Tuesday, 26 September 2017

Autism diagnosis as an "independent risk factor of attempted suicide"

The topic covered in the paper by Mu-Hong Chen and colleagues [1] is unfortunately, a familiar one to this blog examining the association between a diagnosis of autism or autism spectrum disorder (ASD) and suicidality.

Although various research and clinical efforts continue in this area, there remains a worrying association between autism and various aspects of suicidality covering ideation/discussion, attempts and unfortunately, completion in some cases. I might even add in the concept of assisted suicide to such as association (see here). Lives are being lost.

Chen et al once again drew on the 'big data' resource that is the Taiwan National Health Insurance Research Database to look at whether: "ASD independently increases the risk of attempted suicide" on the basis that comorbidity such as depression, has been suggested to exert an influence on suicidality - peripherally or directly - in the context of autism (see here).

Looking at over 5,500 adolescents (12-17 years) and young adults (18-29 years) with a diagnosis of ASD compared to over 22,000 sex- and aged-matched 'not autism' controls, researchers looked for catalogued instances of suicide attempt(s) alongside various other data on participants - "demographic data and psychiatric comorbidities." They observed that suicide attempts were significantly higher in the ASD cohort compared with controls (~4% vs. ~1%) and onward presented with elevated hazard ratios. Those elevated hazard ratios took into account those various demographic and psychiatric comorbidity data, leading the authors to conclude that the diagnosis of ASD was itself an independent risk factor for attempted suicide.

One might um-and-ah about how representative Taiwanese data might be to the rest of the world or indeed, whether with all the strengths of the Taiwanese dataset, there may be psychopathology such as depression that is not recorded in the insurance database on the basis of being sub-clinical for example. But with big participant numbers comes big(ger) confidence that the findings might be generalisable. Knowing also that various types of depression do seem to be over-represented in cases of autism (see here), so one might assume that it would be on the clinical radar no matter what country you come from or are currently living in.

Without trying to simplify the road(s) that lead someone to contemplate suicide (big data Taiwan has also already told us about some of them) I do find some hope in the findings of Chen and colleagues. Their suggestion that autism - the facets of autism - might be an independent risk factor for suicide suggest that if one is able to 'pin down' what specific parts of autism might be linked to a greater risk for suicide, then one could conceivably act upon them. I know some people don't like the idea of 'acting on' autism, but taking the example of another pretty disabling feature of quite a few instances of autism - anxiety - there are indications that acting on core symptoms *might* aid in reducing/dispensing with this quality-of-life-draining clinical feature also (see here). I might also add that even though facets of autism itself might be linked to an elevated risk of suicidality, one shouldn't necessarily assume that comorbid depression is completely off the hook; also keeping in mind that a variety of social factors might play a role in such behaviour(s) (see here)...


[1] Chen MH. et al. Risk of Suicide Attempts Among Adolescents and Young Adults With Autism Spectrum Disorder: A Nationwide Longitudinal Follow-Up Study. J Clin Psychiatry. 2017 Aug 29. pii: 16m11100.


Monday, 25 September 2017

Anxiety prevention meta-analysed and some implications...

"Psychological and/or educational interventions had a small but statistically significant benefit for anxiety prevention in all populations evaluated. Although more studies with larger samples and active comparators are needed, these findings suggest that anxiety prevention programs should be further developed and implemented."

That was the research bottom-line published by Patricia Moreno-Peral and colleagues [1] assessing the collected peer-reviewed literature pertinent to the question: "Are psychological and/or educational preventive interventions for anxiety effective in varied populations?" An accompanying editorial on the Moreno-Peral findings is also worthwhile reading [2].

The methodological name of the game was systematic review and meta-analysis followed by "meta-regression" to boil down data from some 29 studies examining whether "psychological and/or educational interventions are effective in the prevention of anxiety." Said interventions covered some ground but in the most part relied on the use of cognitive behavioral therapy (CBT).

I'm not going to say too much more about the Moreno-Peral findings because I think they speak for themselves. I do however want to make comment on the authors' use of the term 'varied populations' to highlight potential implications for a couple of populations pertinent to this blog: (a) the autism spectrum and (b) those diagnosed with chronic fatigue syndrome/myalgic encephalomyelitis (CFS/ME).

Starting with autism, there are two salient points to make: (i) anxiety is pretty rife in relation to autism (see here and see here) and (ii) treating anxiety in relation to autism already has some peer-reviewed science efforts (see here) but little so far has seemingly been done on the point of potentially heading-off clinically relevant anxiety before it takes hold. I say this mindful of the idea that core symptoms linked to autism might be potential 'anxiety-provokers' (see here). Quite a bit more research is needed to ensure that psychological and/or educational interventions for anxiety currently available are specifically tailored to the wants and needs of those on the autism spectrum (including all of the spectrum!) but this area promises quite a bit. It's also worth appreciating that there may be a place for other types of prevention/intervention when it comes to anxiety (see here for example) in the context of autism (see here).

I also mentioned the [careful] application of the Moreno-Peral findings to CFS/ME. Coincidentally at the time of writing this post, I stumbled across the paper by Sarah Stoll and colleagues [3] asking: 'What treatments work for anxiety in children with chronic fatigue syndrome/myalgic encephalomyelitis (CFS/ME)?' The answer, based on the available literature is 'we don't know yet' with the requirement for more investigations.

I tread very carefully in this area based on the fact that whilst anxiety does seem to be part and parcel of some CFS/ME (see here), suggestions about the possible usefulness of something like CBT to manage anxiety have to viewed in the context of CBT still courting controversy as part of the biopsychosocial 'view' of CFS/ME (see here) (something that is relevant to other recent discussions about CFS/ME). Indeed, one might see the Stoll findings in the context that the 'failure' of interventions like CBT in relation to treating core CFS/ME (see here for what I mean by 'failure') is moving some people along to still try and stick with CBT but re-do and re-apply it in the context of treating more peripheral signs and symptoms accompanying CFS/ME such as anxiety. I might be wrong but...

To close, but keeping the CFS/ME link in mind, I once again note a welcomed U-turn from NICE (National Institute for Health and Care Excellence) on the topic of CFS/ME: "The strong message from stakeholders was that the continuing debate about the causes of this condition and the best approach to treatment argued for a review of the current guideline." I've said it before and will say it again: patient-power has driven this reconsideration (see here)...


[1] Moreno-Peral P. et al. Effectiveness of Psychological and/or Educational Interventions in the Prevention of Anxiety. JAMA Psychiatry. 2017. Sept 6.

[2] Hudson JL. Prevention of Anxiety Disorders Across the Lifespan. JAMA Psychiatry. 2017. Sept 6.

[3] Stoll SVE. et al. What treatments work for anxiety in children with chronic fatigue syndrome/myalgic encephalomyelitis (CFS/ME)? Systematic review. BMJ Open. 2017; 7: e015481.


Saturday, 23 September 2017

Pregnancy antidepressant use and offspring outcomes beyond autism?

I'll say one thing for the British Medical Journal (BMJ), they don't seem to be afraid to cover important issues relating to the *possible* "reproductive safety of drugs" [1] as per their publication of yet another paper looking at antidepressant use during pregnancy and offspring outcomes published by Xiaoqin Liu and colleagues [2]. This follows another paper published in the BMJ and covered on this blog a few weeks back (see here).

