tag:blogger.com,1999:blog-12707236578171721172024-02-22T12:53:42.987-08:00cracking the enigmadrbrocktagonhttp://www.blogger.com/profile/15225859145004971487noreply@blogger.comBlogger77125tag:blogger.com,1999:blog-1270723657817172117.post-52355327943098493672014-02-14T02:27:00.001-08:002014-02-14T02:27:40.348-08:00Autism and the average<table cellpadding="0" cellspacing="0" class="tr-caption-container" style="float: left; margin-right: 1em; text-align: left;"><tbody>
<tr><td style="text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgT_X5lD2DigDvzGrp7yI-2-5aPUW5Nu383VbUdmMIYgra2k0Dj9HZmc4skk29hB7xAr4izQvHEmRqU8R4bcAKSEk8B7E7kbSClsctzX7B0_BgmN-w8TyVZ6vbzDgW4Gg2wT7tY2HtdLzc/s1600/Punctuated1.jpg" imageanchor="1" style="clear: left; margin-bottom: 1em; margin-left: auto; margin-right: auto;"><img border="0" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgT_X5lD2DigDvzGrp7yI-2-5aPUW5Nu383VbUdmMIYgra2k0Dj9HZmc4skk29hB7xAr4izQvHEmRqU8R4bcAKSEk8B7E7kbSClsctzX7B0_BgmN-w8TyVZ6vbzDgW4Gg2wT7tY2HtdLzc/s320/Punctuated1.jpg" height="320" width="215" /></a></td></tr>
<tr><td class="tr-caption" style="text-align: center;">Stephen Jay Gould. Source: <a href="http://www.makify.com/stasis-punctuated-by-change/">Makify.com</a></td></tr>
</tbody></table>
Around this time every year, my <i>almost</i>-namesake, John Brockman, publishes on his website, <a href="http://www.edge.org/">the Edge</a>, a selection of answers to an Annual Question. What have you changed your mind about? What is your favourite deep or beautiful explanation? What <i>should</i> we be worried about?<br />
<br />
This year's question was particularly intriguing. <a href="http://www.edge.org/responses/what-scientific-idea-is-ready-for-retirement">What scientific idea is ready for retirement?</a> Diverse answers include: big data, universal grammar, entropy, string theory, radical behaviourism, common sense, carbon footprints, neuroplasticity, the continuity of time, the idea that science is self-correcting.<br />
<br />
My favourite response, however, came from Nicholas Christasis, a physician and social scientist at Yale University. His answer: <a href="http://www.edge.org/response-detail/25437">the Average</a>.<br />
<blockquote class="tr_bq">
<i>"Ever since the landmark invention of diverse statistical techniques 100 years ago that allow us to properly compare the difference between the averages of two groups, we have deluded ourselves into thinking that it is such differences that are the salient—and often the only—important difference between groups. We have spent a century observing and interpreting such differences. We've become almost obsessed, and we should stop."</i> </blockquote>
As an autism researcher, this is an issue particularly close to my heart. Despite the incessant talk about the "heterogeneity problem" in autism research, most autism studies begin and end with the question of whether or not <i>on average</i> people with autism are different on some measure to people who don't have a diagnosis.<br />
<br />
This carries with it the assumption that it is the average (and <i>not</i> the variation around the average) that matters; that it captures some essential property of autism. It also invariably leads to contradictory findings, where one study finds some interesting difference <i>on average</i> between autistic and non-autistic people - and another finds no difference or even the opposite effect.<br />
<br />
<table align="center" cellpadding="0" cellspacing="0" class="tr-caption-container" style="margin-left: auto; margin-right: auto; text-align: center;"><tbody>
<tr><td style="text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEg-swXxb-BDPUrD4gDOyLk5OTNkUquqz27PdQLKEDsqYgKAC70tWVQ9PdzAQ7KXbJbWa_FP3qAN4lQk8y7_DVNmUt988TQI9R1-XhV_wvIgglF68E_Gxgd_qLk7weilR8BWDIZzHSLLvxc/s1600/Slide10.jpg" imageanchor="1" style="margin-left: auto; margin-right: auto;"><img border="0" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEg-swXxb-BDPUrD4gDOyLk5OTNkUquqz27PdQLKEDsqYgKAC70tWVQ9PdzAQ7KXbJbWa_FP3qAN4lQk8y7_DVNmUt988TQI9R1-XhV_wvIgglF68E_Gxgd_qLk7weilR8BWDIZzHSLLvxc/s1600/Slide10.jpg" height="300" width="400" /></a></td></tr>
<tr><td class="tr-caption" style="text-align: center;"><br /></td></tr>
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My <a href="https://sfari.org/news-and-opinion/columnists/jon-brock/2014/connections-the-elusive-essence-of-autism">latest article</a> for the Simons Foundation Autism Research Initiative elaborates on this point. It was inspired initially by a <a href="http://www.stat.berkeley.edu/users/rice/Stat2/GouldCancer.html">wonderful essay</a> by Stephen Jay Gould, discussing life-expectancy statistics in the context of his own background in evolutionary biology. As Gould wrote:<br />
<blockquote class="tr_bq">
<i>"All evolutionary biologists know that variation itself is nature’s only irreducible essence. Variation is the hard reality, not a set of imperfect measures for a central tendency. Means and medians are the abstractions."</i></blockquote>
This, I argue, is an important lesson for autism research.<br />
<blockquote class="tr_bq">
<i>"We have to take heterogeneity seriously as the object of investigation, rather than an excuse for inconsistent results or an inconvenience in our quest to understand the essence of autism."</i></blockquote>
The search for autism's core essence is something that has driven research ever since Kanner first <a href="https://sfari.org/news-and-opinion/classic-paper-reviews/2007/leo-kanners-1943-paper-on-autism-commentary-by-gerald-fischbach">described</a> autism in 1943. However, seventy years later, we're still not much closer to an answer - as evidenced by the controversies surrounding the latest attempt to redefine autism in DSM-5.<br />
<br />
There's no denying that "autism" is a useful <a href="http://www.urbandictionary.com/define.php?term=meme">meme</a> in terms of raising awareness and in communicating in very broad terms the kinds of difficulties a person may face. "Autism" also serves an important purpose in bringing together likeminded people for support, advocacy, and research.<br />
<br />
Clearly, the symptoms that affect people diagnosed with autism are real and for many present huge challenges. However, autism is not an explanation for those challenges - it <i>is </i>those challenges. And given the incredible diversity within autism, it's not clear that autism is an actual <i>thing</i> to be explained either.<br />
<br />
So, inspired by John Brockman, my question to you is this: Are we now at the point where, as a <i>scientific</i> concept, "autism" is ready for retirement?<br />
<br />
<br />
<b>Related posts:</b><br />
<ul>
<li><a href="http://crackingtheenigma.blogspot.com.au/2012/05/autism-and-art-of-campervan-maintenance.html">Autism and the art of campervan maintenance</a></li>
</ul>
<br />
<br />
<b>Further reading:</b><br />
<ul>
<li>Intellectualizing: <a href="http://intellectualizing.net/2013/12/17/book-rethinking-autism-variation-and-complexity/">Review</a> of <i>Rethinking Autism: Variation and Complexity</i> by Lynn Waterhouse</li>
</ul>
<br />
<br />
<br />drbrocktagonhttp://www.blogger.com/profile/15225859145004971487noreply@blogger.com10tag:blogger.com,1999:blog-1270723657817172117.post-57938459056160165832014-01-30T17:36:00.000-08:002014-01-30T17:41:30.570-08:00The evolution of "autism": Comparing DSM-III and DSM-5<div class="separator" style="clear: both; text-align: center;">
<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgtFb2ISz5Iu5kuw0r0aj3BSbzDYvSEupkc4BUQ1mNWkdD_GMorc7E76ccQZMyeo4bclcFUA6ZALFjkXedF5QpQ7cKXgrO86LwF_tsr06TdhR0AXN-6xTNQ5dbCc3rC0gMZ8NCeM95Z8nc/s1600/dsm3.jpg" imageanchor="1" style="clear: left; float: left; margin-bottom: 1em; margin-right: 1em;"><img border="0" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgtFb2ISz5Iu5kuw0r0aj3BSbzDYvSEupkc4BUQ1mNWkdD_GMorc7E76ccQZMyeo4bclcFUA6ZALFjkXedF5QpQ7cKXgrO86LwF_tsr06TdhR0AXN-6xTNQ5dbCc3rC0gMZ8NCeM95Z8nc/s1600/dsm3.jpg" /></a></div>
It is of course common knowledge that autism rates have steadily increased over the years. The rise in diagnoses is often framed as an "epidemic" or "tidal wave". However, most researchers will tell you that in fact it's hard to know whether there is a real increase or not.<br />
<br />
The reason for caution becomes clear if we compare the current diagnostic criteria with their <a href="http://www.unstrange.com/dsm1.html">historical counterparts</a>.<br />
<br />
Here's the 1980 definition of <i><b>Infantile Autism</b></i> as it appeared in DSM-III.<br />
<blockquote class="tr_bq">
A. Onset before 30 months of age</blockquote>
<blockquote class="tr_bq">
B. Pervasive lack of responsiveness to other people </blockquote>
<blockquote class="tr_bq">
C. Gross deficits in language development </blockquote>
<blockquote class="tr_bq">
D. If speech is present, peculiar speech patterns such as immediate and delayed echolalia, metaphorical language, pronominal reversal </blockquote>
<blockquote class="tr_bq">
E. Bizarre responses to various aspects of the environment, e.g., resistance to change, peculiar interest in or attachments to animate or inanimate objects </blockquote>
<blockquote class="tr_bq">
F. Absence of delusions, hallucinations, loosening of associations, and incoherence as in Schizophrenia.</blockquote>
<br />
And here is how the equivalent items are phrased in the current version, DSM-5, under <i><b>Autism Spectrum Disorder</b></i>:<br />
<blockquote class="tr_bq">
A. <i>Symptoms must be present in the early developmental period (but may not become fully manifest until social demands exceed limited capacities or may be masked by learned strategies later in life).</i> </blockquote>
<blockquote class="tr_bq">
B. <i>Deficits in social-emotional reciprocity</i> must be present (or have been present earlier in development). However, these can range <i>from abnormal social approach and failure of normal back and forth conversation through reduced sharing of interests, emotions, and affect and response to total lack of initiation of social interaction</i></blockquote>
<blockquote class="tr_bq">
C. ASD can be diagnosed <i>with or without accompanying language impairment</i></blockquote>
<blockquote class="tr_bq">
D. "Peculiar speech patterns" are not required for a diagnosis. However, <i>echolalia and idiosyncratic phrases</i> are considered examples of <i>Stereotyped or repetitive movements, use of objects, or speech</i> - one of four nonsocial features (see E below) </blockquote>
<blockquote class="tr_bq">
E. Any two of the following must be present (currently or earlier in development): (1) <i>Stereotyped use of objects</i>; (2) <i>Insistence on sameness, inflexible adherence to routines, or ritualized patterns of verbal or nonverbal behaviour</i>; (3) <i>Highly restricted, fixated interests that are abnormal in intensity or focus</i>; (4) <i>Hyper- or hypo-reactivity to sensory input or unusual interest in sensory aspects of the environment</i></blockquote>
<blockquote class="tr_bq">
F. <i>Hallucinations and delusions, which are defining features of schizophrenia, are not features of ASD</i> </blockquote>
Arguably, item E is as non-specific in DSM-III as it is in DSM-5. In every other respect DSM-5 takes a far broader definition of autism's characteristics. Put another way, it's fair to say that the majority of people whom we would today think of as being "on the spectrum" would not have come close to a diagnosis in the 1980s.<br />
<br />
<br />
<br />
Thanks to Michael Hunsaker for the suggestion:<br />
<blockquote class="twitter-tweet" lang="en">
<a href="https://twitter.com/DrBrocktagon">@DrBrocktagon</a> now cut and paste in the DSM V and your head will explode!<br />
— Michael R. Hunsaker (@mrhunsaker) <a href="https://twitter.com/mrhunsaker/statuses/429021426624897025">January 30, 2014</a></blockquote>
<script async="" charset="utf-8" src="//platform.twitter.com/widgets.js"></script>drbrocktagonhttp://www.blogger.com/profile/15225859145004971487noreply@blogger.com5tag:blogger.com,1999:blog-1270723657817172117.post-17870657962574702842013-12-27T02:15:00.000-08:002013-12-29T20:07:20.061-08:00Autistic brains: Under- or over-connected?<div class="separator" style="clear: both; text-align: center;">
</div>
<table align="center" cellpadding="0" cellspacing="0" class="tr-caption-container" style="margin-left: auto; margin-right: auto; text-align: center;"><tbody>
<tr><td style="text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEi44eMBgZIwPaKKSFTu88AFwV7KkajC7c74kC01V5k0Iy1tbpyuDzhcsu2O_7J5vYkswax19lW-nW6tgxgGd6-aVAYFmMU2c2MfIFDsfm0SSaJdUTPm42mC-A5o8HiqGSSnsqvVqaxGQNE/s1600/journal.pone.0075941.g003.png" imageanchor="1" style="margin-left: auto; margin-right: auto;"><img border="0" height="177" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEi44eMBgZIwPaKKSFTu88AFwV7KkajC7c74kC01V5k0Iy1tbpyuDzhcsu2O_7J5vYkswax19lW-nW6tgxgGd6-aVAYFmMU2c2MfIFDsfm0SSaJdUTPm42mC-A5o8HiqGSSnsqvVqaxGQNE/s400/journal.pone.0075941.g003.png" width="400" /></a></td></tr>
<tr><td class="tr-caption" style="text-align: center;">In Garcia Dominguez et al.'s EEG study, children with autism had increased "coherency" between electrodes overlying the visual cortex <a href="http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0075941">Source</a></td></tr>
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<br />
<i>Note: A Spanish translation of this post can be found at Autismo Diario: <a href="http://autismodiario.org/2013/12/29/cerebros-con-autismo-sub-o-hiper-conectados/">Cerebros con Autismo: ¿Sub o Hiper Conectados?</a></i><br />
<br />
For a while now, the prevailing view has been that the brains of people with autism are "underconnected" and that this lack of communication between different parts of the brain causes at least some of the features of autism. It's an intuitively plausible idea but it was always likely to be an over-simplification.<br />
<br />
Recently, a number of studies have pointed to the exact opposite - an <i>increase</i> in connectivity in autism. The emerging story is that kids with autism have "hyper connected" brains but they become less connected as they get older.<br />
<br />
But this is still just a story. It takes the new brain imaging data, which comes from kids, and tries to reconcile it with the older brain imaging data which mainly involves studies of adults. There are, however, lots of other differences between studies in terms of the methods they used and, perhaps most importantly, the way the data were analysed.<br />
<br />
On top of that, we still don't really understand what many of these "connectivity" measures actually signify. And it's not really clear how changes in connectivity might relate to the development of autism at the behavioural level. Certainly, people with autism change as they get older, but I don't think anyone would argue that autistic adults are the <i>opposite</i> of autistic kids. It's a fascinating area of research but there are still a lot of holes in the plot.<br />
<br />
Earlier this month I contributed to a <a href="http://sfari.org/sfari-community/community-blog/cross-talk/2013/what-to-make-of-contradictions-in-connectivity-findings/">"Cross Talk" </a>feature on the SFARI website, in which Damien Fair, Tal Kenet, John Rubenstein, and I gave our thoughts on an earlier post by Vinod Menon, discussing precisely these issues.<br />
<br />
I was also interviewed by Emily Anthes for a SFARI <a href="http://sfari.org/news-and-opinion/news/2013/autism-brains-are-overly-connected-studies-find">article</a> on two recent papers providing evidence for hyper connectivity in autism: an fMRI study by Kaustubh Supekar and colleagues at Stanford; and an EEG study by Luis Garcia Dominguez and colleagues in Toronto.<br />
<br />
Inevitably, my fairly lengthy answers to Emily's questions were edited down to a couple of short quotes. So, with Emily's permission, I'm posting the full email Q&A. I'd be very interested in other people's thoughts.<br />
<br />
<br />
<b>Regarding the Supekar et al paper: The researchers's use of three independent cohorts seems impressive. Is that notable/unusual?</b><br />
<blockquote class="tr_bq">
This is a really important step, particularly as there are often conflicting findings across studies. It shows that the effect is robust and not just a quirk of the particular sample of children being tested. However, we shouldn't interpret the fact that there are group differences in all three studies as meaning that this is true of all people with autism - or even all people with autism in the studies. </blockquote>
<br />
<b>Also regarding the Supekar paper: What do you think of the suggestion that connectivity may change as children with autism age? Could that help explain some of the contradictory findings in the literature? </b><br />
<blockquote class="tr_bq">
It's possible although I think we need a direct comparison with data from adults analysed in exactly the same way as the data from children.
Given their argument, I'm surprised Supekar et al didn't look to see if there was a correlation with age within the study. If there really is a change from hyperconnectivity in young children to underconnectivity in adolescents and adults then we would expect to see that hyperconectivity is most pronounced in the youngest children. That wouldn't itself be conclusive evidence - we'd need a longitudinal study to test the idea properly, but it would be the obvious starting point. </blockquote>
<br />
<b>The PLoS One paper uses EEG to study connectivity--is this unusual? Does EEG have any particular advantages or disadvantages over MRI when it comes to studying connectivity?</b><br />
<blockquote class="tr_bq">
To me it makes much more sense to use EEG or MEG to look at connectivity. There are lots of studies that have done this before although like the fMRI data the results are quite messy and contradictory.
The big advantage of EEG and MEG is that they have very good time resolution so can pick up on the rapid and dynamic changes in connectivity that are involved in cognitive processes. </blockquote>
<blockquote class="tr_bq">
While people often talk about fMRI connectivity in terms of "communication" between the different parts of the brain, it's more accurate to talk about "coactivation". We're really just talking about brain regions increasing and decreasing their activation together at the roughly the same time, roughly once every second or so. In fact, Supekar et al. make a point of filtering the data to look only at very low frequency changes (0.01 to 0.05 Hz) - so they're looking at the extent to which different brain regions are coactivated at the timescale of minutes. </blockquote>
<blockquote class="tr_bq">
One of the problems with EEG is that the signal from any part of the brain is picked up (to different degrees) by all of the electrodes on the scalp. If you find evidence for synchronization between the response at two different electrodes, it's tempting to assume that this means that the parts of the brain underneath the two electrodes are acting together in synchrony. But it could just be that the two electrodes are measuring the same activity from the same source in the brain.
The Dominguez paper uses a relatively new mathematical technique that is claimed to eliminate this problem. My understanding is that it effectively looks at the parts of the brain response that are nearly but not perfectly synchronized (on the assumption that perfect synchronization is almost certain to reflect the same brain response being measured at two locations).</blockquote>
<br />
<b>Going forward, how can we help clear up some of the contradictions in the literature?</b><br />
<blockquote class="tr_bq">
Researchers need to use the same techniques across different populations. They also need to subject data from the same samples to different analyses. That way we can start to work out how much of the contradictions are due to differences in participant characteristics (eg age, autism severity) and how much is down to the different methods and analyses being used by different research groups.
