Approximately 30% of glioma patients are able to survive beyond one year postdiagnosis. And this short time is often overshadowed by glioma-associated epilepsy. This condition severely impairs the patient’s quality of life and causes great suffering. The genetic, molecular and cellular mechanisms underlying tumour development and epileptogenesis remain incompletely understood, leading to numerous unanswered questions. The various types of gliomas, namely glioblastoma, astrocytoma and oligodendroglioma, demonstrate distinct seizure susceptibility and disease progression patterns. Patterns have been identified in the presence of IDH mutations and epilepsy, with tumour location in cortical regions, particularly the frontal lobe, showing a more frequent association with seizures. Altered expression of TP53, MGMT and VIM is frequently detected in tumour cells from individuals with epilepsy associated with glioma. However, understanding the pathogenesis of these modifications poses a challenge. Moreover, hypoxic effects induced by glioma and associated with the HIF-1a factor may have a significant impact on epileptogenesis, potentially resulting in epileptiform activity within neuronal networks. We additionally hypothesise about how the tumour may affect the functioning of neuronal ion channels and contribute to disruptions in the blood–brain barrier resulting in spontaneous depolarisations.
大约30%的胶质瘤患者在确诊后能够存活超过一年。而这段短暂的时间往往被胶质瘤相关癫痫所笼罩。这种情况严重损害患者的生活质量并带来巨大痛苦。肿瘤发生与癫痫形成的遗传、分子和细胞机制尚未完全阐明，导致诸多未解之谜。不同类型的胶质瘤，即胶质母细胞瘤、星形细胞瘤和少突胶质细胞瘤，表现出不同的癫痫易感性和疾病进展模式。研究已发现IDH突变与癫痫存在关联模式，其中肿瘤位于皮质区域（特别是额叶）与癫痫发作的相关性更为频繁。在胶质瘤相关癫痫患者的肿瘤细胞中，常可检测到TP53、MGMT和VIM的表达改变。然而，理解这些改变的发病机制仍面临挑战。此外，胶质瘤诱导的缺氧效应及其与HIF-1α因子的关联可能对癫痫形成产生重要影响，可能导致神经元网络内出现癫痫样活动。我们还推测肿瘤可能如何影响神经元离子通道功能，并导致血脑屏障破坏从而引发自发性去极化。
Unexplained Causes of Glioma-Associated Epilepsies: A Review of Theories and an Area for Research
肿瘤(癌症)患者之家