"Vanishing" glioblastoma: A case report and review of the literature

Abstract

Contrast enhancement resolution induced by corticosteroids is a phenomenon primarily associated with primary central nervous system lymphoma, while malignant brain gliomas usually maintain a consistent radiological appearance during systemic steroid treatment. Although rare, a few primary and metastatic intracranial lesions have shown similar radiographic changes following corticosteroid therapy. In the case of glioblastomas, corticosteroid therapy is commonly used to alleviate pressure effects from peritumoral edema, but its impact on contrast enhancement is not well-established. A few reported cases in the literature describe reduced contrast enhancement in glioblastomas after corticosteroid treatment. We present a case of corticosteroid-induced regression on imaging of glioblastoma evaluated at our institutionwith the intention to explore the pathogenesis of this response and discuss the therapeutic and prognostic implications of this discovery.

Keywords: Corticosteroids; MRI; Vanishing glioblastoma.

Fig. 1

MRI investigations performed at our institution following tumor protocol comprising fluid attenuated inversion recovery (FLAIR) images (first row), diffusion weighted images (second row), apparent diffusion coefficient (third row), 3D fast spoiled gradient echo (FSPGR) post-contrastographic T1-weighted images (fourth row), dynamic susceptibility contrast perfusion images (fifth row). Initial magnetic resonance imaging on admission (A-E) 2 lesions in the right peritrigonal and temporo-parietal regions characterized by central necrotic areas, restricted diffusion (B and C), and post-contrastographic enhancement (D). Increased intra-lesional rCBV at DSC perfusion due to neoangiogenesis (E). Extensive perilesional edema with compressive effects on the right lateral ventricle and a 13 mm leftward midline shift (A). Brain MR scans after corticosteroid therapy (F-X). A follow-up scan at three weeks post biopsy and initiation of corticosteroid therapy (F-L) revealed a notable decrease in mass effect and contrast enhancement in the surgically untouched pathological tissue of the right peritrigonal region. Elevated perfusion parameters still present (L), with marked reduction of the vasogenic edema and consequently of the compressive effect on the ventricles, leading to a re-expansion of the ventricular trigone and a realignment of the midline (F). Follow-up MR 5 weeks after initiating corticosteroid treatment (N-R) showed a slight further decrease in the post-contrastographic enhancement at the periphery of the remaining pathological tissue (Q), with the other radiological findings remaining stable. Follow-up MR 9 weeks after tapering DEX down to its minimum dosage (2mg a day) and starting adjuvant radio-chemotherapy (T-X) showed tumor recurrence, evident by an increase in both size and extent of post-contrast enhancement (W). Increased perilesional edema (T) with a 5 mm left midline shift. Pathological increase in intralesional rCBV at DSC perfusion (X).

Fig. 2

Glioblastoma characterization: at low power the tumor mass resulted constituted by dense cellular areas (arrow) mixed with prevalent hypoxic necrotic zones (asterisk) showing residual thrombotic vessels (Arrowhead) (A: H&E 100x enlargement). The tumor is histologically characterized by numerous multinucleated giant cells in a background of small astrocytes like cells. Atypical mitotic figures are frequent (arrowhead) (B: H&E 400x): GFAP immunostaining highlights the fusiform structure of the tumor cells (C: GFAP expression 400x). Ki67 immunostaining shows a high proliferative feature sustained by both giant and small cell component (D: Ki67 expression 400x).