Fatal Post COVID mRNA-Vaccine Associated Cerebral Ischemia.

Background: Venous thromboses have been linked to several COVID-19 vaccines, but there is limited information on the Moderna vaccine's effect on the risk of arterial thrombosis. Here we describe a case of post-Moderna COVID-19 vaccination arterial infarct with vaccine-associated diffuse cortical edema that was complicated by refractory intracranial hypertension. Case Summary: 24 hrs after receiving her first dose of the Moderna COVID-19 vaccine, a 30-year-old female developed severe headache. Three weeks later she was admitted with subacute headache and confusion. Imaging initially showed scattered cortical thrombosis with an elevated opening pressure on lumbar puncture. An external ventricular drain was placed, but she continued to have elevated intracranial pressure. Ultimately, she required a hemicraniectomy, but intractable cerebral edema resulted in her death. Pathology was consistent with thrombosis and associated inflammatory response. Conclusion: Though correlational, her medical team surmised that the mRNA vaccine may have contributed to this presentation. The side effects of COVID-19 infection and vaccination are still incompletely understood. Though complications are rare, clinicians should be aware of presentations like this one.

3D Bioprinting in Otolaryngology: A Review.

The evolution of tissue engineering and 3D bioprinting has allowed for increased opportunities to generate musculoskeletal tissue grafts that can enhance functional and aesthetic outcomes in otolaryngology-head and neck surgery. Despite literature reporting successes in the fabrication of cartilage and bone scaffolds for applications in the head and neck, the full potential of this technology has yet to be realized. Otolaryngology as a field has always been at the forefront of new advancements and technology and is well poised to spearhead clinical application of these engineered tissues. In this review, current 3D bioprinting methods are described and an overview of potential cell types, bioinks, and bioactive factors available for musculoskeletal engineering using this technology is presented. The otologic, nasal, tracheal, and craniofacial bone applications of 3D bioprinting with a focus on engineered graft implantation in animal models to highlight the status of functional outcomes in vivo; a necessary step to future clinical translation are reviewed. Continued multidisciplinary efforts between material chemistry, biological sciences, and otolaryngologists will play a key role in the translation of engineered, 3D bioprinted constructs for head and neck surgery.

Parent artery occlusion of a giant internal carotid artery pseudoaneurysm-related direct carotid cavernous fistula: A case report.

Traumatic internal carotid artery injuries can produce direct carotid-cavernous fistulas as well as giant internal carotid artery pseudoaneurysms. Clinical sequelae can include headaches, cranial nerves palsies, proptosis, chemosis and optic neuropathy with visual loss as the most dangerous complication. Herein, we present a case of one of the largest reported internal carotid artery pseudoaneurysms associated with a direct carotid cavernous fistula. We describe the techniques and pitfalls of treatment with parent vessel occlusion.

Cost Comparison for Open Surgery versus Middle Meningeal Artery Embolization in Patients with Chronic Subdural Hematomas: A Propensity Score-Matched Analysis.

BACKGROUND: Chronic subdural hematoma (cSDH) can be treated with conventional surgery or middle meningeal artery embolization (MMAE). The cost profiles of open surgery versus MMAE have never been studied. Therefore, we sought to compare the costs of surgical and MMAE treatment of cSDH. METHODS: Patients treated with open surgery (2006-2019) and MMAE (2018-2020) were identified from the institutional database. Propensity score matching analysis was used to assemble a balanced group of subjects. Detailed hospitalization costs in each group were collected and compared. RESULTS: A total of 341 conventionally treated and 52 MMAE cases were identified. After propensity score matching, 33 patients were included in each group, for a total of 66 patients for analysis. Direct procedural cost was significantly greater in the MMAE group compared with the open surgery group ($38,255 ± $11,859 vs. $11,206 ± $7888; P < 0.001). Medication cost also was greater in the MMAE group ($6888 ± $6525 vs. $4291 ± $3547; P = 0.048). No significant difference was found in costs for intensive care unit care, pharmacy, therapy, laboratory values, and the emergency department. Imaging costs and other miscellaneous costs (e.g., wound care, preoperative, and postanesthesia care unit) were greater in the open surgery group (P < 0.05). Total hospitalization cost was not significantly different between the 2 groups ($60,598 ± 61,315 vs. $71,569 ± $37,813 for open surgery and MMAE respectively, P = 0.385). No significant differences in number of follow ups or total costs for follow up were found (P > 0.05). CONCLUSIONS: Open surgery and MMAE offer an overall equivalent cost-profile for cSDH treatment when matching for potential cost confounders. Direct procedural costs are greater in MMAE; however, total hospitalization costs and follow up costs are not significantly different.

