Hyperactivity and Motoric Activity in ADHD: Characterization, Assessment, and Intervention

Gawrilow, Caterina; Kühnhausen, Jan; Schmid, Johanna; Stadler, Gertraud

doi:10.3389/fpsyt.2014.00171

Cited by 25 publications

(25 citation statements)

References 126 publications

(118 reference statements)

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“…timing, inhibiting responses, tolerating delay) give rise to the highly diverse symptom expression that characterizes ADHD. 13,33 Delayed development within the later maturing areas of the brain has been suggested as a causal mechanism in some theories. 13,34 STRUCTURAL NEUROIMAGING Several recent reviews have detailed structural imaging in children with ADHD.…”

Section: Neurobiologymentioning

confidence: 98%

“…32,34 State (vigilance) regulation theories hypothesize that the core deficit in ADHD is impaired regulation of activation state (arousal). 33,36 Some symptoms are attributed to dysfunctional fluctuations in arousal (e.g. deficits in sustained attention) whereas others are a result of autoregulatory efforts to reach stability by increasing external stimulation (e.g.…”

Section: Neurobiologymentioning

confidence: 99%

“…34 Impaired bottom-up (limbic) regulation of reward-related processing has also been proposed. 13,33,35 Multiple pathway theories postulate that individually variable deficits in multiple core functions (e.g. timing, inhibiting responses, tolerating delay) give rise to the highly diverse symptom expression that characterizes ADHD.…”

Section: Neurobiologymentioning

confidence: 99%

“…8,13,[32][33][34][35] The behavioral neuroenergetics theory postulates neuronal energy insufficiency as a result of inadequate production of lactate by astrocytes. 32,34 State (vigilance) regulation theories hypothesize that the core deficit in ADHD is impaired regulation of activation state (arousal).…”

Section: Neurobiologymentioning

confidence: 99%

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Neurobiology of Adult ADHD: Emerging Evidence for Network Dysfunctions

Jadidian¹,

Hurley²,

Taber³

2015

JNP

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FIGURE 1. Changes in cortical thickness provide one measure of brain maturation. A large longitudinal study found that for most areas of cortex, children with attention deficit hyperactivity disorder (ADHD) reach peak cortical thickness several years later than typically developing children, supporting presence of developmental delay. 1 The rate of cortical thinning also differed between the group who continued to meet diagnostic criteria into adulthood (persistent ADHD) and those who did not (remitted ADHD). 2 Areas of cortex in which the rate of thinning correlated with adult symptom level (green, more symptoms associated with more thinning) are approximated on medial and lateral simplified representations of cortex. 2 An earlier study also identified multiple areas in which cortex was thinner in adults with persistent ADHD compared with controls (orange). 3 In addition, this study noted some areas of thicker cortex in remitted ADHD when compared with persistent ADHD (blue). FIGURE 2. Two recent functional magnetic resonance imaging (fMRI) studies have used cued reaction time tasks to assess differences between adults with a childhood diagnosis of ADHD and controls in task-related activations and functional connectivity. 4,5 Left. One study used the area with the highest level of activation associated with cognitive control (right dorsolateral prefrontal cortex) as the seed to assess functional connectivity associated with cognitive control. 5 The ADHD group had lower connectivity than the control group to multiple areas (orange, left putamen, left inferior frontal gyrus, and bilateral subgenual cingulate cortex), but connectivity was not correlated with symptom severity. Right. The other study assessed thalamocortical functional connectivity and brain activations associated with response preparation. 4 The persistent ADHD group had lower connectivity compared with the remitted ADHD group from the seed region in thalamus to several areas in prefrontal cortex. The locations of the cluster centers (blue, bilateral frontopolar cortex and left dorsolateral prefrontal cortex) are approximated onto a dorsal view of the cortical surface. An unexpected finding was that there were no significant differences between the remitted ADHD group and persistent ADHD in brain activations associated with response preparation. COVER AND FIGURE 3. Left. A resting state fMRI study in adults with a childhood diagnosis of ADHD reported significantly reduced functional connectivity within the default mode network in persistent ADHD. 6 The areas in which either remitted ADHD (blue) or controls (orange) had greater connectivity from the seed region (black, posterior cingulate cortex) compared with persistent ADHD are approximated on a midline MRI. 6 This study also reported that neither ADHD group exhibited the expected negative functional connectivity between the other default mode network seed region (medial prefrontal cortex) and dorsolateral prefrontal cortex . Right. A resting state fMRI study in medication naive adults with ADHD re...

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Section: Neurobiologymentioning

confidence: 98%

Section: Neurobiologymentioning

confidence: 99%

Section: Neurobiologymentioning

confidence: 99%

Section: Neurobiologymentioning

confidence: 99%

See 2 more Smart Citations

Neurobiology of Adult ADHD: Emerging Evidence for Network Dysfunctions

Jadidian¹,

Hurley²,

Taber³

2015

JNP

View full text Add to dashboard Cite

show abstract

“…Two studies using actigraphy reported on gross motor activity in the course of schizophrenia ( 16 , 17 ). Finally, Gawrilow and colleagues summarized the importance of motor activity in ADHD ( 18 ).…”

mentioning

confidence: 99%