Saturday, 25 February 2017

1 in 5 children "met criteria for low language at 7 years"

Although primarily looking at the potential predictors of language outcome, the study results published by Cristina McKean and colleagues [1] revealed the rather important title heading this blog entry: "Almost 19% of children (22/1204;18.9%) met criteria for low language at 7 years."

The source of the finding was a cohort of some 1900 infants "recruited at age 8 to 10 months" who were followed until aged 7 years old and subject to quite a bit of research inspection looking at "early life factors", maternal factors and "child language ability" at various points through the childhood years. I believe this was part of the The Early Language in Victoria Study (ELVS) initiative; something that has previously created a bit of stir in speech and language circles. The authors reported that alongside the quite high percentage of children who met 'low language' criteria (based on standardized receptive or expressive language scores "≥1.25 SD below the mean"): "Child language ability at 4 years more accurately predicted low language at 7 than a range of early child, family, and environmental factors." Said low language abilities at 7 years old were also "associated with a higher prevalence of co-occurring difficulties."

Aside from pointing out that language ability at 4 years old might be quite important to language ability at 7 years old, the question that should be in most people's minds is 'why?' Why are nearly 1 in 5 children presenting with low language ability at 7 years old (and presumably at 4 years old too)? Yes, there are variables such as adverse early life factors (prematurity, birth weight, coming from a non-English speaking background, etc) that will no doubt influence various aspects of language ability, but the authors note that such factors only account for roughly 15% at most of the variation in language scores seen in their cohort (not including "child language scores at ages 2 and 4"). Ergo, there are other factors involved with regards to these findings.

In light of the McKean findings, I'm also going to draw your attention back to another occasion when language ability has been discussed on this blog (see here) and specifically: "At school entry, approximately two children in every class of 30 pupils will experience language disorder severe enough to hinder academic progress." [2] Low language (ability) is not necessarily the same as a diagnosed language disorder, and probably accounts for the variation between the studies (1 in 5 vs. 1 in 15). But in amongst a spectrum of language ability (disorder?) the questions about 'why?' still very much remain (and please, no sweeping generalisations about us 'just being better at diagnosing').

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[1] McKean C. et al. Language Outcomes at 7 Years: Early Predictors and Co-Occurring Difficulties. Pediatrics. 2017 Feb 8. pii: e20161684.

[2] Norbury CF. et al. The impact of nonverbal ability on prevalence and clinical presentation of language disorder: evidence from a population study. Journal of Child Psychology and Psychiatry. 2016. May 16.

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ResearchBlogging.org McKean C, Reilly S, Bavin EL, Bretherton L, Cini E, Conway L, Cook F, Eadie P, Prior M, Wake M, & Mensah F (2017). Language Outcomes at 7 Years: Early Predictors and Co-Occurring Difficulties. Pediatrics PMID: 28179482

Friday, 24 February 2017

Say my name

"At 9 months of age, infants developing ASD [autism spectrum disorder] were more likely to fail to orient to their names, persisting through 24 months."

So said the findings reported by Meghan Miller and colleagues [1] investigating an often over-looked but typically informative question relevant to childhood autism screening and assessment: the response to name. Anyone who knows a little about instruments such as the ADOS (Autism Diagnostic Observation Schedule) will already know about the importance of response to name ("a full response is defined as orientating to and making eye contact with the examiner who calls his name") as part of assessment.

Based on the inclusion of some 150 infants, siblings of children with or without a diagnosis of autism, a response to name task was carried out at various intervals in infancy in this prospective study ("6, 9, 12, 15, 18, and 24 months of age"). At 3 years of age, child participants were "classified into 1 of 3 outcome groups: group with ASD (n = 20), high-risk group without ASD (n = 76), or low-risk group without ASD (n = 60)." As per the opening sentence, consistently not responding to their name was a feature of quite a few of those children who subsequently went on to develop autism. Some but not all. Alongside other findings reported in relation to receptive language for example, the authors concluded: "Infants who consistently fail to respond to their names in the second year of life may be at risk not only for ASD but also for greater impairment by age 3 years."