ADAM10 facilitates rapid neural stem cell cycling and proper positioning within the subventricular zone niche via JAMC/RAP1Gap signaling.

The mechanisms that regulate neural stem cell (NSC) lineage progression and maintain NSCs within different domains of the adult neural stem cell niche, the subventricular zone are not well defined. Quiescent NSCs are arranged at the apical ventricular wall, while mitotically activated NSCs are found in the basal, vascular region of the subventricular zone. Here, we found that ADAM10 (a disintegrin and metalloproteinase 10) is essential in NSC association with the ventricular wall, and via this adhesion to the apical domain, ADAM10 regulates the switch from quiescent and undifferentiated NSC to an actively proliferative and differentiating cell state. Processing of JAMC (junctional adhesion molecule C) by ADAM10 increases Rap1GAP activity. This molecular machinery promotes NSC transit from the apical to the basal compartment and subsequent lineage progression. Understanding the molecular mechanisms responsible for regulating the proper positioning of NSCs within the subventricular zone niche and lineage progression of NSCs could provide new targets for drug development to enhance the regenerative properties of neural tissue.

Laryngopharyngeal reflux: Comparing improvements in reflux symptom index with reflux finding score.

PURPOSE: The objective of this study was to determine the correlation of reported symptom improvement in laryngopharyngeal reflux (LPR) with physical findings on laryngoscopic examination following medical therapy. MATERIALS AND METHODS: This IRB-approved, retrospective, single-institution study included all patients who were diagnosed and medically treated for LPR from Jan. 1, 2015-October 21st, 2019. Only patients who received at least six weeks of treatment with a proton pump inhibitor and those with pre- and post-treatment Reflux Symptom Index; RSI (n = 91) and Reflux Finding Score; RFS (n = 33) were included in the study. RESULTS: A total of 91 patients were included in the analysis (61.54% female). There was a 19.99% improvement in total RSI (p = 0.0034) and a 25.20% improvement in total RFS (p = 0.0011) following at least six weeks of treatment (average = 253 ± 213 SD days). RSI symptoms were significantly decreased between pre- and post-treatment for hoarseness (p = 0.0005), clearing of the throat (p = 0.0066), excess throat mucus or postnasal drip (p = 0.0004), troublesome cough (p = 0.0231), and heartburn/chest pain (p = 0.0053). RFS demonstrated a statistically significant decrease in only subglottic edema (p < 0.0001) and ventricular obliteration (p = 0.0295). Pearson's correlation test did not demonstrate a relationship between RSI and RFS in the pre- and post-treatment analyses alone, but did demonstrate a statistically significant relationship when analyzed across all captured pre and post data (r = 0.265, p = 0.006). CONCLUSIONS: RSI and RFS are complimentary to one another when assessing for treatment response, but improvement in RSI does not correlate with that in RFS.

N-cadherin promotes recruitment and migration of neural progenitor cells from the SVZ neural stem cell niche into demyelinated lesions.

Discrete cellular microenvironments regulate stem cell pools and their development, as well as function in maintaining tissue homeostasis. Although the signaling elements modulating neural progenitor cells (NPCs) of the adult subventricular zone (SVZ) niche are fairly well understood, the pathways activated following injury and the resulting outcomes, are less clear. In the present study, we used mouse models of demyelination and proteomics analysis to identify molecular cues present in the adult SVZ niche during injury, and analyzed their role on NPCs in the context of promoting myelin repair. Proteomic analysis of SVZ tissue from mice with experimental demyelination identified several proteins that are known to play roles in NPC proliferation, adhesion, and migration. Among the proteins found to be upregulated were members of the N-cadherin signaling pathway. During the onset of demyelination in the subcortical white matter (SCWM), activation of epidermal growth factor receptor (EGFR) signaling in SVZ NPCs stimulates the interaction between N-cadherin and ADAM10. Upon cleavage and activation of N-cadherin signaling by ADAM10, NPCs undergo cytoskeletal rearrangement and polarization, leading to enhanced migration out of the SVZ into demyelinated lesions of the SCWM. Genetically disrupting either EGFR signaling or ADAM10 inhibits this pathway, preventing N-cadherin regulated NPC polarization and migration. Additionally, in vivo experiments using N-cadherin gain- and loss-of-function approaches demonstrated that N-cadherin enhances the recruitment of SVZ NPCs into demyelinated lesions. Our data revealed that EGFR-dependent N-cadherin signaling physically initiated by ADAM10 cleavage is the response of the SVZ niche to promote repair of the injured brain.