An interesting case report on autism and diet

Nodding syndrome.

Ever heard of it? Well, up until a few days ago I hadn't. That is before coming across articles on the topic by Richard Idro and colleagues* (open-access) and Angelina Kakooza-Mwesige and colleagues** (open-access). Whilst not specifically my line of expertise or interest, I was intrigued to read about how nodding and other symptoms of the epileptic variety, at least in some cases, seemed to be precipitated by food and showed a potential nutritional angle.

Curving spacetime @ Wikipedia  

Granted, the hows and whys of nodding syndrome are still a mystery, but the first thought that went through my mind was whether any specific types of food(s) might be implicated. Y'know in a similar vein to Marios Hadjivassiliou and the notion of gluten ataxia*** for example? Just speculating...

With all that talk of food and behaviour in mind there are a few things that piqued my attention towards the paper by Herbert & Buckley**** seemingly part of a string of articles looking at the topic of dietary intervention published in the Journal of Child Neurology. The first thing was the title of the paper: "Autism and Dietary Therapy" simply because I have some research interest in this area. Perhaps I might have mentioned it before...

Next was the authorship list, focused on at least one of the authors, Dr Martha Herbert (no disrespect intended to Dr Buckley). Alongside an already distinguished career in autism research, Dr Herbert is also making some waves with her new book: 'The Autism Revolution' co-authored with Karen Weintraub who wrote that very interesting Nature article on autism prevalence a few years back.

Finally, a sentence from the paper abstract: "Over the course of several years following her initial diagnosis, the child’s Childhood Autism Rating Scale score decreased from 49 to 17, representing a change from severe autism to nonautistic, and her intelligence quotient increased 70 points".

Such a dramatic description of change in presentation might once have been received with a very, very sceptical eye. Indeed I assume that still might be the case in some quarters. The publication of the Deborah Fein study (see here and here) on optimal outcome in relation to autism in conjunction with the rising tide of research looking at the potential benefits of early intervention for cases of autism, have perhaps made such observations slightly more 'acceptable', at least to some elements of the autism research community. Indeed I was also very taken by the recent BBC interview of Kristine and Jacob Barnet which discussed similar changes to symptom presentation in a young man now tipped for some absolutely amazing things. The fact that said changes detailed in the Herbert & Buckley paper seemed to occur at the same time that a "gluten-free casein-free ketogenic diet" was being followed is... interesting.

Now round about this time, some people might be thinking what does this study actually show? A case study of a girl / young woman with autism where comorbid epilepsy was controlled both by anti-seizure medication and a ketogenic diet (yes, such a diet has been linked to the control of cases of epilepsy). Said dietary intervention originating in the gluten- and casein-free (GFCF) dietary domain. As time went on, seizures dissipated and over time her clinical scores on the CARS reduced indicative of quite a change in her autism presentation.

One of course might say, a single case study, it means very little in the grand methodological scheme of things. That is unless you think back to the mantra 'if you've met one person with autism, you've met one person with autism' highlighting the power of the N=1 where autism is concerned (see here). That and the interesting viewpoint expressed by people like Gary Mesibov on the issue of evidence-based medicine when applied to a extremely heterogeneous condition like autism, sorry the autisms.

I am interested in the coincidental factors reported in this paper. I have questions: did the (almost) resolution of the epileptic symptoms carry any influence on the presentation of autism? In particular, I'm thinking back to that very interesting piece of research which suggested one particular type of autism (and epilepsy) might be related to a metabolic issue with the branched-chain amino acids (see here). Is this a potential model for that epilepsy-autism relationship for some people on the spectrum? What about the "resolution of morbid obesity" also reported; could this similarly have had any effect on symptom presentation?

I have questions about the role of the diet adopted in this case. A ketogenic diet, as well as finding some value in cases of epilepsy or seizure disorders, has also been looked at with autistic behaviours in mind. Yep, at least one trial***** albeit preliminary, suggested that this might be an option for some people on the spectrum bearing in mind I'm not making any recommendations. Down the years I've also heard anecdotal reports about how the GFCF diet might have aided in the reduction/amelioration of certain signs and symptoms linked to autism. The paper by Stephen Genuis (see this post) is one example. Just before you say something along the lines of 'there is no methodologically sound experimental evidence for dietary effect'; well, yes and no (see here) accepting the need for much more rigorous experimental study and that the evidence is not all one-way (see here).

