Kuwabara Satoshi, Nakata Miho, Sung Jia-Ying, Mori Masahiro, Kato Naoko, Hattori Takamichi, Koga Michiaki, Yuki Nobuhiro
Department of Neurology, Chiba University School of Medicine, 1-8-1 Inohana, Chuo, Chiba 260-8670, Japan.
J Neurol Sci. 2002 Jul 15;199(1-2):89-92. doi: 10.1016/s0022-510x(02)00088-6.
We describe a patient with the acute motor axonal neuropathy (AMAN) form of Guillain-Barré syndrome (GBS), who showed generalized hyperreflexia. A 24-year-old man developed acute paralysis following Campylobacter jejuni enteritis. He showed exaggerated tendon reflexes with abnormal reflex spread to other segments, and was initially diagnosed as having post-infectious myelitis. Nerve conduction studies showed motor axonal degeneration (the AMAN pattern), and increased soleus H-reflex amplitudes. His serum was positive for IgG antibodies to gangliosides GM1b and GalNAc-GD1a. He was treated with plasmapheresis, resulting in rapid recovery. Hyperreflexia was still present 12 months after onset when muscle strength was completely normal. This case provides further evidence that patients with AMAN can develop increased motor neuron excitability, and possible mechanisms for the hyperreflexia are discussed.
我们描述了一名患有格林-巴利综合征（GBS）急性运动轴索性神经病（AMAN）型且表现为全身性反射亢进的患者。一名24岁男性在空肠弯曲菌肠炎后出现急性瘫痪。他表现出腱反射亢进，且异常反射扩散至其他节段，最初被诊断为感染后脊髓炎。神经传导研究显示运动轴索变性（AMAN模式），比目鱼肌H反射波幅增加。他的血清中抗神经节苷脂GM1b和GalNAc-GD1a的IgG抗体呈阳性。他接受了血浆置换治疗，恢复迅速。发病12个月后，当肌肉力量完全正常时，反射亢进仍然存在。该病例进一步证明AMAN患者可出现运动神经元兴奋性增加，并讨论了反射亢进的可能机制。
