Tag: genetic

First Large-Scale Study of Universal Screening for Autism Raises Critical Questions about Accuracy, Equity

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Researchers urge continued screening for all toddlers, while recommending changes to M-CHAT screening method to improve accuracy, address disparities

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Newswise — Philadelphia, September 27, 2019 –

In the first large, real-world study of universal screening for autism spectrum disorder (ASD) in toddlers, researchers at Children’s Hospital of Philadelphia (CHOP) have found that the most widely used and researched screening tool is less accurate than shown in previous studies conducted in research laboratory settings. The new study also revealed significant disparities in detecting early autism symptoms in minority, urban and low-income children. The findings were published online today in the journal Pediatrics.

The American Academy of Pediatrics (AAP) recommends screening all toddlers for ASD at their 18- and 24-month primary care check-ups using the Modified Checklist for Autism in Toddlers with Follow-Up (M-CHAT/F), a two-stage parent survey to determine whether a child may have autism, with the follow-up designed to eliminate false positives. However, most studies to evaluate the accuracy of the M-CHAT/F have been conducted in research settings rather than in real-world clinical settings. Therefore, very little was known about screening in the recommended primary care setting, nor about longer-term outcomes for children who screened negative on the M-CHAT/F. The CHOP study is the first to look at outcomes of truly universal screening in a real-world primary care setting.

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“As part of a large pediatric network implementing universal screening, we found ourselves in a unique position to find answers to critical questions about the accuracy of the M-CHAT, and to determine how many children are missed by early, universal screening,” said lead author Whitney Guthrie, PhD, a clinical psychologist specializing in early diagnosis at CHOP’s Center for Autism Research. “Early intervention has been shown to improve outcomes, potentially into adulthood. We know that early and accurate screening and diagnosis is the crucial first step in helping children access those effective, autism-specific therapies.”

The CHOP research team studied the electronic health records (EHR) of 25,999 patients screened in primary care using the M-CHAT/F between the ages of 16 and 26 months, and systematically followed these children until 4 through 8 years of age using the EHR. Ninety-one percent of these children were screened using the M-CHAT/F, meaning that nearly universal screening of all children in primary care was achieved.

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The study showed that the M-CHAT/F detected only about 40% of children who went on to be diagnosed with ASD. However, children who screened positive were diagnosed seven months earlier than those who screened negative, suggesting that early screening may facilitate early intervention. Overall, 2.2% of children in the study were ultimately diagnosed with ASD, which is consistent with the Centers for Disease Control and Prevention (CDC) estimates nationally.

“Although our findings reveal significant shortcomings in current screening tools, we want to be clear that we are not recommending that pediatricians stop universal screening,” said Guthrie. “Instead, clinicians should continue to screen using the M-CHAT/F, while being aware that this screening tool does miss some children with ASD. Any clinical or parental concerns should be taken seriously, and warrant continued surveillance even if a child screens negative on the M-CHAT/F. And of course, a screen positive on the M-CHAT/F warrants referral so that children with ASD can be diagnosed and receive early intervention.

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“Pediatricians should also be aware of disparities in screening practices and results in children of color and from low-income backgrounds.”

The CHOP study found that the 9% of children who did not receive screening at 18 or 24 months were disproportionately from racial minority groups; from non-English speaking households; and from households with lower median income and who receive Medicaid. When screening was administered, these same children were more likely to receive a false positive result. The M-CHAT was also less accurate in girls than in boys.

“Persistent racial and economic disparities in autism screening and diagnosis are a cause for great concern, and are consistent with previous research showing that black and Hispanic children tend to be diagnosed years later than white children,” said co-author Kate Wallis, MD, MPH, a developmental pediatrician and researcher at CHOP’s PolicyLab who is also studying disparities in referrals for autism services. “This study revealed important limitations and provides us with new knowledge that we can use to make critical improvements to autism screening tools and screening processes, so pediatricians can properly detect and support more children with autism and reduce disparities in diagnosis and care.”

