Department Medical, Surgical, Health Sciences, University of Trieste, Cattinara Hospital, Strada di Fiume, 447, 34149 Trieste, Italy.
Neurological Clinic, Department of Internal Medicine and Neurology, University of Trieste, Cattinara Hospital, Strada di Fiume, 447, 34149 Trieste, Italy.
Int J Mol Sci. 2020 Sep 5;21(18):6506. doi: 10.3390/ijms21186506.
We studied 114 primitive cerebral neoplasia, that were surgically treated, and underwent radiotherapy (RT), and compared their results to those obtained by 190 patients diagnosed with subcortical vascular dementia (sVAD). Patients with any form of primitive cerebral neoplasia underwent whole-brain radiotherapy. All the tumor patients had regional field partial brain RT, which encompassed each tumor, with an average margin of 2.6 cm from the initial target tumor volume. We observed in our patients who have been exposed to a higher dose of RT (30-65 Gy) a cognitive and behavior decline similar to that observed in sVAD, with the frontal dysexecutive syndrome, apathy, and gait alterations, but with a more rapid onset and with an overwhelming effect. Multiple mechanisms are likely to be involved in radiation-induced cognitive impairment. The active site of RT brain damage is the white matter areas, particularly the internal capsule, basal ganglia, caudate, hippocampus, and subventricular zone. In all cases, radiation damage inside the brain mainly focuses on the cortical-subcortical frontal loops, which integrate and process the flow of information from the cortical areas, where executive functions are "elaborated" and prepared, towards the thalamus, subthalamus, and cerebellum, where they are continuously refined and executed. The active mechanisms that RT drives are similar to those observed in cerebral small vessel disease (SVD), leading to sVAD. The RT's primary targets, outside the tumor mass, are the blood-brain barrier (BBB), the small vessels, and putative mechanisms that can be taken into account are oxidative stress and neuro-inflammation, strongly associated with the alteration of NMDA receptor subunit composition.
我们研究了 114 例接受手术治疗和放射治疗（RT）的原始脑肿瘤患者，并将其结果与 190 例皮质下血管性痴呆（sVAD）患者进行了比较。所有患有原始脑肿瘤的患者均接受全脑放疗。所有肿瘤患者均接受区域局部脑 RT，包括每个肿瘤，初始靶肿瘤体积的平均边缘为 2.6 厘米。我们观察到，在接受更高剂量 RT（30-65Gy）的患者中，出现了类似 sVAD 的认知和行为下降，表现为额叶执行功能障碍、淡漠和步态改变，但发病更快，影响更大。多种机制可能参与了放射性认知障碍。RT 脑损伤的活性部位是白质区域，特别是内囊、基底节、尾状核、海马体和侧脑室周围区。在所有情况下，大脑内的辐射损伤主要集中在皮质下额状环路，该环路整合和处理来自皮质区域的信息流，执行功能在那里“详细制定”和准备，然后流向丘脑、下丘脑和小脑，在那里不断完善和执行。RT 驱动的活跃机制与脑小血管疾病（SVD）中观察到的机制相似，导致 sVAD。RT 的主要靶标是肿瘤组织外的血脑屏障（BBB）、小血管，以及可以考虑的潜在机制是氧化应激和神经炎症，它们与 NMDA 受体亚基组成的改变密切相关。
