Autism Diagnoses Spread through Social Networks

EXECUTIVE SUMMARY: A little more than a year ago, a group of sociologists analyzed data from the state of California --- birth records and records from California's Department of Developmental Services --- to look for patterns in where autistic children were most likely to be found. They determined that children living near (defined here as being within 500 meters) a family where one of the children had been diagnosed with autism in the previous year were somewhat (1.26 times) more likely to receive an autism diagnosis themselves. They also found that 1) the effect was stronger for the less severe cases of autism, and also for children who were three years old when they were diagnosed (as opposed to 4, 5, or 6); and 2) children living very close to a family with a recently-diagnosed autistic child were about 28% less likely to be diagnosed with intellectual disability without a concurrent diagnosis of autism. The researchers concluded that parents who know other parents who've had a child diagnosed with autism are more likely to have their own children evaluated, and thus more likely to get a diagnosis for their own children.
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An article published last year in the American Journal of Sociology argues that knowing someone in your neighborhood who has an autistic child makes it likelier that your child, too, will be diagnosed with autism.

The authors' explanation for this is not that autism is "catching," or that people with autistic children are likelier to live in certain places (they investigated both of those possibilities, along with the possibility that some environmental contaminant makes some neighborhoods have more autistic children than others); it's that parents talk to each other about their children, and if one family has an autistic child, and has gotten that child diagnosed and enrolled in services, those parents will tell other parents about that process, and thereby make it easier for other parents to do the same thing. (They may also, by describing their autistic children's behavior, make it more likely that other parents will consider the possibility that their child may be autistic).

What these researchers --- sociologists Peter Shawn Bearman, Marissa D. King (who has conducted a lot of research into autism demographics) and Ka-Yuet Liu --- did to derive this explanation was look at data on all children born in California since 1997, with younger siblings also born in California. (They needed to restrict their sample to children with younger siblings to get information on where the firstborn children spent their early years --- if the family's residence is the same for every child born to that family, the researchers could assume that the firstborn lived in the same place during the years between hir own birth and the birth of hir youngest sibling. That's the information they wanted --- where families lived during their children's early years). This gave them a pool of 533,244 children whose families lived at the same address when they were born as when their younger siblings were born. Then, they used data from the California Department of Developmental Services (I've written about this data set before, in a different context --- it's been used in a lot of studies investigating autism prevalence) to determine which of those children got an autism diagnosis, or a diagnosis of intellectual disability*, between the ages of 2 and 6.

They created a statistical model to see if they could accurately predict which children would end up with a diagnosis of Autistic Disorder**. Their model, which is supposed to predict the odds of any given child being diagnosed with autism in a given year, t, uses the physical proximity of a child diagnosed with autism in the previous year, t - 1, as its predictive variable. They divide this continuous measure --- how far away does [other child with autism] live? --- into six discrete groups: 1 - 250 m; 251 - 500 m; 501 m - 1 km; 1001 m - 2 km; 2001 m - 5 km; and all distances over 5 km. (They used a continuous measure of distance, too). They controlled for a slew of other variables --- sex, maternal age, socioeconomic status (measured by mother's educational attainment and whether she received state assistance with pregnancy- and birth-related medical expenses), proximity to autism-related healthcare services, neighborhood population density, and neighborhood median income --- and predicted that the odds of a child being diagnosed with autism would increase the closer they lived to a child already bearing that diagnosis, and that the odds of a child being diagnosed with intellectual disability independent of any other condition would decrease with increasing proximity to a child diagnosed with autism. They also predicted a pattern in what kind of autistic children would show the greatest change in likelihood of diagnosis: they thought that the "high[est]-functioning" children, who scored the lowest on their measure of autism severity***, would show the greatest effect, along with the youngest children (age 3 or younger). Their reasoning is that, since these are the most ambiguous cases, whether or not their parents knew someone else with an autistic child, and thus got it into their heads to consider whether their child might also be autistic, would make the most difference, since there are less likely to be really obvious, textbook signs of autism. (Or, if signs are present, say, in the very young children, knowing another family with an autistic child might predispose the parents to have their child evaluated sooner, rather than waiting to see if, say, the child is just a late talker).

Sure enough, they found the patterns they'd predicted.

This graph shows the clustering of actual data points around their theoretical curve; you can see it's a pretty close fit.

(Figure 2A, in Bearman, King and Liu, 2010. The x-axis shows distance, in kilometers, from the nearest home with a child with an autism diagnosis, and the y-axis shows the probability that any given child living at that distance will be diagnosed with autism within the next year).

Here's a different representation of the same data:

(Figure 2B, in Bearman, King and Liu, 2010. The x-axis still shows distance, but the y-axis, instead of showing probability of an autism diagnosis in the next year, now shows the odds ratio between each distance category and the reference category, which is 501 m - 1 km. The five different dots in each distance category represent the five different statistical models that were used. You can see that, compared to the middle distance category, the children in the two shorter-distance categories were more likely to receive autism diagnoses, while the children in the three longer-distance categories were less likely to be diagnosed.)

From the Results section:

[W]e also report the effects of proximity as a categorical variable. All odds ratios (ORs) are relative to the reference category of 501 meters - 1 kilometer. ... In figure 2B, we can observe that residing in close proximity to a child diagnosed with autism increases one's chance of being diagnosed with autism in the subsequent year. Compared with children who are 501 meters - 1 kilometer away from their nearest neighbor with autism, those in close proximity (1 - 250 meters) to a child with autism have a 42% higher chance of being diagnosed with autism in the subsequent year. Proximity of 201 - 500 meters increases the chance by 22%. In contrast, being farther away from a child with autism reduces the chance of a diagnosis. Although the last three categories were all significantly associated with the decrease (-21%, -36%, and -49%), there were no statistically significant differences among these three categories. This is consistent with the results in figure 2A, which show that the effect of proximity is strongest within one kilometer, followed by a flat tail.

And here are the graphs showing the effects of proximity to a family with an autistic child on 1) a child being diagnosed with autism (with intellectual disability) rather than with intellectual disability alone ...

(Figure 2C, in Bearman, King and Liu, 2010. The x-axis shows distance; the y-axis shows odds ratios --- compared, again, with the middle-distance "reference" category of 501 m - 1 km --- of being diagnosed with intellectual disability by itself. You can see that living closer to a family with a recently-diagnosed autistic child made it less likely that a given child would be given a sole diagnosis of intellectual disability, although it is only at the farthest distances, 5 kilometers or more, that children become more likely to receive a diagnosis of intellectual disability independent of any other condition).

