Autism in Ireland: Protesting Service Cuts

Shannon Des Roches Rosa
www.thinkingautismguide.com

Updated extensively on 5/28, as the photo in question was removed from all TPGA pages by request of the parent and the photographer, so the photo-linked TPGA Facebook thread this post referred to was also removed -- and now context is needed. -SR

This photo may not mean what you think it means. So let's get that cleared up, because the Irish government is putting autism families and people with disabilities in dire straits, and that's where we need to focus.

The photo was of a little boy at a protest regarding the Irish government's cutback of in-home support services (called entitlements in Ireland) holding up a sign with his own photo and the statement "If you take away my entitlements, can you take away my autisim [sic]?

There's a chance that, like me and like many other literal thinkers, you see this sign as asking "Can you take away my autism?" and supporting a political stance that is harmful to autistic people. This kind of campaigning is unfortunately common in the United States (though I will not give such fear mongerers additional publicity by linking to them). These attitudes are contrary to TPGA's mission, and we speak out firmly against them. I protested the sign vehemently on TPGA Facebook for this reason:

It is not OK to have a child carry a poster that proclaims them broken or damaged. Not ever not ever. This is not support, this is not awareness -- this is public shaming. If you don't understand why, let's talk. -SR

But then I heard that those parents were not trying to demonize autism, and that is not what the sign is meant to say. And this is the information you need to know, and help others understand:

This protest is taking place in Ireland, where sarcasm is part of the cultural fabric -- the sign is not meant to be taken literally, but ironically -- this family believes the entitlements (supports) the Irish government is threatening to take away from Ben (the boy's name) are as much his right as his autism is a part of him. You can't take away his autism, and you can't take away his rights. This is meant to be a message of autism acceptance. (Though I hope folks understand why sarcasm can be problematic in an autism context of frequent literal thinking.)

This sign is protesting widespread Irish government cutbacks to critical services such as in-home support (domiciliary care) for autism families and people with disabilities. Trish Flood has two autistic children and was recently informed that she would no longer receive a carer's allowance for one -- she had to take the matter to High Court. Trish had this to say on TPGA's Facebook page:

"I love my children more than anything and i will do everything in my power to ensure they live happy and independent lives. [But] Without government support, we cannot keep the roof over our heads, as I cannot be a full time carer and hold a job at the same time."

From Inclusion Ireland CEO Deirdre Carroll:

“The situation for people using services is growing increasingly bleak, as services continue to be cut, and charges are introduced in areas such as respite and transport. Given the economic situation, it unfortunately looks like this will continue, which causes massive worry and stress" 

The present and future are worrisome times for people with disabilities in Ireland, and their families. Please let us know what further actions we can take to get the right messages out, and influence the people who need to be influenced.

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However, as I also wrote on the deleted FB thread, I hope Ben's family understands my concerns about the sign's long-term impact:

I think we all understand *in this thread* what the point of the sign was. That's not the issue. The problem is this photo no longer represents the family, or their cause. This photo now belongs to the Internet. You will never be able to remove it [specific instances like TPGA, yes -- in general, no], you will never be able to explain the context every time it appears. And every time someone who wants to cure autism or deny the rights or entitlements of autistic people like Ben or my son and their adults peers Googles for a graphic for an anti-autism diatribe, this photo will appear up with the caption "take away my autism." So while I understand why Ben and his family would be upset by the reaction this photo has generated -- and while I wish it never had to happen -- the potential for harm is very real, long lasting, and is bigger than hurt feelings and cultural crossed wires. -SR

And I also want to express my concern about the way autistic adults who protested the sign were treated. Also from the TPGA FB thread:

I am disturbed by the way this conversation has gone. As an autistic adult I get told to "not judge" and to "not sound so angry" all the time, usually because someone didn't understand the context or look at where I am coming from. Yet I am seeing judging, anger, et cetera [...] from people who tell me not to do this. I don't understand. Nor do I understand how sarcasm is an effective protest technique ... especially because it is hard to catch sarcasm from a sign. -KS [TPGA editor Kassiane Sibley]

Many autistic adults have indeed been bullied -- and in some cases threatened -- over their protesting of this not-at-all-clear sign (though many other folks calmly and clearly stated what the sign's intention was). Bullying and threats are never OK.

