Imaging Modalities for Central Nervous System Tumors
Overview
In the current state of the rapidly developing molecular genetic era of brain tumor diagnosis and classification, the imaging and clinical management of patients with brain tumor are advancing and evolving concurrently, relying heavily on physiologic imaging in addition to high-resolution structural imaging. Imaging remains a powerful noninvasive tool, especially magnetic resonance (MR) imaging, to positively impact the management of patients with brain tumor. While MR imaging remains the most essential imaging method for evaluation of brain tumors, computed tomography (CT) plays an essential role in the emergency setting to detect potential life-threatening complications of brain tumors such as hemorrhage, hydrocephalus, or herniation. In addition to structural imaging, physiology-based MR imaging, such as diffusion-weighted imaging (DWI), perfusion-weighted imaging (PWI), proton spectroscopy, functional imaging, as well as hybrid imaging, such as Positron Emission Tomography-Computed Tomography and Positron Emission Tomography-Magnetic Resonance, provide insights into biologic and physiologic alteration in brain tumors.
|
Computed Tomography
Computed tomography (CT) combines diagnostic X-ray imaging and sophisticated computers to produce multiple images of body, including the brain, in a few minutes using relatively small amounts of ionizing radiation. In patients with brain tumor, head CT is often done as the first imaging study during acute presentation with intracranial symptoms. Unenhanced head CT is an excellent imaging study to exclude acute intracranial hemorrhage, hydrocephalus, mass effect, or herniation of brain. Latest modern CT scanners can provide a complete volume of scan data and generate a complete three-dimensional (3D) volume of data, which in turn allows the creation of multiplanar reconstruction with thick or thin slices using different algorithms. Reconstructed images can highlight abnormalities involving the three main tissue components of the brain—parenchyma, extra-axial space, and bone—to emphasize various tissue
characteristics. Dynamic contrast-enhanced CT angiogram studies can provide high-resolution images of the intracranial arteries and veins that match up to the details provided by catheter angiographic studies but without the invasive catheterization of vessels.
characteristics. Dynamic contrast-enhanced CT angiogram studies can provide high-resolution images of the intracranial arteries and veins that match up to the details provided by catheter angiographic studies but without the invasive catheterization of vessels.
 Figure 1.1. CT vs. MRI in detecting calcified central neurocytoma. A-C. Axial CT unenhanced, brain window: Heavily calcified lateral intraventricular mass. D-F. Axial CT unenhanced, bone window: Internal architecture of the heavily calcified component is better seen. |
 Figure 1.1. (continued) G-I. Axial T2: Heterogeneously hypointense mass. J-L. Axial SWI: Marked susceptibility due to calcium. |
 Figure 1.1. (continued) M-O. Axial T1-precontrast: Heterogeneously hypointense mass. P-R. Axial T1-postcontrast: Minimally enhancing, heterogeneously hypointense mass with small areas of enhancement (white arrows). |
 Figure 1.1. (continued) |
One of the major limitations of CT is limited soft-tissue resolution of brain parenchyma. Brain tumors can be infiltrative, especially diffuse gliomas, and may not be easily detectable on CT. In fact, brain tumors that are isodense to the brain parenchyma may not be detectable at all on CT.