... and 2) being diagnosed with autism at varying levels of severity:

(Figure 3, in Bearman, King and Liu, 2010. The x-axis shows the percent increase in odds of receiving an autism diagnosis associated with proximity to a recently-diagnosed autistic child; the y-axis shows the child's level of disability as assessed by the state's Client Development Evaluation Reports. The highest-scoring, or least impaired, 20% are compared to the bottom, or most seriously impaired, 20%, and to the middle 60%. You can see that the "highest-functioning" group shows a stronger effect of proximity to another autistic child on their chances of being diagnosed than either the middle group or the "lowest-functioning" group, whose chances of being diagnosed with autism were least affected by proximity to another recently-diagnosed autistic child.)

The researchers were pretty well satisfied that the effect they found for proximity wasn't an artifact of shared environmental contamination because they saw the same pattern in a large, diverse sample of neighborhoods. They looked at rural, urban and suburban communities, which would all have their own distinct toxicological profile. (For instance, pesticide exposure would be a likely risk factor in rural areas, and a possible one in suburban areas, but pretty unlikely in urban areas. Similarly, air pollution is probably only a serious factor in dense urban areas.) There were other patterns that would not be explained by shared environmental risk factors or viral transmission, but that do fit with the social-diffusion hypothesis: first, a strong tendency of people coming in for diagnostic evaluations to have been referred there in the way as their nearest neighbor with an autistic child, and second, for people living on or near a border between school districts, the proximity effect was only seen for children living nearby who also attended school in the same district.

So, I find all this pretty supportive of their idea that social networks play a role in determining who is and who is not diagnosed with autism; what is less clear to me is how much of a role they play compared with other factors, like socioeconomic status, parents' ages, male gender, or having an autistic relative.

What Drs. Bearman, King and Liu did to try and answer that question is calculate the population attributable fractions (PAFs) --- the difference any given risk factor makes in the number of people who develop a certain condition --- for proximity to another autistic child, and also for each of three sociodemographic indicators: mother's age at the time of her child's birth, mother's educational attainment, and whether the state of California paid for her prenatal and obstetric care. By this metric, they found a greater role for proximity than for any other factor: living within 500 meters of a family with a recently-diagnosed autistic child raised children's likelihood of being diagnosed with autism in a given year by 16%.

While this may be a larger effect than any of the other, more-established risk factors, it's not larger by all that much, and in absolute size it's also not very big. I would expect that, though --- most children don't have autism, so the most a social diffusion of autism awareness could do is make the parents of those children who do have autism take them in to be evaluated sooner. (Or, maybe for a few families, at all --- but with schools getting more and more proactive about identifying special-needs children, it's not very likely anymore that a child with autism could get all the way through K-12 without being flagged somewhere along the line).

Liu KY, King M, & Bearman PS (2010). Social influence and the autism epidemic. AJS; American journal of sociology, 115 (5), 1387-434 PMID: 20503647

*They tracked this category as well to look for social/spatial patterns of diagnostic substitution --- are children who are more likely to be diagnosed with autism also less likely to be diagnosed with general (i.e., non-autism-associated) intellectual disability?

**They only counted children in this category, and not any other pervasive developmental disorder, because only Autistic Disorder is a category eligible for state services. The researchers felt that parents' main motivation in pursuing a diagnosis would be to gain access to services, so they didn't bother tracking the diagnoses that wouldn't be useful toward that end.

***Their severity measure involved nine items from the California DDS's Client Development Evaluation Report (CDER) on each child. (Here is a PDF of the complete CDER form, if you want to go and look at what exactly these items are measuring). The overall measure was an equally-weighted average of scores on three "scales" --- communication (made up of 3 CDER items: item # 58, word usage; item # 61, receptive language; and item # 62, expressive language), social interaction (made up of 5 CDER items: item # 27, peer interaction; item # 28, interaction with nonpeers; item # 29, friendship formation; item # 30, friendship maintenance; and item # 31, participation in social activities), and a single CDER item, # 42, measuring repetitive and stereotyped behaviors. (I find it a bit odd that they didn't include self-injurious behavior as part of their severity measure --- there are two items on the CDER addressing that, and the presence or absence of self-harm seems to me a more important measure of how "severe" someone's problems are than, say, being able to interact "normally" with one's peers.)

Gene Expression in Autistic Brain Tissue

EXECUTIVE SUMMARY: A recent analysis of mRNA extracted from brain tissue samples taken from brains donated to the Autism Tissue Project and the Harvard Brain Bank, with both sources supplying both autistic and neurotypical brains, found two clusters of genes whose expression differs significantly between autistic and NT brain tissues. One of these clusters, whose component genes primarily encode proteins involved in synapse formation and neurotransmission, is expressed less in the autistic brains than it is in the NT ones. The other cluster includes a lot of immune- and inflammation-related genes, and those genes are expressed to a greater degree in autistic brains. This study also unearthed a gene encoding a protein that seems to be involved in splicing the mRNA transcripts of other genes, and the underexpression of this gene in autism may be part of the reason so many of the other genes in the same cluster are also underexpressed.
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This study, published online at Nature.com last Wednesday, strikes me as an interesting hybrid of two kinds of studies that are frequently used in autism research: gene-expression studies (where researchers compare patterns of gene expression in tissue samples taken from autistic people to those in samples taken from neurotypical people) and neuroanatomical studies (where researchers look at differences in size, structure or activation patterns of various brain structures between autistic and neurotypical subjects).

In this study, the researchers took samples from three different regions of the brain (the prefrontal cortex, superior temporal gyrus and cerebellar vermis), using brains donated to the Autism Tissue Project and the Harvard brain bank. From both of those sources, they ended up with 58 cortex samples (29 from autistic brains; 29 from non-autistic brains) and 21 cerebellar samples (11 autistic; 10 not).

They looked for differences in gene expression between autistic and control tissue samples by measuring the amount of RNA present in each sample corresponding to a given sequence of genomic DNA. (Since the mid-to-late 1990s, a tool has existed to do this at quite a high resolution: the DNA microarray. This is a glass or silicon chip covered in tiny wells where a short sequence of DNA is anchored --- in this case, the DNA probes are short, synthesized 50-base snippets made to match specific parts of each gene contained in the National Center for Biotechnology Information's RefSeq database --- to which your sample DNA or RNA will bind if it contains a complementary sequence).

(What a microarray looks like)

This type of experimental design doesn't really allow direct comparison between RNA extracts from different tissue samples --- instead, each sample (from the same region of the brain of either an autistic or neurotypical donor, or from different regions within the same brain) hybridizes (i.e., forms a new, DNA-RNA "hybrid" helix when heated) to the DNA probes on its own separate array. Researchers then compare the intensity of the signal created by each well across the two arrays --- the brighter the color, the more (fluorescent-dye-treated) sample RNA is present on the chip.

