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Background: Recent work has characterized polysomnographic changes in Alzheimer's Dementia (AD) that correlate with disease severity and precede clinical diagnosis. However, relatively small sample sizes and a paucity of studies examining sleep microarchitecture have been limitations. In this study we examined sleep micro‐ and microarchitectural features in large cohorts of patients with AD and mild cognitive impairment (MCI). Method: Using a database of over 15,000 clinical PSGs with associated clinical metadata, 125 and 173 subjects were identified with mild AD and MCI, respectively. 260 age and sex matched subjects without neurological disease were identified as healthy controls (HC). Sleep staging results were based on AASM criteria, and micro‐architectural features were assessed using an algorithm trained to predict wake (1) or sleep (0) using spectral data from 3 seconds of EEG from a unique healthy adult cohort (Wake EEG Similarity Index, WESI). Result: Sleep fragmentation was apparent in both the MCI and AD cohorts (relative to healthy controls), with AD subjects demonstrating significantly more severe PSG disturbances. Healthy controls demonstrated 400 minutes of total sleep time, in contrast to 374 minutes for MCI subjects and 362 minutes for healthy controls. Healthy subjects demonstrated 33 minutes of wake after sleep onset (WASO), compared to 60 and 67 minutes for MCI and AD subjects, respectively. As has been previously reported in smaller cohorts, wakeful bouts and N1 durations were significantly prolonged for AD and (to a lesser extent) MCI subjects, while N2, N3, and REM durations were reduced (with a pronounced reduction in AD N3 percentage). Sleep microarchitectural features assessed using WESI demonstrated that AD and MCI subjects had markedly higher relative wakefulness in all sleep stages except for N3, which showed the same sleep depth as HC. Conclusion: We confirm increased sleep fragmentation and loss of deeper sleep stages, correlating to disease severity. Spectral features of all sleep stages EXCEPT N3 appear more wakeful in AD and MCI subjects ‐ suggesting microarousals or impaired sleep maintenance contribute to sleep pathology. While N3 duration was markedly reduced, depth of sleep was comparable between populations. PSG findings offer promise as early diagnostic and therapeutic targets. [ABSTRACT FROM AUTHOR]

Objective/Hypothesis: To evaluate clinical outcomes following failed endoscopic extraction of salivary calculi and to assess any relation between clinical outcome and calculi location, number, size, and mobility. If sialendoscopy fails to extract the calculus, subsequent spontaneous passage of the calculus out of the ductoglandular system or secondary effects of sialendoscopy could mitigate the clinical impact of a residual sialolithiasis. Study Design: Prospective observational study. Methods: Prospective comparative study of endoscopic procedures for sialolithiasis performed in the Manukau Surgery Center, in Auckland, New Zealand, from 2010 to 2020. The recurrent symptoms and the variables related to the need for additional surgical intervention for salivary calculi were analyzed. Results: Among the 465 sialendoscopy procedures, 154 (33.1%) were for obstructive sialolithiasis. Among these, there were 30 (19.4%) with unsuccessful stone extraction with re‐operation for these failures performed in 14 of the 27 failed submandibular cases (52%) and 2 of the 3 parotids (66.7%). Location of calculi was a significant factor in predicting the need of further surgery. Patients with perihilar stones were 5 times more likely to have a failed procedure (P =.001). If the stone was intraglandular, the likelihood increased to 8.5 times (P =.005). The likelihood for a revision procedure increased almost 11 times if the stone was intraglandular (P =.004). Calculi size, mobility, multiple calculi, and presence of concurrent stenosis did not correlate with need for further surgery. Conclusions: A significant proportion of "failed" sialendoscopy did not require further intervention. Stone location was a significant factor in predicting a failed procedure and the need for re‐intervention. Laryngoscope, 132:1029–1033, 2022 [ABSTRACT FROM AUTHOR]

Objective: To examine the Manukau Salivary Symptom Score (MSSS) questionnaire as a validated tool to assess obstructive sialadenitis-specific symptoms to both indicate disease severity and assess the outcome after sialendoscopic procedures. Study Design: A prospective observational study was performed from 2010 to 2019 comprising 164 patients undergoing sialendoscopy for nonneoplastic chronic obstructive salivary gland disease (COSGD). Setting: Department of Otolaryngology–Head and Neck Surgery at the Manukau Surgical Centre, Auckland, New Zealand, between June 2010 and September 2019. Methods: A prospective observational study was performed from 2010 to 2019 comprising 164 patients undergoing sialendoscopy for nonneoplastic COSGD. Patients completed the MSSS preoperatively and at postoperative follow-up. Statistical tests were used to compare pre- and postoperative answers. Cronbach's α was used to measure internal consistency. Finally, construct validity was determined by comparing the 5-question MSSS questionnaire to the preexisting 20-question Chronic Obstructive Sialadenitis Symptoms (COSS) questionnaire. Results: Postoperatively, patients had significant improvements in pain, eating, talking, swelling, and quality of life (P <.001). The MSSS questionnaire was found to have high internal consistency (α = 0.938). Questions in the MSSS had a very strong positive correlation with 3 COSS questions, a strong positive correlation with 8, a moderate positive correlation with 4, and a weak positive correlation with 1. Four COSS questions were not considered relevant and were not included in the MSSS questionnaire. Conclusion: The MSSS questionnaire is a simple, validated questionnaire that is useful for assessing the impact of sialendoscopy in patients with COSGD. [ABSTRACT FROM AUTHOR]

The breakdown of the ventricular zone with the presence of blood in cerebrospinal fluid has been shown to increase shunt catheter obstruction in the treatment of hydrocephalus, but the mechanisms by which this occurs are generally unknown. Using a custom‐built incubation chamber, we immunofluorescently assayed cell attachment and morphology on shunt catheters with and without blood after 14 days. Samples exposed to blood showed significantly increased cell attachment (average total cell count 392.0 ± 317.1 vs. control of 94.7 ± 44.5, p < 0.0001). Analysis of the glial fibrillary acidic protein expression showed similar trends (854.4 ± 450.7 vs. control of 174.3 ± 116.5, p < 0.0001). An in vitro model was developed to represent the exposure of astrocytes to blood following an increase in blood–brain barrier permeability. Exposure of astrocytes to blood increases the number of cells and their spread on the shunt. [ABSTRACT FROM AUTHOR]