Anyone who parents or cares about an autistic child needs to think about how they'd like people to speak to their child when that child is grown. And I am writing this as a parent of a non-speaking child who receives the U.S. equivalent of domiciliary services, and as someone who would be on the front lines of the protest, were I to live in Ireland. Asking for respect is not about "severity" or whether or not one's child communicates typically. It is about rights -- the right to not be bullied or threatened as a disabled or autistic person. -SR

IMFAR 2012: NIH and IACC Overview

Susan Daniels

• Acting director of office of autism research coordination at NIH (National Institutes of Health)
• Involved in strategic planning & research at IACC (Interagency Autism Coordinating Committee)

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Dr. Daniels spoke at IMFAR about the IACC and the NIH, on the autism research landscape, and IACC research and data sharing. Any errors or omission are on yours truly. -SR

IACC (Interagency Autism Coordinating Committee)

IACC background: formed under Combating Autism Act of 2006 (CAA) with the goal of accelerating the pace of autism research, and coordinating it as well. The CAA expired Sept 2011, but has been reauthorized.

The IACC consists of Federal and Public members (click photo to enlarge):

List of IACC members, new members are red

The IACC Mission (from the official site, iacc.hhs.gov)

• Provide advice to the Secretary of Health and Human Services regarding Federal activities related to autism spectrum disorder.

• Facilitate the exchange of information on and coordination of ASD activities among the member agencies and organizations.

• Increase public understanding of the member agencies' activities, programs, policies, and research by providing a public forum for discussions related to ASD research and services.

IACC Responsibilities include:

• Advise Department of Health and Human Services Secretary Kathleen Sebelius
• Establish Autism Research Priorities
• IACC strategic plan for ASD research
• Monitor federal activities and monitor research trends
• IACC ASD Research Portfolio analysis
• Communicate advances in the field

IACC Strategic Plan

• The IACC does not fund research
• Resarch Questions in the IACC plan include:
• Diagnosis, biology, treatments, services, lifespan issues*, infrastructure, Data Sharing and surveillance, etc.

Next meeting will be July 2012 - Stay Tuned for details!

• Will be announced on IACC website, listserve, and Twitter
• The IACC welcomes public comments!

More info about the IACC: all public at www.iacc.hhs.gov.

*Lifespan issues used to be a subset of services, but has been broken out because they are separate, important issues.

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NIH (National Institutes of Health) Autism Efforts

Upcoming in 2012: Analysis of 2010 autism spectrum disorders research portfolio across both federal agencies and private organizations.

2010 Total funding across federal & private funding: 480M (Private = $74 M, Fed = $334 M). This is not all more spending, it's better tracking, detailed data from HHS and Dept of Education. Private funding remained similar to 2009 level.

NIH has steadily increased  autism research funding since 1996, though now is plateauing with tight budget times. Compared to diseases, autism research has been on the upswing.

NIH Autism Centers of Excellence

• Encompass centers and networks,
• Foster collaboration between teams of specialists at same facility
• Networks consist of researchers at many facilities

NDAR: National Database for autism research (ndar.nih.gov)

• Contains data from over 25K subject, 200K data elements.
• Data: Imaging, phenotype, genomic, gender, etc. related to human subjects.
• Primary message: We need to build a culture of data sharing to advance autism research!
• If everyone is sharing, then everyone can benefit.
  
• Especially important in this time of tight budgets. 
• Accelerates progress.

NIH Director Tom Insel says: Be smart, share your data -- it will help protect your own research.