(DNA-RNA hybridization)

In this experiment, the researchers found 444 genes that differed significantly between the autistic and control cortex* samples in how much mRNA (the RNA created when DNA is transcribed; used as a template for protein synthesis) there was in a given tissue extract. They decided to concentrate on the 200 most differentially expressed genes for their (more detailed) expression analysis, which included a look into "co-expression networks" of genes whose expression seems to be regulated via the same pathways. They replicated their results by doing a similar microarray experiment on tissue samples from a smaller group of donated brains (nine from autistic donors, five from neurotypical donors), this time taking samples from a different region of the cerebral cortex than either of the cortical regions assayed in the initial experiment.
Figure 1C, in Voineagu et al, 2011 --- scatter plot showing genes found to be up- (red) and down-regulated (green) in both the initial and replication data sets. The bluish lines drawn through each cluster of dots reflects the cutoff for significance; most of the regulation changes are significant, but some aren't. Both axes represent a logarithmic measure of the change from baseline for either data set (Data Set 1, or the initial data, is on the x-axis; Data Set 2, or the replication data, is on the y-axis).
They got additional confirmation of their gene-expression data by using an alternative measure of how much of a given mRNA sequence was present in each tissue extract: for each gene that the microarray experiments identified as being differentially expressed in autistic and non-autistic brain tissues, they made a DNA copy of its array-bound mRNAs, and then amplified those bits of DNA using a process called RT-PCR (real-time polymerase chain reaction). That process uses bacterial enzymes to make huge numbers of copies of a given sequence of DNA, such that the amount of DNA is large enough to be easily quantified. Those amounts could be compared between groups, and thus confirm (or fail to confirm) differences in mRNA production predicted by the microarray experiment.

This figure shows how much more or less mRNA there was from eleven genes whose differential expression levels were validated using PCR:

(Supplementary Figure 2B, in Voineagu et al., 2011 --- top bar graph, in red, shows positive changes in expression of five genes in the tissue samples taken from autistic donors; bottom graph, with green bars, shows the average reduction in expression of six other genes. On both graphs, the numbers on the y-axis represent how many times as much of one kind of mRNA was found in the autistic sample; you can see that the up-regulating produced a more dramatic change --- ten- and twenty-fold, for all but one of the five genes --- than down-regulating, which produced, respectively, one-half, one-fifth, one-eighth, one-third and one-fourth as much mRNA as the control sample).

They found two co-expression modules (networks of genes) whose expression varied in relation to whether the sample came from an autistic or non-autistic donor, and not in relation to any of the other variables they took into account (like age, sex, cause of death, medication history, whether the person also had seizures, and family history of mental illness): M12 and M16.

Here is their drawing of M12, and the relationships between its component genes:
(One of the genes in the middle of this diagram, CNTNAP1, is a close relative of a gene that other genetic studies have tied to autism --- and that I have described on this blog --- CNTNAP2).
... and here is their drawing of M16:
Relative to the samples from neurotypical donors, the brain tissue samples from autistic donors had more mRNA transcripts of genes in M16, and fewer transcripts of genes from M12.

In each of these modules, genes for certain types of proteins predominated: for M12, these are proteins involved in synapse formation, neurotransmission, vesicular transport (importing objects into the cell, or exporting objects from it); while M16 included lots of genes for immune and inflammatory proteins.

One of the major genes in M12, A2BP1, is a splicing regulator. Alternative splicing is one of the ways the cell can make different kinds of proteins from the same mRNA; the mRNA will contain characteristic sequences, called splice sites, where splicing enzymes can bind to it, cut it and put it back together, minus the regions bordered by splice sites.

Like some other instances I've mentioned of proteins playing a role in gene expression themselves being expressed differently in autism, this down-regulation of A2BP1 could have important ramifications for the genes whose transcripts A2BP1 is involved in splicing. The authors of this study thought it would be a good idea to look for A2BP1 splice sites in the RNA samples from those specimens within the autism group with especially low levels of A2BP1 mRNA; to do this, they sequenced all the mRNA from three samples with relatively little A2BP1 mRNA, and also from three control samples with normal A2BP1 expression. They found 212 potential splice sites using this method, which they validated by using RT-PCR (again) to compare relative amounts of various alternatively-spliced mRNAs in autistic and control tissue samples --- first in the same three samples that were sequenced, and then in three other samples from the autism group, which also had low A2BP1 expression. Using this method, they confirmed that the vast majority (85%) of the expected splicing changes were really there in all of the low-A2BP1 samples.

The genes whose alternative splicing depended on A2BP1, and thus whose alternate forms were underexpressed in the low-A2BP1 RNA samples, included a lot of the same genes as the M12 co-expression module. So it looks like, besides finding out that M12 is collectively underexpressed in autism, these researchers have also found at least one of the mechanisms behind this underexpression.
*The cerebellar samples differed significantly in the expression of only two genes, so those data were not included in further analysis.

Irina Voineagu, Xinchen Wang, Patrick Johnston, Jennifer K. Lowe, Yuan Tian, Steve Horvath, Jonathan Mill, Rita M. Cantor, Benjamin J. Blencowe, & Daniel H. Geschwind (2011). Transcriptomic analysis of autistic brain reveals convergent molecular pathology Nature (25 May) : 10.1038/nature10110

Qualified Candidate Barred From Job; U.S. Government Sues Employment Agency

My heart really goes out to Jason O'Dell; he and I seem to be in similar circumstances.

He recently applied for work as a lab technician in Frederick, Maryland, using an employment agency called Randstad US. Everything had been going pretty well --- Randstad had decided that he was exceptionally well-qualified for this particular job, so they "fast-tracked" his application; the company he had applied to had also expressed interest in hiring him --- until O'Dell let it slip that he had Asperger's.

When that happened, the position he had seemed about to get seemed to evaporate. His contacts at Randstad were telling him it had "been put on hold," but really they were continuing to recruit other candidates, and eventually filled the position with someone who was not Jason O'Dell.

In response to this, the U.S. Equal Employment Opportunity Commission is suing Randstad for discrimination --- in pulling O'Dell out of consideration for employment right after he told them about his disability, they violated the Americans with Disabilities Act's prohibition against employers (or employment agencies!) discriminating against qualified people with disabilities in job application procedures, hiring, promotion, pay, training, firing or any other aspect of employment. They're asking for back pay, compensatory and punitive damages for O'Dell, and revisions to Randstad's employment policies to make the kind of discrimination O'Dell experienced Officially Against The Rules.

