International Meeting for Autism Research (London, May 15-17, 2008): Localization of Transverse Relaxation Time Abnormalities in Autism

Thursday, May 15, 2008

Champagne Terrace/Bordeaux (Novotel London West)

10:30 AM

Y. Gagnon , Medical Biophysics, University of Western Ontario, London, ON, Canada

T. Devito , Medical Biophysics, University of Western Ontario, London, ON, Canada

J. Hendry , Medical Biophysics, University of Western Ontario, London, ON, Canada

N. Gelman , Medical Biophysics, University of Western Ontario, London, ON, Canada

N. Rajakumar , Anatomy and Cell Biology, University of Western Ontario, London, ON, Canada

P. Williamson , Psychiatry, University of Western Ontario, London, ON, Canada

D. Drost , Medical Biophysics, University of Western Ontario, London, ON, Canada

R. Nicolson , Psychiatry, University of Western Ontario, London, ON, Canada

Background: Autism is a developmental disorder characterized by social deficits, impaired communication, and restricted and repetitive patterns of behavior. Although there is strong evidence linking autism with abnormal brain development, the anatomical extent and timing of these neurobiological differences are unknown. Transverse relaxation time (T2) is a quantitative parameter of magnetic resonance imaging (MRI) influenced by tissue water compartmentalization and concentration. We reported a global increase of white matter T2 in the first whole brain study of T2 in autism.

Objectives: The purpose of this study was to localize the areas contributing to the previously reported global T2 increase in patients with autism.

Methods: Twenty-one males with autism, aged 6 to 16, and 20 male controls in the same age range underwent a MRI scan at 3 Tesla. T2 data were acquired using a Gradient Echo Sampling of the Free Induction Decay and Echo sequence. The images were spatially normalized and region of interest masks were created to calculate the mean T2 values in the masked regions.

Results: Patients had a global increase in white matter T2 (2.9%; p=0.02) as well as an increase in white matter T2 in the left hemisphere (3.3%; p=0.004). Post-hoc analysis revealed that patients had a significant increase in frontal (3.0%; p=0.03) and parietal white matter (3.1%; p=0.003).

Conclusions: Study limitations include a small sample size and the use of an adult brain template for the spatial normalization of images. Increased T2 could be caused by increased water within the myelin layers, consistent with study data showing larger brains and defective long range brain signaling. The asymmetry of white matter T2 is consistent with findings of abnormal brain lateralization in autism. Future work will focus on specifying the tissue origin of these local T2 differences.

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