If anyone has alternative explanations for the change in symptoms outside of just healthier eating, any placebo effect or just the research attention paid to the participant in question, please feel free to post them in the comments section. That being said, no mumbo-jumbo please like I've being reading today which has been roundly answered by psychiatry. Going back to the Fein study and the promise of more details to come, I'll be interested to see whether they report any of their optimal outcomers were following such a dietary intervention alongside other interventions.

And finally... one of the main points I take from the Herbert & Buckley paper is how it underscores the need for (a) a greater, more controlled look at the potential efficacy of dietary intervention - in whatever form - in relation to cases of autism, including the important categorisation of 'best' and 'non' responders, and (b) mechanisms... how on earth could removal of specific foodstuffs affect the presentation of autism? Leaky gut? Changes to the various populations of our bacterial masters? Allergy or intolerance similar to that noticed in cases of schizophrenia for example? I've talked about some of these potential options in a previous paper (see here******) if you're at all interested. (Sorry about the blatant self-promotion).

----------

* Idro R. et al. Nodding syndrome in Ugandan children—clinical features, brain imaging and complications: a case series. BMJ Open 2013; 3: e002540.

** Kakooza-Mwesige A. et al. Nodding Syndrome in Ugandan Children and Adolescents: Menage A Trios of Epilepsy, Autism, and Pediatric Catatonia. Autism 2012; 2: e112.

*** Hadjivassiliou M. & Grünewald R. The neurology of gluten sensitivity: science vs. conviction. Practical Neurology. 2004; 4: 124–126.

**** Herbert MR. & Buckley JA. Autism and dietary therapy. J Child Neurol. May 2013.

***** Evangeliou A. et al. Application of a ketogenic diet in children with autistic behavior: pilot study. J Child Neurol. 2003; 18: 113-118.

****** Whiteley P. et al. How could a gluten- and casein-free diet ameliorate symptoms associated with autism spectrum conditions? Autism Insights 2010; 2: 39-53.

----------

Herbert, M., & Buckley, J. (2013). Autism and Dietary Therapy: Case Report and Review of the Literature Journal of Child Neurology DOI: 10.1177/0883073813488668

Depression or antidepressant use linked to C.diff infection?

"There's no mystical energy field that controls my destiny". So said a very sceptical Han Solo.

Regular readers might know that I'm a bit of fan of the whole gut-brain axis; indeed other kinds of axes too. I know that to some it might sound a bit daft that what goes on in our deepest, darkest bowels might actually have some important effects on the operations of the grey-pinkish matter floating around in skull central - and vice-versa -  but nonetheless it interests me. The gastrointestinal (GI) tract is not quite the mystical energy field that Captain Solo was referring to, but make no mistake, we are still very much in the infancy of looking at the connection between the two systems*.

Black dog @ Wikipedia  

I've tended to discuss/speculate on the gut-brain relationship with regards to cases of autism spectrum disorder (ASD) on this blog. In this post I'm branching out to look at the paper by Mary Rogers and colleagues** (open-access) on a potentially new dimension to the gut-brain conversation with depression and Clostridium difficile infection in mind.

The Rogers paper is open-access and has also attracted some media attention as a result (see here and here for the press release). The long-and-short of it was that based on two studies - a sort of scientific BOGOF - looking at the rates of C.diff infection (CDI) in participants with and without depression and the potential effects of antidepressant medication use and hospital-acquired CDI, some interesting correlations were noted. Note that word 'correlations'...

Primary among the findings was the suggestion that the chances of CDI were higher in those presenting with depression: "After adjusting for demographic characteristics, comorbidities and frequency of medical visits, there was a 36% increase in the odds of developing CDI for individuals with major depression compared with those without major depression" (CI: 1-06-1.74, p=0.016). Indeed when it came to the label of "emotional, nervous or psychiatric problems", the CDI risk was found to be even higher (OR: 1.47). Certainly some interesting data, made all the more credible by the fact that the total sample size numbered in the thousands.

When it came to medication use, there were some equally interesting associations (not) made. So for example, laboratory confirmed CDI (via stool testing) seemed not to correlate with the majority of medicines participants were also taking at the time of testing. The exceptions were mirtazapine (OR: 2.14) and fluoxetine (OR: 1.92) which were individually associated with an approximate doubling of CDI risk and also carrying some dose-related associations.

