Department of Radiation Oncology & Molecular Radiation Sciences, Johns Hopkins Medicine, 401 North Broadway, Suite 1440, Baltimore, MD, 21287, USA.
Department of Radiation Oncology-National Capitol Region, Johns Hopkins Medicine, 6420 Rockledge Drive Suite 1200, Bethesda, MD, 20817, USA.
Curr Treat Options Oncol. 2023 Jul;24(7):880-891. doi: 10.1007/s11864-023-01078-z. Epub 2023 May 5.
Cranial radiation is ubiquitous in the treatment of primary malignant and benign brain tumors as well as brain metastases. Improvement in radiotherapy targeting and delivery has led to prolongation of survival outcomes. As long-term survivorship improves, we also focus on prevention of permanent side effects of radiation and mitigating the impact when they do occur. Such chronic treatment-related morbidity is a major concern with significant negative impact on patient's and caregiver's respective quality of life. The actual mechanisms responsible for radiation-induced brain injury remain incompletely understood. Multiple interventions have been introduced to potentially prevent, minimize, or reverse the cognitive deterioration. Hippocampal-sparing intensity modulated radiotherapy and memantine represent effective interventions to avoid damage to regions of adult neurogenesis. Radiation necrosis frequently develops in the high radiation dose region encompassing the tumor and surrounding normal tissue. The radiographic findings in addition to the clinical course of the patients' symptoms are taken into consideration to differentiate between tissue necrosis and tumor recurrence. Radiation-induced neuroendocrine dysfunction becomes more pronounced when the hypothalamo-pituitary (HP) axis is included in the radiation treatment field. Baseline and post-treatment evaluation of hormonal profile is warranted. Radiation-induced injury of the cataract and optic system can develop when these structures receive an amount of radiation that exceeds their tolerance. Special attention should always be paid to avoid irradiation of these sensitive structures, if possible, or minimize their dose to the lowest limit.
颅脑放疗在原发性恶性和良性脑肿瘤以及脑转移瘤的治疗中无处不在。放疗靶向和递送的改进导致了生存结果的延长。随着长期生存的改善，我们还关注预防辐射的永久性副作用，并在发生时减轻其影响。这种慢性治疗相关发病率是一个主要问题，对患者和护理人员的生活质量都有重大负面影响。导致放射性脑损伤的确切机制仍不完全清楚。已经引入了多种干预措施来预防、最小化或逆转认知功能恶化。海马保护调强放疗和盐酸美金刚是避免成年神经发生区域损伤的有效干预措施。在包含肿瘤和周围正常组织的高剂量区域经常发生放射性坏死。除了患者症状的临床过程外，还考虑放射影像学表现来区分组织坏死和肿瘤复发。当下丘脑-垂体（HP）轴被包括在放射治疗野中时，辐射引起的神经内分泌功能障碍变得更加明显。需要进行基线和治疗后激素谱评估。当这些结构接收到超过其耐受量的辐射时，白内障和视觉系统的放射性损伤可能会发展。始终应特别注意避免这些敏感结构的照射，或者将其剂量降至最低限度。
