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Background: Deficits characteristic of attention deficit/hyperactivity disorder (ADHD), including poor attention and inhibitory control, are at least partially alleviated by factors that increase engagement of attention, suggesting a hypodopaminergic reward deficit. Lapses of attention are associated with attenuated deactivation of the default mode network (DMN), a distributed brain system normally deactivated during tasks requiring attention to the external world. Task-related DMN deactivation has been shown to be attenuated in ADHD relative to controls. We hypothesised that motivational incentives to balance speed against restraint would increase task engagement during an inhibitory control task, enhancing DMN deactivation in ADHD. We also hypothesised that methylphenidate, an indirect dopamine agonist, would tend to normalise abnormal patterns of DMN deactivation., Method: We obtained functional magnetic resonance images from 18 methylphenidate-responsive children with ADHD (DSM-IV combined subtype) and 18 pairwise-matched typically developing children aged 9-15 years while they performed a paced Go/No-go task. We manipulated motivational incentive to balance response speed against inhibitory control, and tested children with ADHD both on and off methylphenidate., Results: When children with ADHD were off-methylphenidate and task incentive was low, event-related DMN deactivation was significantly attenuated compared to controls, but the two groups did not differ under high motivational incentives. The modulation of DMN deactivation by incentive in the children with ADHD, off-methylphenidate, was statistically significant, and significantly greater than in typically developing children. When children with ADHD were on-methylphenidate, motivational modulation of event-related DMN deactivation was abolished, and no attenuation relative to their typically developing peers was apparent in either motivational condition., Conclusions: During an inhibitory control task, children with ADHD exhibit a raised motivational threshold at which task-relevant stimuli become sufficiently salient to deactivate the DMN. Treatment with methylphenidate normalises this threshold, rendering their pattern of task-related DMN deactivation indistinguishable from that of typically developing children., (© 2010 The Authors. Journal of Child Psychology and Psychiatry © 2010 Association for Child and Adolescent Mental Health.)

Objective: Previous studies have shown smaller brain volume and less gray matter in children with attention-deficit/hyperactivity disorder (ADHD). Relatively few morphological studies have examined structures thought to subserve inhibitory control, one of the diagnostic features of ADHD. We examined one such region, the pars opercularis, predicting a thinner cortex of the inferior frontal gyrus (IFG) in children with ADHD., Method: Structural images were obtained from 49 children (24 control; 25 ADHD combined subtype) aged 9 though 15 years. Images were processed using a volumetric pipeline to provide a fully automated estimate of regional volumes of gray and white matter. A further analysis using FreeSurfer provided measures of cortical thickness for each lobe, and for 13 regions in the frontal lobe., Results: Relative to controls, children with ADHD had smaller whole brain volume and lower gray matter, but not white matter, volumes in all lobes. An analysis of frontal regions showed a significant interaction of group by region. Planned contrasts showed bilateral thinner cortex in the pars opercularis in children with ADHD., Conclusions: Children with ADHD showed both diffuse and regional gray matter abnormalities. Consistent with its putative role in response inhibition, the cortex of the pars opercularis was thinner in children with ADHD who, as expected, had significantly poorer inhibitory performance on a Go/No-go task. These differences held for both hemispheres raising the possibility that a developmental abnormality of IFG might drive development of inhibition difficulties.

The map of the human motor cortex has lacked a representation for the intrinsic musculature of the larynx ever since the electrical stimulation studies of Penfield. In addition, there has been no attempt to localize this area using neuroimaging techniques. Because of the central importance of laryngeal function to vocalization, we sought to localize an area controlling the intrinsic muscles of the larynx by using functional magnetic resonance imaging and to place this area in a somatotopic context. We had subjects perform a series of oral tasks designed to isolate elementary components of phonation and articulation, including vocalization of a vowel, lip movement, and tongue movement. In addition, and for the first time in a neuroimaging study, we had subjects perform "glottal stops," in other words forced closure of the glottis in the absence of vocalizing. The results demonstrated a larynx-specific area in the motor cortex that is activated comparably by vocal and nonvocal laryngeal tasks. Converging evidence suggests that this area is the principal vocal center of the human motor cortex. Finally, the location of this larynx area is strikingly different from that reported in the monkey. We discuss the implications of this observation for the evolution of vocal communication in humans.

