Blunt cerebrovascular injury (BCVI) is a non-penetrating injury to the carotid and/or vertebral artery that may cause stroke in trauma patients. Historically BCVI has been considered rare but more recent publications indicate an overall incidence of 1–2% in the in-hospital trauma population and as high as 9% in patients with severe head injury. The indications for screening, treatment and follow-up of these patients have been controversial for years with few clear recommendations. In an attempt to provide a clinically oriented guideline for the handling of BCVI patients a working committee was created. The current guideline is the end result of this committees work. It is based on a systematic literature search and critical review of all available publications in addition to a standardized consensus process. We recommend using the expanded Denver screening criteria and CT angiography (CTA) for the detection of BCVI. Early antithrombotic treatment should be commenced as soon as considered safe and continued for at least 3 months. A CTA at 7 days to confirm or discard the diagnosis as well as a final imaging control at 3 months should be performed.Electronic supplementary materialThe online version of this article (10.1186/s13049-018-0559-1) contains supplementary material, which is available to authorized users.

OBJECTIVE Vestibular schwannoma (VS) is a benign tumor with associated morbidities and reduced quality of life. Except for mutations in NF2, the genetic landscape of VS remains to be elucidated. Little is known about the effect of Gamma Knife radiosurgery (GKRS) on the VS genome. The aim of this study was to characterize mutations occurring in this tumor to identify new genes and signaling pathways important for the development of VS. In addition, the authors sought to evaluate whether GKRS resulted in an increase in the number of mutations. METHODS Forty-six sporadic VSs, including 8 GKRS-treated tumors and corresponding blood samples, were subjected to whole-exome sequencing and tumor-specific DNA variants were called. Pathway analysis was performed using the Ingenuity Pathway Analysis software. In addition, multiplex ligation-dependent probe amplification was performed to characterize copy number variations in the NF2 gene, and microsatellite instability testing was done to investigate for DNA replication error. RESULTS With the exception of a single sample with an aggressive phenotype that harbored a large number of mutations, most samples showed a relatively low number of mutations. A median of 14 tumor-specific mutations in each sample were identified. The GKRS-treated tumors harbored no more mutations than the rest of the group. A clustering of mutations in the cancer-related axonal guidance pathway was identified (25 patients), as well as mutations in the CDC27 (5 patients) and USP8 (3 patients) genes. Thirty-five tumors harbored mutations in NF2 and 16 tumors had 2 mutational hits. The samples without detectable NF2 mutations harbored mutations in genes that could be linked to NF2 or to NF2-related functions. None of the tumors showed microsatellite instability. CONCLUSIONS The genetic landscape of VS seems to be quite heterogeneous; however, most samples had mutations in NF2 or in genes that could be linked to NF2. The results of this study do not link GKRS to an increased number of mutations.

This study shows that the anatomical distribution of aneurysms is different in SAH patients compared with patients with unruptured aneurysms. Haemodynamic features of the vessel of origin may explain the differences we have found. Furthermore, this study suggests that it is of particular importance to treat patients with incidentally found ACA aneurysms.

Oligodendroglioma poses a biological conundrum for malignant adult human gliomas: it is a tumor type that is universally incurable for patients, and yet, only a few of the human tumors have been established as cell populations in vitro or as intracranial xenografts in vivo. Their survival, thus, may emerge only within a specific environmental context. To determine the fate of human oligodendroglioma in an experimental model, we studied the development of an anaplastic tumor after intracranial implantation into enhanced green fluorescent protein (eGFP) positive NOD/SCID mice. Remarkably after nearly nine months, the tumor not only engrafted, but it also retained classic histological and genetic features of human oligodendroglioma, in particular cells with a clear cytoplasm, showing an infiltrative growth pattern, and harboring mutations of IDH1 (R132H) and of the tumor suppressor genes, FUBP1 and CIC. The xenografts were highly invasive, exhibiting a distinct migration and growth pattern around neurons, especially in the hippocampus, and following white matter tracts of the corpus callosum with tumor cells accumulating around established vasculature. Although tumors exhibited a high growth fraction in vivo, neither cells from the original patient tumor nor the xenograft exhibited significant growth in vitro over a six-month period. This glioma xenograft is the first to display a pure oligodendroglioma histology and expression of R132H. The unexpected property, that the cells fail to grow in vitro even after passage through the mouse, allows us to uniquely investigate the relationship of this oligodendroglioma with the in vivo microenvironment.