Such work continues a theme from some of the authors on the Miller paper [2] and how relatively simple observations during play interaction [3], could be valuable variables when it comes to ascertaining potential risk of developing autism. Of course one needs to be careful that a lack of response to name does not automatically mean that an autism diagnosis is imminent or indicated as per the typical requirement to check a child's hearing for example and to consider the possibility of other diagnoses being applicable. I might also remind readers of the potential effects of regression when it comes to autism (see here) and how not every child presents with autistic features in early infancy (something that needs to be taken into account when it comes to other recent research too).

To close, say my name...

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[1] Miller M. et al. Response to Name in Infants Developing Autism Spectrum Disorder: A Prospective Study. J Pediatr. 2017 Feb 2. pii: S0022-3476(16)31566-9.

[2] Nadig AS. et al. A prospective study of response to name in infants at risk for autism. Arch Pediatr Adolesc Med. 2007 Apr;161(4):378-83.

[3] Trillingsgaard A. et al. What distinguishes autism spectrum disorders from other developmental disorders before the age of four years? Eur Child Adolesc Psychiatry. 2005 Mar;14(2):65-72.

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ResearchBlogging.org Miller M, Iosif AM, Hill M, Young GS, Schwichtenberg AJ, & Ozonoff S (2017). Response to Name in Infants Developing Autism Spectrum Disorder: A Prospective Study. The Journal of pediatrics PMID: 28162768

Thursday, 23 February 2017

"Autoimmune epilepsy is an underrecognized condition..."

"Among adult patients with epilepsy of unknown etiology, a significant minority had detectable serum Abs [autoantibodies] suggesting an autoimmune etiology."

So said the findings reported by Divyanshu Dubey and colleagues [1] continuing a research theme previously discussed on this blog (see here) on how epilepsy / seizure-type disorder(s) for some might have more to do with immune function than many people might think.

OK, a brief bit of background: epilepsy is a blanket term covering a wide variety of different presentations that affect the brain and specifically, 'the electrics' of the brain. Seizures are the most common symptom. Treatment typically comes in the form of anti-epileptic medicines (although other options are being considered for some). It's been known for a while that outside of the 'brain' focus of epilepsy, other biological systems might also play a role in the development/maintenance of the condition(s); specifically the immune system and quite often in cases where traditional anti-epileptic medicines don't seem to be able to control seizures effectively. The details are still a little sketchy but studies like the one from Dubey et al are trying to put some scientific flesh on to the bones of what facets of the immune system are potentially involved, specifically under 'autoimmune' conditions where the body fails to recognise 'self' as self and mounts an immune response against the body's own tissue(s).

Dubey and colleagues looked at a group of participants "presenting to neurology services with new-onset epilepsy or established epilepsy of unknown etiology" and tested donated serum samples "for Abs reported to be associated with autoimmune epilepsy (NMDAR-Ab, VGKCc-Ab, leucine-rich glioma-inactivated protein 1 [LGI1] Ab, GAD65-Ab, γ-aminobutyric acid type B receptor [GABAB] Ab, α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic receptor [AMPAR] Ab, antineuronal nuclear antibody type 1 [ANNA-1 or anti-Hu] Ab, Purkinje cell cytoplasmic antibody type 2 [PCA-2] Ab, amphiphysin Ab, collapsin-response mediator protein 5 [CRMP-5] Ab, and thyroperoxidase [TPO] Ab)." Quite a lot of those autoantibodies probably sound like gibberish to the lay reader but some of them have been discussed in other contexts on this blog (see here and see here for examples).

Results: some (15) of the 127 participants initially enrolled in the study were "subsequently excluded after identification of an alternative diagnosis." This in itself is interesting, as diagnoses such as "hypoxic or anoxic injury following cardiac arrest" and "ischemic stroke" are mentioned, illustrating how several different roads can lead to epilepsy and/or the presentation of seizures.

Then: "Serum Abs suggesting a potential autoimmune etiology were detected in 39 (34.8%) cases." Over a third of the cohort showed serological evidence of autoantibodies and some presented with more than one type of autoantibody as being present. Breaking down those serologically positive participants, we are told that: "19 patients (48.7%) had new-onset epilepsy and 20 patients (51.3%) had established epilepsy." The authors did also subsequently limit their findings to those cases excluding TPO-Ab and low-titer GAD65-Ab (autoantibodies where a specific role to epilepsy is unclear or not specific) but even then reported that: "23 patients (20.5%) with unexplained epilepsy had positive serologic findings strongly suggestive of an autoimmune cause of epilepsy." There is also a final part to the Dubey paper which also merits mention: "Among the 23 patients who were seropositive, 15 (65.2%) received some sort of immunotherapy. Better seizure outcome was associated with use of immunomodulatory therapy... especially with use of intravenous methylprednisolone... or plasmapheresis."

