Current Clinical Brain Tumor Imaging

Abstract

Neuroimaging plays an ever evolving role in the diagnosis, treatment planning, and post-therapy assessment of brain tumors. This review provides an overview of current magnetic resonance imaging (MRI) methods routinely employed in the care of the brain tumor patient. Specifically, we focus on advanced techniques including diffusion, perfusion, spectroscopy, tractography, and functional MRI as they pertain to noninvasive characterization of brain tumors and pretreatment evaluation. The utility of both structural and physiological MRI in the post-therapeutic brain evaluation is also reviewed with special attention to the challenges presented by pseudoprogression and pseudoresponse.

Keywords: Brain tumors; Diffusion MRI; Diffusion tensor imaging; Neuroimaging; Perfusion MRI; Proton magnetic resonance spectroscopy; fMRI.

FIGURE 1.

Diffuse astrocytic tumors. Presurgical MRI of 3 patients included axial T1 postcontrast A, E, I, axial FLAIR B, F, J, axial DWI C, G, K, and axial ASL perfusion D, H, L sequences. MRI of a 52-yr-old man who presented with headaches and word-finding difficulty shows a left middle temporal nonenhancing A, FLAIR hyperintense B, mass without reduced diffusion C, or elevated cerebral blood flow (D) found to be a diffuse astrocytoma (WHO grade II). MRI of a 27-yr-old man who presented with seizure shows a right middle frontal faintly enhancing E, FLAIR hyperintense (F) mass without reduced diffusion G, and increased cerebral blood flow (H) found to be an anaplastic astrocytoma (WHO grade III). MRI of a 76-yr-old man who presented with seizure shows a left anterior temporal heterogeneously enhancing (I) mass with surrounding FLAIR signal hyperintensity J, foci of reduced diffusion K, and elevated cerebral blood flow (L) found to be a glioblastoma (WHO grade IV).

FIGURE 2.

Primary CNS lymphoma. A 33-yr-old woman before (A-D) and after (E-H) steroid therapy. Pretreatment MRI shows extensive FLAIR signal abnormality centered in the left basal ganglia and extending throughout the left hemispheric white matter (A) as well as contrast enhancement (B) associated with reduced diffusion (C, DWI; D, ADC). MRI obtained 14 days after steroid therapy demonstrates a marked reduction in FLAIR signal abnormality E, contrast enhancement F, and reduced diffusion (G, DWI; H, ADC).

FIGURE 3.

Intracranial metastases. Pretreatment MRI of 3 patients included axial T1 precontrast A, E, I, axial FLAIR B, F, J, axial SWI C, G, K, and axial T1 postcontrast D, H, L sequences. MRI of a 50-yr-old woman with breast cancer shows bilateral frontal T1 hypointense (A) masses with surrounding edema B, without susceptibility C, and with peripheral enhancement (D) consistent with multiple nonhemorrhagic metastases. MRI of a 63-yr-old man with lung cancer shows a left parietal mass with intrinsic T1 signal hyperintensity E, minimal surrounding edema F, susceptibility on SWI G, with peripheral enhancement (H) consistent with a hemorrhagic metastasis. Given the susceptibility on SWI, the intrinsic high T1 signal represents blood products in this case. MRI of a 58-yr-old woman with melanoma shows a ventral pontine mass with intrinsic T1 signal hyperintensity I, minimal edema J, minimal peripheral susceptibility K, and no significant enhancement (L) consistent with a melanoma metastasis. Given the relative lack of susceptibility on SWI, the intrinsic high T1 signal represents melanin in this case.

FIGURE 4.

SWI in oligodendroglioma. A 40-yr-old man who presented with loss of consciousness. Presurgical imaging included axial FLAIR A, axial T1 postcontrast B, axial SWI C, and SWI phase (D) sequences as well as axial noncontrast CT E. MRI demonstrates a FLAIR hyperintense A, nonenhancing B, infiltrative mass within the right cingulate gyrus found to represent an oligodendroglioma. A punctate focus of susceptibility (C; white arrow) with high signal intensity on filtered phase images (D; white arrow) corresponds to calcification on CT (E; white arrow).

FIGURE 5.

MRS in glioblastoma. A 65-yr-old man with glioblastoma. Presurgical MRI included axial FLAIR A, coronal FLAIR B, and axial T1 postcontrast (C) sequences as well as multivoxel spectroscopy with Cho/NAA ratios overlaid on T1 postcontrast images D. A dominant, peripherally enhancing (C) right parietal mass with surrounding edema (A) shows an elevated Cho/NAA ratio D. Another subtle focus of FLAIR signal hyperintensity A, B; (white arrows) with minimal enhancement C is also shown to have an abnormally elevated Cho/NAA ratio (D, white arrow) consistent with multifocal glioma.

FIGURE 6.

