Friday, May 13, 2011: 1:45 PM
Douglas Pavilion A (Manchester Grand Hyatt)
1:15 PM
S. Solso1, W. Thompson2, K. Campbell3, C. Ahrens-Barbeau4, R. Stoner5, C. Carter6, M. Weinfeld7, S. Spendlove4, J. Young8, M. Mayo4, J. Kuperman9, D. Hagler9, R. J. Theilmann10, L. T. Eyler11, K. Pierce12, E. Courchesne12 and A. Dale9, (1)Neurosciences, University of California San Diego, UCSD Autism Center of Excellence, San Diego, CA, (2)Psychiatry, University of California San Diego, San Diego, CA, (3)UCSD Autism Center of Excellence, University of California, San Diego, La Jolla, CA, (4)Neurosciences, University of California, San Diego, UCSD Autism Center of Excellence, San Diego, CA, (5)Neurosciences and UCSD Autism Center of Excellence, La Jolla, CA, (6)Neurosciences, University of California, San Diego, UCSD Autism Center of Excellence, La Jolla, CA, (7)Neurosciences, University of California, San Diego, UCSD Autism Center of Exellence, La Jolla, CA, (8)Neuroscinces, University of California, San Diego, UCSD Autism Center of Excellence, San Diego, CA, (9)Radiology, University of California, San Diego, San Diego, CA, (10)University of California, San Diego, La Jolla, CA, United States, (11)Psychiatry and UCSD Autism Center of Excellence, University of California, San Diego, La Jolla, CA, (12)Neurosciences and UCSD Autism Center of Excellence, University of California, San Diego, La Jolla, CA
Background: Autism is a heritable disorder of early brain overgrowth that has been hypothesized, but not demonstrated, to involve abnormal structural development of local and long-distance connectivity and, thus, aberrant functioning (Courchesne & Pierce, 2005). Understanding putative early connectivity defects in autism could aid in the development of animal models, point to significant genetic pathways, and possibly be used as an early biomarker for autism to aid in early diagnosis and treatment. Unfortunately, currently there are no studies of cerebral tracts in the autistic brain at the age of first clinical signs.
Objectives: To identify abnormally as well as normally developing major long-distance cerebral tracts in ASD infants and toddlers.
Methods: We collected 51-angle DTI datasets from N=39 ASD and N=23 typically developing male infants and toddlers (13 months to 43 months) and analyzed FA values in 25 different tracts using a new DTI probabilistic atlas. Subjects were recruited as young as 12-months via the 1-Year Well Baby Check-up approach (Pierce et al., in manuscript) and diagnoses confirmed at later ages.
Results: Logistic regression models show that for multiple cerebral tracts infants and toddlers with greater FA values were more likely to have an ASD diagnosis. Significant tracts included the superior longitudinal fasiculus, forceps minor and uncinate as well as the corpus callosum. Furthermore within these tracts the ability of large FA values to predict ASD was strongest at the youngest ages.
Conclusions: Results are consistent with evidence of early brain overgrowth and suggests that it involves major cerebral white matter tracts as well as cortical gray matter. They are also consistent with MRI evidence of abnormal expansion of specific prefrontal and temporal subregions in ASD infants and toddlers. We theorize that these early developmental defects in connectivity in ASD result from genetic abnormalities in prenatal processes that regulate neuron numbers, migration and neurite outgrowth. We are currently exploring the degree to which DTI profiles could be used alone, or in combination with other imaging indices, as early predictive biomarkers of risk for autism.