The specific class of drugs being examined again are, as I mentioned, the antidepressants and based, yet again, on data from one or more of those wonderful Scandinavian population registries in relation to how pregnancy use of antidepressants *might* impact on risk of risk of various psychiatric disorders in offspring. A diagnosis of autism spectrum disorder (AD) has been a primary focus of previous research in this area; particularly the question of whether the medicines themselves or the condition(s) that the medicines are used for (i.e. maternal psychopathology) might be the more important variables related to enhanced offspring risk of autism. The last paper covered on this blog by Rai and colleagues [3] very cautiously suggested that: "The results of all these analyses, which used different assumptions, seemed to be consistent with each other, suggesting that the association between in utero exposure to antidepressants and autism might not be fully explained by confounding." Cautiously...

This time around the net was widened from just looking at autism as an offspring outcome to "overall risk of psychiatric disorders" including: "autism spectrum disorder... mood disorder... neurotic, stress related, and somatoform disorder... behavioural and emotional disorder... and mental retardation." I might add that these are the authors words not mine and diagnoses were based on ICD-10 criteria and codings.

Looking and following some 900,000 children born between 1998 and 2012 in Denmark until 2014, researchers categorised participants according to their pregnancy antidepressant exposure(s): "unexposed, antidepressant discontinuation (use before but not during pregnancy), antidepressant continuation (use both before and during pregnancy), and new user (use only during pregnancy)" and looked at the frequency of those conditions included for study.

Results: some 2% of children were born to mums who used an antidepressant during pregnancy (n=21,063). Various types of antidepressants were used but the majority were prescribed SSRIs (Selective Serotonin Reuptake Inhibitors) either alone (monotherapy) or in conjunction with other non-SSRI medication.

"We observed increased risks of psychiatric disorders in all three groups of antidepressant users (discontinuation, continuation, and new user groups), compared with the unexposed group." This itself is an important finding but does not yet disentangle whether medicine use or the reason(s) for medicine use might be the more important variable. Then: "we observed an increased risk of psychiatric disorders in children whose mothers continued antidepressant use during pregnancy, compared with mothers who discontinued." Such a statement potentially edges a little closer to some influence of pregnancy antidepressant use on offspring outcomes but, and it is an important but: "These associations could be attributable to the severity of the underlying maternal disorders in combination with in utero antidepressant exposure." In other words, those mums who needed to continue antidepressant use throughout pregnancy probably had to do so because their symptoms either returned or were not controlled properly when medication is not in place. This might imply that more serious maternal psychiatric disorder could be a variable in any enhanced risk of offspring psychiatric disorder.

When it came to looking at specific diagnostic labels for offspring, all but "mental retardation" (I prefer the term learning disability) seemed to be elevated alongside "in utero exposure to antidepressants." The conditions with the highest risk were the mood disorders including diagnoses such as clinical depression and bipolar disorder. Given that antidepressants are typically (but not exclusively) used to treat/manage mood disorders, such a finding of maternal mood disorder potentially transmitting down into offspring mood disorder receives further credence from such results.

The Liu paper and accompanying editorial grapple with the question of whether the *possible* risks from pregnancy use of antidepressants on offspring merit a change to guidance on their use at such a critical time. As I've mentioned on other occasions discussing this topic, antidepressants are not typically just dispensed willy-nilly without appropriate clinical indication. They provide an important service in controlling various types of symptoms; pertinent to the idea that uncontrolled depression during pregnancy for example, can have all-manner of negative outcomes. As all medicines do, yes they may have side-effects but these need to be weighed up against perceived benefits, taking into account any important influence on the developing child. Indeed, the authors note: "any final decision on antidepressant continuation should be individualised and made jointly by health professionals and patients."

And whilst I've mentioned pregnancy antidepressant use and offspring autism risk, yet another review paper enters the scientific fray [4]...


[1] Nordeng H. et al. Prenatal exposure to antidepressants and increased risk of psychiatric disorders. BMJ. 2017; 358: j3950.

[2] Liu X. et al. Antidepressant use during pregnancy and psychiatric disorders in offspring: Danish nationwide register based cohort study. BMJ. 2017; 358: j3668.

[3] Rai. D. et al. Antidepressants during pregnancy and autism in offspring: population based cohort study. BMJ. 2017; 358: j2811.

[4] Andalib S. et al. Maternal SSRI exposure increases the risk of autistic offspring: A meta-analysis and systematic review. Eur Psychiatry. 2017 Jun 20;45:161-166.


Friday, 22 September 2017

SMILE: On the Lightning Process + specialist medical care for chronic fatigue syndrome (CFS)

Even before the publication of the results by Esther Crawley and colleagues [1] I had already seen quite a few discussions on the use of the Lightning Process being applied to the label chronic fatigue syndrome (CFS) (see here for example).

A trial protocol [2] and some additional 'building work' [3] on this topic had already been published in the peer-reviewed domain, talking about how use of the "Phil Parker Lightning Process® (LP)" developed from "osteopathy, life coaching and neuro-linguistic programming" was already reported in the context of CFS (and CFS/ME - myalgic encephalomyelitis) and the requirement to study it given "no reported studies investigating the effectiveness or possible side effects (for example serious adverse events) of the LP."

The theory behind the LP is that of training individuals "to recognize when they are stimulating or triggering unhelpful physiological responses and to avoid these, using a set of standardized questions, new language patterns and physical movements with the aim of improving a more appropriate response to situations." In short, I don't think it's unreasonable to say that the biopsychosocial (BPS) view forms part of the methodological basis for the intervention. Alarm bells were already starting to ring (see here).

The Crawley results have been posted across the lay media, with headlines such as 'Controversial Lightning Process helps children with chronic fatigue syndrome' and 'Chronic fatigue therapy 'could help teenagers', study says.' Interestingly however, various counter viewpoints about the trial have also been included in such reports, as per quotes such as "The over-simplistic and largely psychological model of ME/CFS causation that is being put forward to patients by Lightning Process practitioners is totally out of step with emerging scientific evidence as to its cause." Even expert opinion has it's own worries about the trial and it's subject matter. I'll come back to all that shortly.

So what did the study actually do and find? Well, teens with mild/moderate CFS/ME were the target study group (100 of them): "Children were diagnosed with CFS/ME after a thorough assessment which included screening for other disorders associated with fatigue." The authors noted that recruitment was 'problematic' when it came to this trial as per the note: "Fewer than 30% of eligible children were randomised. We do not know why the majority did not want to take part in the trial but it may be because they did not want to take part in groups or travel for three consecutive days." Diagnosis by the way, I assume followed the NICE guidance on the topic; the same NICE guidance that has seen a U-turn in recent days on the potential need for some reconsideration (see here). Real 'patient power' was behind this decision by the way.

Fifty-one of the 100 participants were allocated to receive specialist medical care (SMC) plus a few days LP training and the remaining 49 just received SMC. SMC by the way, again follows those NICE guidance "focused on improving sleep and using activity management to establish a baseline level of activity (school, exercise and social activity) which is then gradually increased." CBT - cognitive behaviour therapy - is also offered to those with "significant anxiety or low mood" and: "Participants could choose to use physiotherapist-delivered graded exercise therapy, which provides detailed advice about exercise and focuses on an exercise programme rather than other activities." The primary outcome of the trial was scores on the "the 36-Item Short-Form Health Survey Physical Function Subscale (SF-36-PFS)" at baseline and again at 6 months. Various other measures were also included as secondary outcomes looking at "pain, anxiety, depression, school attendance and cost-effectiveness from a health service perspective at 3, 6 and 12 months."

