School-based Screening to Identify Children At Risk for Attention-Deficit/Hyperactivity Disorder: Barriers and Implications.

This report describes a school-based screening project to improve early identification of children at risk for attention-deficit/hyperactivity disorder (ADHD) and communicate these concerns to parents, recommending that they contact their child's primary care provider (PCP). Of 17,440 eligible children in first through fifth grades in five school districts, 47.0% of parents provided required written consent, and teachers completed 70.4% of the online screeners (using the Vanderbilt AD/HD Diagnostic Teacher Rating Scale). Of 5,772 screeners completed, 18.1% of children (n = 1,044) were identified as at risk. Parents of at-risk children were contacted to explain risk status and recommended to visit their child's PCP for further evaluation. It was not possible to contact 39.1% of parents of at-risk children. Of the 636 parents of at-risk children who could be contacted, 53.1% (n = 338) verbally accepted the recommendation to follow-up with their PCP, which was not related to ADHD symptom severity. Parents of children with IEPs or related services were more likely to accept the recommendation to visit the PCP. Our exploration of the potential for school-based screening for ADHD identified a number of barriers to successful execution, but the data also indicated that this is an important problem to address.

Are the parts as good as the whole? A meta-analysis of component treatment studies.

OBJECTIVE: Component studies compare standard treatments to treatments with added components or dismantled components. A previous meta-analysis (Ahn & Wampold, 2001) failed to find any differences in outcome between treatments with more components and those with fewer components, leading the authors to conclude that common factors and not specific ingredients account for therapeutic change. METHOD: The current random effects model meta-analysis of psychotherapy component studies conducted between 1980 and 2010 included more than 3 times as many studies as Ahn and Wampold's (2001) meta-analysis (k = 66). Unlike the previous meta-analysis, this study conducted separate meta-analyses for additive and dismantling studies and also examined treatment outcomes at follow-up. RESULTS: For the dismantling studies, there were no significant differences between the full treatments and the dismantled treatments. For the additive studies, the treatment with the added component yielded a small, but significant, effect at completion (d = 0.14) and a slightly larger effect at follow-up (d = 0.28), but only for the specific problems that were targeted for treatment. Despite the diversity of populations studied, problems treated, and treatments examined, there was little heterogeneity among the results of these studies. CONCLUSION: These findings suggest that added specific ingredients may contribute modestly to treatment outcomes.

Lead and Attention-Deficit/Hyperactivity Disorder (ADHD) symptoms: a meta-analysis.

This meta-analysis examined the association between Attention-Deficit/Hyperactivity Disorder (ADHD) symptoms and lead exposure in children and adolescents. Thirty-three studies published between 1972 and 2010 involving 10,232 children and adolescents were included. There was a small to medium association between inattention symptoms and lead exposure (r=.16, k=27, p<.001) and a similar association between hyperactivity/impulsivity symptoms and lead exposure (r=.13, k=23, p<.001). There was significant heterogeneity among the effect sizes for both inattention symptoms and for hyperactivity/impulsivity symptoms, with studies using hair analysis to assess lead burden yielding substantially larger effect sizes than those using other methods. Excluding the hair analysis studies, the average rs were .14 for inattention (k=23, p<.001) and .12 for hyperactivity/impulsivity (k=21, p<.001). Overall, the relation between lead exposure and ADHD symptoms was similar in magnitude to the relation between lead exposure and decreased IQ and between lead exposure and conduct problems.

Hypoalgesia associated with elevated resting blood pressure: evidence for endogenous opioid involvement.

This study used a placebo-controlled, between-subjects opioid blockade design to evaluate endogenous opioid involvement in the hypoalgesia associated with elevated resting blood pressure (BP) in 163 healthy individuals. Participants were randomly assigned to Drug condition (placebo, naltrexone) and Task Order (computerized maze task with harassment followed by an ischemic pain task or vice versa). Resting BP was assessed, followed by drug administration, and then the pain and maze tasks. A significant Drug x Systolic BP (SBP) interaction was observed on McGill Pain Questionnaire-Affective pain ratings (P < .01), indicating that BP-related hypoalgesia observed under placebo was absent under opioid blockade. A significant Gender x Drug x SBP x Task Order interaction was observed for VAS pain intensity (P < .02). Examination of simple effects comprising this interaction suggested that BP-related hypoalgesia occurred only in male participants who experienced the pain task in the absence of emotional arousal, and indicated that this hypoalgesia occurred under placebo but not under opioid-blockade. Results suggest that under some circumstance, BP-related hypoalgesia may have an endogenous opioid-mediated component in healthy individuals, particularly men.

Endogenous opioids may buffer effects of anger arousal on sensitivity to subsequent pain.

Evidence suggests that anger and pain are related, yet it is not clear by what mechanisms anger may influence pain. We have proposed that effects of anger states and traits on pain sensitivity are partly opioid mediated. In this study, we test the extent to which analgesic effects of acute anger arousal on subsequent pain sensitivity are opioid mediated by subjecting healthy participants to anger-induction and pain either under opioid blockade (oral naltrexone) or placebo. Participants were 160 healthy individuals. A double-blind, placebo-controlled, between-subjects opioid blockade design is used, with participants assigned randomly to one of two drug conditions (placebo or naltrexone), and to one of two Task Orders (anger-induction followed by pain or vice versa). Results of ANOVAs show significant Drug Condition x Task Order interactions for sensory pain ratings (MPQ-Sensory) and angry and nervous affect during pain-induction, such that participants who underwent anger-induction prior to pain while under opioid blockade (naltrexone) reported more pain, and anger and nervousness than those who underwent the tasks in the same order, but did so on placebo. Results suggest that for people with intact opioid systems, acute anger arousal may trigger endogenous opioid release that reduces subsequent responsiveness to pain. Conversely, impaired endogenous opioid function, such as that found among some chronic pain patients, may leave certain people without optimal buffering from the otherwise hyperalgesic affects of anger arousal, and so may lead to greater pain and suffering following upsetting or angry events.