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The present study employed high-density ERPs to examine the effect of induced sad mood on the spatiotemporal correlates of conflict monitoring and resolution in a colour-word Stroop interference task. Neuroimaging evidence and dipole modelling implicates the involvement of the anterior cingulate cortex (ACC) and medial prefrontal cortex (mPFC) regions in conflict-laden interference control. On the basis that these structures have been found to mediate emotion-cognition interactions in negative mood states, it was predicted that Stroop-related cognitive control, which relies heavily on anterior neural sources, would be affected by effective sad mood provocation. Healthy participants (N=14) were induced into transient sadness via use of autobiographical sad scripts, a well-validated mood induction technique (Liotti et al., 2000a, 2002). In accord with previous research, interference effects were shown at both baseline and sad states while Stroop conflict was associated with early (N450) and late (Late Positive Component; LPC) electrophysiological modulations at both states. Sad mood induction attenuated the N450 effect in line with our expectation that it would be susceptible to modulation by mood, given its purported anterior limbic source. The LPC effect was displayed at the typical posterior lateral sites but, as predicted, was not affected by sad mood. However, frontocentral LPC activity-presumably generated from an additional anterior limbic source-was affected at sad state, hinting a role in conflict monitoring. Although the neurophysiological underpinnings of interference control are yet to be clarified, this study provided further insight into emotion-cognition interactions as indexed by Stroop conflict-laden processing., (Copyright © 2012 Elsevier B.V. All rights reserved.)

High-density ERPs were recorded in eight adults with persistent developmental stuttering (PERS) and eight matched normally fluent (CONT) control volunteers while participants either repeatedly uttered the vowel 'ah' or listened to their own previously recorded vocalizations. The fronto-central N1 auditory wave was reduced in response to spoken vowels relative to heard vowels (auditory-vocal gating), but no difference in the extent of such modulation was found in the PERS group. Abnormalities in the PERS group were restricted to the LISTEN condition, in the form of early N1 and late N3 amplitude changes. Voltage of the N1 wave was significantly reduced over right inferior temporo-occipital scalp in the PERS group. A laterality index derived from N1 voltage moderately correlated with the PERS group's assessed pre-experiment stuttering frequency. Source localization with sLORETA (Pascual-Marqui, R. D. (2002). Standardized low-resolution brain electromagnetic tomography (sLORETA): Technical details. Methods & Findings in Experimental & Clinical Pharmacology, 24, 5-12.) revealed that at the peak of the N1 the PERS group displayed significantly greater current density in right primary motor cortex than the CONT group, suggesting abnormal early speech-motor activation. Finally, the late N3 wave was reduced in amplitude over inferior temporo-occipital scalp, more so over the right hemisphere. sLORETA revealed that in the time window of the N3 the PERS group showed significantly less current density in right secondary auditory cortex than the CONT group, suggesting abnormal speech sound perception. These results point to a deficit in auditory processing of speech sounds in persistent developmental stuttering, stemming from early increased activation of right rolandic area and late reduced activation in right auditory cortex., (Copyright © 2010 Elsevier Inc. All rights reserved.)

Somatotopy within the orofacial region of the human motor cortex has been a central concept in interpreting the results of neuroimaging and transcranial magnetic stimulation studies of normal and disordered speech. Yet, somatotopy has been challenged by studies showing overlap among the effectors within the homunculus. In order to address this dichotomy, we performed four voxel-based meta-analyses of 54 functional neuroimaging studies of non-speech tasks involving respiration, lip movement, tongue movement, and swallowing, respectively. While the centers of mass of the clusters supported the classic homuncular view of the motor cortex, there was significant variability in the locations of the activation-coordinates among studies, resulting in an overlapping arrangement. This "somatotopy with overlap" might reflect the intrinsic functional interconnectedness of the oral effectors for speech production.

Background: Theories of attention-deficit/hyperactivity disorder (ADHD) posit either executive deficits and/or alterations in motivational style and reward processing as core to the disorder. Effects of motivational incentives on electrophysiological correlates of inhibitory control and relationships between motivation and stimulant medication have not been explicitly tested., Methods: Children (9-15 years) with combined-type ADHD (n = 28) and matched typically developing children (CTRL) (n = 28) performed a go/no-go task. Electroencephalogram data were recorded. Amplitude of two event-related potentials, the N2 and P3 (markers of response conflict and attention), were measured. The ADHD children were all stimulant responders tested on and off their usual dose of methylphenidate; CTRLs were never medicated. All children performed the task under three motivational conditions: reward; response cost; and baseline, in which points awarded/deducted for inhibitory performance varied., Results: There were effects of diagnosis (CTRL > ADHD unmedicated), medication (on > off), and motivation (reward and/or response cost > baseline) on N2 and P3 amplitude, although the N2 diagnosis effect did not reach statistical significance (p = .1). Interactions between motivation and diagnosis/medication were nonsignificant (p > .1)., Conclusions: Motivational incentives increased amplitudes of electrophysiological correlates of response conflict and attention in children with ADHD, towards the baseline (low motivation) amplitudes of control subjects. These results suggest that, on these measures, motivational incentives have similar effects in children with ADHD as typically developing CTRLs and have additive effects with stimulant medication, enhancing stimulus salience and allocation of attentional resources during response inhibition., (Copyright 2010 Society of Biological Psychiatry. Published by Elsevier Inc. All rights reserved.)

