Nakano Yuta, Kanda Takashi
Department of Neurology and Clinical Neuroscience, Yamaguchi University, Graduate School of Medicine.
Brain Nerve. 2015 Nov;67(11):1329-39. doi: 10.11477/mf.1416200303.
Guillain-Barré syndrome is composed of two distinct clinicopathological entities: acute inflammatory demyelinating polyradiculoneuropathy (AIDP), and acute motor or motor and sensory axonal neuropathy (AMAN and AMSAN). AIDP is characterized by the patchily distributed demyelinative foci throughout the peripheral nervous system (PNS), whereas in AMAN/AMSAN primary axonal degeneration is observed in the PNS, particularly accentuated at the spinal nerve roots. The aim of this article is to provide an overview of previous findings regarding GBS pathology and thus, to elucidate the pathomechanisms of this life-threatening disorder. The most critical cause for AIDP may be the autoimmune attack on the Schwann cell membrane wrapping the myelinated nerve fibers, and that in AMAN/AMSAN may be an antibody-mediated attack on the axolemma at the nodes of Ranvier.
格林-巴利综合征由两种不同的临床病理实体组成:急性炎症性脱髓鞘性多发性神经根神经病(AIDP)和急性运动性或运动与感觉性轴索性神经病(AMAN和AMSAN)。AIDP的特征是整个周围神经系统(PNS)存在散在分布的脱髓鞘病灶,而在AMAN/AMSAN中,PNS可见原发性轴索变性,在脊神经根处尤为明显。本文旨在概述此前关于GBS病理学的研究结果,从而阐明这种危及生命疾病的发病机制。AIDP最关键的病因可能是针对包裹有髓神经纤维的施万细胞膜的自身免疫攻击,而AMAN/AMSAN的病因可能是抗体介导的对郎飞结处轴膜的攻击。