Blümcke I, Löbach M, Wolf H K, Wiestler O D
Department of Neuropathology, University of Bonn Medical Center, D-53105 Bonn, Germany.
Microsc Res Tech. 1999 Jul 1;46(1):53-8. doi: 10.1002/(SICI)1097-0029(19990701)46:1<53::AID-JEMT5>3.0.CO;2-0.
The etiology and pathogenesis of epilepsy-associated local lesions remain largely unknown. Histopathologically, the most frequent lesions comprise gangliogliomas and glioneuronal malformations, i.e., hamartias or hamartomas, with a preferred location in the temporal lobe of young patients. A characteristic histopathological admixture of glial and neuronal elements, the focal appearance and the benign clinical behaviour suggest a malformative nature. So far, no molecular genetic alterations specifically involved in the pathogenesis of these glioneuronal lesions have been identified. However, immunohistochemical analysis revealed distinct distribution patterns of oncofetal antigens. The embryonic form of the neural cell adhesion molecule is present within glioneuronal hamartias, indicating an early migrational disorder. Recently, we have observed immunoreactivity for the stem cell marker CD34 in the majority of gangliogliomas and glioneuronal hamartomas. Based on these findings, we propose a common origin of gangliogliomas and glioneuronal hamartomas from a bipotent precursor that undergoes abnormal glioneuronal development.
癫痫相关局部病变的病因和发病机制在很大程度上仍不清楚。组织病理学上，最常见的病变包括神经节胶质瘤和神经胶质神经元畸形，即错构瘤或错构瘤，好发于年轻患者的颞叶。神经胶质和神经元成分的特征性组织病理学混合、局灶性表现和良性临床行为提示其具有畸形性质。到目前为止，尚未发现特异性参与这些神经胶质神经元病变发病机制的分子遗传学改变。然而，免疫组织化学分析揭示了癌胚抗原的不同分布模式。神经细胞粘附分子的胚胎形式存在于神经胶质神经元错构瘤内，表明存在早期迁移障碍。最近，我们在大多数神经节胶质瘤和神经胶质神经元错构瘤中观察到干细胞标志物CD34的免疫反应性。基于这些发现，我们提出神经节胶质瘤和神经胶质神经元错构瘤起源于一个经历异常神经胶质神经元发育的双能前体细胞。
