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While both NS and NS+budesonide treatments improve QOL for post-FESS patients, neither intervention significantly increases QOL as compared to the other. Olfaction was not significantly improved in either treatment group.

OBJECTIVE To examine the relationship between Cerebrospinal Fluid (CSF) Rhinorrhea and Obstructive Sleep Apnea (OSA). STUDY DESIGN Retrospective chart-review of patients who underwent surgical repair of encephaloceles and/or CSF rhinorrhea at a tertiary medical center over a 12 year period. METHODS Pertinent demographic, clinical and surgical data including age, sex, medical and surgical history was obtained. Patients were classified by etiology of CSF leak into a spontaneous leak group and a non-spontaneous leak group, which included patients with documented trauma, malignancy, or known iatrogenic injury. RESULTS We retrospectively identified126 patients who underwent repair of encephalocele or CSF rhinorrhea. Of these, 70 (55.5%) were found to have a spontaneous etiology, while 56 (44.4%) had a non-spontaneous cause. Patients with spontaneous CSF rhinorrhea were more likely than their non-spontaneous counterparts to have a diagnosis of obstructive sleep apnea (OSA, 30.0% versus 14.3%, p=0.0294) and radiographic evidence of an empty sella on MRI (55.4% vs. 24.3%, p=0.0027). Overall, patients in the spontaneous CSF rhinorrhea group were more likely to be female compared to the non-spontaneous group (84.3% versus 41.1% female, P=0.0001). CONCLUSIONS Our study shows that patients with spontaneous CSF rhinorrhea are significantly more likely to have a diagnosis of OSA compared to those with non-spontaneous causes of CSF leaks, or to the general population (incidence of 1-5% in various population studies). Given the known association between OSA and intracranial hypertension (ICH), it may be prudent to screen all patients with spontaneous CSF rhinorrhea for symptoms of OSA as well as for ICH, and vice versa.

Overall 2- and 5-year survival rates are comparable and sometimes greater than those from open craniofacial resection. Survival rates significantly differ by cancer grade but not stage. Journals and investigators should be encouraged to publish retrospective and prospective case series with staged survival updates based on established guidelines.

The posterior skull base and the nasopharynx have historically represented technically difficult regions to approach surgically given their central anatomical locations. Through continued improvements in endoscopic instrumentation and technology, the expanded endonasal approach (EEA) has introduced a new array of surgical options in the management of pathology involving these anatomically complex areas. Similarly, the transoral robotic surgical (TORS) approach was introduced as a minimally invasive surgical option to approach tongue base, nasopharyngeal, parapharyngeal, and laryngeal lesions. Although both the EEA and the TORS approach have been extensively described as viable surgical options in managing nasopharyngeal and centrally located head and neck pathology, both endonasal and transoral techniques have inherent limitations. Given these limitations, several institutions have published feasibility studies with the combined EEA and TORS approaches for a variety of skull base and nasopharyngeal pathologies. In this article, the authors present their clinical experience with the combined endonasal and transoral approach through a case series presentation, and discuss advantages and limitations of this approach for surgical management of the middle and posterior skull base and nasopharynx. In addition, a presentation is included of a unique, simultaneous endonasal and transoral dissection of the nasopharynx through an innovative intraoperative setup.

Objective: To compare normal saline (NS) vs. NS+budesonide irrigations in post- functional endoscopic sinus surgery (FESS) patients with chronic rhinosinusitis with polyposis (CRSwNP). Currently, no evidence exists for NS+budesonide irrigation over NS irrigation alone. Study design: Prospective, single-blind, randomized controlled trial. Methods: Subjects were prospectively enrolled to NS or NS+budesonide arms. Patients were evaluated at pre-operative and three post-operative visits (POV): POV1 (1-2 weeks post-op), POV2 (3-8 weeks post-op), and POV3 (3-6 months post-op). Patients were evaluated by three quality of life (QOL) questionnaires (SNOT-22, RSOM-31, and RSDI) and two olfaction scores (UPSIT and the PEA test). Results: Fifty patients were randomized, with 25 patients in the NS arm and 25 patients in the NS+budesonide arm. Two patients had unexpected pathology and were excluded from the study. By POV2 and POV3, patients experienced a significant improvement in all three QOL surveys, although the degree of improvement between arms was not significant up through POV3. Neither arm experienced significant olfactory improvement up through POV3. Conclusions: While both NS and NS+budesonide treatments improve QOL for post-FESS patients, neither intervention significantly increases QOL as compared to the other. Olfaction was not significantly improved in either treatment group.

Objective: There is significant evidence for a central role of inflammation in the development of Alzheimer disease (AD). Epidemiological studies indicate that chronic use of nonsteroidal anti‐inflammatory drugs (NSAIDs) reduces the risk of developing AD in healthy aging populations. As NSAIDs inhibit the enzymatic activity of the inflammatory cyclooxygenases COX‐1 and COX‐2, these findings suggest that downstream prostaglandin signaling pathways function in the preclinical development of AD. Here, we investigate the function of prostaglandin E2 (PGE2) signaling through its EP3 receptor in the neuroinflammatory response to Aβ peptide. Methods: The function of PGE2 signaling through its EP3 receptor was examined in vivo in a model of subacute neuroinflammation induced by administration of Aβ42 peptides. Our findings were then confirmed in young adult APPSwe‐PS1ΔE9 transgenic mice. Results: Deletion of the PGE2 EP3 receptor in a model of Aβ42 peptide‐induced neuroinflammation reduced proinflammatory gene expression, cytokine production, and oxidative stress. In the APPSwe‐PS1ΔE9 model of familial AD, deletion of the EP3 receptor blocked induction of proinflammatory gene and protein expression and lipid peroxidation. In addition, levels of Aβ peptides were significantly decreased, as were β‐secretase and β C‐terminal fragment levels, suggesting that generation of Aβ peptides may be increased as a result of proinflammatory EP3 signaling. Finally, deletion of EP3 receptor significantly reversed the decline in presynaptic proteins seen in APPSwe‐PS1ΔE9 mice. Interpretation: Our findings identify the PGE2 EP3 receptor as a novel proinflammatory, proamyloidogenic, and synaptotoxic signaling pathway, and suggest a role for COX‐PGE2‐EP3 signaling in the development of AD. ANN NEUROL 2012;72:788–798

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