Faculty Bibliography

Background/UNASSIGNED:With the uncertainties of COVID-19, people infected by coronavirus present with diverse psychiatric presentations. Some centers have had to manage their patients with existing protocols, others have had to come up with innovations. We aim to report the challenges and good practices recorded in the management of psychiatric conditions and delirium coexisting with COVID-19 and during the COVID-19 era across continents. Material and Methods/UNASSIGNED:Early Career Psychiatrists (ECPs) from across five continents were approached to provide their perspective on the management of psychiatric conditions in patients with COVID-19 and during the current pandemic. Results/UNASSIGNED:We collected information about the experiences from ten countries. Commonalities were similar psychiatric presentations and poor preparedness across countries. Differences were varying innovations and adjustments made in the management of psychiatric conditions coexisting with COVID-19. Good practices which can be adopted by other countries are novel approaches such as telepsychiatry, proactive consultation-liaison units and enhanced community services targeted at circumventing challenges faced yet providing mental health services. Conclusions/UNASSIGNED:This publication highlights the need for global preparedness in the mental health sector during outbreaks of infectious diseases. With our results we can conclude that there is the need for concerted efforts targeted at global and locally sensitive adaptation of existing protocols and the development of new guidelines for the management of psychiatric conditions for the present pandemic and subsequent occurrences.

BACKGROUND:The C8 Science Panel was composed of three epidemiologists charged with studying the possible health effects of PFOA in a highly exposed population in the mid-Ohio Valley. The Panel determined in 2012 there was a 'probable link' (i.e., more probable than not based on the weight of the available scientific evidence) between PFOA and high cholesterol, thyroid disease, kidney and testicular cancer, pregnancy-induced hypertension, and ulcerative colitis. OBJECTIVE:Here, former C8 Science Panel members and collaborators comment on the PFOA literature regarding thyroid disorders, cancer, immune and auto-immune disorders, liver disease, hypercholesterolemia, reproductive outcomes, neurotoxicity, and kidney disease. We also discuss developments regarding fate and transport, and pharmacokinetic models, and discuss causality assessment in cross-sectional associations among low-exposed populations. DISCUSSION/CONCLUSIONS:For cancer, the epidemiologic evidence remains supportive but not definitive for kidney and testicular cancers. There is consistent evidence of a positive association between PFOA and cholesterol, but no evidence of an association with heart disease. There is evidence for an association with ulcerative colitis, but not for other auto-immune diseases. There is good evidence that PFOA is associated with immune response, but uneven evidence for an association with infectious disease. The evidence for an association between PFOA and thyroid and kidney disease is suggestive but uneven. There is evidence of an association with liver enzymes, but not with liver disease. There is little evidence of an association with neurotoxicity. Suggested reductions in birthweight may be due to reverse causality and/or confounding. Fate and transport models and pharmacokinetic models remain central to estimating past exposure for new cohorts, but are difficult to develop without good historical data on emissions of PFOA into the environment. CONCLUSION/CONCLUSIONS:Overall, the epidemiologic evidence remains limited. For a few outcomes there has been some replication of our earlier findings. More longitudinal research is needed in large populations with large exposure contrasts. Additional cross-sectional studies of low exposed populations may be less informative.

BACKGROUND:Nearly half of all mental health disorders develop prior to the age of 15. Early assessments, diagnosis, and treatment are critical to shortening single episodes of care, reducing possible comorbidity and long-term disability. In Norway, approximately 20% of all children and adolescents are experiencing mental health problems. To address this, health officials in Norway have called for the integration of innovative approaches. A clinical decision support system (CDSS) is an innovative, computer-based program that provides health professionals with clinical decision support as they care for patients. CDSS use standardized clinical guidelines and big data to provide guidance and recommendations to clinicians in real-time. IDDEAS (Individualised Digital DEcision Assist System) is a CDSS for diagnosis and treatment of child and adolescent mental health disorders. The aim of IDDEAS is to enhance quality, competency, and efficiency in child and adolescent mental health services (CAMHS). METHODS/DESIGN/METHODS:IDDEAS is a mixed-methods innovation and research project, which consists of four stages: 1) Assessment of Needs and Preparation of IDDEAS; 2) The Development of IDDEAS CDSS Model; 3) The Evaluation of the IDDEAS CDSS; and, 4) Implementation & Dissemination. Both qualitative and quantitative methods will be used for the evaluation of IDDEAS CDSS model. Child and adolescent psychologists and psychiatrists (n = 30) will evaluate the IDDEAS` usability, acceptability and relevance for diagnosis and treatment of attention-deficit/hyperactivity disorder. DISCUSSION/CONCLUSIONS:The IDDEAS CDSS model is the first guidelines and data-driven CDSS to improve efficiency of diagnosis and treatment of child and adolescent mental health disorders in Norway. Ultimately, IDDEAS will help to improve patient health outcomes and prevent long-term adverse outcomes by providing each patient with evidence-based, customized clinical care. TRIAL REGISTRATION/BACKGROUND:ISRCTN, ISRCTN12094788. Ongoing study, registered prospectively 8 April 2020 https://doi.org/10.1186/ISRCTN12094788.

