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Background: Internationally, pediatric depression and suicide are significant issues. Additionally, in the context of the COVID-19 pandemic, pediatric mental health needs are rising astronomically. In light of Child & Adolescent Psychiatrist (CAP) subspecialist shortages in the United States (US), there is an increasing call for primary care physicians in Family Medicine and Pediatrics to address an increasingly broad variety of patient needs. Here we report on the development and preliminary evaluation of medical student and resident perceptions on the "INteractive Virtual Expert-led Skills Training" (INVEST) medical education curriculum, a virtual synchronous CAP curriculum employing active learning strategies, including expert-led discussion and video modeling, and discussion designed to meet those priorities. Methods: In a standardized 60-min training format, our curriculum leverages audience response system polling, video modeling of key clinical skills, and interactive discussion with an expert subspecialist, over a virtual video conferencing platform. The primary educational strategy relies on use of video modeling to demonstrate best practice with CAP led group discussion to solidify and explain important concepts. Five waves of medical students and residents (N = 149) participated in the INVEST curriculum and completed pre- and post-training surveys regarding knowledge and comfort in the management of pediatric patients with depression and suicidality. Results: Trainee participants reported significant positive gains in perceived likelihood of encountering pediatric suicidality as well as knowledge/comfort with depression screening and suicidality assessment in a primary care setting. Across some competency areas, there was an effect of medical learner level. Learners at lower levels generally reported the highest benefit. Medical students reported significant increases in their comfort interpreting and discussing positive depression screens and evidenced the greatest relative benefit in comfort with discussing suicidality. Conclusion: To our knowledge, INVEST is the first fully virtual, multimodal curriculum led by expert CAP subspecialists. Our findings suggest that INVEST shows promise for equipping medical learners with baseline knowledge for caring for patients with pediatric depression and suicidality. This synchronous, virtually delivered curriculum allows for critical training delivered to diverse medical learners regardless of geographic location, a particular benefit during the current COVID-19 pandemic.
RESUMO
Large-scale genetic studies revealed SCN2A as one of the most frequently mutated genes in patients with neurodevelopmental disorders. SCN2A encodes for the voltage-gated sodium channel isoform 1.2 (Nav 1.2) expressed in the neurons of the central nervous system. Homozygous knockout (null) of Scn2a in mice is perinatal lethal, whereas heterozygous knockout of Scn2a (Scn2a+/- ) results in mild behavior abnormalities. The Nav 1.2 expression level in Scn2a+/- mice is reported to be around 50-60% of the wild-type (WT) level, which indicates that a close to 50% reduction of Nav 1.2 expression may not be sufficient to lead to major behavioral phenotypes in mice. To overcome this barrier, we characterized a novel mouse model of severe Scn2a deficiency using a targeted gene-trap knockout (gtKO) strategy. This approach produces viable homozygous mice (Scn2agtKO/gtKO ) that can survive to adulthood, with about a quarter of Nav 1.2 expression compared to WT mice. Innate behaviors like nesting and mating were profoundly disrupted in Scn2agtKO/gtKO mice. Notably, Scn2agtKO/gtKO mice have a significantly decreased center duration compared to WT in the open field test, suggesting anxiety-like behaviors in a novel, open space. These mice also have decreased thermal and cold tolerance. Additionally, Scn2agtKO/gtKO mice have increased fix-pattern exploration in the novel object exploration test and a slight increase in grooming, indicating a detectable level of repetitive behaviors. They bury little to no marbles and have decreased interaction with novel objects. These Scn2a gene-trap knockout mice thus provide a unique model to study pathophysiology associated with severe Scn2a deficiency.
