T2 mapping of the peritumoral infiltration zone of glioblastoma and anaplastic astrocytoma

Abstract

Purpose: To characterise peritumoral zones in glioblastoma and anaplastic astrocytoma evaluating T2 values using T2 mapping sequences.

Materials and methods: In this study, 41 patients with histopathologically confirmed World Health Organization high grade gliomas and preoperative magnetic resonance imaging examinations were retrospectively identified and enrolled. High grade gliomas were differentiated: (a) by grade, glioblastoma versus anaplastic astrocytoma; and (b) by isocitrate dehydrogenase mutational state, mutated versus wildtype. T2 map relaxation times were assessed from the tumour centre to peritumoral zones by means of a region of interest and calculated pixelwise by using a fit model.

Results: Significant differences between T2 values evaluated from the tumour centre to the peritumoral zone were found between glioblastoma and anaplastic astrocytoma, showing a higher decrease in signal intensity (T2 value) from tumour centre to periphery for glioblastoma (P = 0.0049 - fit-model: glioblastoma -25.02± 19.89 (-54-10); anaplastic astrocytoma -5.57±22.94 (-51-47)). Similar results were found when the cohort was subdivided by their isocitrate dehydrogenase profile, showing an increased drawdown from tumour centre to periphery for wildtype in comparison to mutated isocitrate dehydrogenase (P = 0.0430 - fit model: isocitrate dehydrogenase wildtype -10.35±16.20 (-51) - 0; isocitrate dehydrogenase mutated 12.14±21.24 (-15-47)). A strong statistical proof for both subgroup analyses (P = 0.9987 - glioblastoma R² 0.93±0.08; anaplastic astrocytoma R² 0.94±0.15) was found.

Conclusion: Peritumoral T2 mapping relaxation time tissue behaviour of glioblastoma differs from anaplastic astrocytoma. Significant differences in T2 values, using T2 mapping relaxation time, were found between glioblastoma and anaplastic astrocytoma, capturing the tumour centre to the peritumoral zone. A similar curve progression from tumour centre to peritumoral zone was found for isocitrate dehydrogenase wildtype high grade gliomas in comparison to isocitrate dehydrogenase mutated high grade gliomas. This finding is in accordance with the biologically more aggressive behaviour of isocitrate dehydrogenase wildtype in comparison to isocitrate dehydrogenase mutated high grade gliomas. These results emphasize the potential of mapping techniques to reflect the tissue composition of high grade gliomas.

Keywords: Glioblastoma; MRI (magnetic resonance imaging); T2 mapping; glioma; multiparametric imaging.

Figure 1.

Region of interest (ROI) placement in the raw T2 map in accordance with the fluid-attended inversion recovery (FLAIR) sequences. The slice with the largest diameter of peritumoral T2-weighted/FLAIR hyperintensity was chosen, the anatomical centre of the tumour was delineated. Another ROI was placed in the healthy- appearing white matter of the contralateral lobe using an image processing program to ensure reliability of the measurements. The spatial T2 value distribution across the tumour radius was measured at four different locations from the tumour centre to the outer infiltration zone by the placement of three further ROIs.

Figure 2.

Patient, 49 years old, with a non-contrast enhanced (CE) T1-weighted heterogeneous-appearing anaplastic astrocytoma in the left frontal lobe (a) without a significant positive CE in the T1 CE sequence (b). (c) Unilateral surrounding oedema in the fluid-attended inversion recovery sequence. (d) The original raw T2 map. The diagram shows the curve progression from tumour centre to periphery calculated by means of a fit model. As reflected by 15.786x² the curve’s opening angle is positive.

Figure 3.

Patient, 63 years old, with a non-contrast enhanced (CE) T1-weighted heterogeneous glioblastoma in the right temporal lobe (a) and a significant positive CE in the T1 CE sequence (b). (c) A large perifocal oedema in the fluid-attended inversion recovery sequence. (d) The original raw T2 map. The diagram shows the curve progression from tumour centre to periphery calculated by means of a fit model. While the y-axis describes the median T2 values originating out of the T2 map; the x-axis shows the different regions of interest (ROIs) which were placed as follows: 1 – ROI 0: inside the tumour centre; 2 – ROI 1: 0–5 mm of the peritumoral oedema/zone; 3 – ROI 2: 5–10 mm of the peritumoral oedema/zone; 4 – ROI 3: 10–15 mm of the peritumoral oedema/zone and 5 – ROI within healthy brain parenchyma on the contralateral side. As reflected by −25.571x² the curve’s opening angle is negative.

Figure 4.

Patient, 63 years old, with a non-contrast enhanced (CE) T1-weighted homogeneous-appearing anaplastic astrocytoma isocitrate dehydrogenase wildtype in the left parietal lobe (a) with marginal CE in the T1 CE sequence (b). (c) Surrounding oedema in the fluid-attended inversion recovery sequence. (d) The original raw T2 map. The diagram shows the curve progression from tumour centre to periphery calculated by means of a fit model. As reflected by −21.071x² the curve’s opening angle is negative.

Figure 5.

(a) Significant difference between the curve progression for the medians, when the cohort is divided into anaplastic astrocytoma and (b) illustrated with R2 a strong statistical validity for the analyses, when the cohort is subdivided by World Health Organization grade; (c) Significant difference in between curve progression for the medians, when the cohort is divided by isocitrate dehydrogenase (IDH) mutational state; (d) illustrated with R2 a strong statistical validity for the analyses, when the cohort is subdivided into IDH mutated and IDH wildtype high grade glioma.