2000
DOI: 10.1080/026990500120682
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Neuroimaging variables related to development of Secondary Attention Deficit Hyperactivity Disorder after closed head injury in children and adolescents

Abstract: The data support an association between S-ADHD and injury in either or both the thalamus and basal ganglia, but they do not definitively demonstrate whether injury in either structure has an effect on S-ADHD in the absence of injury in the other.

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Cited by 59 publications
(12 citation statements)
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“…Poorer preinjury family function and greater premorbid psychosocial adversity is associated with postinjury ADHD symptoms and SADHD [20, 48, 49]. Brain correlates of SADHD include right putamen or thalamic lesions [50, 51], and orbital frontal gyrus lesions [46]. These anatomical findings suggest that lesions in varied locations along specific cortico-striatal-pallidal-thalamic loops may generate a clinical syndrome of SADHD.…”
Section: Introductionmentioning
confidence: 99%
“…Poorer preinjury family function and greater premorbid psychosocial adversity is associated with postinjury ADHD symptoms and SADHD [20, 48, 49]. Brain correlates of SADHD include right putamen or thalamic lesions [50, 51], and orbital frontal gyrus lesions [46]. These anatomical findings suggest that lesions in varied locations along specific cortico-striatal-pallidal-thalamic loops may generate a clinical syndrome of SADHD.…”
Section: Introductionmentioning
confidence: 99%
“…Trauma to the thalamus and basal ganglia, for example, can produce new-onset ADHD symptoms in children and adolescents (23). Functional imaging studies have shown that activation of distributed portions of CSTC circuits, including the thalamus, is abnormal in individuals with ADHD (6).…”
mentioning
confidence: 99%
“…Herskovits et al [1999] reported an association between lesions within the right putamen detected 3 months after TBI and diagnosis of secondary ADHD 1 year after TBI. In an overlapping cohort, Gerring et al [2000] found that for children with thalamus and/or basal ganglia injury, the odds of developing secondary ADHD were three times higher than among children without injuries identified in those regions. In contrast, other groups have not found associations between number and/or location of injury and development of features of secondary ADHD [Leblanc et al, 2005; Max et al, 2005].…”
Section: Magnetic Resonance Imagingmentioning
confidence: 96%