Regional brain chemical alterations in young children with autism spectrum
disorder
S.D. Friedman, PhD, D.W. Shaw, MD,
A.A. Artru, MD, T.L. Richards, PhD, J. Gardner, PhD,
G. Dawson, PhD, S. Posse, PhD and S.R. Dager, MD
From the Departments of Radiology (Drs. Friedman, Shaw,
Richards, Gardner, and Dager), Anesthesiology (Dr. Artru), Psychology (Dr.
Dawson), Psychiatry (Dr. Dager), and Bioengineering (Drs. Richards and Dager),
University of Washington School of Medicine, Seattle; and Wayne State University
(Dr. Posse), Department of Psychiatry, Detroit, MI.
Address correspondence and reprint requests to Dr. Dager,
Departments of Radiology, Psychiatry & Bioengineering, University of Washington
School of Medicine, 4225 Roosevelt Way NE, Suite 306-C, Seattle, WA 98105-6099;
e-mail: srd@u.washington.edu
Objective: The authors evaluated regional brain
chemistry forevidence of increased neuronal packing density in
autism.
Methods: Forty-five 3- to 4-year-old children with autism
spectrumdisorder (ASD), 13 children with typical development (TD),
and15 children with delayed development (DD) were studied usingdual-echo proton echoplanar spectroscopic imaging (32
x 32 matrix-1cm3
voxels) to measure brain chemical concentrations and relaxation
times. Chemical quantification was corrected for tissue partial
volume and relative measures of chemical relaxation (T2r) werecalculated from the paired echoes. Measures from averaged and
individual regions were compared using analysis of variancecorrected
for multiple comparisons.
Results: ASD subjects demonstrated reduced N-acetylaspartate(NAA) (-10%), creatine (Cre) (-8%), and myo-inositol (-13%)
concentrations compared to TD controls and prolonged NAA T2rrelative to TD (7%) and DD (9%) groups. Compared to DD subjects,children with ASD also demonstrated prolonged T2r for choline(10%) and Cre (9%). Regional analyses demonstrated subtle patternsof chemical alterations in ASD compared to the TD and DD groups.
Conclusions: Brain chemical abnormalities are present in ASDat 3 to 4 years of age. However, the direction and widespread
distribution of these abnormalities do not support hypothesisof
diffuse increased neuronal packing density in ASD.
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