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Nobuhiro Yuki - One of the best experts on this subject based on the ideXlab platform.

  • Neurol Neurosurg Psychiatry Published Online First: [please include Day Month
    2013
    Co-Authors: Br Wakerley, Nobuhiro Yuki, Derek Soon, Yee-cheun Chan, Professor Nobuhiro Yuki
    Abstract:

    Objective Clinical and immunological evaluation of ‘incomplete ’ Bickerstaff brainstem encephalitis (BBE). Methods We studied two patients with postinfectious brainstem syndromes who presented at National University Hospital Singapore. Laboratory work-up included measurement of Antiganglioside Antibodies. Results Both patients displayed hypersomnolence and cerebellar-like ataxia in the absence of external ophthalmoplegia and carried high serum titres of IgG anti-GQ1b Antibodies, strongly indicative of BBE. Conclusions Ophthalmoplegia can be absent or incomplete in BBE, and the absence of this clinical feature should not exclude BBE from the clinicians’ differential. Such cases of incomplete BBE could be defined as ‘ataxic hypersomnolence without ophthalmoplegia’

  • Antiganglioside Antibodies are associated with axonal guillain barre syndrome a japanese italian collaborative study
    Journal of Neurology Neurosurgery and Psychiatry, 2012
    Co-Authors: Yukari Sekiguchi, Nobuhiro Yuki, Antonino Uncini, Sonoko Misawa, Francesca Notturno, Saiko Nasu, Kazuaki Kanai, Yu Ichi Noto, Yumi Fujimaki, Kazumoto Shibuya
    Abstract:

    Background Whether or not Antiganglioside Antibodies are related to axonal or demyelinating Guillain–Barre syndrome (GBS) is still a matter of controversy, as detailed in previous studies conducted in Western and Asian countries. Objective To clarify whether Antiganglioside Antibodies are associated with axonal dysfunction in Japanese and Italian GBS patient cohorts. Methods Clinical and electrophysiological profiles were reviewed for 156 GBS patients collected from Japan (n=103) and Italy (n=53). Serum IgG Antibodies against GM1, GM1b, GD1a and GalNAc-GD1a were measured by ELISA in the same laboratory. Electrodiagnostic criteria and results of serial electrophysiological studies were used for classification of GBS subtypes: acute inflammatory demyelinating polyneuropathy (AIDP) and acute motor axonal neuropathy (AMAN). Results In both Japanese and Italian cohorts, any of the Antibodies were positive in 36% of the patients, and antibody positivity had a significant association with the AMAN electrodiagnosis. Approximately 30% of Japanese and Italian Antiganglioside positive patients showed the AIDP pattern at the first examination whereas sequential studies showed that most finally showed the AMAN pattern. Clinically, seropositive patients more frequently had preceding diarrhoea and pure motor neuropathy in both Japanese and Italian cohorts; vibratory sensation was normal in 97% of Japanese and in 94% of Italian seropositive patients. Conclusions In GBS, clinical and electrophysiological features appear to be determined by Antiganglioside Antibodies, and the Antibodies are associated with motor axonal GBS in both Japan and Italy. Classification of the GBS subtypes as a disease entity should be made, combining the results of Antiganglioside assays and serial electrodiagnostic studies.

  • Antiganglioside Antibodies in guillain barre syndrome and its related conditions
    Expert Review of Neurotherapeutics, 2011
    Co-Authors: Nortina Shahrizaila, Nobuhiro Yuki
    Abstract:

    Guillain-Barre syndrome (GBS) is typically classified into two major subtypes: acute inflammatory demyelinating neuropathy and acute motor axonal neuropathy. Its most recognizable variant is Fisher syndrome. The last two decades have seen considerable advances in our understanding of GBS. Of note, various autoAntibodies against ganglioside antigens have been identified and found to have significant associations with the axonal forms of GBS and Fisher syndrome. In this article, we discuss the different clinical presentations in GBS and the role of Antiganglioside Antibodies in their underlying pathogenesis. We also discuss the impact that Antiganglioside Antibodies have had in the development of experimental models and treatment modalities in GBS.