Here is the relevant part of the ADA:

Sec. 12112. Discrimination

(a) General rule

No covered entity ["covered entity" meaning an employer, employment agency, labor organization or joint labor-management committee] shall discriminate against a qualified individual [someone who can perform the essential functions of the job with reasonable accommodations] on the basis of disability in regard to job application procedures, the hiring, advancement, or discharge of employees, employee compensation, job training, and other terms, conditions, and privileges of employment.

(b) Construction

As used in subsection (a) of this section, the term "discriminate against a qualified individual on the basis of disability" includes

(1) limiting, segregating, or classifying a job applicant or employee in a way that adversely affects the opportunities or status of such applicant or employee

... and here's a handy little page about employment law; it tells you what your rights are under the ADA, and what you can do if you think they've been violated.

The EEOC also mentions in its press release that fiscal year 2010 has been especially bad for discrimination in employment: they had 99,922 claims, of which 25,165 were disability-related. That constitutes an increase of 17.3% over the number of disability claims filed in fiscal 2009.

I hope they win their suit, and that O'Dell gets those damages ... although even more I hope he manages to get a lab job somewhere!

Stigma

I thought this paragraph in the Discussion section of the article I posted about yesterday was so interesting it deserved its own post:

Although researchers have not found cultural variability in phenotypic expression of ASDs, cultural variables may affect prevalence estimates. Indications generally suggest ascertainment bias toward lower prevalence in South Korea since Koreans consider autism to be a stigmatizing hereditary disorder; autism (chap'ae) impugns the child's lineage on both sides and threatens the marriage prospects of unaffected relatives. As a result, autism is often untreated, misdiagnosed as attachment disorder, or unreported in records. Although our total population approach avoided clinical and administrative obstacles associated with stigma, it is possible that some parents, fearing a diagnosis, chose not to report ASD symptoms or to participate in diagnostic evaluations.

I don't know if this blog has any Korean readers --- if any of you are reading, I'd love to hear your thoughts on the accuracy of the quoted passage.

Taking the passage at face value, it seems to me that the difference in stigma associated with autism in the U.S. and in Korea is more a matter of where the stigma is directed than whether a stigma exists at all. Autism is very much a stigmatized condition here; it's just that the family members aren't seen as tainted with faulty genetics (and thus less marriageable) as much as they are alternately pitied and lionized for living with an autistic person. The stigma here is directed almost entirely at the autistic person hirself, although of course parents and caregivers who make choices that don't fit with the current ideas of what's best for an autistic child come in for some serious disapproval, too.

1 in 38?

That's the proportion of school-aged kids found to meet diagnostic criteria for an ASD by this team of mostly Korean researchers --- Drs. Young-Shin Kim, Bennett L. Leventhal, Yun-Joo Koh, Eric Fombonne (who has done a lot of research on the prevalence of autism), Eugene Laska, Keun-Ah Cheon, Soo-Jeong Kim, Young-Key Kim, Dong-Ho Song, and Roy Richard Grinker (the Unstrange Minds guy), along with Eun-Chung Lim and HyunKyung Lee --- when they screened elementary-school children in one district of a fairly large city (Goyang City, pop. 1,073,069; Ilsan district, pop. 488,590) near Seoul, South Korea.

Part of their reasons for doing this study (full text here) was their thought that previous estimates of the prevalence of autism rely too much on documentation from official sources --- national disability offices, special-education registries, autism-specific service providers, etc. --- that wouldn't include children who have not yet been evaluated for ASDs.

To try and get more of a cross-section of Korean children, the researchers recruited from both mainstream elementary schools (41, of which 30 agreed to participate), special-education schools (3), and the city's Disability Registry (all children between 7 and 12 listed as having either ASD or intellectual disability). Children from participating institutions were initially screened for autism using the Autism Spectrum Screening Questionnaire (ASSQ), which parents and/or teachers filled out about each child.

Not surprisingly, the general-population group, recruited from the elementary schools, was much larger than the developmentally-disabled group recruited through the Disability Registry or from special-education schools: in all 30 participating elementary schools, there were 36,592 children between the ages of 7 and 12. Of these, the parents of 23,234 completed the ASSQ and sent it in to the researchers; of the 294 students attending special schools and/or listed in the Disability Registry, 103 had forms submitted for them.

Anyway, following this initial screening, the students who scored high enough on the ASSQ (with a teacher-rated score of at least 10, or a parent-rated score in the top five percentiles*) were offered further diagnostic evaluation. Among the elementary-school students, 1,742 met those screening criteria, and 234 completed the evaluation. All of the special-education students were considered to meet screening criteria, and 52 of them completed the evaluation. Each child was evaluated by two teams, and each team included both Korean- and American-trained practitioners. The evaluators used Korean versions of the Autism Diagnostic Interview (ADI-R), Autism Diagnostic Observation Schedule (ADOS), and two cognitive tests, the WISC-III and a revised version of the Leiter International Performance Scale.

Of the 286 children who were evaluated, 201 met criteria for an ASD**. Just over half of these (101) met criteria for Autistic Disorder; just under half of those (48) had come from the special-education group. All but one of the students in that group who were diagnosed with an ASD were diagnosed with Autistic Disorder, while most of the students in the general-population group were diagnosed with some other ASD, either Asperger's syndrome or PDD-NOS**.

There is one thing I found particularly interesting in their results: the ratio of boys to girls among their ASD "positives" is significantly lower than the 4:1 most commonly cited in the autism literature. These researchers found a ratio of 5.1:1 among the special-education students (who were mostly boys to begin with --- of the 103 special-education students who were screened, 84 were male, so even if *all* of the girls in that group had autism, the ratio would still be skewed in the boys' favor unless relatively few of the boys had it) and a ratio of 2.5:1 among the mainstream elementary-school students.

That number adds some support to the hypothesis that autism remains underdiagnosed among girls --- the lower ratio was only seen in the students who were not flagged as disabled or special-ed, not receiving any services. Among the students known to be developmentally disabled, or already diagnosed with autism (i.e., those registered as ASD in the Disability Registry), the ratio was closer to the current conventional-wisdom ratio of 4:1.

(It also seems like the forms of autism that are most likely to go undiagnosed in girls are the "milder" forms, like Asperger's and PDD-NOS. Very few girls in the general-population sample met criteria for Autistic Disorder; of the 27 children meeting those criteria, only five were female.)

Anyway, back to the number making up the title of this post.

How they got that number is complicated. They divided the number of autistic students they extrapolated there to be based on the number they found (more about this later) by the total number of seven-to-twelve-year-old children living in the Ilsan district of Goyang City, which is 55,266.

So much for the easy part.