Alongside other (independent) studies in this area, the peer-reviewed evidence does seem to growing to suggest that within the wide (and heterogeneous) 'spectrum' that is epilepsy, at least some of that epilepsy might have an important immune component to it. To quote again from Dubey: "The data presented here suggest that autoimmune encephalitis may explain at least 20% of adult-onset epilepsies of unknown etiology." Aside from the importance of screening for said autoantibodies when certain cases of epilepsy appear at clinic, there are a few other potentially important points that could be raised about such data. Autism is area that I would be interested to see some further investigations carried out on with the Dubey findings in mind. Epilepsy is an important comorbidity 'over-represented' when it comes to autism (see here) and given the suggestions down the years that immune function (specifically autoimmunity) might be a facet of 'some' autism (see here for example) it's not beyond the realms of possibility that comorbid epilepsy might be a further facet of any autoimmune processes. Birds of an autoimmune feather tend to stick together and all that (see here). Add in the findings specifically talking about 'anti-NMDA-receptor encephalitis "mimicking an autistic regression"' (see here) and how methlyprednisolone might not be an uncommon medicine for some types of (autoimmune-related autistic presentation) and the hypotheses to be tested are laid out in front of you. By saying that, I don't want to take anything away from the more typical forms of epilepsy that can present (either alone or alongside autism) but rather point to the expanding knowledge base suggesting that immune functions may extend much further than just protecting the host from infection et al...

To close, slightly related to some of the content included in this post, the trailer for the film Brain on Fire (from the book of the same name) is out and looking like required viewing.

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[1] Dubey D. et al. Neurological Autoantibody Prevalence in Epilepsy of Unknown Etiology. JAMA Neurol. 2017 Feb 6.

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ResearchBlogging.org Dubey D, Alqallaf A, Hays R, Freeman M, Chen K, Ding K, Agostini M, & Vernino S (2017). Neurological Autoantibody Prevalence in Epilepsy of Unknown Etiology. JAMA neurology PMID: 28166327

Wednesday, 22 February 2017

History of bipolar disorder = elevated risk of dementia: is vitamin D important?

"History of BD [bipolar disorder] is associated with significantly higher risk of dementia in older adults."

So said the systematic review and meta-analysis published by Breno Diniz and colleagues [1] taking in the accumulated peer-reviewed literature on this topic. Including data for some 3000 individuals diagnosed with bipolar disorder and nearly 200,000 controls (without bipolar disorder), authors calculated something of a significantly higher risk of dementia in those with a documented history of bipolar disorder. They note that there is more research to do in this area, specifically on mechanisms and "to evaluate interventions that may reduce the risk of dementia in this population."

Outside of the literature included in the Diniz study, similar findings have been reported in the science literature. The paper by Almeida and colleagues [2] noted that: "Bipolar disorder in later life is associated with increased risk of dementia" based on their analysis of ~38,000 older men (65-85 years old) and their "13-year risk of dementia." Perhaps more worryingly were their findings that: "Bipolar disorder was also associated with increased mortality" in relation to "death by suicide, accidents, pneumonia or influenza, and diseases of the liver and digestive system." Other data looking more generally at clinical depression paints a similar picture [3] suggesting something of a connection between various types of depression and risk of various types of dementia: "depressive symptomatology is associated with pathological mechanisms associated with neurodegeneration."

I've tackled the topic of dementia a couple of times on this blog; most recently in relation to how incidental vitamin D deficiency *could be* something important when it comes to at least some cases of dementia (see here). Minus any sweeping generalisations and accepting that there may be many different roads leading to dementia and/or bipolar disorder, I am intrigued at the possibility that the sunshine vitamin might be something to consider as a 'connector' between elements of the depression and dementia spectrums as per other findings (see here for example). At the very least, it invites lots more targeted investigation, including whether vitamin D might indeed be a nootropic of choice for some (see here)...