  • continuous spectrum of pharyngeal cervical brachial variant of guillain barre syndrome
    JAMA Neurology, 2007
    Co-Authors: Takahide Nagashima, Michiaki Koga, Koichi Hirata, Masaaki Odaka, Nobuhiro Yuki
    Abstract:

    Background Pharyngeal-cervical-brachial weakness (PCB) is considered a variant of Guillain-Barre syndrome (GBS). Because of its rarity, there have been no studies of large numbers of patients with PCB. Objective To clarify the nosological classification of PCB. Design Retrospective study. Setting Academic research. Patients Medical records were reviewed of patients who manifested progressive weakness of the pharynx, neck, and upper limbs within 4 weeks of initial onset. Main Outcome Measures Clinical features were analyzed, and antecedent infections and Antiganglioside Antibodies were investigated. Results Diagnoses for 100 patients were “pure PCB” (n = 13), PCB with preserved muscle stretch reflexes (n = 8), GBS overlap (n = 48), Fisher syndrome overlap (n = 26), and Bickerstaff brainstem encephalitis overlap (n = 5). Serological test results showed that 31.0% of antecedent infections in PCB were caused by Campylobacter jejuni . Of the Antiganglioside Antibodies tested, anti-GT1a IgG Antibodies were positive in 51.0% of the patients. Anti-GQ1b IgG Antibodies (a serological marker of Fisher syndrome and Bickerstaff brainstem encephalitis) were positive in 39.0%. The IgG Antibodies to GM1, GM1b, GD1a, or GalNAc-GD1a (serological markers of an axonal GBS subtype) were positive in 27.0%. Conclusion This large study identified the clinical profiles of PCB. Clinical overlapping, frequent C jejuni infection, and common Antiganglioside Antibodies present in PCB, GBS, Fisher syndrome, and Bickerstaff brainstem encephalitis provide conclusive evidence that PCB and these conditions form a continuous spectrum.

  • acute facial diplegia and hyperreflexia a guillain barre syndrome variant
    Neurology, 2004
    Co-Authors: Keiichiro Susuki, Michiaki Koga, M Atsumi, Koichi Hirata, Nobuhiro Yuki
    Abstract:

    Two patients with acute facial diplegia and hyperreflexia are described. Both patients had serologic evidence of preceding Campylobacter jejuni infection and Antiganglioside IgG Antibodies as well as other laboratory and electrophysiologic findings suggesting Guillain-Barre syndrome (GBS). IV immunoglobulin produced recovery. Hyperreflexia does not necessarily exclude the diagnosis of a GBS variant. Antiganglioside Antibodies can help with diagnosis in difficult cases.

Isabel Illa - One of the best experts on this subject based on the ideXlab platform.

  • clinical and serological features of acute sensory ataxic neuropathy with Antiganglioside Antibodies
    Journal of The Peripheral Nervous System, 2012
    Co-Authors: Ricard Rojasgarcia, Eduard Gallardo, Luis Querol, Noemi De Luna Salva, Candido Juarez, Mercedes Garces, Eva Fages, Carlos Casasnovas, Isabel Illa
    Abstract:

    There is as yet no consensus for considering pure acute sensory ataxic neuropathy (ASAN) as a variant of Guillain-Barre syndrome (GBS). Reactivity against gangliosides sharing disialosyl epitopes has been reported in these patients. The aim of this study was to determine the spectrum of reactivity against gangliosides in ASAN and to define the clinical pattern. From our database we identified patients with suspicion of ASAN. We defined ASAN as the presence of ataxia of peripheral origin with loss of proprioception, and areflexia, absence of ophthalmoplegia and no or minimal muscle weakness. Patients who met these criteria were retrospectively reviewed for their spectrum of reactivity against gangliosides and clinical features. We identified 12 patients fulfilling pre-defined criteria for ASAN. Reactivity against gangliosides containing disialosyl epitopes was present in seven patients. Concomitant reactivity against other gangliosides was present in 6/7 patients. All patients presented good prognosis and an antecedent illness was present in nine. Our results support the previously described clinico-immunological association between ASAN and disialosyl specificity, and widen the spectrum of reactivity against gangliosides. The acute presentation with a monophasic course, and good prognosis in all cases, together with transient immunoglobulin G Antiganglioside Antibodies and infectious antecedent in 7/12 patients support the inclusion of ASAN as a GBS variant.