Guthrie et al, “Accuracy of Autism Screening in a Large Pediatric Network.” Pediatrics, online 27 September 2019. DOI: 10.1542/peds.2019-0925.

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About Children’s Hospital of Philadelphia: Children’s Hospital of Philadelphia was founded in 1855 as the nation’s first pediatric hospital. Through its long-standing commitment to providing exceptional patient care, training new generations of pediatric healthcare professionals, and pioneering major research initiatives, Children’s Hospital has fostered many discoveries that have benefited children worldwide.  Its pediatric research program is among the largest in the country.  In addition, its unique family-centered care and public service programs have brought the 564-bed hospital recognition as a leading advocate for children and adolescents. For more information, visit http://www.chop.edu

Sex, Lies, and Autism Research

 

How can we get tangible benefit from the millions we spend on autism science?.
Posted Nov 12, 2017

The U.S. government is the world’s biggest funder of autism research.  For the past decade I have had the honor of advising various agencies and committees on how that money should be spent. As an adult with autism, sometimes I’ve been pleased at our government’s choices. Other times I’ve been disappointed. Every now and then I turn to reflect: What have we gotten for our investment?
Autistic people and their parents agree on this: The hundreds of millions we’ve spent on autism research every year has provided precious little benefit to families and individuals living with autism today. Over the past decade the expenditures have run into the billions, yet our quality of life has hardly changed at all.
It would be one thing if massive help was just around the corner, but it’s not. There are no breakthrough medicines or treatments in the pipeline. Autistic people still suffer from GI pain, epilepsy, anxiety, depression, and a host of other issues at the same rates we did before any of this research was funded.
I don’t mean to suggest that nothing has been accomplished.  Scientists have learned a lot. They know more about the biological underpinnings of autism. Researchers have found hundreds of genetic variations that are implicated in autism. We’ve quantified how autistic people are different with thousands of studies of eye gaze, body movement, and more. Scientists are rightly proud of many of their discoveries, which do advance medical and scientific knowledge. What they don’t do is make our lives better today.
Why is that?
In the past I’ve written about the idea that taxpayer-funded research should be refocused on delivering benefit to autistic people. What I have not written about, is why that hasn’t happened, at the most fundamental level.
The answer is simple: Until quite recently, autistic people were not asked what we needed.
There are many reasons for that. Autism was first observed in children and no one expects children to have adult insight and self-reflection. When autism was recognized in adults, they were assumed to be too cognitively impaired to participate in conversations about their condition. Finally, in the spirit of the times, doctors often assumed that they knew best. They were the trained professionals, and we were the patients (or the inmates.)
So doctors studied every question they could imagine, and then some, seldom seeking our opinions except in answer to their research questions. They assumed they knew what “normal” was, and we weren’t it. Countless million$ went down the rabbit hole of causation studies, whether in genetics, vaccines, or other environmental factors. Don’t get me wrong—the knowledge we’ve gotten is valuable for science. It just did not help me, or any autistic person I know.
Millions more have been spent observing us and detailing exactly the ways in which we are abnormal. Only recently have some scientists began to consider a different idea: Perhaps “normal” is different for autistic people, and we are it. Again the studies enhanced the scientists’ knowledge but didn’t do much to help us autistics.
Then there are the educators and psychologists. They observed our “deviations” and then considered therapy to normalize us. That led to ABA and a host of other therapies. Some of those have indeed been beneficial, but the money spent on beneficial therapy is just a drop in the bucket when considering what we taxpayers have funded overall.
Want a different and better outcome? Ask actual autistic people.