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[1] Diniz BS. et al. History of Bipolar Disorder and the Risk of Dementia: A Systematic Review and Meta-Analysis. The American Journal of Geriatric Psychiatry. 2017. Jan 4.

[2] Almeida OP. et al. Risk of dementia and death in community-dwelling older men with bipolar disorder. Br J Psychiatry. 2016 Aug;209(2):121-6.

[3] Cherbuin N. et al. Dementia risk estimates associated with measures of depression: a systematic review and meta-analysis. BMJ Open. 2015 Dec 21;5(12):e008853.

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ResearchBlogging.org Diniz BS, Teixeira AL, Cao F, Gildengers A, Soares JC, Butters MA, & Reynolds CF 3rd (2017). History of Bipolar Disorder and the Risk of Dementia: A Systematic Review and Meta-Analysis. The American journal of geriatric psychiatry : official journal of the American Association for Geriatric Psychiatry PMID: 28161155

Tuesday, 21 February 2017

Neuropsychiatric disorder onset "temporally related to prior vaccinations"?

"Given the modest magnitude of these findings in contrast to the clear public health benefits of the timely administration of vaccines in preventing mortality and morbidity in childhood infectious diseases, we encourage families to maintain vaccination schedules according to CDC guidelines."

The quote opening this post comes from the paper published by Douglas Leslie and colleagues [1] (open-access) and offers not a conclusion from their study looking at the possibility that "the onset of some neuropsychiatric disorders may be temporally related to prior vaccinations in a subset of individuals" but a caution that cause-and-effect were not 'proven' in their study. Anyone with any knowledge about previous occasions where administration of vaccines have been correlated with specific psychiatric or behavioural outcomes (see here and see here for examples) will recognise how important such a caution is, bearing in mind that vaccines are medicines (albeit preventative) and are subject to similar monitoring for safety and the small possibility of adverse effects as other medicines.

Based on the examination of "the MarketScan® Commercial Claims and Encounters database", a US drug and medical insurance claims database, researchers looked at various diagnoses of interest including OCD (obsessive compulsive disorder), AN (anorexia nervosa), anxiety disorder, tic disorder, major depression, bipolar disorder and ADHD (attention-deficit hyperactivity disorder) in children/young adults aged 6-15 years old. This alongside several other classes of diagnosis including broken bones and 'open wounds'. Participants were matched one-to-one with controls without said neuropsychiatric diagnoses and exposure(s) to various vaccinations - "influenza, tetanus and diphtheria (TD), hepatitis A, hepatitis B, meningitis, and varicella" - were 'tracked'. Interestingly, this is not the lead authors' first foray into using the MarketScan database [2], where autism was the previous topic of analysis (specifically healthcare service use and costs).

Results: bearing in mind that samples sizes varied according to those diagnoses under investigation, the authors report: "Receipt of any vaccine in the previous 6 months was highest for children with AN (21.4%), followed by OCD (15.9%) and tic disorder (15.8%), and was lowest for children with open wounds (10.3%)." This information needs to be treated carefully because - again - it tells us nothing about any cause-and-effect relationship, just correlation and trend; trends that could be there for all-manner of different reasons outside of the variables looked at. Further: "HRs [hazard ratioassociated with receipt of any vaccine were highest for children with AN... followed by OCD."

The authors also looked at specific vaccinations in relation to those neuropsychiatric disorders included in their study. They report: "Influenza vaccinations during the prior 3, 6, and 12 months were... associated with incident diagnoses of AN, OCD, and an anxiety disorder." Conversely: "children with major depression were less likely to have received the influenza vaccine in the previous 3 months" and "children with bipolar disorder were also less likely to have received the influenza vaccine in the previous 3 or 6 months."

OK, it is worth reiterating - yet again - that this was a study looking at possible associations and not necessarily cause-and-effect. Indeed, judging by that last paragraph and the table of HRs produced by the authors (see here) one might easily claim that flu vaccination might potentially shield someone from developing major depression as much as 'cause' AN, OCD and/or anxiety disorder. Such is the nature of such studies and the findings being reported. And indeed someone has actually looked at depressive symptoms (symptoms that is, not depression as a clinical diagnosis) before and after an influenza vaccination and found very little...

