Journal of the American Academy of Child & Adolescent Psychiatry RSS feed: Current Issue. Mission Statement Advancing the science of pediatric mental health and promoting the care of youth and their families. Scope The Journal of the American Academy of Child and Adolescent Psychiatry welcomes manuscripts from diverse viewpoints including but not limited to: genetic, epidemiological, neurobiological, psychopathological, cognitive, behavioral, and psychodynamic investigations. The Journal also seeks to promote the well being of children and families by publishing scholarly papers on such subjects as health policy, legislation, advocacy, culture, and service provision as they pertain to the mental health of children and families.http://www.jaacap.com/?rss=yesElsevier Inc.en © 2010 American Academy of Child and Adolescent Psychiatry. Published by Elsevier Inc. All rights reserved. Journal of the American Academy of Child & Adolescent Psychiatry0890-8567499September 2010 © 2010 American Academy of Child and Adolescent Psychiatry. Published by Elsevier Inc. All rights reserved. healthpermissions@elsevier.comhttp://www.jaacap.com/article/PIIS089085671000523X/abstract?rss=yesThis issue of the Journal includes the remainder of the special issue on genetics started in August's installment. In addition, other articles explore potential biomarkers of pediatric depression and obsessive-compulsive disorder (OCD) and interventions for substance misuse that target specific personality traits.In This IssueRoberto B. Sassi10.1016/j.jaac.2010.06.016Journal of the American Academy of Child & Adolescent Psychiatry 49, 9 (2010)2010-09-01Journal of the American Academy of Child & Adolescent Psychiatry2010-09-01499S0890-8567(10)X0009-0Here and There861862http://www.jaacap.com/article/PIIS0890856710002893/abstract?rss=yesObjective: To summarize and evaluate the state of knowledge regarding the role of measured gene-by-environment interactions in relation to attention-deficit/hyperactivity disorder.Method: A selective review of methodologic issues was followed by a systematic search for relevant articles on measured gene-by-environment interactions; the search yielded 16 studies, which are discussed in qualitative fashion.Results: Relatively consistent evidence points to the interaction of genotype with psychosocial factors in the development of attention-deficit/hyperactivity disorder. The next step is to identify the mechanisms on the environment side and the gene combinations on the genetic side accounting for this effect. In contrast, evidence for gene-by-environment interactions involving pre- and perinatal risk factors is generally negative or unreplicated. The aggregate effect size for psychosocial interaction with genotype is more than double that for the interaction of pre- and perinatal risks with genotype. Only a small fraction of candidate environments and gene markers has been studied, and multivariate methods to integrate multiple gene or environment markers have yet to be implemented.Conclusions: Gene-by-environment interaction appears likely to prove fruitful in understanding the etiology of attention-deficit/hyperactivity disorder. Findings to date already suggest new avenues of investigation particularly involving psychosocial mechanisms and their interplay with genotype. Further pursuit of theoretically promising leads is recommended.Measured Gene-by-Environment Interaction in Relation to Attention-Deficit/Hyperactivity DisorderJoel Nigg, Molly Nikolas, S. Alexandra Burt10.1016/j.jaac.2010.01.025Journal of the American Academy of Child & Adolescent Psychiatry 49, 9 (2010)2010-05-06Journal of the American Academy of Child & Adolescent Psychiatry2010-05-06499S0890-8567(10)X0009-0Reviews863873http://www.jaacap.com/article/PIIS0890856710004818/abstract?rss=yesObjective: To describe the utility of twin studies for attention-deficit/hyperactivity disorder (ADHD) research and demonstrate their potential for the identification of alternative phenotypes suitable for genomewide association, developmental risk assessment, treatment response, and intervention targets.Method: Brief descriptions of the classic twin study and