When I was graduating from elementary school, someone on the yearbook committee asked me, “What do you want to be when you grow up?” I will never forget thinking for a moment and then stating “an autism teacher”. In my yearbook, there is a picture of me and under it says “an autism teacher”. You might be thinking this is a very interesting answer for a young child to give, but I had a good reason behind this answer. My twin brother, Robert, has autism and over our lives, I saw the progress he made with many thanks to his incredible teachers. I thought to myself, I would love to be just like them so I can help other children with autism. As I matured and got older, I realized this autism teacher job I wanted really meant that I wanted to be a special education teacher.
When I started college at Hofstra University, I was accepted into the School of Education. I graduated with my bachelor’s degree in Early Childhood and Childhood Education and eventually got a job as a Universal Pre-Kindergarten Teacher in a public school district on Long Island. I had this job for two years while in graduate school for my Master in Early Childhood Special Education and Intervention program, also at Hofstra University. I always knew I wanted to be a special education teacher, however, I had to decide on the age range of students I would work with. I decided to go down this route for my master’s because I fell in love with working with young children. There are so many developmental milestones that a teacher can help young children with disabilities reach. I love teaching and helping children grow their physical, intellectual, emotional, and social development through different fun and engaging activities. By being an early childhood special educator, I am able to accomplish these goals with a variety of different students.
After many endless nights of working and studying, I was able to accept my first position this year as an early childhood special education teacher in an integrated preschool. I finally accepted my dream job! I took a job in an integrated preschool setting specifically because I believe in the importance of integration and having students with disabilities learn with and from their peers. All children with disabilities need to be placed in the proper learning environment that works for them, and I am excited to work in this environment.
I am so thankful that my brother Robert has influenced me to go down the path of special education. I am so proud of him and the progress he has made. He drives my dedication to this career choice everyday. It was definitely not an easy road getting here, but I cannot wait to make a difference in the lives of all the students I work with! I can now smile every time I look in my elementary school yearbook because I followed my dream. Now, I am living it.
Mahir Rahman (MR): Hello, everyone, this is Mahir Rahman. Welcome to the Autism Science Foundation Weekly Science Podcast. I’m subbing in for Alycia for an interview I conducted with Dr. Alex Kolevzon of Mount Sinai. Hope you enjoy the story.
MR: A Mount Sinai research team led by Dr. Alex Kolevzon is investigating if a compound known as insulin-like growth factor 1, also known as IGF-1, can be used as a treatment for autism. Dr. Kolevzon is a child psychiatrist and the clinical director of the Seaver Autism Center in the Icahn School of Medicine at Mount Sinai in New York. He received the Autism Science Foundation Treatment Grant in 2013. He sat down with ASF to discuss his current study. We began the interview by discussing the autism-related disorder Phelan-McDermid syndrome, also known as PMS.
Alex Kolevzon (AK): Phelan-McDermid syndrome is a neurodevelopmental disorder that causes autism. It is due to a deletion or mutation of the SHANK3 gene, which is located at the terminal end of chromosome 22. There’s two copies of the SHANK3 gene, we all have two copies of it. And so, in Phelan-McDermid syndrome, you’re basically missing one copy and that’s called haploinsufficiency.
MR: Are you wondering what happens if you miss one copy of the SHANK3 gene? Well, SHANK3 is a gene that codes for a protein that helps brain cells communicate with each other in order to make useful connections during development. When one copy of the SHANK3 gene is missing, certain brain cells cannot communicate with each other, leading to a number of problems.
AK: So based on very large genetic studies, it seems as if Phelan-McDermid syndrome or SHANK3 deletions and mutations account for about 1% of autism, and not everyone with Phelan-McDermid Syndrome has autism, so there’s going to be additional cases beyond that. So really it’s very common. We’re just now starting to routinely diagnose people.
MR: How can some kids with PMS have autism and others not?
AK: Well, autism is a behavioral diagnosis. It’s really just a collection of symptoms, social impairments, language impairments, restricted and repetitive behaviors, and, you know, many different people with autism look very, very different. So some kids have… with Phelan-McDermid syndrome have a lot of social motivations, social interests, social engagements. And despite being significantly cognitively delayed, the social domain is a relative strength for them, and as a result, they don’t really meet the criteria for an autism spectrum disorder. We’re talking about maybe 15% to 20% of them. So the vast majority of people with Phelan-McDermid syndrome do meet the criteria for autism. But it’s important to understand that if you take a given biological cause of a syndrome, the clinical features of that syndrome could be very, very wide.
