Advanced Imaging Techniques for Newly Diagnosed and Recurrent Gliomas

Abstract

Management of gliomas following initial diagnosis requires thoughtful presurgical planning followed by regular imaging to monitor treatment response and survey for new tumor growth. Traditional MR imaging modalities such as T1 post-contrast and T2-weighted sequences have long been a staple of tumor diagnosis, surgical planning, and post-treatment surveillance. While these sequences remain integral in the management of gliomas, advances in imaging techniques have allowed for a more detailed characterization of tumor characteristics. Advanced MR sequences such as perfusion, diffusion, and susceptibility weighted imaging, as well as PET scans have emerged as valuable tools to inform clinical decision making and provide a non-invasive way to help distinguish between tumor recurrence and pseudoprogression. Furthermore, these advances in imaging have extended to the operating room and assist in making surgical resections safer. Nevertheless, surgery, chemotherapy, and radiation treatment continue to make the interpretation of MR changes difficult for glioma patients. As analytics and machine learning techniques improve, radiomics offers the potential to be more quantitative and personalized in the interpretation of imaging data for gliomas. In this review, we describe the role of these newer imaging modalities during the different stages of management for patients with gliomas, focusing on the pre-operative, post-operative, and surveillance periods. Finally, we discuss radiomics as a means of promoting personalized patient care in the future.

Keywords: PET scanning; glioma; imaging; progression; pseudoprogression; radiomics; recurrence.

FIGURE 1

Glioblastoma, IDH-wildtype. (A) Axial CT without contrast: Ill-defined hypodensity lesion centered in the left superior temporal gyrus; (B) axial DWI: No associated reduced diffusion; (C) axial T1 pre-contrast: hypointense mass; (D) coronal T2: heterogeneous mass with hypointense rim with prominent central necrosis (yellow arrow); (E) axial T2: heterogeneous mass with hypointense rim with prominent central necrosis (yellow arrow); (F) axial SWI: prominent blood products within the mass (black arrow); (G) axial ASL perfusion: marked hyperperfusion (black arrows) within the rim enhancing component of the mass; (H) axial T1 post-contrast: heterogeneous mass with thick rim enhancement (yellow arrows) and prominent central necrosis; (I) coronal T1 post-contrast: heterogeneous mass with thick rim enhancement and prominent central necrosis; (J) sagittal T1 post-contrast: heterogeneous mass with thick rim enhancement and prominent central necrosis. CT, Computed tomography; DWI, Diffusion-weighted imaging; SWI, Susceptibility-weighted imaging; ASL, Arterial spin labeling; MRS, Magnetic resonance spectroscopy.

FIGURE 2

T2/FLAIR mismatch. (A) Axial T2: homogenously hyperintense mass (yellow arrow). (B) Axial FLAIR: hypointense mass (yellow arrow) relative to T2 image with exception of a hyperintense peripheral rim (white arrow).

FIGURE 3

Diffuse astrocytoma, IDH-wildtype. (A) Axial T1 pre-contrast: expansile hypointense left insular mass; (B) Axial T1 post-contrast: No associated enhancement; (C) axial FLAIR: heterogeneous mixed hyper- and hypointense signal intensity within the mass; (D) axial T2: homogeneous hyperintense mass; (E) axial FLAIR: hyperintense region of the tumor (white arrow) in the posterior aspect; (F) axial DWI: associated reduced diffusion in the posterior tumor (white arrow); (G) axial T2: localizer for single voxel MRS targeted to the posterior tumor; (H) proton MRS single voxel: pathologic increase in choline metabolite at 3.2 ppm (yellow arrow) and absent NAA metabolite (arrowhead) at 2 ppm consistent with proliferating process. Biopsy targeted to this region showed cellular astrocytoma. FLAIR, Fluid-attenuated inversion recovery.

FIGURE 4

MR perfusion sequences. (A) Axial DSC perfusion: Marked hyperperfusion within the lateral and posterior aspects of the mass (black arrows); (B) axial DCE perfusion: Marked capillary leakiness within the central aspect of the mass (arrowheads); (C) axial ASL perfusion: Marked hyperperfusion of a neoplasm in the frontal lobe. DSC, Dynamic susceptibility-weighted contrast-enhanced; DCE, Dynamic contrast enhanced; ASL, Arterial spin labeling.