genetic association study methods are provided, with illustrative findings from ADHD research. Biometrical genetics refers to the statistical modeling of data gathered from one or more group of known biological relation; it was apparently coined by Francis Galton in the 1860s and led to the “Biometrical School” at the University of London. Twin studies use genetic correlations between pairs of relatives, derived using this theoretical framework, to parse the individual differences in a trait into latent (unmeasured) genetic and environmental influences. This method enables the estimation of heritability, i.e., the percentage of variance due to genetic influences. It is usually implemented with a method called structural equation modeling, which is a statistical technique for fitting models to data, typically using maximum likelihood estimation. Genetic association studies aim to identify those genetic variants that account for the heritability estimated in twin studies. Measurements other than those used for the clinical diagnosis of the disorder are popular phenotype choices in current ADHD research. It is argued that twin studies have great potential to refine phenotypes relevant to ADHD.Results: Prior studies have consistently found that the majority of the variance in ADHD symptoms is due to genetic factors. To date, genomewide association studies of ADHD have not identified replicable associations that account for the heritable variation. Possibly, the application of genomewide association studies to these alternative phenotypic measurements will assist in identifying the pathways from genetic variants to ADHD.Conclusion: Power to detect associations should be improved by the study of highly heritable endophenotypes for ADHD and by reducing the number of phenotypes to be considered. Therefore, twin studies are an important research tool in the development of endophenotypes, defined as alternative, more highly heritable traits that act at earlier stages of the pathway from genes to behavior. Although genetic variation in liability to ADHD is likely polygenic, the proposed approach should help to identify improved alternative measurements for genetic association studies.Twin Studies and Their Implications for Molecular Genetic Studies: Endophenotypes Integrate Quantitative and Molecular Genetics in ADHD ResearchAlexis C. Wood, Michael C. Neale10.1016/j.jaac.2010.06.006Journal of the American Academy of Child & Adolescent Psychiatry 49, 9 (2010)2010-08-02Journal of the American Academy of Child & Adolescent Psychiatry2010-08-02499S0890-8567(10)X0009-0Reviews874883http://www.jaacap.com/article/PIIS0890856710004934/abstract?rss=yesObjective: Although twin and family studies have shown attention-deficit/hyperactivity disorder (ADHD) to be highly heritable, genetic variants influencing the trait at a genome-wide significant level have yet to be identified. As prior genome-wide association studies (GWAS) have not yielded significant results, we conducted a meta-analysis of existing studies to boost statistical power.Method: We used data from four projects: a) the Children's Hospital of Philadelphia (CHOP); b) phase I of the International Multicenter ADHD Genetics project (IMAGE); c) phase II of IMAGE (IMAGE II); and d) the Pfizer-funded study from the University of California, Los Angeles, Washington University, and Massachusetts General Hospital (PUWMa). The final sample size consisted of 2,064 trios, 896 cases, and 2,455 controls. For each study, we imputed HapMap single nucleotide polymorphisms, computed association test statistics and transformed them to z-scores, and then combined weighted z-scores in a meta-analysis.Results: No genome-wide significant associations were found, although an analysis of candidate genes suggests that they may be involved in the disorder.Conclusions: Given that ADHD is a highly heritable disorder, our negative results suggest that the effects of common ADHD risk variants must, individually, be very small or that other types of variants, e.g., rare ones, account for much of the disorder's heritability.Meta-Analysis of Genome-Wide Association Studies of Attention-Deficit/Hyperactivity