Using microarray technology, we identified novel genes and pathways with a putative role in VSs, confirmed previous candidate genes, and found cancer-related genes with no reported role in VSs. Among these, down-regulation of CAV1 at both the mRNA and protein levels is of particular interest because this tumor suppressor normally is expressed in Schwann cells.

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Background Surgical fixation is recommended for type II and III odontoid fractures (OFx) with major translation of the odontoid fragment, regardless of the patient’s age, and for all type II OFx in patients aged ≥50 years. The level of compliance with this recommendation is unknown, and our hypothesis is that open surgical fixation is less frequently performed than recommended. We suspect that this discrepancy might be due to the older age and comorbidities among patients with OFx. Methods We present a prospective observational cohort study of all patients in the southeastern Norwegian population (3.0 million) diagnosed with a traumatic OFx in the period from 2015 to 2018. Results Three hundred thirty-six patients with an OFx were diagnosed, resulting in an overall incidence of 2.8/100000 persons/year. The median age of the patients was 80 years, and 45% were females. According to the Anderson and D’Alonzo classification, the OFx were type II in 199 patients (59%) and type III in 137 patients (41%). The primary fracture treatment was rigid collar alone in 79% of patients and open surgical fixation in 21%. In the multivariate analysis, the following parameters were significantly associated with surgery as the primary treatment: independent living, less serious comorbidities prior to the injury, type II OFx and major sagittal translation of the odontoid fragment. Conversion from external immobilization alone to subsequent open surgical fixation was performed in 10% of patients. Significant differences the in conversion rate were not observed between patients with type II and III fractures. The level of compliance with the treatment recommendations for OFx was low. The main deviation was the underuse of primary surgical fixation for type II OFx. The most common reasons listed for choosing primary external immobilization instead of primary surgical fixation were an older age and comorbidities. Conclusion Major comorbidities and an older age appear to be significant factors contributing to physicians’ decision to refrain from the surgical fixation of OFx. Hence, comorbidities and age should be considered for inclusion in the decision tree for the choice of treatment for OFx in future guidelines.

Background: The vast majority of hospital admitted patients with traumatic brain injury (TBI) will have intracranial injury identified by neuroimaging, requiring qualified staff and hospital beds. Moreover, increased pressure in health care services is expected because of an aging population. Thus, a regular evaluation of characteristics of hospital admitted patients with TBI is needed. Oslo TBI Registry-Neurosurgery prospectively register all patients with TBI identified by neuroimaging admitted to a trauma center for southeast part of Norway. The purpose of this study is to describe this patient population with respect to case load, time of admission, age, comorbidity, injury mechanism, injury characteristics, length of stay, and 30-days survival. Methods: Data for 5 years was extracted from Oslo TBI Registry-Neurosurgery. Case load, time of admission, age, sex, comorbidity, injury mechanism, injury characteristics, length of stay, and 30-days survival was compiled and compared. Results: From January 1st, 2015 to December 31st, 2019, 2153 consecutive patients with TBI identified by neuroimaging were registered. The admission rate of TBI of all severities has been stable year-round since 2015. Mean age was 52 years (standard deviation 25, range 0-99), and 68% were males. Comorbidities were common; 28% with pre-injury ASA score of ≥3 and 25% used antithrombotic medication. The dominating cause of injury in all ages was falls (55%) but increased with age. Upon admission, the head injury was classified as mild TBI in 46%, moderate in 28%, and severe (Glasgow coma score ≤ 8) in 26%. Case load was stable without seasonal variation. Majority of patients (68%) were admitted during evening, night or weekend. 68% was admitted to intensive care unit. Length of hospital stay was 4 days (median, interquartile range 3-9). 30-day survival for mild, moderate and severe TBI was 98, 94 and 69%, respectively. Conclusions: The typical TBI patients admitted to hospital with abnormal neuroimaging were aged 50-79 years, often with significant comorbidity, and admitted outside ordinary working hours. This suggests the necessity for allhour presence of competent health care professionals.