Objective: To determine if there are differences in the volume of the caudate and anterior cingulate cortex (ACC) between children with attention deficit hyperactivity disorder (ADHD) and controls, and if such differences are related to the subjects' history of stimulant treatment., Methods: We performed a case-control study in an academic medical center. Twenty-one healthy controls, 16 children with ADHD, combined type with a history of stimulant treatment, and 14 children with ADHD, combined type treatment naïve, underwent structural MRI. All children with ADHD were medication-free at the time of the MRI. Regional hemispheric volumes (in cm3) of caudate and anterior cingulate cortex were determined., Results: There were significant differences bilaterally on caudate volume for both ADHD groups vs controls, with no difference between the ADHD groups on either side. In contrast, the right ACC was significantly smaller for the ADHD-treatment naïve (ADHD/TN) group compared to the ADHD-treated (ADHD/Rx) and control group. The volume of left ACC approached significance contrast between ADHD/RX and ADHD/TN. There were no differences found between the ADHD/Rx and controls on the ACC volumes bilaterally., Conclusions: The results from this study indicate a relationship of previous treatment history with caudate and anterior cingulate volumetric changes in children with attention deficit hyperactivity disorder-combined type.

Objective: Difficulty with response inhibition is a cardinal symptom of attention deficit hyperactivity disorder (ADHD), combined type. Prefrontal and cingulate brain regions are known to be involved in inhibitory control. Event-related functional magnetic resonance imaging (fMRI) might establish if these regions differ in their activity in ADHD children relative to healthy comparison subjects., Method: Fifteen healthy comparison subjects and 17 children with ADHD, combined type, completed fMRI studies while performing the Stop Signal Task. Eight ADHD subjects were treatment naive; the remainder had a history of long-term treatment with stimulants, but they were medication free at the time of the fMRI. No subject had a learning disorder or a comorbid psychiatric condition (other than oppositional defiant disorder in the ADHD subjects)., Results: Both the ADHD and comparison subjects activated the right dorsolateral prefrontal cortex on "stop" trials relative to "go" trials; this increase was greater in ADHD subjects. When inhibition was unsuccessful (relative to successful inhibition), healthy comparison subjects strongly activated the anterior cingulate cortex and the left ventrolateral prefrontal cortex. In contrast, the ADHD subjects did not show these differences. Activations in treatment-naive and ADHD subjects treated in the long term did not differ significantly in any brain regions., Conclusions: In relation to comparison subjects, ADHD subjects failed to activate the anterior cingulate cortex and the left ventrolateral prefrontal cortex after unsuccessful inhibition. These findings appear in treatment-naive ADHD individuals and are unlikely to be an artifact of long-term treatment with stimulants or of abrupt termination of stimulants before imaging.

A functional MRI study compared activation in the red nucleus to that in the lateral cerebellar dentate nucleus during passive and active tactile discrimination tasks. The study pursued recent neuroimaging results suggesting that the cerebellum may be more associated with sensory processing than with the control of movement for its own sake. Because the red nucleus interacts closely with the cerebellum, the possibility was examined that activity in red nucleus might also be driven by the requirement for tactile sensory processing with the fingers rather than by finger movement alone. The red and dentate nuclei were about 300% more active (a combination of activation areas and intensities) during passive (non-motor) tactile stimulation when discrimination was required than when it was not. Thus, the red nucleus was activated by purely sensory stimuli even in the absence of the opportunity to coordinate finger movements or to use the sensory cues to guide movement. The red and dentate nuclei were about 70% more active during active tactile tasks when discrimination was required than when it was not (i.e., for simple finger movements alone). Thus, the red nucleus was most active when the fingers were being used for tactile sensory discrimination. In both the passive and active tactile tasks, the observed activation had a contralateralized pattern, with stronger activation in the left red nucleus and right dentate nucleus. Significant covariation was observed between activity in the red nucleus and the contralateral dentate during the discrimination tasks and no significant correlation between the red nucleus and the contralateral dentate activity was detected during the two non-discrimination tasks. The observed interregional covariance and contralateralized activation patterns suggest strong functional connectivity during tactile discrimination tasks. Overall, the pattern of findings suggests that the activity in the red nucleus, as in the lateral cerebellum, is more driven by the requirements for sensory processing than by motor coordination per se.

