I must warn readers that this is probably not the happiest of posts that you will read on this blog. In this post I intend to talk about mortality and a few other not-so-nice things. If you've had a bit of a bad day and really don't want to make it any worse, I won't be offended if you click away now. Might I suggest this link as an alternative?
To quote from the abstract of a recent article appearing in the Journal of Child Neurology: "..there is a higher than expected rate of mortality in individuals with autism and epilepsy than autism alone". Similar studies have confirmed this grim finding related to autism and one of its more frequent co-morbidities. Most people would find it very difficult to say that there are any 'positives' related to having epilepsy or other seizure-type disorder on quality of life either when co-morbid to autism or stand-alone.
Even looking on the Epilepsy Society website there is little to alter such an opinion. Yes, epilepsy can be managed, and managed quite well by things like medication, and yes for the vast majority of people it is not a consistent, on-going problem.
The only thing is that unfortunately people do perish following conditions like status epilepticus and even the anti-epilepsy medications are not without their potential side-effects and developmental effects. [At this point I give a disclaimer on not stopping or altering any medication without seeking medical advice].
Epilepsy and seizure-type disorders have long been associated with autism. The figures are slightly variable as to the extent of the overlap but generally range between 5-40% of people with an autism spectrum condition presenting also with epilepsy at some point in their life. There are lots of different types of epilepsy / seizure-type disorders and quite a few other conditions carrying a higher rate of epilepsy.
With regards to co-morbidity with autism, no-one really knows why there is a heightened risk of epilepsy. There is a correlation, of sorts, between various genetic syndromes presenting with autistic features and epilepsy which could indicate some genetic involvement.
Time of onset of epilepsy in autism might also suggest some variable effect from either environmental or maturational processes. I previously blogged about puberty and autism and a potential relationship there. Other authors have described behavioural regression as being a key correlate with seizure activity onset. I am sure that there are other potential correlates between autism and epilepsy; this article discusses a link between epilepsy and encephalitis following on from the suggestion of a link between autism and viral infection.
Management of epilepsy usually involves medication (as previously discussed) but in some cases can also include things like diet and supplementation of other compounds for certain types of epilepsy. The same kind of diet (ketogenic) has also been suggested for autism without epilepsy; I might come back to this in a future post.
Other, more radical ideas such as the application of vagal nerve stimulation, used for the treatment of epilepsy, to autism remain under investigation.
I apologise again to readers for the grimness of this post. I do stress that epilepsy co-morbid to autism is not an automatic pathway to early mortality - not by any means at all. With the right medicines management, epilepsy can be managed, and managed well.
I suppose the take home message is that epilepsy, in any one of it's many guises, can be common to autism and because of its health implications, really deserves appropriate screening in at-risk groups. Making it a research priority might also be a good idea.
Saturday, 16 April 2011
Friday, 15 April 2011
Its rude to point...
Children have an uncanny nack of picking out details and saying the most embarrassing things sometimes - a lack of 'theory of mind' perhaps? Some examples: moustache - "what's that hairy thing on that man's face?", glasses or spectacles - "why is that woman wearing windows?", the list can go on.
In most of these examples, such questions would probably be followed by a very definite pointing of the index finger towards said object/thing/person, just to make sure that everyone knows what is being described and where it is (for maximum embarrassment impact). The usual response is an awkward smile from the parent / caregiver and a gesture or action for the child to stop pointing (the 'inner child' of many adults is though, also having a secret giggle about such childhood observations no doubt). Pointing in these case is socially undesirable.
A lot has been made about pointing - it's various manifestations and uses - with regards to autism. I was interested in this post as to how pointing is potentially related to autism and the link to things like joint attention. What to do about a failure to point, is also of interest. I might add that I won't be discussing pointing with regards to Facilitated Communication in this post.
