Point-of-Care Ultrasound in United States Pediatric Emergency Medicine Fellowship Programs: The Current State of Practice and Training.

OBJECTIVES: In 2015, the American Academy of Pediatrics (AAP) released a policy statement regarding point-of-care ultrasonography (POCUS) by pediatric emergency physicians, which included recommendations on education and training. In the 3 years since the AAP policy statement and its accompanying technical report were published, it is unclear which aspects of the recommendations set forth by this policy have been instituted by POCUS programs throughout the country. The objective of this study was to conduct a survey of pediatric emergency medicine (PEM) fellowship directors throughout the United States regarding the current state of education and training of POCUS in their department. METHODS: We conducted an online survey of all PEM fellowship program directors in the United States between April 1, 2018, and July 31, 2018. RESULTS: Of the 78 PEM fellowship program directors contacted, 62 (79.5%) responded. The majority reported having an ultrasound curriculum in place to educate their fellows (77%). Fellows are being taught using a variety of educational strategies. The most commonly reported barriers were lack of qualified faculty available for training (62.9%), lack of confidence or comfort in using the existing ultrasound machine(s) in their department (54.8%), and physician resistance to using new technology (50%). The majority of programs reported having processes in place for credentialing (56%) and quality assurance (72.6%). Whereas 77.4% have a system for archiving POCUS studies after they are performed, only half of the programs report utilization of middleware for their archival system. Compliance with documentation varied significantly between programs. CONCLUSIONS: Our survey results demonstrate that, although there is still room for improvement, POCUS programs have succeeded in many of the goals set forth by the 2015 AAP policy statement, such as establishing and growing an ultrasound curriculum and using various strategies to educate PEM fellows.

The 4.1B cytoskeletal protein regulates the domain organization and sheath thickness of myelinated axons.

Myelinated axons are organized into specialized domains critical to their function in saltatory conduction, i.e., nodes, paranodes, juxtaparanodes, and internodes. Here, we describe the distribution and role of the 4.1B protein in this organization. 4.1B is expressed by neurons, and at lower levels by Schwann cells, which also robustly express 4.1G. Immunofluorescence and immuno-EM demonstrates 4.1B is expressed subjacent to the axon membrane in all domains except the nodes. Mice deficient in 4.1B have preserved paranodes, based on marker staining and EM in contrast to the juxtaparanodes, which are substantially affected in both the PNS and CNS. The juxtaparanodal defect is evident in developing and adult nerves and is neuron-autonomous based on myelinating cocultures in which wt Schwann cells were grown with 4.1B-deficient neurons. Despite the juxtaparanodal defect, nerve conduction velocity is unaffected. Preservation of paranodal markers in 4.1B deficient mice is associated with, but not dependent on an increase of 4.1R at the axonal paranodes. Loss of 4.1B in the axon is also associated with reduced levels of the internodal proteins, Necl-1 and Necl-2, and of alpha-2 spectrin. Mutant nerves are modestly hypermyelinated and have increased numbers of Schmidt-Lanterman incisures, increased expression of 4.1G, and express a residual, truncated isoform of 4.1B. These results demonstrate that 4.1B is a key cytoskeletal scaffold for axonal adhesion molecules expressed in the juxtaparanodal and internodal domains that unexpectedly regulates myelin sheath thickness.

Nectin-like proteins mediate axon Schwann cell interactions along the internode and are essential for myelination.

Axon-glial interactions are critical for the induction of myelination and the domain organization of myelinated fibers. Although molecular complexes that mediate these interactions in the nodal region are known, their counterparts along the internode are poorly defined. We report that neurons and Schwann cells express distinct sets of nectin-like (Necl) proteins: axons highly express Necl-1 and -2, whereas Schwann cells express Necl-4 and lower amounts of Necl-2. These proteins are strikingly localized to the internode, where Necl-1 and -2 on the axon are directly apposed by Necl-4 on the Schwann cell; all three proteins are also enriched at Schmidt-Lanterman incisures. Binding experiments demonstrate that the Necl proteins preferentially mediate heterophilic rather than homophilic interactions. In particular, Necl-1 on axons binds specifically to Necl-4 on Schwann cells. Knockdown of Necl-4 by short hairpin RNA inhibits Schwann cell differentiation and subsequent myelination in cocultures. These results demonstrate a key role for Necl-4 in initiating peripheral nervous system myelination and implicate the Necl proteins as mediators of axo-glial interactions along the internode.