We can tell you what our problems are, in many cases very eloquently. I’m not going to re-state all our needs here. I’ll tell you this: Whenever this topic comes up at IACC (the Federal committee that produces the strategic plan for autism for the U.S. government), the priorities of autistic people seem rather different from those of the researchers our government has been funding for so long.
Autistic people have many disparate needs, but they all boil down to one thing: We have major challenges living in American society. Medical problems, communication challenges, learning difficulties, relationship issues, and chronic unemployment are all big deals for us.  The issues are well laid out and many.
Before autistic people began speaking out in great numbers, all we had was parent advocacy. We should not dismiss that, and parents still have a role today, particularly in advocacy for small children and children who are older but unable to effectively advocate for themselves.
Even as we thank parents for their service, it’s time to recognize autistic voices (some of which belong to parents too) should be taking the lead.
As much as parents did for us, they also unwittingly contributed to harm. Parents misinterpreted harmless stimming, and encouraged therapists to suppress it, leaving us scarred in adulthood. Many autistics of my generation remember being placed into programs for troubled children with parental encouragement in hopes we’d become “more normal.” We didn’t. Parents have given us bleach enemas, and some of us have died from misguided chelation and other treatments to “cure” our autism.
I don’t blame parents for any of that. They did their best, given the knowledge of the day. But it’s a different day now. The children who grew up being “normalized” can talk about how it affected them, and parents and clinicians of today would be wise to listen.

Autistic voices are finally speaking in large numbers and it’s time to pay attention. No one else knows life with autism. Parents and nonautistic researchers are sometimes listening. Hard as this may be for them to hear, they are always guessing. With autistics speaking out all over the world, that’s no longer good enough.
For the first time, IACC has recognized this in the 2017 Strategic Plan Update. They say it’s time for a paradigm shift in how we do research. We need to focus on the needs of people living with autism today. That’s a realization that I appreciate, and it’s long overdue.
So what’s the answer to why we’ve gotten so little return on our autism research investment: No one asked the autistic people what we wanted. It’s that simple. Had we been able to articulate our challenges, with the framework of knowledge we have today, and had we been listened to, we’d be in a very different place today.
Today is gone, but tomorrow isn’t here yet, and it can be different.
(c) John Elder Robison
John Elder Robison is an autistic adult and advocate for people with neurological differences. He’s the author of Look Me in the Eye, Be Different, Raising Cubby, and Switched On. He serves on the Interagency Autism Coordinating Committee of the U.S. Dept. of Health and Human Services and many other autism-related boards. He’s co-founder of the TCS Auto Program (a school for teens with developmental challenges), and he’s the Neurodiversity Scholar in Residence at the College of William and Mary in Williamsburg, Virginia, and a visiting professor of practice at Bay Path University in Longmeadow, Massachusetts.
The opinions expressed here are his own. There is no warranty expressed or implied. While reading this essay will give you food for thought, actually printing and eating it may make you sick. 

 John Elder RobisonJohn Elder Robison is the author of Raising CubbyLook Me in the Eye, My Life with Asperger’s, and Be Different – adventures of a free range Aspergian.  John’s books are sold in a dozen languages in over 65 countries. 

Neuroscientists Decrypt the Mystery of Rapid Eye Movements

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504, Leonardo da Vinci made wax castings of the brain and coined the term “cerebellum (link is external)” which is Latin for “little brain.” A groundbreaking study released today reports that Purkinje cells (link is external) in the cerebellum are responsible for controlling the accurate execution of rapid eye movements. Coincidentally, da Vinci also painted the Mona Lisa, which is world-renowned for appearing to have roving eyes that follow viewers around the Louvre. 
My father, Richard M. Bergland, was a neurosurgeon, neuroscientist, nationally ranked tennis player, and author of The Fabric of Mind (Viking). My dad was obsessed with Purkinje cells and the cerebellum. He passed this obsession on to me.
In 2007, my father died unexpectedly of a heart attack leaving his quest to find some type of “holy grail” in neuroscience incomplete. I made a vow at his funeral that I would pick up the torch and try to find answers to his hypotheses about Purkinje cells and the cerebellum. Every morning, I wake up hoping there will be new research that helps to decrypt the mysteries of the cerebellum. Needless to say, I was thrilled to read about the new study on eye movements and Purkinje cells released this morning.