Results: "It is the first trial that has demonstrated the effectiveness of an intervention other than CBT for paediatric CFS/ME." Although it is debatable whether CBT is as 'effective' an intervention for CFS/ME as many people might think (see here for a real world perspective on this from some of the authors on the current paper and see here for other findings), the results did seemingly show a difference between the groups when it came to mean SF-36 physical function scores in favour of the experimental group. The margin of the group difference was significant and authors noted that: "There was little evidence that the effect of LP+SMC compared with SMC on the primary outcome differed according to baseline age, anxiety or school attendance." The caveat to all this is the reliance on patient-reported outcomes and the unblinded nature on the trial that "may have been affected by participants’ knowledge of the group to which they were randomised." As other commentators have noted (see here again) 'positive expectations' seem to be part-and-parcel of the LP method and it's not inconceivable that these might have subsequently affected patient scores. Further comment from the authors that "it would be unethical to have a control group without treatment"as part of their study is to some extent justified but does not discount the idea that other, non-psychological interventions, could have been pitted against both SMC and the LP+SMC (see here for one double-blind, placebo-controlled example). Indeed, I'd like to see more of such comparisons in further study.

When it came to another important part of the study - adverse effects - authors specifically noted that: "Physical function at 6 months deteriorated in nine participants, of whom eight were in the SMC arm." They also reported on a few instances of adverse events but concluded that generally both study arms were considered safe over the course of study.

From a scientific point of view, the Crawley results provide some support for the use of the LP + SMC in the context of [some] teen CFS/ME. The authors noted that they don't know whether their results are likely to generalise to more severe cases of CFS/ME or indeed those younger than 12 years old, and offer little in the way of explanation as to why they got the results that they got (i.e. "Further research is needed to understand why LP improves outcomes at 6 and 12 months and which aspects of the LP contribute to its effectiveness.") I'm not however totally sold on the idea that the LP is "teaching people to use their brain to “stimulate health-promoting neural pathways”" as an explanation for the the findings, but would be willing to concede should the relevant (MRI?) scientific evidence ever emerge. As an aside, quite a lot of the research with a BPS slant to it with regards to CFS/ME could benefit from the odd physiological measures now and again just to see what may or may not be being affected...

Bearing in mind the [long] history of medical involvement in CFS/ME and the often detrimental focus on things like the BPS model [4] with regards to the condition, it's not a surprise that even despite 'positive' results, the SMILE trial has not been received with open arms by quite a few. Problems with trial recruitment? Well, one might opine that this could have had something to do with the subject matter and that BPS-type implication behind the trial potentially putting people off. Other more qualitative reports on the use of the LP in the context of CFS/ME [5] have hinted at issues with things like the "secrecy surrounding it, and feelings of being blamed if the treatment did not work" that hardly provide a great endorsement for getting involved. Yet again, the burden of CFS/ME is seemingly being placed on the person, with only little regard for the fact that there is a growing body of evidence to suggest that biology trumps psychology when it comes to the presentation and perpetuation of symptoms for many (see here). All the positive feelings, thinking and 'reprogramming' in the world are probably not going to fundamentally alter such biological (medical) issues as per other examples in the research literature (see here). Given also that science does not exist in a social or cultural vacuum, and past scientific experiences when it comes to treatment options for CFS/ME (see here) I wonder if perhaps a new direction needs to be taken - particularly here in Blighty - whereby as many resources and research interests are put into trying to understand the biology of the spectrum that is CFS/ME as are seemingly being dedicated to looking at and tackling the psychology of CFS/ME.

Parity in biological and psychological research is the real 'mind-body' stuff when it comes to CFS/ME...


[1] Crawley EM. et al. Clinical and cost-effectiveness of the Lightning Process in addition to specialist medical care for paediatric chronic fatigue syndrome: randomised controlled trial. Archives of Disease in Childhood. 2017. 20 Sept.

[2] Crawley E. et al. Comparing specialist medical care with specialist medical care plus the Lightning Process for chronic fatigue syndrome or myalgic encephalomyelitis (CFS/ME): study protocol for a randomised controlled trial (SMILE Trial). Trials. 2013 Dec 26;14:444.

[3] Crawley E. et al. The feasibility and acceptability of conducting a trial of specialist medical care and the Lightning Process in children with chronic fatigue syndrome: feasibility randomized controlled trial (SMILE study). Trials. 2013 Dec 5;14:415.

[4] Geraghty KJ. & Esmail A. Chronic fatigue syndrome: is the biopsychosocial model responsible for patient dissatisfaction and harm? Br J Gen Pract. 2016 Aug;66(649):437-8.

[5] Reme SE. et al. Experiences of young people who have undergone the Lightning Process to treat chronic fatigue syndrome/myalgic encephalomyelitis – a qualitative study. Br J Health Psychology. 2012; 18: 508-525.


Thursday, 21 September 2017

"the likely effects of autism spectrum disorder on adolescent driving abilities"

"The literature revealed that drivers with autism (particularly males) were less likely to identify social hazards (e.g., pedestrians), had slower reaction times, more tactical driving difficulties, reported more traffic crashes, citations and intentional driving violations, and had poorer situation awareness skills than drivers without autism."

So said the literature review published by Clara Silvi and colleagues [1] looking at how young people diagnosed with an autism spectrum disorder (ASD) manage the multiple tasks involved in driving and how various characteristics linked to autism *might* translate into "driving-related challenges."

I feel I must add a caveat or two before proceeding with this post. First up is the quite widely known about association between age and driving ability (or inability). Younger drivers are, for various reasons, already more likely to be "overrepresented in road crash statistics." Inexperience, more risk-taking driving behaviours combined with the 'overconfidence of youth' are likely to be important reasons for such adverse driving statistics. Second, a diagnosis of autism does not automatically make everyone with autism a poor driver. Granted, here in the Blighty at least, a diagnosis of autism or ASD is something that needs to be considered in the context of licencing for driving (see here) but unlike something like epilepsy - "epileptic attacks, seizures, fits or blackouts" - the condition/label does not automatically disqualify someone from being licensed to drive.

OK, the Silvi review initially took in quite a lot of the literature on this topic, eventually being boiled down to 9 articles. These collected research papers provided various viewpoints on autism and driving behaviours/outcomes including that from parents/caregivers, driving instructors and importantly, young novice drivers with autism. The endpoint reached suggested that "symptoms of autism spectrum disorder can negatively affect the driving abilities of young drivers with autism spectrum disorder, further impacting their ability to drive, and in this way increasing their risk of crashing."

The authors have zoomed in quite a bit on a possible role for situational awareness when it comes to adverse outcomes in the context of autism and driving. Situational awareness combines various elements whereby the 'here and now' of the driving environment is constantly changing and hence drivers require a high degree of perceptual and cognitive flexibility and adaptation to adjust their driving behaviour accordingly. Indeed the authors talk about how: "Poor/underdeveloped situation awareness can represent a lack of mental models and schemas (thought/behavioral patterns)."