The first time I came across pointing as being related to autism was upon reading the ADI-R and ADOS instruments used for assessing autism. In ADOS, pointing forms part of various sections of the schedule including the first-stage module 1 assessment (administered to those with no speech) as an indication of language and communication. In the ADI-R 'pointing to express interest' as part of spontaneous communication of interest is also listed; importantly also including coordinated eye gaze. What this suggests is that pointing, or a lack of it, seems to be quite important during the assessment of autism spectrum conditions. Indeed some authors suggest that it is one of the key markers of symptom onset and potentially tied into regression.
I would add at this point out that there are various forms of pointing (not the construction type) related to what meaning is trying to be conveyed. Pointing to indicate interest - "look over there" is known as proto-declarative. Proto-imperative pointing is the "I want that" form of pointing. Pointing therefore, is a means to an end of direct interest but also serves as an 'attention-grabber' for needs and requirement.
The research on pointing and autism is quite bountiful in terms of communication and use of gestures. What it appears to suggest, specifically with regards to autism, is that proto-declarative pointing, the 'social pointing', seems to be the area of most interest.
I suppose this is to be expected in autism given the emphasis (rightly or wrongly) on the social features being paramount. The thing about proto-declarative pointing also is that it bridges communication and social interaction areas of current diagnostic manuals and is perhaps even the prototype behaviour of the proposals on social affect in DSM V (the words 'pointing' though not appearing in the manual revisions so far). I stress the social and communication domains together because pointing in children with autism seems to differ from pointing in children with a language delay.
The question of what to do about it has also been examined. It appears that you can teach a person to point - at least as part of a joint attention programme. Going back to my point above, the question is whether you are teaching pointing as merely a communicative tool or truly as a social-communicative tool.
In most of these examples, such questions would probably be followed by a very definite pointing of the index finger towards said object/thing/person, just to make sure that everyone knows what is being described and where it is (for maximum embarrassment impact). The usual response is an awkward smile from the parent / caregiver and a gesture or action for the child to stop pointing (the 'inner child' of many adults is though, also having a secret giggle about such childhood observations no doubt). Pointing in these case is socially undesirable.
A lot has been made about pointing - it's various manifestations and uses - with regards to autism. I was interested in this post as to how pointing is potentially related to autism and the link to things like joint attention. What to do about a failure to point, is also of interest. I might add that I won't be discussing pointing with regards to Facilitated Communication in this post.
The first time I came across pointing as being related to autism was upon reading the ADI-R and ADOS instruments used for assessing autism. In ADOS, pointing forms part of various sections of the schedule including the first-stage module 1 assessment (administered to those with no speech) as an indication of language and communication. In the ADI-R 'pointing to express interest' as part of spontaneous communication of interest is also listed; importantly also including coordinated eye gaze. What this suggests is that pointing, or a lack of it, seems to be quite important during the assessment of autism spectrum conditions. Indeed some authors suggest that it is one of the key markers of symptom onset and potentially tied into regression.
I would add at this point out that there are various forms of pointing (not the construction type) related to what meaning is trying to be conveyed. Pointing to indicate interest - "look over there" is known as proto-declarative. Proto-imperative pointing is the "I want that" form of pointing. Pointing therefore, is a means to an end of direct interest but also serves as an 'attention-grabber' for needs and requirement.
The research on pointing and autism is quite bountiful in terms of communication and use of gestures. What it appears to suggest, specifically with regards to autism, is that proto-declarative pointing, the 'social pointing', seems to be the area of most interest.
I suppose this is to be expected in autism given the emphasis (rightly or wrongly) on the social features being paramount. The thing about proto-declarative pointing also is that it bridges communication and social interaction areas of current diagnostic manuals and is perhaps even the prototype behaviour of the proposals on social affect in DSM V (the words 'pointing' though not appearing in the manual revisions so far). I stress the social and communication domains together because pointing in children with autism seems to differ from pointing in children with a language delay.
The question of what to do about it has also been examined. It appears that you can teach a person to point - at least as part of a joint attention programme. Going back to my point above, the question is whether you are teaching pointing as merely a communicative tool or truly as a social-communicative tool.
Thursday, 14 April 2011
Early infant feeding practices
Feeding babies, or more precisely, what to feed babies and young infants has been quite a long-running debate.