MR: To reiterate, it’s important to understand that, like autism, the symptoms of PMS can vary. They can vary enough that some children with PMS don’t meet the criteria for an autism diagnosis, but most of the time, they will. That said, the symptoms seen in autism might be based on biology similar to that of PMS.
AK: Within the broader universe of people with autism, and especially people with autism where there isn’t a known cause — what we call idiopathic autism, it seems as those a subset of them appear clinically, and even on some biological measures, look like people with Phelan-McDermid syndrome.
MR: If two conditions have similar biology, the same treatment may be able to help both. The search for a treatment for PMS and idiopathic autism led Dr. Kolevzon’s team to a group of compounds known as growth factors. Growth factors can help cells grow, change, and make new connections, what scientists call plasticity.
AK: A growth factor can promote growth, promote synaptic plasticity, which is what is essentially absent in Phelan-McDermid syndrome. So we started doing this study with a drug called insulin-like growth factor, which we know crosses into the brain, we know it promotes synaptic maturity, synaptic plasticity, nerve cell growth, and we did a couple of small studies, both of which were very, very promising.
MR: In a pilot clinical trial using IGF-1, Dr. Kolevzon’s team found children with PMS tolerated the drug. They also found that the children treated with IGF-1 had reduced expression of two core symptoms of autism – social withdrawal and repetitive behaviors.
AK: We looked at social symptoms and repetitive behavior symptoms because those are core domains of autism. And those are both studied in this trial using a parent-report measure, and we saw improvement in both those domains in the trial with IGF-1.
MR: Dr. Kolevzon’s team made sure every participant had the opportunity to receive the IGF-1 treatment in the trial by employing a crossover design.
AK: Patients got drugs for 12 weeks, or placebo, and they switched to the other condition, so each patient essentially acted as their own control and treatment was for 12 weeks and placebo was for 12 weeks in random order. We applied the exact same design to the trial in idiopathic autism.
MR: Employing a crossover design was an intentional decision by his team.
AK: One of the biggest obstacles to success in clinical trials is recruitment. One of the biggest obstacles to families wanting to participate is the idea of being on placebo and not getting access to the active treatment. So we purposely designed the trial with everyone getting active treatment.
MR: Based on the findings made by Dr. Kolevzon’s team, IGF-1 appears to be a safe treatment that offers notable improvements in core symptoms of autism, so why is it not considered an effective treatment yet? Dr. Kolevzon hopes to address that question with his current study.
AK: The fear in the field in general is we might be studying an effective medicine but we are not able to show improvement because our measures are not ideal. Either we’re not measuring the right thing, measures aren’t sensitive enough, we’re not able to really account for the placebo effect because they’re so biased. So we’ve been focusing a lot more on more objective, more quantifiable measures, trying to develop new ways of looking at symptoms.
MR: His current study is focusing on sensory reactivity symptoms. Many people with PMS and autism have sensory issues, including varying sensitivity to light and sound and atypical interests in specific textures and temperatures. In order to examine brain activity in general and during periods of sensory reactivity, his lab uses a technique called electroencephalography, or EEG. Dr. Kolevzon’s team will be examining how IGF-1 affects sensory reactivity and brain activity following IGF treatment
AK: That’s really an important symptom, it’s a symptom that’s virtually universal. All kids with Phelan-McDermid syndrome, at least all the kids that we have evaluated, have some sensory reactivity symptoms. Often, they are hyporeactive.
MR: Meaning that these kids often have a decreased response to sensory stimuli. Say a child with sensory hyporeactivity entered a room with very loud speakers. The child might not be bothered by, or let alone react to, the volume. With IGF-1 treatment, Dr. Kolevzon believes his team will be able to observe any change of those sensory reactivity symptoms over the course of the clinical trial.
AK: This is a trial that is pretty burdensome for families because the way that IGF-1 is delivered is through subcutaneous injection. So families are taught to monitor their children’s glucose levels because one of the main side effects can be low blood sugar, and they’re also taught how to inject the children twice a day with small amounts of IGF-1. It’s a very, very small needle and actually, it’s probably the element of the study that people are most concerned about when they first consider it, and it ends up in actually 19 out of 19 cases not to be a really big issue. The children, because they have the sensory hyporeactivity, aren’t especially averse to the shots and the parents become remarkably expert very, very quickly. We give them a big manual with lots of instructions. We show them exactly how big, and in this case, how tiny the needle is, but then, the very first day that they actually get the injection, I give it to them myself.
