Faculty Bibliography

BACKGROUND AND PURPOSE: The National Emergency X-Radiography Utilization Study Low-Risk Criteria were established to identify patients with a low probability of cervical spine injury in whom imaging of the cervical spine was unnecessary. The purpose of this study was to ascertain the number of unnecessary cervical spine CT studies on the basis of proper application of established clinical guidelines and, secondarily, to determine indications for ordering studies in the absence of guideline criteria. MATERIALS AND METHODS: All patients presenting to a level I trauma center for whom a screening cervical spine CT was ordered in the setting of blunt trauma were eligible for enrollment. For each study, the requesting clinician completed a survey regarding study indications. CT examinations were evaluated by a board-certified radiologist blinded to survey data to determine the presence or absence of cervical spine injury. RESULTS: Of 507 CT examinations, 5 (1%) were positive and 497 (98.0%) were negative for acute cervical spine injury. Five studies (1%) were indeterminate for acute injury but demonstrated no abnormality on subsequent imaging and clinical follow-up. Of the 502 studies without cervical spine injury, 81 (16.1%) were imaged despite meeting all 5 NEXUS criteria for nonimaging. Of these, the most common study indication was dangerous mechanism of injury (48.1%) followed by subjective neck pain (40.7%). CONCLUSIONS: Strict application of NEXUS criteria could potentially reduce the number of screening cervical spine CT scans in the setting of blunt trauma; this change would avoid a considerable amount of unnecessary radiation and cost.

Purpose: The purpose of this study was to evaluate whether DTI could demonstrate the water diffusivity changes in the corpus callosum (CC), which were not visible on the morphologic imaging in patients with glioblastoma multiforme (GBM) and brain metastases with no midline CC infiltration. Materials and Methods: Twenty-seven patients with treatment naive unilateral GBM and eleven patients with a solitary brain metastasis with no midline CC infiltration underwent DTI. Ten controls with normal brain MRI were also included. Based on the tensors, the principal diffusion directions, the anisotropy values, and the prior information about the diffusivity pattern in CC, a similarity measure was proposed. Subsequently, the CC was automatically divided into the Witelson subdivisions. Results: We observed significantly decreased fractional anisotropy values in all the regions of CC in the patients with GBM and metastases as compared to those in the controls. The mean diffusivity values showed a significant increase in all the regions of CC, except the splenium in patients with GBM and the isthmus in the patients with metastases, as compared to that in the controls respectively. Conclusion: In conclusion, DTI is more sensitive than the morphologic MR imaging in the evaluation of changes within the CC, in brain tumours which do not infiltrate the CC. However, these changes of the DTI metrics in the CC are due to a Wallerian degeneration rather than a tumour infiltration, as was shown by our results, as similar changes were seen in the GBM as well as the non-infiltrating metastases patients.

BACKGROUND: Clinically significant spontaneous bilateral iliopsoas hematoma is a rare complication of anticoagulation therapy. Definitive treatment of spontaneous iliopsoas hematomas is not well-established and varies between observation and surgical intervention. The intramuscular hematoma causes severe pain, muscle dysfunction, and occasionally nerve palsy with the femoral nerve most commonly affected. Most patients are neurologically normal but when a significant neurological deficit is associated with iliopsoas hematoma, optimal treatment recommendations vary. We report a case of spontaneous bilateral iliopsoas hematomas causing significant bilateral femoral nerve dysfunction. CASE DESCRIPTION: The authors present the case of a 63-year-old female who developed bilateral femoral nerve palsy due to anticoagulation bleeding complication. Magnetic resonance imaging demonstrated large bilateral intramuscular psoas hematomas causing femoral nerve compression. Surgical evacuation and decompression of the femoral nerves was performed with rapid neurological improvement. CONCLUSION: Management recommendations depend on the volume and cause of the hematoma, timing of diagnosis, and the degree of neurological impairment. A conservative approach with bed rest and correction of bleeding abnormalities to allow the hematoma to spontaneously resorb has been utilized for patients with small hematomas and little to no neurological symptoms. In contrast, more aggressive recommendations have been made for patients with large hematomas, severe motor function deficits, or hemodynamic instability.

