Faculty Bibliography

The purpose of this preliminary study is to evaluate if there is a difference between the intelligence quotient (IQ) of 27 adolescent defendants referred to the Bellevue Hospital Center Forensic Psychiatry Clinic after committing violent crimes, and those adolescents in the same age group in the general population of the United States, as defined by the norms of the psychometric testing instrument Wechsler Intelligence Scale for Children, 4th edition (WISC-IV). The IQ scores and sub-scores were compared to IQ scores of the general population (mean = 100, SD = 15) using a Z-test. The mean for the Full Scale IQ was 82.93. The means for the subtests which include Processing Speed Index, Perceptual Reasoning Index, Verbal Comprehension Index, and Working Memory Index, were: 78.48, 87.78, 86.70 (p < 0.05), and 90.78 (p = 0.09) respectively. There is a statistically significant difference in the IQ scores of the violent juveniles studied when compared to the general population

This study examined relations among family environment, cortisol response, and behavior in the context of a randomized controlled trial with 92 children (M = 48 months) at risk for antisocial behavior. Previously, researchers reported an intervention effect on cortisol response in anticipation of a social challenge. The current study examined whether changes in cortisol response were related to later child aggression. Among lower warmth families, the intervention effect on aggression was largely mediated by the intervention effect on cortisol response. Although the intervention also resulted in significant benefits on child engaging behavior, cortisol response did not mediate this effect. These findings demonstrate meaningful associations between cortisol response and aggression among children at familial risk for antisocial behavior

How do infants learn to perceive the backs of objects that they see only from a limited viewpoint? Infants' 3-dimensional object completion abilities emerge in conjunction with developing motor skills--independent sitting and visual-manual exploration. Infants at 4.5 to 7.5 months of age (n = 28) were habituated to a limited-view object and tested with volumetrically complete and incomplete (hollow) versions of the same object. Parents reported infants' sitting experience, and infants' visual-manual exploration of objects was observed in a structured play session. Infants' self-sitting experience and visual-manual exploratory skills predicted looking at the novel, incomplete object on the habituation task. Further analyses revealed that self-sitting facilitated infants' visual inspection of objects while they manipulated them. The results are framed within a developmental systems approach, wherein infants' sitting skill, multimodal object exploration, and object knowledge are linked in developmental time.

Spanning functions from the simplest reflex arc to complex cognitive processes, neural circuits have diverse functional roles. In the cerebral cortex, functional domains such as visual processing, attention, memory, and cognitive control rely on the development of distinct yet interconnected sets of anatomically distributed cortical and subcortical regions. The developmental organization of these circuits is a remarkably complex process that is influenced by genetic predispositions, environmental events, and neuroplastic responses to experiential demand that modulates connectivity and communication among neurons, within individual brain regions and circuits, and across neural pathways. Recent advances in neuroimaging and computational neurobiology, together with traditional investigational approaches such as histological studies and cellular and molecular biology, have been invaluable in improving our understanding of these developmental processes in humans in both health and illness. To contextualize the developmental origins of a wide array of neuropsychiatric illnesses, this review describes the development and maturation of neural circuits from the first synapse through critical periods of vulnerability and opportunity to the emergent capacity for cognitive and behavioral regulation, and finally the dynamic interplay across levels of circuit organization and developmental epochs.

OBJECTIVES: Administration to rats of mood stabilizers approved for bipolar disorder (BD) downregulates markers of the brain arachidonic acid (AA, 20:4n-6) metabolic cascade, including phospholipase A(2) (PLA(2)) and cyclooxygenase (COX) expression. We hypothesized that other agents that target the brain AA cascade, nonsteroidal anti-inflammatory drugs (NSAIDs) and glucocorticoids, also would ameliorate BD symptoms. METHODS: Medication histories on subjects who had been prescribed lithium were collected from the Netherlands PHARMO Record Linkage System. Data were stratified according to drug classes that inhibit PLA(2) and/or COX enzymes, and duration of use. Incidence density (ID) of medication events (dose increase or substance change) was used as a proxy for clinical worsening. ID ratios in patients with the inhibitors plus lithium were compared to ratios in patients using lithium alone. RESULTS: Low-dose acetylsalicylic acid (aspirin) significantly reduced the ID ratio of medication events, independent of use duration. The ID ratios of NSAIDs and glucocorticoids did not differ significantly from 1.0 if prescribed for > or =180 or > or =90 days, but exceeded 1.0 with shorter use. Selective COX-2 inhibitors had no significant effect and multiagent administration increased the ID ratio above 1.0. CONCLUSIONS: Low-dose aspirin produced a statistically significant duration-independent reduction in the relative risk of clinical deterioration in subjects on lithium, whereas other NSAIDs and glucocorticoids did not. These tentative findings could be tested on larger databases containing detailed information about diagnosis and disease course, as well as by controlled clinical trials.