Ramón y Cajal/Public DomainPurkinje Cells in the Cerebellum Control Rapid Eye Movements  

Purkinje cell illustration by Ramón y Cajal.
Source: Ramón y Cajal/Public Domain

The October 2015 study, “Encoding of Action by the Purkinje Cells of the Cerebellum (link is external),” was published in the journal Nature. The researchers found the combined neuronal activity of two seemingly opposite types of Purkinje cell in the brain’s cerebellum appear to control quick eye movements known as saccades.
In a summary of the findings, the editors describe this study saying, “The Purkinje cells are inhibitory neurons in the cerebellum with a central role in coordinating the body’s motor function. It has long been thought that they encode eye motion saccades, but how this is achieved was not known.
Recording from Purkinje cells in monkeys, David Herzfeld et al. find that the combined simple-spike responses of bursting and pausing Purkinje cells, but not either population alone, predicted the real-time speed of the saccade. Moreover, when Purkinje cells were organized according to their complex-spike field, the population responses encoded both speed and direction via a gain field.”
Purkinje cells are named after Johannes Purkinje, who first identified these neurons in 1837. Dr. Purkinje was also the first person to identify the individuality of the human fingerprint. Among many other duties, Purkinje cells are responsible for communicating sensory motor information from the cerebellum to the cerebral cortex.

The Cerebellum Is a Primal Powerhouse

Wikimedia/Life Sciences Database
The cerebellum (red) is only 10% of brain volume but houses over 50% of the brain’s total neurons. 
Source: Wikimedia/Life Sciences Database

The cerebellum is one of our most ancient brain regions. From an evolutionary perspective, the ability to hone in on a target and focus one’s gaze as hunters was necessary for killing prey. The cerebellum is a primitive and intuitive brain region that we relied on to target moving prey with a bow and arrow, or a spear.
Over millenia, both hemispheres of cerebellum have evolved to work seamlessly with both hemispheres of the cerebrum (link is external) to create peak human performance. From an athletic perspective, the cerebellum makes it possible to simultaneously run while locking your eyes onto a moving target. The cerebellum is the primary brain area associated for hand-eye coordination used when catching a baseball, hitting a tennis ball, shooting a hockey puck, etc.

Diagram of the Vestibulo-Ocular Reflex (VOR)
Source: Wikimedia/Creative Commons

Wikimedia/Creative CommonsWhen you shift the direction of your gaze, your head and eye movements are automatically coordinated with each other via the vestibulo-ocular reflex (link is external) (VOR) which is a part of the vestibular system connected to the cerebellum. The VOR is a reflex eye movement that stabilizes images on the retina during head movements by automatically producing an eye movement in the opposite direction of the head movement.
My father often said, “Of this I am absolutely certain, becoming a neurosurgeon was a direct consequence of my eye for the ball.”  When my dad spoke of having an “eye for the ball” he was referring to his VOR system.
The vestibulo-ocular reflex needs to work very quickly to maintain clear vision and focus. Head movements must be compensated for almost immediately—otherwise, your vision would look like a video taken with a shaky hand or in motion. Hypothetically, abnormalities of the VOR would make the world a very disorienting place, as might be the case in people with autism spectrum disorder.
As this most recent study illustrates, the execution of accurate eye movements depends critically on the cerebellum. The combined neuronal activity of two seemingly opposite types of Purkinje cell in the brain’s cerebellum was recently found to control the jerky eye movements known as saccades in monkeys by David Herzfeld et al.

What Is a “Saccade”?