I can kinda see how some of the ways that autism has been defined *might* overlap with the findings talking about how "situation awareness skills were less developed in drivers with autism spectrum disorder." This is something picked up in other research too [2]. I'm not so sure about the whole 'lacking in mental models' thing applied specifically to autism (seemingly harking back to the sweeping generalisation of a 'lack of theory of mind') but can perhaps see a way forward for how cognitive flexibility might be something important in the context of traits related to being rule-bound and highly perseverative.

There is a balance to be struck between the safety of autistic drivers (and indeed, the safety of other road users) and ensuring that personal liberties are not impinged on too much as a result of the Silvi findings. As many drivers will tell you, the freedom that comes with driving a car or other vehicle is something that adds considerably to quality of life; a topic that has already revealed some quite profound issues in relation to some autism [3] (see here for my take). Indeed, if accessibility is a factor in ensuring those on the autism spectrum can live a good quality of life, moves to make driving safer and more readily available to more people on the spectrum should be further [carefully] investigated.


[1] Silvi C. et al. A Literature Review of the Likely Effects of Autism Spectrum Disorder on Adolescent Driving Abilities. Adolescent Research Review. 2017. Sept 2.

[2] Chee DYT. et al. Investigating the driving performance of drivers with and without autism spectrum disorders under complex driving conditions. Disabil Rehabil. 2017 Aug 28:1-8.

[3] Ayres M. et al. A systematic review of quality of life of adults on the autism spectrum. Autism. 2017 Aug 1:1362361317714988.


Wednesday, 20 September 2017

Treating violence in schizophrenia with fish oils?

"Violent schizophrenia patients treated with fish oil (360mg DHA+540mg EPA) demonstrated a decrease in violence."

That was the primary conclusion arrived at in the study results by Yi Qiao and colleagues [1] suggesting that some aspects of nutrition may very well have implications for extremes of behaviour in the context of psychiatric diagnoses. The ClinicalTrials.gov entry for this study can be seen here.

DHA - Docosahexaenoic acid - and EPA - Eicosapentaenoic acid - are categorised as omega-3 fatty acids. In this research instance, Qiao et al divided up their "Fifty inpatients meeting ICD-10 criteria for schizophrenia" such that roughly half received a fish oil for 12 weeks and half received a placebo. I should add that this 'inpatient' group also scored significantly on the Modified Overt Aggression Scale (MOAS) at baseline.

Results: well, fish oil use did not seem to make any significant difference to some of the [positive and negative] signs and symptoms of schizophrenia compared with placebo use. But as per the opening sentence to this post, there did seem to be something significant to see when it came to follow-up of violent behaviour alongside the use of fish oils.

These are interesting findings. My first thoughts on reading the Qiao results harked back to previous work looking at the use of nutrition in the context of a prison population by Bernard Gesch and colleagues [2]. That research concluded that: "Antisocial behaviour in prisons, including violence, are reduced by vitamins, minerals and essential fatty acids" where EPA and DHA were part of the supplement provided under "double-blind, placebo-controlled, randomised trial" conditions; albeit in smaller doses that those used by Qiao and colleagues.

The Qiao results are also not the first time that fish oil use for violence in the context of schizophrenia have been talked about in the peer-reviewed science domain [3]. With the understanding that violence accompanying schizophrenia is probably going to be as complex as violence outside of schizophrenia, such promising results require some further replication and a little more data on possible hows-and-whys. The low cost, pretty favourable safety profile and reports of other potential health benefits associated with fish oil use however, suggest that such an intervention could easily be incorporated into treatment plan for many people fitting a similar profile to those described by Qiao and colleagues.


[1] Qiao Y. et al. Effects of Omega-3 in the treatment of violent schizophrenia patients. Schizophr Res. 2017 Aug 19. pii: S0920-9964(17)30501-7.

[2] Gesch CB. et al. Influence of supplementary vitamins, minerals and essential fatty acids on the antisocial behaviour of young adult prisoners. Randomised, placebo-controlled trial. Br J Psychiatry. 2002 Jul;181:22-8.

[3] Légaré N. et al. Omega-3 and violence in schizophrenia. Schizophrenia Res. 2007; 96: 269.


Tuesday, 19 September 2017

"a heightened co-occurrence rate of ASD [autism spectrum disorder] and GD [gender dysphoria]"

Gender dysphoria "where a person experiences discomfort or distress because there's a mismatch between their biological sex and gender identity" is something that has seemingly risen in research popularity in the context of autism (see here).

The findings reported by Janssen Aron and colleagues [1] (open-access available here) add to the body of research in this area where "endorsement of sex item 110, “wish to be opposite sex,” is 7.76 times more likely among participants with an ASD [autism spectrum disorder] diagnosis than in a nonreferred comparison group." 'Sex item 110' refers to a question item on the Child Behavior Checklist (CBCL) by the way.

Drawing on data derived from almost 500 participants diagnosed with an ASD and some 1600 responses to the CBCL from a 'normative sample', researchers inquired about possible gender variance. Importantly: "In the present study, all CBCL charts had been filled out by the patients' parents" so we need to bear in mind this was a study of proxy reporting albeit from those who probably know the participant pretty well. Researchers observed that some 5% of the ASD cohort "endorsed sex item 110" compared with about half a percent of the control group. Biological gender discussed in terms of 'natal gender' did not suggest that any one gender were more or less likely to endorse that CBCL question and age of participants similarly showed little impact on the endorsement of the questionnaire item.

The authors caution that response to one item on the CBCL does not a gender dysphoria diagnosis make. But they do suggest that further screening could be preferentially offered as and when either autism is diagnosed or indeed screening for autism/autistic traits when gender variance is encountered in the clinic minus any sweeping generalisations. One might also see a need for designing new questionnaires/schedules to specifically ascertain signs of gender dysphoria in cases of autism - indeed, as some have [2] - with a focus on both longitudinal research i.e. how might signs and symptoms change with age/maturation and also taking into account more direct reporting from participants themselves...


[1] Janssen A. et al. Gender Variance Among Youth with Autism Spectrum Disorders: A Retrospective Chart Review. Transgend Health. 2016 Feb 1;1(1):63-68.

[2] George R. & Stokes MA. Gender identity and sexual orientation in autism spectrum disorder. Autism. 2017. Sept 15.


Monday, 18 September 2017

Parent-mediated intervention for autism falls yet again

"We found minimal evidence for main effects of ART [Adapted Responsive Teaching] on child outcomes."

So said the study results reported by Linda Watson and colleagues [1] adding to a bank of studies (and meta-analyses) suggesting that parent delivered early behavioural interventions for autism or cases of 'at-risk for autism' in the most part are not seemingly cutting the scientific mustard (see here). I temper that last sentence with a number of caveats; not least that the methodological quality of the studies in this area still has some way to go and also that parent-mediated interventions covers quite a bit of ground in terms of techniques. The idea however that moves to make parents with children with autism some kind of 'super-parents' (yes, someone did use a term similar to that) to impact on their child's early presentation is not exactly borne out by the scientific data in this area. I would add that many parents of children with autism are already super-parents without any additional help, indications or guidance for the powers-that-be.

