Neural Circuitry Engaged During Unsuccessful Motor Inhibition in Pediatric Bipolar Disorder

Leibenluft, Ellen; Rich, Brendan A.; Vinton, Deborah; Nelson, Eric E.; Fromm, Stephen J.; Berghorst, Lisa H.; Joshi, Paramjit T.; Robb, Adelaide S.; Schachar, Russell; Dickstein, Daniel P.; McClure, Erin B.; Pine, Daniel S.

doi:10.1176/ajp.2007.164.1.52

Cited by 116 publications

(111 citation statements)

References 42 publications

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“…The stop signal task was a rapid, mixed-trial, event-related paradigm, used in previous studies (18, 19). On all trials, a fixation cross appeared centrally against a black background for 500 ms, followed by a white “X” or “O” go signal for 1000 ms.…”

Section: Methodsmentioning

confidence: 99%

“…Performance was measured by (1) go trial accuracy and reaction time, (2) stop trial accuracy, (3) “inhibit delay” or the time interval between the onset of the go and stop signals, (4) the stop signal reaction time (SSRT) calculated as the mean go reaction time minus the mean inhibit delay in subjects who inhibited successfully on 50% of the stop trials (8, 19). If a subject’s stop trial accuracy deviated from 50%, an interpolation algorithm was used to compute SSRT: the mean inhibit delay was subtracted from the go reaction time at the X th percentile of the go reaction times, where X is the subject’s percent accuracy on stop trials.…”

Section: Methodsmentioning

confidence: 99%

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Defining the Neural Substrate of the Adult Outcome of Childhood ADHD: A Multimodal Neuroimaging Study of Response Inhibition

Székely

Sudre

Sharp

et al. 2017

AJP

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Background Understanding the neural processes tied to the adult outcome of childhood attention-deficit/hyperactivity disorder (ADHD) could guide novel interventions to improve its clinical course. It has been argued that normalization of prefrontal cortical activity drives remission from ADHD, while anomalies in subcortical processes are ‘fixed’, present even in remission. Using multimodal neuroimaging of inhibitory processes, we test these hypotheses in adults followed since childhood, contrasting remitted against persistent ADHD. Methods Adult participants (35 persistent ADHD; 47 remitted ADHD; 99 never affected) were scanned with fMRI (n=85), magnetoencephalography (n=33) or both (n=63) during a response inhibition task. Results In fMRI analyses, during inhibition, right caudate anomalies both reflected a childhood ADHD history and were present even among those who remitted. By contrast, differences related to adult outcome emerged in cortical (right inferior frontal and inferior parietal/precuneus) and cerebellar regions. Here, the persistent ADHD group showed under-activation, whereas the remitted ADHD group did not differ significantly from the never-affected group. MEG showed that the association between adult symptom severity and prefrontal neuronal activity was confined to the time window covering the act of inhibition (300–350 ms). Group differences in cerebellar and parietal neuronal activity occurred during the time window of performance monitoring processes (500–600 ms). Conclusions By combining fMRI and MEG we pinpoint the location and time window of neuronal activity that underpins the adult outcome of ADHD. We thus separate the cortico-cerebellar processes tied to clinical course of ADHD from the subcortical processes that are not.

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Defining the Neural Substrate of the Adult Outcome of Childhood ADHD: A Multimodal Neuroimaging Study of Response Inhibition

Székely

Sudre

Sharp

et al. 2017

AJP

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“…BD (n ϭ 22) and control (n ϭ 21) subjects were recruited as described (28,54). The National Institute of Mental Health (NIMH) Institutional Review Board approved the study.…”

Section: Methodsmentioning

confidence: 99%

Limbic hyperactivation during processing of neutral facial expressions in children with bipolar disorder

Rich

Vinton

Roberson‐Nay

et al. 2006

Proc. Natl. Acad. Sci. U.S.A.

