胶质瘤和缺血性脑中风是导致全球患者死亡的两个主要事件。虽然这些条件有不同的生理发生率,〜10%的缺血性中风患者发展为脑癌,尤其是神经胶质瘤,在缺血后阶段。此外,高度扩散,静脉血栓形成和神经胶质瘤块的高凝性增加了血栓栓塞的显著风险,包括缺血性中风.令人惊讶的是,这些事件有几个共同的途径,viz.缺氧,脑部炎症,血管生成,等。,但是这种共现背后的适当机制尚未被发现。卒中患者的高凝状态和D-二聚体水平的存在与非癌症人群不同。其他因素如动脉粥样硬化和凝血障碍参与中风的发病机制部分负责癌症。反过来也是部分正确的。根据临床和神经外科的经验,观察到大脑和脊柱中的神经元结构和功能在导致缺氧和萎缩的缺血进行性发作后发生变化。癌细胞的主要群体不能在排除癌症干细胞(CSC)的不利缺血环境中存活。中风患者的癌细胞已经转移,但是早期癌症患者也有多种原因中风。因此,中风是癌症的早期表现。中风和癌症共有许多因素,导致癌症患者中风风险增加,反之亦然。有癌症和没有癌症的中风的复杂机制是不同的。本综述总结了目前的临床报道,病理生理学,共同发生的可能原因,预后,和治疗的可能性。
Glioma and cerebral ischemic stroke are two major events that lead to patient death worldwide. Although these conditions have different physiological incidences, ~10% of ischemic stroke patients develop cerebral cancer, especially glioma, in the postischemic stages. Additionally, the high proliferation, venous thrombosis and hypercoagulability of the glioma mass increase the significant risk of thromboembolism, including ischemic stroke. Surprisingly, these events share several common pathways, viz. hypoxia, cerebral inflammation, angiogenesis, etc., but the proper mechanism behind this co-occurrence has yet to be discovered. The hypercoagulability and presence of the D-dimer level in stroke are different in cancer patients than in the noncancerous population. Other factors such as atherosclerosis and coagulopathy involved in the pathogenesis of stroke are partially responsible for cancer, and the reverse is also partially true. Based on clinical and neurosurgical experience, the neuronal structures and functions in the brain and spine are observed to change after a progressive attack of ischemia that leads to hypoxia and atrophy. The major population of cancer cells cannot survive in an adverse ischemic environment that excludes cancer stem cells (CSCs). Cancer cells in stroke patients have already metastasized, but early-stage cancer patients also suffer stroke for multiple reasons. Therefore, stroke is an early manifestation of cancer. Stroke and cancer share many factors that result in an increased risk of stroke in cancer patients, and vice-versa. The intricate mechanisms for stroke with and without cancer are different. This review summarizes the current clinical
reports, pathophysiology, probable causes of co-occurrence, prognoses, and treatment possibilities.