DTI tractography in glioblastoma. A 58-yr-old woman with glioblastoma. Presurgical imaging included axial postcontrast T1 sequence with corticospinal tract DTI overlay A-C and optic radiation DTI overlay D. A large right parietotemporal mass splays the corticospinal tract superiorly (A; white arrowheads) and anteriorly displaces the descending tracts (B, C; white arrowheads). The optic radiations are also displaced laterally by tumor (D; black arrowheads).

FIGURE 7.

DTI tractography in recurrent glioblastoma. A 48-yr-old man with glioblastoma before surgical resection (A-D) and 6 mo after completion of chemoradiotherapy E-H. Presurgical axial postcontrast T1 with right corticospinal tract DTI overlay A, B shows a peripherally enhancing right insular tumor separate from the corticospinal fibers (A, B; white arrowheads) and axial FLAIR shows adjacent infiltrative edema C. Sagittal T2 images without and with corticospinal tract DTI overlay show normal signal within the midbrain in the region of the descending corticospinal fibers D. Following chemoradiotherapy, axial postcontrast T1 with right corticospinal tract DTI overlay shows peripherally enhancing recurrent tumor inseparable from the descending corticospinal fibers (E, F; white arrowheads) and increased infiltrative edema along the descending tracts on axial FLAIR G. Sagittal T2 images without and with corticospinal tract DTI overlay now shows abnormal signal within the midbrain in the region of the descending corticospinal fibers (H; black arrowheads).

FIGURE 8.

Task-based fMRI in diffuse astrocytoma. A 22-yr-old man with diffuse astrocytoma. Axial FLAIR (A) and postcontrast T1 (B) MRI shows a nonenhancing right posterior frontal mass. DTI overlay of the corticospinal tract on postcontrast T1 images (B) shows medial displacement of the white matter fibers. Axial (C) and volume rendered (D) BOLD fMRI shows sensorimotor activation lateralized to the right peri-Rolandic cortex in response to left finger tapping with the anterior aspect of sensorimotor activation overlapping with the posterior margin of the mass. Left peri-Rolandic cortical activation is also seen in response to right finger tapping.

FIGURE 9.

Progressive disease. A 38-yr-old man with glioblastoma. Axial postcontrast T1 (A-D) and FLAIR (E-H) images demonstrate a left temporal resection cavity with minimal peripheral residual enhancement (A) and surrounding nonenhancing FLAIR signal abnormality E. At completion of chemoradiotherapy, increased enhancement is seen about the resection cavity, which is decreasing in size (B) and is associated with decreased surrounding FLAIR signal abnormality including decreased mass effect upon the left lateral ventricle F. MRI performed 2 mo later demonstrates increased enhancement (C) and increased ill-defined, mass-like, nonenhancing FLAIR signal abnormality G. Follow-up MRI performed 1 mo later shows continued increase in enhancing mass (D) and extent of expansile, ill-defined, nonenhancing FLAIR signal abnormality (H) consistent with progressive disease.

FIGURE 10.

Pseudoprogression. An 84-yr-old man with glioblastoma. Axial postcontrast T1 (A-C) and FLAIR (D-F) images at levels superior to and at a right parietal resection cavity demonstrate gross total resection of enhancing tumor (A) with minimal surrounding nonenhancing white matter signal abnormality D. At completion of chemoradiotherapy, new pericavity enhancement is seen (B) and extensive edema has developed E. Follow-up imaging 1 mo later without alteration of therapy demonstrates decreased enhancement (C) and edema (F) consistent with pseudoprogression.

FIGURE 11.

Pseudoresponse. A 33-yr-old man with glioblastoma. Axial postcontrast T1 (A-C) and FLAIR (D-F) images demonstrate a left parietal mass with nodular enhancement and infiltrative edema prior to initiation of antiangiogenic therapy A, D. Four weeks after antiangiogenic therapy, a marked decrease in contrast enhancement and edema is seen B, E. Twelve weeks after antiangiogenic therapy, multifocal disease progression is seen in the right periatrial white matter, genu of the corpus callosum, and about the resection cavity C, F.

FIGURE 12.

SMART syndrome. A 44-yr-old woman with previously resected oligodendroglioma treated with adjuvant radiotherapy presented with headaches and aphasia. Coronal postcontrast T1 MRI at presentation demonstrates left temporal gyral enhancement (A; white arrows). Follow-up MRI at 4 wk with resolution of symptoms demonstrates resolution of left temporal gyral enhancement B.

FIGURE 13.

Radiation-associated neoplasm and microhemorrhage. A 52-yr-old man with history of unknown brain tumor treated with irradiation 30 yr prior to presentation. Axial FLAIR (A) and axial (B) and coronal (C) postcontrast T1 MR images demonstrate enhancing extra-axial masses in the right and left frontal convexities with mild underlying parenchymal edema compatible with radiation-associated meningiomas. Axial SWI (D-F) images demonstrate multiple scattered foci of susceptibility compatible with postradiation microvascular injury.