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Glioblastoma (GBM)

Last Updated: March 27, 2020

Figure 1: The avid peripheral enhancement and central necrosis seen in this lesion on post-contrast T1WI (top row left) is typical of a glioblastoma. Infiltrative FLAIR (top row right) hyperintensity extending beyond the enhancing margins usually represent a combination of edema and nonenhancing infiltrative tumor. Areas of low signal intensity in regions of known tumor on ADC (bottom row left) usually indicate hypercellularity. Hemorrhagic foci are also not uncommonly seen on GRE or SWI (bottom row right) as in this patient's GBM.

Basic Description

  • Malignant, rapidly-enlarging astrocytic tumor with microvascular proliferation and necrosis
  • Most common primary intracranial neoplasm

Pathology

  • WHO grade IV
  • Necrosis and microvascular proliferation are characteristic features
  • Develops de novo (primary) or from malignant dedifferentiation of anaplastic astrocytomas (secondary)
    • Uncommonly secondary to prior radiation
    • Primary GBM more aggressive, more common in elderly patients
    • Secondary GBM more common in younger patients
  • Associated with NF-1, Turcot, Li-Fraumeni, and Maffuci syndromes, and Ollier disease

Clinical Features

  • All ages affected (45-75 years most common)
  • Slight male gender predilection
  • Median survival <1 year
    • Better prognosis with younger age, greater extent of resection, and MGMT-positive genetics
  • Presenting symptoms dependent on tumor location

    • Seizures, focal neurologic deficits
  • Treatment: tumor debulking, radiotherapy (XRT), chemotherapy (temozolomide, antiangiogenesis agents)

Imaging

  • General
    • Poorly defined, infiltrating supratentorial white matter mass
      • Neoplastic cells extend beyond areas of signal abnormality
      • Frontal, temporal, and parietal lobes most common
      • Brainstem and cerebellum more common in children
    • Usually solitary but may be multifocal (synchronous tumors) in up to 20% of cases
    • Neovascularity and necrosis are common features
    • Thick, irregularly-enhancing rind with central necrosis
    • Cysts, hemorrhage, fluid-debris levels, and vascular flow voids are common features
    • Commonly spreads along white matter tracts and crosses midline via the corpus callosum, anterior and posterior commissures (“butterfly” glioma)
    • Occasional CSF dissemination
  • CT

    • Irregular hypo- to isodense mass with central hypodensity (necrosis)
    • Surrounding vasogenic edema/tumor with mass effect on adjacent structures
    • Radiodense hemorrhage may be present, calcification rare
    • Irregular, heterogeneous rind of enhancement on contrast-enhanced CT
  • MRI

    • T1WI: irregular, hypointense white matter mass; areas of hyperintensity may represent subacute hemorrhage
    • T2WI: heterogeneously hyperintense; surrounding vasogenic edema and tumor infiltration; presence of flow-voids suggests neovascularity
    • FLAIR: heterogeneously hyperintense
    • T2*GRE: susceptibility artifact related to blood products/hemorrhage
    • DWI: diffusion restriction reflecting hypercellularity is common in solid tumor components
    • T1WI+C: thick, irregular rind of peripheral enhancement; enhancement may be ring, nodular, homogenous, or patchy
    • MR spectroscopy (MRS)/MR perfusion: decreased NAA and myoinositol, increased Cho, lipid/lactate peak (1.3 ppm) indicating anaerobic metabolism of necrosis, increased relative cerebral blood volume (rCBV)) compared with lower-grade astrocytomas
    • Diffusion tensor imaging (DTI) tractography and functional MRI (fMRI) may assist in surgical planning

Imaging Recommendations

  • MRI with contrast; MRS, MR perfusion, DTI and fMRI are often useful adjuncts

For more information, please see the corresponding chapter in Radiopaedia.

Contributor: Rachel Seltman, MD

DOI: https://doi.org/10.18791/nsatlas.v1.03.01.18

References

Arevalo-Perez J, Peck KK, Young RJ. Dynamic contrast-enhanced perfusion MRI and diffusion-weighted imaging in grading of gliomas. J Neuroimaging. 2015;25:792–798.

Blasel S, Zagorcic A, Jurcoane A, et al. Perfusion MRI in the evaluation of suspected glioblastoma recurrence. J Neuroimaging. 2016;26:116-123.

Calli C, et al. Perfusion and diffusion MR imaging in enhancing malignant cerebral tumors. Eur J Radiol. 2006;58:394-403.

Di Costanzo A, et al. Spectroscopic, diffusion and perfusion magnetic resonance imaging at 3.0 Tesla in the delineation of glioblastomas: preliminary results. J Exp Clin Cancer Res. 2006;25:383-390.

Ideguchi M, et al. MRI findings and pathological features in early-stage glioblastoma. J Neurooncol. 2015;123:289-297.

Koukourakis GV, et al. Temozolomide with radiation therapy in high grade brain gliomas: pharmaceuticals considerations and efficacy; a review article. Molecules. 2009;14:1561-1577.

Lacroix M, et al. A multivariate analysis of 416 patients with glioblastoma multiforme: prognosis, extent of resection, and survival. J Neurosurg. 2001;95:190-198.

Louis DN, Ohgaki H, Wiestler OD, Cavenee WK, Burger PC, Jouvet A, et al. The 2007 WHO classification of tumours of the central nervous system. Acta Neuropathol. 2007;114:547.

Osborn, AG, Salzman KL, Jhaveri MD. Diagnostic Imaging (3rd ed). Philadelphia, PA: Elsevier, 2016.

Miletic H, et al. Anti-VEGF therapies for malignant glioma: treatment effects and escape mechanisms. Expert Opin Ther Targets. 2009;13:455-468.

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