various implications.
The paper suggesting that behaviour (in this case, stress) can affect gut bacterial populations implies a few things: (a) gut bacterial populations are dynamic and responsive to our psychology and/or behaviour as well as more physiologically-determined variables such as medication or diet, (b) where gastrointestinal conditions are present and potentially tied into gut bacteria (IBS for example), the mechanism for psychosocial stress impinging on symptoms may well be tied in. This last point in particular may have some relevance for specific cases of autism spectrum conditions where stress and arousal seem to be common. Think also to my recent post covering probably the most undesirable therapy ever invented, fecal transplantation and the implications of a comment posted in jest on the EP blog "..if you ever have a fecal transplant, make sure it is from a slender, non-asthmatic, happy person!".
The other paper detailing the effect of gut bacteria (or lack of it) on behaviour seems to tie in with the growing interest in such a relationship related to autism. Remember that study from Richard Sandler and colleagues from 2000 where short-term administration of a powerful antimicrobial acting on gut bacteria (I assume!) led to some short-term positive behavioural changes in children with autism?
As per the ethos of this blog I have tried to tie the work back to autism, but really these papers potentially show some applicability to lots of different areas. ME/CFS perhaps? How about what happens when we try and change/affect our gut bacterial populations? What happens to behaviour?
This paper was published a few years back and tried just that. Using a double-blind, placebo-controlled methodology, the authors looked at what happened to anxiety symptoms in participants with CFS when a probiotic preparation was taken. The results: a rise in the 'good' bacteria (aerobic predominantly) and a decrease in anxiety symptoms when taking the probiotic over the placebo. Let's be straight though. I am not saying that such an intervention will help everyone with every condition. But all these papers tell us that perhaps we should be looking at our gut bacterial populations a little more closely from a research perspective.
All hail the gut bacteria, ruler of OUR Cosmos!
Despite my previous posts examining a possible relationship between some cases of autism spectrum conditions and 'abnormal' gut bacteria, this post is a little different. Different because it is not looking at gut bacteria in relation to autism per se, but rather some wider research.
Before I start, I want to acknowledge a few sources of information including Emily Deans over at Evolutionary Psychiatry, Maff at the Environmental Illness Resource and the Neurophilosophy blog (I don't want any charges of plagiarism levelled against me).
My attention was turned to two papers published recently on a possible bi-directional relationship between gut bacteria and behaviour in mice. By bi-directional, I mean that gut bacteria could influence behaviour and behaviour could influence gut bacteria. OK I hear you cry, fine if you are a mouse - and you would be absolutely right. But remember that mice are used to build a variety of different models of human functioning including that related to autism (see special edition of the Autism Research journal on mouse models).
Both the papers highlighted have generated quite a bit of discussion on their various implications.
The paper suggesting that behaviour (in this case, stress) can affect gut bacterial populations implies a few things: (a) gut bacterial populations are dynamic and responsive to our psychology and/or behaviour as well as more physiologically-determined variables such as medication or diet, (b) where gastrointestinal conditions are present and potentially tied into gut bacteria (IBS for example), the mechanism for psychosocial stress impinging on symptoms may well be tied in. This last point in particular may have some relevance for specific cases of autism spectrum conditions where stress and arousal seem to be common. Think also to my recent post covering probably the most undesirable therapy ever invented, fecal transplantation and the implications of a comment posted in jest on the EP blog "..if you ever have a fecal transplant, make sure it is from a slender, non-asthmatic, happy person!".
The other paper detailing the effect of gut bacteria (or lack of it) on behaviour seems to tie in with the growing interest in such a relationship related to autism. Remember that study from Richard Sandler and colleagues from 2000 where short-term administration of a powerful antimicrobial acting on gut bacteria (I assume!) led to some short-term positive behavioural changes in children with autism?
As per the ethos of this blog I have tried to tie the work back to autism, but really these papers potentially show some applicability to lots of different areas. ME/CFS perhaps? How about what happens when we try and change/affect our gut bacterial populations? What happens to behaviour?
This paper was published a few years back and tried just that. Using a double-blind, placebo-controlled methodology, the authors looked at what happened to anxiety symptoms in participants with CFS when a probiotic preparation was taken. The results: a rise in the 'good' bacteria (aerobic predominantly) and a decrease in anxiety symptoms when taking the probiotic over the placebo. Let's be straight though. I am not saying that such an intervention will help everyone with every condition. But all these papers tell us that perhaps we should be looking at our gut bacterial populations a little more closely from a research perspective.
All hail the gut bacteria, ruler of OUR Cosmos!
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