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         Miller Fisher Syndrome:     more detail
  1. The Official Patient's Sourcebook on Miller Fisher Syndrome: A Revised and Updated Directory for the Internet Age by Icon Health Publications, 2002-10
  2. Fisher syndrome: An entry from Thomson Gale's <i>Gale Encyclopedia of Neurological Disorders</i> by Bryan, PhD Cobb, 2005

41. Esni - European School Of Neuroimmunology
Autoimmune neuropathy, autoantibodies, Guillain Barre syndrome, Miller Fishersyndrome, gangliosides. Methods. The pathogenesis of miller fisher syndrome.
http://www.esni.org/willison.htm

Research Units
Positions available Personnel support areas
WILLISON Hugh John
Tel.: +44 (0)141 201 1100/2464/2474 Fax: +44 (0)141 201 2993 e-mail: h.j.willison@udcf.gla.ac.uk Address University Department of Neurology Institute of Neurological Sciences Southern General Hospital NHS Trust Glasgow - G51 4TF Scotland Research themes The pathogenesis of autoimmune neuropathy mediated by anti-ganglioside antibodies: clinical and experimental studies. Key words Autoimmune neuropathy, autoantibodies, Guillain Barre syndrome, Miller Fisher syndrome, gangliosides Methods Immunoassays, thin layer chromatography, antibody cloning, immunohistology, animal models Composition of the research group Postdoctoral research scientist Lynne Cochrane Postdoctoral research scientist Jean Veitch Technician Eric Wagner Technician Pat Thomson Technician Shauna Kerr Technician Tyrone Bowes PhD student (joint, Dr J Conner) Rhuari Freil PhD student (joint, Prof M Brown) MD-PhD student (writing-up) Kostas Paparounas MD-PhD student (writing-up) Recent publications
  • Immune-mediated peripheral neuropathies and voltage-gated sodiums channels. Benatar M, Willison HJ, Vincent A.
  • 42. Not Bells Miller Fisher!
    TODAY she was diagnosed with miller fisher syndrome, which is a variantof GuilainBarre syndrome. The clue that finally caught
    http://neuro-www.mgh.harvard.edu/forum/BellsPalsyF/12.9.986.27PMNotBells...Mille
    Not Bells ...Miller Fisher!
    This article submitted by Susan K on 12/9/98.
    Email Address:
    Wanted to share this information in hopes it can help. My Mom, 67, is now at day 16 following a BP diagnosis. But some things weren't adding up. She was incredibly fatigued all the time, lost her appettite, lost feeling/use of her right hand, was having trouble getting around (depending on a walker for support) and complained of occassional loss of balance. I came onto this website a week ago searching for answers because it didn't seem like all this could fit under the BP diagnosis or even be attributed to her other ongoing health problems (which include high blood pressure, high cholerstral and diet-controlled diabetes) TODAY she was diagnosed with Miller Fisher syndrome, which is a variant of Guilain-Barre syndrome. The clue that finally caught the docs attention was that the facial paralysis spread to the other side of her face. Diagnosis was confirmed by a lumbar puncture and the fact that she had lost reflex response! All the other symptoms/complaints fit into this new diagnosis. (Need more info on Guilain-Barre or Miller Fisher? Try www.gbs.org.uk/mfs.html) My advice be AGRESSIVE if you feel there is more to your facial paralysis than can be explained by BP! Mom would have been helped if she had gotten treatment quicker (they are starting plasmapharesis immediately replacing the plasma). Also, if they had done steriod treatment for the BP, it could have made the Miller Fisher WORSE!

    43. Www.panix.com/~donwiss/hoggan/mfs.txt
    miller fisher syndrome unique involvement of opthalmic division of trigeminalnerve Clin Neurol Neurosurg 1995; 97(4) 328331 2. Hughes, RA The spectrum
    http://www.panix.com/~donwiss/hoggan/mfs.txt