IMFAR 2012: Evans - Structural Connectivity in Neurodevelopment

Dr. Evans was a keynote speaker at IMFAR 2012. His talk centered around the work that is being done based on the data collected from the longitudinal study of normal brain development at NIH. He spoke extensively about correlates that can be read from the data, for example, the relationship between cortical structure and things like IQ and testosterone levels. It would be impossible to capture the incredible amount of information in 140 character bites, but as an outline, we hope it can give you a starting point for further research. Errors, omissions and misspellings are mine.-JBM

IMFAR 2012 Roundup: Genetics of Autism and Animal Models

Emily Willingham
www.ThinkingAutismGuide.com

Caveat: All findings discussed here were presented at a conference and have not undergone peer review.

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What is the use of animal models?

I understand the use of animal models like mice to figure out how gene changes affect outcomes in a whole animal, rather than, say, in cells in a dish. I’ve used them myself. Knocking out a gene of interest in a mouse strain, applying an environmental exposure of interest, observing the behavior of the mouse involved -- these tactics can be revealing, sometimes. Say a mouse with a nonfunctioning partner in a gene pair shows a specific behavior -- like vocalizing less to its mother -- and maybe we can interpret that in human terms as being inhibited social communication and assume the gene in question is involved.  The idea is that observing changes linked to the absence or overabundance of a particular gene product can help us home in more on that gene, see what its usual job is and in what pathways, and determine if it could rationally be linked to the human condition in question--in this case, autism.

Studies like this are called “mechanistic” studies because they are the scientific version of opening up the hood and checking the different working parts to see what their function is. Adding a part or taking away a part can often tell us quite a bit about what that part does, what its mechanistic role is in the whole. But I’m feeling a little jaded about animal models in autism because of the genetics and genomics data I saw presented at the conference. With a few exceptions, nothing seems to have emerged as a clear new contender for knocking out or otherwise manipulating in mice. Some of the usual suspects, like SHANK, were there. But the genome-wide association studies, intended to examine a genome for changes associated with a disorder or other condition, are not kicking out a lot of obvious single candidates for genes associated with autism. It’s almost looking like we’d have to make about a thousand animal models of autism to tease out various associations between a gene change and a specific autism-related endpoint.

Genetics and genomics

What studies are kicking out is a mix of information that’s conflicting, suggestive, intriguing, and requiring a lot more refinement. I saw data implicating genes specific to neuronal development or connectivity and data suggesting genetic and biological marker overlap with autism and schizophrenia (and then one suggesting no common, shared gene variants between the two), but possibly tracing to different changes in the genes relative to each condition. The most interesting genetics-related talk I saw referenced microRNA, the tiny molecules in the cell that get to a gene product before the cell can actually use it, and silence it. They’re like the molecular hitmen of the cell. More microRNA generally means less functional product of a given gene. The implication? A gene sequence may be intact and unchanged, but if the microRNA is more abundant, it could be interfering with the pathway well after the gene in question has already completed its work. It is regulation beyond the gene.

Another finding of interest related to maternal genes and their influence in the development of autism. These “maternally acting gene alleles” or MAGAs, have been linked to a number of disorders, including autism, and one conference presentation described using genome-wide association to identify MAGAs potentially involved in autism. That’s an intriguing path to follow.

Awhile back, everyone got pretty excited about genome-wide association studies. These broad-scale but fine-grained analyses were supposed to compare genomic changes between populations and pull out differences that were population specific. The great hope was that these studies would find the needles in the haystack of human gene sequences. Based on what I saw at the conference, in many cases, they’ve just added to the haystack of genes and gene variants implicated autism. On the one hand, given how clearly multifactorial autism is and how little evidence there is for a single gene or even a few genes to be associated with all instances of it, it makes sense that these studies would have confusing results. On the other hand, genome-wide association studies haven’t yielded the clearly writ signposts pointing out research directions that everyone had hoped they would, with some exceptions that apply to a limited segment of the autistic population. That’s not to say we should abandon them. It may be that to really pull the signal from the abundant noise, the number of replications and studies will need to approach biblical proportions before we can see the same candidate genes emerging repeatedly.

