EDITORIAL
Welcome! This, the sixteenth issue of our newsletter, Spectrum, is being sent to provide you with updated information on the activities of the Autism and Developmental Disabilities Research Program at Stanford University. The research program is under the direction of Dr. Antonio Hardan. We appreciated the feedback that we received about our previous issues and look forward to hearing your input on this and future issues. We hope that you will find this newsletter helpful and informative. Please feel free to share this newsletter with family and friends.
|
RECRUITING FOR RESEARCH STUDIES (STANFORD/LPCH)
Click here to see just a few of
our studies that we are recruiting for. For a complete list of all currently recruiting research studies please visit our new website at autism.stanford.edu.
|
Early Support Program for Autism
The Early Support Program for Autism is a collaboration between Stanford Children's Health and the Children's Health Council to provide supportive services at no cost to families after diagnosis.
The services include:
Clinical care coordinator helping families navigate the service system
Parent educator teaching parents play-based strategies to elicit engagement
Call 650.723.ESPA (3772) for more information or email autismsupport@stanford.edu.
|
The 8th Annual Autism Spectrum Disorders Update
Connecting the Dots: Clinical Research for Autism. Making a Difference for our Children
Presented by the Stanford Autism Center at Packard Children's Hospital
Lucile Packard Children's Hospital Stanford is here to help parents find answers. On April 18, 2015 the Stanford Autism Center at Packard Children's Hospital presents its 8th Annual Autism Spectrum Disorders Update, an event that gives members of the community a chance to learn about new autism research and therapies.
Topics Include:
Understanding social deficits and teaching social skills
Managing disruptive behaviors and building social, communication, and emotion regulation skills
Navigating service systems (Early Intervention, Special Education, 504 Plans, Regional Centers, Medical/Mental Health Services)
When: April 18, 2015 from 8:15 a.m. to 4:30 p.m. (Registration and continental breakfast begin at 7:30 am).
Where: McCaw Hall in the Francis C. Arrillaga Alumni Center. 326 Galvez Street, Stanford, California 94035. Parking is free and located at Galvez Field on the corner of Galvez Street and Campus Drive East.
Who Should Attend: Parents, teachers, pediatricians, psychologists, caregivers, media and anyone with an interest in autism are invited to attend.
Registration Fee: The registration fee is $125.00. The fee includes a continental breakfast, buffet lunch and speaker handouts. Register and view the program at: http://childpsychiatry.stanford.edu
Contact: For further information, please contact the Stanford Autism Center at Packard Children's Hospital at (650) 721-6327 or e-mail Maura Chatwell at
chatwell@stanford.edu
|
Special Educational Activity
Autism Spectrum Disorders Parent Education Program
The Stanford Autism Center at Packard Children's Hospital Parent Education Program is offering a half-day parent conference designed to provide parents and caregivers with information about social deficits associated with autism spectrum disorders, and how to build social skills in elementary, middle, and high school age children. The program will be divided into two groups depending on child's age. Please come and join other parents to learn about treatment options, ask questions and share experiences.
Classes are divided between parents of children ages 6-11 years and parents of children/adolescents ages 12-18 years.
Topics Include:
Understanding social deficits and teaching social skills
Managing disruptive behaviors and building social, communication, and emotion regulation skills
Navigating service systems (Early Intervention, Special Education, 504 Plans, Regional Centers, Medical/Mental Health Services)
Date: March 28, 2015
Time: 9:00AM - 12:30PM
Location: Stanford Child Psychiatry, 401 Quarry Rd, Stanford, CA
Cost: $30 per person
How to Register: Online at the Stanford/LPCH Parent Education Program Page or by contacting Maura Chatwell at (650) 721-6327 or
chatwell@stanford.edu
Future Program Dates: June 6, 2015: How to Explain Your Child's Diagnosis/Differences to Your Child, Siblings, and Others
The Stanford Autism Center at Packard Children's Hospital Parent Education Program is offering a half-day parent conference designed to provide parents and caregivers with information about autism, Asperger's disorder, PDD-NOS, other conditions as well as a discussion on when and how to talk to your child and others about these conditions. The program will be divided into two groups depending on child's age. Please come and join other parents to learn about community services, ask questions, and share experiences. |
other events
Autism
Parent Support Group
Sponsored by the Stanford Autism Center at Packard Children's Hospital
Parents of children with autism face a unique set of challenges. The opportunity to connect with other families who have been through similar experiences can be a valuable form of support. Please join our monthly support group! The group will meet from 7:00 PM to 9:00PM. Follow signs in the lobby for room location.
