The Experts below are selected from a list of 3000 Experts worldwide ranked by ideXlab platform

E Nobileorazio - One of the best experts on this subject based on the ideXlab platform.

  • immunosuppressant and immunomodulatory treatments for Multifocal Motor Neuropathy
    Cochrane Database of Systematic Reviews, 2015
    Co-Authors: Thirugnanam Umapathi, R A C Hughes, E Nobileorazio, Jean Marc Leger
    Abstract:

    BACKGROUND: Multifocal Motor Neuropathy is a distinct clinical entity characterised by progressive, predominantly distal, asymmetrical limb weakness and minimal sensory abnormality. The diagnostic feature of this condition is the presence of multiple partial Motor nerve conduction blocks. Controlled trials have demonstrated the efficacy of regular intravenous immunoglobulin infusions. Immunosuppressive agents have been used as primary, second-line or adjunctive agents for its treatment. This review was undertaken to identify and review systematically randomised controlled trials of immunosuppressive agents. The use of intravenous immunoglobulin will be the subject of a separate review. OBJECTIVES: To provide the best available evidence from randomised controlled trials on the role of immunosuppressive agents for the treatment of Multifocal Motor Neuropathy. SEARCH STRATEGY: We searched the Cochrane Neuromuscular Disease Group trials register for all trials of Multifocal Motor Neuropathy published, using 'Multifocal Motor Neuropathy' OR 'chronic inflammatory demyelinating polyradiculoNeuropathy' OR ' conduction block' OR ' Motor Neuropathy' AND 'immunosuppressive agents', 'immunosuppressants', 'corticosteroids', 'plasma exchange', 'azathioprine', 'cyclophosphamide', 'cyclosporin', 'ciclosporin', 'methotrexate', and 'mycophenolate', 'immunomodulatory agents', 'interferon', 'total lymphoid irradiation' or 'bone marrow transplantation' as search terms. In addition we searched MEDLINE, EMBASE for 2000 and 2001 and CINAHL, LILACS for all years. We updated the register search in February 2004 and searched MEDLINE (January 1966 to end May 2004) and EMBASE (January 1980 to end May 2004). SELECTION CRITERIA: All randomised controlled trials and quasi-randomised clinical trials in which allocation was not random but was intended to be unbiased (e.g. alternate allocation) were to have been selected. Since no such trials were discovered, all prospective and retrospective case series were included in the 'background' or 'discussion' sections of the review. DATA COLLECTION AND ANALYSIS: All studies on Multifocal Motor Neuropathy or lower Motor neuron weakness with conduction block and no sensory abnormality were scrutinised for data on patients treated with any form of immunosuppressive agents besides intravenous immunoglobulin. The information on the outcome of treatment was then collated and summarised. MAIN RESULTS: We found no randomised controlled trials of any immunosuppressive agents for Multifocal Motor Neuropathy. We summarised the results of retrospective and prospective case series in the discussion of the review. AUTHORS' CONCLUSIONS: There are no randomised controlled trials to indicate whether immunosuppressive agents are beneficial in Multifocal Motor Neuropathy.

  • autoantibodies to neurofascin 186 and gliomedin in Multifocal Motor Neuropathy
    Journal of Neuroimmunology, 2014
    Co-Authors: Francesca Notturno, E Nobileorazio, Marinella Carpo, Tiziana Di Febo, Nobuhiro Yuki, Blanca Fernandez M Rodriguez, Davide Corti, Angelo De Lauretis, Antonino Uncini
    Abstract:

    Abstract We tested autoantibodies to neurofascin-186 (NF186) and gliomedin in sera from patients with Multifocal Motor Neuropathy (MMN, n = 53) and chronic inflammatory demyelinating polyNeuropathy (CIDP, n = 95) by ELISA. IgG antibodies to NF186 or gliomedin were found in 62% of MMN and 1% of CIDP sera, and IgM antibodies to the same antigens in 12% of MMN and 1% of CIDP sera. These autoantibodies activated complement. Ten percent of the MMN sera without IgM anti-GM1 reactivity had anti-NF186 antibodies. Because NF186 and gliomedin play a crucial role for salutatory conduction, the autoantibodies may contribute to produce Motor nerve conduction block and muscle weakness in MMN.

