Faculty Bibliography

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.

BACKGROUND: This paper presents a three-dimensional (3D) method for segmenting corpus callosum in normal subjects and brain cancer patients with glioblastoma. METHODS: Nineteen patients with histologically confirmed treatment naive glioblastoma and eleven normal control subjects underwent DTI on a 3T scanner. Based on the information inherent in diffusion tensors, a similarity measure was proposed and used in the proposed algorithm. In this algorithm, diffusion pattern of corpus callosum was used as prior information. Subsequently, corpus callosum was automatically divided into Witelson subdivisions. We simulated the potential rotation of corpus callosum under tumor pressure and studied the reproducibility of the proposed segmentation method in such cases. RESULTS: Dice coefficients, estimated to compare automatic and manual segmentation results for Witelson subdivisions, ranged from 94% to 98% for control subjects and from 81% to 95% for tumor patients, illustrating closeness of automatic and manual segmentations. Studying the effect of corpus callosum rotation by different Euler angles showed that although segmentation results were more sensitive to azimuth and elevation than skew, rotations caused by brain tumors do not have major effects on the segmentation results. CONCLUSIONS: The proposed method and similarity measure segment corpus callosum by propagating a hyper-surface inside the structure (resulting in high sensitivity), without penetrating into neighboring fiber bundles (resulting in high specificity).

INTRODUCTION: Meningiomas are typically slow-growing lesions that, depending on the location, can be relatively benign. Knowing their exact rate of growth can be helpful in determining whether surgery is necessary. METHODS: In this study we retrospectively reviewed the meningioma practices of the two senior authors (JR, MR). Our goal was to measure meningioma growth using a variety of methods (linear using diameters, and volumetric using the computer-aided perimeter and cross-sectional diameter methods) to compare rates of growth among the methods. Of 295 meningioma patients seen over an 8-year period, we identified a cohort of 31 patients with at least 30 months of follow-up. Volumes were calculated using medical imaging software with T1 post-contrast magnetic resonance imaging. Doubling times and growth rates were calculated. RESULTS: Of the 31 patients, 26 (84%) were shown to have growing meningiomas. The perimeter methodology measured higher growth rates than the diameter method for both doubling times as well as percentage annual growth (p<0.01). The mean doubling time was 13.4 years (range, 2.1-72.8 years) and 17.9 years (range, 4-92.3 years) comparing perimeter and diameter methods, respectively. The mean percentage of annual growth was 15.2% (range, 1.8-61.7%) and 5.6% (range, 0.7-12.2%), comparing perimeter and diameter methods, respectively. Linear growth was calculated at 0.7 mm/year. CONCLUSION: Overall, we found that computer-aided perimeter methods showed a more accurate picture of tumor progression than traditional methods, which generally underestimated growth.

BACKGROUND AND IMPORTANCE: Temporal bone and skull base pneumatization is a naturally occurring process that begins before birth and continues into early adulthood. Occasionally this process surpasses normal limits, resulting in hyperpneumatization, which is usually obvious, but on rare occasions may mimic more aggressive skull base disorders. An awareness of this rare anatomical variant may help clinicians avoid more extensive investigations. CLINICAL PRESENTATION: We present the case of a 37-year-old man with severe headache and multiple, partially opacified lytic lesions in the skull base noted after minor head trauma. At presentation, a computed tomographic (CT) head scan revealed multiple lucent areas in the skull base after which magnetic resonance imaging (MRI) further suggested the diagnosis of an extensive lytic skull base process associated with a small clival fracture. Needle biopsy revealed nonspecific inflammation. An earlier head CT, not available at the time of admission, demonstrated extensive pneumatized air cells in the basiocciput. During the course of the 2-year follow-up, the originally pneumatized skull base was noted to become permanently opacified with areas of new bone growth. CONCLUSION: We concluded that the skull base abnormality was an anatomical variant associated with a clival fracture and hemorrhage, which led to opacification of the pneumatized air cells. No specific treatment was offered and symptoms resolved completely. Long-term follow-up CT demonstrated opacification of the skull base. This is one of very few cases in the literature reporting the clinical course of a patient with a hyperpneumatized skull base and the subsequent evolution of the disorder after minor head trauma.

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.

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.

Dynamic contrast enhanced T(1)-weighted MRI using the contrast agent gadopentetate dimeglumine (Gd-DTPA) was performed on 10 patients with glioblastoma. Nested models with as many as three parameters were used to estimate plasma volume or plasma volume and forward vascular transfer constant (K(trans)) and the reverse vascular transfer constant (k(ep)). These constituted models 1, 2, and 3, respectively. Model 1 predominated in normal nonleaky brain tissue, showing little or no leakage of contrast agent. Model 3 predominated in regions associated with aggressive portions of the tumor, and model 2 bordered model 3 regions, showing leakage at reduced rates. In the patient sample, v(p) was about four times that of white matter in the enhancing part of the tumor. K(trans) varied by a factor of 10 between the model 2 (1.9 <--> 10(-3) min(-1)) and model 3 regions (1.9 <--> 10(-2) min(-1)). The mean calculated interstitial space (model 3) was 5.5%. In model 3 regions, excellent curve fits were obtained to summarize concentration-time data (mean R(2) = 0.99). We conclude that the three parameters of the standard model are sufficient to fit dynamic contrast enhanced T(1) data in glioblastoma under the conditions of the experiment.