Africa Studios/Shutterstock
Source: Africa Studios/Shutterstock

A saccade is a quick, simultaneous movement of both eyes between two phases of fixation in the same direction. As visual information is received from the retina it is translated into spatial information and then transferred to motor centers for appropriate motor responses.
We rely on the accuracy of saccadic eye movements every millisecond of our lives. During normal day-to-day conditions, you make about 3-5 saccades per second which amounts to about a half-million saccades a day.
Someone with saccadic dysmetria produces uncontrollable eye movements including microsaccades, ocular flutter, and square wave jerks even when the eye is at rest. The cause of dysmetria is thought to be lesions in the cerebellum or lesions in the proprioceptive nerves that lead to the cerebellum. Your cerebellum is responsible for the coordination of visual, spatial and other sensory information with motor control.

What Is the Link Between Purkinje Cells, Eye Movements, and Autism? 

Source: Petr Novak/Wikimedia Commons

Petr Novak/Wikimedia CommonsRecently, there has been a groundswell of research linking Purkinje cells, the cerebellum, and autism spectrum disorders (ASD). The recent findings by Herzfeld et al add to a growing body of evidence that potentially correlates abnormalities of Purkinje cells with autism. Although the recent study by Herzfeld doesn’t refer to autism specifically, the latest findings on the role of Purkinje cells in controlling eye movements supports previous research linking the eye movements, the cerebellum, and autism.
In autism spectrum disorders, the brain consistently shows defects in Purkinje cells, which have a single axon that projects from the cerebellum and creates connectivity from the cerebellum to most other brain regions. Previous research has found cerebellar dysfunction in people with ASD through postmortem studies of brain samples that showed loss of Purkinje cell volume. Over the past few years, a variety of studies have confirmed this phenomenon in the majority of autistic brains.
A 2013 study (link is external), published in the journal Nature, found that eye contact during early infancy may be the earliest indication of ASD. Babies typically begin to focus on human faces within the first few hours of life. Children with autism, however, don’t exhibit interest in making eye contact which makes it difficult to read faces. Learning how to pick up social cues unconsciously by paying attention to another person’s eyes is key to social connectivity.
Another study from August 2013 found that atypical visual orientation in 7-month-olds could be a sign of risk for autism. The study titled “White Matter Microstructure and Atypical Visual Orienting in 7-Month-Olds at Risk for Autism (link is external)” was published in American Journal of Psychiatry. White matter in the corpus callosum connects the left and right hemispheres of your cerebrum.
In 2014, researchers reported that the whites of our eyes communicate important social cues that are key to our bonding and survival both at a conscious and subconscious level. The study, “Unconscious Discrimination of Social Cues from Eye Whites in Infants (link is external),” was published in the online journal Proceedings of the National Academy of Sciences. The researchers from the University of Virginia and Max Planck Institute found that the ability to respond to eye cues typically begins to develop during infancy around the age of seven months.
In another study (link is external) from March 2013, a research team honed in on the gene Tsc2 in Purkinje cells of the cerebellum and found that a loss of Tsc2 in Purkinje cells lead to autistic-like behavioral deficits. The researchers provide compelling evidence that Purkinje cell loss in the cerebellum and/or dysfunction may be an important link between ASD as well as a “general anatomic phenomenon that contributes to the ASD phenotype,” according to researchers.
In August of 2014, Samuel Wang and his colleagues at Princeton University reported that early cerebellum abnormalities hinder neural development and could be a possible root of autism. In August 2014, they published their theory, “The Cerebellum, Sensitive Periods, and Autism (link is external),” in the journal Neuron.
Sam Wang (link is external), Associate Professor of Molecular Biology at Princeton University, is doing fascinating research on information processing in the cerebellum, including its contributions to motor learning, the role of the cerebellum in cognitive and affective function, and autism spectrum disorder.

Conclusion: The Cerebellum May Take Center Stage in the 21st Century

My father often said, “We don’t know exactly what the cerebellum is doing. But whatever its doing, it’s doing a lot of it.” My dad would be thrilled to see the growing new evidence that helps explain everything the powerful and mysterious cerebellum is actually doing.
Purkinje cells and the cerebellum remain enigmatic. That said, neuroscientists are making steady progress using 21st century technology to help us better understand the “little brain” that Leonardo da Vinci first identified over five hundred years ago. We still have a long way to go before completely decrypting these mysteries, therefore, more research is needed.
 

