These results indicate that abnormal dendritic outgrowth or maintenance contributes to reduced neuropil and prefrontal connectivity in schizophrenia. Short postmortem intervals and resulting high tissue quality suggest that these dystrophic changes reflect schizophrenia pathology rather than postmortem artifact.

Researchers and clinicians are increasingly recognizing that psychological and psychiatric disorders are often developmentally progressive, and that diagnosis often represents a point along that progression that is defined largely by our abilities to detect symptoms. As a result, strategies that guide our searches for the root causes and etiologies of these disorders are beginning to change. This review describes interactions between genetics and experience that influence the development of psychopathologies. Following a discussion of normal brain development that highlights how specific cellular processes may be targeted by genetic or environmental factors, we focus on four disorders whose origins range from genetic (fragile X syndrome) to environmental (fetal alcohol syndrome) or a mixture of both factors (depression and schizophrenia). C.H. Waddington's canalization model (slightly modified) is used as a tool to conceptualize the interactive influences of genetics and experience in the development of these psychopathologies. Although this model was originally proposed to describe the 'canalizing' role of genetics in promoting normative development, it serves here to help visualize, for example, the effects of adverse (stressful) experience in the kindling model of depression, and the multiple etiologies that may underlie the development of schizophrenia. Waddington's model is also useful in understanding the canalizing influence of experience-based therapeutic approaches, which also likely bring about 'organic' changes in the brain. Finally, in light of increased evidence for the role of experience in the development and treatment of psychopathologies, we suggest that future strategies for identifying the underlying causes of these disorders be based less on the mechanisms of action of effective pharmacological treatments, and more on increased knowledge of the brain's cellular mechanisms of plastic change.

Objectives: Utilization of emergency departments (EDs) for pediatric mental health (MH) complaints is increasing. These patients require more resources and have higher admission rates than those with nonpsychiatric complaints.Methods: A multistage, multidisciplinary process to reduce length of stay (LOS) and improve the quality of care for patients with psychiatric complaints was performed at a tertiary care children's hospital's ED using Lean methodology. This process resulted in the implementation of a dedicated MH team, led by either a social worker or a psychiatric nurse, to evaluate patients, facilitate admissions, and arrange discharge planning. We conducted a retrospective, before-and-after study analyzing data 1 year before through 1 year after new process implementation (March 28, 2011). Our primary outcome was mean ED LOS.Results: After process implementation there was a statistically significant decrease in mean ED LOS (332 minutes vs. 244 minutes, p < 0.001). An x-bar chart of mean LOS shows special cause variation. Significant decreases were seen in median ED LOS (225 minutes vs. 204 minutes, p = 0.001), security physical interventions (2.0% vs. 0.4%, p = 0.004), and restraint use (1.7% vs. 0.1%, p < 0.001). No significant change was observed in admission rate, 72-hour return rate, or patient elopement/agitation events. Staff surveys showed improved perception of patient satisfaction, process efficacy, and patient safety.Conclusions: Use of quality improvement methodology led to a redesign that was associated with a significant reduction in mean LOS of patients with psychiatric complaints and improved ED staff perception of care.ACADEMIC EMERGENCY MEDICINE 2016;23:440-447 © 2016 by the Society for Academic Emergency Medicine M ental health (MH) disorders are common in children, with an estimated 13%-20% of children in the United States experiencing a mental disorder in a given year.1-5 They also are increasing, with a reported 24% increase in inpatient MH and substance abuse admissions among children from 2007 to 2010 6 and an 80% increase in hospital stays for children with mood disorders from 1997 to 2010. 7 Despite this increasing prevalence, psychiatric services for children in many parts of the country are limited, 8 leaving many with unmet psychiatric care needs. 9Nationally, pediatric emergency department (ED) visits for MH issues increased by over 20% between 2001 and 2010. 10 Pediatric EDs (PEDs) have also seen high volumes of patients presenting with psychiatric crises, with 3.3% of PED visits related to MH issues in one

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From childhood to adolescence, strengthened coupling in frontal, striatal and parieto-temporal regions associated with cognitive control, and increased anticorrelation between task-positive and task-negative circuits, subserve the reshaping of behavior. ADHD is a common condition peaking in adolescence and regressing in adulthood, with a wide variety of cognitive control deficits. Alternate hypotheses of ADHD emphasize lagging circuitry refinement versus categorical differences in network function. However, quantifying the individual circuit contributions to behavioral findings, and relative roles of maturational versus categorical effects, is challenging in vivo or in meta-analyses using task-based paradigms within the same pipeline, given the multiplicity of neurobehavioral functions implicated. To address this, we analyzed 46 positively-correlated and anticorrelated circuits in a multivariate model in resting-state data from 504 age- and gender-matched youth, and created a novel in silico method to map individual quantified effects to reverse inference maps of 8 neurocognitive functions consistently implicated in ADHD, as well as dopamine and hyperactivity. We identified only age- and gender-related effects in intrinsic connectivity, and found that maturational refinement of circuits in youth with ADHD occupied 3-10x more brain locations than in typical development, with the footprint, effect size and contribution of individual circuits varying substantially. Our analysis supports the maturational hypothesis of ADHD, suggesting lagging connectivity reorganization within specific subnetworks of fronto-parietal control, ventral attention, cingulo-opercular, temporo-limbic and cerebellar sub-networks contribute across neurocognitive findings present in this complex condition. We present the first analysis of anti-correlated connectivity in ADHD and suggest new directions for exploring residual and non-responsive symptoms.