  • chronic inflammatory demyelinating polyradiculoNeuropathy and Multifocal Motor Neuropathy treatment update
    Current Opinion in Neurology, 2010
    Co-Authors: E Nobileorazio, Francesca Gallia, Francesco Tuccillo, F Terenghi
    Abstract:

    Purpose of reviewChronic inflammatory demyelinating polyradiculoNeuropathy (CIDP) and Multifocal Motor Neuropathy usually respond to immune therapies including steroids and plasma exchange for CIDP and high-dose intravenous immunoglobulins (IVIgs) for both diseases. Other immune therapies have been

  • Multifocal Motor Neuropathy current concepts and controversies
    Muscle & Nerve, 2005
    Co-Authors: E Nobileorazio, A Cappellari, Alberto Priori
    Abstract:

    Multifocal Motor Neuropathy (MMN) is now a well-defined purely Motor multiNeuropathy characterized by the presence of Multifocal partial Motor conduction blocks (CB), frequent association with anti-GM1 IgM antibodies, and usually a good response to high-dose intravenous immunoglobulin (IVIg) therapy. However, several issues remain to be clarified in the diagnosis, pathogenesis, and therapy of this condition including its nosological position and its relation to other chronic dysimmune neuropathies; the degree of CB necessary for the diagnosis of MMN; the existence of an axonal form of MMN; the pathophysiological basis of CB; the pathogenetic role of antiganglioside antibodies; the mechanism of action of IVIg treatments in MMN and the most effective regimen; and the treatment to be used in unresponsive patients. These issues are addressed in this review of the main clinical, electrophysiological, immunological, and therapeutic features of this Neuropathy.

  • how long is ivig effective in Multifocal Motor Neuropathy
    Neurology, 2004
    Co-Authors: F Terenghi, Marinella Carpo, Anna Bersano, A Cappellari, S Barbieri, E Nobileorazio
    Abstract:

    The authors treated 10 patients with Multifocal Motor Neuropathy (MMN) responding to an initial course of IV immunoglobulin (IVIg) with periodic infusion for 5 to 12 years (mean 8.2 years). At last follow-up, only two patients had maintained the maximal improvement achieved during therapy while eight worsened despite increasing Ig dosage. This decline started after 3 to 7 years (mean 4.8 years) of therapy and correlated with a reduction of distal compound muscle action potential amplitudes ( p

Leonard H Van Den Berg - One of the best experts on this subject based on the ideXlab platform.

  • Multifocal Motor Neuropathy : IVIg and other therapies
    2020
    Co-Authors: Leonard H Van Den Berg
    Abstract:

    Placebo-controlled studies showed that treatment with intravenous human immunoglobulins (IVIg) improves muscle strength of patients with Multifocal Motor Neuropathy. The beneficial effect of IVIg lasts several weeks, and repeated IVIg are necessary to maintain muscle strength. Maintenance IVIg treatment is expensive and may not prevent long-term progression of Motor deficits and axonal degeneration in Multifocal Motor Neuropathy. Frequent infusions may also be burdensome to patients, but at present there is no therapeutic alternative to IVIg therapy. Plasma exchange is probably ineffective, and prednisone may worsen the disease course. Anecdotal reports suggest that cyclophosphamide may be effective as primary therapy or adjunctive therapy to IVIg, but its toxicity may preclude long-term use in relatively young patients. Evaluation in placebo-controlled trials of the efficacy of adjunctive (immunosuppressive) therapy that would allow reduction of IVIg doses is needed.

  • Multifocal Motor Neuropathy controversies and priorities
    Journal of Neurology Neurosurgery and Psychiatry, 2020
    Co-Authors: James P B Dyck, Leonard H Van Den Berg, Matthew C Kiernan, Bruce V Taylor
    Abstract:

    Despite 30 years of research there are still significant unknowns and controversies associated with Multifocal Motor Neuropathy (MMN) including disease pathophysiology, diagnostic criteria and treatment. Foremost relates to the underlying pathophysiology, specifically whether MMN represents an axonal or demyelinating Neuropathy and whether the underlying pathophysiology is focused at the node of Ranvier. In turn, this discussion promotes consideration of therapeutic approaches, an issue that becomes more directed in this evolving era of precision medicine. It is generally accepted that MMN represents a chronic progressive immune-mediated Motor Neuropathy clinically characterised by progressive asymmetric weakness and electrophysiologically by partial Motor conduction block. Anti-GM1 IgM antibodies are identified in at least 40% of patients. There have been recent developments in the use of neuromuscular ultrasound and MRI to aid in diagnosing MMN and in further elucidation of its pathophysiological mechanisms. The present Review will critically analyse the knowledge accumulated about MMN over the past 30 years, culminating in a state-of-the-art approach to therapy.