Authors also reported that polypharmacy - if I can use that word with less than 5 meds being taken - might also impact on CDI risk, as per the "significant interaction between mirtazapine and trazodone" where "the odds of a positive C. difficile test were 5.72 times greater" bearing in mind the small participant numbers who were prescribed these two drugs combined. As per the press on this paper: "People who have been prescribed these types of anti-depressants need to keep taking them unless otherwise advised by their physician"; a viewpoint that I can only echo at this stage.

You can perhaps see why I might be interested in this line of research. There is of course the chicken-and-egg question about which came first: microbial changes which place a person at greater risk of CDI and perhaps depression, or depression leading to changes to the gut microbiota and onwards elevated CDI risk. I'm not going to speculate too much on what came first because I dare say the clinical picture is going to be much more complicated than such a simple question. I've talked before about the possibility of a bi-directional relationship between gut bacteria and behaviour (at least in mice) and my viewpoint has changed very little in the intervening years. Bear also in mind that the hows and whys of depression (in all its forms) are likely to be numerous; perhaps even related to our earliest years****

It's interesting that the authors discuss quite a few important overlapping pieces of research in their summary of their findings related to things like the presence of bowel disease in cases of depression*** and that magical word 'inflammation'*****. To quote: "It is possible that there is a lifelong liaison between the gut microbiota and neurologic response to external stimuli" which certainly does seem to link in with at least some of the current research literature.

Alongside the tentative associations made by Rogers et al on the issue of depression and CDI, I find my mind wandering back to the question of whether such an association might be something which could be translated into therapeutic options. Y'know whether treating the CDI actually had any quantifiable impact on the presentation of depression or vice-versa. Indeed whether one of the more unusual methods suggested to help combat CDI - yep, the fecal transplant - might also impact on depression via changes to the gut microbiota as per the very preliminary reports from other conditions such as chronic fatigue syndrome (CFS)? That and possibility that gut bacteria might, just might, be in cahoots with other more barrier-related issues******, makes for some interesting suggestions for further scientific inquiry*******.

To end, y'know I prefer Constantiople over Istanbul....

----------

* Collins SM. & Bercik P. Gut microbiota: intestinal bacteria influence brain activity in healthy humans. Nature Reviews Gastroenterology and Hepatology. May 2013.

**  Rogers MAM. et al. Depression, antidepressant medications, and risk of Clostridium difficile
infection. BMC Medicine 2013; 11: 121.

*** Graff LA. et al. Depression and anxiety in inflammatory bowel disease: a review of comorbidity and management. Inflamm Bowel Dis. 2009; 15: 1105-1118.

**** Parboosing R. et al. Gestational influenza and bipolar disorder in adult offspring. JAMA Psychiatry. May 2013.

***** Vogelzangs N. et al. Association of depressive disorders, depression characteristics and antidepressant medication with inflammation. Transl Psychiatry. 2012; 2: e79.

****** Maes M. et al. Increased IgA and IgM responses against gut commensals in chronic depression: further evidence for increased bacterial translocation or leaky gut. J Affect Disord. 2012; 141: 55-62.

******* Hughes PA. et al. Immune activation in irritable bowel syndrome: can neuroimmune interactions explain symptoms? Am J Gastroenterol. May 2013

----------

Rogers, M., Greene, M., Young, V., Saint, S., Langa, K., Kao, J., & Aronoff, D. (2013). Depression, antidepressant medications, and risk of Clostridium difficile infection BMC Medicine, 11 (1) DOI: 10.1186/1741-7015-11-121

Does melatonin affect leaky gut? Relevance to autism

Shocker alert: medicines might have more effects than those listed on the patient information leaflet.

I like being surprised. I particularly like being surprised about medicines and health, and how many of the medicines which even reside in the typical household medicines cabinet* might carry the potential to do so much more than that listed on the package insert.

 Leaking? @ Wikipedia  

Take for example the recent paper I bumped into by Sommansson and colleagues** continuing their scientific journey through the potential gastrointestinal effects of melatonin***. Melatonin - as many people with a connection to the autism spectrum disorders (ASD) or more generally neurodevelopmental disorders**** might know - is almost becoming the treatment of choice for issues with sleep disturbance*****. That's not to say it's for everyone, and also not necessarily the only potential option bearing in mind my caveat about not giving medical or any other advice.