  • bulbar involvement in patients with Antiganglioside Antibodies against neunac alpha2 3 gal
    Journal of Neurology Neurosurgery and Psychiatry, 2010
    Co-Authors: Ricard Rojasgarcia, Eduard Gallardo, Candido Juarez, Eva Fages, Carlos Casasnovas, Noemi De Luna, Eugenia Martinezhernandez, Alejandra Carvajal, Pablo Davilagonzalez, Isabel Illa
    Abstract:

    Background Reactivity against terminal NeuNAc(α2–3)Gal, common to several gangliosides such as GD1a, GT1b and GM3, has rarely been reported. The authors recently described a patient with a clinical picture of acute relapsing sensory ataxic neuropathy and bulbar involvement in whom they demonstrated concomitant reactivity against NeuNAc(α2–3)Gal and disialosyl epitopes. The authors suggested a correlation between NeuNAc(α2–3)Gal reactivity and bulbar involvement. Aim To determine the frequency of reactivity against terminal NeuNAc(α2–3)Gal in acute and chronic immune-mediated disorders, and its possible correlation with bulbar involvement. Methods The authors retrospectively reviewed reactivity in the serum of more than 3000 consecutive patients with acute and chronic disorders in which Antiganglioside Antibodies were studied. The authors selected those patients who were simultaneously positive, by ELISA or thin-layer chromatography, for IgG or IgM Antibodies anti-GM3, GD1a and GT1b, and reviewed their clinical features. Results Reactivity against NeuNAc(α2–3)Gal, shared by GM3, GD1a and GT1b gangliosides, was detected in 10 patients: isolated in one patient, and concomitant with reactivity against other gangliosides in the remaining patients. Reactivity against NeuNAc(α2–3)Gal was frequently associated (8/10) with symptoms suggestive of bulbar involvement, such as dysphagia, dysarthria or dysphonia. Severe respiratory failure requiring mechanical ventilation was observed in four patients. Conclusions Reactivity against the NeuNAc(α2–3)Gal epitope is rare and is generally found in association with reactivity against the disialosyl epitope. It can be detected in patients with acute or chronic disorders and could be a serological marker of clinical bulbar involvement and, to a lesser extent, associated with the development of severe respiratory failure.

  • Antiganglioside Antibodies when which and for what
    Neurologia, 2001
    Co-Authors: Eduard Gallardo, Ricard Rojasgarcia, R Belvis, C Serranomunuera, E Ortiz, N Ortiz, Josep M Grau, Isabel Illa
    Abstract:

    Background We report our experience in the study of Antiganglioside Antibodies and define their clinical value establishing associations between clinical syndromes and immunological findings. Methods We analysed 275 sera: Guillain-Barre syndrome (GBS) (78), Miller-Fisher syndrome (MFS) (37), chronic inflammatory demyelinating polyneuroapthy (CIDP) (17), multifocal motor neuropathy (NMM) (42), chronic axonal mixed polyneuropathy (PNP) (54), amyotrophic lateral sclerosis (ALS) (28) and lower motor neuron disease (LMND) (17). We have studied the presence of IgG and IgM Antibodies to 9 gangliosides using ELISA and TLC. Results We have detected anti-GQ1b Antibodies in 36/37 (97,3%) of patients with MFS, being undetectable after 4 weeks in 83%. A 34 % (26/78) of patients with GBS were positive for several Antiganglioside specificities being GalGalNAc the most frequent (54%). Two out of three sera positive for GD1a corresponded to axonal Guillain-Barre. IgM class anti-GM1 Antibodies were positive in 10/12 patients with MMN, while only a 3-9% of patients with ALS, CIDP, PNP and LMND presented Antiganglioside Antibodies. Conclusions Analysis of anti-GQ1b Antibodies confirms the diagnosis of MFS, excluding other acute brainstem pathologies and, in this study, detection of anti-GD1a Antibodies indicates axonal damage in GBS and suggest a worse prognosis. IgM anti-GM1 Antibodies are only found in MMN. These findings confirm a disease specific correlation between specific neuropathies and Antiganglioside Antibodies clinically useful.