Another great hope for tracing the genetic factors of autism was copy number variation (CNV), and that remains in the running. As the name implies, the number of copies of a given DNA sequence can vary from person to person, and sometimes, a difference in copy number can be linked to an outcome, like autism -- and sometimes not. Some of the presentations at the conference offered hints that an accumulation of differences in the genome might be more relevant in autism than one specific gene variant or CNV.

Epigenetics is hot in autism research, as it is in seemingly every other relevant research field. The term refers to the chemical tagging of DNA that either silences the sequence that is tagged or causes it to be used more often. Environment can affect this tagging, so much so that identical twins essentially become quite different in their genetic expression through life, not because their actual gene sequences change, but because lifestyle differences result in different tagging patterns on the DNA. Their sequences are the same, but what they use of those sequences can become quite different. Results in epigenetics studies were mixed and often just the beginning of the adventure. This field looks wide open and poised to complicate autism research even more.

Suggested Directions

The genetics of autism are of interest to me primarily because pinpointing gene variants, gene silencing, and copy number variation as being associated with autism largely extends the host of studies establishing the primarily genetic nature of autism. That’s a purely scientific interest. But with the big analyses, there seems to be a whole lot of noise in the results without much to latch onto. What we need is for genetics studies to focus on the behavioral endpoints of autism that most negatively affect an autistic person’s quality of life. What are the genetic links, for example, to autistic people who engage in self-injurious behaviors? What are the genetic links among autistic people who are nonverbal (some hints here, perhaps)? Most of the populations in these studies are not stratified to that level--they simply include autistic people generally or are divided -- still -- into “low-functioning” and “high-functioning” individuals, which precludes homing in a specific gaps that both groups may share, another draw back of relying on these “functional” divisions.

A few studies at the conference involved efforts to link genes and outcomes, or phenotypes, and even to use this knowledge therapeutically. I’d like to see a lot more of this greater specificity in these analyses because overall, I don’t see “curing” autism as a realistic or even desirable goal, but addressing gaps is both. In addition, the clear heterogeneity of the condition along with still significant overlaps among populations as researchers currently divide them does nothing to clarify all the noise in the results. Rather than taking autism as a complete entity, I’d like to call for research to home in on specific features that directly and negatively influence quality of life of autistic people or even other populations that share these gaps and look for the mechanisms and pathways associated with them. I am not alone in this idea. At the most, a more focused approach could lead to real interventions for the actual negatives associated with autism without necessarily effacing the positives. At the very least, it could save the lives of a whole lot of mice.

Next from Emily: Research with “human subjects,” the research that deserves a “Most Pointless Award,” and why Simon Baron-Cohen (yes, it’s true) may have presented the most interesting results at this conference

IMFAR 2012: Highlights & Takeaways

Shannon Des Roches Rosa
www.ThinkingAutismGuide.com

TPGA editors at IMFAR 2012

We had a great time at IMFAR; it was important that TPGA be present, given our mission to support evidence-based autism information. I wish more autistic people and people whose lives include autism -- personally or professionally -- would or could attend. We'll keep posting summaries and insights for those of you who couldn't go. Here are my general observations and takeaways.

IMFAR 2012 's goal was to present the newest research conducted over last year, with a particular effort to include presenters from outside autism science whose research overlaps with or has implications for autism. This may be why the science often, though not always, seemed a bit softer than 2011. With the result that in some panels, I would just … stop typing after a while, because it was clear the material would not be terribly useful to TPGA readers. (Though some breakout sessions like the Anxiety panel were better than anything I heard at IMFAR 11 -- we'll be reporting on that panel in depth.) 

