Healthcare provider adherence in prescribing antiplatelet therapy for patients with stroke symptoms within 48 hours upon arrival to hospital

Background: According to the Center of Disease Control, stroke accounted for 1 in every 6 cardiovascular-related deaths in the U.S in 2018. This disease is the leading cause of long-term disability and limits mobility in more than half of people who survive stroke older than 65 (Centers for Disease Control and Disease Prevention [CDC], 2020). Due to the difficulty of a full recovery for cerebral vascular accidents, stroke prevention is the top priority in the approach to reduce the mortality and morbidity of the disease. Antiplatelet platelet therapy has been proven to reduce the incidence and complications of an ischemic stroke. Context: A South Florida Hospital is less than excellent in initiating antiplatelet therapy for patients suspected of ischemic stroke. An educational intervention should be provided to healthcare providers to increase compliance to antiplatelet therapy for stroke patients. Purpose: The objective of the quality improvement project is to improve healthcare providers’ knowledge and compliance towards initiating antiplatelet therapy for patients admitted to the hospital with stroke symptoms. Methods: A sample of 13 healthcare providers was provided with a link from the medical director of an acute care hospital in South Florida via email. The link included the pre-test survey, education intervention PowerPoint, and post-test survey. The pre-and post- test measure of knowledge and practice habits related to treating patients with ischemic stroke. Results: There was an 8.9% improvement in scores on the knowledge-based questions in the post-test. Regarding the questions based on practice habits, post-test scores showed a 2% increase when compared to similar pre-test questions. Conclusions: Therefore, it was proven that the education intervention could improve the knowledge of healthcare providers related to increasing compliance for prescribing antiplatelet therapy for patients with stroke symptoms within 48 hours upon arrival to the hospital

Responsible Genes for Neuronal Migration in the Chromosome 17p13.3: Beyond Pafah1b1(Lis1), Crk and Ywhae(14-3-3ε)

The 17p13.3 chromosome region is often deleted or duplicated in humans, resulting in severe neurodevelopmental disorders such as Miller–Dieker syndrome (MDS) and 17p13.3 duplication syndrome. Lissencephaly can also be caused by gene mutations or deletions of a small piece of the 17p13.3 region, including a single gene or a few genes. PAFAH1B1 gene, coding for LIS1 protein, is a responsible gene for lissencephaly and MDS and regulates neuronal migration by controlling microtubules (MTs) and cargo transport along MTs via dynein. CRK is a downstream regulator of the reelin signaling pathways and regulates neuronal migration. YWHAE, coding for 14-3-3ε, is also responsible for MDS and regulates neuronal migration by binding to LIS1-interacting protein, NDEL1. Although these three proteins are known to be responsible for neuronal migration defects in MDS, there are 23 other genes in the MDS critical region on chromosome 17p13.3, and little is known about their functions in neurodevelopment, especially in neuronal migration. This review will summarize the recent progress on the functions of LIS1, CRK, and 14-3-3ε and describe the recent findings of other molecules in the MDS critical regions in neuronal migration

Correction: Liu et al. Responsible Genes for Neuronal Migration in the Chromosome 17p13.3: Beyond <i>Pafah1b1(Lis1)</i>, <i>Crk</i> and <i>Ywhae(14-3-3ε)</i>. <i>Brain Sci.</i> 2022, <i>12</i>, 56

The authors wish to correct the following error in this paper [...

Marsupialization and distal obliteration of a lumbosacral dural ectasia in a nonsyndromic, adult patient

Dural ectasia is frequently associated with connective tissue disorders or inflammatory conditions. Presentation in a patient without known risk factors is rare. Moreover, the literature regarding the treatment options for symptomatic dural ectasia is controversial, variable, and limited. A 62-year-old female presents with intractable, postural headaches for years. A lumbar puncture revealed opening pressure 3 cm of water. A computed tomography myelogram of the spine demonstrated erosion of her sacrum due to a large lumbosacral dural ectasia. An initial surgery was attempted to reduce the size of the expansile dura, and reconstruct the dorsal sacrum with a titanium plate (Depuy Synthes, Westchester, PA, USA) to prevent recurrence of thecal sac dilatation. Her symptoms initially improved, but shortly thereafter recurred. A second surgery was then undertaken to obliterate the thecal sac distal to the S2 nerve roots. This could not be accomplished through simple ligation of the thecal sac circumferentially as the ventral dura was noted to be incompetent and attempts to develop an extradural tissue plane were unsuccessful. Consequently, an abundance of fibrin glue was injected into the thecal sac distal to S2, and the dural ectasia was marsupialized rostrally, effectively obliterating the distal thecal sac while further reducing the size of the expansile dura. This approach significantly improved her symptoms at 5 months follow-up. Treatment of dural ectasia is not well-defined and has been variable based on the underlying manifestations. We report a rare patient without risk factors who presented with significant lumbosacral dural ectasia. Moreover, we present a novel method to treat postural headaches secondary to dural ectasia, where the thecal sac is obliterated distal to the S2 nerve roots using an abundance of fibrin glue followed by marsupialization of the thecal sac rostally. This method may offer an effective therapy option as it serves to limit the expansile dura, reducing the cerebrospinal fluid sump and the potential for intracranial hypotension