Developmental exposure to ethanol has a wide range of anatomical, cellular, physiological and behavioral impacts that can last throughout life. In humans, this cluster of effects is termed fetal alcohol spectrum disorder and is highly prevalent in western cultures. The ultimate expression of the effects of developmental ethanol exposure however can be influenced by post-exposure experience. Here we examined the effects of developmental binge exposure to ethanol (postnatal day 7) in C57BL/6By mice on a specific cohort of inter-related long-term outcomes including contextual memory, hippocampal parvalbumin-expressing neuron density, frontal cortex oscillations related to sleep-wake cycling including delta oscillation amplitude and sleep spindle density, and home-cage behavioral activity. When assessed in adults that were raised in standard housing, all of these factors were altered by early ethanol exposure compared to saline controls except home-cage activity. However, exposure to an enriched environment and exercise from weaning to postnatal day 90 reversed most of these ethanol-induced impairments including memory, CA1 but not dentate gyrus PV+ cell density, delta oscillations and sleep spindles, and enhanced home-cage behavioral activity in Saline- but not EtOH-treated mice. The results are discussed in terms of the inter-dependence of diverse developmental ethanol outcomes and potential mechanisms of post-exposure experiences to regulate those outcomes.

PURPOSE OF REVIEW/OBJECTIVE:We review the state of the literature examining associations between early life stress (ELS), gut microbiota, and neurocognitive development and mental health in animals and humans. We identify gaps in current models and areas for future research. RECENT FINDINGS/RESULTS:ELS is associated with changes in gut microbiota, which correspond to changes in affective and cognitive functioning in both animals and humans. Some of these ELS-induced psychological changes can be remedied by supplementation with probiotics in early life, suggesting a potential area for intervention for ELS-exposed children. Prenatal stress exposure is rarely studied in humans in relation to gut microbiota, but animal work has suggested important associations between prenatal stress and fetal programming that should be tested in humans. The gut microbiota plays an important role in the association between ELS, neurocognitive development, and mental health. More work is needed to fully understand these associations in humans.

BACKGROUND:Family coaggregation of attention-deficit/hyperactivity disorder (ADHD), autism spectrum disorder (ASD), bipolar disorder (BD), major depressive disorder (MDD) and schizophrenia have been presented in previous studies. The shared genetic and environmental factors among psychiatric disorders remain elusive. METHODS:This nationwide population-based study examined familial coaggregation of major psychiatric disorders in first-degree relatives (FDRs) of individuals with ASD. Taiwan's National Health Insurance Research Database was used to identify 26 667 individuals with ASD and 67 998 FDRs of individuals with ASD. The cohort was matched in 1:4 ratio to 271 992 controls. The relative risks (RRs) and 95% confidence intervals (CI) of ADHD, ASD, BD, MDD and schizophrenia were assessed among FDRs of individuals with ASD and ASD with intellectual disability (ASD-ID). RESULTS:FDRs of individuals with ASD have higher RRs of major psychiatric disorders compared with controls: ASD 17.46 (CI 15.50-19.67), ADHD 3.94 (CI 3.72-4.17), schizophrenia 3.05 (CI 2.74-3.40), BD 2.22 (CI 1.98-2.48) and MDD 1.88 (CI 1.76-2.00). Higher RRs of schizophrenia (4.47, CI 3.95-5.06) and ASD (18.54, CI 16.18-21.23) were observed in FDRs of individuals with both ASD-ID, compared with ASD only. CONCLUSIONS:The risk for major psychiatric disorders was consistently elevated across all types of FDRs of individuals with ASD. FDRs of individuals with ASD-ID are at further higher risk for ASD and schizophrenia. Our results provide leads for future investigation of shared etiologic pathways of ASD, ID and major psychiatric disorders and highlight the importance of mental health care delivered to at-risk families for early diagnoses and interventions.

Autism spectrum disorder (ASD) is a class of neurodevelopmental disorders that affects males more frequently than females. Numerous genetic and environmental risk factors have been suggested to contribute to the development of ASD. However, no one factor can adequately explain either the frequency of the disorder or the male bias in its prevalence. Gonadal, thyroid, and glucocorticoid hormones all contribute to normal development of the brain, hence perturbations in either their patterns of secretion or their actions may constitute risk factors for ASD. Environmental factors may contribute to ASD etiology by influencing the development of neuroendocrine and neuroimmune systems during early life. Emerging evidence suggests that the placenta may be particularly important as a mediator of the actions of environmental and endocrine risk factors on the developing brain, with the male being particularly sensitive to these effects. Understanding how various risk factors integrate to influence neural development may facilitate a clearer understanding of the etiology of ASD.

The dorsolateral prefrontal cortex (DLPFC), a key structure in the executive system, has consistently emerged as a crucial element in the pathophysiology of obsessive-compulsive disorder (OCD). However, the neural primacy of the DLPFC remains elusive in this disorder. We investigated the causal interaction (measured by effective connectivity) between the DLPFC and the remaining brain areas using bivariate Granger causality analysis of resting-state fMRI collected from 88 medication-free OCD patients and 88 matched healthy controls. Additionally, we conducted seed-based functional connectivity (FC) analyses to identify network-level neural functional alterations using the bilateral DLPFC as seeds. OCD patients demonstrated reduced FC between the right DLPFC and right orbitofrontal cortex (OFC), and activity in the right OFC had an inhibitory effect on the right DLPFC. Additionally, we observed alterations in both feedforward and reciprocal influences between the inferior temporal gyrus (ITG) and the DLPFC in patients. Furthermore, activity in the cerebellum had an excitatory influence on the right DLPFC in OCD patients. These findings may help to elucidate the psychopathology of OCD by detailing the directional connectivity between the DLPFC and the rest of the brain, ultimately helping to identify regions that could serve as treatment targets in OCD.