This time around nearly 90 young infants "at-risk of later ASD [autism spectrum disorder] diagnoses" were given either ART or REIM (referral to early intervention and monitoring) following other work from this authorship group on this topic [2]. ART by the way, focuses on 'relationships' over a 6 month period where aspects such as engagement, awareness and joint action between parent and child are some of the points of interest. Various facets of functioning were assessed and, assuming the equal use of other early intervention services between the groups, the time, effort and costs of ART did not seemingly provide some wildly significant gains when compared with REIM. In short, yes something like ART is a wonderful aid for things like increasing parental responsiveness to their kids but when it came to important child outcomes - including autism-related outcomes - the intervention did not seemingly fare so well.

What's more to say on this topic? Well, being careful not to hark back to the bad 'ole days where parenting behaviours were 'blamed' for the development of offspring autism, I'm not going to totally poo-poo this area of research and practice. There are some pretty good intervention strategies out there for helping parents to further *connect* with their children in the context of autism and potentially raising the potential and wellbeing of all parties concerned. My issue however is that moves to 'manualise' such interventions in the context of all autism (or rather all 'potential cases' of autism bearing in mind the use of the words 'at-risk') is not a great idea. As I've mentioned before in the context of the pluralised autisms, screening for things like inborn errors of metabolism potentially presenting with autism or autistic features seems a better first use of resources, assuming that underlying biological issues being associated with autism are probably not going to be that amenable to something like parent-mediated intervention or the like as per the example of something like phenylketonuria and autism (see here).


[1] Watson LR. et al. Parent-Mediated Intervention for One-Year-Olds Screened as At-Risk for Autism Spectrum Disorder: A Randomized Controlled Trial. J Autism Dev Disord. 2017 Aug 31.

[2] Baranek GT. et al. Preliminary Efficacy of Adapted Responsive Teaching for Infants at Risk of Autism Spectrum Disorder in a Community Sample. Autism Research and Treatment. 2015: 386951.


Saturday, 16 September 2017

Guess what? Gastrointestinal symptoms are prevalent in autism

The paper by Calliope Holingue and colleagues [1] provides brief blogging fodder today and a topic that has finally found its way into accepted peer-reviewed science when it comes to autism spectrum disorders (ASD): gastrointestinal (GI) issues are an often over-represented comorbidity when it comes to ASD.

Reviewing the peer-reviewed research literature on this topic, the authors concluded that there are some quite wide and sometimes disparate findings on the frequency of functional GI symptoms in the context of autism. Part of the reason for this is the lack of a standardised tool for looking at GI symptoms in relation to the label.

But: "The prevalence range for constipation was 4.3-45.5% (median 22%), for diarrhea was 2.3-75.6% (median 13.0%), and for any or more than one symptom was 4.2-96.8% (median 46.8%)." Median by the way, refers to the middle number (or in this case middle percentage) from the collected datasets and stresses that approaching half of all people on the autism spectrum may present with 'any or more than one' GI symptom of clinical relevance.

I've said it before and will say it again, there is guidance out there for the screening, diagnosis and management of bowel symptoms as and when they occur alongside a diagnosis of ASD [2]. We can um-and-ah about the cause(s) of such issues (stressing that the physiological is likely just as important as any psychological explanations) but at the end of the day, those diagnosed with autism and accompanying bowel issues - both functional and/or pathological - should receive the same care and management for their bowel issues as anyone else, save any further tragedies. Indeed, given the links being made between something like slow intestinal transit and autism for example (see here), preferential screening should perhaps be the order of the day before severe endpoints are reached (see here)...

To close, and not to make light of GI issues in relation to autism, a cautionary tale against 'throwing your poo(p) out of the window because it would not flush'???


[1] Holingue C. et al. Gastrointestinal symptoms in autism spectrum disorder: A review of the literature on ascertainment and prevalence. Autism Res. 2017 Aug 30.

[2] Buie T. et al. Evaluation, diagnosis, and treatment of gastrointestinal disorders in individuals with ASDs: a consensus report. Pediatrics. 2010 Jan;125 Suppl 1:S1-18.


Friday, 15 September 2017

"Children with autism spectrum disorder who improve with fever"

The title of this post mirrors that published by Rebecca Grzadzinski and colleagues [1] looking at an intriguing phenomenon whereby "some children with ASD [autism spectrum disorder] may show behavioral improvements during fever."

I had expected these results to be published given their appearance at this years IMFAR conference (see here) as one of my 'ones to watch' picks. Indeed, the results do not disappoint as the words 'discovery sample' and 'replication sample' are used as per other instances in the peer-reviewed research literature of this methodology (see here for example).

Drawing on data from the Simons Simplex Collection where over 1500 parents with children with autism were asked "whether and in which areas their child improved during fever", researchers randomly assigned participants to either the discovery or replication sample. They took various information - "demographics, medical history, ASD symptoms, adaptive skills, and presence of de novo ASD-associated mutations" - for each child and compared 'fever improvers' with 'fever non-improvers' across those measures for the discovery set.

Results: "Parent reports of 17% of children indicated improvements during fever across a range of domains." Some people might quibble with the reliance on parent report in this study but not me as per other work indicating 'sensitivity to an issue if not necessarily expertise' (see here). That almost a fifth of children with ASD might potentially show some clinical improvement during a fever episode is not to be sniffed at (see here) and hints that previous chatter about 'hot baths and autism' (see here) might not be just some odd idea (albeit with the requirement for further experimental study and with no endorsement from me).

Then: "Discovery and replication analyses revealed that the Improve Group had significantly lower non-verbal cognitive skills (NVIQ) and language levels and more repetitive behaviors." Such results, whilst requiring replication, hint at some interesting future studies to be done with certain parts of the autism spectrum. Lower NVIQ and language levels shouldn't however be just interpreted as just meaning those towards the more 'severe' end of the autism spectrum; even those with spoken language on the autism spectrum can be quite severely disabled by their autism.

"Understanding the profiles of children who improve during episodes of fever may provide insights into innovative treatments for ASD." I find myself in agreement with such sentiments, particularly when set in the context of possible "immunologic and neurobiological pathways, intracellular signaling, and synaptic plasticity" being potentially affected by fever onset [2] in the context of autism.

Music to close: Hüsker Dü - Makes No Sense At All (no reflection of the current research I might add).


[1] Grzadzinski R. et al. Children with autism spectrum disorder who improve with fever: Insights from the Simons Simplex Collection. Autism Res. 2017 Aug 31.

[2] Curran LK. et al. Behaviors Associated With Fever in Children With Autism Spectrum Disorders. Pediatrics. 2007; 120: e1386-92.


Thursday, 14 September 2017

What nearly 1500 patients with ME/CFS actually think about CBT, GET and pacing therapy

Today I'm discussing the findings reported by Keith Geraghty and colleagues [1] (open-access might be available here).

Looking at some interesting data derived from a rather large patient survey, authors examined what people diagnosed with myalgic encephalomyelitis / chronic fatigue syndrome (ME/CFS) actually thought about / experienced when it came to three intervention options: cognitive behavioural therapy (CBT), graded exercise therapy (GET) and pacing therapy (PT). A little bit of context about these interventions can be seen here including reference to some other peer-reviewed published work from members of this authorship group.