    44. NEJM -- Campylobacter Jejuni Infection And Guillain-Barre Syndrome
    We performed a prospective case–control study in a cohort of patients with Guillain–Barrésyndrome (96 patients) or miller fisher syndrome (7 patients
    http://content.nejm.org/cgi/content/short/333/21/1374
    HOME SEARCH CURRENT ISSUE PAST ISSUES ... HELP Previous Volume 333:1374-1379 November 23, 1995 Number 21 Next Campylobacter jejuni
    Jeremy H. Rees, Ph.D., M.R.C.P., Sara E. Soudain, B.Sc., Norman A. Gregson, Ph.D., and Richard A.C. Hughes, M.D. Table of Contents Full Text of this article PDF of this article Related Letters to the Editor ... Related Articles in Medline Articles in Medline by Author: Rees, J. H. Hughes, R. A.C. Medline Citation ABSTRACT Background Although infection with Campylobacter jejuni is recognized the clinical and epidemiologic features of this association are not well understood. Methods (96 patients) or Miller Fisher syndrome (7 patients) who were admitted to hospitals throughout England and Wales between November 1992 and April 1994. Bacteriologic and serologic techniques were used to diagnose preceding C. jejuni infection. Results There was evidence of recent C. jejuni infection in or Miller Fisher syndrome, as compared with 2 percent of household Of the 27 patients with C. jejuni infection, 19 (70 percent) reported having had a diarrheal illness within 12 weeks before the onset of the neurologic illness. No specific serotypes were

    45. Ophthalmoplegia
    miller fisher syndrome Search PUBMED for miller fisher syndrome AllReview Therapy Diagnosis. Ophthalmoplegia, Chronic Progressive
    http://www.ohsu.edu/cliniweb/C11/C11.590.472.html
    Ophthalmoplegia
    Back to previous level

    46. Mioti: Medical Condition
    Main Page Add Website Add Conference Advertising Information Email Mioti. Conditionmiller fisher syndrome. NINDS miller fisher syndrome Information Page.
    http://www.mioti.com/cat/condition/condition.asp?Cat=MillerFisher

    47. COS Post-test
    Canadian Journal of Ophthalmology miller fisher syndrome J. RaymondBuncic, MD, FRCSC October CJO, Volume 37, No. 6, Members of the
    http://cme.cybersessions.com/cos/post-tests/english/main.cfm
    Canadian Journal of Ophthalmology
    Miller Fisher Syndrome
    J. Raymond Buncic, MD, FRCSC
    October CJO, Volume 37, No. 6
    Members of the Royal College of Physicians and Surgeons of Canada may claim section 3 credit for completing this questionnaire. All personal information on the completed form is confidential and will not be released by the Canadian Ophthalmological Society. This questionnaire may not be reproduced without permission.
    Complete the test. Your results will automatically be calculated. Print the result page. Enter this activity into your ongoing CPD record at http://www.mainport.org/ Retain the report for your files in the event you are audited by the Royal College.
    1. What are the characteristic clinical findings in Miller Fisher syndrome?
    a)
    Ataxia, internal ophthalmoplegia and external ophthalmoplegia
    b)
    Ataxia, areflexia and external ophthalmoplegia c) Ataxia, areflexia and internal ophthalmoplegia d) Areflexia, internal ophthalmoplegia and external ophthalmoplegia 2. What is the recommended treatment for patients who do not show spontaneous improvement?

    48. ACTA MEDICA BELGICA AWARD
    Such antibodies were found in most cases (8 out of 9) of miller fisher syndrome,and at very high titres, in one case of GuillainBarré syndrome characterised
    http://www.ulb.ac.be/medecine/loce/Acta_Medica_Belgica/award_98.htm
    ACTA MEDICA BELGICA AWARD
    The prize winners for 1998 are : First prize ex-aequo - (75 000 BEF, each)
    Clinical relevance of the determination of anti-GQ1b antibodies in Miller Fisher and Guillain-Barré syndromes
    S. Goffette , A. Jeanjean, F. Pierret, A. Peeters, C.J.M. Sindic Abstract Anti-GQ1b antibodies were assayed by an enzymelinked immunosorbent assay in sera from patients with non-neurological disorders (N=20), and with various neurological disorders (N=59), including nine cases of Miller Fisher syndromes, 16 cases of Guillain-Barré syndrome and one case of acute post-infectious ophthalmoparesis. Such antibodies were found in most cases (8 out of 9) of Miller Fisher syndrome, and at very high titres, in one case of Guillain-Barré syndrome characterised by an initial ophthalmoparesis, and in the case of isolated post-infectious ophthalmoparesis. The latter was characterised by a long-lasting occurrence of these antibodies. Anti-GQ1b antibodies are specific for an immune-mediated neuropathy of the cranial, especially oculomotor, nerves. Acta Neurol. Belg., 1998, 98, 322-326

    49. NORD - National Organization For Rare Disorders, Inc.
    variants of GBS (acute inflammatory neuropathy or acute inflammatory demyelinatingpolyradiculoneuropathy) are recognized miller fisher syndrome, acute motor
    http://www.rarediseases.org/search/rdbdetail_abstract.html?disname=Guillain Barr

    50. GBS - The Communicator
    Another subtype, the miller fisher syndrome, involves acute onset of ataxia,areflexia, and ophthalmoplegia (paralysis of eye movements).
    http://www.guillain-barre.com/news/2002/main.html?section=article_1