I don't think anyone would really argue with the fact that breast milk is nature's way of providing everything a young infant needs to grow in those tentative early days, weeks and months, packaged up at just the right temperature with no late-night sterilisation of bottles or teats required. Perfect also for the groggy husband who grumbles to himself as he patters downstairs at 3am to do his paternal preparation duties.
Whether or not new mums want to, or can use this 'natural' option is another matter entirely.
I approach this subject with caution being, as I am, the wrong gender to make such a choice. I do however follow quite closely the various guidelines and debates on 'breast vs. bottle' and 'when to start weaning' as a matter of professional interest. Not least because of the link between very early weaning and increased risk of coeliac disease. Not least also because of the possible link between early feeding issues and autism as described in my posts here and here.
In recent times the question of 'when to start weaning' has been the source of some debate. One of the main issues is the age at which infants should start eating solid food and the conflicting advice being offered in this area. Here in the UK the official guidance is very clear: recommending exclusively breast / bottle feeding (or combined) for the first 6 months of life and weaning on to solid foods thereafter. This advice is backed up by the World Health Organisation (WHO) no less.
That would be all well and good if a report from the European Union hadn't mixed things up a little by suggesting that for some children, earlier weaning (from about 4 months onwards) might be OK and possibly advantageous. Added to that an article appearing in BMJ questioning our 6-month rule and again suggesting that there may be a case for revising guidance (backed up by the British Dietetic Association, BDA).
A case perhaps of the head saying do one thing, and the arms and fingers perhaps wanting to do something else.
I have thought about this issue quite a bit. Working backwards from the notion that all babies are different; have different constitutions, raised under different environments, raised by different parents one could argue that the n=1 principle might apply. Thinking also to what happens when research and guidelines get too generalised to a population there may be perhaps some scope for taking on board some of the suggested revisions at least for some infants (although please do not base your decision on my analysis, speak to your physician and healthcare provider about this).
The idea also that there is a window of opportunity for developing tolerance to foods is also an interesting concept. Readers may know of my interest in all things diet and gut-related, and in particular, the concept of the hyperpermeable gut (leaky gut) in connection to lots of things. One of the most interesting parts of how gut hyperpermeability might tie into weaning patterns is trying to ascertain when the gut is 'unpermeable' enough to tolerate food without permeability potentially leading to allergy or intolerance. The infant gut is quite permeable on purpose because: (a) it is still maturing, and (b) it has to allow the passage and absorption of all those goodies in breast milk (and formula) into the CNS, some of which are quite large molecules. Gut hyperpermeability may also have a role to play in producing that lovely soporific effect that babies love following their milk from all those warming opioid peptides and how this may relate to neural growth.
I will be interested to see where this debate goes eventually and how it may (may not) influence guidance and practice.
I don't think anyone would really argue with the fact that breast milk is nature's way of providing everything a young infant needs to grow in those tentative early days, weeks and months, packaged up at just the right temperature with no late-night sterilisation of bottles or teats required. Perfect also for the groggy husband who grumbles to himself as he patters downstairs at 3am to do his paternal preparation duties.
Whether or not new mums want to, or can use this 'natural' option is another matter entirely.
I approach this subject with caution being, as I am, the wrong gender to make such a choice. I do however follow quite closely the various guidelines and debates on 'breast vs. bottle' and 'when to start weaning' as a matter of professional interest. Not least because of the link between very early weaning and increased risk of coeliac disease. Not least also because of the possible link between early feeding issues and autism as described in my posts here and here.
In recent times the question of 'when to start weaning' has been the source of some debate. One of the main issues is the age at which infants should start eating solid food and the conflicting advice being offered in this area. Here in the UK the official guidance is very clear: recommending exclusively breast / bottle feeding (or combined) for the first 6 months of life and weaning on to solid foods thereafter. This advice is backed up by the World Health Organisation (WHO) no less.
