MRI parcellation of the frontal lobe in boys with attention deficit hyperactivity disorder or Tourette syndrome

Dysfunction of frontal–striatal–thalamic–frontal circuitry has been hypothesized to underlie both attention deficit hyperactivity disorder (ADHD) and Tourette syndrome (TS). Several research groups have therefore used anatomic magnetic resonance imaging (aMRI) to obtain volumetric measurements of su...

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Veröffentlicht in:Psychiatry research 2002-11, Vol.116 (1), p.63-81
Hauptverfasser: Kates, Wendy R, Frederikse, Melissa, Mostofsky, Stewart H, Folley, Bradley S, Cooper, Karen, Mazur-Hopkins, Patricia, Kofman, Ora, Singer, Harvey S, Denckla, Martha B, Pearlson, Godfrey D, Kaufmann, Walter E
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Sprache:eng
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Zusammenfassung:Dysfunction of frontal–striatal–thalamic–frontal circuitry has been hypothesized to underlie both attention deficit hyperactivity disorder (ADHD) and Tourette syndrome (TS). Several research groups have therefore used anatomic magnetic resonance imaging (aMRI) to obtain volumetric measurements of subregions of the frontal lobe in these disorders. Most previous studies have relied on subparcellation methods that utilize callosal landmarks to derive subregions of the frontal lobe. In contrast, we present here an investigation of frontal lobe morphometry in ADHD and TS based on a reliable frontal subparcellation protocol that combines contiguous sulcal/gyral boundaries to derive frontal lobe modules based on prior functional studies. This highly reliable procedure subdivides the frontal lobe into five major modules: prefrontal, premotor, motor (precentral gyrus), anterior cingulate, and deep white matter. The first four modules are also segmented into gray and gyral white matter compartments. The protocol was applied to T1-weighted, SPGR coronal MRI images of 13 school-aged boys with ADHD, 13 boys with TS, and 13 age- and gender-matched controls. In ADHD, we found volumetric reductions in both the gray and white matter of the prefrontal cortex. These findings, in conjunction with previous reports on basal ganglia abnormalities, suggest that prefrontal–striatal pathways may be anomalous in ADHD. In TS, we found volumetric decreases in the left deep frontal white matter. Decreases in deep white matter suggest the presence of abnormalities in long associational and projection fiber bundles in TS. The findings of this study both confirm and extend our knowledge of the neurobiology of ADHD and TS, indicating that the reliable parcellation method presented has the potential of increasing our understanding of the role of the frontal lobe in developmental and psychiatric disorders.
ISSN:0925-4927
0165-1781
1872-7506
DOI:10.1016/S0925-4927(02)00066-5