DisorderBenjamin M. Neale, Sarah E. Medland, Stephan Ripke, Philip Asherson, Barbara Franke, Klaus-Peter Lesch, Stephen V. Faraone, Thuy Trang Nguyen, Helmut Schäfer, Peter Holmans, Mark Daly, Hans-Christoph Steinhausen, Christine Freitag, Andreas Reif, Tobias J. Renner, Marcel Romanos, Jasmin Romanos, Susanne Walitza, Andreas Warnke, Jobst Meyer, Haukur Palmason, Jan Buitelaar, Alejandro Arias Vasquez, Nanda Lambregts-Rommelse, Michael Gill, Richard J.L. Anney, Kate Langely, Michael O'Donovan, Nigel Williams, Michael Owen, Anita Thapar, Lindsey Kent, Joseph Sergeant, Herbert Roeyers, Eric Mick, Joseph Biederman, Alysa Doyle, Susan Smalley, Sandra Loo, Hakon Hakonarson, Josephine Elia, Alexandre Todorov, Ana Miranda, Fernando Mulas, Richard P. Ebstein, Aribert Rothenberger, Tobias Banaschewski, Robert D. Oades, Edmund Sonuga-Barke, James McGough, Laura Nisenbaum, Frank Middleton, Xiaolan Hu, Stan Nelson, Psychiatric GWAS Consortium: ADHD Subgroup10.1016/j.jaac.2010.06.008Journal of the American Academy of Child & Adolescent Psychiatry 49, 9 (2010)2010-08-02Journal of the American Academy of Child & Adolescent Psychiatry2010-08-02499S0890-8567(10)X0009-0New Research884897http://www.jaacap.com/article/PIIS089085671000290X/abstract?rss=yesObjective: Genes likely play a substantial role in the etiology of attention-deficit/hyperactivity disorder (ADHD). However, the genetic architecture of the disorder is unknown, and prior genome-wide association studies (GWAS) have not identified a genome-wide significant association. We have conducted a third, independent, multisite GWAS of DSM-IV-TR ADHD.Method: Families were ascertained at Massachusetts General Hospital (MGH; N = 309 trios), Washington University at St. Louis (WASH-U; N = 272 trios), and University of California at Los Angeles (UCLA; N = 156 trios). Genotyping was conducted with the Illumina Human1M or Human1M-Duo BeadChip platforms. After applying quality control filters, association with ADHD was tested with 835,136 SNPs in 735 DSM-IV ADHD trios from 732 families.Results: Our smallest p value (6.7E-07) did not reach the threshold for genome-wide statistical significance (5.0E-08), but one of the 20 most significant associations was located in a candidate gene of interest for ADHD (SLC9A9, rs9810857, p = 6.4E-6). We also conducted gene-based tests of candidate genes identified in the literature and found additional evidence of association with SLC9A9.Conclusions: We and our colleagues in the Psychiatric GWAS Consortium are working to pool together GWAS samples to establish the large data sets needed to follow-up on these results and to identify genes for ADHD and other disorders.Family-Based Genome-Wide Association Scan of Attention-Deficit/Hyperactivity DisorderEric Mick, Alexandre Todorov, Susan Smalley, Xiaolan Hu, Sandra Loo, Richard D. Todd, Joseph Biederman, Deirdre Byrne, Bryan Dechairo, Allan Guiney, James McCracken, James McGough, Stanley F. Nelson, Angela M. Reiersen, Timothy E. Wilens, Janet Wozniak, Benjamin M. Neale, Stephen V. Faraone10.1016/j.jaac.2010.02.014Journal of the American Academy of Child & Adolescent Psychiatry 49, 9 (2010)2010-05-17Journal of the American Academy of Child & Adolescent Psychiatry2010-05-17499S0890-8567(10)X0009-0New Research898905.e3http://www.jaacap.com/article/PIIS089085671000482X/abstract?rss=yesObjective: Although twin and family studies have shown attention-deficit/hyperactivity disorder (ADHD) to be highly heritable, genetic variants influencing the trait at a genome-wide significant level have yet to be identified. Thus additional genomewide association studies (GWAS) are needed.Method: We used case-control analyses of 896 cases with DSM-IV ADHD genotyped using the Affymetrix 5.0 array and 2,455 repository controls screened for psychotic and bipolar symptoms genotyped using Affymetrix 6.0 arrays. A consensus SNP set was imputed using BEAGLE 3.0, resulting in an analysis dataset of 1,033,244 SNPs. Data were analyzed using a generalized linear model.Results: No genome-wide significant associations were found. The most significant results implicated the following genes: PRKG1, FLNC, TCERG1L, PPM1H, NXPH1, PPM1H, CDH13, HK1, and