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anti-MAG neuropathy

Ruben Herrendorff, Pascal Hänggi, Hélène Pfister, Fan Yang, Delphine Demeestere, Fabienne Hunziker, Samuel Frey, Nicole Schaeren-Wiemers, Andreas J Steck, Beat Ernst
Anti-MAG (myelin-associated glycoprotein) neuropathy is a disabling autoimmune peripheral neuropathy caused by monoclonal IgM autoantibodies that recognize the carbohydrate epitope HNK-1 (human natural killer-1). This glycoepitope is highly expressed on adhesion molecules, such as MAG, present in myelinated nerve fibers. Because the pathogenicity and demyelinating properties of anti-MAG autoantibodies are well established, current treatments are aimed at reducing autoantibody levels. However, current therapies are primarily immunosuppressive and lack selectivity and efficacy...
April 17, 2017: Proceedings of the National Academy of Sciences of the United States of America
Philippe Codron, Maud Cousin, Jean-François Subra, Vivien Pautot, Franck Letournel, Christophe Verny, Julien Cassereau
INTRODUCTION: Therapeutic plasma exchange (TPE) can be proposed in the treatment of chronic dysimmune peripheral neuropathies (CDPN). Actual guidelines are however based on few studies, and indications and protocols still remain to be clarified. We conducted a 10-year retrospective study in order to assess the effectiveness and tolerance of TPE in CDPN. METHODS: All patients treated for CDPN with TPE from October 2006 to March 2016 in the university hospital of Angers were included...
March 1, 2017: Journal of Clinical Apheresis
Aude Gesquière-Dando, Emilien Delmont, Mael Launay, Jose Boucraut, Sharham Attarian
OBJECTIVES: To explore clinical-neurophysiological correlations in anti-myelin-associated glycoprotein (anti-MAG) neuropathy. METHODS: Clinical and electrophysiological data of 42 patients with anti-MAG neuropathy were retrospectively analysed. Disability was evaluated using the Overall Neuropathy Limitation Scale (ONLS), motor impairment through MRC sum score and sensory deficiency through INCAT sensory score. Compound motor action potential (CMAP) sum score was calculated adding the distal CMAP amplitude of the median, ulnar, tibial and fibular nerves of both sides...
February 2017: Neurophysiologie Clinique, Clinical Neurophysiology
Emilien Delmont, Fu Liong Hiew, Julien Cassereau, Anne-Catherine Aubé-Nathier, Aude-Marie Grapperon, Shahram Attarian, Yusuf A Rajabally
Our objective was to assess determinants of quality of life (QoL) in anti-myelin associated glycoprotein antibody (MAG) neuropathy. The SF-36 questionnaire was assessed in 55 patients, from Marseille, Angers (France) and Birmingham (UK). Routine clinical evaluations included Medical Research Council (MRC) sum score, inflammatory neuropathy cause and treatment (INCAT) sensory score, inflammatory Rasch-built overall disability score (I-RODS), ataxia score, Jamar grip dynamometry, timed 10-m walk, neuropathic pain symptom inventory (NPSI) score, and fatigue severity score (FSS)...
March 2017: Journal of the Peripheral Nervous System: JPNS
E Delmont
Over the last five years, the management of peripheral neuropathies has become structured by the publication of recognized diagnostic criteria for inflammatory neuropathies and the elaboration of a function score, the R-ODS, used to evaluate the progression of these neuropathies. The concept of nodo-paranodopathy has enriched the concept of peripheral neuropathies, over-riding the classical mechanisms of axonal and demyelinating mechanisms. The structures of the nodes of Ranvier, gangliosides, contractin and neurofascin are preferential targets for auto-antibodies responsible for dysimmune neuropathies...
December 2016: Revue Neurologique
Michael Pt Lunn, Eduardo Nobile-Orazio
BACKGROUND: Serum monoclonal anti-myelin-associated glycoprotein (anti-MAG) antibodies may be pathogenic in some people with immunoglobulin M (IgM) paraprotein and demyelinating neuropathy. Immunotherapies aimed at reducing the level of these antibodies might be expected to be beneficial. This is an update of a review first published in 2003 and previously updated in 2006 and 2012. OBJECTIVES: To assess the effects of immunotherapy for IgM anti-MAG paraprotein-associated demyelinating peripheral neuropathy...
October 4, 2016: Cochrane Database of Systematic Reviews
Taimour Alam, James J P Alix, D Ganesh Rao, Marios Hadjivassiliou
No abstract text is available yet for this article.