STUDY OBJECTIVES: To examine the relationships between parental set bedtimes, sleep duration, and depression as a quasi-experiment to explore the potentially bidirectional relationship between short sleep duration and depression. Short sleep duration has been shown to precede depression, but this could be explained as a prodromal symptom of depression. Depression in an adolescent can affect his/her chosen bedtime, but it is less likely to affect a parent's chosen set bedtime which can establish a relatively stable upper limit that can directly affect sleep duration. DESIGN: Multivariate cross-sectional analyses of the ADD Health using logistic regression. SETTING: United States nationally representative, school-based, probability-based sample in 1994-96. PARTICIPANTS: Adolescents (n = 15,659) in grades 7 to 12. MEASUREMENTS AND RESULTS: Adolescents with parental set bedtimes of midnight or later were 24% more likely to suffer from depression (OR = 1.24, 95% CI 1.04-1.49) and 20% more likely to have suicidal ideation (1.20, 1.01-1.41) than adolescents with parental set bedtimes of 10:00 PM or earlier, after controlling for covariates. Consistent with sleep duration and perception of getting enough sleep acting as mediators, the inclusion of these variables in the multivariate models appreciably attenuated the associations for depression (1.07, 0.88-1.30) and suicidal ideation (1.09, 0.92-1.29). CONCLUSIONS: The results from this study provide new evidence to strengthen the argument that short sleep duration could play a role in the etiology of depression. Earlier parental set bedtimes could therefore be protective against adolescent depression and suicidal ideation by lengthening sleep duration

BACKGROUND: Depression has been found to predict the incidence of hypertension and other adverse cardiovascular events in prospective studies. Insomnia and short sleep duration, which are typical symptoms of depression, have also been shown to increase the risk for hypertension incidence. Insomnia is associated with increased activation of the hypothalamic-pituitary-adrenal axis, and short sleep duration raises average 24-h blood pressure, which over time could lead to structural adaptations that gradually reset the entire cardiovascular system to operate at an elevated pressure equilibrium. No previous published population studies have examined whether insomnia and sleep duration mediate the relationship between depression and hypertension incidence. METHODS: We conducted multivariate longitudinal (1982-1992) analyses stratified by age of the First National Health and Nutrition Examination Survey (NHANES I) (n = 4,913) using Cox proportional hazards models. RESULTS: Middle-aged subjects who suffered from depression at baseline were 44% more likely to be diagnosed with hypertension over the follow-up period after controlling for covariates (hazard ratio (HR) = 1.44, 95% confidence interval (CI) 1.15-1.80). Both short sleep duration and insomnia were also significantly associated with hypertension incidence. Consistent with insomnia and sleep duration acting as mediators of the relationship between depression and hypertension incidence, the inclusion of these variables in the multivariate models appreciably attenuated the association (HR = 1.27, 95% CI 1.00-1.61). Depression, sleep duration, and insomnia were not significantly associated with hypertension incidence in elderly subjects. CONCLUSIONS: These results suggest the hypothesis that treatment of sleep problems in middle-aged individuals suffering from depression could reduce their risk for developing hypertension, and its vascular and cardiac complications

There is increasing consensus that disruptive behavior disorders and syndromes (DBDs) are identifiable in preschool children. There is also concomitant recognition of the limitations of the current DBD nosology for distinguishing disruptive behavior symptoms from the normative misbehavior of early childhood. In particular, there appears to be substantial insensitivity to heterotypic manifestations of this developmental period and problems in identifying meaningful heterogeneity. As a result, the developmental basis for much of the current nosology may be called into question. To address these and other critical issues, this paper reviews the foundational elements of clinical and developmental science pertinent to developmental differentiation of disruptive behavior in the preschool period as paradigmatic for developmental specification across the lifespan and generates an agenda for future research. We begin by reviewing evidence of the validity of DBDs in preschool children. This is followed by an outline of key developmental concepts and a review of the corollary evidence from developmental science. These provide a basis for conceptualizing disruptive behavior in reference to developmental deviation in four core dimensions hypothesized to mark the core features of disruptive behavior syndromes. Finally, we propose a program of research to establish an empirical basis for determining the incremental utility of a developmentally specified nosology. Central to this approach is a contention that the benefits of developmental specification are extensive and outweigh any disadvantages. This is because a developmentally specified approach holds substantial promise for increasing sensitivity and specificity for differentiating disruptive behavior from normative misbehavior and from other related syndromes as well as for improving prediction. Further, more precisely defined, developmentally based phenotypes are likely to elucidate distinct mechanisms within translational studies and to serve as a catalyst for the generation of novel treatments