Faculty Bibliography

BACKGROUND:Arthroscopic shoulder capsulolabral repair using glenoid-based suture anchor fixation provides consistently favorable outcomes for patients with anterior glenohumeral instability. To optimize outcomes, inferior anchor position, especially at the 6-o'clock position, has been emphasized. Proponents of both the beach-chair (BC) and lateral decubitus (LD) positions advocate that this anchor location can be consistently achieved in both positions. HYPOTHESIS:Patient positioning would be associated with the surgeon-reported labral tear length, total number of anchors used, number of anchors in the inferior glenoid, and placement of an anchor at the 6-o'clock position. STUDY DESIGN:Cross-sectional study; Level of evidence, 3. METHODS:test [normal distributions], Wilcoxon rank sum test [nonnormal distributions], and chi-square test [categorical]) were assessed. RESULTS:< .001). CONCLUSION:Surgeons utilizing the LD position for arthroscopic capsulolabral repair in patients with anterior shoulder instability more frequently placed anchors in the inferior glenoid and at the 6-o'clock position. Additionally, surgeon-reported labral tear length was longer when utilizing the LD position. These results suggest that patient positioning may influence the total number of anchors used, the number of anchors used in the inferior glenoid, and the frequency of anchor placement at the 6 o'clock position during arthroscopic capsulolabral repair for anterior shoulder instability. How these findings affect clinical outcomes warrants further study. REGISTRATION:NCT02075775 (ClinicalTrials.gov identifier).

PURPOSE:To identify factors predictive of a large labral tear at the time of shoulder instability surgery. METHODS:As part of the Multicenter Orthopaedic Outcomes Network (MOON) Shoulder Instability cohort, patients undergoing open or arthroscopic shoulder instability surgery for a labral tear were evaluated. Patients with >270° tears were defined as having large labral tears. To build a predictive logistic regression model for large tears, the Feasible Solutions Algorithm was used to add significant interaction effects. RESULTS:After applying exclusion criteria, 1235 patients were available for analysis. There were 222 females (18.0%) and 1013 males (82.0%) in the cohort, with an average age of 24.7 years (range 12 to 66). The prevalence of large tears was 4.6% (n = 57), with the average tear size being 141.9°. Males accounted for significantly more of the large tears seen in the cohort (94.7%, P = .01). Racquet sports (P = .01), swimming (P = .02), softball (P = .05), skiing (P = .04), and golf (P = .04) were all associated with large labral tears, as was a higher Western Ontario Shoulder Instability Index (WOSI; P = .01). Age, race, history of dislocation, and injury during sport were not associated with having a larger tear. Using our predictive logistic regression model for large tears, patients with a larger body mass index (BMI) who played contact sports were also more likely to have large tears (P = .007). CONCLUSIONS:Multiple factors were identified as being associated with large labral tears at the time of surgery, including male sex, preoperative WOSI score, and participation in certain sports including racquet sports, softball, skiing, swimming, and golf. LEVEL OF EVIDENCE:I, prognostic study.

Both primary and metastatic brain tumors carry poor prognoses despite modern advances in medical therapy, radiation therapy, and surgical techniques. Gliomas, including glioblastoma (GBM), are particularly difficult to treat, and high-grade gliomas have poor outcomes. Treatment of brain tumors involves a unique set of scientific and clinical challenges, which are often not present in the treatment of systemic malignancies. With respect to scientific challenges, the anatomy and physiology of brain tumors (including the blood-brain barrier, blood-tumor barrier, and blood-cerebrospinal fluid barrier) prevent adequate drug delivery into the central nervous system. The unique nature of the immune system in the central nervous system as well as the immunosuppressive microenvironment of tumors such as GBM also create therapeutic roadblocks in the treatment of brain tumors. Tumor heterogeneity, particularly in GBM, has classically been believed to contribute to multitherapy resistance; however, recent data suggest that this may not be the case. Clinical challenges include neurologic and medical comorbidities of patients with brain tumor, as well as potential toxicity of tumor-directed treatment. Clinical trials investigating new treatment paradigms are needed, but several roadblocks exist to good and promising clinical trial availability.

Although outcomes for many brain tumors, especially glioblastomas, remain poor, there have been significant advances in clinical and scientific understanding of neuro-oncologic disease. Tumor molecular profiling has become a critical component of clinical practice, allowing more accurate pathologic diagnosis and enhanced clarity of the pathogenesis of both primary and metastatic brain tumors. The development of cerebral organoids carries exciting potential to provide representative models of tumor growth and potential drug efficacy, while new radiology techniques continue to improve clinical decision making. New adaptive trial platforms have been developed to rapidly test therapies and biomarkers with good scientific rationale. Lastly, growth and development of neuro-oncology clinical care teams aim to further improve patients' outcomes and symptoms, especially at the end of life.

Neuro-oncology is a branch of medicine focused on the diagnosis and treatment of primary and secondary tumors of the nervous system as well as the neurologic complications of cancer and cancer treatments. In practice, neuro-oncologists require an intimate knowledge of the neurologic presentation and management of central nervous system tumors, including gliomas, meningiomas, primary central nervous system lymphoma, metastases to the nervous system, and others. The mainstays of treatment for most nervous system tumors include surgical intervention, radiation therapy, and medical treatment with chemotherapy, immunotherapy, and/or targeted therapy. Interdisciplinary collaboration is thus critical to neuro-oncology. The prognosis for many central nervous system tumors, including gliomas and brain metastases, is often poor despite the advent of novel medical therapies. Efforts to develop more effective therapies are ongoing, and patient enrollment in clinical trials assessing the efficacy of new treatments is crucial to improve outcomes.

