Faculty Bibliography

BACKGROUND: Behaviorally inhibited (BI) children who also exhibit enhanced response monitoring might be at particularly high risk for anxiety disorders. The current study tests the hypothesis that response monitoring, as manifest in the error-related negativity (ERN), moderates the association between BI and anxiety. METHODS: Participants (n=113; 73 male) assessed for early-childhood BI were re-assessed as adolescents with a clinical interview and a flanker paradigm that generated behavioral data and event-related potentials (ERPs). Risk for anxiety disorders in adolescents was examined as a function of childhood-BI status and adolescent performance on the flanker paradigm. RESULTS: Adolescents with childhood BI displayed ERP evidence of enhanced response monitoring, manifest as large ERNs. The ERN moderated the relationship between early BI and later clinically significant disorders. CONCLUSIONS: Physiological measures of response monitoring might moderate associations between early-childhood BI and risk for psychopathology. The subset of children with BI and enhanced response monitoring might face greater risk for later-life clinical anxiety than children with either BI or enhanced response monitoring alone.

The authors examined racial/ethnic disparities in mental health service use based on problem type (internalizing/externalizing). A diverse sample of youth in contact with public sectors of care and their families provided reports of youth's symptoms and functional impairment during an initial interview. Specialty and school-based mental health service use during the subsequent 2 years was assessed prospectively. Greater disparities in mental health service receipt were evident for internalizing problems, with non-Hispanic White youth more likely to receive services in response to internalizing symptoms than minority youth. Fewer disparities in rates of unmet need emerged for externalizing problems, but minority youth were more likely to have need for externalizing problems met and African American youth were particularly likely to receive services in response to such problems. Findings highlight the importance of considering problem type when examining racial disparities in mental health services and underscore concerns about the responsiveness of mental health services for minority youth with internalizing disorders.

BACKGROUND: Childhood adversity has been shown to interact with monoamine oxidase-A (MAOA) genotype to confer risk for antisocial behavior. Studies examining this gene-by-environment (G x E) association, however, have produced mixed results. METHODS: Relevant research is reviewed, and results of a study with 114 children (73 maltreated and 41 control subjects) are presented. The maltreated children represent the extreme on a continuum of adversity and were assessed at a time of extreme stress-shortly after removal from their parents' care due to abuse. Measures of aggressive behavior were obtained using standard research instruments, and monoamine oxidase-A MAOA genotypes were obtained from saliva-derived DNA specimens. Population structure was controlled for using ancestral proportion scores computed on the basis of genotypes of ancestry informative markers. RESULTS: Many prior investigations appear to have had reduced power to detect the predicted G x E interaction because of low base rates of maltreatment and antisocial behavior in their samples and failure to use optimal procedures to control for population structure in ethnically diverse cohorts. In this investigation, a significant interaction was detected between exposure to moderate trauma and the 'low-activity' MAOA genotype in conferring risk for aggression. Children with exposure to extreme levels of trauma, however, had high aggression scores regardless of genotype. CONCLUSIONS: Our study suggests that problems in aggressive behavior in maltreated children are moderated by MAOA genotype, but only up to moderate levels of trauma exposure. Extreme levels of trauma appear to overshadow the effect of MAOA genotype, especially in children assessed at time of acute crisis

Background: Parenting practices predict early childhood physical aggression. Preventive interventions that alter parenting practices and aggression during early childhood provide the opportunity to test causal models of early childhood psychopathology. Although there have been several informative preventive intervention studies that test mediation models in older children, no such studies have been conducted with younger children at high risk for psychopathology. Method: Within the context of a randomized controlled trial, we examined whether changes in parenting practices mediate the effects of a family intervention on observed physical aggression among African American and Latino younger siblings of adjudicated youths. Results: Improved parenting practices partially mediated the intervention effect on physical aggression. Improvements in harsh parenting, responsive parenting, and stimulating parenting explained a significant amount of the intervention effect on child physical aggression observed in the context of parent-child interactions. Parenting practices accounted for 38% of the intervention effect on physical aggression. Conclusions: There was support for the hypothesized model of the prevention of physical aggression during early childhood. Intervention benefits on parenting practices partially accounted for intervention effects on physical aggression in young high-risk children

Chronic treatment with selective serotonin reuptake inhibitors (SSRIs) alleviates both anxiety symptoms and associated physiologic disturbances in anxious patients. However, limited research considers the degree to which chronic SSRI treatment influences anxiety in healthy individuals. This study examined the effect of 2-week citalopram treatment on two threat responses: short- and long-duration-potentiated startle. Prior work suggests that these two responses provide neurally and functionally distinct models of fear and anxiety, respectively, in rodents. Healthy volunteers (n=53) received either placebo or citalopram (20 mg per day) for 2 weeks under double-blind conditions. They were each tested twice, before and after treatment. Participants were exposed to three conditions, including one in which predictable aversive shocks were signaled by a cue, a second in which unpredictable shocks were anticipated, and a third in which no shocks were administered. Aversive states were indexed by acoustic startle. Phasic fear-potentiated startle to the threat cue, as well as sustained startle potentiation to the experimental context in the predictable and unpredictable conditions, were investigated. Citalopram affected neither baseline startle nor short-duration fear-potentiated startle to discrete threat cues. However, citalopram reduced long-duration startle potentiation in the predictable conditions. These results are consistent with the hypothesis that short- and long-duration aversive states are mediated by distinct neural systems. They suggest that citalopram alleviates symptoms of anticipatory anxiety, not fear, by acting on mechanisms underlying long-duration aversive states.