Sometimes the science elicited an "Oh please no," as when Ruth Feldman's keynote on Bio-Behavioral Synchrony and the Development of Social Reciprocity. When Dr. Feldman started talking oxytocin and points like:

• The evolution of mammals implies that bio-behavioral synchrony is learned within the "nursing dyad" and the context of mother-infant proximity.
• Synchrony spans the period of early gestation to weaning: in humans early pregnancy to the end of the first year.
• Postpartum maternal behavior is a species-specific repertoire that is needed for growth and development.
• There are two mammalian mechanisms by which the social context impacts the infant's physiology, both of which rely on tactile interactions.

...then even Geri Dawson, Autism Speaks Chief Science Officer, remarked afterward that she too was worried about Feldman dragging us back into Refrigerator Mother territory. Thankfully Feldman stated unequivocally, later in the talk, that while kids with chronic exposure to depressed mothers have higher levels of psychiatric disorders and lower levels of social engagement and empathy, there is no evidence linking maternal depression to autism. However she proposed that oxytocin can have a buffering role.

It seemed reasonable that we encountered much eyebrow-raising science, given that IMFAR generally features pre-peer-review material. We encourage you to keep this qualification in mind as our IMFAR posts appear.

As mentioned in our Press Conference summary, INSAR encouraged autistic people and other community stakeholders to participate at IMFAR 2012, as volunteers, etc. However there was no method for identifying Autistic people at the conference, other than as Stakeholders. And as many of us know, you can't necessarily tell if someone is autistic by looking at or talking with them.

I understand some autistic folks not wanting to identify themselves publicly, but it seems a conference about autism and Autistic people should at least promote the option to do so. (TPGA contributor and self-advocate Corina Becker took matters into her own hands by writing  "AUTISTIC" with an arrow pointing to her name, on her badge.)

We also heard, repeatedly, that many autistic people who would have liked to attend IMFAR weren't able to do so because the conference is really, really expensive. Though there are ways to partially or fully cover costs -- attending as a member of the press, ASF travel grants, INSAR's own IMFAR travel grants -- according to Corina Becker:

"IMFAR [is] financially inaccessible to lots of autistics. I'm going to be in debt for a while [...] I think that the only way I got to IMFAR was due to the fact that it was so local and I do have the privilege of having a credit card, a job, and various other financial resources (I'm working on selling artwork and bracelets locally). I understand that these are privileges that not every one has, and it causes autistics to not be able to attend research meetings.

"However, I think it's not just research meetings like IMFAR that we need to have meaningful inclusion with, but also in participating to conduct research. That being said, IMFAR has been a great chance for me to engage young research students in discussion and I made sure to bring up autistic inclusion in conducting research. From the response I received, most of those I talked to were very enthusiastic about it and my suggestions for the direction of their research."

How many autistics can you count?
(Note that Mr. Shore's answer may be different than yours.)

It was surreal to be sitting among autistic people while, as Estée Klar noted, most researchers spoke to the audience as "us" and about autistics as "them." Our group often handled this disconnect by cackling uncontrollably (to the point where we fretted about being tossed from the panels. Still, I hope the researchers heard us). And irony abounded, as when Marjorie Solomon talked about autistic people having unique strengths, like being less judgmental, and TPGA editor and self-advocate Carol Greenburg judged her with a pronounced eyeroll.

TPGA Science Editor Emily Willingham has specific comments about the oft-flawed relationship between autistics and autism science, with suggestions for improvement:

"Scientists generally seek collaborators out for their expertise in a particular area, and autistic people are the experts, particularly for behavioral/behavior interpretation and qualitative studies of autism, which is where I saw a whole lot of "othering" at this conference. In addition, autistic collaborators would be of great benefit in results interpretation for genomics and genetic studies and even translational studies, as they can provide insights that a neurotypical mind might overlook. I personally found a lack of autistic collaboration in many studies where it clearly would have helped, not to mention an overall impression that many, many researchers are so distanced from their "subjects" or the population they're evaluating that they end up infantilizing, othering, and marginalizing them with their language and interpretations without even realizing it."

