PhD Nobuhiro Yuki MD

Dokkyo Medical University, Tochigi, Tochigi-ken, Japan

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Publications (4)38.04 Total impact

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    ABSTRACT: A 49-year-old woman developed acute left facial, hypoglossal, and phrenic nerve palsies, as well as dysphagia and weakness in the neck and arms. Electrophysiologic studies showed an acute motor axonal neuropathy. Serum anti-GM1 IgG antibody was positive. Intavenous immunoglobulin treatment resulted in good clinical recovery. The present report indicates that the cranial and phrenic nerves may be affected unilaterally in Guillain–Barré syndrome, and that there is clinical variability in the axonal subtype of this syndrome. © 2002 John Wiley & Sons, Inc. Muscle Nerve 25: 297–299, 2002 DOI 10.1002/mus.10041
    Muscle & Nerve 02/2002; 25(2):297 - 299. DOI:10.1002/mus.10041 · 2.31 Impact Factor
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    ABSTRACT: Some humans develop the axonal form of Guillain-Barré syndrome after receiving bovine brain ganglioside. On sensitization with the ganglioside mixture, all of a group of rabbits injected developed high anti-GM1 IgG antibody titers, flaccid limb weakness of acute onset, and a monophasic illness course. Pathological findings for the peripheral nerves showed predominant Wallerian-like degeneration, with neither lymphocytic infiltration nor demyelination. IgG was deposited on the axons of the anterior roots, and GM1 was proved to be present on the axons of peripheral nerves. Sensitization with purified GM1 also induced axonal neuropathy, indicating that GM1 was the immunogen in the mixture. A model of human axonal Guillain-Barré syndrome has been established that uses inoculation with a bovine brain ganglioside mixture or isolated GM1. This model may help to clarify the molecular pathogenesis of the syndrome and to develop new treatments for it.
    Annals of Neurology 06/2001; 49(6):712 - 720. DOI:10.1002/ana.1012 · 11.91 Impact Factor
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    ABSTRACT: GM1b is a minor ganglioside in human peripheral nerves. Serum anti-GM1b antibodies frequently are present in patients with Guillain-Barré syndrome (GBS). In this collaborative study, we investigated the antecedent infections, clinical features, and response to treatment of GBS patients with anti-GM1b antibodies. Of 132 GBS patients who participated in the Dutch GBS trial that compared the effect of intravenous immunoglobulins and plasma exchange, 25 (19%) patients had anti-GM1b antibodies. IgM antibodies were present in 14, IgG antibodies in 15, and both isotypes in 4 patients. The 25 patients with anti-GM1b antibodies had a clinical pattern distinct from that of the other 107 GBS patients. They more often had an episode of gastrointestinal illness and frequently showed serological evidence of recent infection by Campylobacter jejuni. The anti-GM1b–positive subgroup was marked by more rapidly progressive, more severe, and predominantly distal weakness. Cranial nerve involvement and sensory deficits were less common in the patients with anti-GM1b antibodies. The presence of anti-GM1b antibodies was associated with slower recovery. The clinical manifestations predominantly were associated with anti-GM1b antibodies of the IgG isotype. Fourteen (56%) of the 25 patients with anti-GM1b antibodies also had anti-GM1 antibodies. The group of patients with both antibodies was clinically more homogeneous and had a more rapidly progressive, pure motor neuropathy. The subgroup of anti-GM1b–positive GBS patients responded well to treatment with immunoglobulins but not to plasmapheresis. The distinctive clinical features of the patients with anti-GM1b antibodies show that acute motor neuropathy represents a specific subgroup within GBS and that recognizing these patients may have consequences as to the choice of therapy. Ann Neurol 2000;47:314–321
    Annals of Neurology 02/2000; 47(3):314 - 321. DOI:10.1002/1531-8249(200003)47:3<314::AID-ANA6>3.0.CO;2-C · 11.91 Impact Factor
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    ABSTRACT: To clarify the relations of the axonal form of Guillain-Barré syndrome (GBS) to anti-ganglioside antibodies and Campylobacter jejuni infection, 86 consecutive Japanese GBS patients were studied. Electrodiagnostic criteria showed acute inflammatory demyelinating polyneuropathy in 36% of the patients and acute motor axonal neuropathy (AMAN) in 38%. Frequent anti-ganglioside antibodies were of the IgG class and against GM1 (40%), GD1a (30%), GalNAc-GD1a (17%), and GD1b (21%). Identified infections were C. jejuni (23%), cytomegalovirus (10%), Mycoplasma pneumoniae (6%), and Epstein-Barr virus (3%). There was a strong association between AMAN and IgG antibodies against GM1, GD1a, GalNAc-GD1a, or GD1b. Almost all the patients with at least one of these antibodies had the AMAN pattern or rapid resolution of conduction slowing/block possibly because of early-reversible changes on the axolemma. C. jejuni infection was frequently associated with AMAN or anti-ganglioside antibodies, but more than half of the patients with AMAN or anti-ganglioside antibodies were C. jejuni–negative. These findings suggest that the three phenomena “axonal dysfunctions (AMAN or early-reversible conduction failure),” “IgG antibodies against GM1, GD1a, GalNAc-GD1a, or GD1b,” and “C. jejuni infection” are closely associated but that microorganisms other than C. jejuni frequently trigger an anti-ganglioside response and elicit axonal GBS. Ann Neurol 2000;48:624–631
    Annals of Neurology 01/2000; 48(4):624 - 631. DOI:10.1002/1531-8249(200010)48:4<624::AID-ANA9>3.0.CO;2-O · 11.91 Impact Factor