HKDC1.Conclusions: The current analyses are a useful addition to the present literature and will make a valuable contribution to future meta-analyses. The candidate gene findings are consistent with a prior meta-analysis in suggesting that the effects of ADHD risk variants must, individually, be very small and/or include multiple rare alleles.Case-Control Genome-Wide Association Study of Attention-Deficit/Hyperactivity DisorderBenjamin M. Neale, Sarah Medland, Stephan Ripke, Richard J.L. Anney, Philip Asherson, Jan Buitelaar, Barbara Franke, Michael Gill, Lindsey Kent, Peter Holmans, Frank Middleton, Anita Thapar, Klaus-Peter Lesch, Stephen V. Faraone, Mark Daly, Thuy Trang Nguyen, Helmut Schäfer, Hans-Christoph Steinhausen, Andreas Reif, Tobias J. Renner, Marcel Romanos, Jasmin Romanos, Andreas Warnke, Susanne Walitza, Christine Freitag, Jobst Meyer, Haukur Palmason, Aribert Rothenberger, Ziarih Hawi, Joseph Sergeant, Herbert Roeyers, Eric Mick, Joseph Biederman, IMAGE II Consortium10.1016/j.jaac.2010.06.007Journal of the American Academy of Child & Adolescent Psychiatry 49, 9 (2010)2010-08-06Journal of the American Academy of Child & Adolescent Psychiatry2010-08-06499S0890-8567(10)X0009-0New Research906920http://www.jaacap.com/article/PIIS0890856710005265/abstract?rss=yesObjective: Many investigators now routinely classify children with fragile X syndrome (FXS) according to whether or not they also meet diagnostic criteria for autism. To determine whether this classification is appropriate, we examined the profiles of autistic behaviors shown by boys and girls with FXS.Method: Individuals with FXS, aged 5 to 25 years, were assessed on two established measures of autism, the Social Communication Questionnaire (SCQ) and the Autism Diagnostic Observation Schedule (ADOS).Results: We found that 35.1% of boys and 4.3% of girls with FXS scored in the “autism” category on both instruments. Analysis of the symptom profile indicated that both boys and girls with FXS showed lower rates of impairment on communication and reciprocal social interaction items than the reference autism samples on the measures. Furthermore, a regression model showed that IQ was significantly negatively associated with the SCQ total score in both boys and girls with FXS, when controlling for age, medication use, and FMRP levels.Conclusions: These data suggest that there are significant differences in the profile of social and communicative symptomatology in FXS compared with individuals diagnosed with idiopathic autism. Given these differences, the implementation of standard autism interventions for individuals with FXS may not be optimal. Maintaining the conceptual distinction between FXS (an established biological disease) and idiopathic autism (a phenomenologically defined behavioral disorder) may also facilitate the development of more targeted and thus effective interventions for individuals with FXS in the future.Autism in Fragile X Syndrome: A Category Mistake?Scott S. Hall, Amy A. Lightbody, Melissa Hirt, Ava Rezvani, Allan L. Reiss10.1016/j.jaac.2010.07.001Journal of the American Academy of Child & Adolescent Psychiatry 49, 9 (2010)2010-08-02Journal of the American Academy of Child & Adolescent Psychiatry2010-08-02499S0890-8567(10)X0009-0New Research921933http://www.jaacap.com/article/PIIS0890856710004247/abstract?rss=yesObjective: Sleep disturbances are common in major depressive disorder (MDD), although polysomnographic (PSG) abnormalities are more prevalent in adults than in children and adolescents with MDD. Sleep spindle activity (SPA) is associated with neuroplasticity mechanisms during brain maturation and is more abundant in childhood and adolescence than in adulthood, and as such, may be a more sensitive measure of sleep alteration than PSG in early-onset depression. This study investigated SPA changes related to early-onset MDD, comparing individuals already ill with MDD and individuals at high-risk for MDD with healthy nondepressed controls.Method: The study included 63 participants (8 to 15 years of age): 21 currently depressed individuals, 21 individuals at high risk for MDD based on positive family