National Institute of Mental Health NIMH

Mesa, MD, United States

National Institute of Mental Health NIMH

Mesa, MD, United States
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Britton J.C.,National Institute of Mental Health NIMH | Bar-Haim Y.,Tel Aviv University | Clementi M.A.,National Institute of Mental Health NIMH | Sankin L.S.,National Institute of Mental Health NIMH | And 6 more authors.
Developmental Cognitive Neuroscience | Year: 2013

Attention Bias Modification Treatment (ABMT), an emerging treatment for anxiety disorders, is thought to modify underlying, stable patterns of attention. Therefore, ABMT research should take into account the impact of attention bias stability on attention training response, especially in pediatric populations. ABMT research typically relies on the dot-probe task, where individuals detect a probe following an emotional-neutral stimulus pair. The current research presents two dot-probe experiments relevant to ABMT and attention-bias stability. In Experiment 1, anxious youth receiving 8-weeks of cognitive-behavioral therapy (CBT) were randomly assigned to ABMT that trains attention towards happy faces (n = 18) or placebo (n = 18). Two additional comparison groups, anxious youth receiving only CBT (n = 17) and healthy comparison youth (n = 16), were studied. Active attention training towards happy faces did not augment clinician-rated response to CBT; however, individuals receiving training exhibited reductions on self-report measures of anxiety earlier than individuals receiving CBT only. In Experiment 2, healthy youth (n = 12) completed a dot-probe task twice while undergoing functional magnetic resonance imaging. Intra-class correlation demonstrated stability of neural activation in response to attention bias in the ventrolateral prefrontal cortex and amygdala. Together, these two studies investigate the ways in which attention-bias stability may impact future work on ABMT. © 2012 Elsevier Ltd.


Witkowski M.,University of Tübingen | Garcia-Cossio E.,University of Tübingen | Garcia-Cossio E.,Radboud University Nijmegen | Chander B.S.,University of Tübingen | And 5 more authors.
NeuroImage | Year: 2016

Transcranial alternating current stimulation (tACS), a non-invasive and well-tolerated form of electric brain stimulation, can influence perception, memory, as well as motor and cognitive function. While the exact underlying neurophysiological mechanisms are unknown, the effects of tACS are mainly attributed to frequency-specific entrainment of endogenous brain oscillations in brain areas close to the stimulation electrodes, and modulation of spike timing dependent plasticity reflected in gamma band oscillatory responses. tACS-related electromagnetic stimulator artifacts, however, impede investigation of these neurophysiological mechanisms. Here we introduce a novel approach combining amplitude-modulated tACS during whole-head magnetoencephalography (MEG) allowing for artifact-free source reconstruction and precise mapping of entrained brain oscillations underneath the stimulator electrodes. Using this approach, we show that reliable reconstruction of neuromagnetic low- and high-frequency oscillations including high gamma band activity in stimulated cortical areas is feasible opening a new window to unveil the mechanisms underlying the effects of stimulation protocols that entrain brain oscillatory activity. © 2015 Elsevier Inc.


Luking K.R.,State University of New York at Stony Brook | Pagliaccio D.,National Institute of Mental Health NIMH | Luby J.L.,Washington University in St. Louis | Barch D.M.,Washington University in St. Louis
Trends in Cognitive Sciences | Year: 2016

Striatal response to reward has been of great interest in the typical development and psychopathology literatures. These parallel lines of inquiry demonstrate that although typically developing adolescents show robust striatal response to reward, adolescents with major depressive disorder (MDD) and those at high risk for MDD show a blunted response to reward. Understanding how these findings intersect is crucial for the development and application of early preventative interventions in at-risk children, ideally before the sharp increase in the rate of MDD onset that occurs in adolescence. Robust findings relating blunted striatal response to reward and MDD risk are reviewed and situated within a normative developmental context. We highlight the need for future studies investigating longitudinal development, specificity to MDD, and roles of potential moderators and mediators. Offspring of depressed mothers are at increased risk for developing depression and show blunted responses to reward, relative to low-risk peers, within the dorsal and ventral striatum.The strongest evidence for the relationship between depression risk and blunted striatal response to reward has been found during mid-adolescence, a time in development when healthy low-risk groups show maximal striatal response to reward.Blunted striatal response to reward is not simply a consequence of experiencing depression because both never-depressed high-risk adolescents and currently depressed adolescents show a similarly blunted striatal response to reward relative to low-risk controls.Blunted striatal response to reward may specifically relate to maternal depression, and not to maternal anxiety.Blunted striatal response to reward may co-occur with enhanced responses to loss of reward or punishment in high-risk groups. © 2016 Elsevier Ltd.