February 2017: Muscle & Nerve
Pierre Lozeron, Vincent Ribrag, David Adams, Marion Brisset, Marguerite Vignon, Marine Baron, Marion Malphettes, Marie Theaudin, Bertrand Arnulf, Nathalie Kubis
To report the frequency of the different patterns of sensory and motor electrophysiological demyelination distribution in patients with anti-MAG neuropathy in comparison with patients with IgM neuropathy without MAG reactivity (IgM-NP). Thirty-five anti-MAG patients at early disease stage (20.1 months) were compared to 23 patients with IgM-NP; 21 CIDP patients and 13 patients with CMT1a neuropathy were used as gold standard neuropathies with multifocal and homogeneous demyelination, respectively. In all groups, standard motor and sensory electrophysiological parameters, terminal latency index and modified F ratio were investigated...
September 2016: Journal of Neurology
Jean-Michel Vallat, Laurent Magy, Jonathan Ciron, Philippe Corcia, Gwendal Le Masson, Stéphane Mathis
INTRODUCTION: IgM monoclonal gammopathy with anti-MAG (myelin associated glycoprotein) antibodies is associated with demyelinating polyneuropathy. MAG mediates adhesion between the Schwann cell membrane (non-compact myelin) and axons. Various drugs have been tried in this form of neuropathy, with varying responses, but to date there is no consensus on the treatment of this disease. AREAS COVERED: Based on the medical literature and the experience of our group of clinicians, we offer some proposals for the management of anti-MAG neuropathy...
September 2016: Expert Review of Neurotherapeutics
Giuliana Galassi, Manuela Tondelli, Alessandra Ariatti, Francesca Benuzzi, Paolo Nichelli, Franco Valzania
AIM OF THE STUDY: Neuropathy associated with IgM monoclonal gammopathy (MGUS) represents distinctive clinical syndrome, characterized by male predominance, late age of onset, slow progression, predominantly sensory symptoms, deep sensory loss, ataxia, minor motor impairment. More than 50% of patients with neuropathy-associated MGUS possess antibodies against myelin-associated glycoprotein (MAG). Purpose of our study was to assess effects on disease progression of demographic, clinical and neurophysiological variables in our large cohort of patients...
May 2017: International Journal of Neuroscience
Ioanna M Athanasopoulou, Maria Rasenack, Christine Grimm, Hubertus Axer, Michael Sinnreich, Bernhard F Décard, Alexander Grimm
OBJECTIVE: To investigate the use of peripheral nerve ultrasound (PNUS) in addition to nerve conduction studies (NCS) in the diagnosis of paraproteinemic neuropathies (PN). METHODS: PNUS/NCS of predefined peripheral nerves and the 5th/6th cervical roots were performed in patients with chronic inflammatory demyelinating polyneuropathy (CIDP) (+/-paraprotein), patients with anti-MAG neuropathy, and patients with neuropathy and multiple myeloma or monoclonal gammopathy of uncertain significance (MGUS) - summarized as M-protein associated neuropathies (MPAN) and compared to controls (+/-paraprotein)...
March 15, 2016: Journal of the Neurological Sciences
Brian C Callaghan, Raymond S Price, Kevin S Chen, Eva L Feldman
IMPORTANCE: Peripheral neuropathy is a prevalent condition that usually warrants a thorough history and examination but has limited diagnostic evaluation. However, rare localizations of peripheral neuropathy often require more extensive diagnostic testing and different treatments. OBJECTIVE: To describe rare localizations of peripheral neuropathy, including the appropriate diagnostic evaluation and available treatments. EVIDENCE REVIEW: References were identified from PubMed searches conducted on May 29, 2015, with an emphasis on systematic reviews and randomized clinical trials...
December 2015: JAMA Neurology
Mary L Vo, Peter Martin, Norman Latov
Gait impairment is a common presentation in patients with IgM anti-myelin-associated glycoprotein (anti-MAG) antibody demyelinating neuropathy. However, current methods used to assess gait are limited. We report spatiotemporal gait parameters captured by GAITRite, a computerized walkway with embedded pressure sensors. The patient worsened after treatment with rituximab and subsequently improved with intravenous immunoglobulin. Serial gait assessments were performed at baseline and after treatment. Spatiotemporal gait parameters correlated with Medical Research Council sum score, Inflammatory Neuropathy Cause and Treatment disability score, and grip strength...
September 2015: Journal of Clinical Neuromuscular Disease
Mariëlle H J Pruppers, Ingemar S J Merkies, Nicolette C Notermans
PURPOSE OF REVIEW: This review aims to provide an overview of all randomized trials performed in IgM Anti-Myelin Associated Glycoprotein related peripheral neuropathy (MGUSP) with emphasis on the applied outcome measures including the rationale for their choice and possible limitations, emphasizing new advances in modern clinimetrics. RECENT FINDINGS: All clinical trials performed in patients with MGUSP have been negative, which raises many unanswered questions: were the sample sizes too small, the duration of the trials too short, the chosen medical interventions not aggressive enough, the definition of being a responder inadequate, and, last but not least, the outcome measures used improper? Only recently has attention been directed towards the possibility of using suboptimal outcome measures as a potential factor that may have contributed to the negative results in MGUSP...