MR: Dr. Kolevzon and his team understand that they’re asking a lot from the families choosing to participate in the study. They take great strides in order to prepare and help the families throughout the recruitment and trial process.
AK: For me to say things like, “Oh, this is not a big deal,” isn’t helpful. Obviously, this is a big deal, we acknowledge that on the onset, but for me to also encourage them and say, “Look, it’s going to feel scary and then you’re going to be quite good at it.” That’s one thing. I think the other thing is that they don’t feel alone in this, right? They don’t have to make decisions on their own. They don’t have to worry about dosing on their own. You know, if they see anything concerning, they don’t need to decide what to do about that. They have unfettered access to me. We exchange cell phone numbers early on and then, the other thing I say to them is, “You know, if you have any concerns at all, skip the dose. That’s it. You get to control that. If you don’t want to give your child the does for whatever reason, just skip the dose. There will not be any harm in that.” Then, we just take it from there.
MR: For those autism families that are listening, Dr. Kolevzon has a message for you.
AK: “Come participate!” I’d say that if you’re not convinced that a clinical trial is a good idea, that’s okay also. Come just to get to know us. Let us get to know you. And then, you know, we’ll figure it out. Nobody has ever required anybody to participate in a clinical trial. We definitely respect how scary it can be and how hard it can be. So it’s really all about just the fit.
MR: You can learn more about this study on asfpodcast.org. Thanks for listening.
Life is a sensory experience! We touch, hear, feel our muscles, move our bodies, taste, and smell and use vision to take in information from the environment, process and integrate it to act and interact as well as to learn and grow. Upwards of 80% of persons with Autism Spectrum Disorder (ASD) experience differences in the way they perceive and process sensory information. This impacts the ways in which they participate in functional tasks such as speaking, moving, eating, dressing, interacting with others, playing, learning and working. These sensory features are now part of the diagnosis of autism in the DSM5.
As an occupational therapist and a neuroscientist, my interest in the sensory features of ASD developed from working with children and families who often articulated how decreased sensory perception, integration or sensory sensitivities affected their everyday lives. As we worked together to improve independence and skill in daily life activities, success at school and to foster social engagement, it became clear that we needed to address these sensory differences in order to achieve their desired goals. We used the principles of sensory integration (Ayres, 2005; Bundy, et al, 2001) to target these issues and saw positive results! To share our knowledge and test this approach we received funding to write a manualized protocol (Schaaf & Mailloux, 2015), test its effectiveness, and publish our findings (Schaaf, et al, 2014). This study showed that children with ASD who received the occupational therapy using sensory integration treatment performed significantly better in functional skills and individual goals compared to controls.
We are now conducting a larger, more comprehensive study and are seeking families who have a child with ASD aged 6-9.5 years who may want to participate in the study. This study is a collaboration with Thomas Jefferson University and Albert Einstein Medical Center and is located in the Bronx, NY. Children will receive a full diagnostic battery and then be randomized to one of the treatments (Sensory Integration or a behavioral intervention) and will receive 3 one-hour sessions/week for a total of 30 treatments. Parents must be willing to travel to Albert Einstein College of Medicine (1225 Morris Park Avenue, Suite 1-C, Bronx, NY 10461). Participants will receive a total of $250 and a report of the child’s performance and assessment data at the end of the study. Children have a 1/3 chance of being randomized into the “No Treatment” arm of the study but will still receive all assessments and stipends for participation.
The report will indicate whether the child performed below, at, or above average in the last round of the following tests:
Wechsler Abbreviated Scale of Intelligence (WASI-II)
Autism Diagnostic Observation Schedule (ADOS-2)
Sensory Integration and Praxis Tests (SIPT)
Assessment of Motor and Process Skills (AMPS)
Evaluation of Social Interaction (ESI)
Aberrant Behavior Checklist (ABC)
Restrictive and Repetitive Behaviors Rating Scale Revised (RBS-R)
Pediatric Evaluation of Disability Inventory Computer Adaptive Test (PEDI-CAT)
More and more, researchers and clinicians are thinking about how advances in technology can be leveraged for interventions for children with autism. Tablets, computers, and video games have become increasingly available to children in their daily lives. At the same time, the American Academy of Pediatrics has put forth clear screen time guidelines for children, and many parents worry about their children spending too much time in front of a screen or with devices.
In the autism field, technology is providing promising avenues for early detection and intervention. For example, a recent study describes the use of mobile technology to screen for autism in young children. Others have developed apps and virtual reality systems through which treatments can be delivered. But what good are advances in technology-based interventions if parents aren’t interested in utilizing them?