Based on the results of a survey offered by one of the premier UK organisations devoted to ME/CFS - certainly the one I tend to use when it comes to defining the spectrum that is ME/CFS - Geraghty et al add something to a body of research looking at the 'real world' impact (or not) of the various interventions currently advised for 'treating' CFS/ME (at least here in the UK). Their analyses suggested that: "While a small percentage of patients report some benefit from either CBT or GET, the majority experience no benefit." Even worse: "GET brings about a substantive deterioration in symptoms for almost half of patients"; something important to mention in the context of other, similar, intervention results being published earlier this year (see here).

At this point, I'll also refer you to other discussions of the Geraghty paper (see here).

Details are important to the Geraghty results. Including quite a sizeable cohort (N=1428) and asking over 200 questions "regarding treatment, particularly CBT, GET or PT", results were also compared against other patient survey results in the context of the intervention(s) being scrutinised. The combined results painted a similar sort of picture when it comes to experiences of the interventions insofar as "CBT brought about improvement in symptoms for approximately 35 per cent of respondents (65% unchanged/worse)" and "25 per cent of GET reported improvement in symptoms (17% unchanged/54% worse)." All this needs to be read in the context of the primary medical tenet: first, do not harm.

Geraghty et al acknowledge that there are limitations to their study results; not least that recall bias might be a potentially important issue and also that delivery of said interventions  might not have been carried out in "a uniform manner" (something also mentioned in the paper by Collin & Crawley [2]). With all due respect to the respondents, I might also add that independent confirmation of their diagnosis - knowing how important this - might also have provided some further methodological strength to the results too.

But in the context that patient surveys "offer a valuable insight into the ‘patient experience’" and how controversial some (all?) of these intervention options have been/continue to be in relation to CFS/ME (see here), these latest results represent an important research voice. They suggest yet again, that blanket recommendations for treating CFS/ME may have lots of potential effects (some positive but also quite a few negative) for many, many people diagnosed with such debilitating conditions. And once again, in the words of Jonathan Edwards [3] "If they [those diagnosed with ME/CFS] are still ill, presumably these approaches have failed and the priority is to find something more effective." Indeed (but don't hold your breath at least here in Blighty).


[1] Geraghty K. et al. Myalgic encephalomyelitis/chronic fatigue syndrome patients' reports of symptom changes following cognitive behavioural therapy, graded exercise therapy and pacing treatments: Analysis of a primary survey compared with secondary surveys. J Health Psychol. 2017 Aug 1:1359105317726152.

[2] Collin SM. & Crawley E. Specialist treatment of chronic fatigue syndrome/ME: a cohort study among adult patients in England. BMC Health Serv Res. 2017 Jul 14;17(1):488.

[3] Edwards J. PACE team response shows a disregard for the principles of science. J Health Psychol. 2017 Aug;22(9):1155-1158.


Wednesday, 13 September 2017

Autism portrayed in the movies: pleasing some of the people some of the time...

Things have come a long way since the first real mainstream appearance of autism on the silver screen (Rain Man). Nowadays, not a week seems to go by when autism doesn't feature in one form or another on a television show or new film/movie; even appearing in Sesame Street. I see this as a good thing when it comes to bringing autism further into the public psyche and hopefully preventing headlines such as 'Mother sent 'hurtful' letter about 'screechy' son with autism' from making many more appearances.

The downside however, is that with every representation of autism, there are typically comments galore about how autism is not being accurately portrayed or represented. A case in point is a new series called Atypical which has, according to one commentator, invited the same-old-same-old from some quarters (see here). Indeed, the old tenet: 'you can please some of the people some of the time, but not all of the people all of the time' seems to be tailor-made when it comes to views and opinions on the representation of autism on the screen.

It's timely that a new paper looking at the representation of autism in film and TV has also been published by Anders Nordahl-Hansen and colleagues [1]. Starting on the basis that: "Inaccurate portrayals [of autism] are a concern as they may lead to increased stereotypes toward the condition" authors concluded that many characters portraying autism seemed to "align unrealistically well with DSM-5 diagnostic criteria." They mention that those 'savant skills' (a.k.a 'a superpower') that every person with autism is supposed to have(!) were VERY well represented in the media content they surveyed. The authors go on to talk about the educational value of such portrayals and "the notion of authenticity in representing the autistic experience."

As I mentioned a few sentences back, I see autism appearing in more TV and films as a good thing. It makes an often invisible condition a lot more visible and helps to spread the idea that children/adults who were traditionally 'hidden away' deserve the same rights as anyone else. Insofar as the notion of 'authenticity' there have been quite a few, quite authentic portrayals of autism on TV shows. 'The A Word' was one of them (see here) (although I don't doubt some might disagree). Of course, there are always going to be creative processes acting on the fictional portrayal of autism; this goes for just about anything to do with creative media - soap operas do this all the time in the constant chase for viewer ratings. Indeed, one should never forget that TV shows and movies are in a constant state of chasing viewer ratings and not always necessarily produced with authenticity in mind.

In the context of autism also being an extremely heterogeneous condition (y'know, those 'autisms' that I keep going on about), I find it nigh on impossible that any single representation of autism is going to please all of the people all of the time. 'Authentic' is always going to be a matter of perspective...


[1] Nordahl-Hansen A. et al. Mental health on screen: A DSM-5 dissection of portrayals of autism spectrum disorders in film and TV. Psychiatry Res. 2017. Aug 22.


Tuesday, 12 September 2017

Facial phenotypes of autism continued

Quite a few years back, I talked on this blog about research suggesting that the structure of faces might be an important research area when it comes to at least some autism (see here). As per that blogging occasion, I cautioned that one has to be a little careful in this area of science so as not to make too many sweeping generalisations from any findings, but that there may some important *associations* to be noted. Such associations may, for example, be particularly important in the context of various genetic syndromes manifesting specific facial features as well as expressing autism or autistic traits.

In recent times I've noticed a couple of articles emerging on this topic from the University of Western Australia under the guidance of Prof. Andrew Whitehouse. Research from Prof. Whitehouse has been discussed before on this blog (see here and see here for examples) and I have to say I'm quite a fan of some of his, and his teams, efforts.

This time around I'm blogging about the papers by Maryam Boutrus and colleagues [1] and Diana Weiting Tan and colleagues [2] who talked about applying "a hypothesis-driven approach" to the study of facial phenotypes when it comes to autism and then offered up one such hypothesis: "comparing the facial masculinity/femininity of boys and girls with ASD [autism spectrum disorder] to that of typically-developing children" in the context of elevated prenatal testosterone exposure being *associated* with autism (albeit probably not universally so). I yet again hasten to add that the term 'typically-developing' is the authors' choice not mine.

The Tan paper talks about 3D imaging of faces from "a normative sample of 48 boys and 53 girls" which built up a kind of composite image to differentiate boy faces from girl faces. Some 21 facial landmarks were initially used but eventually this was boiled down into 11 selected facial features: "three linear distances (alar-base width, nose height and upper lip height) and eight geodesic distances (outer-canthal width, forehead width, forehead height, right upper cheek height, nasal tip protrusion, nose height, upper lip height, and nasal bridge length)."

The second part of the study then applied these 11 parameters deemed useful for differentiating "the faces of typically-developing boys and girls" and used them to compare faces of children diagnosed with ASD compared with those with no diagnosis - "54 autistic and 54 control boys... and also for 20 autistic and 60 control girls." This involved the application of "an overall facial masculinity/femininity index" providing a scale scoring between extreme masculinity and extreme femininity.