history of MDD, and 21 healthy control individuals with no personal or family history of psychiatric illness. All participants maintained a regular sleep/wake schedule for 5 days, followed by 2 nights in the laboratory. SPA was analyzed in Stage 2 of non–rapid eye movement sleep.Results: SPA differed significantly between groups, particularly in the late part of the night (F2,62 = 7.3, p = .001). Although the difference was greatest between the MDD and healthy control groups, both the MDD (p = .0004) and at high-risk groups (p = .02) had significantly lower SPA compared with healthy controls. SPA deficit was more prominent in females than in males (F5,62 = 5.19, p = .005).Conclusions: Low SPA characterizes youths with MDD and those at high risk for MDD, particularly girls, suggesting that early-onset depression and risk for the MDD are associated with decreased neuroplasticity.Reduced Sleep Spindle Activity in Early-Onset and Elevated Risk for DepressionJorge Lopez, Robert Hoffmann, Roseanne Armitage10.1016/j.jaac.2010.05.014Journal of the American Academy of Child & Adolescent Psychiatry 49, 9 (2010)2010-07-26Journal of the American Academy of Child & Adolescent Psychiatry2010-07-26499S0890-8567(10)X0009-0New Research934943http://www.jaacap.com/article/PIIS0890856710004168/abstract?rss=yesObjective: Deficits in cognitive flexibility and response inhibition have been linked to perturbations in cortico-striatal-thalamic circuitry in adult obsessive-compulsive disorder (OCD). Although similar cognitive deficits have been identified in pediatric OCD, few neuroimaging studies have been conducted to examine its neural correlates in the developing brain. In this study, we tested hypotheses regarding group differences in the behavioral and neural correlates of cognitive flexibility in a pediatric OCD and a healthy comparison (HC) sample.Method: In this functional magnetic resonance imaging (fMRI) study, a pediatric sample of 10- to 17-year-old subjects, 15 with OCD and 20 HC, completed a set-shifting task. The task, requiring an extradimensional shift to identify a target, examines cognitive flexibility. Within each block, the dimension (color or shape) that identified the target either alternated (i.e., mixed) or remained unchanged (i.e., repeated).Results: Compared with the HC group, the OCD group tended to be slower to respond to trials within mixed blocks. Compared with the HC group, the OCD group exhibited less left inferior frontal gyrus/BA47 activation in the set-shifting contrast (i.e., HC > OCD, mixed versus repeated); only the HC group exhibited significant activation in this region. The correlation between set shifting-induced right caudate activation and shift cost (i.e., reaction time differential in response to mixed versus repeated trials) was significantly different between HC and OCD groups, in that we found a positive correlation in HC and a negative correlation in OCD.Conclusions: In pediatric OCD, less fronto-striatal activation may explain previously identified deficits in shifting cognitive sets.Cognitive Inflexibility and Frontal-Cortical Activation in Pediatric Obsessive-Compulsive DisorderJennifer C. Britton, Scott L. Rauch, Isabelle M. Rosso, William D.S. Killgore, Lauren M. Price, Jennifer Ragan, Anne Chosak, Dianne M. Hezel, Daniel S. Pine, Ellen Leibenluft, David L. Pauls, Michael A. Jenike, S. Evelyn Stewart10.1016/j.jaac.2010.05.006Journal of the American Academy of Child & Adolescent Psychiatry 49, 9 (2010)2010-06-30Journal of the American Academy of Child & Adolescent Psychiatry2010-06-30499S0890-8567(10)X0009-0New Research944953http://www.jaacap.com/article/PIIS0890856710004521/abstract?rss=yesObjective: This trial examined the efficacy of teacher-delivered personality-targeted interventions for alcohol-misuse over a 6-month period.Method: This randomized controlled trial randomly allocated participating schools to intervention (n = 11) or control (n = 7) conditions. A total of 2,506 (mean age, 13.7 years) were assessed for elevated levels of personality risk factors for substance misuse: sensation-seeking, impulsivity, anxiety sensitivity, and hopelessness. Six hundred ninety-six