That would be all well and good if a report from the European Union hadn't mixed things up a little by suggesting that for some children, earlier weaning (from about 4 months onwards) might be OK and possibly advantageous. Added to that an article appearing in BMJ questioning our 6-month rule and again suggesting that there may be a case for revising guidance (backed up by the British Dietetic Association, BDA).
A case perhaps of the head saying do one thing, and the arms and fingers perhaps wanting to do something else.
I have thought about this issue quite a bit. Working backwards from the notion that all babies are different; have different constitutions, raised under different environments, raised by different parents one could argue that the n=1 principle might apply. Thinking also to what happens when research and guidelines get too generalised to a population there may be perhaps some scope for taking on board some of the suggested revisions at least for some infants (although please do not base your decision on my analysis, speak to your physician and healthcare provider about this).
The idea also that there is a window of opportunity for developing tolerance to foods is also an interesting concept. Readers may know of my interest in all things diet and gut-related, and in particular, the concept of the hyperpermeable gut (leaky gut) in connection to lots of things. One of the most interesting parts of how gut hyperpermeability might tie into weaning patterns is trying to ascertain when the gut is 'unpermeable' enough to tolerate food without permeability potentially leading to allergy or intolerance. The infant gut is quite permeable on purpose because: (a) it is still maturing, and (b) it has to allow the passage and absorption of all those goodies in breast milk (and formula) into the CNS, some of which are quite large molecules. Gut hyperpermeability may also have a role to play in producing that lovely soporific effect that babies love following their milk from all those warming opioid peptides and how this may relate to neural growth.
I will be interested to see where this debate goes eventually and how it may (may not) influence guidance and practice.
Registering research: present Sir.
Another quick post just to drop in a few interesting links.
The title of the post refers to the increasingly important use of clinical trial registries in research. Our ScanBrit trial looking at the use of gluten- and casein-free diets for children with autism was registered with the US National Institutes of Health (NIH) trial registry - ClinicalTrials.gov.
The reason being that many scientific journals nowadays make clinical trial registry a pre-requisite before even entertaining the thought of publishing a paper. It also allows a degree of transparency of trial protocol, outcomes, and even posting of results for everyone to see.
There are other trial registries such as this one from the World Health Organisation (WHO) - the International Clinical Trials Registry Platform.
All these registries are searchable and often provide a wealth of information about studies recruiting, underway or completed on a specific topic. I am particularly interested in this and this trial related to autism when they eventually report.
A new clinical trial register has also joined the party - the EU Clinical Trials Register. As part of a directive from the European Medicines Agency there is now a commitment to further transparency in European-produced research (I don't suppose the fact that everyone was registering with the NIH or WHO had anything to do with it!)
I would encourage readers to use these valuable resources. They are all open-access and really do make science accessible and provide an important window into the inner workings of evidence-based practice.
The title of the post refers to the increasingly important use of clinical trial registries in research. Our ScanBrit trial looking at the use of gluten- and casein-free diets for children with autism was registered with the US National Institutes of Health (NIH) trial registry - ClinicalTrials.gov.
The reason being that many scientific journals nowadays make clinical trial registry a pre-requisite before even entertaining the thought of publishing a paper. It also allows a degree of transparency of trial protocol, outcomes, and even posting of results for everyone to see.
There are other trial registries such as this one from the World Health Organisation (WHO) - the International Clinical Trials Registry Platform.
All these registries are searchable and often provide a wealth of information about studies recruiting, underway or completed on a specific topic. I am particularly interested in this and this trial related to autism when they eventually report.
A new clinical trial register has also joined the party - the EU Clinical Trials Register. As part of a directive from the European Medicines Agency there is now a commitment to further transparency in European-produced research (I don't suppose the fact that everyone was registering with the NIH or WHO had anything to do with it!)
I would encourage readers to use these valuable resources. They are all open-access and really do make science accessible and provide an important window into the inner workings of evidence-based practice.
Wednesday, 13 April 2011
Diagnostic substitution and autism prevalence
I don't know if it is still part of the autism debate, but I remember a while back there was a lot of interest in whether or not diagnostic substitution was a factor in the increasing prevalence of autism spectrum conditions.
