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Background: The recommended treatment for cervical spinal cord injury (cSCI) is surgical decompression and stabilization within 24 h after injury. The aims of the study were to estimate our institutional compliance with this recommendation and identify potential factors associated with surgical delay. Methods: Population-based retrospective database study of patients operated for cSCI in 2015-2022 within the South-East Norway Health Region (3.1 million inhabitants). Data extracted were demographics, injury description, management timeline, place of primary triage [local hospital (LH) or neurotrauma center (NTC)]. Main outcome variables were: (1) time from injury to surgery at NTC, (2) time from injury to admission NTC, and (3) time from admission NTC to surgery. Results: We found 243 cSCI patients having acute neck surgery. Their median age was 63 years (IQR 47-74 years), 77% were male, 48% were =65 years old. Primary triage at an LH occurred in 150/243 (62%). The median time from injury to acute surgery was 27.8 h (IQR 15.4-61.9 h), and 47% had surgery within 24 h. The median time from injury to NTC admission was 5.6 h (IQR 1.9-19.4 h), and 67% of the patients were admitted to the NTC within 12 h. Significant factors associated with increased time from injury to NTC admission were transfer via LH, severe preinjury comorbidities, less severe cSCI, time of injury other than night, absence of multiple injuries. The median time from NTC admission to surgery was 16.7 h (IQR 9.5-31.0 h), and 70% had surgery within 24 h. Significant factors associated with increased time from NTC admission to surgery were increasing age and non-translational injury morphology. Conclusion: Less than half of the patients with cSCI were operated on within the recommended 24 h time frame after injury. To increase the fraction of early surgery, we suggest the following: (1) patients with clinical suspicion of cSCI should be transported directly to the NTC from the scene of the accident, (2) MRI should be performed only at the NTC, (3) at the NTC, surgery should commence on the same calendar day as arrival or as the first operation the following day. [ABSTRACT FROM AUTHOR]

Abstract Background Intracranial arachnoid cysts (AC) are membranous sacs filled with CSF-like fluid that are commonly found in the temporal fossa. The majority of ACs are congenital. Typical symptoms are headache, dizziness, and dyscognition. Little is known about genes that contribute to the formation of the cyst membranes. Methods In order to identify differences in gene expression between normal arachnoid membrane (AM) and cyst membrane, we have performed a high-resolution mRNA microarray analysis. In addition we have screened DNA from AC samples for chromosomal duplications or deletions using DNA microarray-based copy number variation analysis. Results The transcriptome consisting of 33096 gene probes showed a near-complete similarity in expression between AC and AM samples. Only nine genes differed in expression between the two tissues: ASGR1, DPEP2, SOX9, SHROOM3, A2BP1, ATP10D, TRIML1, NMU were down regulated, whereas BEND5 was up regulated in the AC samples. Three of the AC samples had unreported human DNA copy number variations, all DNA gains. Conclusions Extending results of previous anatomical studies, the present study has identified a small subset of differentially expressed genes and DNA alterations in arachnoid cysts compared to normal arachnoid membrane.

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. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

Objective: Cerebral venous thrombosis (CVT) is increasingly recognized in traumatic brain injury (TBI), but its complications and effect on outcome remain undetermined. In this study, the authors characterize the complications and outcome effect of CVT in TBI patients., Methods: In a retrospective, case-control study of patients included in the Oslo University Hospital trauma registry and radiology registry from 2008 to 2014, the authors identified TBI patients with CVT (cases) and without CVT (controls). The groups were matched regarding Abbreviated Injury Scale 1990, update 1998 (AIS'98) head region severity score 3-6. Cases were identified by AIS'98 or ICD-10 code for CVT and CT or MR venography findings confirmed to be positive for CVT, whereas controls had no AIS'98 or ICD-10 code for CVT and CT venography or MR venography findings confirmed to be negative for CVT. All images were reviewed by a neuroradiologist. Rates of complications due to CVT were recorded, and mortality was assessed both unadjusted and in a multivariable logistic regression analysis adjusting for initial Glasgow Coma Scale score, Rotterdam CT score, and Injury Severity Score. Complications and mortality were also assessed in prespecified subgroup analysis according to CVT location and degree of occlusion from CVT. Lastly, mortality was assessed in an exploratory subgroup analysis according to the presence of complications from CVT., Results: The CVT group (73 patients) and control group (120 patients) were well matched regarding baseline characteristics. In the CVT group, 18% developed venous infarction, 11% developed intracerebral hemorrhage, and 19% developed edema, all representing complications secondary to CVT. Unadjusted 30-day mortality was 16% in the CVT group and 4% in the no-CVT group (p = 0.004); however, the difference was no longer significant in the adjusted analysis (OR 2.24, 95% CI 0.63-8.03; p = 0.215). Subgroup analysis by CVT location showed an association between CVT location and rate of complications and an unadjusted 30-day mortality of 50% for midline or bilateral CVT and 8% for unilateral CVT compared with 4% for no CVT (p < 0.001). The adjusted analysis showed a significantly higher mortality in the midline/bilateral CVT group than in the no-CVT group (OR 8.41, 95% CI 1.56-45.25; p = 0.032)., Conclusions: There is a significant rate of complications from CVT in TBI patients, leading to secondary brain insults. The rate of complications is dependent on the anatomical location of the CVT, and midline and bilateral CVT is associated with an increased 30-day mortality in TBI patients.

A right-handed woman of 90, taking aspirin 160 mg daily, suffered acute neck pain radiating to the shoulders, with right side hemiparesis and numbness occurring minutes thereafter. On admission 2.5 hrs later, examination showed paresis and hyporeflexia of the right limbs accompanied by neck stiffness and vertebral tenderness in level C7. Acute stroke was the initial working diagnosis. Cerebral CT was normal. Symptoms progressed with left arm numbness and left ancle clonus, and eight hours after symptom onset there was bilateral plantar inversion, reduced skin prick sensibility below C4, bladder paresis and anal sphincter hypotonia. CT myelography revealed an intraspinal mass extending from C2 to C6. 14 hours after symptom onset, a spinal epidural haematoma was removed by spinal laminectomy. Recovery and functional outcome was good. Symptoms, work-up and treatment are discussed with reference to previous publications.