Comparison of Hands-On Versus Online Learning in Teaching Ultrasound Skills for Achilles Tendon Rupture: A Pilot Study.

Introduction In the emergency department, the diagnosis of an Achilles tendon rupture (ATR) is reportedly missed in greater than 20% of cases. A limited number of studies evaluate the use of cadaver models as a potential ultrasound teaching and training modality. We hypothesize that emergency medicine residents can effectively utilize point-of-care ultrasound (POCUS) on cadaver models and a focused teaching intervention to assess their ability to detect ATRs. Methods A prospective study of 23 EM residents was performed. All participants in the study were divided into two learner groups: (a) independent and (b) hands-on. The independent learner group received a 30-minute online didactic lecture demonstrating how to diagnose ATRs. The hands-on learner group received direct instruction on cadaver lower leg models with a ruptured and normal Achilles tendon (AT). Both groups then participated in identifying either normal or ruptured ATs on six cadaver lower leg models. Results The sensitivity and specificity were 89% and 82% in the independent learner group 96% and 100% in the hands-on learner group, respectively. The overall sensitivity and specificity were 91% and 88%, respectively. There was a trend toward successful identification with increased years of residency training. Conclusions In this study, lower leg and ankle cadaver models were found to be as effective as an independent learner model for potential POCUS teaching and training modality in both novice and more advanced trainees.

Paranodal interactions regulate expression of sodium channel subtypes and provide a diffusion barrier for the node of Ranvier.

The node of Ranvier is a distinct domain of myelinated axons that is highly enriched in sodium channels and is critical for impulse propagation. During development, the channel subtypes expressed at the node undergo a transition from Nav1.2 to Nav1.6. Specialized junctions that form between the paranodal glial membranes and axon flank the nodes and are candidates to regulate their maturation and delineate their boundaries. To investigate these roles, we characterized node development in mice deficient in contactin-associated protein (Caspr), an integral junctional component. Paranodes in these mice lack transverse bands, a hallmark of the mature junction, and exhibit progressive disruption of axon-paranodal loop interactions in the CNS. Caspr mutant mice display significant abnormalities at central nodes; components of the nodes progressively disperse along axons, and many nodes fail to mature properly, persistently expressing Nav1.2 rather than Nav1.6. In contrast, PNS nodes are only modestly longer and, although maturation is delayed, eventually all express Nav1.6. Potassium channels are aberrantly clustered in the paranodes; these clusters are lost over time in the CNS, whereas they persist in the PNS. These findings indicate that interactions of the paranodal loops with the axon promote the transition in sodium channel subtypes at CNS nodes and provide a lateral diffusion barrier that, even in the absence of transverse bands, maintains a high concentration of components at the node and the integrity of voltage-gated channel domains.

Pergolide restores sleep maintenance but impairs sleep EEG synchronization in patients with restless legs syndrome.

BACKGROUND: The treatment with the long-acting dopamine D1/D2 receptor agonist pergolide has been proven as very effective in lowering the frequency of periodic leg movements (PLM) in patients with restless legs syndrome (RLS). To further investigate the influence of this potent dopaminergic drug on the microstructure of rapid eye movement (REM) and non-REM sleep EEG we established a quantitative analysis of the EEG data. METHODS: The study group consisted of 15 patients with primary RLS (mean age 57.1+/-10.1 years) who were a subgroup of patients within a double-blind randomized crossover treatment study with pergolide versus placebo. The polysomnographic recordings were analyzed visually and submitted to a quantitative EEG analysis (fast Fourier transformation). RESULTS: The pergolide treatment induced a significant reduction of the spectral power in the delta range (0.78-3.9 Hz; P<0.05; t-test) during SWS, as well as a significant reduction of PLMs. In addition, we observed a decrease in the sigma EEG activity (12.1-14.8 Hz; P<0.03) during non-REM sleep and stage 2 sleep. The visual sleep scoring revealed a significant increase in stage 2 sleep (P<0.005), whereas wakefulness was markedly diminished (P<0.001). The REM sleep parameters including the EEG power spectrum remained unchanged. CONCLUSIONS: The treatment with pergolide markedly improved the sleep quality in RLS patients but did not restore SWS including the spectral power in the lower frequencies. Our results suggest that the dopamine agonist pergolide interferes with the subcortical mechanisms regulating the process of EEG synchronization during non-REM sleep.