There were several steps involved in correcting for the large proportion of nonresponders; first, and easiest, they guesstimated the likely full scores of the people who turned in partial ASSQs. (The simplest method they had for doing this was simply to take the average single-item score on a form in which only some of the items are answered and multiply it by the number of items on the full questionnaire, which is 27). Just doing that gave them 264 more subjects meeting initial screening criteria for an ASD. They also added in all the children listed in the Disability Registry as having ASD who did not participate in this study; this would add 101 subjects to the confirmed-ASD pool. (They left out all the non-participating children listed as having intellectual disability).

They also did some statistical manipulations that I don't understand (I had minimal coursework in statistics, and not even good old Google can tell me what a "weigh-back procedure"*** is) to correct for their only having given some of the people meeting their minimum screening criteria the opportunity for furthere evaluation. (See the Methods section and this supplemental section for their discussion of these techniques).

At the end of all of this, they ended up with an adjusted prevalence figure of 2.64%, or the 1 in 38 referred to in the post title. There are several ways in which this might be an overestimate: chief among them, the researchers assumed that the proportion of children meeting screening criteria who also meet diagnostic criteria for an ASD would be the same for the nonresponders as it was for the responders --- i.e., about 70%. Their basis for this assumption is a logistical regression model they created to try and predict parental consent to, and participation in, diagnostic evaluations. They found that since none of the co-variates they'd chosen for this missing "latent variable" --- child's age, sex and ASSQ score --- predicted whether a given child would end up with an ASD diagnosis or not, that parental willingness to have more tests done did not vary with the likelihood that their child is autistic. But all of those variables are somewhat crude proxies --- even the ASSQ score, when you consider that all of the "screen-positive" children had scores clustered within the same narrow window, and thus variation between them would be minuscule. So I think it's reasonable to think that maybe the model was wrong, and the parents who chose to have their children evaluated might have a higher proportion of autistic children than the parents who opted out.

However, there are just as many reasons to suspect that their numbers are an underestimate --- after all, they did write off all the nonparticipants labeled intellectually disabled, even though their own results show a substantial proportion of intellectually-disabled responders having autism. The authors also suspect underreporting of possible autism by both parents and teachers, because autism is stigmatized in South Korea (thus making parents less likely to want to admit that their child has it) and because the South Korean school day is so rigorous and structured (making teachers less likely to notice the social dysfunction that the ASSQ tests for, because there is so little socializing during a typical school day in Korea).

But the need to extrapolate so much data to make up for low response rates is a serious flaw in this study, though, as Prometheus points out, even when you restrict your gaze to the data that they actually have, you still see that the majority of confirmed ASD cases were in the general-population group, among children who had never seen a mental-health professional before.

Other bloggers posting about this study: Steven Novella at Science-Based Medicine; Sullivan at Left Brain/Right Brain and the Autism Science Foundation blog; Rose at Hard Won Wisdom; Michelle Diament at Disability Scoop; Paul Whiteley at Questioning Answers; Polly Palumbo at Momma Data; Aspie Editorial; Raphael Fraser at Music, Medicine & the Mind; Prometheus at A Photon in the Darkness; and MJ at Autism Jabberwocky (who has a detailed explanation of the ASSQ and its inherent biases)

*Only some of these children were referred for further evaluation: all the children scoring in the top two percentiles, half the children (chosen randomly, not by score) in the percentile third from the top, and one-third of the children in the percentiles fourth and fifth from the top.

**There's another interesting asymmetry within the general-population-derived ASD cases: a much greater proportion of those whose final diagnosis was Autistic Disorder had histories of psychiatric or psychological treatment. A majority (26 of 48) of students attending mainstream elementary schools who both met criteria for an ASD and had seen a psychiatrist or psychologist in the past ended up being diagnosed with Autistic Disorder, while the ASD students from mainstream elementary schools who had never seen a mental-health professional were mostly diagnosed with the other ASDs (27 of 104 with Autistic Disorder; 77 of 104 with either Asperger's or PDD-NOS).

***Perhaps it is how Mr. Peabody travels back in time?

Kim, Y., Leventhal, B., Koh, Y., Fombonne, E., Laska, E., Lim, E., Cheon, K., Kim, S., Kim, Y., Lee, H., Song, D., & Grinker, R. (2011). Prevalence of Autism Spectrum Disorders in a Total Population Sample American Journal of Psychiatry DOI: 10.1176/appi.ajp.2011.10101532

Non-Blog Happenings: Turkey Creek Fest

Last Saturday, I made my first attempt at selling my jewelry out in the real world. I bought a vendor space at the Merriam Turkey Creek Festival, which includes a fairly large arts-and-crafts market.

Here's what my booth looked like, more or less:
(I say "more or less" because this picture was taken some time before the event, at my house rather than at the actual site. The festival organizers wanted to see what everyone's setup would look like, so I took some pictures in advance. I did not take any pictures on festival day, so this is all I have).

Here's a closer view of the sign I made:
And here's one of my display elements that I think looks cool, although it's really annoying to set up:Unfortunately, I didn't do well at all in terms of selling stuff --- I only sold two items*, and failed even to make back what I had spent on registration fees! Apparently this year's festival had lackluster turnout compared with what the organizers were expecting; they had planned for 10,000 people showing up, and I didn't think there were anywhere near that many. Most of the other vendors I talked to also had poor sales, although a few did really well. I think one of the reasons I had such bad luck was that there were so many other jewelry vendors --- whoever wanted to buy jewelry had maybe a dozen or more places to do it, and had probably already bought some elsewhere before they got around to my booth.

I don't think it was a total loss, because I had fun, distributed some business cards and learned a few things about picking the right festival to sell what you make --- people are more willing to buy stuff near the holidays, when they are looking for gifts, and different festivals attract different kinds of people, some of whom are more likely than others to want fancy beaded jewelry.

You don't find this stuff out if you never try.

*One of the things I sold was the asymmetrical blue necklace with the circular shell beads shown at the bottom of this post; I made two of those and sold one to my sister a while ago, and now someone has bought the other one, too. I was really proud of the design on that one, so I was gratified to see someone take it (even though it means I can't dig it out and wear it anymore).

Autistic Woman Writes Terrible Column; Speculation About Her Capacity for Empathy Ensues

There's this woman, Penelope Trunk, who writes about climbing the corporate ladder on her blog, and in her book Brazen Careerist: The New Rules for Success. She's founded several startup companies, has worked in marketing and is now a full-time writer, focusing on career advice for young people.

She also has Asperger syndrome.

A few days ago, she wrote a column about Dominique Strauss-Kahn, the former head of the International Monetary Fund who is accused of sexually assaulting a hotel maid. In her column, Trunk advances the bizarre hypothesis that women who occupy the lowest rungs of the socioeconomic ladder, who work low-paying, menial jobs with no possibility of advancement, have greater freedom than higher-paid, professional women do to report sexual abuse by bosses, co-workers or clients.

