Incidence of high grade gliomas presenting as radiographically non-enhancing lesions: experience in 111 surgically treated non-enhancing gliomas with tissue diagnosis.

PURPOSE: Although non-enhancing lesions suspicious for glioma are usually assumed to be low grade glioma (LGG), some high grade glioma (HGG) do not enhance, which may lead to a delay in biopsy and/or resection, diagnosis, and treatment initiation. Thus, there is a clear need for a large-sample study that quantifies the rate of malignant, non-enhancing gliomas. METHODS: We retrospectively reviewed our series of 561 consecutive surgically treated gliomas with tissue diagnosis, 111 of which were non-enhancing, to determine the prevalence of high-grade histology in radiographically presumed LGG. Relative expression of tumor markers were also reported for non-enhancing lesions to investigate genetic correlates. RESULTS: We identified 561 surgically treated gliomas with tissue diagnosis from August 2012 to July 2018 and found that 111 patients (19.8%) demonstrated non-enhancing lesions suspicious for glioma on preoperative MRI. Thirty-one (27.9%) of the non-enhancing lesions were classified as HGGs (WHO Grade III or IV). Non-enhancing lesions were four times more likely to be HGG in patients older than 60 years than patients younger than 35 years (41.2% vs. 11.4%, Pearson Chi2 p < 0.001). Binomial logistic regression showed a significant inverse effect of age on the presence of IDH mutation in non-enhancing HGGs (p = 0.007). CONCLUSION: A clinically significant proportion (27.9%) of non-enhancing lesions were found to be HGG on final pathologic diagnosis. Thus, in patients with good functional and health status, especially those older than 60 years, we recommend obtaining tissue diagnosis of all lesions suspected to be glioma, even those that are non-enhancing, to guide diagnosis as well as early initiation of chemotherapy and radiation therapy.

Social Media Presence Across U.S. Neurosurgical Residency Programs and Subspecialties.

OBJECTIVE: U.S. neurosurgery programs are increasingly using social media accounts. We performed a search and analysis of social media accounts across all U.S. neurosurgical training programs with an attempt at understanding the relative utilization by various subspecialties. METHODS: We compiled a list of all Accreditation Council for Graduate Medical Education-accredited U.S. neurosurgery programs and the faculty. Each faculty member was classified on the basis of their subspecialty. Next, the Twitter, Facebook, and Instagram profiles were extensively searched for the number of followers and posts. RESULTS: We analyzed 110 programs with 1829 clinical faculty. Programs with a larger number of faculty (P = 0.035; χ2 = 13.528) and residents (P = 0.003; χ2 = 11.865) were more likely to have a social media account. Likewise, faculty and resident numbers had a positive correlation to Twitter (P = 0.037 for faculty size; P = 0.008 for residents' size) and Instagram followers (P = 0.003 for faculty size; P < 0.001 for residents' size). We additionally found a significant association between subspecialty type and the presence of a Twitter and Instagram account (P = 0.001; P = 0.028) and the number of followers (P = 0.004; P = 0.013), especially the vascular and oncology subspecialties. CONCLUSIONS: Many U.S. neurosurgical programs have social media accounts with larger programs likely to have social media accounts. While there is a larger percentage of spine faculty within individual departments, vascular and oncology subspecialties are more likely to have a Twitter account. We suggest the need for increased engagement among spine faculty across social media platforms.

Targeting Microglial Polarization to Improve TBI Outcomes.

Traumatic Brain Injury (TBI) is still the worldwide leading cause of mortality and morbidity in young adults. Improved safety measures and advances in critical care have increased chances of surviving a TBI, however, numerous secondary mechanisms contribute to the injury in the weeks and months that follow TBI. The past 4 decades of research have addressed many of the metabolic impairments sufficient to mitigate mortality, however, an enduring secondary mechanism, i.e. neuroinflammation, has been intractable to current therapy. Neuroinflammation is particularly difficult to target with pharmacological agents due to lack of specificity, the blood brain barrier, and an incomplete understanding of the protective and pathologic influences of inflammation in TBI. Recent insights into TBI pathophysiology have established microglial activation as a hallmark of all types of TBI. The inflammatory response to injury is necessary and beneficial while the death of activated microglial is not. This review presents new insights on the therapeutic and maladaptive features of the immune response after TBI with an emphasis on microglial polarization, followed by a discussion of potential targets for pharmacologic and non-pharmacologic treatments. In aggregate, this review presents a rationale for guiding TBI inflammation towards neural repair and regeneration rather than secondary injury and degeneration, which we posit could improve outcomes and reduce lifelong disease burden in TBI survivors.