- •Contents
- •Contributors
- •Brain Tumor Imaging
- •1 Introduction
- •1.1 Overview
- •2 Clinical Management
- •3 Glial Tumors
- •3.1 Focal Glial and Glioneuronal Tumors Versus Diffuse Gliomas
- •3.3 Astrocytomas Versus Oligodendroglial Tumors
- •3.4.1 Diffuse Astrocytoma (WHO Grade II)
- •3.5 Anaplastic Glioma (WHO Grade III)
- •3.5.1 Anaplastic Astrocytoma (WHO Grade III)
- •3.5.3 Gliomatosis Cerebri
- •3.6 Glioblastoma (WHO Grade IV)
- •4 Primary CNS Lymphomas
- •5 Metastatic Tumors of the CNS
- •References
- •MR Imaging of Brain Tumors
- •1 Introduction
- •2 Brain Tumors in Adults
- •2.1 Questions to the Radiologist
- •2.2 Tumor Localization
- •2.3 Tumor Malignancy
- •2.4 Tumor Monitoring
- •2.5 Imaging Protocol
- •Computer Tomography
- •2.6 Case Illustrations
- •3 Pediatric Brain Tumors
- •3.1 Standard MRI
- •3.2 Differential Diagnosis of Common Pediatric Brain Tumors
- •3.3 Early Postoperative Imaging
- •3.4 Meningeal Dissemination
- •References
- •MR Spectroscopic Imaging
- •1 Methods
- •1.1 Introduction to MRS
- •1.2 Summary of Spectroscopic Imaging Techniques Applied in Tumor Diagnostics
- •1.3 Partial Volume Effects Due to Low Resolution
- •1.4 Evaluation of Metabolite Concentrations
- •1.5 Artifacts in Metabolite Maps
- •2 Tumor Metabolism
- •3 Tumor Grading and Heterogeneity
- •3.1 Some Aspects of Differential Diagnosis
- •4 Prognostic Markers
- •5 Treatment Monitoring
- •References
- •MR Perfusion Imaging
- •1 Key Points
- •2 Methods
- •2.1 Exogenous Tracer Methods
- •2.1.1 Dynamic Susceptibility Contrast MRI
- •2.1.2 Dynamic Contrast-Enhanced MRI
- •3 Clinical Application
- •3.1 General Aspects
- •3.3 Differential Diagnosis of Tumors
- •3.4 Tumor Grading and Prognosis
- •3.5 Guidance for Biopsy and Radiation Therapy Planning
- •3.6 Treatment Monitoring
- •References
- •Diffusion-Weighted Methods
- •1 Methods
- •2 Microstructural Changes
- •4 Prognostic Marker
- •5 Treatment Monitoring
- •Conclusion
- •References
- •1 MR Relaxometry Techniques
- •2 Transverse Relaxation Time T2
- •4 Longitudinal Relaxation Time T1
- •6 Cest Method
- •7 CEST Imaging in Brain Tumors
- •References
- •PET Imaging of Brain Tumors
- •1 Introduction
- •2 Methods
- •2.1 18F-2-Fluoro-2-Deoxy-d-Glucose
- •2.2 Radiolabeled Amino Acids
- •2.3 Radiolabeled Nucleoside Analogs
- •2.4 Imaging of Hypoxia
- •2.5 Imaging Angiogenesis
- •2.6 Somatostatin Receptors
- •2.7 Radiolabeled Choline
- •3 Delineation of Tumor Extent, Biopsy Guidance, and Treatment Planning
- •4 Tumor Grading and Prognosis
- •5 Treatment Monitoring
- •7 PET in Patients with Brain Metastasis
- •8 Imaging of Brain Tumors in Children
- •9 Perspectives
- •References
- •1 Treatment of Gliomas and Radiation Therapy Techniques
- •2 Modern Methods and Strategies
- •2.2 3D Conformal Radiation Therapy
- •2.4 Stereotactic Radiosurgery (SRS) and Radiotherapy
- •2.5 Interstitial Brachytherapy
- •2.6 Dose Prescription
- •2.7 Particle Radiation Therapy
- •3 Role of Imaging and Treatment Planning
- •3.1 Computed Tomography (CT)
- •3.2 Magnetic Resonance Imaging (MRI)
- •3.3 Positron Emission Tomography (PET)
- •4 Prognosis
- •Conclusion
- •References
- •1 Why Is Advanced Imaging Indispensable for Modern Glioma Surgery?