We also need to look at individual as well as group differences - and for that we need to know how reliable these measures are (ie if you test the same person twice, do you get the same result).</blockquote>
<b><br /></b>
<b>References: </b><br />
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=PloS+one&rft_id=info%3Apmid%2F24098409&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=The+imaginary+part+of+coherency+in+autism%3A+differences+in+cortical+functional+connectivity+in+preschool+children.&rft.issn=&rft.date=2013&rft.volume=8&rft.issue=10&rft.spage=&rft.epage=&rft.artnum=&rft.au=Garc%C3%ADa+Dom%C3%ADnguez+L&rft.au=Stieben+J&rft.au=P%C3%A9rez+Vel%C3%A1zquez+JL&rft.au=Shanker+S&rfe_dat=bpr3.included=1;bpr3.tags="><br /></span>
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=PloS+one&rft_id=info%3Apmid%2F24098409&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=The+imaginary+part+of+coherency+in+autism%3A+differences+in+cortical+functional+connectivity+in+preschool+children.&rft.issn=&rft.date=2013&rft.volume=8&rft.issue=10&rft.spage=&rft.epage=&rft.artnum=&rft.au=Garc%C3%ADa+Dom%C3%ADnguez+L&rft.au=Stieben+J&rft.au=P%C3%A9rez+Vel%C3%A1zquez+JL&rft.au=Shanker+S&rfe_dat=bpr3.included=1;bpr3.tags=">García Domínguez L, Stieben J, Pérez Velázquez JL, & Shanker S (2013). The imaginary part of coherency in autism: differences in cortical functional connectivity in preschool children. <span style="font-style: italic;">PloS one, 8</span> (10) PMID: <a href="http://www.ncbi.nlm.nih.gov/pubmed/24098409" rev="review">24098409</a></span><br />
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=Cell+reports&rft_id=info%3Apmid%2F24210821&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=Brain+hyperconnectivity+in+children+with+autism+and+its+links+to+social+deficits.&rft.issn=&rft.date=2013&rft.volume=5&rft.issue=3&rft.spage=738&rft.epage=47&rft.artnum=&rft.au=Supekar+K&rft.au=Uddin+LQ&rft.au=Khouzam+A&rft.au=Phillips+J&rft.au=Gaillard+WD&rft.au=Kenworthy+LE&rft.au=Yerys+BE&rft.au=Vaidya+CJ&rft.au=Menon+V&rfe_dat=bpr3.included=1;bpr3.tags=Medicine%2CNeuroscience%2CCognitive+Neuroscience%2C+%2C+Developmental+Neuroscience%2C+Neurology%2C+Psychiatry%2C+Autism"><br /></span>
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=Cell+reports&rft_id=info%3Apmid%2F24210821&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=Brain+hyperconnectivity+in+children+with+autism+and+its+links+to+social+deficits.&rft.issn=&rft.date=2013&rft.volume=5&rft.issue=3&rft.spage=738&rft.epage=47&rft.artnum=&rft.au=Supekar+K&rft.au=Uddin+LQ&rft.au=Khouzam+A&rft.au=Phillips+J&rft.au=Gaillard+WD&rft.au=Kenworthy+LE&rft.au=Yerys+BE&rft.au=Vaidya+CJ&rft.au=Menon+V&rfe_dat=bpr3.included=1;bpr3.tags=Medicine%2CNeuroscience%2CCognitive+Neuroscience%2C+%2C+Developmental+Neuroscience%2C+Neurology%2C+Psychiatry%2C+Autism">Supekar K, Uddin LQ, Khouzam A, Phillips J, Gaillard WD, Kenworthy LE, Yerys BE, Vaidya CJ, & Menon V (2013). Brain hyperconnectivity in children with autism and its links to social deficits. <span style="font-style: italic;">Cell reports, 5</span> (3), 738-47 PMID: <a href="http://www.ncbi.nlm.nih.gov/pubmed/24210821" rev="review">24210821</a></span>
<br />
<br />
<br />
<b>SFARI links:</b><br />
<br />
<ul>
<li><a href="http://sfari.org/news-and-opinion/news/2013/autism-brains-are-overly-connected-studies-find">Autism brains are overly connected, studies find</a></li>
<li><a href="http://sfari.org/sfari-community/community-blog/cross-talk/2013/what-to-make-of-contradictions-in-connectivity-findings/">What to make of contradictions in connectivity findings?</a></li>
<li><a href="http://sfari.org/news-and-opinion/viewpoint/2013/more-or-less-connected-in-autism-compared-to-what">More or less connected in autism, compared to what?</a></li>
<li><a href="http://sfari.org/news-and-opinion/specials/2013/connectivity">Connectivity special report</a></li>
</ul>
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<br />drbrocktagonhttp://www.blogger.com/profile/15225859145004971487noreply@blogger.com2tag:blogger.com,1999:blog-1270723657817172117.post-2949078073438956412013-12-17T15:14:00.001-08:002013-12-18T12:55:52.990-08:00Science in action. Or "This is the plant I yelled at"<div class="separator" style="clear: both; text-align: center;">
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As Jacob Bronowski once said, "The hand is the cutting edge of the mind". We learn not so much by detached thinking but by acting and then observing the consequences of our actions. Science is just a more formal version of this process: act, observe, and update your ideas accordingly.<br />
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These principles were much in evidence at the recent science fair at our local primary school, which I had the honour and privilege of judging. In the weeks beforehand, the kids had each come up with a question and then designed and carried out an experiment at home to try and answer it.<br />
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On the big day, everyone brought posters of their experiment into school. We, the judges, asked them questions. What did you do? Did it answer your question? Can you explain your results a different way? What next?<br />
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Then we gave them post-stick notes with comments like "Awesome experiment!" "Cool science!" and "I'm glad you didn't try that on a real dog!"<br />
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Of course, everyone was a winner, but here are a few of my favourites (click each one to enlarge).<br />
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<table align="center" cellpadding="0" cellspacing="0" class="tr-caption-container" style="margin-left: auto; margin-right: auto; text-align: center;"><tbody>
<tr><td style="text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEj1dtDTCtVtz2mI8ipOEYZJjQs0C48K0mkfcW3H8xajtL_VN14Z8CrN0jTVAQ5OGa_Jc0bvmZsC76iqyqeuUoC_mOzsq-uOAta4qNCKAu5Aqd7ahJXSr6HqeIDbcvKzzyWryS5-FAWgX4w/s1600/171020132946.jpg" imageanchor="1" style="margin-left: auto; margin-right: auto;"><img border="0" height="300" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEj1dtDTCtVtz2mI8ipOEYZJjQs0C48K0mkfcW3H8xajtL_VN14Z8CrN0jTVAQ5OGa_Jc0bvmZsC76iqyqeuUoC_mOzsq-uOAta4qNCKAu5Aqd7ahJXSr6HqeIDbcvKzzyWryS5-FAWgX4w/s400/171020132946.jpg" width="400" /></a></td></tr>
<tr><td class="tr-caption" style="text-align: center;">Do all rocks sink? No, pumice doesn't because it has holes in it full of air!</td></tr>
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<table align="center" cellpadding="0" cellspacing="0" class="tr-caption-container" style="margin-left: auto; margin-right: auto; text-align: center;"><tbody>
<tr><td style="text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgBEvrwJLH26BhA9oLSYdh7rq9CXgFvxC4zmtSFem3HCYl08iHAAczV-o_aiSyrJI03xssXLdoDirTHBQfFxi7dHUl_GDxryHQUdmNkUH8kB5sXxszPkK_uSnBN7YppCiB56g2uG8AoEIQ/s1600/171020132947.jpg" imageanchor="1" style="margin-left: auto; margin-right: auto;"><img border="0" height="400" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgBEvrwJLH26BhA9oLSYdh7rq9CXgFvxC4zmtSFem3HCYl08iHAAczV-o_aiSyrJI03xssXLdoDirTHBQfFxi7dHUl_GDxryHQUdmNkUH8kB5sXxszPkK_uSnBN7YppCiB56g2uG8AoEIQ/s400/171020132947.jpg" width="300" /></a></td></tr>
<tr><td class="tr-caption" style="text-align: center;">Can you make stalagmites and stalactites without having to wait thousands of years? And how do you remember which one is which?</td></tr>
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<table align="center" cellpadding="0" cellspacing="0" class="tr-caption-container" style="margin-left: auto; margin-right: auto; text-align: center;"><tbody>
<tr><td style="text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjcqhTPKNcsF8IxuOuxXuiHduPYKXFd0QwERX48xZ5CnasdEnXWxVnfK22vZ_-CGqIsezdT-CAvBBOZTTOF13LGFB246TfbtflCTesxktuvYRl9wIU-SwTG3LTJOcCXz2xYzM3FeXDhpKk/s1600/171020132948.jpg" imageanchor="1" style="margin-left: auto; margin-right: auto;"><img border="0" height="300" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjcqhTPKNcsF8IxuOuxXuiHduPYKXFd0QwERX48xZ5CnasdEnXWxVnfK22vZ_-CGqIsezdT-CAvBBOZTTOF13LGFB246TfbtflCTesxktuvYRl9wIU-SwTG3LTJOcCXz2xYzM3FeXDhpKk/s400/171020132948.jpg" width="400" /></a></td></tr>
<tr><td class="tr-caption" style="text-align: center;">Can girls do more skips than boys? Yes on average, but some boys are really good at skipping too!</td></tr>
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<tr><td style="text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjUcAhR5q4UvaoYfPrtVQhSHjIteHTQ6grv_WuF4hEvCe9HZFLTbqWM1iZeehyphenhyphenCRJ-wJuFNFplfSxjgXMB2etNCddx0LVis2qY_baabUw_0NwJ_BbPOteLFinEs3d2jZr80Eh56URwwIB8/s1600/171020132951.jpg" imageanchor="1" style="margin-left: auto; margin-right: auto;"><img border="0" height="300" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjUcAhR5q4UvaoYfPrtVQhSHjIteHTQ6grv_WuF4hEvCe9HZFLTbqWM1iZeehyphenhyphenCRJ-wJuFNFplfSxjgXMB2etNCddx0LVis2qY_baabUw_0NwJ_BbPOteLFinEs3d2jZr80Eh56URwwIB8/s400/171020132951.jpg" width="400" /></a></td></tr>
<tr><td class="tr-caption" style="text-align: center;">Does talking nicely to your plants help them grow? The caption says "This is the plant I yelled at"</td></tr>
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<table align="center" cellpadding="0" cellspacing="0" class="tr-caption-container" style="margin-left: auto; margin-right: auto; text-align: center;"><tbody>
<tr><td style="text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEiVSNGi2KUQQ2n-1OBwCE8WTdq23xljd2TRBVd4jnkIRmAPs7FJLZoS5nN1ytL8M2PC3ycz480waibs7uRJn9Lw2SJjbCJTFocRJyeLE2vXR43jftLw7bZ2eCyyRWVkpntLu2xn4n9wtO4/s1600/171020132952.jpg" imageanchor="1" style="margin-left: auto; margin-right: auto;"><img border="0" height="300" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEiVSNGi2KUQQ2n-1OBwCE8WTdq23xljd2TRBVd4jnkIRmAPs7FJLZoS5nN1ytL8M2PC3ycz480waibs7uRJn9Lw2SJjbCJTFocRJyeLE2vXR43jftLw7bZ2eCyyRWVkpntLu2xn4n9wtO4/s400/171020132952.jpg" width="400" /></a></td></tr>
<tr><td class="tr-caption" style="text-align: center;">Which sand is the squeakiest? These kids couldn't get home because of a bushfire so went to the beach and did a science! </td></tr>
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<table align="center" cellpadding="0" cellspacing="0" class="tr-caption-container" style="margin-left: auto; margin-right: auto; text-align: center;"><tbody>
<tr><td style="text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjg3myKTMePuZuuAO0x5bL_FWlvknmASJnszll27sNqAZV3MW6pyTZGbfuaPqNgBij-fSwwde8uTjbFGN5UR7zHErBQK66XYsrWdWSECqFj0uVwzj3cysgAvmPy_KgoubrnvZWkMltcEW0/s1600/1392957_10151757665164389_1173705227_n.jpg" imageanchor="1" style="margin-left: auto; margin-right: auto;"><img border="0" height="300" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjg3myKTMePuZuuAO0x5bL_FWlvknmASJnszll27sNqAZV3MW6pyTZGbfuaPqNgBij-fSwwde8uTjbFGN5UR7zHErBQK66XYsrWdWSECqFj0uVwzj3cysgAvmPy_KgoubrnvZWkMltcEW0/s400/1392957_10151757665164389_1173705227_n.jpg" width="400" /></a></td></tr>
<tr><td class="tr-caption" style="text-align: center;">How do you make a rainbow? Easy - cheat and use an old CD!</td></tr>
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That last one is my boy's effort. To be honest, we were completely disorganised and did it all the night before. Not exactly optimal rainbow-making conditions. We also didn't realise quite what an effort everyone else was going to. But the important thing is that we had great fun doing it and in trying and failing we got closer to working out what causes a rainbow.</div>
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I've <a href="http://crackingtheenigma.blogspot.com.au/2012/05/clouds.html">written before</a> about the joy of sharing with my son some of the amazing things that humans have learned through science. How scientific understanding enhances rather than detracts from the wonder of the world around him. But truth told, the best part of all is seeing him figure things out for himself.</div>
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Probably my favourite memory of this year was when, after swimming lessons one Saturday, we stopped off for a hot chocolate in the cafe at Ku-ring-gai National Park and spent a happy hour or so beside the river, testing our evolving theories of why some things float and others things don't. By the time we left for home, we'd progressed from "heavy things sink" to "things that you can break will probably float". Given the materials available, it was a reasonable working hypothesis.<br />
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In fact, I like that we left the experiment hanging. To be continued… Science after all is the journey not the destination. More a verb than a noun. As our junior scientists so ably demonstrated, it really is the taking part that counts.<br />
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drbrocktagonhttp://www.blogger.com/profile/15225859145004971487noreply@blogger.com1tag:blogger.com,1999:blog-1270723657817172117.post-45590948768573130092013-12-06T13:14:00.002-08:002013-12-15T15:58:05.391-08:00Does a baby's eye gaze really predict future autism?<div class="separator" style="clear: both; text-align: center;">
<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgc4mXmTqBdRTkni0UyLztEkaLwWTkAg5ddpXvG17OkENvGKy6Y_h-gLNqkpxhthlhHeudALQykVSe9XQ4Z7lSznEFNLMIrbr7eKmYMObkJhXijqdqbTnNWaOwYLwlf1n8pNXEXqwDoqyg/s1600/132_10900095407_235_n.jpg" imageanchor="1"><img border="0" height="323" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgc4mXmTqBdRTkni0UyLztEkaLwWTkAg5ddpXvG17OkENvGKy6Y_h-gLNqkpxhthlhHeudALQykVSe9XQ4Z7lSznEFNLMIrbr7eKmYMObkJhXijqdqbTnNWaOwYLwlf1n8pNXEXqwDoqyg/s400/132_10900095407_235_n.jpg" width="400" /></a></div>
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<i>Note: Due to the considerable interest in this post, I've <a href="http://figshare.com/articles/Does_a_baby_s_eye_gaze_really_predict_future_autism_/878085">uploaded</a> a PDF version at figshare.com. This can be cited as:</i><br />
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<i>Brock, Jon (2013): Does a baby's eye gaze really predict future autism?. figshare.
http://dx.doi.org/10.6084/m9.figshare.878085 </i></blockquote>
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<a href="http://well.blogs.nytimes.com/2013/11/06/a-babys-gaze-may-signal-autism-study-finds/?_r=0">Baby's gaze may signal autism, study finds</a>. That was the headline in the New York Times. The BBC declared that <a href="http://www.bbc.co.uk/news/health-24837462">Autism signs present in first months of life</a>. Turning the hype up to 11, a Canadian website boldly announced that <a href="http://Researchers prove that autism can be diagnosed right at the infant stage and intervention is possible">Researchers prove that autism can be diagnosed right at the infant stage and that intervention is possible</a>.<br />
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Nature, the journal that published the study, ran with <a href="http://www.nature.com/news/autism-symptoms-seen-in-babies-1.14117">Autism symptoms seen in babies</a>, summarising the findings thus:<br />
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Children with autism make less eye contact than others of the same age, an indicator that is used to diagnose the developmental disorder after the age of two years. But a paper published today in Nature reports that infants as young as two months can display signs of this condition, the earliest detection of autism symptoms yet.</blockquote>
Certainly, being able to identify infants who were likely to develop autism would be a ground breaking advance, opening up the possibility of very early diagnosis and intervention. It would also allow researchers to study the very earliest stages of autism development.<br />
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But, as with many studies that receive the full media treatment, there are caveats a-plenty. In fact, it could be argued that the results show the exact <i>opposite</i> of what the authors and the media coverage has suggested.<br />
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<iframe allowfullscreen="" frameborder="0" height="315" mozallowfullscreen="" scrolling="no" src="http://embed.ted.com/talks/ami_klin_a_new_way_to_diagnose_autism.html" webkitallowfullscreen="" width="400"></iframe></div>
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The study was conducted by Warren Jones and Ami Klin from Emory University. Back in 2002, Klin and colleagues published a <a href="http://archpsyc.jamanetwork.com/article.aspx?articleid=206705">study</a> showing that adolescents with autism spent less time looking at the eyes of people in a movie clip than did typically developing adolescents. Although, like all things autism, this seems to be true of some <a href="http://psych.brookes.ac.uk/publications/norbury2009.pdf">but not all</a> people with a diagnosis.<br />
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Since then, Klin and Jones have reported <a href="http://www.pediatrics.emory.edu/divisions/marcus/Jones_Carr_Klin_2008.pdf">similar results</a> in two-year-old children with autism. Their new study was an attempt to push that all the way back to the very earliest months of life.<br />
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Jones and Klin began with a sample of 64 infant boys, 38 of whom had an older sibling with autism, putting them at increased risk of having autism themselves [1]. They also tested 46 girls but later excluded all of them from the analyses [2].<br />
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At various time points between the ages of 2 months and 2 years, the infants were eye-tracked as they viewed short video clips of a female caregiver’s face and upper body.<br />
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<table align="center" cellpadding="0" cellspacing="0" class="tr-caption-container" style="margin-left: auto; margin-right: auto; text-align: center;"><tbody>
<tr><td style="text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhZjXc8I-2Pyv69aVIVvx0uT0VuvQ5lv9h68IABK7GJIaGRRwCSmHMPLfInOYOlsKBkasznLHz5CcS6aiDoVi5vy3ZTnvS3unHjZ3yNQZwr8Eo1H006Z00rvlRxT-wqdOXtEiUiWH_Z_7I/s1600/JonesKlin_Scanpaths.png" imageanchor="1" style="margin-left: auto; margin-right: auto;"><img border="0" height="277" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhZjXc8I-2Pyv69aVIVvx0uT0VuvQ5lv9h68IABK7GJIaGRRwCSmHMPLfInOYOlsKBkasznLHz5CcS6aiDoVi5vy3ZTnvS3unHjZ3yNQZwr8Eo1H006Z00rvlRxT-wqdOXtEiUiWH_Z_7I/s400/JonesKlin_Scanpaths.png" width="400" /></a></td></tr>
<tr><td class="tr-caption" style="text-align: center;"><span class="Apple-style-span" style="font-family: Verdana; font-size: 10px;">Sample scanpaths for a baby later diagnosed with autism (red) and a typically developing control (blue). Reprinted by permission from Macmillan Publishers Ltd: NATURE, doi:10.1038/nature12715, copyright 2013</span></td></tr>
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Then, at 3 years of age, the by-now toddlers were assessed for autism [3]. 11 boys (10 from the high risk group) were identified as having an autism spectrum disorder (ASD). They were then compared with the remaining 25 typically developing (TD) boys from the low-risk group.