I note that with specific regard to the influenza vaccine and the findings that "children with AN, OCD, or a tic disorder were more likely to have received the influenza vaccine in the preceding periods" the authors head into the research talking about narcolepsy and the "AS03-adjuvanted H1N1 vaccine" as a possible template for their findings. This despite not covering the diagnosis of narcolepsy in their study (they could have). I've touched upon this area of research before on this blog (see here) (something that continues to appear in media discussions) and whilst not disputing the findings, do for example, wonder why in the work of Szakács and colleagues [3] ADHD was picked up as a comorbidity present in their "post-H1N1 vaccination (PHV) narcolepsy group" but in the Leslie data the HRs showed little evidence of any relationship. Yes, H1N1 vaccination is not necessarily the same as influenza vaccination reported in the Leslie data (we don't actually know what specific influenza vaccines were administered), but surely if discussions turn to an 'autoimmune' element as a possible mechanistic feature potentially linking vaccination and [some] neuropsychiatric disorder(s), one would expect to see the same/similar pattern of conditions being represented and reported? For balance, I should also point out that other independent study has talked about eating disorders potentially having "immune-mediated mechanisms" connected, particularly those associated with autoimmunity [4] although I don't doubt such a connection is likely complicated and probably not universally applicable.

It's not difficult to find issues with the Leslie paper and no doubt these will be emphasised in any further discussions about the data reported even when the authors stress throughout that "findings do not demonstrate a causal role of vaccination in the pathoetiology of any of these conditions." The strengths of the data - e.g. the use of that administrative database for confirming diagnoses and vaccine exposure - are worth mentioning again in light of other debates on data sources from other 'disappearing' manuscripts in this area. I might also add that by focusing in on various diagnoses but not autism (which again, they could have done) and not a certain vaccine, the authors seem well aware of the history in this area - "the association of the measles, mumps, and rubella vaccine with autism spectrum disorder has been convincingly disproven" - and probably either thought nothing more of it or chose to steer well clear of it (or perhaps a combination of both).

Is there a 'where next' when it comes to the Leslie data? To quote again from the paper: "findings require replication in a larger population-based sample, possibly including assessments of various potentially important host factors, e.g., the individual’s genomic and epigenomic background, the individual’s microbiome, their history of antecedent psychosocial stress, infections, as well as other potentially simultaneously administered vaccinations, the differences in vaccine types, and the route of administration (e.g., intramuscular or intranasal administration of influenza vaccine)." The scientific literature also provides some other avenues for further study in this area [5]. But science does not happen in a social vacuum; any further research needs to be done with care and focus. Mindful of both the important reliance on vaccination in protecting both the individual and population at large and mindful that sweeping generalisations (often emanating from scientific study) need to be minimised.

And on the topic of the research of Douglas Leslie, I'll be coming to another recent paper he published on the important issue of depression in parents of children diagnosed with autism [6] quite soon...

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[1] Leslie DL. et al. Temporal Association of Certain Neuropsychiatric Disorders Following Vaccination of Children and Adolescents: A Pilot Case-Control Study. Front Psychiatry. 2017 Jan 19;8:3.

[2] Wang L. et al. Healthcare Service Use and Costs for Autism Spectrum Disorder: A Comparison Between Medicaid and Private Insurance. Journal of autism and developmental disorders. 2013;43(5):1057-1064.

[3] Szakács A. et al. Psychiatric comorbidity and cognitive profile in children with narcolepsy with or without association to the H1N1 influenza vaccination. Sleep. 2015 Apr 1;38(4):615-21.

[4] Raevuori A. et al. The increased risk for autoimmune diseases in patients with eating disorders. PLoS One. 2014 Aug 22;9(8):e104845.

[5] Sadarangani SP. et al. "Let there be light": the role of vitamin D in the immune response to vaccines. Expert Rev Vaccines. 2015;14(11):1427-40.

[6] Cohrs AC. & Leslie DL. Depression in Parents of Children Diagnosed with Autism Spectrum Disorder: A Claims-Based Analysis. J Autism Dev Disord. 2017 Feb 18.

