Fig. 1

Glioblastoma is a tumor of a high degree of malignancy, a heterogeneous structure with central necrosis, rapid infiltrative growth, perifocal edema and the worst prognosis among all gliomas.


Fig. 2

Glioblastoma multiforme, may develop from a diffuse astrocytoma or an anaplastic astrocytoma but more commonly presents de novo without evidence of a less malignant precursor.

Histologically, this tumor is an anaplastic, cellular glioma composed of poorly differentiated, often pleomorphic astrocytic tumor cells with marked nuclear atypia and brisk mitotic activity.

Secondary glioblastoma is the term used to describe a glioblastoma developed from a diffuse astrocytoma or an anaplastic astrocytoma.

Glioblastoma is the most frequent brain tumor and accounts for 12–15% of all brain tumors and 50–60% of all astrocytic tumors.

The peak incidence occurs between the ages of 45 and 70 years. Glioblastoma primarily affects the cerebral hemispheres. Two histologic variants include giant cell glioblastoma and gliosarcoma.

Glioblastomas are seen in mismatch repair–associated Turcot syndrome type 1. Glioblastomas are among the most aggressively malignant human neoplasms, with a mean total length of disease in patients with primary glioblastoma of less than 1 year.

The usual appearance of a GBM or anaplastic astrocytoma on MRI is that of a contrast-enhancing lesion causing mass effect.

On CT and MRI has the appearance of a region with a central necrosis zone, formed by rapid growth of the tumor (mitotic activity and metabolic needs exceed proliferative angiogenesis).

Thus, the cells of the outer part of the tumor infiltrate the surrounding tissues, and the cells of the central part are consumed again by emerging ones.

External borders of the tumor can not be determined, since its edges extend far from the visible areas.

The visible edges of the tumor have → the MR signal and → the density of the brain substance, and the central part of the tumor ↓ by T1, ↑ by T2 and Flair, by CT ↓. The periphery of the tumor is surrounded by perifocal vasogenic edema.

It is often very difficult to distinguish a GBM from a contrast-enhancing anaplastic astrocytoma lesion by MRI alone. GBMs characteristically spread along the white matter tracts of the corpus callosum to invade the contralateral hemisphere (“butterfly” appearance).

Up to 95% of GBMs demonstrate contrast enhancement, and they are usually associated with high signal on T2-weighted imaging. Anaplastic astrocytomas also exhibit heterogeneous signal intensity on noncontrast MRI, but the frequency of contrast enhancement is less than in GBM.

Large GBM lesions may demonstrate prominent areas of central necrosis with peritumoral edema, while others may show metastasis.

The author of the article: radiologist, Ph.D. Vlasov Evgeniy Alexandrovich

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