Her notion is that someone working a low-paying job will not have the same incentive to hold onto that job that someone with a better job would have:

It has been clear for at least a decade that women who want to have a high-flying career should not report sexual harassment. I have written about this a zillion times, and before you argue with me, read the quotes from all the labor lawyers (representing plaintiffs) who agree.

The bottom line is that just about every woman who has entered the workplace has experienced sexual harassment, but the women who report it face retribution. ... [W]omen who complain about harassment generally lose their jobs in some convoluted but ultimately predictable way.
...
But, what about women who don't care if they get fired? Those women hold a lot of power in this equation.

It used to be that women with low-level jobs did not have the socioeconomic backing to stand up for themselves in the face of harassment. Today, women feel more empowered - even women in a low pay grade. And women across the economic spectrum can identify what crosses the line.

These women have nothing to lose when they report men who cross the line sexually. So the maid reported. And then, it turns out, all sorts of women in higher-up positions spoke up against Strauss-Kahn. The women wouldn't report the harassment on their own. They don't want to suffer retribution. But now there will be no retribution, so it's safe to come forward.

This is why men are going to focus harassment at the higher ranks of the corporate ladder. These are the women who have to keep their mouths shut if they want to keep climbing the ladder.

But God help the guy who harasses a woman with nothing to lose.

It's a great moment in history. Poor women are empowered to fight against lecherous men, and rich women can finally come out of the sexual-harassment closet because of it.

Matt Yglesias at Think Progress and Amanda Marcotte at Pandagon have both covered why this is astonishingly, massively wrong --- not just off, but actually the opposite of what's really true, which is that poorer women working menial jobs are more, not less, vulnerable to exploitation and abuse at work, and have fewer options for escaping or combating it. In believing otherwise, Trunk seems to have forgotten that, for some people, losing a job means not being able to pay rent, not having enough money to buy enough food, having to put off needed medical treatments or go without needed medications because they can't pay for them.

She also assumes that, if one quits a menial job, one can quickly and easily find another. This is just not true in an economy where almost one-tenth of all people in the U.S. are officially unemployed, and many more are working fewer hours than they'd like to. These low-wage service jobs are actually really competitive right now, since there are relatively few of them (since companies have mostly been weathering the Great Recession by laying off all the employees they could conceivably do without) and lots of people needing work.

There's a lot of other important stuff she leaves out, but I think the most important failing in her article is her assumption that women working low-paying jobs don't need those jobs. As a commenter on Pandagon noted, it's as if she's assuming that everyone has well-off relatives who can support them for a time, or has a trust fund or significant savings to fall back on. She doesn't seem to understand what poverty is.

Anyway, enough about Trunk. She's ignorant, naive and starry-eyed, and her good fortune and financial security have given her the (mistaken) impression that life is as easy for everyone as it has been for her.

Now, I want to talk about her critics.

It shouldn't surprise anyone reading this blog that commenters on both Pandagon and Yglesias's site have brought up her autism as a possible explanation for her failure to grasp basic economic and social realities.

From Pandagon:

Penelope Trunk's deal is that she has Asperger's and spends a great deal of time and energy figuring out the "rules" for social interaction. (Note: she is open about this and has written a great deal about it.) I got reading her because her perspective can bring some real insight into human interactions. But she can also get things dead, dead wrong.

If Ms. Trunk actually suffers from an illness which damages her ability to feel empathy, that both absolves her (partially) and leads to the next question --- why is she indistinguishable from the average conservative/libertarian?

My understanding is that while the inability to read nonverbal cues is quite acute, the practical effect of Asperger's also includes a lesser capacity for empathy, especially in relatively swift interactions.

From Yglesias's:

Trunk is wrong, obviously. But Asperger's Syndrome makes what she's trying to do here --- put herself in both DSK's and the maid's position and see who's right --- incredibly difficult. This isn't Tom Friedman telling us we gotta say "suck on that" to Iraq b/c he's a dick, this is someone with a legitimate medical condition exercising poor judgment by choosing to comment on something it's very hard for her to understand given that condition.

These comments are actually not representative of the threads in which they appear; these four comments are the only comments on both websites to blame Trunk's classism on her Asperger's diagnosis, and both threads also include other comments telling the quoted commenters that they are wrong to do so.

But it still depresses me that her diagnosis comes up at all in a discussion of why her article is wrong. One of the reasons it depresses me is because --- as the last comment I quote indicates --- it effectively bars all autistic people from participating* in discussions about workplace harassment. "Oh, you're autistic, you don't understand how normal people act." Because our "condition" prevents us from understanding other people, nothing we say about anything other people do --- even things they do to us --- has to be taken seriously. This is especially troubling when it's workplace (or school) harassment we're talking about, since autistic people are especially likely to be targeted for such harassment. (Indeed, we are often blamed for being bullied --- it's our own fault for being so weird, we're told as children.)

It also depresses me somewhat to see Trunk's excessive optimism about most people's ability to quit jobs at will, and find new jobs quickly and easily, attributed to her Asperger's rather than to her having a lot of resources at her disposal that she takes for granted, when most people with autism, when they can work, have terrible trouble finding jobs, and then holding on to those jobs for longer than a few weeks. If anything, we probably have a keener grasp than most people do of the risks inherent in quitting a job, because those risks are heightened for us.

I'd also like to point out, in two of those comments --- both written by the same person --- the use of autism as a metaphor for a self-serving political philosophy.

I've seen this once before, in an article on CommonDreams.org:

The language used in this passage --- citing "self-centered" behavior as the characteristic feature of autism, for example, or saying autistic people lack "linguistic, social, cultural or logical constraints to manage [our] lives" --- draws strong, if implicit, parallels between autism (a neurological condition) and selfishness (a moral quality).

These comments do a similar thing, with the "lack of empathy" that is so often cited as the core deficit of Asperger's syndrome. In the psychological literature on autism, the "empathy" being spoken of is usually cognitive --- we are unable to understand non-autistic people's behavior, feelings or states of mind, even though we are perfectly capable of caring about them. Yet, in the comment quoted above, the implication is that this lack of understanding also entails a lack of feeling for these incomprehensible others.

Autism is not a moral failing. Autistic people have moral failings, but they have them because they are people, not because they are autistic.

*Not in the literal sense of "You are not allowed to speak," but in the more nebulous sense of "You can speak, but if I know that you're autistic, I will attribute everything you say to your being autistic, and if any of it conflicts with what I think is true, or right, I will disregard whatever you say because your mind is diseased and mine is not."

Memento Mori: Thoughts of Mortality Can Subtly Bias People's Ideas about Human Origins

Death, be not proud, though some have callèd thee
Mighty and dreadful, for thou art not so;
For those, whom thou think'st thou dost overthrow,
Die not, poor Death, nor yet canst thou kill me.

