Okoukoni Catherine, McTyre Emory R, Ayala Peacock Diandra N, Peiffer Ann M, Strowd Roy, Cramer Christina, Hinson William H, Rapp Steve, Metheny-Barlow Linda, Shaw Edward G, Chan Michael D
Department of Radiation Oncology, Wake Forest School of Medicine, Winston-Salem, North Carolina.
Department of Biomedical Engineering, Wake Forest School of Medicine, Winston-Salem, North Carolina.
Adv Radiat Oncol. 2017 Aug 30;2(4):624-629. doi: 10.1016/j.adro.2017.08.013. eCollection 2017 Oct-Dec.
Radiation-induced cognitive decline is relatively common after treatment for primary and metastatic brain tumors; however, identifying dosimetric parameters that are predictive of radiation-induced cognitive decline is difficult due to the heterogeneity of patient characteristics. The memory function is especially susceptible to radiation effects after treatment. The objective of this study is to correlate volumetric radiation doses received by critical neuroanatomic structures to post-radiation therapy (RT) memory impairment.
Between 2008 and 2011, 53 patients with primary brain malignancies were treated with conventionally fractionated RT in prospectively accrued clinical trials performed at our institution. Dose-volume histogram analysis was performed for the hippocampus, parahippocampus, amygdala, and fusiform gyrus. Hopkins Verbal Learning Test-Revised scores were obtained at least 6 months after RT. Impairment was defined as an immediate recall score ≤15. For each anatomic region, serial regression was performed to correlate volume receiving a given dose (V) with memory impairment.
Hippocampal V to V significantly predicted post-RT memory impairment ( < .05). Within this range, the hippocampal V was the most significant predictor ( = .004). Hippocampal V of 0%, 25%, and 50% was associated with tumor-induced impairment rates of 14.9% (95% confidence interval [CI], 7.2%-28.7%), 45.9% (95% CI, 24.7%-68.6%), and 80.6% (95% CI, 39.2%-96.4%), respectively.
The hippocampal V is a significant predictor for impairment, and a limiting dose below 55 Gy may minimize radiation-induced cognitive impairment.
在原发性和转移性脑肿瘤治疗后,辐射诱发的认知衰退相对常见;然而,由于患者特征的异质性,识别可预测辐射诱发认知衰退的剂量学参数具有难度。记忆功能在治疗后尤其易受辐射影响。本研究的目的是将关键神经解剖结构所接受的体积辐射剂量与放射治疗(RT)后的记忆损害相关联。
2008年至2011年期间,在我们机构进行的前瞻性临床研究中,53例原发性脑恶性肿瘤患者接受了常规分割放疗。对海马体、海马旁回、杏仁核和梭状回进行剂量体积直方图分析。在放疗后至少6个月获得霍普金斯词语学习测验修订版分数。损害定义为即时回忆分数≤15。对于每个解剖区域,进行系列回归以将接受给定剂量(V)的体积与记忆损害相关联。
海马体V至V显著预测放疗后的记忆损害(P<0.05)。在此范围内,海马体V是最显著的预测因子(P = 0.004)。海马体V为0%、25%和50%时,分别与肿瘤诱发的损害率14.9%(95%置信区间[CI],7.2%-28.7%)、45.9%(95%CI,24.7%-68.6%)和80.6%(95%CI,39.2%-96.4%)相关。
海马体V是损害的显著预测因子,低于55 Gy的限制剂量可能会使辐射诱发的认知损害最小化。