Community violence exposure is a common stressor, known to compromise youth cognitive and emotional development. In a diverse, urban sample of 22 adolescents, participants reported on community violence exposure (witnessing a beating or illegal drug use, hearing gun shots, or other forms of community violence) in early adolescence (average age 12.99), and underwent a neuroimaging scan 3-5 years later (average age 16.92). Community violence exposure in early adolescence predicted smaller manually traced left and right hippocampal and amygdala volumes in a model controlling for age, gender, and concurrent community violence exposure, measured in late adolescence. Community violence continued to predict hippocampus (but not amygdala) volumes after we also controlled for family aggression exposure in early adolescence. Community violence exposure was also associated with stronger resting state connectivity between the right hippocampus (using the manually traced structure as a seed region) and bilateral frontotemporal regions including the superior temporal gyrus and insula. These resting state connectivity results held after controlling for concurrent community violence exposure, SES, and family aggression. Although this is the first study focusing on community violence in conjunction with brain structure and function, these results dovetail with other research linking childhood adversity with smaller subcortical volumes in adolescence and adulthood, and with altered frontolimbic resting state connectivity. Our findings suggest that even community-level exposure to neighborhood violence can have detectable neural correlates in adolescents.
This study used an emotional go/no-go task to explore inhibitory spillover (how intentional cognitive inhibition ‘spills over’ to inhibit neural responses to affective stimuli) within 23 adolescents. Adolescents were shown emotional faces and asked to press a button depending on the gender of the face. When asked to inhibit with irrelevant affective stimuli present, adolescents recruited prefrontal cognitive control regions (rIFG, ACC) and ventral affective areas (insula, amygdala). In support of the inhibitory spillover hypothesis, increased activation of the rIFG and down-regulation of the amygdala occurred during negative, but not positive, inhibition trials compared with go trials. Functional connectivity analysis revealed coupling of the rIFG pars opercularis and ventral affective areas during negative no-go trials. Age was negatively associated with activation in frontal and temporal regions associated with inhibition and sensory integration. Internalizing symptoms were positively associated with increased bilateral IFG, ACC, putamen and pallidum. This is the first study to test the inhibitory spillover emotional go/no-go task within adolescents, who may have difficulties with inhibitory control, and to tie it to internalizing symptoms.
In the original article there was an error in the beta value reporting the association between left amygdala volume calculated with manual segmentation and family aggression exposure in early life. The correct version of Table 3 appears below. In the "Results" section, sub section "Manual Segmentation, " the second sentence has been added stating the following: A positive relationship between left amygdala volume and family aggression exposure using manual segmentation was approaching significance (b = 0.39, p = 0.09).
Individual treatments for chronic low back pain (CLBP) have small magnitude effects. Combining different types of treatments may produce larger effects. This study used a 2x2 factorial randomized controlled trial (RCT) design to combine procedural and behavioral treatments for CLBP. The study aims were to: (1) assess feasibility of conducting a factorial RCT of these treatments; and (2) estimate individual and combined treatment effects of (a) lumbar radiofrequency ablation (LRFA) of the dorsal ramus medial branch nerves (vs. a simulated LRFA control procedure) and (b) Activity Tracker-Informed Video-Enabled Cognitive Behavioral Therapy program for CLBP (AcTIVE-CBT) (vs. an educational control treatment) on back-related disability at 3 months post-randomization. Participants (n=13) were randomized in a 1:1:1:1 ratio. Feasibility goals included an enrollment proportion ≥30%, a randomization proportion ≥80%, and a ≥80% proportion of randomized participants completing the 3-month Roland-Morris Disability Questionnaire (RMDQ) primary outcome endpoint. An intent-to-treat analysis was used. The enrollment proportion was 62%, the randomization proportion was 81%, and all randomized participants completed the primary outcome. Though not statistically significant, there was a beneficial, moderate-magnitude effect of LRFA vs. control on 3-month RMDQ (-3.25 RMDQ points; 95% CI: -10.18, 3.67). There was a significant, beneficial, large-magnitude effect of AcTIVE-CBT vs. control (-6.29, 95% CI: -10.97, -1.60). Though not statistically significant, there was a beneficial, large effect of LRFA+AcTIVE-CBT vs. control (-8.37; 95% CI: -21.47, 4.74). We conclude that it is feasible to conduct an RCT combining procedural and behavioral treatments for CLBP.
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