I've talked about melatonin with autism in mind quite a few times on this blog (see here for example). Not only because the source material for melatonin (in the body) is tryptophan, one of those truly remarkable aromatic amino acids, but also because outside of the traditional sleep-wake link, melatonin might be quite the molecular 'handyman'****** (or handywoman). Indeed it is with the ethos of that last study by Boga and colleagues in mind that I head into the two Sommansson reports.

The first thing to note about the the Sommansson reports is that they are both studies on rats. I know that in recent times, there has been some chatter about using rodents to model conditions like autism (see here) focused in particular on the dangermouse that is the BTBR mouse model. In the current studies, the variable of rodent behaviour is not relevant given that the authors were looking at the physiological data pertaining to intestinal permeability (leaky gut) with melatonin as the primary variable.

Ah yes, intestinal permeability aka leaky gut. The same leaky gut that a recent NHS Choices entry described as being expounded by "largely nutritionists and practitioners of complementary and alternative medicine". Just for the record I am neither of those two occupational options but I am a believer in the concept in relation to quite a few conditions. And you can perhaps understand why I'm so interested in the Sommansson reports whereby leaky gut - or gut hyperpermeability - seems to be positively affected (i.e. reduced) by the introduction of melatonin, at least in rats. Indeed how this might fall into line with other observations of leaky gut being defined in cases of ASD (see here) and very possibly in a mouse model of autism (see here). A part of the effect of melatonin administration in cases of autism?

I'm not by the way falling hook, line and sinker for the author's observations that "melatonin reduces ethanol- and wine-induced increases in duodenal paracellular permeability partly via enteric neural pathways involving nicotinic receptors" being the same conditions as that found in cases of autism or any other condition. As far as I am aware children with autism are not knocking back copious amounts of alcohol, so one has to be careful about extrapolating such specific conclusions to the population with such tentative data. That and the fact that we currently know so little about gut barrier issues in cases of autism; assuming that people like this chap (yes, you Alessio Fasano with your zonulin et al) might shed some light on it in the near future. Oh and should I also mention the suggested link******* between melatonin being a modifier of toll-like receptor signalling too?

But... if anything the Sommansson papers might lead us to ask some pertinent questions about responses to melatonin both in general and also with autism in mind. A simple-ish experiment: two groups, randomised to melatonin or placebo, looking at the traditional responses to melatonin in terms of sleep and quality of sleep, at the same time some before and after measures of the lactulose:mannitol ratio and whether there is any correlation between supplementation, response and gut permeability. All fairly noninvasive by all accounts but if you really wanted to go to town you might also want to look at other measures like glutathione for example******** which has also found a spot in autism research.

But don't listen to my ramblings... listen instead to the these guys who are still going strong.

----------

* Berk M. et al. Aspirin: a review of its neurobiological properties and therapeutic potential for mental illness. BMC Medicine 2013; 11: 74.

** Sommansson A. et al. Melatonin inhibits alcohol-induced increases in duodenal mucosal permeability in rats in vivo. Am J Physiol Gastrointest Liver Physiol. May 2013.

*** Sommansson A. et al. Melatonin decreases duodenal epithelial paracellular permeability via a nicotinic receptor-dependent pathway in rats in vivo. J Pineal Res. 2013; 54: 282-291.

**** Gringras P. et al. Melatonin for sleep problems in children with neurodevelopmental disorders: randomised double masked placebo controlled trial. BMJ. 2012; 345: e6664.

***** Malow BA. et al. A practice pathway for the identification, evaluation, and management of insomnia in children and adolescents with autism spectrum disorders. Pediatrics. 2012; 130: S106-S124.

****** Boga JA. et al. Beneficial actions of melatonin in the management of viral infections: a new use for this "molecular handyman"? Rev Med Virol. 2012; 22: 323-338.

******* Kang JW. et al. Melatonin protects liver against ischemia and reperfusion injury through inhibition of toll-like receptor signaling pathway. J Pineal Res. 2011; 50: 403-411.

******** Swiderska-Kołacz G. et al. The effect of melatonin on glutathione and glutathione transferase and glutathione peroxidase activities in the mouse liver and kidney in vivo. Neuro Endocrinol Lett. 2006 ; 27: 365-368.

