Morphological Abnormalities of the Thalamus in Youths With Attention Deficit Hyperactivity Disorder

The role of the thalamus in the genesis of attention deficit hyperactivity disorder (ADHD) remains poorly understood. The authors used anatomical MRI to examine the morphology of the thalamus in youths with ADHD and healthy comparison youths

A Functional Imaging Study of Self-Regulatory Capacities in Persons Who Stutter

<div><p>Developmental stuttering is a disorder of speech fluency with an unknown pathogenesis. The similarity of its phenotype and natural history with other childhood neuropsychiatric disorders of frontostriatal pathology suggests that stuttering may have a closely related pathogenesis. We investigated in this study the potential involvement of frontostriatal circuits in developmental stuttering. We collected functional magnetic resonance imaging data from 46 persons with stuttering and 52 fluent controls during performance of the Simon Spatial Incompatibility Task. We examined differences between the two groups of blood-oxygen-level-dependent activation associated with two neural processes, the resolution of cognitive conflict and the context-dependent adaptation to changes in conflict. Stuttering speakers and controls did not differ on behavioral performance on the task. In the presence of conflict-laden stimuli, however, stuttering speakers activated more strongly the cingulate cortex, left anterior prefrontal cortex, right medial frontal cortex, left supplementary motor area, right caudate nucleus, and left parietal cortex. The magnitude of activation in the anterior cingulate cortex correlated inversely in stuttering speakers with symptom severity. Stuttering speakers also showed blunted activation during context-dependent adaptation in the left dorsolateral prefrontal cortex, a brain region that mediates cross-temporal contingencies. Frontostriatal hyper-responsivity to conflict resembles prior findings in other disorders of frontostriatal pathology, and therefore likely represents a general mechanism supporting functional compensation for an underlying inefficiency of neural processing in these circuits. The reduced activation of dorsolateral prefrontal cortex likely represents the inadequate readiness of stuttering speakers to execute a sequence of motor responses.</p></div

Morphological Biomarkers in the Amygdala and Hippocampus of Children and Adults at High Familial Risk for Depression

Major Depressive Disorder (MDD) is highly familial, and the hippocampus and amygdala are important in the pathophysiology of MDD. Whether morphological markers of risk for familial depression are present in the hippocampus or amygdala is unknown. We imaged the brains of 148 individuals, aged 6 to 54 years, who were members of a three-generation family cohort study and who were at either high or low familial risk for MDD. We compared surface morphological features of the hippocampus and amygdala across risk groups and assessed their associations with depression severity. High- compared with low-risk individuals had inward deformations of the head of both hippocampi and the medial surface of the left amygdala. The hippocampus findings persisted in analyses that included only those participants who had never had MDD, suggesting that these are true endophenotypic biomarkers for familial MDD. Posterior extension of the inward deformations was associated with more severe depressive symptoms, suggesting that a greater spatial extent of this biomarker may contribute to the transition from risk to the overt expression of symptoms. Significant associations of these biomarkers with corresponding biomarkers for cortical thickness suggest that these markers are components of a distributed cortico-limbic network of familial vulnerability to MDD

Activation Maps.

<p>(A) Representative axial–oblique slices depict greater activation of stutterers relative to healthy controls in frontostriatal regions when resolving Simon conflict (activation contrast: incongruent trials immediately preceded by a congruent trial versus congruent trials immediately preceded by a congruent trial). Abbreviations: ACC = anterior cingulate cortex; Cau = caudate; IPC = inferior parietal cortex; SMA = supplementary motor area. (B) Axial–oblique views of attenuated activation in the dorsolateral prefrontal cortex of stutterers as compared to healthy controls during response to incongruent trials under the influence of congruency of preceding trial (context-dependent adaptation, activation contrast: incongruent trials immediately preceded by an incongruent trial versus incongruent trials immediately preceded by a congruent trial). Abbreviations: DLPFC = dorsolateral prefrontal cortex. Statistical maps were displayed at a threshold of p<0.025 with a cluster extent of 30 voxels (P<0.05, corrected). The left-hand sides of the images correspond to the left side of the brain. The color bars indicate the t-values. The coordinates in Montreal Neurological Institute space are defined in millimeters.</p

Granger Causality Analyses for the Anterior Cingulate Cortex and Dorsolateral Prefrontal Cortex during Performance of the Simon Task.

<p>Abbreviations: ACC, anterior cingulate cortex; BA, Brodmann area; DLPFC, dorsolateral prefrontal cortex.</p>†<p>Granger causality indices (mean±standard deviation) of functional connectivity between the ACC and DLPFC subregions, including BA46, 44, 8, and 45. The ACC seed region was an 8 mm-radius sphere centered at the voxel (x = −6, y = 28, z = 31) in which stuttering speakers activated more strongly relative to fluent speakers during conflict resolution. The DLPFC seed regions were defined using 8 mm spheres placed at the foci of activation (BA46, x = −48, y = 30, z = 16; BA44, x = −54, y = 12, z = 15; BA8, x = −46, y = 10, z = 40; BA45, x = −53, y = 23, z = 14) in which stuttering speakers showed blunted activation during context-dependent adaptation.</p>††<p>Between-group comparisons of Granger causality indices.</p

Experimental design of the Simon Spatial Incompatibility Task.

<p>Experimental design of the Simon Spatial Incompatibility Task.</p

Brain Regions of Group-Level Differences during Performance of the Simon Task.

<p>Abbreviations: BA, Brodmann area; L, left; MNI, Montreal Neurological Institute; R, right.</p

Severity correlation.

<p>Axial–oblique views of brain regions in stutterers show negative correlations between the magnitude of brain activation during conflict resolution and stuttering severity as measured with the ACES and OASES. The scatter plot illustrates the negative association in the ACC between the standardized severity score and the parameter estimate of brain responses during conflict resolution (r = −0.33, p<0.025). Abbreviations: ACC = anterior cingulate cortex.</p

Behavioral results. Mean reaction times (± standard errors) of stutterers and healthy controls for current trial congruency were plotted under modulation of preceding trial congruency.

<p>Abbreviations: cC = congruent trials immediately preceded by a congruent trial; cI = incongruent trials immediately preceded by a congruent trial; iC = congruent trials immediately preceded by an incongruent trial; iI = incongruent trials immediately preceded by an incongruent trial.</p