L. Zwaigenbaum
,
Department of Pediatrics, University of Alberta, Edmonton, AB, Canada
W. Stone
,
Vanderbilt Children's Hospital, Vanderbilt University, Nashville, TN
K. Dobkins
,
Psychology, UC San Diego, La Jolla, CA
R. Urbano
,
Vanderbilt Kennedy Center for Research on Human Development, Vanderbilt University, Nashville, TN
W. Lambert
,
Vanderbilt Kennedy Center for Research on Human Development, Vanderbilt University, Nashville, TN
S. E. Bryson
,
Pediatrics and Psychology, Dalhousie University/IWK Health Centre, Halifax, NS, Canada
K. Chawarska
,
Child Study Center, Yale University School of Medicine, New Haven, CT
J. N. Constantino
,
Psychiatry, Washington University School of Medicine
G. Dawson
,
University of Washington, Seattle, WA
A. Klin
,
Yale Child Study Center, Yale School of Medicine, New Haven, CT
R. Landa
,
Center for Autism and Related Disorders, Kennedy Krieger Institute, Johns Hopkins Medical School, Baltimore, MD
S. Ozonoff
,
Psychiatry, University of California at Davis, Sacramento
S. J. Rogers
,
The M.I.N.D. Institute, UC Davis, Sacramento, CA
M. Sigman
,
Depts. of Psychiatry and Psychology, UCLA, Los Angeles, CA
T. B. S. R. C. (BSRC)
,
Autism Speaks/NICHD
Background: Increased head circumference is the most consistently replicated biological marker of autism since the disorder was first described by Kanner in 1943. Recent analyses of data from medical records have suggested that accelerated head growth has an onset during the first year of life, although the apparent timing of this phenomenon varies between studies. To date, there are no
prospective data on whether atypical trajectories of head growth are predictive of ASD.
Objectives: To assess prospectively whether children with ASD identified from a cohort of high-risk infants (siblings of children with ASD) exhibit accelerated head growth relative to non-diagnosed high-risk infants and low-risk comparison infants (no family history of ASD).
Methods: Head circumference (HC) was measured prospectively on a total of 761 high-risk and 400 low-risk infants from 11 sites across North America and supplemented by data from health records (25% of total dataset). Analyses compared head growth between high-risk infants diagnosed with ASD at age 24 months (DSM-IV clinical best estimate based on developmental history and symptoms observed on the ADOS) to non-diagnosed high-risk and low risk infants. Growth trajectories were assessed using mixed longitudinal models, assessing change in HC as a function of time (linear growth) and time-squared (acceleration/deceleration), including sex as a fixed covariate, and height as a time-varying covariate.
Results: Mean HC at birth (model-based estimates) did not differ significantly between the three groups (p=0.08). However, there were significant differences between the ASD and both non-ASD groups in HC growth rate (growth rate 0.06 cm/month faster in ASD group compared to non-diagnosed high-risk and low-risk infants; p=.021 and p=.017, respectively), and in deceleration rate (deceleration rate 0.002 cm/month higher in ASD group; p=.018 and p=.021, respectively).
Conclusions: Prospectively measured head growth rates differentiate infants subsequently diagnosed with ASD from non-diagnosed high-risk and low-risk infants.
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