The argument went something like this: 20-odd years ago, children were diagnosed with intellectual disability (ID) even though they may have presented with either autism or autistic features. In more recent times, said children who would have been diagnosed with ID would now be classified as having autism or an autism spectrum condition as a primary diagnosis. The shift is due to either a greater awareness of autism, changing diagnostic criteria for autism or clinicians getting better and more accurately diagnosing autism.
I have to say that I always had mixed feelings about this argument. Mixed feelings because this would suggest that despite autism being included in the diagnostic manuals for quite a few years, clinicians were basically, pardon my language, either crap at diagnosing it during the 80s and 90s (perhaps into the noughties) or were so swayed by the diagnostic 'fads' of the time that they did not diagnose it. I know a few clinicians and have to say that I can't buy this being such a universal phenomena. If anything else what does this tell us about the criteria for autism being used?
On the other side of argument is the various research which has more than hinted at a reduction of ID diagnoses corresponding with an increase in autism diagnoses. It is not just in the US that this trend has been noted, but also in Canada. The 'Californa data' has been pivotal in this argument / debate.
The common consensus is that diagnostic substitution has probably contributed to the increase in autism prevalence (at least in the USA and Canada); as a percentage roughly ranging from anywhere between a quarter to about a half of cases.
I say all this because an interesting paper has emerged on PLoS ONE titled: Autism and intellectual disability are differentially related to sociodemographic background at birth. The full-text of the paper is happily available here.
You are right - the paper does not, from the title, seem like it is going to deal with the issue of diagnostic substitution, but look further, particularly at Figure 1 and there are some interesting numbers to crunch.
I think it is worthwhile stating at this point that this paper looked at Australian trends in diagnosis so we cannot really say too much other than this is what happened to Australian trends. I have talked about Australian prevalence trends in a previous post.
From Figure 1: mild-moderate ID diagnostic prevalence (without autism) by birth year peaked in 1992 and by 1999 was quite a few orders lower. Severe ID (without autism) by contrast seemed to show a quite unstable pattern throughout the whole period of study (1984-1999) with lots of peaks and troughs.
Autism (with or without ID) grew in prevalence up to 1996. At that point autism and no ID seemed to drop off (I wonder if this was a change point where Asperger syndrome became more 'fashionable' a diagnostic label to use?) whilst autism with ID continued its steady climb upwards.
The conclusion: well it is a complicated picture. It does appear as though there are some 'opposite' trends in ID and autism diagnoses but the relationship is not completely straight forward.
This is of course just my own interpretation of the figures; complete with my own biases et al. Others have their own take on the data and results. I would encourage readers to take a look at the figures themselves and draw their own conclusions on this very complicated part of the autism debate.
The argument went something like this: 20-odd years ago, children were diagnosed with intellectual disability (ID) even though they may have presented with either autism or autistic features. In more recent times, said children who would have been diagnosed with ID would now be classified as having autism or an autism spectrum condition as a primary diagnosis. The shift is due to either a greater awareness of autism, changing diagnostic criteria for autism or clinicians getting better and more accurately diagnosing autism.
I have to say that I always had mixed feelings about this argument. Mixed feelings because this would suggest that despite autism being included in the diagnostic manuals for quite a few years, clinicians were basically, pardon my language, either crap at diagnosing it during the 80s and 90s (perhaps into the noughties) or were so swayed by the diagnostic 'fads' of the time that they did not diagnose it. I know a few clinicians and have to say that I can't buy this being such a universal phenomena. If anything else what does this tell us about the criteria for autism being used?
On the other side of argument is the various research which has more than hinted at a reduction of ID diagnoses corresponding with an increase in autism diagnoses. It is not just in the US that this trend has been noted, but also in Canada. The 'Californa data' has been pivotal in this argument / debate.
The common consensus is that diagnostic substitution has probably contributed to the increase in autism prevalence (at least in the USA and Canada); as a percentage roughly ranging from anywhere between a quarter to about a half of cases.