-- John Donne, from Holy Sonnet X (also called "Death, Be Not Proud")

BPS Research Digest described a recent study in which a group of psychologists looked at the influence of thoughts of one's own death on people's attitudes toward two different ideas about human origins: evolutionary theory and the variant of creationism known as Intelligent Design.
The researchers --- Dr. Jessica L. Tracy, who is an assistant professor of social and personality psychology at the University of British Columbia's Vancouver campus, where she is also director of the Emotion and Self Lab, Dr. Joshua J. Hart, who is an assistant professor of psychology at a small liberal arts college in New York called Union College, and UBC graduate student Jason Martens --- went to rather more trouble than is usual in these social-psychology studies in their search for a diverse study population.

Too often, these studies make claims about "people" based on surveys of psychology undergraduates at one university. In this study, one of the five mini-experiments involved people from all over the US who filled out surveys online. They ranged in age from 18 to 75, with a median age of 37, so most of them were substantially older than the college students questioned in the other four experiments. They also came from (one assumes) a broader distribution of socioeconomic classes; socioeconomic data are not given for any of the student groups, but the general-population group includes people from a wide range of income levels: 12% of respondents reported making less than $20,000 a year, 25% made between $20,000 and $40,000, 20% made between $40,000 and $60,000, 11% made between $60,000 and $80,000, 8% made between $80,000 and $100,000, and 9% made more than $100,000 a year. (Fifteen percent of respondents chose not to say how much money they made). The general-population sample also included people with more widely varying educational backgrounds: 26% had a high school diploma or less, 33% had been to college but hadn't gotten a degree, 32% had a college degree, and 9% had a postgraduate degree.

The other four groups consisted entirely of college students; two of the groups were all psychology students recruited from either UBC or Union College, one group was college students recruited online from all over the U.S. and Canada, and the last group was natural-science students* from UBC and Union College.
Each group of participants was asked to specify their religion and rate how religious they thought they were, and then to read a passage written by either Richard Dawkins or Michael Behe discussing either evolution or Intelligent Design, and rate their attitudes toward the two belief systems and their representative authors.

Right before they did this, they were asked to imagine one of two unpleasant things (death vs. painful dental work) and write briefly about their feelings. The reason for including this morbid exercise was to see if bringing mortality to the forefront of people's minds had any effect on their preference for a naturalistic or deistic worldview.
They found that, for most people, being reminded of death does tend to make you more receptive to Intelligent Design and more hostile to evolution. This is true regardless of one's educational attainment, religion or religiosity. It was also true regardless of one's attitude toward evolution as measured before the experiment.
(Some more explanation of that last sentence: yes, being more religious meant you were more likely to be receptive to Intelligent Design whether you were asked to contemplate death or not; likewise with being Christian rather than belonging to any other religious tradition, or claiming no religion. But within each category, the researchers saw the same effect of the memento mori nudging people toward Intelligent Design and away from evolutionary theory. Oddly, being reminded of death did not prompt people to rate themselves as more religious, even though it had a noticeable effect on their ideas about human origins.)

While how much education a person had didn't make any difference in how they responded to the memento mori, the type of education did have some dampening effects. Compared to the general-population and general-student-population groups, the psychology students expressed less hostility to evolutionary theory in response to the memento mori, although they showed the same increase in receptivity to Intelligent Design.

Resistance to these effects was strongest in the natural-science students, who actually responded in the opposite way to the memento mori; when confronted with the thought of death, they reported feeling a stronger affirmation of evolution and repudiation of creationism.

The authors hypothesized that people would react to the thought of death by looking for something that confers some lasting meaning on human life; for most people, a divine Creator fills that role readily enough. One of their experiments --- one of the two using psychology undergraduates as guinea pigs --- addressed this hypothesis directly: they compared the responses of students who had read a passage by Carl Sagan aimed at dispelling fears that the scientific understanding of the universe is nihilistic with those of students who did not read this humanistic passage, looking to see if exposure to a Middle Way between deism and nihilism didn't moderate the shift toward Intelligent Design prompted by the students' meditating on their own deaths.

Here is the Sagan passage:

It is very reasonable for humans to want to understand something of our context in a broader universe, awesome and vast. It is also reasonable for us to want to understand something about ourselves. And understanding the nature of the world and the nature of ourselves is, to a very major degree, I believe, what the human enterprise is about. Truth should be pursued, and science helps us pursue it; science gives us meaning. All we have to do is maintain some tolerance for ambiguity, because right now science does not have all the answers. This tolerance goes with the courageous intent to greet the universe as it really is, not to foist our emotional predispositions on it but to courageously accept what our explorations and knowledge tell us. The more likely we are to assume that the solution comes from something outside science, the less likely we are to solve our problems ourselves. If we are merely matter that is intricately assembled, is this really demeaning? If there's nothing in here but atoms, does that make us less, or does that make matter more? We make our purpose. And we have to work out what that is, for ourselves.

Ahhh. Humanism. (Go on, bask in it!)

Sure enough, students who read this passage did seem to be less threatened by evolution, even with thoughts of their own individual mortality foremost in their minds: they responded to the thought of death by reporting less of a warm feeling for Intelligent Design, and more for evolutionary theory.

Here is the authors' summation of their findings:

The present findings demonstrate that reminders of one's mortality --- inducing a state of mortality salience --- promote relative support for [Intelligent Design Theory], and skepticism toward [Evolutionary Theory]. Individuals respond to existential threat by becoming more accepting of a theory that offers a greater sense of meaning by depicting human life as having ultimate purpose (while appearing consistent with the scientific worldview), and/or less supportive of the theory that is the true mainstay of the scientific worldview but seems to offer little in the way of existential comfort. These findings also suggest that a desire to find greater meaning in human life accounts for this effect (at least the effect of mortality salience on belief in IDT), because it is reversed by making ET more meaningful, and among natural-science students for whom ET is already meaningful. The findings are notable because they (a) help explain why some people are motivated to believe in IDT and doubt ET in terms of fundamental psychological drives; (b) account for the underlying causal process; and (c) emerged regardless of preexisting religious ideologies, religious affiliation, or (with one highly limited exception, discussed below) views of evolution. The last point suggests that although religion influences baseline beliefs in IDT and ET, it cannot account for the impact of MS on these views. Given previous research suggesting that many MS effects are heightened, or occur only, among individuals with certain preexisting belief systems or cultural associations, the fact that we found no moderators of MS effects --- other than the extent to which naturalism is seen as meaningful --- suggests that embracing IDT or rejecting ET may be a unique, broadly appealing mechanism that addresses the existential concerns of religious and, for the most part, more scientifically oriented individuals alike. In contrast, explicitly religious ideologies tend to be fairly parochial, limiting their appeals and making them viable defenses only for those who already believe in a supernatural god.