----------

Sommansson A, Wan Saudi WS, Nylander O, & Sjöblom M (2013). Melatonin inhibits alcohol-induced increases in duodenal mucosal permeability in rats in vivo. American journal of physiology. Gastrointestinal and liver physiology PMID: 23639810

The ESSENCE of autism comorbidity?

Like Charlie Bucket looking through the sweet shop window at the delicious chocolates produced by the workforce of a certain Mr Willy Wonka (the candyman no less), I am always quite interested in the goings-on at the IMFAR autism research conference.

  The candyman can... @ Wikipedia  

This year (2013) proved to be a bit of a vintage, as once again the great and the good presented their Wonka bars of autism research; thus hinting at the direction of future autism research and what you can expect to read on this blog in the coming months. Oh, and something about poodles(?) (thanks Carol).

I've been hearing quite a bit of chatter about the keynote speech given by Prof. Christopher Gillberg which seemed to quite strongly hint that the autism research community should be paying rather more attention to the add-ons which seem to accompany a diagnosis of autism, rather than seeing autism as just existing stand-alone in a diagnostic vacuum.

Far be it from me to say 'I told you so', but comorbidity and overlap, and the often far-reaching effects on quality of life of certain comorbidity, has been a theme running through many posts on this blog and not just the more behaviourally-defined type of comorbidity. So for example the question of 'significantly over-represented' and all that autism's' chatter (note the plural) immediately come to mind. Indeed I don't actually believe that many people in the know would view the autisms as just being the total sum of the triad (very soon to be dyad). Or would they?

Mention of the word ESSENCE - Early Symptomatic Syndromes Eliciting Neurodevelopmental Clinical Examinations* - has apparently been made in Prof. Gillberg's address denoting "the reality of children (and their parents) presenting in clinical settings with impairing child symptoms before age 3 (-5) years in the fields of (a) general development, (b) communication and language, (c) social inter-relatedness, (d) motor coordination, (e) attention, (f) activity, (g) behaviour, (h) mood, and/or (i) sleep". Before proceeding, I would perhaps suggest that Gillberg seems to have some interest in the use of acronyms in autism research and beyond as per the example of DAMP and MBD**.

Anyhow, a quick scan of the peer-reviewed research literature does indeed see a small but growing body of work discussing ESSENCE and its use in autism research circles. I note for example this paper by Prof. Brian Neville*** who highlights an essential part of the use of ESSENCE: that the presentation of behaviour in infants and young children is often complex, and the "problems are their multiplicity". Common sense perhaps?

Perhaps one of the best (so far) papers discussing the concept of ESSENCE in a real-world clinical setting is this one from Lotta Höglund Carlsson and colleagues**** (open-access) (which includes Gillberg as part of the authorship team). The paper is free for all to read so no great dissection required from me. That being said, I would highlight the fact that based on examination of just over 100 children diagnosed with an autism spectrum disorder (ASD), "a mean of 3.2 coexisting disorders or problems" were reported, including a third of children presenting with "severe hyperactivity/ADHD".

I was particularly interested in this autism-ADHD link given some other recent research on the overlap*****. That and the fact that additional reports have indicated even higher levels of overlap between autism and ADHD (see this post) calls into question whether the two labels may intersect even more than we perhaps have appreciated.

One of the potential implications of the co-occurrence of autism and ADHD is with regards to intervention and therapeutic options. Without trying to hijack the association with my dietary mumbo-jumbo, I would draw your attention to a previous post I published a while back on food and ADHD and some potential lesson for autism (see here). The suggestion there - and it was only a suggestion - was that some of the observations made when looking at the impact of a dietary intervention for autism actually working on some of the symptoms associated with ADHD might imply that targeting such comorbidity might eventually impact on more core autism presentation. A shocker I know that children being described as less impulsive and attending better might actually have better outcome.

I'm finishing shortly but before I do, I want to draw your attention to another ESSENCE mention in the paper by Stephanie Plenty and colleagues****** (open-access) who looked at the retrospective application of the concept in cases of adult ASD and ADHD. They similarly reported: "Although differences were observed between ADHD and ASD patients in the core diagnostic areas, these syndromes also shared a number of childhood difficulties".

The wave of research and opinion which is seemingly directing everyone to this idea that autism is not a stand-alone label is growing. Add into the mix the recent announcement that even before the introduction of DSM-V the NIMH prefer an even broader view of behaviour and psychiatry (RDoC) ('reorienting' apparently) and that autism-ADHD-[insert other] spectrum is starting to feel more and more like a giant tapestry.