I say all this because an interesting paper has emerged on PLoS ONE titled: Autism and intellectual disability are differentially related to sociodemographic background at birth. The full-text of the paper is happily available here.
You are right - the paper does not, from the title, seem like it is going to deal with the issue of diagnostic substitution, but look further, particularly at Figure 1 and there are some interesting numbers to crunch.
I think it is worthwhile stating at this point that this paper looked at Australian trends in diagnosis so we cannot really say too much other than this is what happened to Australian trends. I have talked about Australian prevalence trends in a previous post.
From Figure 1: mild-moderate ID diagnostic prevalence (without autism) by birth year peaked in 1992 and by 1999 was quite a few orders lower. Severe ID (without autism) by contrast seemed to show a quite unstable pattern throughout the whole period of study (1984-1999) with lots of peaks and troughs.
Autism (with or without ID) grew in prevalence up to 1996. At that point autism and no ID seemed to drop off (I wonder if this was a change point where Asperger syndrome became more 'fashionable' a diagnostic label to use?) whilst autism with ID continued its steady climb upwards.
The conclusion: well it is a complicated picture. It does appear as though there are some 'opposite' trends in ID and autism diagnoses but the relationship is not completely straight forward.
This is of course just my own interpretation of the figures; complete with my own biases et al. Others have their own take on the data and results. I would encourage readers to take a look at the figures themselves and draw their own conclusions on this very complicated part of the autism debate.
Bacteria, PANDAS and anti-psychotics
I don't know why but I seem to be repeatedly seeking out the most spine-tingling things to blog about. First it was gut parasites and fecal transplantation and now I am moving on to parasites "controlling" the mind. I really do need to cut out the horror flicks and drink more relaxing cups of tea.
This post stems from a programme broadcast on BBC Radio 4 titled: Voodoo wasps and Zombie worms. I attach a link to the programme here (bearing in mind that this link might change to something else in the not too distant future when a new programme uses the same link - so don't be surprised if I just linked to 'butter vs. margarine: the debate' or something like that).
The crux of the programme is that parasitic organisms might have the ability to affect the mind as well as the body. The programme uses the example of Toxoplasma gondii and how the bacteria might affect rats to relinquish their fear of cats, thus making them easier prey, and with it aiding the transfer of the bacteria (bacterium?) from rat to cat. T gondii (to those in the know) is then discussed in relation to schizophrenia, the manufacture of dopamine and just possibly, how some of the anti-psychotics might stop T gondii from replicating in the brain. This article from Faith Dickerson and colleagues sums it up.
I don't know about you but all that just gave me a chill down my spine. Real Sci-Fi stuff.
I had heard about T gondii before in relation to toxoplasmosis and why pregnant women should not handle used kitty litter. Those who remember that interesting film Trainspotting might also remember the link between one of the protagonists and death by toxoplasmosis following IV drug use.
The notion that bacterial or viral agents can conceivably affect the mind and behaviour has been mentioned in relation to lots of things, including autism spectrum conditions; think encephalitis for example. I even found this paper with onset of autistic symptoms and a possible temporal association post-malaria (remembering the adage 'correlation does not imply causation').
I say autism, but one of the most interesting areas relates to something called PANDAS. Before you start questioning why I am talking about those lovable, bamboo-eating bears, I will stop you and say I am not. PANDAS stands for Pediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcal infections.
PANDAS is a controversial concept. There are quite a few reports on the web talking about PANDAS and how it affected people. The suggestion is that a particular type of strep infection for one reason or another starts to manifest behavioural symptoms quite rapidly, possibly following a mechanism to that described in Sydenham's chorea. The basal ganglia is a target in PANDAS - as it is in autism also.
I find this whole area absolutely fascinating. The same kind of fascinating when studies suggest for example, that gut bacteria can affect behaviour. What it suggests is that we may think that 'we' control our actions and behaviour, but the question is, to what extent?
Coming back to autism, and assuming that there may be a specific 'type' of autism tied into such a mechanism, what are the possible implications? Well for one thing, it suggests that presentation of somatic conditions (moderated by viral or bacterial infection) in autism might be doing more than just affecting the physical body.