Autism researchers should also read the Autistic Self-Advocacy Network's Operational Policy on Research Inquiries. Excerpt:

The Autistic Self Advocacy Network welcomes opportunities to assist researchers with grant proposals and research projects that utilize Community Based Participatory Research (CBPR or PAR) methodologies. The CBPR approach brings together professionals and community members to serve as equal partners throughout the research process, focusing on research that is relevant to the community.

Self-advocate Stephen Shore stood up at the Stakeholders' lunch and talked about this kind of meaningful inclusion for Autistic people. As many of the people who make IMFAR happen were in the audience, I hope they listened to and absorbed Stephen's message.   

I was also extremely pleased when Wrong Planet's Alex Plank interviewed Corina Becker -- Corina had much to say about autistic people and inclusion, and her interview video will round out Wrong Planet's channel nicely.

Carol Greenburg & Alex Plank talk to Simon Baron-Cohen

Our editors and contributors were constantly engaging with researchers and influencers regarding inclusion and other TPGA mission matters, and having intense discussions all over the conference -- Carol with Simon Baron-Cohen and Autism Speaks's Dana Marnane, Emily with John Elder Robison, Shannon and Jen with DSM-5 task force chair Sue Swedo -- to whom we gave a copy of the TPGA book, and whom we think could gain much insight from reading our TPGA Slice of Life series. Several discussions led to interview agreements that we believe will enrich this site and your brains.

I came away from IMFAR with a renewed desire to see more non-scientists attend -- not just autistics from outside the research community, but anyone with a deep autism connection, whether personal or professional. It is crucial to forge connections with autism researchers, because insurance companies, schools, and policy makers rely heavily on those researchers' findings. So it was wonderful to see the Boston Higashi School's Executive Director Michael Kelly and Principal Deborah Donovan attending IMFAR. Sadly, word on the street is they're the exception rather than the rule. I'd like to see that change. And hopefully more inclusion and attendance opportunities will be available for next year's IMFAR 2013 conference in San Sebastián, Spain.

IMFAR 2012: Decompression Interlude

We'll be posting about IMFAR 2012 over the next week or so, once we all catch our breath. In the mean time, see if you can identify the four people in this photo, which was taken when said folk peered over an iPad after nearly an hour of intense discussion. (Hint: All four have contributed original writing to this site.)

IMFAR 2012: An Update on the ASD DSM-5 Recommendations

Sue Swedo M.D. 
Chair, DSM-5 Neurodevelopmental Disorders Workgroup

An Update on the DSM-5 Recommendations for Autism Spectrum Disorder and Other Neurodevelopmental Disorders

We spoke with Sue at length both at the IMFAR Stakeholder's lunch, and after her IMFAR talk. Any errors or omissions in this summary of her talk are on TPGA. -SR

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The goal of the new DSM-5 is clearer criteria, changing all PDDs (Pervasive Developmental Disorders) to ASDs (Autism Spectrum Disorders). This is group's thoughts on what they are and are not concerned about.

In addition to 11 full time members of DSM 5 task force, they have 2 dozen advisors. It's been a five-year process. She's deeply appreciative to all of her colleagues.

They never expected to be making headlines, the DSM is a bit dry if you sit down and read it. They were shocked when the headlines became about stealing services from 2/3 of the people with autism, when they were being accused of fudging numbers to make diagnoses go away. But their intention: Do no harm, do NOT overlook individuals with ASD.

It is not their intent for Aspergers' folk to be removed from the DSM-5. There will be no subtype for Asperger's as there is in the DSM-4, but there will be a number of specifiers to help identify affected subjects.

DSM-5 is really not that different from DSM-4. But they are trying to improve diagnosis sensitivity, especially for older kids & young adults, women, underserved and minority populations. It is possible that under the new criteria, the number of individuals with autism will actually increase.