adolescents were invited to participate in teacher-delivered personality-targeted interventions, and 463 were assigned to the nontreatment condition. Primary outcomes were drinking, binge-drinking status, quantity by frequency of alcohol use, and drinking-related problems.Results: School delivery of the personality-targeted intervention program was associated with significantly lower drinking rates in high-risk students at 6-month follow-up (odds ratio, 0.6), indicating a 40% decreased risk of alcohol consumption in the intervention group. Receiving an intervention also predicted significantly lower binge-drinking rates in students who reported alcohol use at baseline (odds ratio, 0.45), indicating a 55% decreased risk of binge-drinking in this group compared with controls. In addition, high-risk intervention-school students reported lower quantity by frequency of alcohol use (β = −.18) and drinking-related problems (β = −.15) compared with the nontreatment group at follow-up.Conclusion: This trial replicates previous studies reporting the efficacy of personality-targeted interventions and demonstrates that targeted interventions can be successfully delivered by teachers, suggesting potential for this approach as a sustainable school-based prevention model.Clinical trial registration information—Personality-Targeted Interventions for Adolescent Alcohol Misuse, URL: http://www.clinicaltrials.gov, unique identifier: NCT00344474.Personality-Targeted Interventions Delay Uptake of Drinking and Decrease Risk of Alcohol-Related Problems When Delivered by TeachersMaeve O'Leary-Barrett, Clare J. Mackie, Natalie Castellanos-Ryan, Nadia Al-Khudhairy, Patricia J. Conrod10.1016/j.jaac.2010.04.011Journal of the American Academy of Child & Adolescent Psychiatry 49, 9 (2010)2010-08-02Journal of the American Academy of Child & Adolescent Psychiatry2010-08-02499S0890-8567(10)X0009-0New Research954963.e1http://www.jaacap.com/article/PIIS0890856710003928/abstract?rss=yesThings ain't what they used to be and probably never was.—Will Rogers It seems more difficult than ever to be a child or adolescent in the 21st century. Each day the news reports on more youth in difficulty or “in crisis.” Aside from the media storm generated by some high-profile reports, what does this actually mean? What do many children and adolescents struggle with in quieter moments?Laura M. Prager, Anita Chu10.1016/j.jaac.2010.04.010Journal of the American Academy of Child & Adolescent Psychiatry 49, 9 (2010)2010-09-01Journal of the American Academy of Child & Adolescent Psychiatry2010-09-01499S0890-8567(10)X0009-0Book Forum964964http://www.jaacap.com/article/PIIS0890856710004193/abstract?rss=yes Books with titles that include words such as essential regularly do not live up to their names, but this edited text by Mary Nixon and Nancy Heath actually does. It is indeed, as the editors claim, “…the first [book] to bring together a wealth of expertise from psychiatry, psychology, counseling, and community health…wherein leaders in each field share their knowledge directly with practitioners to improve practice.…” (p. 317). Truly multidisciplinary in focus and authorship, this comprehensive guide offers detailed, evidence-based, and compassionate information for anyone working with adolescents who engage in NSSI. It is not often that a single text can provide such depth and scope on a topic, particularly one that is too frequently talked about in an unbalanced or incomplete manner. Kudos to Nixon and Heath for giving us a very usable and useful guide!Robin E. Connors10.1016/j.jaac.2010.05.009Journal of the American Academy of Child & Adolescent Psychiatry 49, 9 (2010)2010-09-01Journal of the American Academy of Child & Adolescent Psychiatry2010-09-01499S0890-8567(10)X0009-0Book Forum964965http://www.jaacap.com/article/PIIS089085671000420X/abstract?rss=yes As early as 1970, the famous developmentalist Urie Bronfenbrenner warned that without thoughtful and coordinated action by whole integrated communities, we would begin to witness increased antagonism and indifference in the younger generation from all segments of society—the middle-class and the disadvantaged. Since