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<tr><td style="text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEizW-6MrIGzS0oSb_QzUdAAFBzGOwK7Z-itVSmzthQv3u2ozc9sqgr2uHtKwaCxze1sOid6UOyZFY-DrhyphenhyphenKUP7EUYvL6v8P2U9xxcwuRfmm05rVY2RHtq6zg21PHA58qGIfGoyGObqki6A/s1600/KlinJones_Participants.png" imageanchor="1" style="margin-left: auto; margin-right: auto;"><img border="0" height="171" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEizW-6MrIGzS0oSb_QzUdAAFBzGOwK7Z-itVSmzthQv3u2ozc9sqgr2uHtKwaCxze1sOid6UOyZFY-DrhyphenhyphenKUP7EUYvL6v8P2U9xxcwuRfmm05rVY2RHtq6zg21PHA58qGIfGoyGObqki6A/s400/KlinJones_Participants.png" width="400" /></a></td></tr>
<tr><td class="tr-caption" style="text-align: center;">The 64 boys were divided into 4 groups at their 3-year assessment: ASD; low risk typically developing (TD); high-risk with some autism symptoms (BAP); and high-risk with no autism symptoms (no-Dx). Forty-six girls were also tested but were not included in the reported analyses.</td></tr>
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Jones and Klin began their analyses by building developmental trajectories for the two groups, similar to the growth charts that doctors use to tell, for example, whether a baby is putting on sufficient weight or not. Except here, what mattered was the percentage of time the babies were looking at the eyes in the video.<br />
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What they found was that the ASD boys showed a steady decline in eye gaze across time. However, there were no significant differences between the trajectories of the two groups until the final test session at 24 months [4].<br />
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<tr><td style="text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEiTgw9yOZc5IBTrgmxiQNpJpZsiG0-3n3Ju2IrnjqxzHLx_4Y3l_PjZo9nMSmW2F1VdJlTsQjchtqGr310qNo8NsVG_gnt1C3juhCYHBbEQyxsSp7l_Dow86pmv7_0BFsHtBVLncenHNUI/s1600/JonesKlinFig2_Trajectory.png" imageanchor="1" style="margin-left: auto; margin-right: auto;"><img border="0" height="220" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEiTgw9yOZc5IBTrgmxiQNpJpZsiG0-3n3Ju2IrnjqxzHLx_4Y3l_PjZo9nMSmW2F1VdJlTsQjchtqGr310qNo8NsVG_gnt1C3juhCYHBbEQyxsSp7l_Dow86pmv7_0BFsHtBVLncenHNUI/s400/JonesKlinFig2_Trajectory.png" width="400" /></a></td></tr>
<tr><td class="tr-caption" style="text-align: center;"><div style="font: 9.6px Verdana; margin: 0.0px 0.0px 0.0px 0.0px;">
Reprinted by permission from Macmillan Publishers Ltd: NATURE, doi:10.1038/nature12715, copyright 2013</div>
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The obvious interpretation of these data is that, in fact, eye gaze in infancy does <b><i>not</i></b> predict which infants will go on to develop autism (at least using Jones and Klin's set-up). Both from a practical and a theoretical point of view, that's an important finding. [5]<br />
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So how do we end up with "Baby's eye gaze signals autism"?<br />
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Having failed to find evidence for reduced eye gaze in ASD infants, Jones and Klin looked instead at the slopes of the developmental trajectories. In other words, not the <i>amount</i> of eye gaze at a particular time but the <i>change</i> in eye gaze relative to earlier and later time points. Here, they did find significant differences throughout the early months.<br />
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<tr><td style="text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjlNNS8K0cCGFgqxibaVTg2WIQTsSx_oNCPhpK7XxwajqADRkSx5Di-LjKWnsZr6SiH-vT99oTFeQZNZ0eYLKG7Sl_z1e3UHV5Wa1i1fD07gPOr6C66HVxNshyphenhyphen8j3mNL-j1puFi7Hw5Yho/s1600/JonesKlinExtFig2_Slopes.png" imageanchor="1" style="clear: left; margin-bottom: 1em; margin-left: auto; margin-right: auto;"><img border="0" height="320" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjlNNS8K0cCGFgqxibaVTg2WIQTsSx_oNCPhpK7XxwajqADRkSx5Di-LjKWnsZr6SiH-vT99oTFeQZNZ0eYLKG7Sl_z1e3UHV5Wa1i1fD07gPOr6C66HVxNshyphenhyphen8j3mNL-j1puFi7Hw5Yho/s320/JonesKlinExtFig2_Slopes.png" width="195" /></a></td></tr>
<tr><td class="tr-caption" style="text-align: center;"><span class="Apple-style-span" style="font-family: Verdana; font-size: 10px;">Reprinted by permission from<br />Macmillan Publishers Ltd: NATURE, <br />doi:10.1038/nature12715<br />copyright 2013</span></td></tr>
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When the analyses were restricted to the data from 2 to 6 months, the boys who developed autism showed a negative slope (declining eye gaze) while the low-risk boys had a positive slope (increasing eye gaze).<br />
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This, in essence, is what all the excitement is about. The study suggests that if you measure a baby's eye gaze at multiple time points before the age of 6 months and notice a decline over time, then that baby is at heightened risk for developing autism. It doesn't matter how awkward the data collection process or convoluted the analysis, there's <i>information</i> about autism in a babies' eye gaze.<br />
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However, there was always something about this story that didn't quite add up for me - and it's taken a while to put my finger on it. But before I get to that, there are a few other more obvious points that need to be mentioned.<br />
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First of all, the final sample size is very small. This is understandable because, even with a high risk sample, you need to test a lot of babies just to get a dozen or so who develop ASD. But it doesn't change the fact that a study with only 11 participants in one group has to be considered preliminary at best. It wouldn't have taken much to get wildly different results and we really need a replication of this before we get excited.<br />
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Second, the most useful comparison would be between the high risk children who develop autism and the high risk children who don't. That's because, in practice, it's very unlikely that such an eye-tracking measure would be rolled out as a universal screening measure. Not only would that be extremely expensive and time-consuming (especially if babies had to be tested on multiple occasions under highly controlled conditions to work out the slope of their trajectory), it would also throw up a <a href="http://crackingtheenigma.blogspot.com.au/2012/09/a-genetic-test-for-autism.html">huge number </a>of false positives - babies who the eye-tracking test said were likely to develop autism but were never really at risk. So, in reality, only babies with a family history of autism would be tested. Unfortunately, Jones and Klin don't report this direct comparison [6].<br />
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But the biggest issue for me is this: The claim is that babies who develop ASD start off with typical eye gaze but it's the <i>decline</i> in eye gaze in the first 6 months that is the signal of impending autism. However, if the ASD babies start off at the same level as the TD babies then there should also be a significant difference in the <i>amount</i> of eye gaze at 6 months. In fact, the two groups are almost identical in terms of their eye gaze at 6 months. And the only reason there's a difference in slope is that the ASD babies actually start off with <i>greater</i> eye gaze than the TD babies [7]. </div>
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It would be incredibly interesting if this were true - if boys who go on to develop autism make <i>more</i> eye contact at 2 months than is typical. However, we have to be very careful because, despite the media coverage focusing on the fact that the babies were tested from 2 months, there is in fact very little data from 2-month-olds in either group.</div>
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How do we know this?</div>
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Figure 1d in the paper includes the data from a single ASD baby. Each dot corresponds to the amount of time spent gazing at the caregiver's eyes in a single video clip.<u> There are I think 16 data points for this baby at 2 months.</u><br />
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Matching this up with Supplementary Figure 2b, which combines the data from all the ASD babies, we can see that <u>there are a total of 24 data points. This means that the remaining 10 babies provided just 8 data points between them at 2 months. </u> <strike>this one boy provides the majority of the data points at 2 months. This in turn suggests that there are only two, perhaps three boys with data at 2 months .</strike> <br />
<br />
<u>It could be that these 8 points all come from one baby. It could also be that they come from lots of babies all providing one data point but, given how much our first baby's eye gaze varies from video clip to video clip, this is going to be an extremely unreliable measure of eye gaze </u>[8]</div>
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<table align="center" cellpadding="0" cellspacing="0" class="tr-caption-container" style="margin-left: auto; margin-right: auto; text-align: center;"><tbody>
<tr><td style="text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEiKm-HP3U3COHVHS_g4oev_dR5v05aJVJWT6lEnPYil6ikuevMSNdWe7_PXwafhqD9wrbr-aXQdflofxrMG0HpOpTj-GhSgt8mvXiTlXs5HC_tvG8pNizS4R7qQd4YbhjsF_aas6JH9VJw/s1600/JonesKlin_2monthData.png" imageanchor="1" style="margin-left: auto; margin-right: auto;"><img border="0" height="300" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEiKm-HP3U3COHVHS_g4oev_dR5v05aJVJWT6lEnPYil6ikuevMSNdWe7_PXwafhqD9wrbr-aXQdflofxrMG0HpOpTj-GhSgt8mvXiTlXs5HC_tvG8pNizS4R7qQd4YbhjsF_aas6JH9VJw/s400/JonesKlin_2monthData.png" width="400" /></a></td></tr>
<tr><td class="tr-caption" style="text-align: center;"><span class="Apple-style-span" style="font-family: Verdana; font-size: 10px;">Adapted by permission from Macmillan Publishers Ltd: NATURE, doi:10.1038/nature12715 copyright 2013</span></td></tr>
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<u>Extended Data Figure 9 in the paper shows the trajectories excluding the data from the recording at 2 months. With the trajectories now beginning at 3 months, there is hardly any difference between the two groups before 6 months. In other words, everything hangs on the rather sketchy data from the babies at 2 months.</u><br />
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<tr><td style="text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgiUt1wpYi41Fqy4nKpBKNyMdfWOpMcPkRXLvuMRD1CljE59nauUKWStClyKqaRQbzyxsa62OsPP1-Y0VbW8cgF3qKu7gI8iyQUz5dOlRKm0cqI2m9F9yj0QVtqtjffTDhq5zbbWVzNHOg/s1600/JonesKlin+TrajectoriesOverlaid.png" imageanchor="1" style="margin-left: auto; margin-right: auto;"><img border="0" height="260" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgiUt1wpYi41Fqy4nKpBKNyMdfWOpMcPkRXLvuMRD1CljE59nauUKWStClyKqaRQbzyxsa62OsPP1-Y0VbW8cgF3qKu7gI8iyQUz5dOlRKm0cqI2m9F9yj0QVtqtjffTDhq5zbbWVzNHOg/s400/JonesKlin+TrajectoriesOverlaid.png" width="400" /></a></td></tr>
<tr><td class="tr-caption" style="text-align: center;"><span class="Apple-style-span" style="font-family: Arial, Helvetica, sans-serif; font-size: x-small;">Here I've overlaid Extended Data Figure 9a (TD in blue) and 9b (ASD in red) and faded out the irrelevant data, leaving the trajectories for eye gaze based on data from 3 to 24 months (ie excluding data collected at 2 months). Adapted by permission from Macmillan Publishers Ltd: NATURE, doi:10.1038/nature12715 copyright 2013</span></td></tr>
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So, to sum up, it's far too early to be declaring that baby's eye gaze predicts future autism. <u>Given that I've been pulling the paper apart, I probably haven't emphasised enough quite how ground-breaking and sophisticated Jones and Klin's study is. It's </u>an extremely impressive effort to answer an important question. It suggests that, <u>contrary to expectations, </u>there is in fact very little difference between babies who do and don't develop autism in terms of their eye gaze (at least when the eyes are on a computer screen). <u>This is something that appears to emerge very gradually over the first two years of life.</u><br />
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Future studies beginning even earlier and having even larger sample sizes may uncover evidence of atypical eye gaze <u>in infancy</u> - and there's a tantalising and intriguing suggestion that ASD babies may actually begin life with <i>excessive</i> eye gaze. [9]</div>
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However, not for the first time - and certainly not the last - the headlines obscure a far messier reality.<br />
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<b>Reference:</b></div>
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<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=Nature&rft_id=info%3Apmid%2F24196715&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=Attention+to+eyes+is+present+but+in+decline+in+2-6-month-old+infants+later+diagnosed+with+autism.&rft.issn=0028-0836&rft.date=2013&rft.volume=&rft.issue=&rft.spage=&rft.epage=&rft.artnum=&rft.au=Jones+W&rft.au=Klin+A&rfe_dat=bpr3.included=1;bpr3.tags=Psychology%2CNeuroscience%2CCognitive+Neuroscience%2C+Developmental+Neuroscience%2C+Abnormal+Psychology%2C+Cognitive+Psychology%2C+Developmental+Psychology%2C+Autism">Jones W, & Klin A (2013). Attention to eyes is present but in decline in 2-6-month-old infants later diagnosed with autism. <span style="font-style: italic;">Nature</span> PMID: <a href="http://www.ncbi.nlm.nih.gov/pubmed/24196715" rev="review">24196715</a></span></div>
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<b>Other coverage:</b><br />
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<li>SFARI: <a href="https://sfari.org/news-and-opinion/news/2013/classic-sign-of-autism-appears-in-early-infancy-study-says/news_view">Classic sign of autism appears in early infancy, study says</a></li>
<li>NHS Choices: <a href="http://www.nhs.uk/news/2013/11November/Pages/Can-autism-really-be-detected-in-babies.aspx">Can autism really be detected in babies? </a></li>
<li>Research the headlines: <a href="http://researchtheheadlines.org/2013/11/25/can-autism-be-identified-as-young-as-2-months-old/">Can autism be identified as young as 2 months old?</a></li>
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<b>Discussion:</b><br />
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Some great comments below the line. See also the <a href="http://www.reddit.com/r/science/comments/1sm3hw/does_a_babys_eye_gaze_really_predict_future/">discussion thread on reddit</a> started by Noah Gray, one of the Nature editors, and the comments on the <a href="https://www.facebook.com/thinkingpersonsguidetoautism/posts/631913960183268">Thinking Person's Guide to Autism</a> Facebook page.<br />
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<b>Footnotes:</b><br />
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1. It's usually the case in these studies that "low-risk" infants have older non-autistic siblings but this isn't explicitly stated.<br />
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2. It's not clear why the authors went to the trouble of testing 46 girls for 3 years only to exclude them later. The rationale given was that only 2 developed ASD, but this should have been expected given that autism is much less common in girls. My suspicion is that reviewers made them take the girls out of the analyses - but this is another reason why having an open peer review process is important.<br />
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<b>Update 09/12/13: </b>Ami Klin has informed me that more girls are being tested and their data will be analysed when the sample size is sufficiently large.<br />
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3. The ADOS was used as a severity measure in one analysis so was presumably included as part of the assessment. Beyond that, I can't find anywhere in the paper that actually says how the the authors determined which kids had autism.<br />
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<b>Update 09/12/13: </b>My mistake here. Although in my defence Nature doesn't make things easy by having three variations on the Methods section, each of increasing level of detail. Full details of diagnosis are buried in the <i>Supplementary Information</i> (which is separate from the <i>Methods</i> supplement, which is where I was searching for diagnostic information). In short, diagnosis was a clinical best estimate based on all available information, including ADI-R and ADOS scores (and direct or recorded observation of the ADOS session), language and cognitive assessments, history, and "any other relevant information". Diagnoses were made by independently by two experienced clinicians and positive diagnoses were reviewed by a third clinician.<br />
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4. This is based on the lower panel of Figure 2e<br />
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5. It's certainly possible that eye gaze discriminates between ASD and TD infants earlier than the 24 months reported and that the lack of statistical significant is just a reflection of the small sample sizes. With more babies tested, perhaps there would be a significant reduction much earlier. But that is speculation based on data that we currently don't have.<br />
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6. The high risk kids who didn't meet the ASD criteria were divided further into two subgroups - those who had no diagnosis (noDx) and those were had the "broader autism phenotype" (ie some autism symptoms) but didn't meet the full ASD criteria (BAP). The noDx group appear to resemble the TD group (at least in terms of their trajectory between 2 and 6 months) while the BAP group are intermediate between the TD and ASD groups. Unfortunately, nowhere does the paper say how the BAP was defined or whether the cut-offs were decided upon before the study started.<br />
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<b>Update 09/12/13: </b>Again, there were in fact details provided in the <i>Supplementary Information. </i>BAP infants were those for whom there were clinical concerns documented at any one of the clinical assessments. They differed significantly from the noDx group in terms of their ADOS Total scores. It would still have been useful to include a direct comparison between the high-risk babies who did develop ASD and those who didn't.<br />
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7. Based on the lower panel of Figure 2e this increase in eye gaze is statistically significant.<br />
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8. It seems as though one of the reviewers spotted this issue because the supplement to the paper includes a re-analysis looking at just the data from 3 to 6 months. This suggests that there was still a difference in the slope between the two groups , but this was barely significant. This is based on the Receive Operating Curves (ROCs) in Extended Data Figure 9d, where the 95% confidence intervals include chance at low levels of sensitivity (high specificity) but not a high levels (low specificity).<br />
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<b>Update 09/12/13: </b>I hadn't noticed that Extended Data Figure 9a has the trajectories based on data from 3 to 24 months. With the data from 2 months excluded, the early trajectories look very similar. For the ASD group, there's a drop from about 47.5% eye gaze at 3 months to 45% eye gaze at 6 months. The TD group are steady at about 45% throughout. If there is a real difference, it's <i>very</i> subtle.<br />
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9. By this I mean "more than is typical".</div>
drbrocktagonhttp://www.blogger.com/profile/15225859145004971487noreply@blogger.com18tag:blogger.com,1999:blog-1270723657817172117.post-32998544674385737292013-11-26T21:38:00.000-08:002013-11-28T19:09:58.123-08:00Beeps burps and brains: A thesis in three minutes<div class="separator" style="clear: both; text-align: center;">
<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEj-BaVwm8SadkmLmdX_XItsLWP0afUDyW49TTox9frdRusGVyOMDd9351CJX3L4jQHEBs5Kp02eTqYDWn9RO41AJH4sZkGZaQaqBV6gaQHKW00hyphenhyphenYVY0OkVSdznJlM55J6yRSfqcdvu5NA/s1600/Shu3MT.jpeg" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" height="266" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEj-BaVwm8SadkmLmdX_XItsLWP0afUDyW49TTox9frdRusGVyOMDd9351CJX3L4jQHEBs5Kp02eTqYDWn9RO41AJH4sZkGZaQaqBV6gaQHKW00hyphenhyphenYVY0OkVSdznJlM55J6yRSfqcdvu5NA/s400/Shu3MT.jpeg" width="400" /></a></div>
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Last month I had the pleasure of attending the Trans-Tasman finals of the 3-minute thesis competition, where students representing 42 universities from across Australia and New Zealand each gave a 3-minute presentation on the topic of their PhD thesis.</div>
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Representing Macquarie University was my student, <a href="http://www.cogsci.mq.edu.au/members/profile.html?memberID=537">Shu Yau</a>.<br />
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Having got through three rounds of competition (department, faculty, and then whole university) to win the Macquarie nomination, Shu made it all the way to the last eight of the finals.<br />
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Shu's presentation focused on a small part of her PhD research in which she measured the brain responses to sounds of an 8-year-old girl with autism. What makes this girl different to other kids taking part in our study (and other similar studies) is that she is completely nonverbal. She communicates via iPad but has never spoken a word.<br />
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There's an interesting story in how this study came about (and a lesson for me in underestimating nonverbal people with autism). But I'll leave all that for Shu to tell herself - once she's submitted her actual thesis.<br />
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The fact that we were able to test this girl is pretty cool in itself. As Shu notes in her presentation, there's hardly any research on these kinds of kids. But we also noticed a stark difference in her brain responses to the speech sounds compared to the other sounds - far greater than any of the other typically developing or (verbal) autistic kids we've tested.<br />
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Shu is currently writing this up as a case study for publication. It's obviously very preliminary data and we really have no idea how her findings might generalise to other autistic kids with minimal language skills. This is something we're planning on following up in the very near future.<br />
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For now, you can just enjoy the video of Shu's presentation in the final. All three minutes of it!<br />
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<iframe allowfullscreen='allowfullscreen' webkitallowfullscreen='webkitallowfullscreen' mozallowfullscreen='mozallowfullscreen' width='320' height='266' src='https://www.youtube.com/embed/WsZAFKraZbE?feature=player_embedded' frameborder='0'></iframe></div>
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Although we were primarily there to support Shu, the whole day was a fantastic advertisement for research in Australia and New Zealand. Topics ranged from optimal control of feral cats to a socio-cultural analysis of vaginal plastic surgery - and everything in between.<br />
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Particularly in Australia right now, there is a lot of concern about the sidelining of science - and research in general. The students at the three-minute thesis competition represent the next generation of researchers and it was heartening to see so many who were able to distil their research into a 3-minute soundbite and convey its importance to a general audience.<br />
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You can watch the whole of the final below. All eight talks are fantastic. But if you're short of time, fast forward to 43 minutes and watch Kelsey Kennedy's presentation, <i>"Feeling for cancer: an imaging tool to make breast cancer surgery more effective" </i>- a deserving winner.<br />
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<iframe frameborder="0" height="246" scrolling="no" src="http://cdn.livestream.com/embed/uwslive?layout=4&clip=pla_c576e0ce-df26-49a3-99fd-824b39cee307&color=0xe7e7e7&autoPlay=false&mute=false&iconColorOver=0x888888&iconColor=0x777777&allowchat=true&height=193&width=300" style="border: 0; outline: 0;" width="400"></iframe><br />
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Watch <a href="http://www.livestream.com/?utm_source=lsplayer&utm_medium=embed&utm_campaign=footerlinks" streaming="" title="live" video="">live streaming video</a> from <a at="" href="http://www.livestream.com/uwslive?utm_source=lsplayer&utm_medium=embed&utm_campaign=footerlinks" livestream.com="" title="Watch" uwslive="">uwslive</a> at livestream.com</div>
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Finally, a big thanks to the University of Western Sydney for hosting the event and for supplying the video of Shu's presentation.
