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

Kates, Wendy R.; Frederikse, Melissa; Mostofsky, Stewart H.; Folley, Bradley S.; Cooper, Karen L.; Mazur-Hopkins, Patricia; Kofman, Ora; Singer, Harvey S.; Denckla, Martha B.; Pearlson, Godfrey D.; Kaufmann, Walter E.

doi:10.1016/s0925-4927(02)00066-5

Cited by 154 publications

(114 citation statements)

References 57 publications

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“…A smaller rostral corpus callosum in ADHD children had been reported relative to controls (see review (Giedd et al 2001)). It has also been suggested that the cortical-striatial circuitry is impaired in ADHD patients (Amen and Carmichael 1997;Casey et al 1997;Giedd et al 2001;Kates et al 2002). Our resting CBF data in the corpus callosum is consistent with these findings.…”

Section: Resting Cerebral Blood Flow Differences Between Shr and Wky supporting

confidence: 91%

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Quantitative regional cerebral blood flow MRI of animal model of attention-deficit/hyperactivity disorder

Danker

Duong

2007

Brain Research

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The spontaneously hypertensive rat (SHR) has been widely used as an animal model for attentiondeficit/hyperactivity disorder (AD/HD), a developmental disorder that affects 3-5% of school-age children. Quantitative high-resolution (180×180×1500 μm) perfusion magnetic resonance imaging was performed to evaluate regional CBF in AD/HD rats (SHR, n=7) and control Wistar Kyoto rats (WKY, n=9) in the frontal cortex, motor cortex, sensory cortex, corpus callosum, hippocampus, thalamus, globus pallidus, caudoputamen and whole brain. The accuracy of repeated cerebral blood flow (CBF) measurements within animals in these brain regions ranged from 3 to 10% (7 repeated measures) and across animals ranged from 15 to 18% (n = 7 rats), respectively, indicating highly accurate and reproducible CBF measurements. Regional CBF of the SHR were statistically different from those of the WKY rats in all structures analyzed (P<0.05) except for the caudate putamen (P=0.09) and the globus pallidus (P=0.12). Whole brain CBF of the SHR (1.5±0.2ml/gram/min, mean ±SD) was ∼25% higher than that of the WKY rats (1.2±0.2ml/gram/min), likely due to the hypertensive nature of the AD/HD rat model. Following normalization to eliminate global CBF differences, CBF in the medial prefrontal cortex, a structure thought to be the equivalent of the human dorsolateral prefrontal cortex and widely implicated in AD/HD, was found to be higher in SHR compared to WKY rats (P<0.05). The only other structure that was found to be statistically different after normalization is the corpus callosum (P<0.05). Since resting cerebral blood flow is intricately coupled to resting neural activity, these results suggest that there was abnormal resting neural activity in the medial prefrontal cortex and the corpus callosum between the control and AD/HD animals, consistent with the hyperactivity, impulsivity, inattention, and other AD/HD-like behaviors in this animal model.

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Section: Resting Cerebral Blood Flow Differences Between Shr and Wky supporting

confidence: 91%

“…A plethora of structures have been identified to be associated with ADHD. Some of these prominent structures are the frontal lobes, basal ganglia, cerebellum, and frontal-basal ganglia circuitry (Amen and Carmichael 1997;Casey et al 1997;Giedd et al 2001;Kates et al 2002). Prefrontal volume has been found to be 8.3% smaller in ADHD boys .…”

Section: Introductionmentioning

confidence: 99%

Quantitative regional cerebral blood flow MRI of animal model of attention-deficit/hyperactivity disorder

Danker

Duong

2007

Brain Research

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“…These have generally helped establish that in ADHD, there are widespread abnormalities in the volumes of brain circuitry relevant to attention and ADHD and attention networks G Bush .......................................................................................................................................................... motor control. In addition to relatively consistent findings of decreased total cerebral volume of B3 to 5% (Castellanos, 2001;Castellanos et al, 1996Castellanos et al, , 2002Seidman et al, 2005;Valera et al, 2007), volumetric studies have also found more specific abnormalities within defined regions of the lateral prefrontal cortex, cingulate cortex, striatum, cerebellum, and corpus callosum (Castellanos et al, 1996;Kates et al, 2002;Overmeyer et al, 2001;Semrud-Clikeman et al, 2000).…”