FIGURE 5

Molecular glioblastoma. (A) Axial FLAIR: homogeneously hyperintense mass; (B) axial T1 post-contrast: mild enhancement within the mass without distinct area of necrosis; (C) axial DSC perfusion: marked hyperperfusion within the lateral and posterior aspects of the mass (black arrows); (D) axial DCE perfusion: marked capillary leakiness within the central aspect of the mass (arrowheads); (E) axial ASL perfusion: marked increase in cerebral blood flow and hyperperfusion of tumor in the frontal lobe (different tumor than the one depicted in panels A–D).

FIGURE 6

Diffuse glioma, IDH-mutant. (A) Axial FLAIR: Expansile hyperintense mass in the right medial temporal lobe; (B) axial T1 pre-contrast: hypointense mass; (C) axial T1 post-contrast: no associated enhancement within the mass; (D) axial SWI: no blood products or calcium within the mass; (E) axial DWI: linear reduced diffusion (white arrows) in the right hippocampus due to recent seizure activity; (F) axial ASL perfusion: Marked hyperperfusion within the right hippocampus and medial temporal lobe due to recent seizure activity (yellow arrow).

FIGURE 7

Recurrent glioblastoma in right posterior insula (FMISO PET-MR). (A) Axial FLAIR: Ill-defined hyperintense area in the right posterior insula (black arrow); (B) axial T1 post-contrast: mild enhancement in the right posterior insula (white arrow); (C) axial ¹⁸F-FMISO PET: avid uptake of FMISO tracer in the right posterior insular (yellow arrow). Biopsy targeted to this region showed recurrent glioblastoma. ¹⁸F-FMISO, Fluoromisonidazole; PET, Positron emission tomography.

FIGURE 8

Tractography corticospinal tract. Corticospinal tractography (yellow arrows) spanning from the superior motor cortex to pons overlaid on axial T1 post-contrast images showing enhancing necrotic glioblastoma (white arrows) in the left posterior parahippocampal gyrus.

FIGURE 9

Tractography: arcuate fasciculus. Arcuate fasciculus tractography (yellow arrows) overlaid on sagittal T2 images.

FIGURE 10

Tractography: optic radiations. (A) Optic radiation tractography (yellow arrows) overlaid on axial T1 post-contrast images showing enhancing necrotic glioblastoma (white arrows) centered in the left posterior parahippocampal gyrus; (B) optic radiation tractography (yellow arrows) overlaid on sagittal T2 images.

FIGURE 11

Tractography: inferior fronto-occipital fasciculus. (A) Inferior fronto-occipital fasciculus tractography (yellow arrows) overlaid on sagittal T2 images. Left temporal glioblastoma (white arrows) is adjacent to but does not invade the tract. (B) Inferior fronto-occipital fasciculus tractography (yellow arrows) overlaid on axial T1 post-contrast images. Left temporal glioblastoma (white arrows) is adjacent to but does not invade the tract.

FIGURE 12

Tractography: superior longitudinal fasciculus. Sagittal T2-weighted images show glioblastoma centered in the hippocampus and parahippocampal gyrus (white arrows). Overlay of tractography of superior longitudinal fasciculus (yellow arrows) demonstrates sparing of the tract by the tumor.

FIGURE 13

Pseudoprogression in glioblastoma. (A) Immediate pre-radiotherapy: axial T1 post-contrast images show rim enhancing and centrally necrotic left frontoparietal glioblastoma. (B) Eight-week follow up: Immediate post-radiotherapy axial T1 post-contrast images show marked increase in enhancement and necrosis. (C) Dynamic susceptibility-weighted contrast-enhanced perfusion MRI shows mild increase in blood volume along the posterior rim (black arrows). Single voxel proton spectroscopy targeted to the posterior component shows markedly increased lipid peak suggesting tissue necrosis. (D) Three-months follow up: axial T1 post-contrast images show marked decrease in enhancement and necrosis of the treated glioblastoma.