Abstract

The aim of this study was to assess the feasibility of sparing contralateral hippocampus during partial brain radiotherapy in high grade gliomas. 20 previously treated patients were replanned to 60 Gy in 30 fractions with sparing intensity-modulated radiotherapy (IMRT) and volumetric modulated arctherapy (VMAT) using the following planning objectives: 100 % of PTV covered by 95% isodose without violating organs at risk (OAR) and hot spot dose constraints. For each, standard intensity-modulated radiotherapy (IMRT) plans were generated, as well as sparing IMRT and VMAT plans which spared contralateral (hemispheric cases) hippocampus. When the three plans were compared, there was equivalent PTV coverage, homogeneity, and conformality. Sparing IMRT significantly reduced maximum, mean, V20, V30 and V40 hippocampus doses compared with standart IMRT and VMAT (p < 0.05). VMAT significantly reduced maximum left lens and mean eye doses compared with standart IMRT and sparing IMRT (p < 0.05). Brainstem, chiasm, left and right optic nerves, right eyes and lens doses were similar. VMAT significantly reduced monitor units compared with standart IMRT and sparing IMRT (p < 0.05). It is possible to spare contralateral hippocampus during PBRT for high grade gliomas using IMRT. This approach may reduce late cognitive sequelae of cranial radiotherapy.

Highlights

  • The prognosis of the patients with high grade gliomas had improved with the combination of radiotherapy and chemotherapy

  • All intensity-modulated radiotherapy (IMRT) and volumetric modulated arctherapy (VMAT) plans were able to meet the constraints placed on the organs at risk (OAR), as well as PTV

  • The PTV coverage, conformality, and homogeneity were equivalent with VMAT and IMRT

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Summary

Introduction

The prognosis of the patients with high grade gliomas had improved with the combination of radiotherapy and chemotherapy. Side effects are more frequent in children after partial brain radiotherapy (PBRT) These side effects include cognitive dysfunctions, endocrine dysfunctions, visual loss, hearing loss, myelopathy, vasculopathies and the induction of secondary tumours including gliomas (high and low grade), sarcomas and meningiomas (Merchant et al 2005; Nandagopal et al 2008; Kondoh et al 2003; Douw et al 2009; Crossen et al.1994; Kortmann et al 2003) Clear dose–volume relationships exist for many of these late adverse events. No clear dose–response relationships have been proven for cognitive dysfunction and secondary tumour induction (Merchant et al 2005; Marks et al 1981) These side effects are seen less often in elderly patients (Douw et al 2009).

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