- •2 Preoperative Imaging Strategies
- •2.4 Preoperative Imaging of Function and Functional Anatomy
- •2.4.1 Imaging of Functional Cortex
- •2.4.2 Imaging of Subcortical Tracts
- •3 Intraoperative Allocation of Relevant Anatomy
- •Conclusions
- •References
- •Future Methods in Tumor Imaging
- •1 Special Editing Methods in 1H MRS
- •1.1 Measuring Glycine
- •2 Other Nuclei
- •2.1.1 Spatial Resolution
- •2.1.2 Measuring pH
- •2.1.3 Measuring Lipid Metabolism
- •2.1.4 Energy Metabolism
- •References
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E. Hattingen and M. Warmuth-Metz |
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Fig. 5 Schematic illustration of extracerebral versus intracerebral tumors is shown in (a). In meningiomas with irregular enhancement and marked intracerebral edema, (b) the extracerebral location might be difficult to evaluate. However, broad and sometimes umbilicated basis to the thickened dura (arrow in c) and the shifted cortex (arrow in b) may help to correctly diagnose extracerebral tumor
Second Question: Intracerebral (Intra-axial) or Extracerebral (Extra-axial)?
Signs indicating an extracerebral tumor are illustrated in Fig. 5.
The next question addresses the number of tumors. Singular large intracerebral tumors are mostly glial tumors; otherwise metastases should be suspected.
Finally, the possibility of a cerebral lymphoma should be considered. Corticosteroids should be withheld if a lymphoma is a differential diagnosis based on the imaging findings until a stereotactic needle biopsy has been performed (Fig. 6). Lympholytic activity of corticosteroids makes the histopathological diagnosis more difficult or even
impossible. Therefore, radiologists should be familiar with imaging features of this tumor entity (Bühring et al. 2001).
Third Question: Is Cerebral Lymphoma Possible?
2.2Tumor Localization
The description of tumor localization should consider two aspects: the precise anatomical localization and the spatial relation to functional representations of motor and language skills. Anatomical designation not only means the lobe and gyrus but also the relationship to white and gray matter
MR Imaging of Brain Tumors |
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Fig. 6 Typical primary CNS lymphoma (PCNSL) showing features of a tumor with dense-packed tumor cells. The tumor is almost isointense to the gray matter in T2WI and T1WI (a) and enhances contrast agent
Fig. 7 Diffuse infiltrating gliomas often infiltrate the cortical gray matter (left and also right frontal lobe in a), resulting in a swelling and blurring gray-white matter interface (“ribbon sign”). In contrast, vasogenic edema (b) respects the gray-white matter interface and white matter tracts, extends finger-like into the gyri (black arrows), and demasks the optic radiation (white arrow)
with a patchy appearance. On CCT the tumor is isodense to gray matter (b). DWI signal is bright due to the narrowed extracellular space (c) and corresponding ADC values are low (d)
18 |
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E. Hattingen and M. Warmuth-Metz |
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Table 2 Cerebral anatomy with respect to brain function |
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Spatial |
Distortions and |
Tumor related |
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resolution |
signal loss |
dislocation |
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Sectional MRI |
+ |
GE >> SE |
Anatomical |
White matter tracts |
Anatomical |
Variance between |
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|
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distortions in |
mostly invisible |
interindividual |
function and |
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large tumors |
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variances |
anatomy |
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(edema) |
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3D MRI |
++ |
Due to GE |
Anatomical |
White matter tracts |
Anatomical |
Variance between |
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distortions in |
mostly invisible |
interindividual |
function and |
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large tumors |
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variances |
anatomy |
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(edema) |
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Surface |
++ |
Minimal |
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White matter not |
Contorted proportions |
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reformatting |
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depicted |
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fMRI |
Reduced |
Skull base, blood |
False-negative or |
Discrepancy |
Task dependent |
Needs intact |
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products, metal, |
positive |
between vascular |
activation depicts |
neurovascular |
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mineral |
activations |
response and |
only part of language |
coupling |
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neuronal activity |
function |
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DTI |
Reduced |
Skull base, blood |
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products, metal, |
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mineral |
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Tractography |
Reduced |
See DTI |
May assume tract |
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Different |
Significantly |
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damage |
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methodologies |
affected by the |
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method |
structures. The infiltration of the cortical ribbon (cortical ribbon sign) and thickening of the corpus callosum are typical features of infiltrative glial tumors which help to differentiate them from vasogenic edema (Fig. 7).
