Conventional and advanced magnetic resonance imaging in patients with high-grade glioma

Abstract

Magnetic resonance imaging is integral to the care of patients with high-grade gliomas. Anatomic detail can be acquired with conventional structural imaging, but newer approaches also add capabilities to interrogate image-derived physiologic and molecular characteristics of central nervous system neoplasms. These advanced imaging techniques are increasingly employed to generate biomarkers that better reflect tumor burden and therapy response. The following is an overview of current strategies based on advanced magnetic resonance imaging that are used in the assessment of high-grade glioma patients with an emphasis on how novel imaging biomarkers can potentially advance patient care.

Figure 1.

—Glioblastoma and mimics. Axial post-contrast T1-weighted images of the brain in 6 patients. All patients demonstrate a ring-enhancing lesion. Histopathologic diagnoses were toxoplasmosis (A), neurocysticercosis (B), tuberculosis (C), tumefactive multiple sclerosis (D), primary CNS lymphoma in an immunocompromised patient (E) and glioblastoma (F).

Figure 2.

—Diffusion tensor tractography for surgical planning. Axial (A) and sagittal (B) T2-weighted images of the brain with superimposed color-coded DTI-derived tractographic images. Note displacement of fiber tracts by the tumor (red arrow).

Figure 3.

—Pseudoprogression identified with perfusion imaging. Axial post-contrast T1-weighted images (A, C, D, F) and axial rCBV maps (B, E) of the brain. For patient 1 (A-C), the initial image shows an enhancing periventricular lesion (A, oval), with low rCBV (B, oval). Follow-up imaging (C) shows resolution of enhancement (oval) compatible with the lesion representing pseudoprogression on the initial images. Conversely, for patient 2 an initial enhancing lesion (D, oval), shows markedly elevated rCBV (E, oval) and the lesion progresses on follow-up imaging (F, oval), compatible with true progression.

Figure 4.

—Pseudoresponse and diffusion imaging. Axial post-contrast T1-weighted (A, C), T2-weighted (B, D), and DWI(E) images of a patient with glioblastoma. On initial presentation the patient had a left cerebral ring-enhancing mass (A, arrow) with surrounding vasogenic edema seen as T2-hyperintese areas (B). Following biopsy and 1 week of anti-angiogenic therapy with bevacizumab, tumor-related enhancement nearly resolved (C, arrow). However, diminished but still abundant T2 hyperintensity (D) corresponded to areas of DWIsignal abnormality (E, arrows) with low ADC(not shown), compatible with residual non-enhancing tumor. Such rapid resolution of contrast enhancement independent of substantial tumor shrinkage is compatible with pseudoprogression.

Figure 5.

—Persistent diffusion restriction after anti-angiogenic treatment. Axial diffusion (A, E), T2-weighted (B, F), T1-weighted (C, G) and post-contrast T1-weighted images of a patient with glioblastoma treated with bevacizumab. At the first time point show (A-D) the patient had developed a DWI and T2 bright (A and B arrow) peri-ventricular lesion with restricted diffusion that demonstrated an intrinsically T1-hyperintense rim (C, arrow) and little or no contrast enhancement (D). Follow-up imaging nearly 1 year later showed little interval change in the lesion (arrow, E-H) and no evidence of progression compatible with the lesion representing treatment effect rather than growing tumor.

Figure 6.

—ADC as predictive biomarker for high grade glioma response to anti-angiogenic therapy. Pre-contrast T1-weighted images are subtracted from post-contrast T1-weighted images to generate T1-subtraction maps which are then segmented and overlaid on the ADC Map (process illustrated in part A). Voxels from the enhancing region are used to generate an ADC histogram fitted with a 2-normal curve with a lower (ADCL) and higher (ADCH) component (part B). A larger volume of ADCL<1.24 μm²/ms is associated with shorter survival (part C, red graph) in glioblastoma patients treated with anti-angiogenic therapy (from Ellingson et al.).

Figure 7.

—Magnetic resonance spectroscopy for identifying IDH1 mutant gliomas. Axial fluid-attenuated inversion recovery (FLAIR) images (A, B) of two anaplastic astrocytomas (WHO grade III) show areas of abnormal hyperintensity compatible with tumor. Comparison of representative MR spectra from the IDH1 mutant (C) versus wild-type (D) glioma. Note the extra peaks in the region of Glu/Gln/2-HG(centered at 2.25 ppm) that are increased in the IDH1 mutant tumors (from Pope et al.).