Two Worlds

Hey, I’m just back from a meeting in Europe! Pediatric neurology. Couple of observations:
The Europeans are certainly interested in autism. Witness the debates in France about whether it’s the mother’s fault or not. But European physicians tend to put a somewhat different frame about it than we do.
Here, autism counts as a distinct disease. There, it’s really just a chapter in the mental retardation story. And European physicians tend to talk about “MR” rather than autism. Of course all children with the autism diagnosis are not retarded. That’s the purpose of “Asperger’s Disease,” meaning autism with normal or higher intelligence. But over there, “MR” continues to be a valid category while here the term has become taboo.
Why is that?
It’s because American physicians are running scared in the face of a very powerful parents’ lobby. Parents of developmentally disabled children hate the term “mental retardation” because of the pall of hopelessness that enshrouds it. The term is heavy with odium and somehow “autism,” though not a gateway to the sunny uplands, is less stigmatizing. This is why “MR” has virtually vanished from U. S. pediatric centers, and even though many of the autistic children will have subnormal intelligence, this is not the focus. Rather, the classic autistic characteristics of social isolation and a tin-ear for social cues occupy center stage, and intelligence is simply not dwelt upon.
In a way, this is progress. It gets attention off brain power and onto social issues that are much more important to the child. The mania for intelligence testing that gripped US society in the first half of the twentieth century is now easing as we become more interested in helping children fit in than in prepping them for exams. The contrasts between the US and China or Korea could not be more dramatic: There, exam-passing is everything and subnormal intelligence represents a humiliation for the family. The children are kept indoors and experience social death. Here we believe that every child is precious.
So, this is progress. But it is not science. There is nothing wrong with accommodating parents’ very real and very bruise-able sensitivities. But to reduce the complex world of developmental disorders to “autism” makes it harder to do research. The patient population becomes too heterogeneous to study.
Look at what has happened to “depression.” The term has swollen so badly out of shape that anyone the least bit dysphoric will be diagnosed as “depressed” and given “antidepressants” that, in many cases, are quite useless. Lots of different disorders are at play here, some quite poorly defined, and rather than throwing everyone into the depression tub we should be trying to make distinctions in order to come up with specific treatments.
Similarly with “autism”: When every child on the pediatric service becomes “autistic,” the term loses its meaning: genetics and social causation become jumbled together. Treatment responsiveness is lost sight of. For example, lots of kids with the autism diagnosis also have symptoms of catatonia, including self-injurious behavior (SIB). SIB is quite treatment-responsive. So are other forms of catatonia. “Autism” is not highly treatment-responsive, though various psychotherapies may relieve some of its symptoms.
There is a huge irony here. Autism was well described in the European psychiatric literature in the 1920s, and it was certainly differentiated from mental retardation. But the autism craze over here was initiated in 1943 by Leo Kanner, at Johns Hopkins University, a European who claimed to be describing a new disease. Kanner included no references in his paper, although he was Austrian-born and read German (Shorter & Wachtel, 2013 (link is external)).
So as the autism star rose here, the MR star fell. In Europe by contrast, the two diagnoses existed side by side. (It is true that in Europe after the Second World War, developmental psychology and psychiatry were swallowed up by the Freudians, who were more interested in toilet training than in social communication and isolation.) And to this day in Europe, “MR” is a respectable diagnosis.
So what you gain on the swings, you lose on the roundabouts. Here “autism” now rules the developmental roost. There, “MR” is still au courant, though the diagnosis—however scientific—is a cruel and unfeeling one. Here, physicians are cowed by the political power of the parents’ movement. There, the authority of the “Herr Professor Doktor” is unchallenged. Two worlds. 

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