then, a growing number of scholars, pundits, youth advocates, parents, and policy makers have sounded the alarm. Alongside theories about the decay of youth morals and the growing epidemic of parental ineptitude comes the charge that corrosive elements in popular culture and social processes are simultaneously thwarting the potential for positive youth development and the capacity of important socializing agents (families, neighborhoods, schools, and communities) to buffer youth from caustic effects in the larger environment.Janis Whitlock10.1016/j.jaac.2010.05.010Journal of the American Academy of Child & Adolescent Psychiatry 49, 9 (2010)2010-09-01Journal of the American Academy of Child & Adolescent Psychiatry2010-09-01499S0890-8567(10)X0009-0Book Forum966967http://www.jaacap.com/article/PIIS0890856710004211/abstract?rss=yesWhen the lid was put back on the jar, Elpis [Hope] was kept inside. That is why Elpis [Hope] alone is still found among the people, promising that she will bestow on each of us the good things that have gone away.—Aesop, Fables 526 (from Babrius 58, translated by Laura Gibbs, Greek fable 6th century B.C.)Benjamin Sugar, Sarah Furlong10.1016/j.jaac.2010.05.011Journal of the American Academy of Child & Adolescent Psychiatry 49, 9 (2010)2010-09-01Journal of the American Academy of Child & Adolescent Psychiatry2010-09-01499S0890-8567(10)X0009-0Book Forum968969http://www.jaacap.com/article/PIIS0890856710004223/abstract?rss=yes Since the 1920s, gun-related tragedies have occurred in primary and secondary schools and on college campuses, yet within the past 20 years, the frequency and severity of these attacks have increased. Accordingly, our intellectual curiosity about what drives these events has also grown: much research has examined the psychology of the perpetrators, the environments in which they occur, and how to prevent future attacks. This book joins this growing body of literature and proposes that “school shooters” (the author's term for the individuals responsible for the violence) derive from one of three psychological typologies: the psychopathic, psychotic, or traumatized personality. Clinical psychologist Langman analyzes documents related to eight school shootings that occurred between 1997 and 2007 (including, most notoriously, the Columbine and Virginia Tech tragedies) as he gathers evidence for these typologies. His conclusions lead him to refute popularly held notions that school shooters are disproportionately subjected to bullying and ridicule by their peers and that they are isolated, lonely, and eccentric. The book concludes with a concise, 10-item list of recommendations for preventing school shootings.Abigail E.V. Wilson10.1016/j.jaac.2010.05.012Journal of the American Academy of Child & Adolescent Psychiatry 49, 9 (2010)2010-09-01Journal of the American Academy of Child & Adolescent Psychiatry2010-09-01499S0890-8567(10)X0009-0Book Forum969971http://www.jaacap.com/article/PIIS0890856710005915/abstract?rss=yesSeptember 2010 CME10.1016/j.jaac.2010.08.001Journal of the American Academy of Child & Adolescent Psychiatry 49, 9 (2010)2010-09-01Journal of the American Academy of Child & Adolescent Psychiatry2010-09-01499S0890-8567(10)X0009-0CME972973http://www.jaacap.com/article/PIIS089085671000568X/abstract?rss=yesEditorial Board10.1016/S0890-8567(10)00568-XJournal of the American Academy of Child & Adolescent Psychiatry 49, 9 (2010)2010-09-01Journal of the American Academy of Child & Adolescent Psychiatry2010-09-01499S0890-8567(10)X0009-0FrontmatterA1A1http://www.jaacap.com/article/PIIS0890856710005691/abstract?rss=yesCouncil Page10.1016/S0890-8567(10)00569-1Journal of the American Academy of Child & Adolescent Psychiatry 49, 9 (2010)2010-09-01Journal of the American Academy of Child & Adolescent Psychiatry2010-09-01499S0890-8567(10)X0009-0FrontmatterA2A2http://www.jaacap.com/article/PIIS089085671000571X/abstract?rss=yesTable of Contents10.1016/S0890-8567(10)00571-XJournal of the American Academy of Child & Adolescent Psychiatry 49, 9 (2010)2010-09-01Journal of the American Academy of Child & Adolescent Psychiatry2010-09-01499S0890-8567(10)X0009-0FrontmatterA4A5