Time- and dose-dependent volume decreases in subcortical grey matter structures of glioma patients after radio(chemo)therapy

Publikation: Beitrag in FachzeitschriftForschungsartikelBeigetragenBegutachtung

Beitragende

Abstract

BACKGROUND AND PURPOSE: Radiotherapy (RT) is an adjuvant treatment option for glioma patients. Side effects include tissue atrophy, which might be a contributing factor to neurocognitive decline after treatment. The goal of this study was to determine potential atrophy of the hippocampus, amygdala, thalamus, putamen, pallidum and caudate nucleus in glioma patients having undergone magnetic resonance imaging (MRI) before and after RT.

MATERIALS AND METHODS: Subcortical volumes were measured using T1-weighted MRI from patients before RT (N = 91) and from longitudinal follow-ups acquired in three-monthly intervals (N = 349). The volumes were normalized to the baseline values, while excluding structures touching the clinical target volume (CTV) or abnormal tissue seen on FLAIR imaging. A multivariate linear effects model was used to determine if time after RT and mean RT dose delivered to the corresponding structures were significant predictors of tissue atrophy.

RESULTS: The hippocampus, amygdala, thalamus, putamen, and pallidum showed significant atrophy after RT as function of both time after RT and mean RT dose delivered to the corresponding structure. Only the caudate showed no dose or time dependant atrophy. Conversely, the hippocampus was the structure with the highest atrophy rate of 5.2 % after one year and assuming a mean dose of 30 Gy.

CONCLUSION: The hippocampus showed the highest atrophy rates followed by the thalamus and the amygdala. The subcortical structures here found to decrease in volume indicative of radiosensitivity should be the focus of future studies investigating the relationship between neurocognitive decline and RT.

Details

OriginalspracheEnglisch
Seiten (von - bis)99-105
Seitenumfang7
FachzeitschriftClinical and translational radiation oncology
Jahrgang36
PublikationsstatusVeröffentlicht - Sept. 2022
Peer-Review-StatusJa

Externe IDs

PubMedCentral PMC9363945
Scopus 85135414186
ORCID /0000-0003-1776-9556/work/171065756

Schlagworte

Bibliotheksschlagworte