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 acquisition of volitional control depends, in part, on developing the ability to countermand a planned action. Many tasks have been used to tap the efficiency of this process, but few studies have investigated how it may be modulated by participants' motivation. Multiple mechanisms may be involved in the deliberate exercise of caution when incentives are provided. For example, control may involve modulation of the efficiency of the countermanding process, and/or inhibitory modulation of the impulse to go. One of the most commonly used paradigms to assess control of action is the Stop Signal Task, in which a primary Go stimulus is occasionally followed by a countermanding Stop signal, allowing a Stop Signal Reaction Time (SSRT) to be inferred as the outcome of a "horse race" between the go and countermanding processes. Here, we present a computational model in which high task motivation modulates proactive pre-stimulus inhibition of the go response. This allows responses to be calibrated so as to fall within a time-window that maximizes the probability of success, regardless of trial type, but does not decrease the observed SSRT. We report empirical support for the model from a sample of typically developing children, and discuss the broader implications for operationalizing measures of volitional control.

Magnetoencephalography (MEG) was recorded while 5-7 year-old children were performing a visual-spatial memory recognition task. Full-term children showed greater gamma-band (30-50 Hz) amplitude in the right temporal region during the task, than children who were born extremely preterm. These results may represent altered brain processing in extremely preterm children who escape major impairment.

Background: A core deficit in inhibitory control may account for a wide range of dysfunctional behaviors in attention-deficit/hyperactivity disorder (ADHD)., Methods: Event-related potentials were measured in 10 children with ADHD and 10 healthy children during a task specifically involving response inhibition (Stop signal task)., Results: In response to all Stop signals, control participants produced a large negative wave at 200 msec (N200) over right inferior frontal cortex, which was markedly reduced in ADHD children. The N200 amplitude was significantly correlated across subjects with response-inhibition performance. In response to the Go stimuli, ADHD children showed a reduced slow positive wave (250-500 msec) in anticipation of failed inhibitions over right frontal scalp regions., Conclusions: ADHD children appear to have an abnormality in an early-latency, right inferior frontal processing component critical to the initiation of normal response-inhibition operations. They also appear to have a right frontal abnormality associated to the covert processing of Go stimuli preceding failed inhibitions. By providing timing and processing component specificity, these results extend the findings of recent functional MRI studies of inhibitory control reporting right frontal abnormalities in ADHD.

Background: Affective disorders are associated with comorbidity of depression and anxiety symptoms. Positron emission tomography resting-state studies in affective disorders have generally failed to isolate specific symptom effects. Emotion provocation studies in healthy volunteers have produced variable results, due to differences in experimental paradigm and instructions., Methods: To better delineate the neural correlates of sad mood and anxiety, this study used autobiographical memory scripts in eight healthy women to generate sadness, anxiety, or a neutral relaxed state in a within-subject design., Results: Sadness and anxiety, when contrasted to a neutral emotional state, engaged a set of distinct paralimbic-cortical regions, with a limited number of common effects. Sadness was accompanied by specific activations of the subgenual cingulate area (BA) 25 and dorsal insula, specific deactivation of the right prefrontal cortex BA 9, and more prominent deactivation of the posterior parietal cortex BAs 40/7. Anxiety was associated with specific activations of the ventral insula, the orbitofrontal and anterior temporal cortices, specific deactivation of parahippocampal gyri, and more prominent deactivation of the inferior temporal cortex BAs 20/37., Conclusions: These findings are interpreted within a model in which sadness and anxiety are represented by segregated corticolimbic pathways, where a major role is played by selective dorsal cortical deactivations during sadness, and ventral cortical deactivations in anxiety.

Several lines of evidence suggest impaired right hemisphere function in depression. In order to further investigate this phenomenon, simple reaction times (RTs) to lateralized visual stimuli were studied in patients with mild unipolar depression, in patients with chronic anxiety, and in medical patients free of psychiatric symptoms. The results showed a marked slowing of RTs to left visual field (right hemisphere) stimuli in depressed patients. Anxious patients showed a trend toward an opposite asymmetry, with slower responses to right field (left hemisphere) stimuli. In the nonpsychiatric group no visual field differences were present. The results are discussed in light of two alternative interpretations: depression may engage the right hemisphere's mechanisms, interfering with its functioning at a premotor level, or it may influence the regulation of performance by arousal and vigilance mechanisms lateralized to the right hemisphere, possibly operating at an earlier sensory stage.