drbrocktagonhttp://www.blogger.com/profile/15225859145004971487noreply@blogger.com1tag:blogger.com,1999:blog-1270723657817172117.post-14895007338867589082013-10-07T08:35:00.000-07:002013-10-08T20:52:50.747-07:00This study lacked an appropriate control group: Two stars<table align="center" cellpadding="0" cellspacing="0" class="tr-caption-container" style="margin-left: auto; margin-right: auto; text-align: center;"><tbody>
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<tr><td class="tr-caption" style="text-align: center;">Margaret and David's journal club <a href="http://www.abc.net.au/atthemovies/txt/s3552384.htm">Source</a></td></tr>
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In a recent article in the Observer newspaper, veteran film critic, Mark Kermode, <a href="http://www.theguardian.com/film/2013/sep/29/hatchet-jobs-anonymity-internet-kermode">discussed</a> his changing role in the internet age - a time when anyone with a blog can be an amateur critic, and when "recommendations" used in film advertising often come, not from established critics like himself, but from anonymous and potentially untraceable twitter accounts. Kermode's musings led him to conclude that what matters above all is reputation. The critic must have something at stake if his or her critique is to be of any worth:</div>
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<i>"criticism without risk to the critic has no value whatsoever – [...] an opinion is only worth as much as its author has to lose: their good name; their reputation; their audience; their job."</i></blockquote>
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Reading Kermode's article, I couldn't help but think of the parallels with professional criticism in science - otherwise known as peer review.</div>
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Before a paper can be published in a scientific journal it's first sent to a small number of experts in the field, who report back to the journal's editor. He or she then decides whether to publish the paper, ask the authors to change it to address the reviewers' comments, or reject the paper entirely.<br />
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Typically the reviewers are anonymous, uncredited as well as unpaid. The only reward is the good karma associated with contributing towards the broader endeavour of scientific progress. The main rationale for anonymity is that it allows you as the reviewer to say what you might be reluctant to say if everyone knew who you were. The authors of the paper you've just criticized might soon be reviewing your next paper or grant proposal or sitting on your hiring committee. Perhaps you'd be tempted to mince your words for fear of retribution or repercussions down the line.<br />
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Of course, this works both ways. Hiding behind the veil of anonymity, you can be as mean and unprofessional as you like. If you so desired, you could sabotage the paper of a competitor or someone you dislike personally. You could give the paper a cursory glance, pick out something that doesn't sit with your preconceptions and, rather than consider the authors' careful justification of their approach, dismiss the paper out of hand for being "fundamentally flawed". Alternatively, the same cursory glance could lead you to write a positive review that misses the crucial details that really do make the paper problematic. A good, constructive review takes time, thought, and effort. But again, apart from the karma, there's not a whole lot of motivation or incentive to do a good job.<br />
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Last week, Science magazine <a href="http://www.sciencemag.org/content/342/6154/60.full">published an article</a> highlighting further problems with the current peer review system. In an elaborate sting operation, investigative journalist, John Bohannon sent out variations on a fake microbiology paper to 304 journals, more than half of which accepted the paper, despite its obvious flaws.<br />
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As it happened, all of the journals targeted were open access - anyone can read them without having to pay a subscription. In some cases, this means the authors pay the journal a fee to cover the costs associated with publication. The implication of Bohannon's article was that, if publishers have a financial motivation to accept a paper (they only get paid if that happens) then they will inevitably let through a lot of rubbish. This is a genuine concern. But, as many commenters were quick to point out, we have no idea how many closed access journals would have also accepted the paper because none of them were targeted in the sting.<br />
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If there's a lesson here, it's that peer review itself is becoming a devalued product. When anyone can set up a "peer reviewed" journal; but nobody other than the journal editor knows who the reviewers are; and when only they and the authors know what the reviews say (or if they even exist), we eventually arrive at a situation where the fact of publication means next to nothing at all.<br />
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As Kermode's discussion suggests, reputation is what matters. Established journals have their reputations and dare not lose them. New journals, open access or otherwise, have reputations to establish. And so too should we, as reviewers have reputations to build. Clearly, this is only possible if, like film critics, our reviews are attributable:<br />
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<i>"if no one knows (or cares) who you are or what you have done, then what have you invested in your review? What do you have to lose?"</i></blockquote>
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A reviewer who consistently fails to spot glaring problems in a paper will soon develop a reputation as a sloppy scientist. On the other hand, a reviewer who is always constructively critical will become known as someone whose opinion matters. A review with their signature will come to mean more - just as a review from Mark Kermode or his like should carry more weight than one from Julie, 23, on twitter.</div>
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The analogy is imperfect. For a start, film critics generally sit outside the film-making process. As reviewers of scientific articles, we are taking a break from our normal role in the "production" side of the science industry to become a temporary critic. This does introduce some conflicts of interest, but it's not clear that anonymity solves them.<br />
<br />
And this closer involvement - knowing that the shoe will soon be on the other foot - should lead to a more constructive approach to review. As Kermode points out, it's relatively easy as a critic to do a hatchet job on a film, to produce a pithy negative review that translates into a succinct headline. Saying what's good about a film makes you vulnerable:<br />
<blockquote class="tr_bq">
<i>On some level, saying you love a film is a bit like admitting you have a crush on someone – it opens you up to accusations of foolishness, setting you up for inevitable heartbreak.</i></blockquote>
Anyone who's ever been in a journal club and ventured the opinion that they "actually quite liked the paper" will empathise with this view. Picking holes is easy. Finding the true value in a paper is the real difficult art. But this after all is what we want from peer review. We want to know that someone whose opinion we value has studied the paper in depth, has thought about it, and has concluded that it's worth our while taking a closer look.<br />
<br />
<br />
<b>Related posts:</b><br />
<ul>
<li><a href="http://crackingtheenigma.blogspot.com.au/2011/10/on-peer-review.html">Peer review - is it all it's cracked up to be?</a></li>
</ul>
<br />
<b>Further reading:</b><br />
<ul>
<li>Curt Rice: <a href="http://curt-rice.com/2012/12/17/open-evaluation-11-sure-steps-and-2-maybes-towards-a-new-approach-to-peer-review/">Open Evaluation: 11 sure steps – and 2 maybes – towards a new approach to peer review</a></li>
<li>Bob O'Hara: <a href="http://www.theguardian.com/science/grrlscientist/2013/oct/08/1">The scientific publishing sting: A missed opportunity</a></li>
</ul>
drbrocktagonhttp://www.blogger.com/profile/15225859145004971487noreply@blogger.com3tag:blogger.com,1999:blog-1270723657817172117.post-88331245275085301192013-09-19T04:19:00.000-07:002013-09-19T04:19:38.437-07:00Does psychology belong in the science club?<table align="center" cellpadding="0" cellspacing="0" class="tr-caption-container" style="margin-left: auto; margin-right: auto; text-align: center;"><tbody>
<tr><td style="text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjblTG_sCGHe66K1a20_b5jFeDLVK4AqrpvKrU4kVAiqiwr0IXOeuYzVU7c7GP7DgjszOtsN2fJjkxN9hXQUT5L-XbOTTeMkx5p3DbvZuq7g7OadARHVqiHS5IdhuuxEmkAinUq0UUzYYA/s1600/H4000039-Watson-and-Crick_cropped-by-CM-v1-1440x866.jpg" imageanchor="1" style="margin-left: auto; margin-right: auto;"><img border="0" height="240" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjblTG_sCGHe66K1a20_b5jFeDLVK4AqrpvKrU4kVAiqiwr0IXOeuYzVU7c7GP7DgjszOtsN2fJjkxN9hXQUT5L-XbOTTeMkx5p3DbvZuq7g7OadARHVqiHS5IdhuuxEmkAinUq0UUzYYA/s400/H4000039-Watson-and-Crick_cropped-by-CM-v1-1440x866.jpg" width="400" /></a></td></tr>
<tr><td class="tr-caption" style="text-align: center;">Crick and Watson with their Nobel-winning model of DNA. <a href="http://www.nobelweekdialogue.org/?attachment_id=364">Source</a> </td></tr>
</tbody></table>
<br />
First, a disclaimer: I’m the proud holder of a Bachelor of Science (upper second class) in experimental psychology. So you shouldn’t be too surprised when I tell you <a href="http://blogs.scientificamerican.com/psysociety/2013/08/13/psychology-is-a-science/">psychology is a science</a>. But for many other people, particularly scientists from other disciplines, psychology is at best a “soft” science. It doesn’t belong in the same exalted company as physics, chemistry, or, dare I say, neuroscience.<i></i><br />
<i><img alt="The Conversation" height="1" src="//counter.theconversation.edu.au/content/17429/count.gif" width="1" /></i><br />
The long-standing debate about psychology’s <a href="https://theconversation.com/is-psychology-a-science-10126">scientific credentials</a> was reignited last year by microbiologist and founding editor of RealClearScience, Alex Berezow. In a provocative article entitled <a href="http://www.realclearscience.com/blog/2012/07/keep-psychology-out-of-science-club.html">Keep psychology out of the science club</a>, Berezow argued:<br />
<blockquote>
The dismissive attitude that scientists have toward psychologists […] is […] rooted in the failure of psychologists to acknowledge that they don’t have the same claim on secular truth that the hard sciences do.</blockquote>
Left unanswered was the question of how science arrives at this so-called “secular truth”. More to the point: how is psychology any different when it comes to interrogating reality?<br />
<br />
<h3>
<b>Models in mind</b></h3>
<b><br /></b>
In the introductory chapter of his most recent book, <a href="http://books.google.com.au/books?id=2J18mryOM2YC&printsec=frontcover&dq=the+magic+of+reality&hl=en&sa=X&ei=9_UZUviUBaPZigeLlYCwCA&ved=0CEAQ6AEwAA#v=onepage&q&f=false">The Magic of Reality</a>, evolutionary biologist Richard Dawkins discusses how we know what is real. Most obviously, we can use our senses. If we can see or hear or feel something, if we can touch it or taste it, then we know that it’s real. We can also use machines to enhance and expand our senses. Bacteria are invisible to the naked eye but we can see them with a microscope. We can’t perceive radio waves, but we can have them translated into sounds we can hear.<br />
<br />
But as Dawkins notes:<br />
<blockquote>
There is a less familiar way in which a scientist can work out what is real when our five senses cannot detect it directly. This is through a model of what might be going on, which can then be tested […]<br />
We look carefully at the model and predict what we ought to see or hear, etc. if the model were correct. Then we look to see whether the predictions are right or wrong. If they are right, this increases our confidence that the model really does represent reality […]. If our predictions are wrong, we reject the model, or modify it and try again.</blockquote>
Dawkins illustrates this point with some famous examples of scientific modelling. Crick and Watson, for instance, didn’t <i>see</i> the double-helix shape of DNA: they <a href="http://www.nobelprize.org/educational/medicine/dna_double_helix/readmore.html">built a model</a> (literally, with cardboard) and saw that its predictions were consistent with observations made by another scientist, <a href="http://www.sdsc.edu/ScienceWomen/franklin.html">Rosalind Franklin</a>.<br />
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<br />
From genetics to <a href="http://arstechnica.com/science/2013/09/why-trust-climate-models-its-a-matter-of-simple-science/">climate change</a>, building, testing, and improving models of reality is an entirely legitimate way of doing science – and that’s precisely how psychology works. We can’t measure memories, beliefs or attitudes directly. But we <i>can</i> measure behaviour. And we can use those measurements to test the predictions of our psychological theories – our models of the mind.<br />
Psychology is a science. But the connection goes far deeper.<br />
<br />
<h3>
</h3>
<h3>
The science of thought</h3>
<br />
In his 1951 book <a href="http://crackingtheenigma.blogspot.com.au/2012/05/common-sense-of-science.html">The Common Sense of Science</a>, Jacob Bronowski argued that science should be thought of just like any other form of human thought: “science is made by people, and it has their style.”<br />
<br />
Bronowski would doubtless be fascinated to learn of subsequent <a href="https://www.ncbi.nlm.nih.gov/m/pubmed/23663408/?i=6&from=/16257103/related">developments</a> in psychology research. At every turn, we find analogs between science and everyday human cognition.<br />
<br />
A good example comes from the work of vision scientist <a href="http://www.richardgregory.org/">Richard Gregory</a>, who argued the way our visual system works is akin to the scientific process. Making sense of the light patterns hitting our retina involves <a href="http://www.richardgregory.org/papers/knowl_illusion/knowledge-in-perception.htm">generating hypotheses</a> about the objects in the world around us that could have given rise to that sensory “data”. These perceptual “hypotheses” are only revealed on those rare occasions when they are wrong – when the hypothesis doesn’t match reality and we experience an illusion.<br />
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<br />
Similar analogs apply in theories of language. When reading a story or listening to someone speak, we make sense of the incoming stream of words by building up a <a href="http://www3.nd.edu/~memory/Reprints/Zwaan%20&%20Radvansky%201998%20%28Psychological%20Bulletin%29.pdf">model of the situation</a> being described and <a href="http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2854821/">making predictions</a> about what will be heard or read next.<br />
<br />
Perhaps the most compelling analogy comes from the study of young children. Developmental psychologist <a href="http://www.alisongopnik.com/">Alison Gopnik</a> refers to children as the the “Research and Development Section of the Human Species”, learning by exploring, playing, and trying out new ideas. Adult scientists, she suggests, are really just kids who haven’t grown up!<br />
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<br />
<h3>
The psychology of science</h3>
<br />
The scientific nature of everyday thinking has important implications for understanding the <a href="http://www.psychologicalscience.org/index.php/news/releases/a-new-discipline-emerges-the-psychology-of-science.html">human element</a> of science. What leads to new discoveries and ideas? Why do some catch on while others are <a href="http://books.google.com.au/books?hl=en&lr=&id=SgCSC2P1IToC&oi=fnd&pg=PT90&ots=5UETtTl6Fz&sig=sqJjhCqEsaMaB3tXRq7dlGHa-fU&redir_esc=y#v=onepage&q&f=false">neglected</a>? What does it take to abandon a cherished theory, to <a href="http://www.theguardian.com/science/2012/aug/19/thomas-kuhn-structure-scientific-revolutions">change the scientific model</a>? These are all questions for psychology.<br />
<br />
Perhaps most importantly, psychology has a crucial role to play in the effective communication of science. As we’ve seen, people will <a href="http://www.britishscienceassociation.org/people-science-magazine/march2013/scientific-view-non-scientific-beliefs">interpret</a> each new piece of evidence in the light of their existing models of the world. It’s <a href="http://www.bbc.co.uk/news/science-environment-18709587">not enough</a> to simply expose people to science and hope for the best.<br />
<br />
Science is our best tool for understanding reality and predicting the future. But if science is to have a genuine influence in human affairs, if our decisions are to be guided by the best scientific evidence, scientists will have to start taking psychology seriously.<br />
<i><br /></i>
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<i>This article was originally published at <a href="http://theconversation.com/">The Conversation</a>. Read the <a href="http://theconversation.com/does-psychology-belong-in-the-science-club-17429">original article</a>.</i></div>
<h3>
Further reading:</h3>
<ul>
<li>Melanie Tanenbaum: <a href="http://blogs.scientificamerican.com/psysociety/2013/08/13/psychology-is-a-science/">Psychology's brilliant beautiful scientific messiness</a></li>
<li>Vaughan Bell: <a href="http://mindhacks.com/2013/08/20/dont-panic-but-psychology-isnt-always-a-science/">Don't panic but psychology isn't always a science</a></li>
<li>Neuroskeptic: <a href="http://blogs.discovermagazine.com/neuroskeptic/2013/08/19/is-psychology-science-is-the-wrong-question/#.UjhLSGS9MU8">"Is psychology science?" is the wrong question</a></li>
<li>Aidan Horner: <a href="http://aidanhorner.blogspot.com.au/2013/08/what-are-experimental-psychologists.html">What are experimental psychologists good for?</a></li>
<li>Alex Berezow: <a href="http://www.realclearscience.com/articles/2012/05/30/what_separates_science_from_non-science_106278.html">What separates science from non-science?</a></li>
</ul>
drbrocktagonhttp://www.blogger.com/profile/15225859145004971487noreply@blogger.com1tag:blogger.com,1999:blog-1270723657817172117.post-77359190344145218192013-09-10T19:20:00.003-07:002013-09-10T19:37:16.474-07:00Come to Sydney! Jobs and PhD scholarships in Cognitive Science at Macquarie Uni<div class="separator" style="clear: both; text-align: center;">
<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgLBrSkX0BtCWIxp7TJkcntI0EqMrNC71pP_TWPNDoZ7xXKMJyI-noTLDB58jwIcxi-Ca0wJNIUISV6pMXjnTchQR8Q5zf5CRyVtAduI3389y3ZkXSW4Fk_rl55xElz6ukG2zM_XM2tOTc/s1600/1918_108600840407_9902_n.jpg" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" height="237" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgLBrSkX0BtCWIxp7TJkcntI0EqMrNC71pP_TWPNDoZ7xXKMJyI-noTLDB58jwIcxi-Ca0wJNIUISV6pMXjnTchQR8Q5zf5CRyVtAduI3389y3ZkXSW4Fk_rl55xElz6ukG2zM_XM2tOTc/s400/1918_108600840407_9902_n.jpg" width="400" /></a></div>
<br />
<br />
We've got a number of positions going here in the <a href="http://www.cogsci.mq.edu.au/">Cognitive Science</a> department at Macquarie Uni in sunny Sydney. These include four post-doctoral fellowships and a fixed term lectureship. We're also looking for a technically minded person to run our Brain Research Lab, which has <i>three</i> MEG systems.<br />
<br />
In addition, there are a range of PhD scholarships available to international and domestic students.<br />
<br />
Some of the deadlines are pretty tight, so if you're interested, get cracking!<br />
<br />
<a href="http://jobs.mq.edu.au/cw/en/job/493353/cognitive-science-research-fellowships"><b>Cognitive Science Research Fellowships</b></a><br />
Two fixed-term three-year research fellowships are available in the Department of Cognitive Science, Macquarie University. The appointees will be outstanding researchers and will build strength in emerging interdisciplinary research fields in the Department. While the areas of research specialization are open, areas of special focus are: hearing and cognition; <b>autism and developmental disorders</b>; memory and aging; and computational neurology and computational neuroscience.<br />
<br />
<a href="http://jobs.mq.edu.au/cw/en/job/493354/ccd-postdoctoral-research-fellow"><b>CCD Postdoctoral Research Fellowships</b></a><br />
An opportunity for two postdoctoral research positions exists within the Language Program of the ARC Centre of Excellence in Cognition and its Disorders (CCD). The Language Program investigates the development of language in children, and how language is impaired in children and adults with language disorders (e.g., specific language impairment, aphasia).<br />
<br />
<a href="http://jobs.mq.edu.au/cw/en/job/493390/senior-scientific-advisor"><b>Senior Scientific Advisor</b></a><br />
The role will involve technical support and logistical planning of the MEG Laboratory, training staff and students in MEG system hardware and software, performing routine tests for specific research projects, providing recommendations and reports to the MEG Committee and advising them on options for resolution of technical problems. Importantly, the incumbent will be motivated to develop his/her own research into new analysis methods and enhanced MEG signal quality. <br />
<br />
<a href="http://jobs.mq.edu.au/cw/en/job/493352/lecturer-cognitive-science"><b>Lecturer in Cognitive Science</b></a><br />
A fixed-term Level B (Lecturer) teaching and research position is available for three years in the Department of Cognitive Science, Macquarie University. As well as undertaking research in one or more component fields of the cognitive sciences, the appointee will assist the Head of Department in the coordination and development of the Department's teaching program.<br />
<br />
<b><a href="http://www.hdr.mq.edu.au/information_about/scholarships/hdr_scholarships_domestic_and_international">International PhD Scholarships</a> </b>(see also other scholarships on the same page)<br />
Three full-time PhD International Macquarie University Research Excellence Scholarships are available in the ARC Centre of Excellence in Cognition and it’s Disorders. Scholarships are available in the areas of Belief Formation, Language, and Reading, however, outstanding applications from other related areas of cognitive science will be considered.<br />
<br />
Australian students should also check out these additional <a href="http://www.hdr.mq.edu.au/information_about/scholarships/hdr_scholarships_domestic_candidates_only">PhD scholarship opportunities</a>.<br />
<br />drbrocktagonhttp://www.blogger.com/profile/15225859145004971487noreply@blogger.com0tag:blogger.com,1999:blog-1270723657817172117.post-78595708838951975032013-08-07T07:13:00.000-07:002013-08-07T07:18:45.997-07:00For Pinker in 2013, read Bronowski 1951Steven Pinker has a wonderful essay in the New Republic. Entitled <i><a href="http://www.newrepublic.com/article/114127/science-not-enemy-humanities#">Science is not your Enemy</a>, </i>it's a passionate defence of "scientism" - a term often used in a derogatory fashion by those who see science as a threat, but which Pinker seeks to repurpose.<br />
<br />
Pinker's main focus is the fraught relationship between science and the humanities. Reading it on the train home this evening, I couldn't help but be reminded of Jacob Bronowski's <i>The Common Sense of Science</i>, which I read and <a href="http://crackingtheenigma.blogspot.com.au/2012/05/common-sense-of-science.html">reviewed</a> last year. The difference is that <i>Common Sense</i> was first published over 60 years ago. It's interesting as well as disheartening to see how little things have progressed in the interim.<br />
<br />
So before you go off and <a href="http://www.newrepublic.com/article/114127/science-not-enemy-humanities#">read Pinker</a> (if you haven't already done so), a few choice Bronowski quotes:<br />
<br />
<br />
On modernity:<br />
<blockquote class="tr_bq">
<i>Many people affect to believe that science has progressively strangled the arts, or distorted them into some unpleasant 'modern' form; and therefore that the arts can be revived only by throwing over science. Often of course this is merely an elderly sentiment in favour of the art of our younger days, and real scapegoat is not science but change. </i>(p 12)</blockquote>
<br />
On values:<br />
<blockquote class="tr_bq">
<i>Science changes our values in two ways. It injects new ideas into the familiar culture. And it subjects it to the pressure of technical change... So the invention of photography has made the painter and the patron lose interest in the likeness and transfer it to some more formal pattern. Our whole sensibility has been re-created by such subtle shifts. </i>(p 16)</blockquote>
<br />
On truth:<br />
<blockquote class="tr_bq">
<i>It is at least odd that science should be called amoral, and this by people who in their own lives set a high value on being truthful. For whatever else may be held against science, this cannot be denied, that it takes for ultimate judgement one criterion alone, that it shall be truthful. </i>(p 128)</blockquote>
<blockquote class="tr_bq">
<i>The truth of science is not truth to fact, which can never be more than approximate, but the truth of the laws that we see within the facts. And this kind of truth is as difficult and as human as the sense of truth in a painting which is not a photograph, or the feeling of emotional truth in a movement in music.</i> <i>When we speak of truth, we make a judgement between what matters and what does not... We do this as much in science as we do in the arts or in daily life. </i>(p 135)</blockquote>
<br />
Towards a reconciliation:<br />
<blockquote class="tr_bq">
<i>Science and the arts shared the same language at the Restoration. They no longer seem to do so today. But the reason is that they share the same silence: they lack the same language. And it is the business of each of us to try and remake that one universal language which alone can unite art and science, and layman and scientist, in a common understanding. </i>(p 17)</blockquote>
<br />drbrocktagonhttp://www.blogger.com/profile/15225859145004971487noreply@blogger.com0tag:blogger.com,1999:blog-1270723657817172117.post-16289854186647958462013-06-20T06:17:00.001-07:002013-06-21T16:45:14.168-07:00Registered report<table align="center" cellpadding="0" cellspacing="0" class="tr-caption-container" style="margin-left: auto; margin-right: auto; text-align: center;"><tbody>
<tr><td style="text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhNerCvqMId8WBe_Ph-QA1ZyvIkZFV9X6xogGPabB3XFUIgjQRto9ItZ5pRBsXdxTEZblVZnjguT0NIKGjfxwRp6LhNjS4rZUrmT_uUovac-8AowhbetjKw13qR48QjxdgRGiHZBdIuTmc/s1600/cartoon400.jpg" imageanchor="1" style="margin-left: auto; margin-right: auto;"><img border="0" height="241" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhNerCvqMId8WBe_Ph-QA1ZyvIkZFV9X6xogGPabB3XFUIgjQRto9ItZ5pRBsXdxTEZblVZnjguT0NIKGjfxwRp6LhNjS4rZUrmT_uUovac-8AowhbetjKw13qR48QjxdgRGiHZBdIuTmc/s400/cartoon400.jpg" width="400" /></a></td></tr>
<tr><td class="tr-caption" style="text-align: center;">Cartoon courtesy of Hilda Bastian's <a href="http://statistically-funny.blogspot.com.au/">Statistically Funny</a> blog</td></tr>
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Until fairly recently, I'd naively assumed that, if a finding was statistically significant, that meant it was probably true. There might be alternative explanations for the effect, but the existence of the effect itself wasn't in doubt.<br />
<br />
However, it turns out that it's actually much easier than I ever imagined to achieve a significant result just by chance. The main reason is that statistical analyses don't take into account the number of possible analyses that can be conducted. The more you poke around with your data, the more likely you are to find <i>something </i>that's statistically<i> </i>significant, even if there's really nothing going on.<br />
<br />
I've got a <a href="http://sfari.org/news-and-opinion/columnists/jon-brock/2013/connections-registered-reports">new post</a> over at the Simons Foundation Autism Research Initiative (SFARI) blog discussing these issues, and looking at a recent publishing initiative, the "registered report" that aims to cut down the number of false results that are published. Or, to put it in a more positive light, to identify those studies in which we can have the greatest confidence.<br />
<blockquote class="tr_bq">
These are fast-moving times for autism research. Every week brings a new swath of research findings that promise fresh insights into the causes of autism, its diagnosis and treatment. Yet, beneath the flurry of publications, the reality is that progress has been painstakingly slow. </blockquote>
<blockquote class="tr_bq">
One reason, unfortunately, is that many published studies contain results that turn out not to be true. This isn’t because scientists are lying or fabricating their data. It is a consequence of the way science is done and the pressures on researchers to produce results.</blockquote>
Read the rest of the post at <a href="http://sfari.org/news-and-opinion/columnists/jon-brock/2013/connections-registered-reports">SFARI</a><br />
<br />
<br />
For a more technical look at these issues in relation to EEG studies and analysis of variance, check out Dorothy Bishop's excellent post on <a href="http://deevybee.blogspot.com.au/2013/06/interpreting-unexpected-significant.html">interpreting unexpected significant results</a>. Also related, Neuroskeptic has a great discussion of ethical issues in what he calls <a href="http://blogs.discovermagazine.com/neuroskeptic/2013/06/20/the-trolley-problem-with-science/">The Science "Trolley Problem"</a>.<br />
<br />drbrocktagonhttp://www.blogger.com/profile/15225859145004971487noreply@blogger.com0tag:blogger.com,1999:blog-1270723657817172117.post-40379295847808301672013-06-04T16:13:00.000-07:002013-06-10T23:15:09.240-07:00Transforming Autism Research: Reflections on IMFAR, RDoC, and DSM-5 <div class="separator" style="clear: both; text-align: center;">