Barker T.V.,University of Maryland University College | Troller-Renfree S.,University of Maryland University College | Pine D.S.,National Institute of Mental Health NIMH | Fox N.A.,University of Maryland University College
Cognitive, Affective and Behavioral Neuroscience | Year: 2015

The error-related negativity (ERN) is an event-related potential that occurs approximately 50 ms after an erroneous response. The magnitude of the ERN is influenced by contextual factors, such as when errors are made during social evaluation. The ERN is also influenced by individual differences in anxiety, and it is elevated among anxious individuals. However, little research has examined how individual differences in anxiety interact with contextual factors to impact the ERN. Social anxiety involves fear and apprehension of social evaluation. In the present study, we explored how individual differences in social anxiety interact with social contexts to modulate the ERN. The ERN was measured in 43 young adults characterized as being either high or low in social anxiety, while they completed a flanker task in two contexts: alone and during social evaluation. The results revealed a significant interaction between social anxiety and context, such that the ERN was enhanced in a social relative to a nonsocial context only among highly socially anxious individuals. Furthermore, the degree of such enhancement significantly correlated with individual differences in social anxiety. These findings demonstrate that social anxiety is characterized by enhanced neural activity to errors in social-evaluative contexts. © 2015, Psychonomic Society, Inc.


Leopold D.A.,National Institute of Mental Health NIMH | Leopold D.A.,U.S. National Institutes of Health
Annual Review of Neuroscience | Year: 2012

The primary visual cortex (V1) is the principal telencephalic recipient of visual input in humans and monkeys. It is unique among cortical areas in that its destruction results in chronic blindness. However, certain patients with V1 damage, though lacking visual awareness, exhibit visually guided behavior: blindsight. This phenomenon, together with evidence from electrophysiological, neuroimaging, and psychophysical experiments, has led to speculation that V1 activity has a special or direct role in generating conscious perception. To explore this issue, this article reviews experiments that have used two powerful paradigms-stimulusinduced perceptual suppression and chronicV1ablation-each of which disrupts the ability to perceive salient visual stimuli. Focus is placed on recent neurophysiological, behavioral, and functional imaging studies from the nonhuman primate that shed light on V1's role in conscious awareness. In addition, anatomical pathways that relay visual information to the cortex during normal vision and in blindsight are reviewed. Although the critical role of V1 in primate vision follows naturally from its position as a bottleneck of visual signals, little evidence supports its direct contribution to visual awareness. © 2012 by Annual Reviews. All rights reserved.


Guilloux J.-P.,University of Pittsburgh | Guilloux J.-P.,University Paris - Sud | Douillard-Guilloux G.,University of Pittsburgh | Kota R.,University of Pittsburgh | And 6 more authors.
Molecular Psychiatry | Year: 2012

Women are twice as likely as men to develop major depressive disorder (MDD) and are more prone to recurring episodes. Hence, we tested the hypothesis that the illness may associate with robust molecular changes in female subjects, and investigated large-scale gene expression in the post-mortem brain of MDD subjects paired with matched controls (n21 pairs). We focused on the lateral/basolateral/basomedian complex of the amygdala as a neural hub of mood regulation affected in MDD. Among the most robust findings were downregulated transcripts for genes coding for γ-aminobutyric acid (GABA) interneuron-related peptides, including somatostatin (SST), tachykinin, neuropeptide Y (NPY) and cortistatin, in a pattern reminiscent to that previously reported in mice with low brain-derived neurotrophic factor (BDNF). Changes were confirmed by quantitative PCR and not explained by demographic, technical or known clinical parameters. BDNF itself was significantly downregulated at the RNA and protein levels in MDD subjects. Investigating putative mechanisms, we show that this core MDD-related gene profile (including SST, NPY, TAC1, RGS4 and CORT) is recapitulated by complementary patterns in mice with constitutive (BDNF-heterozygous) or activity-dependent (exon IV knockout) decreases in BDNF function, with a common effect on SST and NPY. Together, these results provide both direct (low RNA/protein) and indirect (low BDNF-dependent gene pattern) evidence for reduced BDNF function in the amygdala of female subjects with MDD. Supporting studies in mutant mice models suggest a complex mechanism of low constitutive and activity-dependent BDNF function in MDD, particularly affecting SST/NPY-related GABA neurons, thus linking the neurotrophic and GABA hypotheses of depression. © 2012 Macmillan Publishers Limited All rights reserved.


Mueller S.C.,National Institute of Mental Health NIMH | Mueller S.C.,Ghent University | Aouidad A.,University Pierre and Marie Curie | Gorodetsky E.,Mood and Anxiety Disorders Program NIMH | And 3 more authors.
Journal of the American Academy of Child and Adolescent Psychiatry | Year: 2013

Objective: Minimal research links anxiety disorders in adolescents to regional gray matter volume (GMV) abnormalities and their modulation by genetic factors. Prior research suggests that a brain-derived neurotrophic factor (BNDF) Val66Met polymorphism may modulate such brain morphometry profiles. Method: Using voxel-based morphometry and magnetic resonance imaging, associations of BDNF and clinical anxiety with regional GMVs of anterior cingulate cortex, insula, amygdala, and hippocampus were examined in 39 affected (17 Met allele carriers, 22 Val/Val homozygotes) and 63 nonaffected adolescents (33 Met allele carriers, 41 Val/Val homozygotes). Results: Amygdala and anterior hippocampal GMVs were significantly smaller in patients than in healthy comparison adolescents, with a reverse pattern for the insula. Post-hoc regression analyses indicated a specific contribution of social phobia to the GMV reductions in the amygdala and hippocampus. In addition, insula and dorsal-anterior cingulate cortex (ACC) GMVs were modulated by BDNF genotype. In both regions, and GMVs were larger in the Val/Val homozygote patients than in individuals carrying the Met allele. Conclusions: These results implicate reduced GMV in the amygdala and hippocampus in pediatric anxiety, particularly social phobia. In addition, the data suggest that genetic factors may modulate differences in the insula and dorsal ACC.