Yet, an exception emerged in Study 5, where individuals whose life goals require strong acceptance of ET showed the opposite responses. Like those explicitly taught, in Study 4, to view naturalism as a source of meaning, natural-science students responded to MS with stronger antagonism toward IDT. This provides converging support for the causal process found in Study 4, and suggests that rejecting IDT can be a source of existential comfort for a limited population of individuals. These individuals are not simply those steeped in the scientific cultural worldview --- presumably psychology undergraduates fall into that category --- but rather those who more specifically view evolution as a critical part of their understanding of the world and a source of meaning and purpose.

They also point out in the final section of the article that these results might shed some light on why creation-vs.-evolution has remained such an intractable social issue: rather than being solely determined by religious doctrine, political ideology or (lack of) scientific literacy, people's embrace of creationism is also a response to the fear of death. Merely cataloguing the evidence for evolution doesn't address these underlying emotional issues; it tears away the defense mechanism while providing nothing to replace it. To my mind, that goes a long way toward explaining not only the deadlock between sides but also the rancor in this debate.

(Of course, many evolution-defending speakers do emphasize the existential perks of their worldview: a sense of wonder at being part of such a beautiful, intricate, ever-changing universe; the feeling of joy as you discover deeper and deeper layers of life's complexity; a stronger sense of kinship with other forms of animal life, etc. Why, even Richard Dawkins, the theorist featured in this study as representative of the godless, naturalistic worldview, has written a lot --- most notably in his book Unweaving the Rainbow --- about the beauties and benefits of that worldview. So the emotional angle isn't all there is to this, though I think it is important and not usually given the prominence it deserves).

*The authors do not explain what fields are included in this umbrella category "natural sciences." As it is commonly used, it encompasses fields having nothing whatsoever to do with evolution, like physics, or chemistry, or astronomy or geology. So I would quibble a bit with their assertion that strong acceptance of evolutionary theory is necessary for one to progress in the "natural sciences" --- it is quite possible to complete a degree in a non-biological science field without ever encountering it.


Tracy, J., Hart, J., & Martens, J. (2011). Death and Science: The Existential Underpinnings of Belief in Intelligent Design and Discomfort with Evolution PLoS ONE, 6 (3) DOI: 10.1371/journal.pone.0017349

Coming Unstuck in Time

Neuroskeptic posted about this case study of two autistic young men who experience "time slips" --- extremely vivid memories, as if they are reliving the past instead of just remembering it:

CASE 1

Case 1, a male patient, was 16 years old at the time of his first visit to our hospital. He had not shown any delay in language development but had been isolated and unable to make friends since his infancy. In addition, he was extremely clumsy. He was extremely afraid of developing liver dysfunction. He had been bullied by a classmate when he was in the 8th grade; thereafter he refused to go to school and began to stay indoors. One day, he clearly recalled bullying incident that had occurred a few years earlier and re-experienced the feelings of fear and frustration as if he were once again experiencing that event. Thereafter, he often had similar experiences, even though he did not purposely intend to recall the event, and he became strongly distressed. He and his family stated that the recalled content was always the same. He thought that the distress could only be relieved by obtaining revenge on the boy who had bullied him, and he visited the boy's house with a knife. He was subsequently admitted to the emergency ward of our hospital.
...
The patient continued to experience the [time slip] even after he was hospitalized. If he saw any man with an appearance similar to that of the boy who had bullied him, he recalled the same experience of being bullied and became violent. The patient's doctor and the ward staff observed that the patient made no effort to avoid the recall stimuli but instead seemed to approach the stimuli. ...

CASE 2

Case 2, a male patient, was 27 years old at the time of his first visit. He had shown no marked clinical signs of delayed language development. However, since an early age, he had exhibited disturbed reciprocal sociality and did not have any close friendships. His interest was limited to collecting figures of comic characters. He began to be bullied during junior high school. He entered senior high school but quit during the second year. Thereafter, he tended to seclude himself at home. One day, he watched his neighbor discarding a cigarette butt in front of his home. Thereafter, he began to be annoyed by that memory. Almost every time he heard the voice of that neighbor or saw that man, he would leave his home and curse at the neighbor. His behavior became more violent and he eventually threatened the neighbor with a wooden sword. Because of this event, his family brought him to our hospital as an emergency patient.
...
In this case, an acoustic or visual stimulus (the voice or appearance of the neighbor) provoked the [time slip] resulting in the recollection of the same visual scene accompanied by the vivid emotions that he had experienced at the actual time. He took no measures to avoid remembering the event and tended to advance closer to the neighbor.

The authors of the paper observed four cases of time-slipping autistic patients in all; two of the troublesome recurring memories involved bullying at school, and two involved bad experiences with neighbors. All of the instances of time slipping that they heard about were bad; the memories triggered strong, unpleasant emotions and drove all four young people (three male and one female) to violence.

I mentioned in the comment thread at Neuroskeptic's blog that I experience this kind of vivid, immersive reminiscence --- it can be like those described in the article, where I remember being bullied or some other unpleasant experience with no buffers between me and it, but most often the things that come up are emotionally neutral, and not even necessarily episodes from my life; they might just be something I've seen before.

An example of the latter sort of memory might be my remembering, for decades, a random doodle I drew in preschool. Even now I can call it up --- a monster's face, with scraggly green teeth and a huge lumpy oval of a head. I even remember what color markers I used to draw it. I have similarly clear memories of making colored spinners out of paper plates, cutting off the edges, using a compass to bore a hole through the middle, and drawing a checkered pattern of concentric rings in contrasting colors. I would string a long piece of yarn through it, with a big, bulky knot on one end, and then spin it so that it would climb up the string and into the air, like a brightly colored UFO. This would captivate me for hours; I probably spent most of my schooldays in fifth or sixth grade doing this.

Most of these are really fragmentary, though; a single image, or a single multisensory impression. I don't really have flashbacks where I relive an incident, as the guys in the article seem to be doing. Even when I do recall an episode, it's only fragmented impressions that come back with this immediacy; the whole episode I have to reconstruct with narrative memory, as most people do.

I said on Neuroskeptic's blog that I considered my randomly retrieved archived sensory impressions to be a visual analogue to echolalia --- I hear echoes in my head of many of the things I hear, and sometimes I feel compelled to repeat them aloud; these memories are like visual echoes. However old they are, they persist, and sometimes they'll find their way into my conscious mind and I will hear the sound, or see the image, again. Even if I first saw it ten, fifteen, or twenty years ago.