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. 2009 Nov 15;66(10):942-9.
doi: 10.1016/j.biopsych.2009.07.007. Epub 2009 Sep 2.

Amygdala enlargement in toddlers with autism related to severity of social and communication impairments

Affiliations

Amygdala enlargement in toddlers with autism related to severity of social and communication impairments

Cynthia Mills Schumann et al. Biol Psychiatry. .

Abstract

Background: Autism is a heterogeneous neurodevelopmental disorder of unknown etiology. The amygdala has long been a site of intense interest in the search for neuropathology in autism, given its role in emotional and social behavior. An interesting hypothesis has emerged that the amygdala undergoes an abnormal developmental trajectory with a period of early overgrowth in autism; however this finding has not been well established at young ages nor analyzed with boys and girls independently.

Methods: We measured amygdala volumes on magnetic resonance imaging scans from 89 toddlers at 1-5 years of age (mean = 3 years). Each child returned at approximately 5 years of age for final clinical evaluation.

Results: Toddlers who later received a confirmed autism diagnosis (32 boys, 9 girls) had a larger right (p < .01) and left (p < .05) amygdala compared with typically developing toddlers (28 boys, 11 girls) with and without covarying for total cerebral volume. Amygdala size in toddlers with autism spectrum disorder correlated with the severity of their social and communication impairments as measured on the Autism Diagnostic Interview and Vineland scale. Strikingly, girls differed more robustly from typical in amygdala volume, whereas boys accounted for the significant relationship of amygdala size with severity of clinical impairment.

Conclusions: This study provides evidence that the amygdala is enlarged in young children with autism; the overgrowth must begin before 3 years of age and is associated with the severity of clinical impairments. However, neuroanatomic phenotypic profiles differ between males and females, which critically affects future studies on the genetics and etiology of autism.

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Conflict of interest statement

Disclosures

Dr. Lord receives royalties from the ADI-R and ADOS; as per agreement with the University of Michigan, all proceeds go to charity. The other authors reported no biomedical financial interests or potential conflicts of interest.

Figures

Figure 1
Figure 1
Three-dimensional reconstruction of images (a) in which lines indicate the position though the cerebrum of the coronal plane (b), sagittal plane (c), and transverse (horizontal) plane (d). A, amygdala; H, hippocampus; P, putamen.
Figure 2
Figure 2
Amygdala volume (in cubic centimeters) for all participants by diagnostic group (*p<0.05; **p<0.01 significantly different from gender matched controls). Length of box is the interquartile range computed from Tukey’s hinges. Line inside box is median and whiskers represent entire value range.
Figure 3
Figure 3
Linear regression scatter plots showing a positive correlation for right (r=.52, p=.001) and left (r=.57, p<.001) amygdala volume (in cubic centimeters) and ADI-R Social score in ASD males.
Figure 4
Figure 4
Linear regression scatter plots showing a positive correlation for right (r=-.38, p<.05) and left (r=.34, p<.05) amygdala volumes (in cubic centimeters) and Vineland Communication score in ASD males.

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