Subjective and physiologic effects of 33% inhaled Xe were measured with 15O-water positron emission tomography (PET) in 3 subjects at rest and during visual stimulation. The procedure was well tolerated. Robust functional activations of the visual cortex were obtained after xenon (Xe) inhalation as well as air breathing. However, Xe inhalation was followed by smaller size, but significant decreases of regional cerebral blood flow (rCBF) in visual cortex relative to the air-breathing baseline, both during visual stimulation and at rest. No such decreases were found in other sensory or motor regions.

Background Patients in recovery following episodes of major depressive disorder (MDD) remain highly vulnerable to future recurrence. Although psychological determinants of this risk are well established, little is known about associated biological mechanisms. Recent work has implicated the default mode network (DMN) in this vulnerability but specific hypotheses remain untested within the high risk, recovered state of MDD. Aims To test the hypothesis that there is excessive DMN functional connectivity during task performance within recovered-state MDD and to test for connected DMN cortical gyrification abnormalities. Method A multimodal structural and functional magnetic resonance imaging (fMRI) study, including task-based functional connectivity and cortical folding analysis, comparing 20 recovered-state patients with MDD with 20 matched healthy controls. Results The MDD group showed significant task-based DMN hyperconnectivity, associated with hypogyrification of key DMN regions (bilateral precuneus). Conclusions This is the first evidence of connected structural and functional DMN abnormalities in recovered-state MDD, supporting recent hypotheses on biological-level vulnerability. [ABSTRACT FROM AUTHOR]

BackgroundRecent models of major depressive disorder (MDD) have proposed the rostral anterior cingulate (rACC) and dorsomedial prefrontal cortex (dmPFC) as nexus sites in the dysfunctional regulation of cognitive-affective state. Limited evidence from remitted-state MDD supports these theories by suggesting that aberrant neural activity proximal to the rACC and the dmPFC may play a role in vulnerability to recurrence/relapse within this disorder. Here we present a targeted analysis assessing functional activity within these two regions of interest (ROIs) for groups with identified vulnerability to MDD: first, remitted, high predicted recurrence-risk patients; and second, patients suffering observed 1-year recurrence.MethodBaseline T2* images sensitive to blood oxygen level-dependent (BOLD) contrast were acquired from patients and controls during a Go/No-Go (GNG) task incorporating negative feedback, with 1-year patient follow-up to identify recurrence. BOLD contrast data for error commission (EC) and visual negative feedback (VNF) were used in an ROI analysis based on rACC and dmPFC coordinates from the literature, comparing patients versus controls and recurrence versus non-recurrence versus control groups.ResultsAnalysis of patients (n = 20) versus controls (n = 20) showed significant right dmPFC [Brodmann area (BA) 9] hypoactivity within the patient group, co-localized during EC and VNF, with additional significant rACC (BA 32) hypoactivity during EC. The results from the follow-up analysis were undermined by small groups and potential confounders but suggested persistent right dmPFC (BA 9) hypoactivity associated with 1-year recurrence.ConclusionsConvergent hypoactive right dmPFC (BA 9) processing of VNF and EC, possibly impairing adaptive reappraisal of negative experience, was associated most clearly with clinically predicted vulnerability to MDD. [ABSTRACT FROM PUBLISHER]