Results: "autistic boys had significantly lower gender scores for their faces (i.e., more masculine) when compared to the control boys." Also: "For girls, ANOVA showed that gender scores were significantly lower (i.e., less feminine) for the ASD group compared to the control group." These findings were accompanied by some equally interesting observations in relation to how the gender context of facial features seemed to tie into aspects of autistic presentation. Specifically: "increased facial masculinity in the ASD group correlated with more social-communication difficulties based on the Social Affect score derived from the Autism Diagnostic Observation Scale-Generic (ADOS-G)." No such relationship was reported in relation to the other part of the diagnostic dyad currently used to diagnose autism - Restricted and Repetitive Behaviours (RRBs).

Obviously, more needs to be done in this area. The sample size for both parts of the study reported by Tan et al is preliminary at best and replication is most definitely the name of the research game. I have to say that outside of the sexing/gendering of faces with autism in mind, I'm particularly interested in how facial masculinity might be linked to greater issues with social affect. One wonders whether this might for example, extend to the more general population and indeed, sub-clinical signs and symptoms of autism such as that noted in the broader autism phenotype (BAP)?

To close, although unrelated to the material covered today, facial phenotyping is starting to ask some other interesting questions too...


[1] Boutrus M. et al. Investigating facial phenotype in autism spectrum conditions: The importance of a hypothesis driven approach. Autism Res. 2017 Aug 17.

[2] Tan DW. et al. Hypermasculinised facial morphology in boys and girls with Autism Spectrum Disorder and its association with symptomatology. Sci Rep. 2017; 7: 9348.


Monday, 11 September 2017

On drinking water lithium content and dementia risk

"Lithium in tap water may cut dementia" went the BBC website headline reporting the study results published by Lars Vedel Kessing and colleagues [1]. The authors relied on some of those oh-so important Scandinavian population registries and other data to examine a possible connection between drinking water lithium levels and risk of "diagnosis of dementia in a hospital inpatient or outpatient contact."

Alongside looking at data for some 70,000 people diagnosed with dementia and nearly three-quarters of a million non-diagnosed controls, researchers estimated lithium exposure via drinking water based on data from over 150 waterworks. The relationship they observed between lithium in drinking water and risk of dementia diagnosis was not altogether straight-forward as "higher long-term lithium exposure from drinking water may be associated with a lower incidence of dementia" but the relationship was described as "nonlinear." Nonlinear meant that those with drinking water levels of lithium at moderate levels - between 5.1 and 10 micrograms per litre - actually showed an increased risk of dementia compared to those who had low levels of lithium (below 5 micrograms per litre) in their drinking water. The authors add: "Nonlinear dose-response associations are often found in medicine, with a gradual increase in drug response at the lower doses and gradual leveling off in response at the highest doses."

The authors do caution about their results and the various limitations attached to the findings. Not least is their reliance on a diagnosis of dementia as a starting point and how factors such as "accessibility to health care services that vary geographically" may have influenced such results. Indeed they note: "accessibility to health care services is increased in eastern regions of Denmark, where lithium levels generally are higher, and decreased in western regions, specifically in Jutland, where lithium levels generally are lower." They also found: "a direct inverse association with increasing risk of dementia in rural areas" as part of a sensitivity analysis, and as noted in some other studies [2]. More investigation is definitely required.

But these remain interesting results. Lithium is a treatment of choice when it comes to conditions such as bipolar disorder (see here). I've also talked about this stuff in connection to some other important research looking at suicide reduction too (see here) based on quite a body of research [3] (and growing all the time [4]) but minus simplifying something like suicide ideation, attempts or completion all down to lithium 'deficiency'. In relation to the possible effects on dementia risk, this is not the first time that lithium has been discussed as per findings looking at dementia risk in cases of lithium treated bipolar disorder [5] (something else that has been discussed on this blog - see here).

Questions still however remain. The mechanism of effect(s) is still to be suitably deciphered and one also needs to keep in mind the safety profile of lithium [6] as a balance to any risk-reduction effects on dementia or anything else. This is particularly relevant to those who might be at particular risk for dementia [7]. I'll also add that any focus on lithium intake and dementia also needs to keep in mind other *associations* that have been previously discussed in the peer-reviewed research literature such as that talking about vitamin D deficiency and dementia risk for example (see here) as part of a wider research interest in vitamin D and cognitive functions in the context of ageing (see here).


[1] Kessing LV. et al. Association of Lithium in Drinking Water With the Incidence of Dementia. JAMA Psychiatry. 2017 Aug 23.

[2] Contador I. et al. Childhood and Adulthood Rural Residence Increases the Risk of Dementia: NEDICES Study. Curr Alzheimer Res. 2015;12(4):350-7.

[3] Cipriani A. et al. Lithium in the prevention of suicide in mood disorders: updated systematic review and meta-analysis. BMJ. 2013 Jun 27;346:f3646.

[4] Kanehisa M. et al. Serum lithium levels and suicide attempts: a case-controlled comparison in lithium therapy-naive individuals. Psychopharmacology (Berl). 2017 Aug 28.

[5] Gerhard T. et al. Lithium treatment and risk for dementia in adults with bipolar disorder: population-based cohort study. Br J Psychiatry. 2015 Jul;207(1):46-51.

[6] Albert U. et al. Lithium treatment and potential long-term side effects: a systematic review of the literature. Riv Psichiatr. 2014 Jan-Feb;49(1):12-21.

[7] Holroyd S. & Rabins PV. A Retrospective Chart Review of Lithium Side Effects in a Geriatric Outpatient Population. Am J Geriatr Psychiatry. 1994 Autumn;2(4):346-351.


Saturday, 9 September 2017

School refusal is 'pervasive' in students with autism

The findings reported by Ellen Kathrine Munkhaugen and colleagues [1] make for worrying reading when it comes to the concept of school refusal in the context of autism spectrum disorders (ASD). Detailing how school refusal - where a child/young adult refuse to attend school because of the anxiety or distress it causes - was quite a bit more common among students with ASD compared with non-ASD students over a 20-day inspection period, the authors highlight an important issue. Indeed, an issue that has already been noted in the peer-reviewed literature [2] and has accompanying advice from the one of the larger autism organisations here in Blighty (see here).

As I've mentioned a few times on this blog, school can be a significant source of stress for many children on the autism spectrum (see here). We can for example, um-and-ah about the merits of inclusive vs. specialised education settings in the context of autism or how bullying seems to be something that quite a few children unfortunately, have to contend with (see here), but the bottom line is that stress is a likely passenger for many children with autism as they navigate the complicated world that is the childhood education system. And it is therefore perhaps unsurprising that for some children/young adults with autism, school might not be a place they necessarily want to spend a lot of time in.

One of the worries (among the many) that I have about results such as the ones from Munkhaugen et al is how, in these days of real focus on 'bottoms on seats' in school at least here in Blighty, such findings have the potential to single out families. If one reads the guidance from the UK Department of Education on the topic of school attendance (see here) for example, it's not difficult to see how tools like 'parenting contracts' and even 'parenting orders' might be something not unfamiliar in the context of school refusal. I say this bearing in mind that quite a few parents are already having to fight their child's corner when it comes to schools and local authorities providing appropriate school resources and allowances (see here) also potentially impacting on school refusal.

