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Background Dolichoectasia is defined as elongation and dilatation of a blood vessel. In the intracranial circulation, the basilar artery is affected in 80% of cases. These are challenging lesions with an aggressive natural history, and treatment carries a relatively high rate of morbidity and mortality. We describe a case of multimodal treatment including endovascular, open microsurgical, and endoscopic endonasal approach (EEA) for management. Objective To describe the technical nuance of the addition of the EEA for management of posterior circulation dolichoectasia. Methods A 44-yr-old Hispanic woman with a 2-mo history of progressive headaches, gait disturbance, and lower cranial nerve dysfunction presented with acute neurologic decline. MRI demonstrated a dolichoectatic vertebrobasilar system with a giant 4.5-cm fusiform basilar aneurysm. Results She underwent concomitant endovascular bilateral vertebral artery sacrifice with suction decompression and trapping by clip ligation distal to the lesion. Postoperatively, she developed symptomatic pontine compression. She was then taken for a transclival EEA for intra-aneurysmal thrombectomy. Thereafter, she made a significant functional recovery. Conclusion The addition of endoscopic reconstruction to the treatment of a dolichoectatic basilar aneurysm is an operative nuance that can be employed in treating these highly morbid lesions. This case describing a multimodal treatment paradigm including EEA reconstruction can serve as an example for the future of treatment select cases of dolichoectasia of the vertebrobasilar complex.

BACKGROUND: Critical examination of the quality and validity of available allergic rhinitis (AR) literature is necessary to improve understanding and to appropriately translate this knowledge to clinical care of the AR patient. To evaluate the existing AR literature, international multidisciplinary experts with an interest in AR have produced the International Consensus statement on Allergy and Rhinology: Allergic Rhinitis (ICAR:AR). METHODS: Using previously described methodology, specific topics were developed relating to AR. Each topic was assigned a literature review, evidence-based review (EBR), or evidence-based review with recommendations (EBRR) format as dictated by available evidence and purpose within the ICAR:AR document. Following iterative reviews of each topic, the ICAR:AR document was synthesized and reviewed by all authors for consensus. RESULTS: The ICAR:AR document addresses over 100 individual topics related to AR, including diagnosis, pathophysiology, epidemiology, disease burden, risk factors for the development of AR, allergy testing modalities, treatment, and other conditions/comorbidities associated with AR. CONCLUSION: This critical review of the AR literature has identified several strengths; providers can be confident that treatment decisions are supported by rigorous studies. However, there are also substantial gaps in the AR literature. These knowledge gaps should be viewed as opportunities for improvement, as often the things that we teach and the medicine that we practice are not based on the best quality evidence. This document aims to highlight the strengths and weaknesses of the AR literature to identify areas for future AR research and improved understanding.

Background Environmental factors such as inhaled pollutants like cigarette smoke may play a significant role in diseases of the upper airway including chronic rhinosinusitis (CRS). Recent studies have shown that cigarette smoke causes impaired airway epithelial cell barrier function likely through environmental oxidative stress related pathways. The purpose of this study is to explore whether enhancing nuclear factor erythroid 2 [NF-E2]-related factor 2 [Nrf2], the body's master antioxidant system, can ameliorate cigarette smoke–induced sinonasal epithelial cell (SNEC) barrier dysfunction. Methods Human SNECs (HSNECs) were grown from control patients at the air-liquid interface (ALI). HSNECs were stimulated with cigarette smoke extract (CSE) with and without pharmacologic activation of Nrf2. HSNECs were then stained for the epithelial cell junctional proteins zonula occludens 1 (ZO-1) and junctional adhesion molecule A (JAM-A) using confocal microscopy. In addition, transepithelial electrical resistance (TER) was measured in cultures before and after stimulation with CSE. Results CSE stimulation caused a global disruption of the epithelial junctional proteins ZO-1 and JAM-A along with an associated decrease in TER levels. Enhancing Nrf2 levels prior to stimulation with CSE was associated with increased localization of ZO-1 and JAM-A levels at the cell surface and statistically significant increases in TER levels. Conclusion This is the first study to demonstrate that cigarette smoke induced SNEC barrier dysfunction is reversible by Nrf2 activation. The Nrf2 antioxidant pathway may represent a potential therapeutic target for cigarette smoke–associated sinonasal inflammation.

