Pretreatment Volume of MRI-Determined White Matter Injury Predicts Neurocognitive Decline After Hippocampal Avoidant Whole-Brain Radiation Therapy for Brain Metastases: Secondary Analysis of NRG Oncology Radiation Therapy Oncology Group 0933.
Journal
Advances in radiation oncology
ISSN: 2452-1094
Titre abrégé: Adv Radiat Oncol
Pays: United States
ID NLM: 101677247
Informations de publication
Date de publication:
Historique:
received:
22
04
2019
revised:
26
06
2019
accepted:
08
07
2019
entrez:
2
11
2019
pubmed:
2
11
2019
medline:
2
11
2019
Statut:
epublish
Résumé
NRG Oncology's RTOG 0933 demonstrated benefits to memory preservation after hippocampal avoidant whole-brain radiation therapy (HA-WBRT), the avoidance of radiation dose to the hippocampus (using intensity modulated radiation planning and delivery techniques) during WBRT, supporting the hypothesis of hippocampal radiosensitivity and associated memory specificity. However, some patients demonstrated cognitive decline, suggesting mechanisms outside hippocampal radiosensitivity play a role. White matter injury (WMI) has been implicated in radiation therapy-induced neurocognitive decline. This secondary analysis explored the relationship between pretreatment WMI and memory after HA-WBRT. Volumetric analysis of metastatic disease burden and disease-unrelated WMI was conducted on the pretreatment magnetic resonance image. Correlational analyses were performed examining the relationship between pretreatment WMI and Hopkins Verbal Learning Test-Revised (HVLT-R) outcomes at baseline and 4 months after HA-WBRT. In the study, 113 patients received HA-WBRT. Of 113 patients, 33 underwent pretreatment and 4-month posttreatment HVLT testing and pretreatment postcontrast volumetric T1 and axial T2/fluid-attenuated inversion recovery magnetic resonance imaging. Correlation was found between larger volumes of pretreatment WMI and decline in HVLT-R recognition (r = 0.54, In patients receiving HA-WBRT for brain metastases, extent of pretreatment WMI predicts posttreatment memory decline, suggesting a mechanism for radiation therapy-induced neurocognitive toxicity independent of hippocampal stem cell radiosensitivity. Stability or improvement in HVLT after HA-WBRT for patients with higher pretreatment intracranial metastatic burden supports the importance of WBRT-induced intracranial control on neurocognition.
Identifiants
pubmed: 31673651
doi: 10.1016/j.adro.2019.07.006
pii: S2452-1094(19)30090-9
pmc: PMC6817553
doi:
Types de publication
Journal Article
Langues
eng
Pagination
579-586Subventions
Organisme : NCI NIH HHS
ID : U10 CA180868
Pays : United States
Organisme : NCI NIH HHS
ID : UG1 CA233163
Pays : United States
Organisme : NCI NIH HHS
ID : U10 CA180822
Pays : United States
Organisme : NCI NIH HHS
ID : UG1 CA233193
Pays : United States
Organisme : NCI NIH HHS
ID : UG1 CA189852
Pays : United States
Informations de copyright
Crown Copyright © 2019 Published by Elsevier Inc. on behalf of American Society for Radiation Oncology.
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