  • Antiganglioside Antibodies in neuropathies and motor neuronopathies
    Neurologia, 1996
    Co-Authors: Eduard Gallardo, C Serrano, C Prat, Isabel Illa
    Abstract:

    The presence of Antiganglioside Antibodies is associated with several neurologic disorders. These Antibodies recognize several epitopes, generally saccharides present in these glucolipids. The presence of antiGM Antibodies has been described in certain clinical syndromes, the main one being multifocal motor neuropathy with and without conduction blocks. The frequency of antiGM1 class IgM antibody falls between 20 and 80% in this disease. Axon predominant Guillain-Barre syndrome is also associated with high titers of antiGM1 Antibodies, although in this case class IgG is implicated. The most important association to date has been established between Miller-Fisher syndrome and the presence of antiGQ1b Antibodies. Several authors have reported molecular similarities among these gangliosides and bacterial lipopolysaccharides, mainly Campylobacter iejuni. The principal aims in the study of Antiganglioside Antibodies are to establish their pathogenic role as well as the clinical usefulness of analyzing for them, and to discover new specificities that aid in the diagnosis and classification of neuropathies, whether they are predominantly motor disorders or chronic sensory ones.

Susumu Kusunoki - One of the best experts on this subject based on the ideXlab platform.

  • effects of acidic phospholipids on Antiganglioside Antibodies in guillain barre syndrome role of the disialosyl residue
    Clinical and Experimental Neuroimmunology, 2013
    Co-Authors: Masami Ueda, Minako H Yamada, Shoji Tsuji, Susumu Kusunoki
    Abstract:

    Objectives The activities of anti-GM1 immunoglobulin G (IgG) Antibodies in Guillain–Barre syndrome (GBS) are increased when a mixture of acidic phospholipids, such as phosphatidic acid (PA) and the ganglioside GM1, is used as an antigen in an enzyme-linked immunosorbent assay (ELISA). In contrast, no obvious enhancing effect is seen on the activities of anti-GQ1b Antibodies in Fisher syndrome. The cause of these different results remains to be determined. We investigated whether it is caused by the difference in the pathogens of the preceding infections or by that in the physicochemical properties of GM1 and GQ1b. Methods The effects of the phospholipid on the antibody activities in ELISA were compared between the cases preceded by respiratory infections and those by gastrointestinal infections. We examined the effects of the phospholipids on anti-GD1b IgG Antibodies and compared the effects on GD1b-specific Antibodies and those on Gal-GalNAc epitope-specific Antibodies. Results The effects of the phospholipids on the average of the antibody activities, either anti-GM1 or anti-GQ1b antibody, did not differ between patients with antecedent gastrointestinal infections and those with respiratory infections. The anti-GD1b IgG activity in GBS patients with anti-Gal-GalNAc specificity increased when a mixture of GD1b and a phospholipid, such as PA, was an antigen; whereas the activity of monospecific anti-GD1b IgG did not increase. Conclusions The enhancing effect of such a phospholipid as PA appears not to be a result of the presence of a particular phospholipid within the pathogen for the antecedent infection. It might depend on the presence of a negatively charged disialosyl residue in the ganglioside antigen.