  • mri shows thickening and altered diffusion in the median and ulnar nerves in Multifocal Motor Neuropathy
    European Radiology, 2017
    Co-Authors: Leonard H Van Den Berg, Wieke Haakma, Bas A Jongbloed, Martijn Froeling, Stephan H Goedee, Alexander Leemans, Jeroen Hendrikse
    Abstract:

    Objectives To study disease mechanisms in Multifocal Motor Neuropathy (MMN) with magnetic resonance imaging (MRI) and diffusion tensor imaging (DTI) of the median and ulnar nerves.

  • immune pathogenesis and treatment of Multifocal Motor Neuropathy
    Journal of Clinical Immunology, 2013
    Co-Authors: Leonard H Van Den Berg, Elisabeth A Cats, Lotte Vlam, Sanneke Piepers
    Abstract:

    Multifocal Motor Neuropathy (MMN) is a rare, probably immune-mediated chronic disorder characterized by asymmetric distal limb weakness and conduction block. The exact pathogenesis of MMN is still unclear, but IgM anti-GM1 antibodies, which can be detected in sera from approximately half of all MMN patients, are thought to play an important role. Treatment with intravenous immunoglobulin (IVIG) is effective in the vast majority of patients, but, despite IVIG maintenance treatment, many patients experience a slowly progressive decline in muscle strength. In this review we will summarize the results from studies on pathogenesis. We will discuss current treatment strategies of MMN and how insight into MMN pathogenesis may translate into novel therapies in the future.

  • Multifocal Motor Neuropathy diagnosis pathogenesis and treatment strategies
    Nature Reviews Neurology, 2012
    Co-Authors: Lotte Vlam, Elisabeth A Cats, Hessel Franssen, Dirk C G Straver, Sanneke Piepers, Leonard H Van Den Berg
    Abstract:

    Multifocal Motor Neuropathy (MMN) is a rare inflammatory disorder that features slowly progressive, asymmetric distal limb weakness. Leonard van den Berg and colleagues describe the diagnostic criteria for MMN, which are important for distinguishing this disease from mimic disorders such as amyotrophic lateral sclerosis. The authors also discuss the pathophysiology of MMN, emphasizing the role of GM1-specific autoantibodies, and outline current treatment options and possible new therapeutic strategies.

R. Kaji - One of the best experts on this subject based on the ideXlab platform.

  • Multifocal Motor Neuropathy
    Handbook of Clinical Neurophysiology, 2020
    Co-Authors: R. Kaji
    Abstract:

    Publisher Summary This chapter describes Multifocal Motor Neuropathy (MMN), which is a disease of the lower Motor neurons or Motor nerves and produces asymmetric muscle weakness, often in association with fasciculations and cramping. MMN not only challenges the electromyographer to make differential diagnosis from a fatal disease but also provides an opportunity to reconsider the mechanism of conduction block in demyelinating neuropathies. Conduction block or slowing is not always a consequence of demyelination. Because myelinating Schwann cells mediate the spacing of sodium channel clusters by excluding the channels from the contact surface of Schwann cells and the axon, the lack of normal axo-glial contact in chronic inflammatory demyelinating polyNeuropathy (CIDP) may lead to an abnormal clustering of the channels that affects channel densities at the node. In MMN, CIDP, and other demyelinating neuropathies, axonal dysfunction associated with demyelinating lesions must be considered for full understanding of the pathophysiology.

  • cervical root sonography to differentiate Multifocal Motor Neuropathy from als
    The Journal of Medical Investigation, 2016
    Co-Authors: Hiroyuki Nodera, Yuishin Izumi, Naoko Takamatsu, R. Kaji
    Abstract:

    To explore suggestive evidence of focal proximal demyelination in Multifocal Motor Neuropathy (MMN) without overt evidence of conduction block, we conducted sonographical assessment of cervical nerve roots in 9 MMN patients, 22 ALS patients, and 17 control subjects. The mean diameters of the C5 and C6 roots in MMN patients were significantly larger than those in ALS and controls, especially on the clinically dominant side. Although non-specific, sonography can be a potentially useful diagnostic procedure to support the diagnosis of MMN, even when overt conduction block is lacking.

