Nuclear accidents and acts of terrorism have the potential to expose thousands of people to high-dose total-body iradiation (TBI). Those who survive the acute radiation syndrome are at risk of developing chronic, degenerative radiation-induced injuries [delayed effects of acute radiation (DEARE)] that may negatively affect quality of life. A growing body of literature suggests that the brain may be vulnerable to radiation injury at survivable doses, yet the long-term consequences of high-dose TBI on the adult brain are unclear. Herein we report the occurrence of lesions consistent with cerebrovascular injury, detected by susceptibility-weighted magnetic resonance imaging (MRI), in a cohort of non-human primate [(NHP); rhesus macaque, Macaca mulatta] long-term survivors of high-dose TBI (1.1–8.5 Gy). Animals were monitored longitudinally with brain MRI (approximately once every three years). Susceptibility-weighted images (SWI) were reviewed for hypointensities (cerebral microbleeds and/or focal necrosis). SWI hypointensities were noted in 13% of irradiated NHP; lesions were not observed in control animals. A prior history of exposure was correlated with an increased risk of developing a lesion detectable by MRI (P = 0.003). Twelve of 16 animals had at least one brain lesion present at the time of the first MRI evaluation; a subset of animals (n = 7) developed new lesions during the surveillance period (3.7–11.3 years postirradiation). Lesions occurred with a predilection for white matter and the gray–white matter junction. The majority of animals with lesions had one to three SWI hypointensities, but some animals had multifocal disease (n = 2). Histopathologic evaluation of deceased animals within the cohort (n = 3) revealed malformation of the cerebral vasculature and remodeling of the blood vessel walls. There was no association between comorbid diabetes mellitus or hypertension with SWI lesion status. These data suggest that long-term TBI survivors may be at risk of developing cerebrovascular injury years after irradiation.

核事故和恐怖主义行为有可能使成千上万的人受到高剂量全身辐射 (TBI) 的影响。那些在急性辐射综合征中幸存下来的人有发生慢性、退行性辐射引起的伤害[急性辐射延迟效应 (DEARE)] 的风险，这可能会对生活质量产生负面影响。越来越多的文献表明，在可存活的剂量下，大脑可能容易受到辐射损伤，但高剂量 TBI 对成人大脑的长期影响尚不清楚。在这里，我们报告了一组非人类灵长类动物 [(NHP); 磁共振成像 (MRI) 检测到的与脑血管损伤一致的病变的发生。恒河猴，猕猴] 高剂量 TBI (1.1–8.5 Gy) 的长期幸存者。用脑MRI纵向监测动物（大约每三年一次）。检查磁敏感加权图像 (SWI) 的低信号（脑微出血和/或局灶性坏死）。13% 的辐照 NHP 出现 SWI 低信号；在对照动物中未观察到损伤。既往暴露史与发生 MRI 可检测到的病变的风险增加相关（P= 0.003)。在第一次 MRI 评估时，16 只动物中有 12 只至少存在一个脑损伤；一部分动物（n = 7）在监测期间（照射后 3.7-11.3 年）出现了新的病变。病变好发于白质和灰白质交界处。大多数有病变的动物有 1 到 3 次 SWI 低信号，但有些动物有多灶性疾病 (n = 2)。队列中已故动物（n = 3）的组织病理学评估显示脑血管系统畸形和血管壁重塑。合并糖尿病或高血压与 SWI 病变状态之间没有关联。这些数据表明，长期 TBI 幸存者可能在照射后数年有发生脑血管损伤的风险。