Kanner talked about strep infection in one of his original cases - 'Alfred' - who was frequently ill with 'chickenpox, strep and impetigo'. Yes it could be coincidence; maybe, maybe not. Impetigo is something that I have been interested in for quite a while now - here and here - in relation to autism (or more accurately Asperger syndrome). I don't think I can make any link on the basis of the available data, but it is still interesting.
There might also be some implication for treatment of said infections and how it impacts on behavioural presentation. Remember Sandler and colleagues who reported on anti-microbial use impacting on the presentation of autistic behaviour? That combined with the suggestion that some of the anti-psychotic medications may impact on parasitic infections opens up a whole new world of possibilities.
In the words of Nick Ross ex-presenter from Crimewatch - "don't have nightmares".
This post stems from a programme broadcast on BBC Radio 4 titled: Voodoo wasps and Zombie worms. I attach a link to the programme here (bearing in mind that this link might change to something else in the not too distant future when a new programme uses the same link - so don't be surprised if I just linked to 'butter vs. margarine: the debate' or something like that).
The crux of the programme is that parasitic organisms might have the ability to affect the mind as well as the body. The programme uses the example of Toxoplasma gondii and how the bacteria might affect rats to relinquish their fear of cats, thus making them easier prey, and with it aiding the transfer of the bacteria (bacterium?) from rat to cat. T gondii (to those in the know) is then discussed in relation to schizophrenia, the manufacture of dopamine and just possibly, how some of the anti-psychotics might stop T gondii from replicating in the brain. This article from Faith Dickerson and colleagues sums it up.
I don't know about you but all that just gave me a chill down my spine. Real Sci-Fi stuff.
I had heard about T gondii before in relation to toxoplasmosis and why pregnant women should not handle used kitty litter. Those who remember that interesting film Trainspotting might also remember the link between one of the protagonists and death by toxoplasmosis following IV drug use.
The notion that bacterial or viral agents can conceivably affect the mind and behaviour has been mentioned in relation to lots of things, including autism spectrum conditions; think encephalitis for example. I even found this paper with onset of autistic symptoms and a possible temporal association post-malaria (remembering the adage 'correlation does not imply causation').
I say autism, but one of the most interesting areas relates to something called PANDAS. Before you start questioning why I am talking about those lovable, bamboo-eating bears, I will stop you and say I am not. PANDAS stands for Pediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcal infections.
PANDAS is a controversial concept. There are quite a few reports on the web talking about PANDAS and how it affected people. The suggestion is that a particular type of strep infection for one reason or another starts to manifest behavioural symptoms quite rapidly, possibly following a mechanism to that described in Sydenham's chorea. The basal ganglia is a target in PANDAS - as it is in autism also.
I find this whole area absolutely fascinating. The same kind of fascinating when studies suggest for example, that gut bacteria can affect behaviour. What it suggests is that we may think that 'we' control our actions and behaviour, but the question is, to what extent?
Coming back to autism, and assuming that there may be a specific 'type' of autism tied into such a mechanism, what are the possible implications? Well for one thing, it suggests that presentation of somatic conditions (moderated by viral or bacterial infection) in autism might be doing more than just affecting the physical body.
Kanner talked about strep infection in one of his original cases - 'Alfred' - who was frequently ill with 'chickenpox, strep and impetigo'. Yes it could be coincidence; maybe, maybe not. Impetigo is something that I have been interested in for quite a while now - here and here - in relation to autism (or more accurately Asperger syndrome). I don't think I can make any link on the basis of the available data, but it is still interesting.
There might also be some implication for treatment of said infections and how it impacts on behavioural presentation. Remember Sandler and colleagues who reported on anti-microbial use impacting on the presentation of autistic behaviour? That combined with the suggestion that some of the anti-psychotic medications may impact on parasitic infections opens up a whole new world of possibilities.
In the words of Nick Ross ex-presenter from Crimewatch - "don't have nightmares".
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