BACKGROUND AND PURPOSE: Integration of imaging and genomic data is critical for a better understanding of gliomas, particularly considering the increasing focus on the use of imaging biomarkers for patient survival and treatment response. The purpose of this study was to correlate CBV and PS measured by using PCT with the genes regulating angiogenesis in GBM. MATERIALS AND METHODS: Eighteen patients with WHO grade IV gliomas underwent pretreatment PCT and measurement of CBV and PS values from enhancing tumor. Tumor specimens were analyzed by TCGA by using Human Gene Expression Microarrays and were interrogated for correlation between CBV and PS estimates across the genome. We used the GO biologic process pathways for angiogenesis regulation to select genes of interest. RESULTS: We observed expression levels for 92 angiogenesis-associated genes (332 probes), 19 of which had significant correlation with PS and 9 of which had significant correlation with CBV (P < .05). Proangiogenic genes such as TNFRSF1A (PS = 0.53, P = .024), HIF1A (PS = 0.62, P = .0065), KDR (CBV = 0.60, P = .0084; PS = 0.59, P = .0097), TIE1 (CBV = 0.54, P = .022; PS = 0.49, P = .039), and TIE2/TEK (CBV = 0.58, P = .012) showed a significant positive correlation; whereas antiangiogenic genes such as VASH2 (PS = -0.72, P = .00011) showed a significant inverse correlation. CONCLUSIONS: Our findings are provocative, with some of the proangiogenic genes showing a positive correlation and some of the antiangiogenic genes showing an inverse correlation with tumor perfusion parameters, suggesting a molecular basis for these imaging biomarkers; however, this should be confirmed in a larger patient population.

We have tested the predictive value of apparent diffusion coefficient (ADC) histogram analysis in stratifying progression-free survival (PFS) and overall survival (OS) in bevacizumab-treated patients with recurrent glioblastoma multiforme (GBM) from the multi-center BRAIN study. Available MRI's from patients enrolled in the BRAIN study (n = 97) were examined by generating ADC histograms from areas of enhancing tumor on T1 weighted post-contrast images fitted to a two normal distribution mixture curve. ADC classifiers including the mean ADC from the lower curve (ADC-L) and the mean lower curve proportion (LCP) were tested for their ability to stratify PFS and OS by using Cox proportional hazard ratios and the Kaplan-Meier method with log-rank test. Mean ADC-L was 1,209 x 10(-6)mm(2)/s +/- 224 (SD), and mean LCP was 0.71 +/- 0.23 (SD). Low ADC-L was associated with worse outcome. The hazard ratios for 6-month PFS, overall PFS, and OS in patients with less versus greater than mean ADC-L were 3.1 (95 % confidence interval: 1.6, 6.1; P = 0.001), 2.3 (95 % CI: 1.3, 4.0; P = 0.002), and 2.4 (95 % CI: 1.4, 4.2; P = 0.002), respectively. In patients with ADC-L <1,209 and LCP >0.71 versus ADC-L >1,209 and LCP <0.71, there was a 2.28-fold reduction in the median time to progression, and a 1.42-fold decrease in the median OS. The predictive value of ADC histogram analysis, in which low ADC-L was associated with poor outcome, was confirmed in bevacizumab-treated patients with recurrent GBM in a post hoc analysis from the multi-center (BRAIN) study.

Acute calcific longus colli tendinitis (LCT) has been reported as an unusual cause of acute-onset neck pain, dysphagia, and headache.(1-5) As described in most of the published reports, LCT traditionally manifests on computed tomography (CT) imaging as paramidline calcium hydroxyapatite crystal deposits anterior to the C1 and C2 vertebral bodies. However, recent studies have brought attention to the disease existing at the C4-C5 and C5-C6 levels.(6,7) Acute LCT is considered relatively benign, typically resolving on its own within several weeks.

Distinguishing tumor progression from radiation necrosis after treatment in patients with brain tumors presents a clinical dilemma. A well-characterized, orthotopic rodent model of radiation-induced brain necrosis including a tumor is not currently available The objective of the study was to create focal radiation necrosis in rat brain bearing human glioblastoma (GBM) using stereotactic radiosurgery and confirm it by immuno-histological analysis. Nude rats implanted with primary GBM cells were irradiated using a stereotactic setup (n = 3) or received no radiation (n = 3). Ten weeks after the implantation, growth of the tumor was confirmed by magnetic resonance imaging (MRI). For each animal, MRI and contrast-enhanced CT images were obtained and fused using registration software. The tumor was identified and delineated using the fused CT/MR images. A treatment plan was generated using a 4 mm radiosurgery cone such that one portion of the tumor receives 100% dose of 60 Gy sufficient to cause necrosis, whereas the tumor edge at depth receives only 50% or less dose, allowing for regrowth of the tumor. The brains were collected 10 weeks after irradiation and immuno-histological analysis was performed. Hematoxylin and eosin staining showed central liquefaction necrosis in the high dose region consistent with necrosis and viable tumor in the peripheral low dose region. Ki-67 staining showed highly proliferative tumor cells surrounding the necrotic parts of the tumor. Luxol fast blue and lectin staining showed demyelination and vascular injury in brain tissue consistent with radiation necrosis. We have developed a novel model of radiation necrosis in rats bearing glioma.