Pender M P
J Neuroimmunol. 1987 May;15(1):11-24. doi: 10.1016/0165-5728(87)90003-8.
Because of the reported absence of demyelination in some animals with neurological signs of experimental allergic encephalomyelitis (EAE), it has been suggested that these signs are not due to demyelination. The present study demonstrates that there is ample demyelination in the central nervous system (CNS) and peripheral nervous system (PNS) to account for the neurological signs in rats with myelin basic protein (MBP)-induced acute EAE as well as in rats and rabbits with whole-spinal-cord-induced acute EAE. The main reasons for failure to detect demyelination in animals with neurological signs of EAE appear to be inadequate histological techniques and incomplete examination of the nervous system, particularly the PNS and the lumbar, sacral and coccygeal segments of the spinal cord.
由于有报道称，一些出现实验性变应性脑脊髓炎（EAE）神经症状的动物不存在脱髓鞘现象，因此有人提出这些症状并非由脱髓鞘引起。本研究表明，在中枢神经系统（CNS）和周围神经系统（PNS）中存在大量脱髓鞘现象，这足以解释髓鞘碱性蛋白（MBP）诱导的急性EAE大鼠以及全脊髓诱导的急性EAE大鼠和兔子的神经症状。在出现EAE神经症状的动物中未能检测到脱髓鞘的主要原因似乎是组织学技术不足以及对神经系统，特别是PNS和脊髓腰段、骶段和尾段的检查不完整。