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ResearchBlogging.org Leslie DL, Kobre RA, Richmand BJ, Aktan Guloksuz S, & Leckman JF (2017). Temporal Association of Certain Neuropsychiatric Disorders Following Vaccination of Children and Adolescents: A Pilot Case-Control Study. Frontiers in psychiatry, 8 PMID: 28154539

Monday, 20 February 2017

Catatonic symptoms and autism

"Catatonic symptoms are more prevalent in young people with autism than previously thought" said the article recently published by Breen and Hare [1]. Continuing a research theme of at least one of the authors [2], the idea that catatonic symptoms - primarily manifesting as stupor, unresponsiveness to light, noise or touch, mutism, etc - might be over-represented when it comes to autism is not a new one by any means.

Breen & Hare set about looking for "the presence and nature of such attenuated behaviours in children and adolescents with autism" based on something called the Attenuated Behaviour Questionnaire. This was delivered to parents/caregivers online alongside looking at information from other measures based on the presence of repetitive behaviour and depression.

"Attenuated behaviour indicative of catatonia was relatively common in young people with autism with up to 20.2% having an existing diagnosis of catatonia and evidence of a relationship between attenuated behaviours and measures of depression and repetitive and restricted behaviours." Such findings as I said, are by no means novel but once again highlight how a diagnosis of autism or autism spectrum disorder (ASD) is seemingly protective of nothing when it comes to comorbidity. To quote another author on this topic: "an unabashed drumroll for increased recognition and treatment of catatonia in autism spectrum disorders (ASD)" [3] is needed.

Catatonia appearing alongside [some] autism leads into a number of areas in relation to the 'closeness' of any relationship (some people have talked about 'autistic catatonia') and the management strategies that may be subsequently indicated. On the issue of management, guidance is available [4] albeit including a strategy - electroconvulsive therapy (ECT) - that is probably not going to win any awards in terms of popularity given its historical basis. Accepting that still today ECT as an 'intervention' option when it comes to autism still courts heated discussion (see here), there is the requirement for much greater study of catatonic symptoms in relation to autism and whether there may be several presentations ripe for more novel intervention [5] (in light of a growing area of research interest). Said intervention might also take into account the plurality of autism too (see here)...

To close, yet another song for my brood and a very proud father who saw some real talent in the karate competition yesterday (those first place trophies are proof that team kata and team kumite are definitely the way forward)...

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[1] Breen J. & Hare DJ. The nature and prevalence of catatonic symptoms in young people with autism. J Intellect Disabil Res. 2017 Feb 1.

[2] Hare DJ. & Malone C. Catatonia and Autistic Spectrum Disorders. Autism. 2004; 8: 183-195.

[3] Dhossche DM. Decalogue of Catatonia in Autism Spectrum Disorders. Frontiers in Psychiatry. 2014;5:157.

[4] Mazzone L. et al. Catatonia in patients with autism: prevalence and management. CNS Drugs. 2014 Mar;28(3):205-15.

[5] Kiani R. et al. Anti-NMDA-receptor encephalitis presenting with catatonia and neuroleptic malignant syndrome in patients with intellectual disability and autism. BJPsych Bull. 2015 Feb;39(1):32-5.

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ResearchBlogging.org Breen J, & Hare DJ (2017). The nature and prevalence of catatonic symptoms in young people with autism. Journal of intellectual disability research : JIDR PMID: 28150394

Saturday, 18 February 2017

Social interaction and autism: it takes two to tango

Psychology experiments are not generally fodder for this blog when it comes to autism. The main reason being that quite a few appearing in the peer-reviewed literature tend to look at quite abstract features perhaps somewhat removed from the daily lives of autistic people and their significant others. A few also seem to struggle with the idea that grand over-arching psychological theories (that seem to inevitably follow psychological findings in particular) are not required when it comes to autism in these days of heterogeneity and plurality.

I am making an exception today however with the paper by Noah Sasson and colleagues [1] (open-access) and their findings suggesting advocating "for a broader perspective of social difficulties in ASD [autism spectrum disorder] that considers both the individual’s impairments and the biases of potential social partners." In other words, it takes two to [socially, interactively] tango. I might add that a doctoral thesis by one of the co-authors on the Sasson paper (Daniel Faso) is also available for further inspection too (see here).