  • Diagnosis and treatment of Multifocal Motor Neuropathy
    Current Treatment Options in Neurology, 2008
    Co-Authors: R. Kaji
    Abstract:

    Multifocal Motor Neuropathy (MMN) is a unique disease mimicking Motor neuron disease, but it is treatable with intravenous immunoglobulins. Anti-GM1 IgM antibody titers are not sensitive enough to predict the outcome. Electrodiagnosis is essential for the diagnosis of MMN. Conduction block has been suggested as the best diagnostic marker, but it is not found in all treatable cases. Activity-dependent conduction changes, as revealed by comparing conduction before and after maximal voluntary contraction of the muscle, are a convenient and promising tool. Treatment options include various immunosuppressants (including cyclophosphamide), but there has not been ample evidence in favor of any of these agents in randomized controlled trials. Intravenous immunoglobulins remain the mainstay for treating MMN.

  • Pathophysiology of Multifocal Motor Neuropathy
    2007
    Co-Authors: R. Kaji
    Abstract:

    Multifocal Motor Neuropathy is a unique disease that not only challenges the electromyographer to make differential diagnosis from a fatal disease but also provides an opportunity to reconsider the mechanism of conduction block in demyelinating neuropathies. Conduction block or slowing is not always a consequence of demyelination, but can be due to membrane hyperpolarisation or depolarisation, as well as sodium channel blockage. Recent pieces of evidence suggest that clinical features of Multifocal Motor Neuropathy, such as fasciculations, muscle fatigue, cold paralysis, sensory sparing and secondary axonal degeneration, can be explained by depolarisation and hyperpolarisation block in addition to focal demyelination.

  • activity dependent conduction block in Multifocal Motor Neuropathy magnetic fatigue test
    Neurology, 2006
    Co-Authors: Hiroyuki Nodera, Hugh Bostock, Yuishin Izumi, Kazumi Nakamura, Ryo Urushihara, Takashi Sakamoto, Nagako Murase, Hideki Shimazu, Susumu Kusunoki, R. Kaji
    Abstract:

    BACKGROUND: Multifocal Motor Neuropathy (MMN) is often misdiagnosed as Motor neuron disease, especially when overt evidence of conduction block (CB) is lacking. Activity-dependent CB (ADCB), defined as transient CB induced by brief exercise, has been recently found in MMN but not in ALS. METHODS: To test the diagnostic utility of ADCB for differentiating MMN from ALS, the authors recorded the compound muscle action potentials (CMAPs) from small hand muscles by magnetically stimulating nerve roots before and after 1 minute of maximal voluntary contraction (magnetic fatigue test). They examined nine patients with MMN with unequivocal clinical responses to IV immunoglobulins (IVIgs), yet lacked CB according to the conventional criteria. RESULTS: Six MMN patients had postexercise CB/temporal dispersion maximum in the immediate postexercise period. ADCB in an MMN patient improved after IVIg. Further analysis revealed that prolongation of the duration from the onset to the positive peak of the CMAP was the most sensitive indicator for MMN, presumably because the phase cancellation obscures the abnormalities of the other parameters. CONCLUSION: The magnetic fatigue test is useful in detecting mild conduction block presumably located in a proximal nerve segment in patients with Multifocal Motor Neuropathy who do not fulfill its conventional electrodiagnostic criteria.

Vinay Chaudhry - One of the best experts on this subject based on the ideXlab platform.

  • treatment of Multifocal Motor Neuropathy
    Current Treatment Options in Neurology, 2014
    Co-Authors: Madhavi Jinka, Vinay Chaudhry
    Abstract:

    Multifocal Motor Neuropathy (MMN) is a treatable immune disorder of the peripheral nerves that is characterized clinically by slowly progressive or stepwise asymmetric distal > proximal, upper > lower limb weakness in multiple Motor nerve distributions; electrophysiologically by Multifocal Motor demyelination, specifically partial Motor conduction block; laboratory evidence of high serum anti-GM1 IgM antibodies; and remarkable treatment response to intravenous immunoglobulin (IVIG). IVIG has become the treatment of choice, and the U.S. Food and Drug Administration (FDA) has approved Gammagard Liquid 10 % [immune globulin infusion (human)] as a treatment for Multifocal Motor Neuropathy (MMN). Response to IVIG in MMN is dose- and frequency-dependent, most patients needing high (2 g/kg) and frequent (every 4–8 weeks) doses for several years. Over time, response to IVIG may decrease despite higher and more frequent dosing of IVIG treatment. Subcutaneous immunoglobulin (dose equivalent to IVIG) given in weekly fashion has recently been used with equal efficacy and fewer side effects. There are some case reports and non-randomized trials suggesting variable results from therapeutic or adjunctive use of other immunosuppressive or immunomodulatory agents such as cyclophosphamide, cyclosporine, methotrexate, azathioprine, interferon beta-1a, and rituximab. Of these, cyclophosphamide and rituximab are the only immune treatments that have shown some benefits in case reports. One randomized controlled trial of mycophenolate mofetil used as adjunctive agent did not prove efficacious in altering the disease course. Although MMN, like chronic inflammatory demyelinating polyNeuropathy (CIDP), is a chronic immune-mediated demyelinating Neuropathy, the use of corticosteroids and plasma exchange – two other therapies used in CIDP – is not beneficial for MMN. Further investigations are warranted to evaluate the immunopathogenesis of MMN and to explore options for dose, frequency, and duration of IVIG treatment as well as the use of alternative immunomodulatory agents either as primary therapeutic or adjunctive agents.

  • Worsening of Multifocal Motor Neuropathy during pregnancy
    Neurology, 2002
    Co-Authors: Vinay Chaudhry, Diana M. Escolar, David R Cornblath
    Abstract:

    Three women with Multifocal Motor Neuropathy (MMN) were treated during pregnancy. Compared with their pregestation strength, the women became weaker in previously involved muscles and showed new weakness in previously unaffected muscles. All were treated with IV immunoglobulin during pregnancy and improved in strength. After pregnancy, strength in all patients returned to the prepregnancy state. The authors conclude that pregnancy may worsen MMN.

  • sensory nerve pathology in Multifocal Motor Neuropathy
    Annals of Neurology, 1996
    Co-Authors: Andrea M Corse, Vinay Chaudhry, Thomas O Crawford, David R Cornblath, Ralph W Kuncl, John W Griffin
    Abstract:

    : The nosological status of Multifocal Motor Neuropathy remains controversial. The clinical and electrodiagnostic hallmarks suggest selective Motor fiber involvement. In this study, we asked to what extent sensory nerves might be involved pathologically in Multifocal Motor Neuropathy. Examination of sensory nerve biopsy specimens from 11 patients did reveal pathological findings in all, but they were very mild. An increased number of thinly myelinated, large-caliber fibers was the unifying feature common to each specimen. By electron microscopy, each biopsy specimen had thinly myelinated fibers surrounded by minor onion bulbs. Active demyelination, though scant, was seen in 3 nerves. Myelinated fiber density was normal. Subperineurial edema and inflammation were not present. We conclude that Multifocal Motor Neuropathy is not an exclusively Motor abnormality, although it appears to be so clinically and electrophysiologically. The frequent, albeit mild, pathological abnormalities in sensory fibers suggest that the demyelinating pathophysiology also affects sensory fibers, but to a lesser degree than Motor fibers. Some investigators maintain that Multifocal Motor Neuropathy is within the spectrum of chronic inflammatory demyelinating polyNeuropathy. The very mild degree of sensory fiber involvement, the absence of inflammation or edema, and the distinctive clinical features support the concept of Multifocal Motor Neuropathy as distinct from chronic inflammatory demyelinating polyNeuropathy.

  • Multifocal Motor Neuropathy electrodiagnostic features
    Muscle & Nerve, 1994
    Co-Authors: Andrea M Corse, Vinay Chaudhry, David R Cornblath, Ralph W Kuncl, Miriam Freimer, John W Griffin
    Abstract:

    Diagnosis of Multifocal Motor Neuropathy (MMN), a syndrome characterized by progressive asymmetric weakness with intact sensation, is important because the disorder often responds to treatment. Multifocal partial Motor conduction block (PMCB) has been emphasized as a cardinal feature in the diagnosis of this syndrome, but detailed nerve conduction studies are not available. Nine patients, ages 28–58, had chronic, progressive, asymmetric, predominantly distal limb weakness for 5–18 years. Sensation was normal and reflexes were reduced asymmetrically. Although all 9 demonstrated PMCB localized to short nerve segments, additional features of Multifocal Motor demyelination were present, including temporal dispersion (5 patients), segmentally reduced Motor nerve conduction velocity (7 patients), prolonged distal Motor latency (4 patients), and prolonged F-wave latency (9 patients). The strength of all patients improved after treatment with human immune globulin. A reduction in the degree of PMCB or an increase in the distal Motor amplitude or both accompanied the clinical improvement. These studies suggest that patients with MMN demonstrate widespread evidence of Motor demyelination in addition to the well-described PMCB, and that reduction of PMCB accounts for the increase in strength following therapy. © 1994 John Wiley & Sons, Inc.