The primary motor, sensory, auditory, and visual cortices are assigned at the brain surface. However, surface relief may be difficult to recognize in sectional images and anatomy might be distorted by the tumors. The identification of surface anatomy is easier with interactive observation of 3D objects. Further, planar reformatting of the brain surface helps to delineate the central sulcus which marks the perirolandic region with the primary sensorimotor cortex (Table 2) (Figs. 8 and 9).
However, this direct allocation of anatomy to function and vice versa is only true for primary cortical areas: the variance increases with the complexity of brain function. One of the most investigated functions is the language since neurosurgeons have the primary goal of preserving the language during tumor resection. Another critical issue is to protect important white matter tracts. To achieve these goals, functional MRI (fMRI) and tractography are well-established components of presurgical imaging (Fig. 10). MR tractography virtually dissects functionally critical white matter tracts, such as the corticospinal tract and the arcuate fascicle (Fig. 11), enabling the neurosurgeon to plan the surgical approach which best preserves the tract during resection. However, uncritical and inexpertly handling of these methods bears the imminent danger of misinterpretations (Jellison et al. 2004).
Therefore, the main indication and the undoubted strength of fMRI and DTI is the presurgical planning. Functional language MRI can localize language dominant hemisphere (Ruff et al. 2008; Roux et al. 2003; Kim et al. 2009; Spreer et al. 2002) (Fig. 11). However, surgical resection of tumors in the language areas of the dominant hemispheres still requires awake craniotomy and direct brain mapping to prevent postsurgical aphasia (Kim et al. 2009). Tractography may depict the relation between tumor and white matter tract, but it should not determine the extent of resection during surgery.
2.3Tumor Malignancy
The imaging criteria of malignancy include blurring tumor margins, tumor edema, necroses, and contrast enhancement. However, these signs of malignancy are not as reliable as they allow the definite categorization into lowand high-grade tumors. Diffuse gliomas infiltrate the brain tissue by definition. Therefore, they mainly do not have sharp margins. In contrast, metastases and also highly malignant PNETs often have sharply delineated margins between tumor and edema (Fig. 12). Low-grade neuroepithelial glioneuronal tumors like gangliogliomas and DNETs may be associated with cortical dysplasia which may blur anatomical structures. Further, especially gangliogliomas may show areas of contrast enhancement (Fig. 13). Necroses are difficult to differentiate from tumor cysts; in both, the
MR Imaging of Brain Tumors |
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Fig. 8 The surface-reformatted image (a) shows both hemispheres from the interhemispheric fissure to the Sylvian fissure, displaying the entire central sulcus. The space-occupying lesion is located in the postcentral gyrus, shifting the precentral sulcus forward. The fMRI with
motor activation of the hand (b) and intraoperative monitoring confirmed this localization. It was an epidermoid with characteristic very hyperintense signal in T2WI (c) and very high signal on DWI (see also Fig. 1)
margins may enhance. However, cysts enhance linearly in contrast to the often partially nodular enhancement at the margins of tumor necroses.
Malignant gliomas generate tumor vessels with impaired blood-brain barrier. The higher vascular permeability causes extravasal accumulation of contrast agent with consecutive signal increase on T1WI. Therefore, contrast enhancement is one important hallmark of tumor malignancy. Considering that most of the WHO grade I astrocytomas and a larger
amount of grade II oligodendroglioma (White et al. 2005) may also enhance due to higher vasculature, this sign of malignancy has a limited value (Fig. 14). On the other side, about 30 % of high-grade WHO III astrocytomas do not enhance contrast agent (Scott et al. 2002; Muragaki et al. 2008; Chaichana et al. 2009) (Fig. 15).
Although the histopathological WHO classification still is the gold standard to categorize tumor entity and their malignancy, the molecular genetic profile of a brain tumor