Topics for discussion will include:
Advocating for your child
Dealing with impact on family
Navigating school and learning
issues
Investigating treatment options and
resources
Please note that the support group is not intended to serve as therapy or other mental health services.
Upcoming
meetings:
March 12, 2015
April 9, 2015
May 14, 2015
June 11, 2015
Location: 401 Quarry Road, Room 2209, Stanford, CA (Map)
Facilitated by Annie Darrow, Leslie Stafford
RSVP: Maura Chatwell, (650) 721-6327 or chatwell@stanford.edu
Walk-ins are welcome!
|
Web and facebook pages
Visit
our website and "like" us on
facebook!
autism.stanford.edu
|
|
Issue 16, FEBRUARY 2015
RECENT PUBLICATIONS
Longitudinal patterns of repetitive behavior in toddlers with autism. (Wolff J.J. et al., 2014; Journal of Child Psychology and Psychiatry)
Although restricted, repetitive behaviors (RRBs) are quintessential to past and present clinical definitions of ASD, relatively little is known about the nature and course of these behaviors prior to diagnosis. Once thought to emerge after core social symptoms, recent findings raise the possibility that RRBs may be among the earliest behavioral manifestations of ASD. The repetitive behavior domain includes topographies ranging from motor stereotypies to circumscribed preoccupations with highly idiosyncratic interests. There is increasing evidence that repetitive behaviors manifest prior to age 2 in children who develop ASD at levels above and beyond those associated with typical or delayed development. Based on retrospective parent-report data, significantly elevated RRBs have been described relative to typically developing (TD) children as early as 10 months of age and to children who were TD or developmentally delayed (DD) at 12 months of age. This study sought to clarify the development of repetitive behavior from 12 to 24 months among TD children and high-risk siblings who did and did not meet criteria for ASD at 2 years of age. The authors examined longitudinal parent-reported patterns of repetitive behavior in typically developing toddlers and toddlers at familial high risk for ASD, a subset of whom met criteria for the disorder, at ages 12 and 24 months of age. They found significant group effects for all subtypes of RRBs over this age interval. The effect of Time was significant for compulsive and ritual/sameness behaviors from 12 to 24 months of age, in-line with previous work finding that higher-order RRBs increase over time. This age-related effect is likely related in part to a child's increasing ability to perform complex behaviors. This adds to a growing body of work suggesting that repetitive behavior may be an early emerging symptom of ASD. It further raises the possibility that a simple, inexpensive parent-report measure of repetitive behavior could predict risk by pulling for disorder-specific differences early in development. The authors also found that RRBs were present across a continuum of cognitive ability in toddlers with ASD, and not restricted to children who were lower functioning. The sole exception to this was for restricted behavior, which was modestly negatively correlated with Mullen ELC and NVDQ at 12 months of age. This finding is consistent with previous reports suggesting that the relationship between RRBs and cognitive measures develops over time.
Plasma oxytocin concentrations and OXTR polymorphisms predict social impairments in children with and without autism spectrum disorder. (Parker K.J. et al., 2014; Proceedings of the National Academy of Sciences of the United States)
The neuropeptide oxytocin (OXT) and its receptor (OXTR) regulate social functioning in animals and humans. Initial clinical research suggests that dysregulated plasma OXT concentrations and/or OXTR genetic variations, Single Nucleotide Polymorphisms (SNPs), may be biomarkers of social impairments in autism spectrum disorder (ASD). We do not know, however, whether OXT dysregulation is unique to ASD or whether OXT biology influences social functioning more generally, thus contributing to, but not causing ASD. To distinguish between these possibilities, the investigators examined in a sample of children with ASD , their unaffected siblings and unrelated neurotypical controls (ages 3–12 y; n = 193), whether plasma OXT concentrations and OXTR genetic variations (SNPs) (i) interact to produce ASD phenotypes, (ii) exert differential phenotypic effects in ASD vs. non-ASD children, or (iii) have similar phenotypic effects independent of disease status. In the largest cohort tested to date, the investigators found no evidence to support the OXT deficit hypothesis of ASD. Rather, OXT concentrations strongly and positively predicted theory of mind and social communication performance in all groups. Furthermore, OXT concentrations showed significant heritability between ASD-discordant siblings; a heritability estimate on par with that of height in humans. Finally, carriers of the "G" allele of rs53576 showed impaired affect recognition performance and carriers of the "A" allele of rs2254298 exhibited greater global social impairments in all groups. These findings indicate that OXT biology is not uniquely associated with ASD, but instead exerts independent, additive, and highly heritable influences on individual differences in human social functioning, including the severe social impairments which characterize ASD.
back to top
|
.gif)
