Faculty Bibliography

Being a victim or perpetrator of school bullying, the most common type of school violence, has been frequently associated with a broad spectrum of behavioral, emotional, and social problems. Suicide is third leading cause of mortality in children and adolescent in the United States of America and around the world. This paper provides a systematic review of the previous 37 studies conducted in children and adolescents from communities, as well as in special populations that examined the association between bullying experiences and suicide, with an emphasis on the strengths and limitations of the study designs. Despite methodological and other differences and limitations, it is increasingly clear that any participation in bullying increases the risk of suicidal ideations and/or behaviors in a broad spectrum of youth

Bullying is a very toxic psychosocial stressor associated with serious health problems and death, affecting both the victims and the bullies. This form of abuse or maltreatment occurs around the world and along the lifespan. Health professionals have the unique responsibility of promoting the development of community initiatives for the prevention of bullying and related health problems. This effort must include ongoing programs with elements of primary, secondary, and tertiary prevention. These programs should be supported and monitored by a public health policy with a strategy aimed at developing a whole community awareness about bullying and the related health risks, prohibiting bullying, and developing emotionally and physically safe environments in schools and workplace settings. Public health policy should mandate the monitoring, detection, and reporting of bullying incidents; provide guidance for school intervention; and offer guidelines for medical consultation

Reports identified the neuronal glutamate transporter gene, SLC1A1 (OMIM 133550, chromosome 9p24), as a positional and functional candidate gene for obsessive-compulsive disorder (OCD). The presence of obsessions and compulsions similar to OCD in autism, the identification of this region in a genome-wide linkage analysis of individuals with autism spectrum disorders (ASDs), and the hypothesized role of glutamate in ASDs make SLC1A1 a candidate gene for ASD as well. To test for association between SLC1A1 and autism, we typed three single nucleotide polymorphisms (SNPs, rs301430, rs301979, rs301434) previously associated with OCD in 86 strictly defined trios with autism. Family-Based Association Tests (FBAT) with additive and recessive models were used to check for association. Additionally, an rs301430-rs301979 haplotype identified for OCD was investigated. FBAT revealed nominally significant association between autism and one SNP under a recessive model. The G allele of rs301979 was undertransmitted (equivalent to overtransmission of the C allele under a dominant model) to individuals with autism (Z=-2.47, P=0.01). The G allele was also undertransmitted in the T-G haplotype under the recessive model (Z=-2.41, P=0.02). Both findings were also observed in the male-only sample. However, they did not withstand correction for multiple comparisons

The authors assessed the reliability of the Autism Diagnostic Interview (ADI-R). Seven Clinical Examiners evaluated a three and one half year old female toddler suspected of being on the Autism Spectrum. Examiners showed agreement levels of 94-96% across all items, with weighted kappa (K(w)) between .80 and .88. They were in 100% agreement on 74% of the items; in excellent agreement on 6% of the items (93-96%, with K(w) between .78 and .85); in good agreement on 7% (89-90%, with K(w) between .62 and 0.68); and in fair agreement on 3% (82 - 84%, with K(w) between .40 and .47). For the remaining 10% of ADI-R items, examiners showed poor agreement (50-81% with K(w )between -.67 and .37)

The current study examined the persistence and phenotypic presentation of inattention/overactivity (I/O) into early adolescence, in a sample of institution reared (IR) children adopted from Romania before the age of 43 months. Total sample comprised 144 IR and 21 non-IR Romanian adoptees, and a comparison group of 52 within-UK adoptees, assessed at ages 6 and 11 years. I/O was rated using Rutter Scales completed by parents and teachers. I/O continued to be strongly associated with institutional deprivation, with continuities between ages 6 and 11 outcomes. There were higher rates of deprivation-related I/O in boys than girls, and I/O was strongly associated with conduct problems, disinhibited attachment and executive function but not IQ more generally, independently of gender. Deprivation-related I/O shares many common features with ADHD, despite its different etiology and putative developmental mechanisms. I/O is a persistent domain of impairment following early institutional deprivation of 6 months or more, suggesting there may be a possible pathway to impairment through some form of neuro-developmental programming during critical periods of early development