Background Chronic rhinosinusitis is an inflammatory disorder in which the role of bacteria remains uncertain. While sinus outflow obstruction is often an initiating event, mucosal inflammation and dysbiosis may persist or develop in sinuses with widely patent surgical openings. Understanding of the relationship between dysbiosis and chronic sinus inflammation is obfuscated by inter-individual microbiota variability and likely intra-individual temporal variation that has yet to be defined. In this study, long-term microbiota stability is investigated within surgically-opened maxillary sinuses of individuals with and without sinus inflammatory disease. Methods Maxillary sinus swabs were performed in 35 subjects with longstanding maxillary antrostomies. Subjects with and without active chronic maxillary sinusitis were included. Repeat swabs were obtained from the same sinuses after a prolonged interval (mean 719 ± 383 days). Patients were categorized based on the inflammatory status of the sinus mucosa at times of sample collection, as assessed by nasal endoscopy. Total DNA from swab eluents was extracted, and the microbiota characterized using 16S rRNA gene sequencing followed by taxonomic classification. Prevalence and abundance of genera were determined by analysis of 16S rRNA gene sequences. Taxa were identified that were stably present between two time points in individual subjects. Results The overall proportion of stable taxa across time points was 24.5 ± 10.6%. This stability index was consistent across patient groups and not correlated with clinical parameters. Highly prevalent taxa, including Staphylococcus, Corynebacterium, Propionibacterium, and Pseudomonas, were often stably present, but varied in relative abundance. Janthinobacterium, Enterobacter, Lactobacillus, and Acinetobacter were prevalent and moderately abundant taxa in healthy sinuses, but not in inflamed sinuses. Moraxella and Haemophilus were present at low prevalence and proportional abundance in chronically or intermittently inflamed sinuses, but not in healthy sinuses. Conclusions A relatively small component of the post-antrostomy maxillary sinus microbiota exhibits long-term stability in individual subjects. Stable bacteria include a limited number of highly prevalent and a larger number of lower prevalence taxa, which vary widely in proportional abundance. The concept of individual-specific core sinus microbiota, durable over time and medical therapy, but fluctuating in proportional abundance, has implications for understanding the role of bacteria in CRS pathogenesis. Electronic supplementary material The online version of this article (10.1186/s12879-018-3272-9) contains supplementary material, which is available to authorized users.

Environmental factors such as inhaled pollutants like cigarette smoke may play a significant role in diseases of the upper airway including chronic rhinosinusitis (CRS). Recent studies have shown that cigarette smoke causes impaired airway epithelial cell barrier function likely through environmental oxidative stress related pathways. The purpose of this study is to explore whether enhancing nuclear factor erythroid 2 [NF-E2]-related factor 2 [Nrf2], the body's master antioxidant system, can ameliorate cigarette smoke-induced sinonasal epithelial cell (SNEC) barrier dysfunction.Human SNECs (HSNECs) were grown from control patients at the air-liquid interface (ALI). HSNECs were stimulated with cigarette smoke extract (CSE) with and without pharmacologic activation of Nrf2. HSNECs were then stained for the epithelial cell junctional proteins zonula occludens 1 (ZO-1) and junctional adhesion molecule A (JAM-A) using confocal microscopy. In addition, transepithelial electrical resistance (TER) was measured in cultures before and after stimulation with CSE.CSE stimulation caused a global disruption of the epithelial junctional proteins ZO-1 and JAM-A along with an associated decrease in TER levels. Enhancing Nrf2 levels prior to stimulation with CSE was associated with increased localization of ZO-1 and JAM-A levels at the cell surface and statistically significant increases in TER levels.This is the first study to demonstrate that cigarette smoke induced SNEC barrier dysfunction is reversible by Nrf2 activation. The Nrf2 antioxidant pathway may represent a potential therapeutic target for cigarette smoke-associated sinonasal inflammation.

BACKGROUND AND PURPOSE: It remains unclear whether SSCD syndrome, characterized by onset of vestibular symptoms in the setting of loud noises, is a congenital or acquired condition. The purpose of this investigation was to assess the prevalence of SSCD on imaging among multiple age groups to determine whether this condition is more likely to be congenital or acquired. MATERIALS AND METHODS: Following approval of the institutional review board, 306 consecutive temporal bone CT examinations performed between July 2005 and March 2007 were retrospectively reviewed. Of these, 2 patients were eliminated due to destructive processes in the inner ear. Patients ranged in age from 7 months to 89 years. Images were independently evaluated by 2 neuroradiologists, and the superior semicircular canal was characterized as normal, thin, or frankly dehiscent in each temporal bone. Any discrepancies were resolved by consensus. The patient list was then subcategorized into 5 age groups, and the prevalence of SSCD was calculated for each group. RESULTS: Twenty-four patients were identified with SSCD, of which 6 demonstrated dehiscence bilaterally. One hundred thirty-seven subjects were identified with thinning, of which 50 demonstrated thinning bilaterally. Each successively older age category experienced a 93% increase (95% CI, 30%–187%) in the prevalence of SSCD ( P = .001) and a 9% increase (95% CI, −5%–25%) in the prevalence of thinning ( P = .21). Neither crude nor age-adjusted models demonstrated a significant association between thinning and contralateral dehiscence or vice versa. CONCLUSIONS: The increased radiologic prevalence of SSCD among older age groups suggests that this is more commonly an acquired rather than congenital condition.