To close, for the second time in this post I'm going to direct you to the genius of Sammy Davis Jnr - the Candyman can y'know.

---------

* Gillberg C. The ESSENCE in child psychiatry: Early Symptomatic Syndromes Eliciting Neurodevelopmental Clinical Examinations. Res Dev Disabil. 2010; 31: 1543-1551.

** Gillberg C. Deficits in attention, motor control, and perception: a brief review. Arch Dis Child 2003; 88: 904-910.

*** Neville B. Role of ESSENCE for preschool children with neurodevelopmental disorders. Brain Dev. 2013; 35: 128-132.

**** Höglund Carlsson L. et al. Coexisting disorders and problems in preschool children with autism spectrum disorders. Scientific World Journal. 2013: 213979.

***** Cooper M. et al. Autistic traits in children with ADHD index clinical and cognitive problems. Eur Child Adolesc Psychiatry. April 2013.

****** Plenty S. et al. Applying an ESSENCE Framework to Understanding Adult Autism Spectrum Disorder and ADHD: Retrospective Parent Reports of Childhood Problems. Scientific World Journal. 2013: 469594.

----------

Höglund Carlsson, L., Norrelgen, F., Kjellmer, L., Westerlund, J., Gillberg, C., & Fernell, E. (2013). Coexisting Disorders and Problems in Preschool Children with Autism Spectrum Disorders The Scientific World Journal, 2013, 1-6 DOI: 10.1155/2013/213979

Surgery following self-injurious behaviour

Discussions on self-injurious behaviour (SIB) or auto-aggression are not normally for the faint-hearted.

Indeed, as I intimated on a previous post on SIB and autism, when such behaviours are witnessed in children and young adults - even older adults, one does wonder what the effects might be not only on the person themselves but also on a parent or a sibling as they watch their own flesh and blood banging their head on a wall or pulling their hair out or trying to gouge their eyes out. I can't put myself in their place without thinking of how it might affect me if it were one of my brood showing such behaviours.

In this post I'm drawing your attention to a paper by Robert Sisk and colleagues* (open-access) on surgical outcomes following the repair of detached retinas in young adults with intellectual disability (ID) and SIB. Due credit should go to Harold Doherty of the Facing Autism in New Brunswick blog for bringing this paper to my attention. I'm not going to deconstruct the paper in any statistical sense because the paper speaks for itself in terms of observations and outcomes of those nine patients described. Some of the language used is also a little too technical for me.

The long-and-short of it was that in a largely non-verbal subject group, where autism is mentioned as being some part of 6 cases, the outcome of surgery for detached retina is reported. I just want to clarify one thing about retinal detachment, we aren't talking eye-balls hanging out of eye-sockets or anything like that, but rather when the retina comes away from the support tissue. Nevertheless it is a medical emergency and can have profound consequences if not treated in time.

There are a few points and quotes from the Sisk paper worthy of some comment.

• Surgery was reported to be successful in all cases but that's not to say retinal detachment (RD) did not occur more than once for a few of the participants and at least partially because SIB didn't just miraculously stop following the first episode. 
• "RDs from self-injurious behaviors were observed during puberty, coinciding with the onset or worsening of self-injurious behaviors". Ah yes, puberty and the wonders it brings for everyone. Indeed, what puberty can mean to those with autism and/or intellectual disability for example (see here).
• "Self-injurious behaviors also worsened when visual performance declined and served as an indicator to family members and health care providers to investigate for RD". This is an important point about SIB. It kinda tells us that there is nearly always a reason for SIB and one shouldn't for example just assume that it's naturally part and parcel of autism or ID presentation (just like another comorbidity). It also suggests that those findings by Ikeda and colleagues on ophthalmologic disorder and autism (40%) are to be taken very, very seriously save any more health inequality appearing.
• "The management of RD in patients with severe cognitive impairment and persistent self-injurious behaviors was challenging". Indeed in some cases things did not stop at RD in terms of both repeat episodes and the onset of other symptoms such as glaucoma as a result of the long-term use of silicone oil tamponade as part of the treatment.