Based on the idea that issues with social interaction "quantity and quality" might not be something exclusively under the control of those diagnosed with autism, Sasson et al devised a series of experiments to test their hypothesis: "three studies conceived and conducted independently by three research groups assessing observers’ first impressions of—and intentions to socially engage with— children and adults with ASD based upon “thin slices” of their real-world social behavior." I'm not going to go into too much detail about the experiments because the paper is open-access and you can read about them for yourselves. 'Thin slices' in the context of the experiments carried out referred to media that were rated pertinent to "observers’ first impressions of individuals with ASD engaging in real-world social behavior."

The results make for some important reading as across the different experiments undertaken the key messages were that: "first impressions of individuals with ASD are significantly less favorable than those of matched TD [typically developing] controls, and are associated with greater reluctance on the part of observers to pursue social engagement." Further: "social interaction difficulties in ASD are not solely an individual impairment but also a relational one, and consideration of both of these factors is necessary for a full understanding of social impairment in ASD." I relay all of that bearing in mind that these were experiments carried out under controlled conditions (I don't know about you, but I don't generally rate people at first contact using a "0-3Likert scale or a "non-graduated slider" on 'how approachable' they were or the likelihood of a friendship developing).

Although important, I don't think anyone should be too surprised by the results reported in the context of how first impressions count and how people are generally quick to judge from "personality and character traits" whether social engagement with a person or group of people is going to be a short or longer-term thing. I say this also bearing in mind that minus any psychobabble, people generally take into account things like context, familiarity and similarity when it comes to their social interaction decisions too [if for example, you happen to be a fan of Star Wars or a Shotokan karateka, I might be more inclined to chat with you than say if you talked about the goings-on on various reality TV shows]. Indeed, the authors note: "these studies present only group-wise comparisons and do not address individual differences among those with ASD, nor whether individual characteristics of the raters (e.g., gender, personality, etc.) affect the results reported here." I'd also forward the idea that they might also include important concepts such as self-monitoring for example when it comes to future studies in this area. Similarly, it would also be handy to see if 'comorbidity counts' when it comes to further investigations on this topic in light of expanding links between different labels and traits (see here).

The question of what to do about the Sasson findings similarly provide some food for thought. The authors suggest that: "intervention and education approaches that target both those with ASD as well as their TD [typically developing] peers may offer a more comprehensive approach for improving social and functional outcomes in autism." In the context of other studies looking at social interaction and autism particularly in the school setting (see here) I can see how this might work in terms of raising awareness of how people are not always the same when it comes to the presentation of their social persona. Intervening with a wider group (i.e. peers) and taking the onus off 'just the person with autism' is a win-win situation and will no doubt have other positive knock-on effects in terms of self-esteem and helping to remove barriers around the 'disability' framing of autism. I might add that in these days of the potential virality of personality traits, it makes sense to include everyone.

In a wider context - outside of school - and in the big, wide [adult] world however, I'm slightly less sure of how such intervention is going to be achieved. Yes, we would all love people to be more understanding and less 'judgemental' in their first (and subsequent) impressions, but when it comes to influencing aspects such as views on "awkwardness, attractiveness, [and] likability" I'm not so sure that this can be universally achieved. Indeed, facets such as attractiveness and likability are probably going to be influenced by lots of variables outside of those just linked to an autism diagnosis and its presentation (frank or not). By saying all that, I'm not suggesting that we shouldn't try to educate and perhaps even move people away from the whole 'first impressions last' [2] thing, but rather am looking at the realistic prospect of achieving such a societal goal, mindful that it takes two to tango...

And on the topic of first impressions, at least get the handshake right (i.e. let go)...

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[1] Sasson NJ. et al. Neurotypical Peers are Less Willing to Interact with Those with Autism based on Thin Slice Judgments. Sci Rep. 2017 Feb 1;7:40700.

[2] Gunaydin G. et al. Impressions Based on a Portrait Predict, 1-Month Later, Impressions Following a Live Interaction. Social Psychological and Personality Science. 2017. 8: 36-44.

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ResearchBlogging.org Sasson NJ, Faso DJ, Nugent J, Lovell S, Kennedy DP, & Grossman RB (2017). Neurotypical Peers are Less Willing to Interact with Those with Autism based on Thin Slice Judgments. Scientific reports, 7 PMID: 28145411