 Figure 1.2. Pitfall of CT in detecting isodense mass, meningioma. A-C. Axial CT, unenhanced: Midline anterior cranial fossa meningioma is hardly detectable. |
 Figure 1.2. (continued) D-E. Axial T2: Homogeneously hypointense meningioma is clearly visible. G-I. Axial T1-postcontrast: Homogeneous and avid enhancement within meningioma. |
 Figure 1.2. (continued) |
 Figure 1.3. CT and MRI of hemorrhagic glioblastoma. A-C. Axial CT, unenhanced: Hemorrhagic right basal ganglia mass. D-F. Axial CT, enhanced: Discontinuity of right middle cerebral artery (black arrow) along the anterior margin of the mass. |
 Figure 1.3. (continued) G. CT angiogram: Occlusion of right middle cerebral artery (black arrow) is confirmed. H. Axial DWI: Large area of acute infarct in the right middle cerebral artery territory. I. Axial ADC: Large area of acute infarct in the right middle cerebral artery territory. J-L. Axial FLAIR: Right basal ganglia mass is better delineated (black arrows), and the additional non-enhancing glioma (white arrows) in the left occipital lobe is more clearly seen. |
 Figure 1.3. (continued) M-O. Axial T1 postcontrast: Heterogeneously enhancing right basal ganglia mass. |
Cerebral Angiography
Cerebral angiography, also called cerebral angiogram, is a minimally invasive procedure that can provide a detailed, real-time imaging of blood flow, arterial supply, venous drainage, and other hemodynamics within a vascular brain tumor such as meningioma. Although safe, cerebral angiography can be associated with less than 1% incidence of neurological deficits and other non-neurological complications.
In brain tumors, cerebral angiography is not used as the primary diagnostic tool to characterize tumor location, size, or type. It is primarily used to assess tumor vascularity and to consider preoperative embolization to reduce tumor blood supply. Depending on the types of feeding vessels, the tumor’s artery blood supply can be safely and precisely reduced or closed down using endovascular embolization technique prior to surgery to facilitate surgical removal of the tumor and to reduce intraoperative blood loss and operative times. Meningiomas are the most common brain tumors to undergo cerebral angiography, followed by embolization. One of the most commonly used embolic agents is polyvinyl alcohol particles, which expand in an aqueous solution due to their sponge-like quality. Other embolic agents include porous cellulose beads, hydroxyapatite, gelfoam, N-butyl cyanoacrylate, and platinum microcoils.
 Figure 1.4. Digital subtraction angiogram (DSA) of CNS lymphoma. A. Axial CT, enhanced: Large destructive left parietal skull mass with intracranial dural, intraparenchymal, and extracranial extension. B. Axial CT, bone window: Osseous lytic destruction of the involved skull. |
 Figure 1.4. (continued) C. Axial T2: Heterogeneous mixed intensity mass with intraparenchymal invasion (black arrows). D. Axial T1-precontrast: Mostly isointense mass. E. Axial FLAIR: Heterogeneously isointense mass. F. Axial DWI: Heterogeneously reduced diffusion within the mass. G. Axial T1-postcontrast: Heterogeneous but avid enhancement within the mass. H. Coronal T1-postcontrast: Heterogeneous but avid enhancement within the mass. |
 Figure 1.4. (continued) I. Sagittal T1-postcontrast: Heterogeneous but avid enhancement within the mass. J-L. DSA, left common carotid artery injection: Hypervascular mass with dominant arterial supply from the external carotid artery, particularly branches of the left middle meningeal artery (black arrow), superficial temporal artery (red arrow), deep temporal artery (yellow arrow), and occipital artery (white arrow). |
 Figure 1.5. DSA of meningioma, pre- and post-embolization. A. Axial T2: Heterogeneously isointense dural based right frontal mass. B. Coronal T1-postcontrast: Avid tumor enhancement. |
 Figure 1.5. (continued) C. Axial T1-postcontrast: Avid tumor enhancement. D. DSA, right external carotid artery injection (arterial phase): Hypervascular right frontal mass with primary arterial supply from the anterior division of right middle meningeal artery (white arrows), and right superficial temporal artery (red arrow). E. DSA, right external carotid artery injection (delayed venous phase): Hypervascular right frontal tumor with persistent intratumoral contrast staining. F. DSA, right external carotid artery injection (arterial phase, post-embolization): Markedly diminished flow following embolization of the right middle meningeal artery anterior division and right superficial temporal artery using Polyvinyl Alcohol (PVA) particles (355-500 µm) and proximal coil occlusion (black arrow).
WordPress theme by UFO themes
|