Requires impairments that interfere with functioning. Trying to avoid people getting "mild" diagnoses and then agencies, schools, insurance thinking that those ASD folks don't need support.

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Recommendations for Changes to the PDDs

• Three diagnoses will become two: 
• Social communication
• Restricted & repetitive interests
• Rett disorder and other etiology subgroups will be described by use of Specifiers: Associated with Know Medical or Genetic Condition or Environmental Factor.
• PDD will be replaced by ASD
• Individual diagnoses will be merged into a single, behaviorally defined disorder*

*Has resulted in most controversy, push back etc.

Bottom line: Can't distinguish on basis of DSM-4 between ASD & Asperger's. In DSM-4 Asperger's should be more significant than ASD -- has significant impairments, ASD has qualitative impairments

Sensitivity & specificity of proposed DSM-5 diagnostic criteria for ASD

Rememeber that current DSM5 criteria are *recommendations*. New DSM hasn't been written yet.

In head-to-head comparison, DSM-5 is more inclusive -- it picks up more individuals than short list of specific behaviors -- junior high schoolers, college students, etc.

Some folks say we'll be picking up fewer toddlers with new DSM-5 criteria. But this has to do with timing of onset: Symptoms may not fully manifest in a child until social pressures exceed capacity. May not happen until they are older.

Decision not to include Asperger's

• Lack of specificity & sensitivity in separating ASD diagnoses.
• Lack of accurate historical information about very early language development puts emphasis on current speech (trainable) e.g., monologue about Pokemon is not conversation
• Overlap in samples when VIQ (Verbal IQ) controlled
• Considerattion of access to services

Specificities

• Severity of ASD symptoms
• Pattern of onset and clinical course
• Etiologic factors
• Associated conditions
• Individual weaknesses and strengths

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Swedo said it hurt like hell when she was accused of trying to hurt kids & adults with autism by trying to deny them services. Her team started this five-year process with the caveat of "first do no harm." With the goal that people with Asperger's would remain eligible -- but also "wanted to give consideration for 'Aspies' who don't want to be diagnosed."

DSM5 task force continuing to do work, the are meeting again in June.

Question from the audience for Task Force Team

Q: Did screeners get same results from DSM-4 & DSM-5?

A: Mostly, Handful missed by each test -- but may be explained by changes in behavior w age.

DSM-4 not the gold standard for ASD diagnosis, if it was, Swedo & task force wouldn't have been asked to fix it. Have been working on this for over 5 years now, haven't yet done own prospective data collection -- will now look at that to establish validity.

No point in using DSM-3 or DSM-4 data/diagnoses -- need to rediagnose folks with DSM-5 criteria, and expert clinical judgement. Make sure descriptions are rich enough to provide descriptors of function across the lifespan AND spectrum.

Q for Swedo from transgender self-advocate: Concerned that task force will be erasing Asperger's identities by erasing diagnoses. Asperger's made her a success, not a burden. Many folks will feel lost, in limbo, without Asperger's diagnosis. Implores Swedo directly to not remove from #DSM5

A: Swedo says DSM-5 will not remove Asperger's, will be retained in rich, detailed specifiers. Asperger's will be a specifier. But not a subtypes, e.g., PDD-NOS will be removed as well. All will be "autism."

Q: Will loss of Asperger's diagnsosis make things problematic with insurance companies?

A: Mostly, up to insurance companies. But they're hoping for a smooth transition with the new, clearer criteria, in changing all PDDs to ASDs
   
Geri Dawson came to the mic and made a statement: How will this affect prevalence? Dawson says we don't know, but AS is funding study with CDC where prospectively will be comparing DSM-5 against DSM-4, and how this will affect prevalence and case identification -- based on case records, hopefully this will answer some of these questions as we make this transition, provide continuity. (Dr. Dawson noted afterward that this study is in the process of being board approved.)