Andreas Weishaupt - One of the best experts on this subject based on the ideXlab platform.

  • contactin 1 and neurofascin 155 186 are not targets of auto antibodies in Multifocal Motor Neuropathy
    PLOS ONE, 2015
    Co-Authors: Kathrin Doppler, Luise Appeltshauser, Heidrun H Kramer, Judy King Man Ng, Edgar Meinl, Carmen Villmann, Peter J Brophy, Sulayman D Dibhajj, Stephen G Waxman, Andreas Weishaupt
    Abstract:

    Multifocal Motor Neuropathy is an immune mediated disease presenting with Multifocal muscle weakness and conduction block. IgM auto-antibodies against the ganglioside GM1 are detectable in about 50% of the patients. Auto-antibodies against the paranodal proteins contactin-1 and neurofascin-155 and the nodal protein neurofascin-186 have been detected in subgroups of patients with chronic inflammatory demyelinating polyNeuropathy. Recently, auto-antibodies against neurofascin-186 and gliomedin were described in more than 60% of patients with Multifocal Motor Neuropathy. In the current study, we aimed to validate this finding, using a combination of different assays for auto-antibody detection. In addition we intended to detect further auto-antibodies against paranodal proteins, specifically contactin-1 and neurofascin-155 in Multifocal Motor Neuropathy patients’ sera. We analyzed sera of 33 patients with well-characterized Multifocal Motor Neuropathy for IgM or IgG anti-contactin-1, anti-neurofascin-155 or -186 antibodies using enzyme-linked immunosorbent assay, binding assays with transfected human embryonic kidney 293 cells and murine teased fibers. We did not detect any IgM or IgG auto-antibodies against contactin-1, neurofascin-155 or -186 in any of our Multifocal Motor Neuropathy patients. We conclude that auto-antibodies against contactin-1, neurofascin-155 and -186 do not play a relevant role in the pathogenesis in this cohort with Multifocal Motor Neuropathy.

  • Contactin-1 and Neurofascin-155/-186 Are Not Targets of Auto-Antibodies in Multifocal Motor Neuropathy.
    PloS one, 2015
    Co-Authors: Kathrin Doppler, Luise Appeltshauser, Heidrun H Kramer, Judy King Man Ng, Edgar Meinl, Carmen Villmann, Peter J Brophy, Stephen G Waxman, Sulayman D Dib-hajj, Andreas Weishaupt
    Abstract:

    Multifocal Motor Neuropathy is an immune mediated disease presenting with Multifocal muscle weakness and conduction block. IgM auto-antibodies against the ganglioside GM1 are detectable in about 50% of the patients. Auto-antibodies against the paranodal proteins contactin-1 and neurofascin-155 and the nodal protein neurofascin-186 have been detected in subgroups of patients with chronic inflammatory demyelinating polyNeuropathy. Recently, auto-antibodies against neurofascin-186 and gliomedin were described in more than 60% of patients with Multifocal Motor Neuropathy. In the current study, we aimed to validate this finding, using a combination of different assays for auto-antibody detection. In addition we intended to detect further auto-antibodies against paranodal proteins, specifically contactin-1 and neurofascin-155 in Multifocal Motor Neuropathy patients' sera. We analyzed sera of 33 patients with well-characterized Multifocal Motor Neuropathy for IgM or IgG anti-contactin-1, anti-neurofascin-155 or -186 antibodies using enzyme-linked immunosorbent assay, binding assays with transfected human embryonic kidney 293 cells and murine teased fibers. We did not detect any IgM or IgG auto-antibodies against contactin-1, neurofascin-155 or -186 in any of our Multifocal Motor Neuropathy patients. We conclude that auto-antibodies against contactin-1, neurofascin-155 and -186 do not play a relevant role in the pathogenesis in this cohort with Multifocal Motor Neuropathy.