Background and aims: Routine examinations for patients with stroke include clinical assessment using the National Institute of Health Stroke Scale (NIHSS). Although this score accurately predicts the outcome of stroke, the NIHSS is weighted for anterior circulation. No reliable clinical assessment tool has been established for predicting the functional outcome of posterior circulation ischemic stroke. We aimed to develop a stroke scale based on clinical assessment that can increase the yield of detection of posterior circulation ischemic strokes in acute settings, the Langone Augmented Posterior-fossa Stroke Scale (LAPSS).
Method(s): A retrospective, dual campus, single center record review of patients that have been diagnosed with posterior fossa circulation strokes between 12/2018-11 /2019 will be conducted. We will catalog the presenting symptoms, calculate their prevalence, and use this information to adjust the current proposed LAPSS. The validity of the LAPSS will then be tested by retrospectively applying it to all patients that presented with symptoms of posterior fossa ischemic strokes.
Result(s): We project 120 patients will fit the inclusion criteria. The sensitivity, specificity, positive predictive value, and negative predictive value of LAPSS will be calculated. Inter-rater reliability will be assessed using ANOVA to define an intraclass correlation coefficient. Primary clinical outcome in patients with suspected posterior fossa stroke will be independent functional outcome (mRS 2).
Conclusion(s): The NIHSS has been shown to detect <60% of posterior circulation strokes in previous studies. We anticipate that the LAPSS will increase the sensitivity of the NIHSS to increase the overall yield of detection of posterior circulation strokes.
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Background and aims: Intracranial arterial calcification (IAC) has been identified as an independent risk factor for ischemic stroke. The predictive value of calcification severity for the underlying pathophysiological mechanism of an ischemic stroke remains undetermined. We aimed to assess the degree of intracranial artery calcification in patients with ischemic stroke and evaluate its correlation with intracranial artery atherosclerotic disease as the underlying mechanism.
Method(s): Two hundred and eleven patients with strokes attributed to large vessel atherosclerotic disease from the NYU Ischemic Stroke Database, determined by two independent vascular neurologists, were enrolled. Patients with tandem lesions or competing pathophysiologic mechanisms were excluded. Head CT scans for each patient were reviewed. The degree of calcification of each vertebral and basilar artery was determined by two physicians using the Woodcock Score (interrater reliability score of kappa = 0.88).
Result(s): The highest prevalence of calcification was seen in the left vertebral artery (47%), and less commonly in the basilar artery (15%). There was a trend towards higher prevalence of moderate-severe IAC in patients with stroke due to intracranial atherosclerosis than patients with stroke due to extracranial atherosclerosis (40% vs. 28%, P = 0.073). The most common risk factors were hypertension (42 vs. 26%, p = 0.890), dyslipidemia (25 vs. 19%, p = 0.496), and type 2 diabetes (21 vs. 13%, p = 0.415), in patients with stroke due to intracranial atherosclerosis vs extracranial atherosclerosis, respectively.
Conclusion(s): There may be a positive correlation between the severity of vertebrobasilar atherosclerotic disease as determined by the Woodcock score and the likelihood that the underlying pathophysiological mechanism of an ischemic stroke is intracranial atherosclerotic disease.
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Background and Aims: Knowledge about assumed causes and subsequent treatment in patients with atrial fibrillation (AF) and ischemic stroke despite anticoagulant therapy is limited.
Method(s): Retrospective analysis of patients with known AF and acute ischemic stroke despite therapy with vitamin-K-antagonists (VKA) or direct oral anticoagulants (DOAC). We determined probable stroke cause (s) as either (a)competing etiology other than AF (e.g. large artery atherosclerosis), (b)medication error (subtherapeutic DOAClevel or off-label DOAC-dosing/INR<2.0 or reported non-adherence) or (c)cardoembolic stroke despite anticoagulation (absence of medication error and competing etiology) and subsequent prevention therapies. The composite of recurrent ischemic stroke, intracranial hemorrhage, or allcause death was assessed at 3 months.
Result(s): We analyzed 2, 949 patients from 11 centers (age 81years, IQR [76-86], 48%Female, NIHSS 6, IQR[2-14], 57% DOAC, 913 with DOAClevels, median CHA2DS2-VASc score 4, IQR[4, 6]). Of those, 24% had competing etiology (DOAC vs VKA: 28% vs 20%, aOR1.3, 95%CI 0.96-1.7), 32% medication error (23% vs 43%, aOR0.5, 95%CI 0.4-0.6) and 44% cardoembolic stroke despite anticoagulation (49% vs 37%, aOR1.6, 95%CI 1.2-2.1). After index stroke, anticoagulant drug was changed in 45.8% of patients (1317/2877), antiplatelets were added in 7.1% (203/ 2873), 3.4% (94/2776) received carotid revascularization therapies and 1%(17/1764) underwent left atrial appendage occlusion. Eight centers collected 3-month outcome data (2, 084 patients). In those, stroke recurred in 4.6% (84/1844; completeness 88.5%). The composite outcome occurred in 27% (516/1908, completeness 91.6%), and no specific prevention strategy reduced its odds.
Conclusion(s): Stroke despite anticoagulation comprises heterogeneous causes with 1/3 of strokes potentially preventable and 1/4 attributable to competing etiologies. Recurrence rate is high and the optimal secondary prevention strategy needs to be determined. (Table Presented)