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<tr><td style="text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgP1lG0M1GOkkbu2m6Qn2xZvTfo3ejyRf5lhEEwKqhdWzFRM83KSp6K2PR9YXD_jJvzlLmUPLUvcvXO8QnYqQeN2vx6xsGFilaqsqOiKFco5BDotcEPXaf2a0jHizhYVOVATI5Konhu5s0/s1600/800px-San_Sebastian_Kursaal_noche.jpg" imageanchor="1" style="margin-left: auto; margin-right: auto;"><img border="0" height="300" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgP1lG0M1GOkkbu2m6Qn2xZvTfo3ejyRf5lhEEwKqhdWzFRM83KSp6K2PR9YXD_jJvzlLmUPLUvcvXO8QnYqQeN2vx6xsGFilaqsqOiKFco5BDotcEPXaf2a0jHizhYVOVATI5Konhu5s0/s400/800px-San_Sebastian_Kursaal_noche.jpg" width="400" /></a></td></tr>
<tr><td class="tr-caption" style="text-align: center;">The Kursaal Centre, San Sebastian. Venue for IMFAR 2013. <a href="http://en.wikipedia.org/wiki/File:San_Sebastian_Kursaal_noche.jpg">Source</a></td></tr>
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<i>“In many scientific problems, the difficulty is to state the question rightly; once that is done it may almost answer itself.” </i>Jacob Bronowski<br />
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<div style="text-align: center;">
<b>*</b></div>
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A year, it seems, is a long time in autism research. In May 2012, the International Meeting for Autism Research (IMFAR) in Toronto was all about DSM-5 and the proposed changes to autism diagnosis contained therein. Up for discussion were the abolition of Asperger syndrome as a distinct condition, the introduction of a new (and still mysterious) diagnosis of “social communication disorder”, and the feared exclusion of many people from autism-specific support and interventions.<br />
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Those concerns have not gone away. But 12 months later, at IMFAR 2013 in San Sebastian, the DSM-5 debate was notable by its absence. People had apparently agreed to disagree. And the manual had long since gone to the printers.<br />
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Discussion turned instead to comments by Thomas Insel, director of the National Institute of Mental Health (NIMH). In a <a href="http://www.nimh.nih.gov/about/director/2013/transforming-diagnosis.shtml">blogpost</a> entitled "Transforming Diagnosis", Insel announced that the institute would be “re-orienting its research away from DSM categories”. “Patients”, he argued, “deserve better”.<br />
<br />
Insel's proposed solution is a new research framework - <a href="http://www.nimh.nih.gov/research-priorities/rdoc/index.shtml">Research Domain Criteria</a> or RDoC. The aim of RDoC is to make connections across different levels of analysis, from genes and neurotransmitters through to brain circuits and behavior. But rather than basing research on existing diagnostic categories, RDoC focuses on broad constructs such as ‘social communication’, ‘cognitive control’, or ‘anxiety’ that cut across existing diagnostic boundaries.<br />
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*</div>
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As Insel pointed out, the DSM’s great weakness is “a lack of validity”. This doesn’t mean that it's useless or a waste of time. The key point is that there’s little independent evidence to suggest that people who are diagnosed with the same condition really do belong together - and should be treated differently to people with other diagnoses. We don’t know that their symptoms have the same underlying cause, and we can’t say that their outcomes will be similar, or that they should be offered the same interventions.<br />
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These issues were front and centre in the opening address of IMFAR 2013. Focusing on the problem of “comorbidity”, Christopher Gillberg noted that people with autism often meet criteria for several other DSM diagnoses, including ADHD, specific language impairment, and developmental coordination disorder. These, Gillberg argued, are not discrete syndromes, so it is inappropriate to research them separately or to diagnose one condition without considering the implications of the others.<br />
<br />
Daniel Geschwind's keynote address on Day 2 raised similar problems with the validity of autism. Reviewing the latest in autism genetics, Geschwind noted that, according to current projections, autism is linked to upwards of 1000 different genetic variations. Although these appear to converge on a smaller number of pathways, most of the genetic risk factors discovered so far also increase the likelihood of other, supposedly unrelated disorders.<br />
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Like so many other conditions in the DSM, autism is a mess.<br />
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<b>*</b></div>
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Insel's comments, arriving just days before DSM-5’s publication, were widely seen as a final blow to the DSM’s credibility and a major snub to its publishers, the American Psychiatric Association. Media coverage spoke of a civil war within psychiatry. But the reality is that the aims of RDoC actually align closely with those of the APA.<br />
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Back in 2002, in a document entitled “<i>A Research Agenda for DSM-V</i>”, Dennis Charney and colleagues stated:<br />
<blockquote class="tr_bq">
<i>“It is our goal to translate basic and clinical neuroscience research relating brain structure, brain function, and behavior into a classification of psychiatric disorders based on etiology and pathophysiology. It is possible, even likely, that such a classification will be radically different from the current DSM-IV approach.</i></blockquote>
It soon became clear, however, that this radical new approach to diagnosis was not ready for primetime. As Insel noted, the controversy surrounding DSM-5 belies the fact that the changes from DSM-IV have been relatively modest. In the case of autism, the reworking of diagnostic criteria may yet have profound consequences in terms of who receives interventions and services. But conceptually, little has changed. Seventy years after it was first identified, autism is still diagnosed in terms of the collection of behavioral symptoms that also define the condition.<br />
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In the absence of reliable alternatives, clinicians will continue to rely on the DSM. But researchers do not have the same excuse. Holding up the current diagnostic criteria as the ‘gold standard’ for research makes it impossible to discover better alternatives.<br />
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Writing for the Dana Foundation in 2011, DSM-5 panel member, Steven Hyman, <a href="http://www.dana.org/news/cerebrum/detail.aspx?id=32066">concluded</a>:<br />
<blockquote class="tr_bq">
<i>“it is critical that the scientific community escape the artificial diagnostic silos that control so much research, ultimately to our detriment.”</i></blockquote>
Lynn Waterhouse reached a similar conclusion in her 2012 book, “<a href="http://books.google.com.au/books?id=zOC-qfqCGZUC&pg=PA48&lpg=PA48&dq=rethinking+autism+waterhouse&source=bl&ots=BhJAu4WAYU&sig=Oe8EwiY5ZHfnZ6W6ugFPpws3gwk&hl=en&sa=X&ei=aOGuUfznCojIlQXrsoHgBQ&ved=0CHsQ6AEwCQ#v=onepage&q=rethinking%20autism%20waterhouse&f=false">Rethinking Autism</a>”:<br />
<blockquote class="tr_bq">
<i>“The only viable scientific path… requires researchers to abandon the use of the diagnosis of autism as a basis for research.”</i></blockquote>
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<b>*</b></div>
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Last year on my journey home from Toronto, I spent the flight reading Jacob Bronowski’s “<a href="http://crackingtheenigma.blogspot.com.au/2012/05/common-sense-of-science.html">The Common Sense of Science</a>”, a 1951 history of science that I’d picked up for a few dollars in our local second hand bookstore. I took it with me for no reason other than that it fitted neatly into my hand luggage. But the ideas seemed particularly relevant in the light of the drama and intrigue of the IMFAR meeting.<br />
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According to Bronowski, the first step towards scientific understanding is to “order” things into groups, as he put it, “not of identical things, but of things which seem to be or behave alike”. This “ordering” process is necessary if we are to generalize our narrow scientific observations towards a broader understanding of the world. Initially, the “throwing into groups” has to be intuitive, but these intuitions must be tested. If the evidence doesn’t fit, then we should be prepared to refine or even abandon our intuitions and (literally) regroup:<br />
<blockquote class="tr_bq">
<i>“We order by likeness, and we choose those likenesses which we first judge <b>and then find </b>to have significance” </i>[emphasis added]</blockquote>
Since Kanner, the idea of a discrete condition, “autism”, has made intuitive sense to researchers and clinicians alike. We could metaphorically throw a wide range of people into that group because, although they were different from one another in many ways, they seemed to have something essential in common. What was learned about one sample of autistic people could, we assumed be generalised to others. However, as more evidence has come in, the concept of autism as a coherent entity has been found wanting. This is the “validity” issue that so undermines the DSM.<br />
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Insel’s bet is that the “domains” of RDoC <i>do</i> have validity, that they <i>will</i> map better onto underlying biological mechanisms and, crucially, that they <i>will</i> provide clearer insights into appropriate treatments and interventions for individuals. RDoC represents an alternative “ordering” of the human mind. But like the DSM, it needs to be empirically tested, refined, and, if necessary, rejected.<br />
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<b>*</b></div>
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After all the controversy surrounding DSM-5, RDoC represents a fresh start, and a much-needed reframing of the scientific problem. At present, however, it’s little more than a statement of intent, describing how research could and perhaps should proceed. The goals are long term. And while the idea of looking beyond DSM categories is a welcome move, there’s no guarantee that RDoC will succeed in its primary objectives of linking behavioural symptoms back to their underlying biological origins.<br />
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Identifying risk genes and their immediate relevance to neural function is likely to be the easy part. The greater challenge will come in working out how these differences interact with other genetic and environmental risk factors, such that some individuals develop into autism, whereas others have completely different outcomes. Given the complexities, both known and unknown, that are yet to be addressed, it seems essential that any biological approach to autism is complemented by research with more immediate benefits to the autism community.</div>
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For me, the highlight of IMFAR 2013 was Maureen Durkin's <a href="http://crackingtheenigma.blogspot.com.au/2013/05/the-epidemiology-of-autism-spectrum.html">keynote address</a> on the final morning, focusing on the discrepancies in autism diagnosis across countries, cultures, and social classes. In her closing remarks, Durkin emphasized an important distinction - between the current emphasis on autism as an impairment and the alternative view of autism as a disability. Practical strategies for assisting people with sensory and physical disabilities often have the indirect consequence of increasing social participation. It follows, Durkin argued, that research on autism should address similar practical solutions that might lead to greater inclusion of people with autism in society.<br />
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<b>*</b></div>
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DSM-5 has been a long and painful process. Only time will tell if the changes represent a net improvement on DSM-IV. But the debates generated within the scientific community and beyond have served an important purpose, laying bare the questionable assumptions that underpin contemporary autism research. Whatever your views on the specifics of DSM-5 and RDoC, Dr Insel was certainly right about one thing. There is room for improvement. We can do better. Autistic people deserve better.
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<br />
<b>Reference:</b><br />
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=American+Journal+of+Psychiatry&rft_id=info%3Adoi%2F10.1176%2Fappi.ajp.2010.09091379&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=Research+Domain+Criteria+%28RDoC%29%3A+Toward+a+New+Classification+Framework+for+Research+on+Mental+Disorders&rft.issn=0002-953X&rft.date=2010&rft.volume=167&rft.issue=7&rft.spage=748&rft.epage=751&rft.artnum=http%3A%2F%2Fajp.psychiatryonline.org%2Farticle.aspx%3FarticleID%3D102361&rft.au=Insel%2C+T.&rft.au=Cuthbert%2C+B.&rft.au=Garvey%2C+M.&rft.au=Heinssen%2C+R.&rft.au=Pine%2C+D.&rft.au=Quinn%2C+K.&rft.au=Sanislow%2C+C.&rft.au=Wang%2C+P.&rfe_dat=bpr3.included=1;bpr3.tags=Medicine%2CPsychology%2CNeuroscience%2CCognitive+Neuroscience%2C+Psychiatry%2C+Autism"><br /></span>
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=American+Journal+of+Psychiatry&rft_id=info%3Adoi%2F10.1176%2Fappi.ajp.2010.09091379&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=Research+Domain+Criteria+%28RDoC%29%3A+Toward+a+New+Classification+Framework+for+Research+on+Mental+Disorders&rft.issn=0002-953X&rft.date=2010&rft.volume=167&rft.issue=7&rft.spage=748&rft.epage=751&rft.artnum=http%3A%2F%2Fajp.psychiatryonline.org%2Farticle.aspx%3FarticleID%3D102361&rft.au=Insel%2C+T.&rft.au=Cuthbert%2C+B.&rft.au=Garvey%2C+M.&rft.au=Heinssen%2C+R.&rft.au=Pine%2C+D.&rft.au=Quinn%2C+K.&rft.au=Sanislow%2C+C.&rft.au=Wang%2C+P.&rfe_dat=bpr3.included=1;bpr3.tags=Medicine%2CPsychology%2CNeuroscience%2CCognitive+Neuroscience%2C+Psychiatry%2C+Autism">Insel, T., Cuthbert, B., Garvey, M., Heinssen, R., Pine, D., Quinn, K., Sanislow, C., & Wang, P. (2010). Research Domain Criteria (RDoC): Toward a New Classification Framework for Research on Mental Disorders <span style="font-style: italic;">American Journal of Psychiatry, 167</span> (7), 748-751 DOI: <a href="http://dx.doi.org/10.1176/appi.ajp.2010.09091379" rev="review">10.1176/appi.ajp.2010.09091379</a></span><br />
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<b>Further reading:</b><br />
<ul>
<li>Simons Foundation: <a href="http://sfari.org/news-and-opinion/news/2013/funding-agency-shifts-focus-away-from-diagnostic-groups">Funding agency shifts focus away from diagnostic groups</a></li>
<li>SFARI <a href="http://sfari.org/sfari-community/community-blog/2013/live-dsm-5-discussion?utm_source=Autism+research+news+from+SFARI.org&utm_campaign=b6575560fa-SFARI_Newsletter_130604&utm_medium=email&utm_term=0_0a60ccb345-b6575560fa-381152246">web-chat</a> with Tom Insel, Cathy Lord, and Helen Tager-Flusberg</li>
<li>The Neurocritic: <a href="http://neurocritic.blogspot.com.au/2013/05/what-rdoc-research-might-look-like.html">What RDoC research might look like</a></li>
<li>Russ Poldrack: <a href="http://www.russpoldrack.org/2013/05/the-dimensional-approach-to-studying.html">The dimensional approach to studying mental illness</a></li>
<li>The Neurocritic: <a href="http://neurocritic.blogspot.com.au/2013/05/rdoc-dimensional-approach-for-research.html">RDoC dimensional approach for research vs DSM-5 for diagnosis</a></li>
<li>Sanjay Srivastrava: <a href="http://hardsci.wordpress.com/2013/05/24/where-is-rdoc-headed-a-look-at-the-eating-disorders-foa/">Where is RDoC Heading? A look at the eating disorders FOA</a></li>
<li>Squirreled Thoughts: <a href="http://squirreledthoughts.wordpress.com/2013/05/16/a-framework-for-mental-health-research-rdoc/">A framework for mental health research</a></li>
<li>Maia Szalavitz: <a href="http://healthland.time.com/2013/05/17/viewpoint-my-case-shows-whats-right-and-wrong-with-psychiatric-diagnoses/">My case shows what's right - and wrong - with psychiatric diagnoses</a></li>
<li>David Dobbs: <a href="http://daviddobbs.net/smoothpebbles/the-book-of-woe-gary-greenbergs-romp-of-a-read-about-the-dsm-disaster/?utm_source=rss&utm_medium=rss&utm_campaign=the-book-of-woe-gary-greenbergs-romp-of-a-read-about-the-dsm-disaster">“The Book of Woe” – Gary Greenberg’s Romp of a Read About the DSM Debacle</a></li>
<li>Steven Novella: <a href="http://www.sciencebasedmedicine.org/index.php/dsm-5-and-the-fight-for-the-heart-of-psychiatry/">DSM-5 and the Fight for the Heart of Psychiatry</a></li>
</ul>
drbrocktagonhttp://www.blogger.com/profile/15225859145004971487noreply@blogger.com0tag:blogger.com,1999:blog-1270723657817172117.post-38498201371310371032013-05-06T12:50:00.000-07:002013-07-19T14:34:00.510-07:00The Epidemiology of Autism Spectrum Disorder: Toward a More Inclusive World<div class="separator" style="clear: both; text-align: center;">
<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgfcJaUSJZrQOeTmcbTjQ5bd1rfmbndJx1gI4iMIQw6WoAfrwOFeUfFEoc1ehtJadTluidl7q19YviwClFb-fmOyHtiOFfWKFdwayQYsObxha9JWoV_3rP1-QU1v_DD9Bhzjuw1IumYNw0/s1600/Durkin_IMFAR05042013.png" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" height="298" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgfcJaUSJZrQOeTmcbTjQ5bd1rfmbndJx1gI4iMIQw6WoAfrwOFeUfFEoc1ehtJadTluidl7q19YviwClFb-fmOyHtiOFfWKFdwayQYsObxha9JWoV_3rP1-QU1v_DD9Bhzjuw1IumYNw0/s400/Durkin_IMFAR05042013.png" width="400" /></a></div>
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<br />
On Saturday, Maureen Durkin gave a brilliant keynote address at the International Meeting for Autism Research in San Sebastian. Entitled <i>The Epidemiology of Autism Spectrum Disorder: Toward a More Inclusive World</i>, it really put the International into IMFAR.<br />
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Durkin began with an overview of recent trends in autism epidemiological research, including the increases in autism numbers, the make-up of the autism population, and the variation in those numbers across countries and socio-economic status. She then moved on to consider more political issues, including the impact of copyright restrictions on access to diagnostic tools and the need to broaden the focus of epidemiological research beyond considering only autistic impairments.<br />
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I understand that the slides (and possibly the video) of the talk will be made available. <b>Update: slides available to download <a href="http://www.disabilitymeasures.org/durkin-imfar/">here</a></b>. In the meantime, here are the (lightly edited) notes I made during the talk. Be aware that they may not be a completely accurate record. If you notice any inaccuracies or major omissions, please comment. Also, the notes don't do the talk much justice, so it's well worth looking out for it when it becomes available.<br />
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<ul>
<li>Elsabbagh et al in Autism Research provide a valuable review of autism prevalence by year and country </li>
<li>Pre 2000 – 1/3 of children with ASD had IQs in normal range. In studies since 2000 the rate is around 2/3 </li>
</ul>
<ul>
<li>Autism is the most expensive form of special education with an estimated cost of $11000 per year – double that of other special education</li>
<li>Lifetime costs are huge. Parents should be referred for financial counselling at diagnosis</li>
</ul>
<ul>
<li>Autism rates differ by socio-economic status (SES)</li>
<li>Wing 1980 noted that educated parents are more likely to obtain an autism diagnosis for their child </li>
<li>Autism rates are significantly higher in higher SES groups – the opposite of other disabilities where rates are higher in less well-to-do social groups </li>
<li>The SES effect is present in all races (Durkin et al 2010 PLoS ONE) </li>
<li>If we assume this is due to differences in ascertainment then it follows that (a) there are disparities in access to service and (b) many kids with autism are being missed </li>
<li>Disparities may also be due in part to clinicians’ bias.</li>
<li>Clinicians are more likely to assign autism diagnoses when given descriptions of children from high SES background than when given description of child showing same features but from low SES background (Cuccuro et al 96 JADD) </li>
<li>Latino kids are half as likely to receive ABA, due to later diagnosis (Magana) </li>
<li>Despite improving identification of autistic kids, there is no evidence of the prevalence disparity decreasing </li>
<li>SES gradient is not found in Sweden. In fact it trends in the opposite direction (ie like other disorders) (Rai) </li>
</ul>
<ul>
<li>Media images of autism are still almost exclusively of white boys</li>
</ul>
<ul>
<li>Most assessments are copyrighted, preventing translations to other languages </li>
<li>To avoid copyright restrictions, clinicians currently have to reinvent the wheel to develop new diagnostic tools </li>
<li>The R-statistics package could be a useful model for how an open source approach to autism diagnosis might work </li>
<li><a href="http://www.disabilitymeasures.org/">DisabilityMeasures.org</a> provides a list of free and open disability measurement tools </li>
</ul>
<ul>
<li>The International Classification of Functioning Disability and Health distinguishes between (a) impairment, (b) activity limitations, and (c) restrictions </li>
<li>Epidemiology currently looks only at impairment </li>
<li>But there may be a limited amount that can be done regarding impairment so it’s important to look at activity limitations and restrictions </li>
<li>Lessons can be drawn from physical and sensory disabilities where enhancing participation of people with disabilities indirectly improves their social participation </li>
</ul>
<ul>
<li>The World Health Organization coordinated an international study on the course and outcome of schizophrenia </li>
<li>“Extraordinary finding that subjects in developing world were generally better off than their counterparts in developed world”
This despite the frequency of schizophrenia being the same </li>
<li>This suggests possibility that might find better models for dealing with schizophrenia in developing countries </li>
<li>Should be open to possibility that this might also be true of autism </li>
</ul>
<ul>
<li>UN Conventions on rights of the child and rights of persons with disabilities provides an important framework, seeing people with disabilities less as objects of charity (and more as valued members of society) </li>
</ul>
<ul>
<li>Future of autism – shaped by convergence of ideas (open collaboration, emphasis on participation in society) and new technologies</li>
</ul>
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<div>
<b>Links:</b></div>
<div>
<ul>
<li><a href="http://sfari.org/sfari-community/community-blog/2013/reactions-from-imfar">Response</a> from Francesca Happe</li>
<li><a href="http://www.autismspeaks.org/blog/2013/05/08/understanding-autism-toward-more-inclusive-world">Response</a> from Michael Rosanoff of Autism Speaks</li>
<li><a href="https://sfari.org/news-and-opinion/viewpoint/2013/a-global-vision-for-autism-with-community-solutions">A global vision for autism with community solutions</a>: Fantastic SFARI post from Mayada Elsabbagh</li>
</ul>
</div>
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drbrocktagonhttp://www.blogger.com/profile/15225859145004971487noreply@blogger.com0tag:blogger.com,1999:blog-1270723657817172117.post-89947783062201720892013-05-01T03:44:00.001-07:002013-05-01T03:48:30.684-07:00Come and find me at IMFAR 2013<a href="http://www.autism-insar.org/imfar-annual-meeting/imfar-2013">IMFAR</a>, the International Meeting for Autism Research, begins in tomorrow in the beautiful city of San Sebastian in northern Spain. The <a href="https://imfar.confex.com/imfar/2013/webprogram/start.html">program</a> looks pretty good and I'm surprising myself at how excited I am!<br />
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As well as sampling the rioja and pinchos, I'm presenting two posters. Please do drop by and say hello if you're attending.<br />
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<b>108.143: Oscillatory neural responses to speech and nonspeech sounds in a nonverbal child with autism</b><br />
<i>Thursday 12pm, Poster 143</i><br />
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<tr><td style="text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgYTXedwtBzOst_gwGcQM1iAFNfqSpEPV8nEJ5Xxv3ChzGkCZjA1vDMypRo3-VWl3Y41QF76LKwDXKj15LSilsAC_DEBNRfg8bXt7nxM-dZhxQjwWWWKuSiuwSK6wDiFYDcHHE6IaFPSmw/s1600/ShuPoster.png" imageanchor="1" style="clear: right; margin-bottom: 1em; margin-left: auto; margin-right: auto;"><img border="0" height="320" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgYTXedwtBzOst_gwGcQM1iAFNfqSpEPV8nEJ5Xxv3ChzGkCZjA1vDMypRo3-VWl3Y41QF76LKwDXKj15LSilsAC_DEBNRfg8bXt7nxM-dZhxQjwWWWKuSiuwSK6wDiFYDcHHE6IaFPSmw/s320/ShuPoster.png" width="224" /></a></td></tr>
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On Thursday I'm presenting a case study conducted by Shu Yau as part of her PhD research. Shu couldn't come so I get to stand next to her poster and waffle instead.<br />
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The study involves G, an autistic girl who has never spoken. Shu used magnetoencephalo-graphy (MEG) to record the magnetic fields produced by G's brain while she listened to different sounds.<br />
<br />
Interestingly, G showed a very weak response to speech sounds, but an extremely strong response to nonspeech sounds. This was unlike any of the other children we've tested - either typically developing children or verbal autistic children.<br />
<br />
We're not sure what to make of the data so would love any feedback. Given G's profound language difficulties, it's tempting to assume that her differential brain response to the two sounds is related to the differences in "speechiness" of the sounds. But we don't know that for sure. It's also unclear at this stage how representative G is of other kids like her.<br />
<br />
Nonetheless, we think these are interesting preliminary findings. At the very least they show that it's possible to conduct MEG studies with nonverbal kids, who are usually excluded from neuroimaging research.<br />
<br />
<br />
<b>144.148: Individual differences in homograph reading amongst Hebrew-speaking autistic children</b><br />
<i>Friday 3pm, Poster 148</i><br />
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On Friday I'm presenting a study of homograph reading in Hebrew-speaking kids with autism, conducted with colleagues Nufar Sukenik and Naama Friedmann from Tel Aviv University.<br />
<br />
Homographs are written words that have multiple meanings and, sometimes different pronunciations. For example, the word "tear" is pronounced differently depending on whether the context is crying or ripping.<br />
<br />
One of the more consistent findings in autism research is that people with autism tend to be bad at working out which pronunciation of the homograph to use. This is seen as key evidence for the "weak central coherence" account, which attributes many features of autism to an inability to use contextual information.<br />
<br />
The advantage of conducting the study in Hebrew is that there are many more suitable homographs in Hebrew than in English - mainly because written Hebrew doesn't really bother with vowels! This meant we could give the kids lots of homographs to read, so our data should be much more reliable than previous studies conducted in English.<br />
<br />
Our main finding was that there were statistically reliable individual differences in homograph reading skills within our autism group. In other words, only a subgroup had difficulties. And importantly those differences couldn't be explained away in terms of boring things like older kids or kids with generally stronger reading skills being better at the task.<br />
<br />
In fact, the best predictor of homograph reading was performance on a picture naming task. The numbers in the study are relatively small, so again need to be treated with caution - but they suggest (to me at least) an alternative view of homograph reading difficulties in autism. Perhaps the problem is less to do with comprehension of the sentence context and more to do with selecting the right word to say when speaking or reading aloud.<br />
<br />
<br />
<b>Conference updates:</b><br />
<br />
SFARI (the Simons Foundation Autism Research Initiative) will be <a href="http://sfari.org/sfari-community/community-blog/2013/reactions-from-imfar">live-blogging</a> the conference. You can also follow the <a href="https://twitter.com/search/realtime?q=%23IMFAR2013&src=hash">#IMFAR2013</a> hashtag on Twitter.drbrocktagonhttp://www.blogger.com/profile/15225859145004971487noreply@blogger.com2tag:blogger.com,1999:blog-1270723657817172117.post-64020839075036263392013-04-04T20:04:00.001-07:002013-04-07T20:49:30.900-07:00An exception to prove the ruleI’ve often had cause to query the wisdom of old sayings. One that has always seemed particularly nonsensical is the phrase “The exception that proves the rule”. There is a rule; you find something that breaks the rule; and that somehow proves that the rule was correct? This is not the kind of logic to be encouraging. It turns out, however, that I (and I suppose many others) have misinterpreted that particular phrase, and that those ancient purveyors of wisdom were onto something all along.<br />
<br />
In his essay, “Death Before Birth”, Stephen J Gould notes that the word “prove” derives from the Latin, <i>probare</i>, to test or probe. An exception tests a rule; it doesn’t necessarily confirm it. Another old saying, “The proof of the pudding is in the eating”, is perhaps less easy to miscomprehend. Gould was an evolutionary biologist and his writing focused on the quirks of nature that put evolutionary theory to the test. From the panda’s inelegant “thumb” (actually, an outgrowth of the wrist) to the hero of the essay, a mite that impregnates his sisters and dies before being born, all are difficult to reconcile with the idea of a divine creator (unless He or She had a particularly warped sense of humour), yet make perfect sense when seen through the lens of evolution. But, as the existence of the old saying suggests, the principle extends far beyond biology. Ideas should be tested by looking at exceptional cases.