Researchers at the UC Davis MIND Institute on the UC Davis Medical Center campus in Sacramento are conducting a study of parental perceptions of use of technology in treatment of impulsivity in 4 to 7-year-olds with autism spectrum disorder. Parents of 4 to 7-year-old children who have been diagnosed with autism spectrum disorder (ASD) can participate. Families can expect to complete of several online questionnaires about: Your family, your opinions about technology in treatment, and your child’s behavior. These questionnaires will take about 10 minutes of your time.
내 생각에, 나는 꽤 평범한 한국의 대학생이지만, 내 삶을 그리 일반적이지 않게 만드는 것이 있다. 바로 나보다 2살 많은 자폐성 장애인인 오빠이다. 좀 낯설게 들릴 수도 있겠지만, 적어도 한국에서 자폐성 장애인의 형제자매로서의 삶은 다른 사람들의 그것과는 상당한 차이가 있다고 본다.
2009년 7월의 어느 여름 날, 나는 한국 자폐인 사랑협회(ASK)에서 주최하는 여름 캠프에 참가하게 되었다. 많은 장애 아동과 그 가족이 캠프에 참가했고, 프로그램들은 장애 아동, 부모, 그리고 그 형제자매들을 대상으로 나눠져 있었다. 그 캠프에서 나는 처음으로 비슷한 경험을 가진 비장애 형제들을 만날 수 있었다. 몇몇은 그들의 가족, 특히 그들의 장애 형제들에 대해 말하는 것이 낯설어 보였기 때문에 그 중 가장 나이가 많았던 나는 내 이야기를 먼저 나누며 그 친구들이 자유롭게 얘기할 수 있는 분위기를 만들었다. 깊은 공감을 나타내며 그들이 이야기를 듣고 있을 때, 머뭇거리던 한 꼬마 아이가 나에게 물었다.
“어떻게 그렇게 잘 이해해요?”
그 순간, 처음으로 비장애 형제들이 서로의 경험을 나누고 공감할 수 있는 자조 모임이 필요하다는 것을 깨닫고, 언젠가 한국에 비장애 형제 자조모임을 만들겠다는 결심을 했다.
2016년 1월 초, 나는 내 또래의 비장애 형제 4명을 만났다. 만났던 첫 날, 우리는 얘기하느라 시간이 가는 줄 몰랐고 서로에게 꽤 많은 공통점이 있다는 것을 깨달았다. 각자 형제들의 장애와 증상은 다르지만, 우리는 비슷한 경험과, 걱정과, 생각을 가지고 있었다. 어렸을 때, 가족 내에서 혹은 부모에게서 소외당했다고, 심지어는 무시당했다고 느낀 적이 있었고, 장애 형제들에 대해 이해할 수 없는 부분들이 많았지만 누구에게도 물어볼 수 없었다. 형제와, 그들의 장애와, 부모님에게 분노를 느끼기도 했었고 결국 그 분노가 자기 자신을 향하기도 했다. 또, 나를 포함한 몇몇은 인정 받고 싶은 욕구를 강하게 느끼며 다른 사람들에게 사랑 받기 위해 기대를 충족시키고 뛰어넘으려는 경향을 보였다. 우리의 삶에 대해 얘기하면서, 우리는 “나는”이라는 이름으로 한국의 첫 번째 비장애 형제 자조모임을 만들자고 결심했다.
“나는”이 시작된 후, 다른 비장애 형제들과의 많은 모임을 가졌고, 그 모임에서 우리는 장애 형제와 부모, 그리고 특히 자신에 대해 자유롭게 얘기할 수 있었다. 모임을 통해 많은 이야기들을 모아 2018년 3월 우리의 이야기를 담은 책을 출판하기도 했다. “나는”을 통해 책 출판 이외에도 많은 목표들을 이룰 수 있었다. 첫째로, 한국에는 장애인 당사자들을 위한 관심과 담론 자체가 부족하기 때문에 장애인의 가족, 특히 그들의 형제들에 대한 관심 또한 기대하기 힘든데, “나는”을 통해 장애인의 형제 자매의 존재를 인식시킬 수 있었다. 또한, 살면서 처음으로 장애 형제나 부모가 아닌 우리 자신에 대해 더 많은 관심을 가질 수 있었다. 그 무엇보다 우리 자신에게 집중 하는 것은 살면서 느껴왔던, 그리고 느끼고 있는 수많은 감정들을 마주하고 인정함으로써 비장애 형제로서의 소외감과 불안 등을 해소하는 데 도움이 되었다.