Section: Selected Adhd Imaging Datamentioning

confidence: 74%

Attention-Deficit/Hyperactivity Disorder and Attention Networks

Bush

2009

Neuropsychopharmacol

298

251

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Research attempting to elucidate the neuropathophysiology of attention-deficit/hyperactivity disorder (ADHD) has not only shed light on the disorder itself, it has simultaneously provided new insights into the mechanisms of normal cognition and attention. This review will highlight and integrate this bidirectional flow of information. Following a brief overview of ADHD clinical phenomenology, ADHD studies will be placed into a wider historical perspective by providing illustrative examples of how major models of attention have influenced the development of neurocircuitry models of ADHD. The review will then identify major components of neural systems potentially relevant to ADHD, including attention networks, reward/feedbackbased processing systems, as well as a 'default mode' resting state network. Further, it will suggest ways in which these systems may interact and be influenced by neuromodulatory factors. Recent ADHD imaging data will be selectively provided to both illustrate the field's current level of knowledge and to show how such data can inform our understanding of normal brain functions. The review will conclude by suggesting possible avenues for future research.

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“…Author manuscript; available in PMC 2008 January 1. . Such disturbances are reflected in structural abnormalities of the basal ganglia and frontal cortex (Fredericksen et al, 2002;Kates et al, 2002;Ludolph et al, 2006) and in abnormal levels of dopamine, a crucial neurotransmitter crucial in frontal/basal-ganglia circuits (for review and discussion, see Albin, 2006;Kienast & Heinz, 2006;Mink, 2006;Rauch & Savage, 1997;Singer & Wendlandt, 2001). The frontal/basal-ganglia abnormalities are thought to result in decreased inhibition of frontal activity, leading to a hyperkinetic behavioral profile and an inability to suppress tics (Albin & Mink, 2006;Osmon & Smerz, 2005).…”

Section: Author Manuscriptmentioning

confidence: 99%

Speeded processing of grammar and tool knowledge in Tourette's syndrome

2007

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Tourette's syndrome (TS) is a developmental disorder characterized by motor and verbal tics. The tics, which are fast and involuntary, result from frontal/basal-ganglia abnormalities that lead to unsuppressed behaviors. Language has not been carefully examined in TS. We tested the processing of two basic aspects of language: idiosyncratic and rule-governed linguistic knowledge. Evidence suggests that idiosyncratic knowledge (e.g., in irregular past-tense formation; bring-brought) is stored in a mental lexicon that depends on the temporal-lobe-based declarative memory system that also underlies conceptual knowledge. In contrast, evidence suggests that rule-governed combination (e.g., in regular past-tenses; walk + -ed) takes place in a mental grammar that relies on the frontal/ basal-ganglia based procedural memory system, which also underlies motor skills such as how to use a hammer. We found that TS children were significantly faster than typically-developing control children at producing rule-governed past-tenses (slip-slipped, plim-plimmed, bring-bringed) but not irregular and other unpredictable past-tenses (bring-brought, splim-splam). They were also faster than controls at naming pictures of manipulated (hammer) but not non-manipulated (elephant) items. These data were not explained by a wide range of potentially confounding subject-and item-level factors. The results suggest that the processing of procedurally-based knowledge, both of grammar and of manipulated objects, is particularly speeded in TS. The frontal/basal-ganglia abnormalities may thus lead not only to tics, but to a wider range of rapid behaviors, including in the cognitive processing of rule-governed forms in language and other types of procedural knowledge. Keywords procedural memory; morphology; basal ganglia; picture naming; past tense; regular inflection Tourette's syndrome (TS) is a developmental disorder characterized by the presence of verbal and motor tics (APA, 1994). Tics, which may be expressed as "simple" or "complex" motor movements or vocalizations (e.g., "simple" grunting, or "complex" shouting of phrases), are both fast and involuntary (see references below and Tulen, Groeneveld, Romers, De Vries, & Van De Wetering, 2001). The tics appear to be caused by disturbances of the basal-ganglia and closely connected regions of cortex, especially motor and cognitive regions of the frontal lobes (Albin & Mink, 2006;Albin, Young, & Penney, 1989;Bradshaw, 2001;Singer & Wendlandt, *Corresponding author. Address: Brain and Language Lab, Department of Neuroscience, Georgetown University, Box 571464, Washington, DC 20057-1464, Tel: (202) Fax: (202) 687-6914, E-mail: michael@georgetown.edu Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note t...

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

Cited by 154 publications

References 57 publications

Quantitative regional cerebral blood flow MRI of animal model of attention-deficit/hyperactivity disorder

Quantitative regional cerebral blood flow MRI of animal model of attention-deficit/hyperactivity disorder

Attention-Deficit/Hyperactivity Disorder and Attention Networks

Speeded processing of grammar and tool knowledge in Tourette's syndrome

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