<br />
<br />
Psychology is a comparatively new science that currently lacks the kind of over-arching theory that Darwin has provided for biologists, but there is clearly much to be learned from the investigation of exceptional minds. And this, I suspect, is at least part of the reason why autism holds such fascination, both to researchers and to the public at large. Autism affects language, it affects the ability to organise behaviour. Most notably, it affects the ability to interact with other humans, to infer their unobservable beliefs and motivations. These are all qualities that we tend to think of as being uniquely human. Autism, it follows, offers a window into the human mind.<br />
<br />
The danger, however, is that the study of autism makes autistic people appear somehow less than human. It’s not difficult to find examples, both in the scientific literature and the popular media, where this impression is given. Clearly, this is wrong, and not merely for reasons of political correctness or the avoidance hurt feelings. Again, I think we can draw lessons from the biological sciences. As Gould and many others have pointed out, one of Darwin’s great insights was that members of a species should not be seen merely as deviations from an abstract ideal of what that species should be. Individuals matter. It is the variation that defines a species, not the average or the norm. And it is the variation amongst people that defines the human species.<br />
<br />
Autism is a disability and we shouldn’t pretend away the challenges faced by autistic people and their families. We can try and understand the causes of autism, its genetics and neurobiology; we can investigate how autistic people think, how they perceive the world; and we can try and work out the best ways to help autistic individuals lead fulfilling lives. But whether we refer to autistic people or people with autism, we can do all this whilst still recognizing that autism is part of who they are as human beings. Autistic people are exceptional people. If we understand autism then we are a step closer to understanding what it means to be human. drbrocktagonhttp://www.blogger.com/profile/15225859145004971487noreply@blogger.com18tag:blogger.com,1999:blog-1270723657817172117.post-55859217549618112962013-03-25T23:56:00.000-07:002013-03-25T23:56:44.930-07:00Six questions for connectivity theory researchIn my latest <a href="http://sfari.org/news-and-opinion/columnists/jon-brock/2013/connections-six-questions-for-connectivity-theory-research">column for the Simons Foundation Autism Research Initiative</a>, I list six questions for the “connectivity” account of autism. “Underconnectivity” is arguably the leading account of the neurobiology of autism at present. It makes a lot of sense intuitively (in fact, the idea has been around since at least the 1960s). But, while the advent of various neuroimaging techniques has now made it possible to investigate neural connections in autism, we’re still a long way from really understanding how the brain of autistic people are wired up (not that we have a much of better idea for non-autistic people).<br />
<br />
The article is part of a <a href="http://sfari.org/news-and-opinion/specials/2013/connectivity/connectivity-special-report">Special Report on connectivity in autism</a>, featuring contributions from a range of top neuroimaging researchers (and me). A recurring theme in the series is the need for better methods - to make sure that group differences in measured connectivity really do reflect differences in the brains of autistic versus non-autistic participants and not, for example, the fact that one group are less able to lie still in the scanner. A related issue, raised by Dan Kennedy, is the problem of publication bias, where only studies that find evidence for underconnectivity end up being published, thereby distorting the literature. Finally, there's a need for the theory to get more specific - to be more precise about what is meant by local and global connectivity, and to specify which particular connections might be involved.<br />
<br />
<b>Further reading:</b><br />
<br />
There have been a couple of good reviews of connectivity in autism in the last few years. I'd particularly recommend Sam Wass's <a href="http://www.cbcd.bbk.ac.uk/people/sam/BrainCog">2011 paper</a> in Brain and Cognition, which raises many of the same questions as my post.<br />
<br />
<b>Related posts:</b><br />
<br />
<ul>
<li><a href="http://crackingtheenigma.blogspot.com.au/2010/12/networks-in-autistic-brain.html">Networks in the autistic brain: insights from graph theory</a></li>
<li><a href="http://crackingtheenigma.blogspot.com.au/2010/11/genes-for-autism-or-genes-for.html">Genes for autism or genes for connectivity?</a></li>
<li><a href="http://crackingtheenigma.blogspot.com.au/2011/08/on-neural-correlates-and-causation.html">On neural correlates and causation</a></li>
<li><a href="http://crackingtheenigma.blogspot.com.au/2012/01/datathief-and-superior-longitudinal.html">The Adventures of DataThief</a></li>
<li><a href="http://crackingtheenigma.blogspot.com.au/2011/07/autism-temporal-binding-and.html">Autism, temporal binding... and chiropractic</a></li>
</ul>
drbrocktagonhttp://www.blogger.com/profile/15225859145004971487noreply@blogger.com5tag:blogger.com,1999:blog-1270723657817172117.post-62394984135117633892013-03-05T20:47:00.000-08:002013-03-06T18:06:08.493-08:00Perfect matchI've got a <a href="https://sfari.org/news-and-opinion/columnists/jon-brock/2013/connections-perfect-match">new post</a> over on the SFARI (Simons Foundation Autism Research Initiative) blog discussing the use of control groups in autism research.<br />
<blockquote class="tr_bq">
Control groups are an essential part of autism research, providing a benchmark against which to assess those with autism. Finding, for instance, that participants with autism score an average of 68 percent on a test is meaningless if you don’t know how people who don’t have autism do on the same test. </blockquote>
<blockquote class="tr_bq">
A control group can also be used to try and rule out alternative and perhaps uninteresting explanations for group differences.
The logic is simple: If two groups are matched on one measure, such as intelligence or age, then this can’t explain differences on another measure, such as performance on an emotion recognition test, that is under investigation. </blockquote>
<blockquote class="tr_bq">
Despite its widespread use, there are many issues to consider when designing an experiment with matched controls or when reading and attempting to evaluate such a study. Who should be in the control group? On what measures should they be matched? And how do we decide if the groups are truly matched? </blockquote>
The post focuses on this last question and a recent paper by Sara Kover and Amy Atwood, which I think makes some pretty sensible recommendations.<br />
<br />
Be warned, it involves statistics and made-up data.<br />
<br />
<br />
<b>Reference:s</b><br />
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=American+journal+on+intellectual+and+developmental+disabilities&rft_id=info%3Apmid%2F23301899&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=Establishing+equivalence%3A+methodological+progress+in+group-matching+design+and+analysis.&rft.issn=1944-7515&rft.date=2013&rft.volume=118&rft.issue=1&rft.spage=3&rft.epage=15&rft.artnum=&rft.au=Kover+ST&rft.au=Atwoo+AK&rfe_dat=bpr3.included=1;bpr3.tags=Medicine%2CPsychology%2CNeuroscience%2CCognitive+Neuroscience%2C+Abnormal+Psychology%2C+Cognitive+Psychology%2C+Developmental+Psychology%2C+Intelligence%2C+Language%2C+Psychiatry"><br /></span>
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=American+journal+on+intellectual+and+developmental+disabilities&rft_id=info%3Apmid%2F23301899&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=Establishing+equivalence%3A+methodological+progress+in+group-matching+design+and+analysis.&rft.issn=1944-7515&rft.date=2013&rft.volume=118&rft.issue=1&rft.spage=3&rft.epage=15&rft.artnum=&rft.au=Kover+ST&rft.au=Atwoo+AK&rfe_dat=bpr3.included=1;bpr3.tags=Medicine%2CPsychology%2CNeuroscience%2CCognitive+Neuroscience%2C+Abnormal+Psychology%2C+Cognitive+Psychology%2C+Developmental+Psychology%2C+Intelligence%2C+Language%2C+Psychiatry">Kover ST, & Atwoo AK (2013). Establishing equivalence: methodological progress in group-matching design and analysis. <span style="font-style: italic;">American journal on intellectual and developmental disabilities, 118</span> (1), 3-15 PMID: <a href="http://www.ncbi.nlm.nih.gov/pubmed/23301899" rev="review">23301899</a></span><br />
<br />
Mervis, C. B., & Klein-Tasman, B. (2004). Methodological Issues in Group-Matching Designs: α Levels for Control Variable Comparisons and Measurement Characteristics of Control and Target Variables. Journal of Autism and Developmental Disorders, 24, 7-17. <a href="http://infantlab.fiu.edu/articles/Mervis%20%26%20Klein-%20Tasman,%202004%20JADD.pdf">PDF</a>drbrocktagonhttp://www.blogger.com/profile/15225859145004971487noreply@blogger.com0tag:blogger.com,1999:blog-1270723657817172117.post-52279376377759549422013-01-21T13:26:00.000-08:002013-02-09T13:32:06.752-08:00Goodbye PDD-NOS, hello SCDAmidst all the furore about the loss of the Asperger syndrome label and the potential drop-off in autism diagnoses, the proposed introduction of a new diagnosis in DSM-5, <a href="http://crackingtheenigma.blogspot.com.au/2011/06/social-communication-disorder-new.html">Social Communication Disorder</a>, (SCD) has been largely overlooked. When, late last year, it was announced that DSM-5 had been ratified, SCD didn't even warrant a mention. However, it's clearly going ahead.<br />
<br />
The APA website now hosts a <a href="http://www.psychiatry.org/File%20Library/Practice/DSM/DSM-5/DSM-5-Social-Communication-Fact-Sheet.pdf">downloadable PDF describing SCD</a> as follows:<br />
<blockquote class="tr_bq">
SCD is characterized by a persistent difficulty with verbal and nonverbal communication that cannot be explained by low cognitive ability. Symptoms include difficulty in the acquisition and use of spoken and written language as well as problems with inappropriate responses in conversation. The disorder limits effective communication, social relationships, academic achievement, or occupational performance. Symptoms must be present in early childhood even if they are not recognized until later when speech, language, or communication demands exceed abilities.</blockquote>
Further details are provided in an accompanying <a href="http://psychnews.psychiatryonline.org/newsarticle.aspx?articleid=1558424">article in Psychiatric News</a>:<br />
<blockquote class="tr_bq">
The criteria describe “persistent difficulties in the social use of verbal and nonverbal communication” in four areas: using communication for social purposes such as greeting or exchanging information; changing communication to match context or the needs of the listener; following rules for conversation or storytelling, such as taking turns in conversation; and understanding what is not explicitly stated and nonliteral or ambiguous meanings of language.</blockquote>
This sounds a lot like autism (at least at the "high functioning" end of the spectrum). In fact the main difference between SCD and ASD in DSM-5 is not some subtle distinction in the type of social communication impairment involved but the fact that an ASD diagnosis also requires evidence of repetitive and restricted behaviours:<br />
<blockquote class="tr_bq">
while autism spectrum disorder (ASD) does encompass communication problems, it also includes restricted, repetitive patterns of behavior, interests or activities and gives equal weight to both communication issues and repetitive behaviors.</blockquote>
As Will Mandy and colleagues have <a href="http://crackingtheenigma.blogspot.com.au/2011/05/what-is-pdd-nos.html">pointed out</a>, many (if not most) kids accurately diagnosed with PDD-NOS conform to this profile. And it seems as though SCD is essentially a rebranding of PDD-NOS.<br />
<blockquote class="tr_bq">
Because the symptoms described in SCD were not defined in previous editions of DSM, many individuals with such symptoms may have been lumped under the not otherwise specified category of pervasive development disorder. </blockquote>
In Psychiatric News, Sue Swedo from the DSM-5 Neurodevelopmental Work Group says this:<br />
<blockquote class="tr_bq">
“We believe social communication disorder will capture those children who have in the past been diagnosed with PDD-NOS as a way of drawing attention to the patient’s social communication impairments despite the absence of restrictive interests and repetitive behaviors.”</blockquote>
This is confusing, because the line all along has been that PDD-NOS would be "folded into" ASD. From the same Psychiatric News article:<br />
<blockquote class="tr_bq">
Possibly the most significant change is... the consolidation of DSM-IV criteria for autism, Asperger’s, childhood disintegrative disorder, and pervasive developmental disorder-not otherwise specific (PDD-NOS)—into one diagnostic category called autism spectrum disorder (ASD). </blockquote>
It also contradicts the APA line that ASD prevalence won't be affected by DSM-5 changes. This is repeated in another new <a href="http://www.psychiatry.org/File%20Library/Practice/DSM/DSM-5/DSM-5-Autism-Spectrum-Disorder-Fact-Sheet.pdf">downloadable PDF</a> from the APA website, describing Autism Spectrum Disorder.<br />
<blockquote class="tr_bq">
The DSM-5 criteria were tested in real-life clinical settings as part of <a href="http://crackingtheenigma.blogspot.com.au/2012/12/dsm-5-field-trials-leave-many-questions.html">DSM-5 field trials</a>, and analysis from that testing indicated that there will be no significant changes in the prevalence of the disorder.</blockquote>
<blockquote class="tr_bq">
More recently, the largest and most up-to-date study, published by <a href="http://crackingtheenigma.blogspot.com.au/2012/10/more-dsm-5-confusion.html">Huerta, et al</a>... found that DSM-5 criteria identified 91 percent of children with clinical DSM-IV PDD diagnoses, suggesting that most children with DSM-IV PDD diagnoses will retain their diagnosis of ASD using the new criteria. [2]</blockquote>
However, the same article hints at the fact that some people <i>will</i> be re-assigned:<br />
<blockquote class="tr_bq">
Anyone diagnosed with one of the four pervasive developmental disorders (PDD) from DSM-IV should still meet the criteria for ASD in DSM-5 <i>or another, more accurate DSM-5 diagnosis</i> [italics added]. While DSM does not outline recommended treatment and services for mental disorders, determining an accurate diagnosis is a first step for a clinician in defining a treatment plan for a patient.</blockquote>
The implication is that people who meet these criteria will be better off with an SCD diagnosis than they would have been with an ASD diagnosis. Put another way, people with similar social communication difficulties should receive different treatments depending on whether or not they also have restricted and repetitive behaviours.<br />
<br />
Even if this made sense in theory and even if there was evidence to support it, the main problem from a practical viewpoint is that there are currently no services provided for people with an SCD diagnosis - because it doesn't yet exist. PDD-NOS may have been an inelegant and poorly defined diagnosis, but at least in some (not all) places, it actually meant something in terms of access to support. Those battles will all have to be refought. And even if SCD does eventually become recognised, it is classified in DSM-5 as a form of language disorder, completely separate from ASD, so service provision is likely to be at the same level as that for other language disorders (i.e., not good).<br />
<br />
One of the main reasons cited for ditching the distinction between PDD-NOS, Asperger's and autism was a study by Cathy Lord and colleagues indicating that the use of these different diagnoses varies widely across different clinics in different states. As these authors admitted, this variability was likely to be driven at least by regional differences in service provision for the different diagnoses (I think I'm right in saying that the main outlier was California where PDD-NOS and Asperger's diagnoses were never given). DSM-5 was supposed to fix that problem but the worry is that it's going to make things a whole lot worse.<br />
<br />
<br />
<i>A Spanish translation of this article can be found at <a href="http://autismodiario.org/2013/01/24/adios-tgd-ne-bienvenido-scd/">Autismo Diario</a>.</i><br />
<i><br /></i>
<i><br /></i>
<b>Links:</b><br />
<br />
<a href="http://news.msn.com/science-technology/what-does-the-end-of-aspergers-mean">MSN News article</a> featuring quotes from Fred Volkmar, Temple Grandin, Cathy Lord, and Ari Ne'eman.drbrocktagonhttp://www.blogger.com/profile/15225859145004971487noreply@blogger.com12tag:blogger.com,1999:blog-1270723657817172117.post-10816019977912686572012-12-13T14:12:00.000-08:002012-12-13T14:12:10.074-08:00Sydney Autism Science<div class="separator" style="clear: both; text-align: center;">
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<br />
Last week at Macquarie University, as a prelude to the <a href="http://asfar.org.au/conference/">Australasian Society for Autism Research Conference</a>, we held an afternoon and evening of research presentations and discussions around the question "What is autism?" The event was I think a big success - despite the fact that three of the presenters had their morning flights cancelled and the running order was torn up and replaced with whoever's-here-presents-next.<br />
<br />
One thing that has become really obvious, both through organising the event and the feedback afterwards, is that a lot of people in Sydney have a deep interest in autism - either because they are themselves on the spectrum or have a family member who is autistic, or because they work with autistic people in the community. And then of course there are researchers and research students scattered across various departments of different universities - and to be honest, none of us have a great idea what the others are doing.<br />
<br />
As a first step to getting something a bit more concrete going, we recently set up a website, <a href="http://sydneyautismscience.com/">sydneyautismscience.com</a> It's a work in progress, but so far has information about autism research events (like the one last week as well as uni seminars) and recruitment adverts for autism studies being run in the Sydney area. There are also links to homepages of local autism researchers, with a student page to come.<br />
<br />
So if you're in Sydney or nearby and want to get involved in autism research, please take a look at the website and sign up to the email alerts. And we'll hopefully see you at the next event.drbrocktagonhttp://www.blogger.com/profile/15225859145004971487noreply@blogger.com1tag:blogger.com,1999:blog-1270723657817172117.post-63147752129368265552012-12-07T15:29:00.001-08:002012-12-09T10:27:14.189-08:00DSM-5 field trials leave many questions unansweredLast weekend, the American Psychiatric Association announced that the DSM-5 has been <a href="http://leftbrainrightbrain.co.uk/2012/12/01/dsm-5-has-been-approved/">ratified</a> and that changes to the diagnosis of various “mental disorders” would go ahead as planned early next year.