Dickstein D.P.,Brown University | Leibenluft E.,National Institute of Mental Health NIMH
Israel Journal of Psychiatry and Related Sciences | Year: 2012

From the mid-1990s through the present, studies have demonstrated a significant rise in the numbers of children and adolescents diagnosed with bipolar disorder (BD). Why is this? The present manuscript reviews several possibilities, most notably ambiguity in the diagnostic criteria for mania and how they may apply to children with functionally-impairing irritability. Furthermore, we discuss ongoing phenomenological and affective neuroscience research approaches to address those children most on the fringes of our current psychiatric nosology. In summary, these studies suggest that BD youths may be distinguished on some measures from those with chronic irritability and severe mood dysregulation, although the two groups also have some shared deficits.


News Article | January 27, 2017
Site: www.techtimes.com

Researchers from the University of Texas Health Science Center at Houston have made an amazing discovery, which could be a potential game changer for the treatment and diagnosis of bipolar disorder and other mental health issues. Bipolar disorder, otherwise known as manic-depressive illness, is a brain condition that causes drastic shifts in a person's mood, energy, and activity. These mood swings are basically classified into three categories: manic episodes (feeling extremely ecstatic and energized), depressive episodes (feeling miserable, hopeless, and suicidal), and hypomanic episodes (less severe manic episode). These radical changes in mood can greatly affect a person's sleep, activities, and way of thinking, and often inhibit them from having a normal life. The exact reason why bipolar disorder occurs in people is still unknown, although experts believe that several factors can trigger the illness or increase one's risk, These include genetics, family history, and brain structure and functioning. Using a combination of magnetic resonance imaging and an advanced segmentation approach, researchers evaluated the differences in the volumes of subfields of the hippocampus, the seahorse-shaped region in the brain's medial temporal lobe. The hippocampus, an essential part of the limbic system, controls our memories and emotional behavior. The researchers discovered that the study participants with bipolar disorder had volume reduction in certain parts of their hippocampus. The portion of the tail, two cellular layers, and subfield 4 of the cornu ammonis all displayed lower volumes. The reduced volume was more pronounced in subjects with bipolar I disorder than those with other mood disorders. Additionally, the researchers found that patients with bipolar I disorder displayed lower volumes of certain hippocampus areas the longer the period of their illness became. Volumes of other CA areas and hippocampal tail, on the other hand, decreased more in subjects with more manic episodes. The entirety of the study can be found in the journal Molecular Psychiatry. Bo Cao, first and corresponding author of the study and a post-doctoral fellow in the Department of Psychiatry and Behavioral Sciences at McGovern Medical School at UTHealth, is hopeful that the results of their study, funded partly through a grant from the National Institute of Mental Health NIMH), will pave the way for further in-depth research aimed at more accurate diagnosis and positive treatment response of the puzzling brain disorder. "Our study is one of the first to locate possible damage of bipolar disorder in specific subfields within the hippocampus," Cao stated. "This is something that researchers have been trying to answer. The theory was that different subfields of the hippocampus may have different functions and may be affected differently in different mood disorders, such as bipolar disorder and major depression disorder." © 2017 Tech Times, All rights reserved. Do not reproduce without permission.


Lahat A.,McMaster University | Lamm C.,University of New Orleans | Chronis-Tuscano A.,University of Maryland College Park | Pine D.S.,National Institute of Mental Health NIMH | And 2 more authors.
Journal of the American Academy of Child and Adolescent Psychiatry | Year: 2014

Objective Behavioral inhibition (BI) is an early childhood temperament characterized by fearful responses to novelty and avoidance of social interactions. During adolescence, a subset of children with stable childhood BI develop social anxiety disorder and concurrently exhibit increased error monitoring. The current study examines whether increased error monitoring in 7-year-old, behaviorally inhibited children prospectively predicts risk for symptoms of social phobia at age 9 years. Method A total of 291 children were characterized on BI at 24 and 36 months of age. Children were seen again at 7 years of age, when they performed a Flanker task, and event-related potential (ERP) indices of response monitoring were generated. At age 9, self- and maternal-report of social phobia symptoms were obtained. Results Children high in BI, compared to those low in BI, displayed increased error monitoring at age 7, as indexed by larger (i.e., more negative) error-related negativity (ERN) amplitudes. In addition, early BI was related to later childhood social phobia symptoms at age 9 among children with a large difference in amplitude between ERN and correct-response negativity (CRN) at age 7. Conclusions Heightened error monitoring predicts risk for later social phobia symptoms in children with high BI. Research assessing response monitoring in children with BI may refine our understanding of the mechanisms underlying risk for later anxiety disorders and inform prevention efforts.

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