In this article the authors reflect on the role of executive function (EF) deficits and delay aversion (DAv) in the diagnosis of attention deficit hyperactivity disorder (ADHD). The authors, empirical review shows clearly that EF deficits and DAv are implicated in ADHD, although neither is necessary for ADHD nor specific to it. The constructs are somewhat dissociable from one another so that each may represent a distinctive feature associated with an ADHD subsample. The authors argue that neither EF deficits nor DAv add much value to the diagnosis of ADHD as it is currently conceptualized, but may be crucial in helping to partition heterogeneity in the condition, leading to the refinement of ADHD nosology

Examination of spontaneous intrinsic brain activity is drawing increasing interest, thus methods for such analyses are rapidly evolving. Here we describe a novel measure, 'network homogeneity', that allows for assessment of cohesiveness within a specified functional network, and apply it to resting-state fMRI data from adult ADHD and control participants. We examined the default mode network, a medial-wall based network characterized by high baseline activity that decreases during attention-demanding cognitive tasks. We found reduced network homogeneity within the default mode network in ADHD subjects compared to age-matched controls, particularly between the precuneus and other default mode network regions. This confirms previously published results using seed-based functional connectivity measures, and provides further evidence that altered precuneus connectivity is involved in the neuropathology of ADHD. Network homogeneity provides a potential alternative method for assessing functional connectivity of specific large-scale networks in clinical populations

Mother-infant attachment is facilitated in altricial rodents through unique neural mechanisms that include impaired neonatal fear conditioning until the time that pups first begin to leave the nest (sensitive period). Here, we confirmed the developmental emergence of odor fear conditioning in neonatal rat pups, and examined synaptic plasticity of inputs to the basolateral amygdala in vitro. Coronal slices through the amygdala were obtained from sensitive (<10 days) and post-sensitive (>10, <19 days) period pups. Field potentials were recorded in the basolateral amygdala in response to stimulation of either the external capsule (neocortical inputs) or fibers from the cortical nucleus of the amygdala (olfactory inputs). The effects of tetanic stimulation were examined in each pathway. In both pathways, tetanic stimulation induce significant long-term synaptic plasticity in post-sensitive period pups, but no significant plasticity in sensitive period pups incapable of learning odor aversions. GABA(A) receptor blockade in post-sensitive period slices reverts synaptic plasticity to sensitive period characteristics. The results suggest that sensitive period deficits in fear conditioning may be related to impaired amygdala synaptic plasticity and the immature state of GABAergic inhibition and/or its modulation in the neonatal amygdala

BACKGROUND: Pediatric anxiety disorders, although highly prevalent, are understudied with little known about their pathophysiology. Intolerance of uncertainty (IU) is a trait associated with worry, a key characteristic of these disorders. Neural responses to uncertainty in healthy subjects involve the same frontal-limbic circuits that are hyper-responsive in pediatric anxiety. As such, the present study examines the relationship between IU and neural responses to uncertainty in anxious adolescents. METHODS: Sixteen adolescents (ages 13-17) diagnosed with generalized anxiety disorder and/or social phobia (ANX) and 13 non-anxious control subjects completed a decision-making task while functional magnetic resonance imaging scans were acquired. RESULTS: The ANX group endorsed greater task-related anxiety and less certainty than control subjects on a post-task questionnaire. Compared with control subjects, the ANX group did not demonstrate hyper-responsivity of brain regions as hypothesized. Across groups, IU was positively correlated with activity in several frontal and limbic regions. Further analyses identified subgroups within the ANX group: those with high IU activated frontal/limbic regions, whereas those with low IU and less anxiety during the task deactivated the same regions in response to uncertainty. CONCLUSIONS: Results substantiate the hypothesized link between IU and neural responses to uncertainty in some adolescents with anxiety disorders. Our findings, if replicated, suggest that trait measures, such as IU, can significantly improve our understanding of the neurobiological basis of pediatric anxiety disorders