하지만 가장 크게 이룬 것은 바로 우리가 혼자가 아니라는 점을 깨달았다는 점이다. 내 경우, 자폐성 장애인의 동생으로서 분노와 공포, 죄책감을 나 혼자만 느끼고 있는 건 아닐까 생각했고, 아무도 나를 이해하지도, 나에게 공감하지도 않을까봐 걱정했다. 하지만, “나는”을 결성하고 다른 비장애 형제들을 만나면서 내가 혼자가 아니라는 사실을 깨달았다. 또, ‘내가 혼자가 아니라는 사실’을 깨달은 것은 비단 나뿐만이 아니었다. 우리는 다른 많은 비장애 형제들과 같이, “함께”하는 힘으로 좀 더 성숙하기 위한 한 발을 내딛는다.
In my opinion, I am a quite ordinary university student in South Korea. However, there is a feature that has made my life unusual: my older brother. He is two years older than me, and has autism. This may sound strange, but at least in South Korea, living as a sibling of an autistic person is considerably different from others.
A summer day of July 2009, I had a chance to participate a summer camp held by Autism Society Korea (ASK). In the camp, there were many families of children with special needs, and the programs were divided into three parts; for the children, for the parents, and for the siblings. That was the first time for me to meet other children who had had similar experience being siblings without disabilities. Some of them seemed to be unfamiliar with talking about their family members, especially their brothers and sisters. I was the oldest among them, so I shared my story and tried to make them feel free to talk about their experience. When I listened to them and expressed my empathy, a little boy hesitated for a moment and asked me a question.
“How can you understand me that well?”
That was the first moment that I realized the necessity of supporting groups for siblings where they could share their experience and empathize with one another. Also, I made my mind to make a sibling supporting group in South Korea someday.
In the beginning of January 2016, I met four other siblings of my age. On the first day we met, we even lost track of time talking about our lives and realized that we had quite a few things in common. Even though our siblings with special needs had different symptoms and aspects in detail, we had similar experience, concerns, and thoughts. When we were children, we had felt left out in our families or from our parents, and even felt ignored by them. There were a lot of things that we couldn’t understand about our brothers and sisters, but there was almost no one whom we could ask. Some of us used to feel resentment toward our siblings themselves, the disabilities of our siblings, and parents, which led us to feel guilty about the anger. Some people, including me, had a tendency to strongly desire to be acknowledged and used to tried hard to exceed expectations from others to be loved. Talking about our lives, we decided to form the first sibling supporting group in South Korea, and named it as “Nanun,” which means “It’s about me.”
From the beginning, we have had dozens of meetings with other siblings. In the meetings, they felt free to talk about their brothers and sisters, parents, and especially themselves. Having gathered diverse episodes from those meetings, finally, we published a book containing our stories in March 2018. Not only did we get a success in the publication, but we also achieve a lot of things in “Nanun.” Firstly, there is a lack of attention to people with disabilities in South Korea, so it’s hard to expect concerns for their family members, especially the siblings. We made it possible for people to realize the existence of siblings of people with special needs. Additionally, for the first time in our lives, we had a chance to be more concerned with ourselves, not the brothers and sisters or parents. We tried to concentrate on ourselves, face and admit the various emotions. It helped us to relieve our anxiety or alienation as siblings without disabilities.
But the most important thing that we fulfilled was to recognize that we are not alone. In my case, I had felt alone and strange because I had thought that I might be the only one who had anger, fears, and guilt being a sister of an autistic person. I was afraid that there might be no one that understand me and empathize with me. However, forming the supporting group and meeting siblings, I finally realized that I was not the only one. Also, I am not the only one who does not feel alone anymore. Standing with many other siblings, we understand the power of being together and make a next step to be mature.
ASF funded fellow Nick Goeden from USC examines the role of the placenta.
Blog written by Priyanka Shah, ASF intern
Many researchers are studying various factors during pregnancy that can lead to an increased risk of autism and other neurodevelopmental disorders in children. Maternal infection and inflammation have been shown to be risk factors for autism and schizophrenia. For example, in recent news, we have seen how expecting mothers infected with the Zika virus have given birth to babies with a high-risk for brain damage and other abnormalities. So, studying how maternal health (in this case, a viral infection) affects the fetus can help us predict for possible disorders and possibly even prevent them.