Reiterating my starting sentence to this post on SIB not being great dinner party conversation, I'd like to think there are some lessons that could be learned from papers like the one from Sisk. That for example, autism is a very, very heterogeneous spectrum with lots of shades of presentation is an important point that should not be forgotten. That those on the more 'severe' end of the spectrum might be at greater risk of comorbidity as a result of things like SIB - and importantly not always able to communicate the reasons why - should automatically mean a greater focus on health screening and the potential outcomes from things like SIB (not just the eyes and vision). It's not that we might not have clues as to at least some of the circumstances around SIB**.

Presenting SIB as potentially occurring in cases of autism*** should perhaps also be an important part of the autism awareness message. Alongside other physical comorbidity which might also reflect on behaviour (see here and here), and where it can lead (see here), adding SIB to the long list of potential correlates to autism can only serve to heighten awareness of the importance of these factors and how we might go about dealing with them to improve quality of life. I'll being continuing this chatter about the 'ESSENCE' of comorbidity in a post next week...

To finish and without making light of the topic matter covered today, I believe it is customary to celebrate Star Wars day (May 4th) in a particular way... and we have the late Margaret Thatcher to thank for this???

-----------

* Sisk RA. et al. Surgical Outcomes Following Repair of Traumatic Retinal Detachments in Cognitively Impaired Adolescents With Self-Injurious Behavior. Journal of Pediatric Ophthalmology and Strabismus. 2013; 50: 20-26.

** Duerden EG. et al. Risk factors associated with self-injurious behaviors in children and adolescents with autism spectrum disorders. J Autism Dev Disord. 2012; 42: 2460-2470

*** Richards C. et al. Self-injurious behaviour in individuals with autism spectrum disorder and intellectual disability. J Intellect Disabil Res. 2012; 56: 476-89.

----------

Sisk RA, Motley WW 3rd, Yang MB, & West CE (2013). Surgical outcomes following repair of traumatic retinal detachments in cognitively impaired adolescents with self-injurious behavior. Journal of pediatric ophthalmology and strabismus, 50 (1), 20-6 PMID: 23061560

Autism research at IMFAR 2013

"Kaixo!" That's hello by the way in Basque, or at least I think it is.

The beautiful Basque Country is currently welcoming the 2013 IMFAR conference and its delegates to its shores, as once again one of the premier autism research conferences brings together the minds (and souls) of many an autism researcher.

San Sebastian @ Wikipedia  

As per my previous posts on the IMFAR conference series - the 2011 conference and 2012 conference - hopes are high that more advances are being made into the autisms, their aetiology and pathology, and importantly those all-important real-world applicable findings to help improve quality of life for those on the spectrum, and their loved ones.

Well, the request for press coverage certainly looks interesting... including something about Kelly the Robot(!) and already some discussion on arbaclofen (see here), a drug which has already graced this blog. Indeed I am sad not to be able to attend the event.

With my research blogging hat on, IMFAR offers a tantalising look at what peer-reviewed research publications one might expect to see appearing in the coming months and onwards what I can expect to be discussing on this blog in the not-too-distant-future.

Enough of the chatter, a few sessions and abstracts which caught my eye from the searchable abstract finder:

• Session: 'The Role of Environmental Exposures in Autism Etiology: A Retrospective of the Last Decade, New Results and Frontiers for the Future' which includes an interesting title on insecticides and risk for autism.
• Session: 'Measuring Treatment Change in Core Symptoms: Novel Methods, Meaningful Outcomes' which I hope will be asking some important questions on just how we understand 'what works' when it comes to the myriad of intervention options on offer (see this post).
• Session: 'Epidemiology' which by all accounts seems to cover a lot more than just the numbers game; instead talking about (i) comorbidity and autism, (ii) the perinatal epigenome, (iii) maternal cholesterol and the topic of (iv) immunisation.
• Session: '30-Year Follow-Up of Autism in Adulthood' which promises some interesting observations about aging and autism (see here). 
• And finally... this abstract on a topic close to my research heart, the gut microbiome, which might just build on some other very interesting work (see here). That and Paul Patterson talking gastrointestinal symptoms, probiotics and mouse models (see here) as per his recent findings in this area.

No doubt there will be more to see and hear from the conference over the coming days. To close, hopefully no-one will need to use this phrase whilst in the Basque Country, but just in case... "Abokatu batekin hitz egin nahi dut". [roughly translated: "I want to talk to a lawyer".] Agur!

P.S. Jon Brock over at Cracking The Enigma is also presenting a couple of posters.