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Isolated absence of F waves and proximal axonal dysfunction inGuillain-Barré syndrome with antiganglioside antibodies

机译:孤立的F波缺失和近端轴索功能障碍。抗神经节苷脂抗体的格林-巴利综合征

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摘要

OBJECTIVES—To investigate the pathophysiology of selective absence of F waves and its relation with antiganglioside antibodies in Guillain-Barré syndrome (GBS). Some patients with GBS show the absence of F waves as an isolated conduction abnormality, which has been interpreted as demyelination in the proximal nerve segments.
METHODS—In 62 consecutive patients with GBS, sequential nerve conduction and F wave studies were reviewed, and antibodies against ganglioside GM1, GM1b, GD1a, GalNAc-GD1a, GD1b, and GQ1b were measured by an enzyme linked immunosorbent assay.
RESULTS—In the first electrophysiological studies, isolated absence of F waves was found in 12 (19%) patients. Sequential studies in 10 of these patients showed two electrophysiological sequel patterns; rapid restoration of F waves (six patients), and persistent absence of F waves with distal motor nerve degeneration (acute motor axonal neuropathy, four patients). None of the 10 patients showed evidence of demyelination in the proximal, intermediate, or distal nerve segments throughout the course. Of the 62 patients, IgG antibodies against GM1, GM1b, GalNAc-GD1a, or GD1b were significantly associated with the electrodiagnosis of acute motoraxonal neuropathy, and patients with these antibodies more often hadisolated absence of F waves than patients without them (11 of 36 (31%)v one of 26 (4%);p<0.01). Eleven of the 12 patients withisolated absence of F waves had positive serology for one or moreantiganglioside antibodies.
CONCLUSIONS—In GBSwith antiganglioside antibodies, isolated absence of F waves is afrequent conduction abnormality especially in the early phase of thedisease, and may be caused by axonal dysfunction, such as physiologicalconduction block or axonal degeneration at the nerve roots.

机译:目的—研究在格林-巴利综合征(GBS)中选择性缺乏F波的病理生理及其与抗神经节苷脂抗体的关系。一些GBS患者显示出F波没有作为孤立的传导异常,这被解释为近端神经节段脱髓鞘。
方法-在62例连续的GBS患者中,进行了顺序神经传导和F波研究,并通过酶联免疫吸附法测量了针对神经节苷脂GM1,GM1b,GD1a,GalNAc-GD1a,GD1b和GQ1b的抗体。
结果-在最初的电生理研究中,发现12个单独的F波缺失( 19%)患者。在其中的10位患者中进行的顺序研究显示了两种电生理学后遗症模式。快速恢复F波(6例患者),并持续存在F波并没有远端运动神经变性(急性运动轴索神经病,4例患者)。在整个过程中,这10例患者中没有一个显示近端,中间或远端神经节脱髓鞘的迹象。在这62例患者中,针对GM1,GM1b,GalNAc-GD1a或GD1b的IgG抗体与急性运动的电诊断显着相关轴突性神经病,并且使用这些抗体的患者更常患有与没有F波的患者相比,孤立的F波缺失(36中的11人(31%)v 26(4%)之一;p <0.01)。 12例患者中有11例患有孤立的F波缺失对一个或多个血清学呈阳性抗神经节苷脂抗体。
结论—GBS中用抗神经节苷脂抗体,孤立的F波消失是频繁的传导异常,尤其是在早期疾病,并且可能是由轴突功能障碍(例如生理性疾病)引起的神经根的传导阻滞或轴突变性。

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