The implications for autism are still unclear. <a href="https://theconversation.edu.au/redefining-autism-in-the-dsm-5-6385">Most of the published studies</a> suggest a reduction in autism rates. However, the argument from the DSM-5 working group responsible for autism has always been that everyone should wait for the official field trials to be published before jumping to any conclusions.<br />
<br />
The field trials were finally released a couple of weeks ago, with methods and results spread across three articles in the American Journal of Psychiatry, the APA’s own journal. If ever there were a case for scientific documents to be made freely available, this would be it. Instead, they’re hidden behind a paywall, costing $35 to “rent” each article for 24 hours.
It’s taken me a couple of weeks to get my head around them (luckily my university library has paid for unlimited access to the journal). For those who are interested but don’t want to spend the kids’ Christmas present money on journal articles, I’ve done my best to summarise the study – at least those parts that are relevant to autism.<br />
<br />
The field trials were spread across 11 sites, all in North America. But only two – Baystate and Stanford - were involved in trialling autism diagnoses.
Both centres were also assessing a number of other diagnoses, so autistic kids only made up a small proportion of those assessed. At Baystate, 23% of kids in their sample of 569 met DSM-IV criteria for an ASD (i.e., they already had a diagnosis of autistic disorder, Asperger syndrome, or PDD-NOS). At Stanford, the figure was 26% from a sample of 463.
<br />
<br />
The main aim of the field trials was <a href="http://www.psychologytoday.com/blog/dsm5-in-distress/201211/you-cant-turn-sows-ear-silk-purse">to assess reliability</a> – whether two different clinicians would give the same person the same diagnosis. This meant that, to be included in the final sample, each child had to be assessed twice and, as a result, only a small fraction of the children initially screened into the study were included in the final analysis. At Baystate, 146 of 569 kids made it all the way through. At Stanford the figure was 149 out of 463.<br />
<br />
This is where things start to get complicated. In an effort to make sure they had enough kids for each of the diagnoses, the kids were assigned to various “strata” corresponding to the DSM-5 diagnoses under investigation. To be in the ASD stratum, a child had to have a DSM-IV diagnosis of ASD. However, some of the kids with ASD also met criteria for other strata and some were assigned to those strata rather than ASD. At Baystate, this happened to 20 of the 132 ASD kids. At Stanford, 21 of 119 ASD kids were reassigned. However, there is no indication of which strata they were assigned to.<br />
<br />
<table align="center" cellpadding="0" cellspacing="0" class="tr-caption-container" style="margin-left: auto; margin-right: auto; text-align: center;"><tbody>
<tr><td style="text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEiR9KQSjCGPv4_iicSMu1q8_Xzum4UMUqR7xtEqZ7prkof5vNw7NW_Nis1E_BoKlHQLv2XFN4ZqJOmjUdtU-eV6rW6JjOnPFaGzPzrEnmXSaaIpIX7gTPLEssMrHEuK2aPNrvdbPv_8xGU/s1600/Clarke+Regier+Table.png" imageanchor="1" style="margin-left: auto; margin-right: auto;"><img border="0" height="192" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEiR9KQSjCGPv4_iicSMu1q8_Xzum4UMUqR7xtEqZ7prkof5vNw7NW_Nis1E_BoKlHQLv2XFN4ZqJOmjUdtU-eV6rW6JjOnPFaGzPzrEnmXSaaIpIX7gTPLEssMrHEuK2aPNrvdbPv_8xGU/s400/Clarke+Regier+Table.png" width="400" /></a></td></tr>
<tr><td class="tr-caption" style="text-align: center;">First 6 columns taken from Paper I (Clarke et al.). Columns 7 and 8 calculated by me. Column 9 take from Paper II (Regier et al)</td></tr>
</tbody></table>
<br />
Because of this biased sampling, the authors employed a complicated formula to estimate DSM-5 prevalence. This essential piece of information can be found in Footnote E of Table 1 of the second paper.<br />
<br />
Calculating the ASD prevalence was effectively done as follows:<br />
<br />
<ol>
<li>The authors calculated the proportion of kids in each stratum who met DSM-5 criteria for ASD (kids who were diagnosed with ASD by one clinician but not the other were effectively treated as half an ASD kid). </li>
<li>They then multiplied this by a weighting factor, which corresponds to the proportion of kids in the original sample who were assigned to that stratum. </li>
<li>Having done this for all the strata, they added up all the values to get the prevalence. </li>
</ol>
<br />
At Baystate, estimated prevalence was 24%, a slight increase from DSM-IV (23%). At Stanford, estimated prevalence went down fairly dramatically to 19%, compared with 26% under DSM-IV.<br />
<br />
One of the slightly weird consequences of this approach is that different kids would have ended up contributing different amounts to the ASD prevalence depending on which stratum they’d been assigned to. For example, at Baystate, a child assigned to the non-suicidal self-injury strata would have been “worth” double a child assigned to the bipolar disorder strata.
Having scratched my head about this for a while, I think it does make sense – but only if sampling really was deliberate. If it wasn’t, then there’s no reason to weight a child with ASD differently just because they weren’t assigned to the ASD stratum.<br />
<br />
My suspicions here are raised by the non-suicidal self-injury stratum. Despite being one of the rarest target diagnoses, this was wildly under-sampled. This suggests that sampling was really a process of assessing as many kids as possible before time ran out. In that case, the formula could seriously distort the true DSM-5 prevalence.<br />
<br />
A much simpler and more transparent way to compare DSM-IV and DSM-5 rates would have been to look only at the kids in the final sample and ask how many had an ASD diagnosis under each diagnostic scheme. The authors told me that, across both centres, 79 of the kids in the final group met DSM-IV criteria for ASD (note that only 64 of these were in the ASD stratum, which is why most reports have mistakenly said there were 64 ASD kids in total).
However, the authors haven't responded to my question about numbers in DSM-5.<br />
<br />
One thing they did tell me is that another paper is being prepared that looks in more detail at the autism results. In addition to the actual numbers of kids diagnosed under DSM-IV and DSM-5, we’re also currently missing information about the make-up of the autism groups at both centres. This is critical to know because, if anyone is going to miss out on ASD diagnosis, it’s likely to be the less clear-cut cases – those who'd meet criteria for Asperger’s or PDD-NOS under DSM-IV. Even without the concerns I've already mentioned, the numbers are pretty meaningless without that information.<br />
<br />
The authors cheerfully conclude that children missing out on an ASD diagnosis will be better served by the new Social Communication Disorder (SCD) diagnosis:<br />
<blockquote class="tr_bq">
"A careful review of data from both sites showed that the decrease at the Stanford site was offset by movement into a new DSM-5 diagnosis called social (or pragmatic) communication disorder (data not shown). Since autism spectrum disorder requires both deficits in social communication and fixated interests/repetitive movement, the more specific deficit assessments in DSM-5 should facilitate more focused treatments for those with social communication deficits only."</blockquote>
Given that <strike>most</strike> many autism interventions are targeted at social and communication difficulties, it's not clear what "more focused treatments" the authors have in mind. And, as many people have noted, there is currently no mandated provision for SCD anywhere in the real world. Indeed, the press release announcing the ratification of DSM-5 made no mention of SCD - despite the fact that it would be a major change to diagnostic practice. As with so many other aspects of DSM-5, your guess is as good as mine.<br />
<br />
<br />
<b>References:</b><br />
<br />
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=The+American+journal+of+psychiatry&rft_id=info%3Apmid%2F23111546&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=DSM-5+Field+Trials+in+the+United+States+and+Canada%2C+Part+I%3A+Study+Design%2C+Sampling+Strategy%2C+Implementation%2C+and+Analytic+Approaches.&rft.issn=0002-953X&rft.date=2012&rft.volume=&rft.issue=&rft.spage=&rft.epage=&rft.artnum=&rft.au=Clarke+DE&rft.au=Narrow+WE&rft.au=Regier+DA&rft.au=Kuramoto+SJ&rft.au=Kupfer+DJ&rft.au=Kuhl+EA&rft.au=Greiner+L&rft.au=Kraemer+HC&rfe_dat=bpr3.included=1;bpr3.tags=Medicine%2CCognitive+Neuroscience%2C+Psychiatry">Clarke DE, Narrow WE, Regier DA, Kuramoto SJ, Kupfer DJ, Kuhl EA, Greiner L, & Kraemer HC (2012). DSM-5 Field Trials in the United States and Canada, Part I: Study Design, Sampling Strategy, Implementation, and Analytic Approaches. <span style="font-style: italic;">The American journal of psychiatry</span> PMID: <a href="http://www.ncbi.nlm.nih.gov/pubmed/23111546" rev="review">23111546</a></span><br />
<br />
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=The+American+journal+of+psychiatry&rft_id=info%3Apmid%2F23111466&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=DSM-5+Field+Trials+in+the+United+States+and+Canada%2C+Part+II%3A+Test-Retest+Reliability+of+Selected+Categorical+Diagnoses.&rft.issn=0002-953X&rft.date=2012&rft.volume=&rft.issue=&rft.spage=&rft.epage=&rft.artnum=&rft.au=Regier+DA&rft.au=Narrow+WE&rft.au=Clarke+DE&rft.au=Kraemer+HC&rft.au=Kuramoto+SJ&rft.au=Kuhl+EA&rft.au=Kupfer+DJ&rfe_dat=bpr3.included=1;bpr3.tags=Medicine%2CNeuroscience%2CPsychiatry">Regier DA, Narrow WE, Clarke DE, Kraemer HC, Kuramoto SJ, Kuhl EA, & Kupfer DJ (2012). DSM-5 Field Trials in the United States and Canada, Part II: Test-Retest Reliability of Selected Categorical Diagnoses. <span style="font-style: italic;">The American journal of psychiatry</span> PMID: <a href="http://www.ncbi.nlm.nih.gov/pubmed/23111466" rev="review">23111466</a></span>
<br />
<br />
<b>Update:<br />
</b><br />
I now have it on good authority (via Twitter) that Social Communication Disorder <i>will</i> be included in DSM-5. Implications still unclear.<br />
<br />
<blockquote class="twitter-tweet" data-in-reply-to="277273917213777920"><p>@<a href="https://twitter.com/autismcrisis">autismcrisis</a> @<a href="https://twitter.com/drbrocktagon">drbrocktagon</a> it is still in. Have been asked to write about it for JCPP...</p>— Courtenay Norbury (@lilacCourt) <a href="https://twitter.com/lilacCourt/status/277800413267374080" data-datetime="2012-12-09T15:42:34+00:00">December 9, 2012</a></blockquote>
<script src="//platform.twitter.com/widgets.js" charset="utf-8"></script>drbrocktagonhttp://www.blogger.com/profile/15225859145004971487noreply@blogger.com5tag:blogger.com,1999:blog-1270723657817172117.post-11769290521321485262012-11-30T19:15:00.002-08:002012-12-07T21:32:48.761-08:00The autism "epidemic" - a plea at least for consistency of logicOn Friday at the <a href="http://www.thinkingautismguide.com/2012/11/congressional-autism-hearing-recap.html">Congressional Autism Hearing</a>, Bob Wright, founder of Autism Speaks <a href="http://www.autismspeaks.org/advocacy/advocacy-news/bob-wright-tells-congress-face-crisis?utm_source=social-media&utm_medium=text-link&utm_campaign=espeaks">testified</a> to a "growing autism epidemic". He backed this up with figures from the Centre for Disease Control in the United States estimating that <a href="http://www.cdc.gov/mmwr/preview/mmwrhtml/ss6103a1.htm?s_cid=ss6103a1_w">1 in 88 Americans</a> are autistic, an increase from the previous estimate of 1 in 110 reported six years previously.<br />
<br />
He then proceeded to argue that the 1 in 88 figure is likely to be an underestimate, with the true rate being closer to the 1 in 38 reported in a <a href="http://www.guardian.co.uk/science/blog/2011/jun/07/how-common-autism-diagnosis">study in South Korea</a>.<br />
<br />
However, the CDC report also showed huge differences across the various states sampled, and huge variation across different ethnic groups in terms of both the current numbers and the rate of change. If, like Bob, you take the overall rise in autism rates at face value as evidence for an epidemic, you also need to take at face value the geographical and ethnic variations. You need to take seriously the possibility that <a href="http://www.cdc.gov/mmwr/preview/mmwrhtml/ss6103a1.htm?s_cid=ss6103a1_w#Tab2">white kids from Utah really are 28 times more likely to be autistic than Hispanic kids from Alabama</a>. And that <a href="http://www.cdc.gov/mmwr/preview/mmwrhtml/ss6103a1.htm?s_cid=ss6103a1_w#Tab5">rates among Hispanic kids in Missouri really did go up 460% in 6 years</a> [1].<br />
<br />
And if, like Bob, you're going to argue that the CDC figure of 1 in 88 is a gross underestimation, you're acknowledging that the CDC data speak to the number of kids flagged by health and education records, as opposed to the number of actual autistic people. And so you <i>can't</i> take the increase at face value as evidence for an increase in the number of autistic people.<br />
<br />
<div style="margin-bottom: 0px; margin-left: 0px; margin-right: 0px; margin-top: 0px;">
As the CDC report concluded, there is a need to "focus on understanding disparities in the identification of ASDs among certain subgroups and on how these disparities have contributed to changes in the estimated prevalence of ASDs".</div>
<div style="margin-bottom: 0px; margin-left: 0px; margin-right: 0px; margin-top: 0px;">
<br /></div>
<div style="margin-bottom: 0px; margin-left: 0px; margin-right: 0px; margin-top: 0px;">
Underlying all of those disparities, there may be a true increase in the number of autistic people - and it's important to be open-minded. But it's also important to be consistent in your logic.</div>
<div style="margin-bottom: 0px; margin-left: 0px; margin-right: 0px; margin-top: 0px;">
<br />
<br />
<b>Footnote:</b><br />
<br />
[1] Even at the lower end of the 95% confidence interval, rates in 2008 were 3.4 times what they were in 2002.<br />
<br />
<br />
<b>More on the Congressional Autism Hearing:</b><br />
<br />
The Thinking Person's Guide to Autism has <a href="http://www.thinkingautismguide.com/2012/11/congressional-autism-hearing-recap.html">full coverage</a> of the Congressional Autism Hearing. They highlight the testimony of Ari Ne'eman from the Autistic Self Advocacy Network, including this particularly striking except:</div>
<blockquote class="tr_bq">
Of the approximately $217 million dollars that the National Institutes of Health (NIH) invested in autism research in 2010 (the most recent year for which data is available), only a meager 2.45% went towards improving the quality of services and supports available to Autistic people and our families. Only 1.5% went towards research that addresses the needs of Autistic adults. When compared to research on questions of causation, etiology and biology and diagnosis, the percentage of the autism research agenda focused on the actual needs of Autistic people in order to improve their quality of life is miniscule. We are pro-research, but the research agenda must be re-balanced to incorporate both causation and quality of life.</blockquote>
<br />
<b>More on autism prevalence:</b><br />
<br />
<ul>
<li>Paul Whiteley <a href="http://questioning-answers.blogspot.com.au/2012/12/autism-prevalence-increasing-in-new-jersey.html">reviews</a> a new study looking into the changes in prevalence in New Jersey</li>
<li>Guest post on the SFARI blog: <a href="https://sfari.org/news-and-opinion/blog/2012/guest-blog-utah-revisited">Utah, revisited</a></li>
</ul>
drbrocktagonhttp://www.blogger.com/profile/15225859145004971487noreply@blogger.com5tag:blogger.com,1999:blog-1270723657817172117.post-58053074100058724182012-10-26T05:56:00.000-07:002012-11-01T13:58:28.419-07:00Redefining autism in the DSM-5I've got an <a href="http://theconversation.edu.au/redefining-autism-in-the-dsm-5-6385">article out in The Conversation</a>.this week on changes to autism diagnosis in the DSM-5. It's part of a series called <a href="https://theconversation.edu.au/pages/matters-of-the-mind">Matters of the Mind</a>, discussing similar issues across a range of "mental disorders". For those who aren't familiar, The Conversation is an Australian online newspaper with articles written mainly by academics - but edited by professionals to make them readable! It's a great initiative and there have been some pretty <a href="http://theconversation.edu.au/no-youre-not-entitled-to-your-opinion-9978">stellar articles</a> of late. So I'm excited to be involved.<br />
<div style="margin-bottom: 0px; margin-left: 0px; margin-right: 0px; margin-top: 0px;">
<br />
In the last year or so there has been a glut of studies comparing DSM-IV and DSM-5. I've listed below all the ones I know of, but there may be even more. In the article, I focus on three of these: the Yale study from earlier this year that I covered <a href="http://crackingtheenigma.blogspot.com.au/2012/03/how-will-dsm-5-affect-autism-rates-yale.html">here</a> and <a href="http://crackingtheenigma.blogspot.com.au/2012/03/autism-and-intellectual-disability-in.html">here</a>; the recent Cornell study that I <a href="http://crackingtheenigma.blogspot.com.au/2012/10/more-dsm-5-confusion.html">critiqued</a> earlier this week; and another newish study from Autism Spectrum Australia that, unlike other studies, actually looked at DSM-5 in a clinical context, rather than re-coding old data.<br />
<br />
We're still waiting for the results of the official DSM-5 field trials. But, to be honest, the more studies I read, the less convinced I am that we can predict DSM-5's impact in advance. The obvious problem is that there is no objective test of whether or not someone is autistic, so it's difficult to say whether DSM-5 is an improvement on DSM-IV. But much will also depend on the interpretation of the new rules by clinicians; the reaction of governments and insurers to resulting changes in autism numbers and to new diagnoses such as Social Communication Disorder; and ultimately the extent to which an autism diagnosis continues be a stepping stone to services. These are all in themselves difficult to predict.<br />
<br />
There is also the broader question of whether it makes sense to base research and clinical practice on the notion of an autism "syndrome". We have the strange situation where, for example, someone can be denied support for social and communication difficulties because they don't have sufficient repetitive behaviours for an autism diagnosis. Or, as one commenter <a href="https://theconversation.edu.au/redefining-autism-in-the-dsm-5-6385#comment_86398">noted</a>, a child with specific language difficulties is unable to access speech therapy that is available to an autistic child <i>without</i> language difficulties. From the research perspective, we're still all just relying on an intuition that the behaviours that define autism actually constitute a coherent syndrome. As scientists we should be always challenging our intuitions but in effect the DSM serves only to formalise and reinforce them.<br />
<br />
<br />
<b>Further reading:</b><br />
<br />
Emily Singer has a <a href="http://www.nature.com/nature/journal/v491/n7422_supp/full/491S12a.html">comprehensive review</a> of DSM-5 issues as part of a free supplement in Nature.<br />
<br />
<br />
<b>References:</b><br />
<br />
Frazier TW, Youngstrom EA, Speer L, Embacher R, Law P, Constantino J, Findling RL, Hardan AY, Eng C (2012). <a href="http://www.ncbi.nlm.nih.gov/pubmed/22176937">Validation of proposed DSM-5 criteria for autism spectrum disorder</a>. Journal of the American Academy of Child and Adolescent Psychiatry, 51, 28–40 </div>
<br />
Gibbs V, Aldridge F, Chandler F, Witzlsperger E, Smith K (2012). <a href="http://www.ncbi.nlm.nih.gov/pubmed?term=Brief%20Report%3A%20An%20Exploratory%20Study%20Comparing%20Diagnostic%20Outcomes%20for%20Autism%20Spectrum%20Disorders%20Under%20DSM-IV-TR%20with%20the%20Proposed%20DSM-5%20Revision">Brief Report: An Exploratory Study Comparing Diagnostic Outcomes for Autism Spectrum Disorders Under DSM-IV-TR with the Proposed DSM-5 Revision</a>. Journal of Autism and Developmental Disorders, 42, 1750-1756.<br />
<br />
Huerta M, Bishop SL, Duncan A, Hus V, Lord C (2012). <a href="http://www.ncbi.nlm.nih.gov/pubmed?term=Application%20of%20DSM-5%20Criteria%20for%20Autism%20Spectrum%20Disorder%20to%20Three%20Samples%20of%20Children%20With%20DSM-IV%20Diagnoses%20of%20Pervasive%20Developmental%20Disorders">Application of DSM-5 Criteria for Autism Spectrum Disorder to Three Samples of Children With DSM-IV Diagnoses of Pervasive Developmental Disorders</a>. American Journal of Psychiatry, 169, 1056-64.<br />
<br />
McPartland JC, Reichow B, Volkmar FR: <a href="http://Sensitivity and specificity of proposed DSM-5 diagnostic criteria for autism spectrum disorder">Sensitivity and specificity of proposed DSM-5 diagnostic criteria for autism spectrum disorder</a>. Journal of the American Academy of Child and Adolescent Psychiatry, 51, 368–383.<br />
<br />
Matson JL, Kozlowski A, Hattier MA, Horovitz M, Sipes M (2012). <a href="http://www.ncbi.nlm.nih.gov/pubmed?term=DSM-IV%20vs%20DSM-5%20diagnostic%20criteria%20for%20toddlers%20with%20Autism.%20Developmental%20Neurorehabilitation">DSM-IV vs DSM-5 diagnostic criteria for toddlers with Autism. Developmental Neurorehabilitation</a>, 15, 3, 185-190.<br />
<br />
Mattila ML, Kielinen M, Linna SL, Jussila K, Ebeling H, Bloigu R,
Joseph RM, Moilanen I (2011). <a href="http://www.ncbi.nlm.nih.gov/pubmed?term=Autism%20spectrum%20disorders%20according%20to%20DSM-IV-TR%20and%20comparison%20with%20DSM-5%20draft%20criteria%3A%20an%20epidemiological%20study">Autism spectrum disorders according to DSM-IV-TR and comparison with DSM-5 draft criteria: an epidemiological study</a>. Journal of the American Academy of Child and Adolescent Psychiatry, 50, 583–592.<br />
<br />
Mazefsky CA, McPartland JC, Gastgeb HZ, Minshew NJ. (in press). <a href="http://www.ncbi.nlm.nih.gov/pubmed?term=Comparability%20of%20DSM-IV%20and%20DSM-5%20ASD%20Research%20Samples">Comparability of DSM-IV and DSM-5 ASD Research Samples</a>. Journal of Autism and Developmental Disorders
<br />
<br />
Worley JA, Matson JL (2012). <a href="http://www.blogger.com/Brief%20report:%20an%20exploratory%20study%20comparing%20diagnostic%20outcomes%20for%20autism%20spectrum%20disorders%20under%20DSM-IV-TR%20with%20the%20proposed%20DSM-5%20revision.">Comparing symptoms of autism spectrum disorders using the current DSM-IV-TR diagnostic criteria and the proposed DSM-V diagnostic criteria</a>. Research in Autism Spectrum Disorders, 6, 965-970.