There are no easy or universal solutions to the issue of school refusal in the context of autism. Yes, schools can perhaps make provisions to help a child, but this needs to be set in the context that they have a school full of children who are similarly relying on them to provide the best educational experience that they can. The current cash-flow situation that many schools are faced with is also pertinent (see here). The other option is to try to manage school refusal behaviours particularly when chronic. This might first include investigations relevant to comorbid conditions that might also impact on school refusal [3] and then looking to strategies to help minimise the possible causes of school refusal [4] (tailoring them to the individual of course). Anxiety seems to be a key feature of school refusal (see here) and hence, moves to address this issue - and the core symptoms that seemed to be linked to it - should probably be part of any intervention strategy (see here). I hold back from making a big case for moving a child to a new school or into home education because this should really be a very last resort and come with their own potential issues.


[1] Munkhaugen. EK. et al. School refusal behaviour: Are children and adolescents with autism spectrum disorder at a higher risk? Research in Autism Spectrum Disorders. 2017; 41-42: 31-38.

[2] Kurita H. School refusal in pervasive developmental disorders. J Autism Dev Disord. 1991 Mar;21(1):1-15.

[3] Egger HL. et al. School Refusal and Psychiatric Disorders: A Community Study. Journal of the American Academy of Child & Adolescent Psychiatry. 2003; 42: 797-807.

[4] Kearney CA. & Silverman WK. A Preliminary Analysis of a Functional Model of Assessment and Treatment for School Refusal Behavior. Behavior Modification. 1990; 14: 340-366.


Friday, 8 September 2017

On puzzle pieces and autism

At first reading I was a little confused by the paper published by Morton Ann Gernsbacher and colleagues [1] talking about how puzzle pieces used as part of various organisations insignia concerned with autism might stir up the wrong kind of sentiments about the diagnosis. Confused because, with all the pressing needs related to autism research and practice - diagnosis, services, comorbidities, quality of life, happiness! - it seemed a little trivial to publish a research paper on what symbols an organisation might wish to choose and their subsequent connotations.

With a little more thought, my opinion of this research softened slightly as I can see how there might be some important psychological forces at work based on the imagery used to represent autism. Indeed, the puzzle piece and autism has been the topic of quite a few discussions in various quarters (see here) reflective of how some views and opinions about autism have changed down the years.

On this particular research occasion authors questioned some 400 people about the associations the general public might make regarding the use of the puzzle piece in the context of autism. They concluded that: "Puzzle pieces, both those used as autism logos and those used more generically, evoked negative implicit associations... and negative explicit associations" onward to associations with words like "incompleteness, imperfection, and oddity." Authors even concluded that: "If an organization's intention for using puzzle-piece imagery is to evoke negative associations, our results suggest the organization's use of puzzle-piece imagery is apt." Whoa. Where did that come from I wonder?

I've kinda approached this topic before on this blog in the context of how associations between organisations here in Blighty and brands such as Thomas the Tank Engine might have similar connotations when it comes to the perception of autism (see here). I suppose one could equally suggest that whilst something like Thomas the Tank Engine is enjoyed by many children on the autism spectrum (as well as many children not on the autism spectrum!) there is always a risk that it might feed into a stereotype. In the case of trains, one can see the old 'systemising' link coming through and onward the shadow of the 'extreme male brain' thingy-majig that has, I think, been rather overplayed in the context of autism (see here). Indeed, with the classical association between trains and boys ('boys and their toys') one might be inclined to ask what such an association might mean for the the perception of the presentation of autism in females for example? And onward what imagery/association would be most appropriate in the context of female autism minus any sweeping generalisations?

Of course, one can find meaning in any imagery used in the context of any organisation linked to a specific diagnosis or condition. At least some opinions on this topic are likely also to reflect specific viewpoints about the organisation in question as per the MSSNG project funded by Autism Speaks (who coincidentally use a puzzle piece in their logo) and how that has been interpreted in some quarters. I do think we have to be quite careful in this area not to slide from one extreme to another in relation to how wide the autism spectrum is and indeed, ensuring representation of the entire autism spectrum when it comes to public perceptions (see here). I have one suggestion: with all the creative talent out there on the autism spectrum, perhaps organisations linked to autism should ask their members with autism to help design new logos...

To close, some artwork from a rather talented chap who might be able to help.


[1] Gernsbacher MA. et al. Do puzzle pieces and autism puzzle piece logos evoke negative associations? Autism. 2017 Aug 1:1362361317727125.


Thursday, 7 September 2017

Epilepsy (or comorbidity?) impacts on academic achievement

The results of the systematic review from Wo and colleagues [1] highlight something of an important trend in the peer-reviewed science domain looking at how epilepsy may have various important implications for all manner of different issues outside of just the presence of seizures. This time around the focus was on academic achievement.

Drawing on data from 20 studies that "assessed the prevalence of academic difficulties in children with epilepsy (CWE) of normal intelligence, and its associating factors" researchers concluded that nearly three-quarters of studies found that CWE "had significantly lower academic achievement scores" compared with controls or population norms. The authors added that despite improvements in seizure frequency for some, issues with academic achievement still remained.

There were also some more positive points to take from the Wo findings: "Higher parental education and children with higher IQ, and [who] had better attention or had a positive attitude towards epilepsy, were associated with higher academic achievement score." I can't readily explain how (and indeed whether) a 'positive attitude' towards ones epilepsy might influence academic achievement but one might see how children with a high IQ, nurtured under the right circumstances, might have somewhat more protection against 'lower academic achievement scores'.

I think it is important to take a step back here before any sweeping generalisations are made. Not every study included for review by Wo et al indicated a relationship between epilepsy and academic achievement. This is an important point, and stresses how under the very heterogeneous label of epilepsy - some types more readily associated with conditions such as learning (intellectual) disability - not everyone is going to be potentially 'disadvantaged' in an academic sense as a result. This also bearing in mind that academic achievement is not always a great 'marker' when it comes to what one might define as a successful life; plenty of people do alright / make it big without great academic achievement scores.

Added to the Wo study, I also want to introduce the findings reported by Gillberg and colleagues [2] providing something of an example of how many other factors might potentially affect academic achievement in the context of epilepsy. Gillberg et al once again refer to their ESSENCE description - early symptomatic syndromes eliciting neurodevelopmental clinical examinations - to denote how diagnoses affecting behaviour and development rarely appear in isolation to one and another. They observed that: "The rate of ESSENCE in febrile seizures and epilepsy was significantly higher than in the total population without seizures" based on the examination over 27,000 parent reports of twins. I might venture further into their suggestion that: "Febrile seizures alone could be seen as a marker for a broader ESSENCE phenotype in some cases" specifically in the context of autism on a separate blogging occasion (see here) but for now, the message is that epilepsy probably does not appear (diagnostically) alone and said comorbidity *might* also be important to academic achievement and no doubt, other outcomes too.


[1] Wo SW. et al. The impact of epilepsy on academic achievement in children with normal intelligence and without major comorbidities: A systematic review. Epilepsy Res. 2017 Jul 20;136:35-45.

[2] Gillberg C. et al. Febrile Seizures and Epilepsy: Association With Autism and Other Neurodevelopmental Disorders in the Child and Adolescent Twin Study in Sweden. Pediatr Neurol. 2017 Jun 8. pii: S0887-8994(17)30178-9.