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Purpose of review This review illustrates the evolution and progress with standardization of fellowship education in neuroanesthesiology. It provides a structured discussion around the need for curricula and framework which individual training programs in neuroanesthesiology can use to meet defined educational standards thus meeting criteria for accreditation. Recent findings Neuroanesthesiology training has traditionally been heterogenous around the world but international efforts from the community of neuroanesthesiology have culminated in the development of an international council for perioperative training in neuroscience in anesthesiology(ICPNT). This serves not only as an accrediting body but also creates a platform through their neuroanesthesia program relations committee for collaboration and engagement between various training programs internationally, increasing the educational standards of the individual programs and collectively increasing the overall level of standards for neuroanesthesia training. Standardized curriculum and competency-based assessments and milestones would help with narrowing the focus to quality education in neuroanesthesiology. Summary Structured training around the three pillars of neuroanesthesiology with concomitant accreditation is expected to lead to higher education standards with better patient care. The SNACC created milestones for neuroanesthesiology training during residency and the ICPNT can now use this as a foundation for fellowship training. Having a council to accredit and standardize will likely become indispensable in creating a set path for training in neuroanesthesiology. Additionally, the flexibility built in due to the international nature would allow modified and variable pathways depending upon individual capabilities and interests. The path forward will include widespread adoption of standardization supporting the overarching goal of excellent patient outcomes around the world.

Background and Purpose— Identification of single-nucleotide polymorphisms (SNPs) associated with increased risk of new intracranial hemorrhage (ICH) after brain arteriovenous malformation (BAVM) diagnosis would facilitate risk stratification and identify potential targets for therapeutic intervention. Methods— Patients with BAVM were longitudinally followed. Primary outcome was new ICH after diagnosis; censoring events were last follow-up or any BAVM treatment. We genotyped 4 promoter SNPs in 2 inflammatory cytokine genes: interleukin-6 (IL-6–174G>C; IL-6–572G>C) and tumor necrosis factor-α (TNF-α–238G>A; TNF-α–308G>A). Association of genotype with risk of new ICH was screened using χ 2 ; SNPs associated with new ICH were further characterized using Cox proportional hazards. Results— We genotyped 280 patients (50% female; 59% white, mean±SD age at diagnosis 37±17 years; 40% presenting with ICH). TNF-α–238G>A was associated with increased risk of new ICH after diagnosis (χ 2 ; P =0.003). After adjusting for age, race/ethnicity, and clinical presentation, the risk of new ICH was increased for patients with TNF-α–238 AG genotype (hazard ratio, 4.01; P =0.015). No other SNP was found to be associated with new ICH. Conclusion— A TNF-α SNP was associated with increased risk of new ICH in the natural course of BAVMs. The role of inflammatory cytokines in the pathogenesis of BAVM hemorrhage merits further study.

Male Sprague-Dawley rats were exposed on 7 consecutive days for 8 h a night to 0.6 ppm ozone, 10.8 ppm NO2 or a mixture of the two gases. Cumulative labeling indices were measured in the epithelium of the terminal bronchioles and the adjacent centriacinar region. An excellent correlation in labeling indices between the two sites was found. It is concluded that the labeling index in the terminal bronchioles represents a sensitive measurement for ozone-induced lung injury.

Brain arteriovenous malformations (BAVM) have high matrix metalloproteinase-9 (MMP-9) expression, the source of which is unclear. We hypothesized MMP-9 production might be due to inflammation in BAVM. Compared to control brain tissues (n = 5), BAVM tissue (n = 139) had a higher expression (by ELISA) of myeloperoxidase (MPO) (193 +/- 189 vs. 6 +/- 3, ng/mg, P < .001), MMP-9 (28 +/- 32 vs. 0.7 +/- 0.6, ng/mg, P < .001), and IL-6 (102 +/- 218 vs. 0.1 +/- 0.1, pg/mg, P < .001), but not eNOS (114 +/- 87 vs. 65 +/- 9, pg/mg, P = .09). MMP-9 expression in BAVM highly correlated with myeloperoxidase (R2 = .76, P < .001), as well as with IL-6 (R2 = .32, P < .001). In contrast, MMP-9 in BAVM poorly correlated with the endothelial marker, eNOS (R2 = .03, P = .05), and CD31 (R2 = .004, P = .57). Compared to non-embolized patients (n = 46), patients with pre-operative embolization (n = 93) had higher levels of myeloperoxidase (236 +/- 205 vs. 106 +/- 108, ng/mg, P < .001) and MMP-9 (33 +/- 35 vs. 16 +/- 20, ng/mg, P < .001), however the correlation between MMP-9 and myeloperoxidase was equally strong for both groups (R2 = .69, n = 93, P < .001, for both). MMP-9 expression correlated with the lipocalin-MMP-9 complex, suggesting neutrophils as the MMP-9 source. MPO co-localized with majority of MMP-9 signal by immunohistochemistry. Our data suggest that inflammation is a prominent feature of BAVM lesional phenotype, and neutrophils appear to be a major source of MMP-9 in these lesions.

Background and Purpose— A better understanding of angiogenic factors and their effects on cerebral angiogenesis is necessary for the development of effective therapeutic strategies for ischemic brain injury. Vascular endothelial growth factor (VEGF) has been shown to induce angiogenesis in the adult mouse brain. However, the function of angiopoietin-2 (Ang-2) in cerebral angiogenesis has not been clarified. The goal of this study was to identify the combined effects of VEGF and Ang-2 on cerebral angiogenesis and the blood–brain barrier (BBB). Methods— Six groups of 6 adult male CD-1 mice underwent AdlacZ (viral vector control), AdVEGF, AdAng2, VEGF protein, VEGF protein plus AdAng2, or saline (negative control) injection. Microvessels were counted using lectin staining on tissue sections after 2 weeks of treatment. Matrix metalloproteinase-9 (MMP-9) activity was determined by zymography. The presence of zonula occludens-1 (ZO-1) protein was determined by Western blot and immunohistochemistry. Results— Mice treated with VEGF protein infusion plus AdAng-2 significantly increased microvessel counts relative to all other groups ( P P Conclusions— Our study demonstrates that the combination of VEGF and Ang-2 promotes more angiogenesis compared with VEGF alone. Furthermore, the combination of VEGF and Ang-2 may lead to BBB disruption because it increases MMP-9 activity and inhibits ZO-1 expression.