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Reflecting a paradigm shift in clinical neuroscience, many chronic psychiatric illnesses are now hypothesized to result from perturbed neural development. However, most work in this area focuses on schizophrenia. Here, we extend this paradigm to pediatric bipolar disorder (BD), thus demonstrating traction in the developmental psychobiology perspective. To study amygdala dysfunction, we examined neural mechanisms mediating face processing in 22 youths (mean age 14.21 ؎ 3.11 yr) with BD and 21 controls of comparable age, gender, and IQ. Event-related functional MRI compared neural activation when attention was directed to emotional aspects of faces (hostility, subjects' fearfulness) vs. nonemotional aspects (nose width). Compared with controls, patients perceived greater hostility in neutral faces and reported more fear when viewing them. Also, compared with controls, patients had greater activation in the left amygdala, accumbens, putamen, and ventral prefrontal cortex when rating face hostility, and greater activation in the left amygdala and bilateral accumbens when rating their fear of the face. There were no between-group behavioral or neural differences in the nonemotional conditions. Results implicate deficient emotion-attention interactions in the pathophysiology of BD in youth and suggest that developmental psychobiology approaches to chronic mental illness have broad applicability.amygdala ͉ faces ͉ functional MRI R ecently, psychology and psychiatry have witnessed a major paradigm shift: virtually all chronic adult mental illnesses are now thought to result from long-term perturbations in neural development. Two lines of research support this perspective: family-based͞longitudinal studies and neurobiological studies. Family-based and longitudinal studies implicate developmental perturbations in a range of conditions, including behavior disorders, substance abuse, mood disorders, and psychoses (1-3). However, virtually all research on developmental neurobiology focuses on schizophrenia, where data implicate a neural circuit connecting the dorsolateral prefrontal cortex, striatum, and hippocampus (4, 5). Neurocognitive correlates of schizophrenia, such as deficient working memory, are thought to result from dysfunction in this circuit (6). An important next step is the extension of the developmental neurobiological approach to other mental illnesses and other neural systems associated with information processing and emotion regulation.For several reasons, bipolar disorder (BD) is an ideal illness in which to expand the emerging developmental paradigm by conducting neurobiologically oriented developmental research. BD causes marked disruption in social, academic, and family function. Major questions persist concerning the boundaries of the condition in children; neurobiological data might ultimately resolve them. Most importantly, research in adult patients and animals implicates a circuit encompassing the amygdala, striatum, and ventral prefrontal cortex (VPFC) in the pathophysiology of BD (7). This circu...

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“…A shift away from PVC in depression, might suggest a change in the regulatory skills in depressed patients (110, 111). On the contrary, reduced behavioral regulation, associated with altered fronto-striatal activation, has been found in BD and MDD during response inhibition and working memory tasks (112) (113, 114). However, unlike MDD, BD is typically characterized by increased reward-seeking behavior (115).…”

Section: Current Research Of Circuit Interactions In Mood Disordersmentioning

confidence: 97%

Current Neural and Behavioral Dimensional Constructs Across Mood Disorders

Langenecker

Jacobs

Passarotti

2014

Curr Behav Neurosci Rep

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Our understanding of the underlying neurobiology for mood disorders is still limited. We present an integrated model for conceptualizing and understanding mood disorders drawing upon a broad literature pertinent to mood disorders. The integrated model of emotion processing and regulation incorporates the linguistic constructs of the Research Domain Criteria (RDoC) initiative. In particular, we focus on the Positive Valence domain/circuit (PVC), highlighting recent reward research and the Negative Valence domain/circuit (NVC), highlighting rumination. Furthermore, we also illustrate the Cognitive Control and Problem Solving (CCaPS) circuit, which is heavily involved in emotion regulation, as well as the default mode network (DMN) and interactions between circuits. We conclude by proposing methods for addressing challenges in the developmental study of mood disorders including using high-risk design that incorporates risk for many disorders.

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Neural Circuitry Engaged During Unsuccessful Motor Inhibition in Pediatric Bipolar Disorder

Cited by 116 publications

References 42 publications

Defining the Neural Substrate of the Adult Outcome of Childhood ADHD: A Multimodal Neuroimaging Study of Response Inhibition

Defining the Neural Substrate of the Adult Outcome of Childhood ADHD: A Multimodal Neuroimaging Study of Response Inhibition

Limbic hyperactivation during processing of neutral facial expressions in children with bipolar disorder

Current Neural and Behavioral Dimensional Constructs Across Mood Disorders

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