drbrocktagonhttp://www.blogger.com/profile/15225859145004971487noreply@blogger.com5tag:blogger.com,1999:blog-1270723657817172117.post-7634938356076207562012-10-23T21:14:00.000-07:002012-10-24T06:19:17.604-07:00More DSM-5 confusionOne of the big concerns about forthcoming changes to autism diagnosis in DSM-5 is that the new rules may miss out a sizeable chunk of the autism population, particularly those who, under current diagnostic guidelines, would be considered to have Asperger’s Disorder or PDD-NOS. A number of studies published over the last year or so seemed to confirm those fears, although each of those studies had its limitations.<br />
<br />
Earlier this month, a study in the American Journal of Psychiatry by Marisela Huerta and colleagues appeared to show quite conclusively that almost every autistic person, including people in the PDD-NOS bracket, would qualify for an Autism Spectrum Disorder diagnosis in DSM-5.<br />
<br />
Emily Singer has a nice <a href="http://sfari.org/news-and-opinion/news/2012/proposed-guidelines-wont-miss-autism-cases-study-says">summary</a> on the SFARI blog, complete with interviews with various researchers all agreeing that the study really seems to have settled the issue.<br />
<br />
However, I'm not so sure. Here's my attempt to explain why.<br />
<br />
Huerta et al.'s approach was to map items from the ADI-R and ADOS diagnostic tests onto "symptoms" in the DSM-IV and DSM-5 criteria. They then looked to see whether, for each individual assessed, the combination of symptoms qualified them for a diagnosis under DSM-IV or DSM-5. It's important to note that they didn't use the official algorithms for translating item scores into diagnoses. Instead, they asked whether, for each symptom, there was evidence from at least one item in ADI-R or ADOS.<br />
<br />
Next, they compared the diagnostic outcome of the DSM-IV and DSM-5 recodings to what they call "clinical best estimate diagnosis". I was a little unsure what this meant, so I emailed Dr Huerta, who confirmed that this was essentially the opinion of experienced clinicians at the time of the original assessment. The diagnosis was guided by DSM-IV and was based partly on outcomes of the ADOS and ADI-R, as well as developmental history and performance on some standardized tests.<br />
<br />
Have a look at Table 2 below. This is actually just the top third of the table as the data Huerta et al used comes from three different sources. For now, we're just looking at data supplied by the Collaborative Programs of Excellence in Autism.<br />
<br />
<br />
<table align="center" cellpadding="0" cellspacing="0" class="tr-caption-container" style="margin-left: auto; margin-right: auto; text-align: center;"><tbody>
<tr><td style="text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgKQ2iuqKviFiG1Zp0EF5_c5tv-ZfifTydllA7mkdhGtadWIulfNf5zTisXPzlht5279eg28TRYDp2lure8il9wRrkk_DkR8UVxGiqnkRzACfR37kkh_2XWGCp92NanLoY4eFedgFP1NsY/s1600/Huertaetal2012b.jpg" imageanchor="1" style="margin-left: auto; margin-right: auto;"><img border="0" height="307" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgKQ2iuqKviFiG1Zp0EF5_c5tv-ZfifTydllA7mkdhGtadWIulfNf5zTisXPzlht5279eg28TRYDp2lure8il9wRrkk_DkR8UVxGiqnkRzACfR37kkh_2XWGCp92NanLoY4eFedgFP1NsY/s400/Huertaetal2012b.jpg" width="400" /></a></td></tr>
<tr><td class="tr-caption" style="text-align: center;">Table 2 from Huerta et al (2012). Click to enlarge.</td></tr>
</tbody></table>
<div class="separator" style="clear: both; text-align: center;">
<br /></div>
<div class="separator" style="clear: both; text-align: center;">
<br /></div>
We're interested here in the kids with best estimate diagnoses of PDD-NOS or Asperger syndrome. I've highlighted in red the row entitled "Either parent or clinical measure". This means that a symptom box could be ticked if it was present in either the parent measure (ADI-R) or clinical measure (ADOS).<br />
<br />
The first column of figures shows the sensitivity and specificity according to the proposed DSM-5 criteria (columns to the right of this show outcomes for potential tweaks to the DSM-5 criteria). In this sample, 94% of kids with best estimate diagnoses of Asperger’s or PDD-NOS met the DSM-5 criteria for Autism Spectrum Disorder (see blue oval). Across the three datasets, the value was 96%.<br />
<br />
But now look at the column headed "Autistic Disorder". This shows the proportion of kids meeting DSM-IV criteria for Autistic Disorder according to the recoding. In this case, the figure is 84% (green oval).<br />
<br />
This is distinctly odd. According to DSM-IV, PDD-NOS and Asperger's disorder should only be diagnosed if Autistic Disorder has been ruled out. But the authors are reporting that, of the kids with a best estimate diagnosis of PDD-NOS or Asperger's disorder, 84% actually met criteria for Autistic Disorder under the recoding. <br />
<br />
For the other two datasets, it's even more extreme. The corresponding figures are 90% and 97%. Overall, it works out that 94% of kids diagnosed with PDD-NOS or Asperger's actually meet criteria for Autistic Disorder.<br />
<br />
<div style="margin-bottom: 0px; margin-left: 0px; margin-right: 0px; margin-top: 0px;">
Now look at the specificity, highlighted in orange. Across the three datasets, specificity for DSM-5 was 33% (purple oval). In other words, two thirds of the non-PDD kids met DSM-5 criteria for Autism Spectrum Disorder. We're not talking about autism risk here. This relates to actual diagnosis. 33% specificity would be terrible.</div>
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<br /></div>
<div style="margin-bottom: 0px; margin-left: 0px; margin-right: 0px; margin-top: 0px;">
For DSM-IV it's even worse. Specificity is 10%. That means that 90% of the non-PDD kids met criteria for PDD-NOS (in fact two thirds of them met criteria for Autistic Disorder). </div>
<br />
Something is not right. 94% of kids who were considered by clinicians to have PDD-NOS or Asperger's ended up meeting criteria for Autistic Disorder under the recoding. And 90% of kids who weren't considered autistic at all ended up meeting criteria for PDD-NOS.<br />
<br />
One possibility is that the clinical best estimates are wrong. If this were the case, it would completely undermine the claim that most kids with PDD-NOS or Asperger's will meet DSM-5 criteria - because the study didn't actually include any such kids. Or at least, if it did, they were all in the non-PDD group!<br />
<br />
More likely I think is that the coding scheme used in this study is far more liberal than best estimate clinical diagnosis. Getting a diagnosis from a real life clinician requires more than just a single example of each relevant behaviour. If this is the case then it again undermines the study's conclusions. If the recoding is too liberal, if boxes are being ticked that would not ever be ticked by a clinician conducting a real best estimate diagnosis, then we can't trust the DSM-IV coding. And by the same token, we can't trust the DSM-5 coding either.<br />
<br />
Emily Singer's article has an interesting <a href="http://sfari.org/news-and-opinion/news/2012/proposed-guidelines-wont-miss-autism-cases-study-says">quote</a> from Cathy Lord, who's a member of the workgroup responsible the DSM-5 changes to autism diagnosis, as well as being a co-author on the Huerta et al. paper.<br />
<br />
<blockquote class="tr_bq">
"It's still not the same thing as taking the new criteria and testing them out, which is why we didn't do this analysis before," says Lord. "But clearly people have been analyzing much more restricted datasets, so we thought we better get in here and do it."</blockquote>
<br />
I think she's absolutely right to worry about the limitations of recoded data. But we need to be skeptical whether or not the results support DSM-5.<br />
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<b>Reference:</b><br />
<br />
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=The+American+journal+of+psychiatry&rft_id=info%3Apmid%2F23032385&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=Application+of+DSM-5+Criteria+for+Autism+Spectrum+Disorder+to+Three+Samples+of+Children+With+DSM-IV+Diagnoses+of+Pervasive+Developmental+Disorders.&rft.issn=0002-953X&rft.date=2012&rft.volume=169&rft.issue=10&rft.spage=1056&rft.epage=64&rft.artnum=&rft.au=Huerta+M&rft.au=Bishop+SL&rft.au=Duncan+A&rft.au=Hus+V&rft.au=Lord+C&rfe_dat=bpr3.included=1;bpr3.tags=Medicine%2CNeuroscience%2CAutism%2C+Psychiatry%2C+Diagnosis">Huerta M, Bishop SL, Duncan A, Hus V, & Lord C (2012). Application of DSM-5 Criteria for Autism Spectrum Disorder to Three Samples of Children With DSM-IV Diagnoses of Pervasive Developmental Disorders. <span style="font-style: italic;">The American journal of psychiatry, 169</span> (10), 1056-64 PMID: <a href="http://www.ncbi.nlm.nih.gov/pubmed/23032385" rev="review">23032385</a></span>drbrocktagonhttp://www.blogger.com/profile/15225859145004971487noreply@blogger.com0tag:blogger.com,1999:blog-1270723657817172117.post-67144803103183643282012-10-15T04:03:00.000-07:002012-10-15T04:03:00.810-07:00Free autism research event: 5th December at Macquarie University<table align="center" cellpadding="0" cellspacing="0" class="tr-caption-container" style="margin-left: auto; margin-right: auto; text-align: center;"><tbody>
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<br />
In December, at Macquarie University (Sydney), we're hosting the <a href="http://asfar.org.au/conference/">first scientific meeting</a> of the Australasian Society for Autism Research. Seeing as there are going to be so many great autism researchers in town, we're also putting on a public autism research event.<br />
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Things will kick off on <b>Wednesday 5th December at 2pm</b> with a workshop, loosely around the theme of "What is Autism?" It's a question that I think everyone has a slightly different answer to, so should provoke some interesting discussion.<br />
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Starting off, we have Giacomo Vivanti talking about social cognition, and Nicole Rinehart on motor difficulties as an example of non-diagnostic features of autism. Then we have Rhoshel Lenroot on the overlap between autism and other developmental disorders and Andrew Whitehouse on lessons for autism research from cerebral palsy - I'm as intrigued as you are by that!<br />
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Next up will be Thomas Kuzma, a young man with Asperger syndrome, telling us about his first-hand experience of being on the autism spectrum. He's followed by Liz Pellicano, visiting from London, talking about the importance of actively involving autistic people in autism research.<br />
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The workshop will then conclude with a panel discussion of changes to autism diagnosis in DSM 5.<br />
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At 6pm, there will be a cheese and wine reception. Then the headline event - a public lecture by Prof Kevin Pelphrey from Yale University entitled "Searching for Autism in the Social Brain". Kevin is one of the world's leading autism researchers (and dad to two autistic kids) and will be presenting his lab's work on the social brain in typical development and autism.<br />
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The good news is that the whole thing is free. It's being sponsored by the Faculty of Human Sciences at Macquarie University and the Australian Research Council Centre of Excellence in Cognition and its Disorders. The bad news is that places are limited so if you're in the Sydney area and would like to come, <a href="http://www.ccd.edu.au/events/conferences/2012/whatisautism/index.html">visit this link and register as soon as possible</a>.<br />
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Hope to see you there.drbrocktagonhttp://www.blogger.com/profile/15225859145004971487noreply@blogger.com2tag:blogger.com,1999:blog-1270723657817172117.post-81197123085942727022012-09-14T09:13:00.000-07:002013-10-23T04:51:30.548-07:00A genetic test for autism?This week's <a href="http://www.heraldsun.com.au/news/breaking-news/genetic-test-for-autism-developed/story-e6frf7kf-1226472754450">big autism story</a> was a genetic test able to predict with 70% accuracy [1] whether or not a child had autism. Rather than looking for a specific gene that might differentiate autistic from non-autistic people, Stan Skafidas and colleagues from Melbourne University developed the test by combining information about many different genetic variations. Critically, having developed the test based on one set of genetic data, they then tested the test on genetic data from a <a href="http://www.nature.com/mp/journal/vaop/ncurrent/fig_tab/mp2012126f1.html#figure-title">completely new set</a> of people.<br />
<br />
I don't want to take anything away from the basic science. And it would, of course, be incredibly useful to know early on whether or not a child is likely to develop autism. But the headlines are misleading. The unfortunate truth is that we're still a long way from a genetic test for autism. A screening measure with 70% accuracy would only be slightly better than completely useless.<br />
<br />
Here's why.<br />
<br />
Say you had 1000 kids and you ran the genetic test to see which ones would become autistic. <br />
<br />
If we assume that the rate of autism in the population is around 1% then we'd expect 10 of the 1000 kids to be autistic. Given 70% accuracy, we'd expect 7 to show up on the genetic test as autistic.<br />
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The problem is the other 990 who aren't autistic. 70% accuracy means that 30% would be incorrectly diagnosed as autistic. 30% of 990 is 297.<br />
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Putting those together, our genetic test thinks that 304 of the 1000 children are autistic. Of those, only 7 really are autistic, the other 297 have been mis-diagnosed.<br />
<br />
In other words, if your child took the test and the test came out positive, there would still be a 98% chance that your child was <i>not</i> autistic.<br />
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<u>[</u><u>Edit </u><u>15/9]: The researchers <a href="http://www.abc.net.au/worldtoday/content/2012/s3588670.htm">describe</a> the test as a test of autism <i>risk </i>rather than a diagnostic test<i>.</i> In those terms, what it tells you is whether you have a 2% risk, as opposed to the usual 1% risk.</u><br />
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This <strike>screener's</strike> <a href="http://en.wikipedia.org/wiki/Base_rate_fallacy">base rate fallacy</a> is a well known problem. <a href="http://deevybee.blogspot.com.au/2010/07/difference-between-p-05-and-screening.html">Dorothy Bishop</a> covered it when discussing screening for autism based on speech recordings and MRI scans. <a href="http://www.badscience.net/2009/02/datamining-would-be-lovely-if-it-worked/">Ben Goldacre</a> talked about it in relation to screening for terrorists. It's a problem any time you're looking for something that's relatively rare. Even a really good test gets torpedoed by a disasterous rate of false positives.<br />
<br />
To be fair, the researchers did <a href="http://www.news-medical.net/news/20120911/Genetic-test-predicts-risk-for-Autism.aspx">suggest</a> that the test would be most useful for parents who already had one autistic child. The latest <a href="http://pediatrics.aappublications.org/content/early/2011/08/11/peds.2010-2825.abstract">research</a> suggests that, if you have an autistic child, the chances of a second autistic child may be as high as 19%. Even in that situation, you'd still expect roughly two thirds of the kids picked up by the test to actually be non-autistic. <u>[Edit 17/9]: And that's assuming 70% accuracy. In fact, the test was much poorer at discrimination between siblings with and without autism, suggesting that it's predictive value in the real world will be much lower.</u><br />
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<b>Update (15/09/12)</b><br />
<br />
On Twitter, Emily asked whether such a test could ever be useful.<br />
<blockquote class="twitter-tweet" data-in-reply-to="246643264961265664">
@<a href="https://twitter.com/drbrocktagon">drbrocktagon</a> how high would the detection rate need to be to be useful? Given rarity of <a href="https://twitter.com/search/%23autism">#autism</a> would any test escape false positive issue?<br />
— Emily (@mosaicofminds) <a data-datetime="2012-09-14T16:31:16+00:00" href="https://twitter.com/mosaicofminds/status/246647313399939072">September 14, 2012</a></blockquote>
<script charset="utf-8" src="//platform.twitter.com/widgets.js"></script>As a population screening test, I think the answer would have to be no. Let's assume that the sensitivity (ability to detect true cases) goes up hand in hand with the specificity (ability to reject non-cases). Then for each level of accuracy, we can plot your autism risk if you test positive for autism. Even if the test was 90% accurate, you've still only got an 8% risk of autism if you test positive.<br />
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<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEj6qxQeCllpoy_aQzkKqhoR6BvBbndALRXJSA_c_py8KucTX6OHohUfelYyzcMIoSVnX__ULBq8_B6Oo9BwI11EUPW8yvBiAFAp7TyKdZ9C8-ZY9Ls14Ffv7L96vkM-HWCq-WUC7Ilej3o/s1600/ScreeningGraph.jpg" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" height="261" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEj6qxQeCllpoy_aQzkKqhoR6BvBbndALRXJSA_c_py8KucTX6OHohUfelYyzcMIoSVnX__ULBq8_B6Oo9BwI11EUPW8yvBiAFAp7TyKdZ9C8-ZY9Ls14Ffv7L96vkM-HWCq-WUC7Ilej3o/s320/ScreeningGraph.jpg" width="320" /></a></div>
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<b>Update (17/09/12): </b>Stan Skafidas has <a href="http://crackingtheenigma.blogspot.com.au/2012/09/a-genetic-test-for-autism.html?showComment=1347777989025">responded</a> (at length!) in the comments.<br />
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<b>Update (06/06/13):</b> Dan Geschwind and colleagues have written a critical commentary of the paper in Molecular Psychiatry. See <a href="http://blogs.discovermagazine.com/neuroskeptic/2013/04/05/genetic-test-for-autism-criticized/">Neuroskeptic</a> for coverage.<br />
<b><br /></b>
<b><br />Update (23/10/13): </b>Robinson et al have published another critical <a href="http://www.nature.com/mp/journal/vaop/ncurrent/full/mp2013125a.html">letter</a>, in which they describe a failure to replicate Skafidis et al.'s results. See <a href="http://questioning-answers.blogspot.com.au/2013/10/put-it-in-autism-science-replicator.html">Questioning Answers</a> for coverage.<br />
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<b><br /></b>
<b>Notes</b><br />
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[1] "Positive and negative predictive accuracies were <a href="http://www.nature.com/mp/journal/vaop/ncurrent/full/mp2012126a.html">70.8 and 71.8%</a> respectively"<br />
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<b>Reference</b><br />
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<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=Molecular+psychiatry&rft_id=info%3Apmid%2F22965006&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=Predicting+the+diagnosis+of+autism+spectrum+disorder+using+gene+pathway+analysis.&rft.issn=1359-4184&rft.date=2012&rft.volume=&rft.issue=&rft.spage=&rft.epage=&rft.artnum=&rft.au=Skafidas+E&rft.au=Testa+R&rft.au=Zantomio+D&rft.au=Chana+G&rft.au=Everall+IP&rft.au=Pantelis+C&rfe_dat=bpr3.included=1;bpr3.tags=Biology%2CMedicine%2CHealth%2CNeuroscience%2CCognitive+Neuroscience%2C+Genetics%2C+Autism">Skafidas E, Testa R, Zantomio D, Chana G, Everall IP, & Pantelis C (2012). Predicting the diagnosis of autism spectrum disorder using gene pathway analysis. <span style="font-style: italic;">Molecular psychiatry</span> PMID: <a href="http://www.ncbi.nlm.nih.gov/pubmed/22965006" rev="review">22965006</a> <a href="http://www.nature.com/mp/journal/vaop/ncurrent/full/mp2012126a.html">Full Text</a></span><br />
<br />
<b>Related post</b><br />
<br />
<ul>
<li><a href="http://crackingtheenigma.blogspot.com.au/2010/08/describing-brain-in-autism-in-five.html">Can MRI scans be used to diagnose autism?</a></li>
</ul>
drbrocktagonhttp://www.blogger.com/profile/15225859145004971487noreply@blogger.com25