Liu H M, Maurer H S, Vongsvivut S, Conway J J
Hum Pathol. 1978 Nov;9(6):635-48. doi: 10.1016/s0046-8177(78)80047-1.
The present report is a neuropathologic study of three patients who died from a severe form of necrotizing encephalopathy following intrathecal methotrexate therapy and craniospinal irradiation for acute lymphoblastic leukemia. During the early phase the lesion presented as multifocal coalescing areas of coagulation necrosis in the deep white matter. In the diseased areas the myelin was lost and the axons were severely swollen and fragmented. During the late stage the white matter was reduced to a thin gliotic calcified layer. The pathogenesis of this lesion is unclear, but the preferential involvement of the white matter with sparing of the cortical gray matter and basal ganglia makes it unlikely that direct chemical injury is the cause. The distribution of the lesion suggests a vascular disturbance due to endothelial injury caused by interaction of the methotrexate with tissue infiltrated by leukemic cells and altered by irradiation.
本报告是对三名因鞘内注射甲氨蝶呤治疗和颅脑脊髓照射急性淋巴细胞白血病后死于严重坏死性脑病的患者进行的神经病理学研究。在疾病早期，病变表现为深部白质中多灶性融合的凝固性坏死区域。在病变区域，髓鞘丢失，轴突严重肿胀和断裂。在疾病后期，白质减少为一层薄薄的胶质化钙化层。这种病变的发病机制尚不清楚，但白质优先受累而皮质灰质和基底神经节未受累表明直接化学损伤不太可能是病因。病变的分布提示由于甲氨蝶呤与白血病细胞浸润并经照射改变的组织相互作用导致内皮损伤而引起的血管紊乱。
