1998
DOI: 10.1046/j.1468-1331.1998.510067.x
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The striatum in a putative cerebral network activated by verbal awareness in normals and in ADHD children

Abstract: The aim of the present study was to evaluate the striatum's involvement in verbal awareness (semantic processing and supra-modal attention) in normals and children with attention deficit hyperactivity disorder (ADHD). Our previous finding of striatal hypoperfusion in ADHD at rest, supports our prediction that the striatum will also show reduced activation in response to tasks requiring verbal awareness. Regional cerebral blood flow (rCBF) was studied with the Xenon133 SPECT method in 12 boys with ADHD and six … Show more

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Cited by 42 publications
(19 citation statements)
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“…pB, raclopride binding potential. A second line of evidence for deficiency in dopaminergic pathways was the early demonstration with 133 Xe in single PET of dysfunctional striatum in ADHD (Lou et al 1984), confirmed in an independent patient group (Lou et al 1998). This discovery established ADHD as the first member of a class of neurodevelopmental disorders of frontal-subcortical-cortical circuits controlling behaviour.…”
Section: Discussionmentioning
confidence: 94%
“…pB, raclopride binding potential. A second line of evidence for deficiency in dopaminergic pathways was the early demonstration with 133 Xe in single PET of dysfunctional striatum in ADHD (Lou et al 1984), confirmed in an independent patient group (Lou et al 1998). This discovery established ADHD as the first member of a class of neurodevelopmental disorders of frontal-subcortical-cortical circuits controlling behaviour.…”
Section: Discussionmentioning
confidence: 94%
“…For instance, striatal hypoperfusion is found in ADHD at rest using SPECT, and the right striatum has low activation in a verbal awareness task in ADHD [80] . In a stop signal task, patients show lower power of response in the left caudate [10] .…”
Section: Basal Gangliamentioning
confidence: 99%
“…9 As discussed earlier, there is also evidence of disruption in DAT levels in subjects with ADHD, although the findings are inconsistent (reviewed 5 ) and difficult to interpret because DAT levels are a function of both the density of DA terminals and the number of DATs per terminal. Decreased DA release could also reflect prefrontal pathology, which has been consistently documented in ADHD (reviewed 28,29 ) since frontal-striatal glutamatergic circuits regulate striatal DA release. 30,31 However, prefrontal pathology in ADHD could also indicate improper dopaminergic regulation of frontal regions.…”
Section: Decreased Da Releasementioning
confidence: 99%