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From the aMRI Analysis Laboratory (Dr. Kaufmann and K. Fredericksen, K. Cooper, and D. Lanham), Kennedy Krieger Institute (Drs. Cutting, Mostofsky, Denckla, and Kaufmann, and K. Frederickson, K. Cooper, and D. Lanham), and the Departments of Psychiatry (Drs. Kates, Mostofsky, Denckla, and Kaufmann), Neurology (Drs. Singer, Denckla, and Kaufmann), Pediatrics (Drs. Singer, Denckla, and Kaufmann), Pathology (Dr. Kaufmann), and Radiology (Dr. Kaufmann), Johns Hopkins University School of Medicine, Baltimore, MD.
Address correspondence and reprint requests to Dr. Walter E. Kaufmann, Department of Developmental Cognitive Neurology, The Kennedy Krieger Institute, 707 N. Broadway, Room 522, Baltimore, MD 21205; e-mail: wekaufma{at}jhmi.edu
Objective: Based on previous findings implicating abnormalities of cortico–striatal–thalamo–cortical circuitry in Tourette syndrome (TS), the authors performed a volumetric analysis of frontal and nonfrontal tissue (gray + white matter) in boys with TS, with and without attention deficit hyperactivity disorder (ADHD).
Methods: Frontal and nonfrontal gray and white matter compartment volumes, obtained by a MRI protocol, were analyzed with a 2 x 2 factorial multivariate analysis of variance approach for associations with a TS or ADHD factor in 11 boys with TS only, 14 with TS + ADHD, 12 with ADHD only, and 26 healthy boys.
Results: In subjects with TS, the right frontal lobe showed a larger proportion of white matter. In addition, results were consistent with previous reports of reduced frontal lobe volumes associated with ADHD. Our analyses suggested these reductions to be mainly the consequence of smaller gray matter volumes, particularly on the left.
Conclusions: These findings, suggesting the volumetric composition of frontal lobe tissue to be different in TS, support the hypothesis proposing frontostriatal pathway involvement in the pathophysiology of the disorder. Differences in composition of right frontal lobe attributable to white matter do not definitively implicate the hypothesized fiber pathways; however, considered in the context of the unilateral directionality of frontal–striatal circuitry, these results suggest the white matter connections as one explanation for basal ganglia anomalies (loss of normal left > right asymmetry) in TS.
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