October 2015: Current Opinion in Neurology
Laurent Magy, Raphaël Kaboré, Stéphane Mathis, Prisca Lebeau, Karima Ghorab, Christiane Caudie, Jean-Michel Vallat
Polyneuropathy associated with IgM monoclonal gammopathy and anti-myelin associated glycoprotein (MAG) antibodies is an immune-mediated demyelinating neuropathy. The pathophysiology of this condition is likely to involve anti-MAG antibody deposition on myelin sheaths of the peripheral nerves and it is supposed to be distinct from chronic inflammatory demyelinating neuropathy (CIDP), another immune-mediated demyelinating peripheral neuropathy. In this series, we have retrospectively reviewed clinical and laboratory findings from 60 patients with polyneuropathy, IgM gammopathy, and anti-MAG antibodies...
2015: Journal of Immunology Research
Marta Campagnolo, Sergio Ferrari, Chiara Dalla Torre, Ilaria Cabrini, Mario Cacciavillani, Marta Lucchetta, Susanna Ruggero, Elisabetta Toffanin, Tiziana Cavallaro, Chiara Briani
IgM paraproteins often present reactivity to myelin-associated glycoprotein (MAG) and sulfatide. We describe the clinical and neurophysiological findings, and therapy response in 21 patients with IgM paraproteinemic neuropathy (15 with anti-MAG antibodies, 1 with anti-sulfatide antibodies, and 5 with both reactivity), and in 2 with anti-sulfatide positivity and no hematological disease. All patients complained of sensory symptoms, the majority had demyelinating neuropathy. Indirect immunofluorescence on human normal sural nerves disclosed different staining patterns...
April 15, 2015: Journal of Neuroimmunology
Pierre R Bourque, Jodi Warman Chardon, Rami Massie
Peripheral nervous system axons and myelin have unique potential protein, proteolipid, and ganglioside antigenic determinants. Despite the existence of a blood-nerve barrier, both humoral and cellular immunity can be directed against peripheral axons and myelin. Molecular mimicry may be triggered at the systemic level, as was best demonstrated in the case of bacterial oligosaccharides. The classification of immune neuropathy has been expanded to take into account specific syndromes that share unique clinical, electrophysiological, prognostic and serological features...
September 20, 2015: Clinica Chimica Acta; International Journal of Clinical Chemistry
Satoshi Kuwabara
This review described current status and perspectives of treatment for immune-mediated neuropathies, such as Guillain-Barre syndrome, chronic inflammatory demyelinating polyneuropathy (CIDP), multifocal motor neuropathy, and demyelinating neuropathy with anti-MAG neuropathy. corticosteroids, immunoglobulin therapy, and plasmapheresis are conventional treatments for these neuropathies, but the responsiveness to the treatments significantly differ among the disorders. Promising new treatment options include anti-complement monoclonal antibody (Eculizumab, anti-C5) for Guillain-Barre syndrome, and rituximab (anti-CD20) for anti-MAG neuropathy...
2014: Rinshō Shinkeigaku, Clinical Neurology
C Giannotta, D Di Pietro, F Gallia, E Nobile-Orazio
BACKGROUND AND PURPOSE: Anti-sulfatide immunoglobulin M (IgM) antibodies have been associated with different forms of neuropathies but their diagnostic role in neuropathy remains unclear. METHODS: The clinical association of increased titers of anti-sulfatide IgM antibodies in 570 patients with neuropathy and related disorders examined in our laboratory since 2004 was reviewed. Sera were tested by enzyme-linked immunosorbent assay at the initial serum dilution of 1:32,000 and titrated by serial two-fold dilution...
May 2015: European Journal of Neurology: the Official Journal of the European Federation of Neurological Societies
Ali Al-Zuhairy, Henrik Daa Schrøder, Torben Plesner, Niels Abildgaard, Søren H Sindrup
BACKGROUND AND PURPOSE: For several decades an association between MGUS, IgM-MGUS in particular, and peripheral neuropathy has been suspected. Several histopathology studies have shown binding of IgM to myelin and a secondary widening of myelin lamellae in cutaneous nerves and in the sural nerve of patients with IgM-MGUS, or Waldenström's Macroglobulinaemia (WM), and peripheral neuropathy. In this retrospective study we investigated the value of skin biopsy examination in the diagnosis of MGUS- and WM-associated peripheral neuropathy...
February 15, 2015: Journal of the Neurological Sciences
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