In particular, at the University of Southern California, Nick Goeden and colleagues studied how the placenta was affected after the mother experienced inflammation. The placenta is a tissue in a woman’s uterus that provides nourishment to the fetus through the umbilical cord. The placenta also produces an important chemical messenger, called serotonin, which is transmitted to the fetus and plays a role in organizing the brain during development. After birth, it helps regulate emotions and has been implicated in depression and anxiety.
Researchers decided to use a mouse model to see how maternal inflammation can affect the production of serotonin in the placenta and brain development in the fetus. To do this, they used a chemical that induces inflammation in pregnant mice, and mimics flu-like conditions seen in humans. They found that the amount of serotonin in the placenta drastically increased, leading to increased amounts of serotonin in the fetal brain. During brain development, brain cells migrate and become connected together like an electric network. The formation of certain brain cells that specifically help move serotonin around was disrupted, which means that the fetus’ brain became wired differently. Because of this, some of the behaviors serotonin helps control could have been affected. And in fact, other studies have shown how maternal infection during pregnancy can lead to increased anxiety or depression-like symptoms in the offspring.
This study shows thateven mild inflammation during pregnancy can induce a series of events that eventually disrupts the development of the fetal brain. Although these children will have a higher risk for known mental disorders such as ASD or schizophrenia, these diagnoses are not guaranteed. Our next steps in this line of research should be to see the long-term effects of inflammation on the serotonin-specific brain cells and related behaviors. Researchers should also look at how other infections and viruses might be changing the production of other chemical messengers or molecules in the placenta. Understanding the biological mechanisms of the placenta and of fetal brain development can help direct new research into prevention and therapy for neurodevelopmental disorders in children.
The results are not surprising: autistics are bullied more often. While this may not come as a shock, having this data is the first step to effecting change. And, yes, autistics can play the role of the bully, but often with different motivations than their non-autistic peers. This figure from the preliminary report says a great deal: a much higher (about 3x more) percentage of autistics were bullied.
Those with Asperger syndrome were reported as being bullied more often than those with other ASD diagnoses. The preliminary report also lists behaviors and traits that increased the likelihood of bullying:
•Rigid rule keeping (enforcing adults’ rules when other children would not)
•Continuing to talk about a favorite topic even when others are bored or annoyed
•Inflexibility or rigidity
Sadly, one group that was frequently bullied was children with ASD who wanted to interact with other children, but had a hard time making friends. Of these, 57% were bullied, compared to only 25% of children who prefer to play alone and 34% of children who will play, but only if approached. The one slightly bright spot was that children who had learned to make friends successfully were bullied at a lower rate: 34%.
While autistics bully more often than their non-autistic peers, they mostly play the role of “bully-victims”. From the preliminary report: Unlike victims who are more passive, bully-victims insult their tormentors or otherwise try to fight back in a way that only makes the situation worse.
Again, IAN has an excellent discussion of this study. It is worth noting that a study creates awareness in the research community and provides the type of data from which questions can be formed. Just as we can hope that this study will spark further work, we can hope that the UJA Adult with ASD Survey will provide a basis for more work, and some solutions to the issues uncovered.
OBJECTIVE: : Bullying has become a major national concern, particularly as it affects children with disabilities. The current study aimed to determine the association between psychiatric comorbid conditions, involvement in bullying (victim, bully, or bully-victim), and the immediate psychological correlates of bullying among children with autism spectrum disorders (ASDs).
METHODS: : A national sample of 1221 parents completed a survey dedicated to the bullying and school experiences of their child with ASD, reporting on the immediate consequences of bullying involvement, including their child’s psychological well-being and any psychiatric comorbidity. Multivariate logistic regressions were performed to determine whether specific psychiatric comorbidities were associated with an increased risk of involvement as victim, bully, or bully-victim. Analyses of variance determined the relationship between bullying frequency and psychological functioning. All models adjusted for child and school covariates.
RESULTS: : Children who were frequently victimized were more likely to present with internalizing symptoms, whereas children who frequently bullied others were more likely to exhibit emotion regulation problems. Children who were identified as frequent bully-victims presented with both internalizing symptoms and emotion regulation problems. Children with attention-deficit hyperactivity disorder (ADHD) and depression were more likely to have been victimized, whereas children with conduct disorder (CD) or oppositional defiant disorder (ODD) were more likely to have bullied other children. Children identified as bully-victims were more likely to have ADHD, CD, or ODD.
CONCLUSIONS: : Children with ASDs who had displayed bullying behaviors in the past month exhibited psychological impairments, including psychiatric comorbidity. The frequency of bullying behaviors was significantly associated with the level of impairment.