  • Antibodies to gangliosides and ganglioside complexes in guillain barre syndrome and fisher syndrome mini review
    Journal of Neuroimmunology, 2010
    Co-Authors: Kenichi Kaida, Susumu Kusunoki
    Abstract:

    Antiganglioside Antibodies play a pathogenic role in the pathophysiology of Guillain-Barre syndrome (GBS) and Fisher syndrome (FS). Antiganglioside antibody-mediated nerve injury is likely to result from nerve damage through complement activation or dysfunction of molecules such as voltage-gated sodium and calcium channels. Clustered epitopes of complexes of two gangliosides in the cell membrane can be targeted by serum Antibodies in GBS and FS and may regulate the accessibility and avidity of Antiganglioside Antibodies. The glycolipid environment or the specific distribution of target gangliosides in the peripheral nervous system may also influence the pathogenic effect of Antiganglioside Antibodies in GBS and FS. Structural and functional analyses of glycoepitopes of ganglioside complexes in membranes will provide new vistas on antibody-antigen interaction in GBS and shed light on microdomain function mediated by carbohydrate-carbohydrate interactions, which may lead to novel treatments for GBS and FS.

  • clinicopathological study of an autopsy case with sensory dominant polyradiculoneuropathy with Antiganglioside Antibodies
    Muscle & Nerve, 1999
    Co-Authors: Tomokazu Obi, Susumu Kusunoki, Toshikazu Murakami, M Takatsu, Masahiro Serizawa, Kouichi Mizoguchi, Reiko Koike, Yoshiro Nishimura
    Abstract:

    A previously reported patient presenting sensory-dominant neuropathy with Antiganglioside Antibodies, bound preferentially to polysi- alogangliosides including GD1b, was autopsied. While axonal degeneration was predominant in the sural nerve, many demyelinated fibers were present in the spinal roots. Dorsal roots had undergone significant damage. These pathological findings were well correlated with the electrophysiological results showing decreased F-wave conduction velocities and conduction blocks in motor nerves and decreased or absent sensory action potentials in sensory nerves, with distribution of GD1b in nerve tissues such as dorsal root ganglia and paranodal myelin in the ventral and dorsal roots. © 1999 John Wiley & Sons, Inc. Muscle Nerve 22: 1426–1431, 1999

  • a case of pharyngeal cervical brachial variant of guillain barre syndrome with positive anti galactocerebroside gal c igm antibody
    Rinshō shinkeigaku Clinical neurology, 1999
    Co-Authors: J Kasuya, T Miyazono, Satoshi Takenaga, Kimiyoshi Arimura, Mitsuhiro Osame, Susumu Kusunoki
    Abstract:

    A 49-year-old man presented with hoarseness, dysphagia, muscle atrophy and weakness of deltoid, trapezius, sternocleidomastoid, rhomboid, anterior serratus, infraspinatus and supraspinatus. Anti-Gal-C IgM antibody was positive in the serum. The other Antiganglioside Antibodies (GM1, GM2, GM3, GD1a, GD1b, GD3, GT1a, GT1b, GQ1b, GA1, GalNAc-GD1a, GM1b) were negative. Patient contracted pneumonia but whether it was due to mycoplasma was not evident. Plasmapheresis improved his clinical state including a decrease of the antibody. This case was diagnosed pharyngeal-cervical-brachial variant of Guillain-Barre syndrome, and anti-Gal-C antibody seemed to be correlated with the pathogenesis of this syndrome. Gal-C is a major glycolipid of myelin and the cell membrane of the myelin-forming cell (oligodendrocytes and Schwann cells) and is free of specific localization and distribution. The mechanism how the anti-Gal-C IgM antibody induced bulbar paralysis and the symptoms localizing neck and upper limbs remains to be known.

  • Antiganglioside Antibodies in the pathogenesis of autoimmune neuropathies
    Rinshō shinkeigaku Clinical neurology, 1999
    Co-Authors: Susumu Kusunoki
    Abstract:

    Antiganglioside Antibodies are frequently detected in sera from patients with autoimmune neuropathies, such as Guillain-Barre syndrome, Miller Fisher syndrome, IgM paraproteinemic neuropathy, chronic inflammatory demyelinating polyneuropathy, and multifocal motor neuropathy. In the acute phase sera from GBS patients, Antiganglioside Antibodies are detected in 60-70%. Ganglioside antigens recognized by serum Antibodies are varied from case to case. IgG antibody against GQ1b ganglioside is specifically raised in sera from patients with Miller Fisher syndrome and Guillain-Barre syndrome with ophthalmoplegia. That antibody may bind to the paranodal myelin of oculomotor, trochlear and abducens nerves, where GQ1b ganglioside is specifically localized, to cause ophthalmoplegia. IgM M-protein which recognizes the disialosyl residue of GD1b is specifically associated with sensory ataxic neuropathy. The IgM M-protein may bind to the primary sensory neurons, where GD1b ganglioside is localized, to cause sensory disturbance. After we confirmed the localization of GD1b in the rabbit primary sensory neurons, we sensitized rabbits with GD1b and induced sensory ataxic neuropathy in them. This is the first established animal model of autoimmune neuropathy induced by sensitization with ganglioside. Some Antiganglioside Antibodies may determine the clinical phenotype of neuropathy by binding specifically to the ganglioside antigens which have unique localization.

P.a. Van Doorn - One of the best experts on this subject based on the ideXlab platform.

  • Antiganglioside Antibodies in polyneuropathy associated with monoclonal gammopathy.
    Neurology, 2001
    Co-Authors: M. Eurelings, Nicolette C. Notermans, C. W. Ang, P.a. Van Doorn, B. C. Jacobs, Leonard H. Van Den Berg
    Abstract:

    Antibody reactivity to GA1, GM1, GM2, GD1a, GD1b, and GQ1b gangliosides was measured in 87 patients with polyneuropathy associated with monoclonal gammopathy (60 IgM, 25 IgG, 2 IgA) and 42 control patients with monoclonal gammopathy without polyneuropathy (21 IgM, 21 IgG). Of these 87 patients, 30% had anti-myelin-associated glycoprotein Antibodies and 15% had Antiganglioside Antibodies. Antiganglioside Antibodies were significantly associated with demyelinating neuropathy and with IgM monoclonal gammopathy. Anti-GD1b and anti-GQ1b Antibodies were significantly associated with predominantly sensory ataxic neuropathy.

  • guillain barre syndrome and miller fisher syndrome associated campylobacter jejuni lipopolysaccharides induce anti gm1 and anti gq1b Antibodies in rabbits
    Infection and Immunity, 2001
    Co-Authors: C. W. Ang, B. C. Jacobs, M De Klerk, Hubert P Endtz, Jon D Laman, F G A Van Der Meche, P.a. Van Doorn
    Abstract:

    Campylobacter jejuni infections are thought to induce Antiganglioside Antibodies in patients with Guillain-Barre syndrome (GBS) and Miller Fisher syndrome (MFS) by molecular mimicry between C. jejuni lipopolysaccharides (LPS) and gangliosides. We used purified LPS fractions from five Campylobacter strains to induce Antiganglioside responses in rabbits. The animals that received injections with LPS from GBS-associated strains developed anti-GM1 and anti-GA1 Antibodies. Animals injected with LPS from one MFS-related C. jejuni strain produced anti-GQ1b Antibodies. Rabbits that were injected with Penner O:3 LPS had a strong anti-LPS response, but no Antiganglioside reactivity was observed. The Antiganglioside specificity in the rabbits reflected the specificity in the patients from whom the strains were isolated. In conclusion, our results indicate that an immune response against GBS- and MFS-associated C. jejuni LPS results in Antiganglioside Antibodies. These results provide strong support for molecular mimicry as a mechanism in the induction of Antiganglioside Antibodies following infections.

Koichi Hirata - One of the best experts on this subject based on the ideXlab platform.

  • continuous spectrum of pharyngeal cervical brachial variant of guillain barre syndrome
    JAMA Neurology, 2007
    Co-Authors: Takahide Nagashima, Michiaki Koga, Koichi Hirata, Masaaki Odaka, Nobuhiro Yuki
    Abstract:

    Background Pharyngeal-cervical-brachial weakness (PCB) is considered a variant of Guillain-Barre syndrome (GBS). Because of its rarity, there have been no studies of large numbers of patients with PCB. Objective To clarify the nosological classification of PCB. Design Retrospective study. Setting Academic research. Patients Medical records were reviewed of patients who manifested progressive weakness of the pharynx, neck, and upper limbs within 4 weeks of initial onset. Main Outcome Measures Clinical features were analyzed, and antecedent infections and Antiganglioside Antibodies were investigated. Results Diagnoses for 100 patients were “pure PCB” (n = 13), PCB with preserved muscle stretch reflexes (n = 8), GBS overlap (n = 48), Fisher syndrome overlap (n = 26), and Bickerstaff brainstem encephalitis overlap (n = 5). Serological test results showed that 31.0% of antecedent infections in PCB were caused by Campylobacter jejuni . Of the Antiganglioside Antibodies tested, anti-GT1a IgG Antibodies were positive in 51.0% of the patients. Anti-GQ1b IgG Antibodies (a serological marker of Fisher syndrome and Bickerstaff brainstem encephalitis) were positive in 39.0%. The IgG Antibodies to GM1, GM1b, GD1a, or GalNAc-GD1a (serological markers of an axonal GBS subtype) were positive in 27.0%. Conclusion This large study identified the clinical profiles of PCB. Clinical overlapping, frequent C jejuni infection, and common Antiganglioside Antibodies present in PCB, GBS, Fisher syndrome, and Bickerstaff brainstem encephalitis provide conclusive evidence that PCB and these conditions form a continuous spectrum.

  • acute facial diplegia and hyperreflexia a guillain barre syndrome variant
    Neurology, 2004
    Co-Authors: Keiichiro Susuki, Michiaki Koga, M Atsumi, Koichi Hirata, Nobuhiro Yuki
    Abstract:

    Two patients with acute facial diplegia and hyperreflexia are described. Both patients had serologic evidence of preceding Campylobacter jejuni infection and Antiganglioside IgG Antibodies as well as other laboratory and electrophysiologic findings suggesting Guillain-Barre syndrome (GBS). IV immunoglobulin produced recovery. Hyperreflexia does not necessarily exclude the diagnosis of a GBS variant. Antiganglioside Antibodies can help with diagnosis in difficult cases.

  • Antiganglioside Antibodies in various episodes in a patient with recurrent guillain barre syndrome
    Journal of Neurology Neurosurgery and Psychiatry, 1998
    Co-Authors: Yumi Tagawa, Nobuhiro Yuki, Koichi Hirata
    Abstract:

    Guillain-Barre syndrome is defined as an acute, monophasic polyneuropathy. It recurs in 2%-5% of patients.1 Both the initial and recurrent episodes are preceded by an infection. Antibodies against several gangliosides are often present in the acute phase in serum samples from patients with Guillain-Barre syndrome.2 There have been no previous reports, however, on anti-ganglioside Antibodies in patients with recurrent disease. We report finding anti-ganglioside Antibodies in a patient with recurrent Guillain-Barre syndrome during the third and fourth episodes. Ten days after a bout of upper respiratory tract infection, a 26 year old man noted paraesthesias in his fingers and toes, and rapidly developed limb weakness. He had bulbar palsy and areflexic tetraparesis on day 1, and underwent three sessions of plasmapheresis on days 3, …

  • ability to remove immunoglobulins and Antiganglioside Antibodies by double filtration plasmapheresis in guillain barre syndrome is it equivalent to plasma exchange
    Therapeutic Apheresis, 1997
    Co-Authors: Nobuhiro Yuki, Yumi Tagawa, Koichi Hirata
    Abstract:

    : The value of plasma exchange (PE) in Guillain-Barre syndrome (GBS) is well established. In Japan, patients with GBS and related diseases often receive double filtration plasmapheresis (DFPP) as well as PE. No comparative trials between PE and DFPP, however, have been conducted. We compared their abilities to remove immunoglobulins and Antiganglioside Antibodies to find out whether DFPP is equivalent to PE. The ability to remove immunoglobulins and Antiganglioside Antibodies was compared between PE and DFPP using plasma samples from 41 patients with GBS and related diseases before and after each treatment session. The ability of DFPP to remove both IgGs and Antiganglioside IgG Antibodies were significantly inferior to those of PE. There is a less theoretical basis for selecting DFPP as the first choice of plasmapheresis for GBS and related disorders.—