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000062197 0247_ $$2DOI$$a10.1097/CHI.0b013e3181676545
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000062197 041__ $$aeng
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000062197 084__ $$2WoS$$aPsychology, Developmental
000062197 084__ $$2WoS$$aPediatrics
000062197 084__ $$2WoS$$aPsychiatry
000062197 1001_ $$0P:(DE-HGF)0$$aHuebner, T.$$b0
000062197 245__ $$aMorphometric brain abnormalities in boys with conduct disorder
000062197 260__ $$aKidlington [u.a.]$$bElsevier$$c2008
000062197 300__ $$a540 - 547
000062197 3367_ $$0PUB:(DE-HGF)16$$2PUB:(DE-HGF)$$aJournal Article
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000062197 440_0 $$018041$$aJournal of the American Academy of Child and Adolescent Psychiatry$$v47$$x0890-8567$$y5
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000062197 520__ $$aChildren with the early-onset type of conduct disorder (CD) are at high risk for developing an antisocial personality disorder. Although there have been several neuroimaging studies on morphometric differences in adults with antisocial personality disorder, little is known about structural brain aberrations in boys with CD.Magnetic resonance imaging and voxel-based morphometry were used to assess abnormalities in gray matter volumes in 23 boys ages 12 to 17 years with CD (17 comorbid for attention-deficit/hyperactivity disorder) in comparison with age- and IQ-matched controls.Compared with healthy controls, mean gray matter volume was 6% smaller in the clinical group. Compared with controls, reduced gray matter volumes were found in the left orbitofrontal region and bilaterally in the temporal lobes, including the amygdala and hippocampus on the left side in the CD group. Regression analyses in the clinical group indicated an inverse association of hyperactive/impulsive symptoms and widespread gray matter abnormalities in the frontoparietal and temporal cortices. By contrast, CD symptoms correlated primarily with gray matter reductions in limbic brain structures.The data suggest that boys with CD and comorbid attention-deficit/hyperactivity disorder show brain abnormalities in frontolimbic areas that resemble structural brain deficits, which are typically observed in adults with antisocial behavior.
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000062197 650_2 $$2MeSH$$aAdolescent
000062197 650_2 $$2MeSH$$aAmygdala: pathology
000062197 650_2 $$2MeSH$$aAntisocial Personality Disorder: diagnosis
000062197 650_2 $$2MeSH$$aAntisocial Personality Disorder: physiopathology
000062197 650_2 $$2MeSH$$aAttention Deficit Disorder with Hyperactivity: diagnosis
000062197 650_2 $$2MeSH$$aAttention Deficit Disorder with Hyperactivity: physiopathology
000062197 650_2 $$2MeSH$$aBrain: pathology
000062197 650_2 $$2MeSH$$aChild
000062197 650_2 $$2MeSH$$aComorbidity
000062197 650_2 $$2MeSH$$aConduct Disorder: diagnosis
000062197 650_2 $$2MeSH$$aConduct Disorder: physiopathology
000062197 650_2 $$2MeSH$$aDominance, Cerebral: physiology
000062197 650_2 $$2MeSH$$aFrontal Lobe: pathology
000062197 650_2 $$2MeSH$$aHippocampus: pathology
000062197 650_2 $$2MeSH$$aHumans
000062197 650_2 $$2MeSH$$aImage Processing, Computer-Assisted
000062197 650_2 $$2MeSH$$aMagnetic Resonance Imaging
000062197 650_2 $$2MeSH$$aMale
000062197 650_2 $$2MeSH$$aParahippocampal Gyrus: pathology
000062197 650_2 $$2MeSH$$aParietal Lobe: pathology
000062197 650_2 $$2MeSH$$aPrefrontal Cortex: pathology
000062197 650_2 $$2MeSH$$aRisk Factors
000062197 650_2 $$2MeSH$$aTemporal Lobe: pathology
000062197 650_7 $$2WoSType$$aJ
000062197 65320 $$2Author$$aconduct disorder
000062197 65320 $$2Author$$amorphometry
000062197 65320 $$2Author$$amagnetic resonance imaging
000062197 65320 $$2Author$$alimbic system
000062197 7001_ $$0P:(DE-HGF)0$$aVloet, T. D.$$b1
000062197 7001_ $$0P:(DE-HGF)0$$aMarx, I.$$b2
000062197 7001_ $$0P:(DE-HGF)0$$aKonrad, K.$$b3
000062197 7001_ $$0P:(DE-Juel1)131720$$aFink, G. R.$$b4$$uFZJ
000062197 7001_ $$0P:(DE-HGF)0$$aHerpertz, S.$$b5
000062197 7001_ $$0P:(DE-HGF)0$$aHerpertz-Dahlmann, B.$$b6
000062197 773__ $$0PERI:(DE-600)2022051-0$$a10.1097/CHI.0b013e3181676545$$gVol. 47, p. 540 - 547$$p540 - 547$$q47<540 - 547$$tJournal of the American Academy of Child and Adolescent Psychiatry$$v47$$x0890-8567$$y2008
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