    51. PNS Meeting Platform Abstracts - Inflammatory Neuropathies
    EVIDENCE FOR A COMBINED PRE AND POSTSYNAPTIC BLOCKADE OF NEUROMUSCULAR TRANSMISSIONBY ANTI-GQ1B ANTIBODIES FROM PATIENTS WITH miller fisher syndrome (MFS).
    http://pns.ucsd.edu/Plat1.abstracts.html
    Back to Program PNS Home
    Inflammatory Neuropathies Abstracts
    Platform 1
    THE MEMBRANE ATTACK COMPLEX OF COMPLEMENT (C5b-9) RESCUES SCHWANN CELLS (SchC) FROM APOPTOSIS IN EXPERIMENTAL ALLERGIC NEURITIS (EAN). Hafer-Macko C.E. Koski C.L. University of Maryland, Baltimore, Maryland, USA. MEMBRANE ATTACK COMPLEX OF COMPLEMENT (C5b9) INDUCES PROLIFERATION AND RESCUE FROM APOPTOSIS OF SCHWANN CELLS (SchC) Dashiell S.M., Rus H., Koski C.L University of Maryland, Baltimore, Maryland, USA C5b-9 deposition on SchC of GBS patients or EAN rats does not induce cytolysis secondary to complement regulatory protein expression. To determine if sublytic C5b-9 induces SchC mitogenesis and survival in vitro, rat SchC in serum free medium (N2) were stimulated with C5b-9 assembled from purified proteins (C5,6,7,8,9) or b -neuregulin (NRG). C5b-9 increased 3H-thymidine incorporation 10-fold by 24 hrs over N2 alone or N2 with heat inactivated C5b-9. Cell cycle analysis with propidium iodide and FACS showed SchC in N2 were synchronized in G1/G0 at 24 hrs. C5b-9 shifted 50% of SchC into S phase similar to NRG (100 ng/ml). C5b-9 stimulated SchC doubling as assessed by vital dye exclusion. Pertussis toxin and PD098,059, but not a PKA inhibitor, prevented C5b-9 mediated thymidine incorporation suggesting signal transduction was mediated via Gi proteins and ERK kinase. ERK1 activity, increased 2-fold by 20 min. Serum withdrawal and culture in N2 that caused 40-50% of SchC to undergo apoptosis was prevented by NRG. Likewise, C5b-9 inhibited the number of apoptotic cells and reduced TUNEL-positive SchC. C5b-9, like NRG, is a potent trophic factor stimulating SchC mitogenesis and apoptotic rescue and may contribute to peripheral nerve repair following immune-mediated demyelination.

    52. Platform 1
    EVIDENCE FOR A COMBINED PRE AND POSTSYNAPTIC BLOCKADE OF NEUROMUSCULAR TRANSMISSIONBY ANTI GQ1B ANTIBODIES FROM PATIENTS WITH miller fisher syndrome (MFS).
    http://pns.ucsd.edu/Platform1.html
    Platform 1: Inflammatory Neuropathies
    Thursday July 22, 1999 THE MEMBRANE ATTACK COMPLEX OF COMPLEMENT (C5b-9) RESCUES SCHWANN CELLS (SchC) FROM APOPTOSIS IN EXPERIMENTAL ALLERGIC NEURITIS (EAN). Hafer-Macko CE, Koski CL MEMBRANE ATTACK COMPLEX OF COMPLEMENT (C5b-9) INDUCES PROLIFERATION AND RESCUE FROM APOPTOSIS OF SCHWANN CELLS. Dashiell SM, Rus H, Koski CL T CELL RECOGNITION OF NON PROTEIN ANTIGENS IN GUILLAIN BARRE SYNDROME. Cooper JC , Hughes S, Ben-Smith A, Savage COS, Winer JB EXPOSURE TO NITRIC OXIDE DONORS CAN CAUSE AXONAL DEGENERATION: ELECTRICALLY ACTIVE AXONS ARE ESPECIALLY SUSCEPTIBLE. Smith KJ , Kapoor R, Hall SM, Davies M. EVIDENCE FOR A COMBINED PRE- AND POSTSYNAPTIC BLOCKADE OF NEUROMUSCULAR TRANSMISSION BY ANTI GQ1B ANTIBODIES FROM PATIENTS WITH MILLER FISHER SYNDROME (MFS). Buchwald B , Bufler J, Carpo M, Nobile-Orazio E, Toyka KV ANTI-GQ1B ANTIBODIES CLONED FROM MICE IMMUNISED WITH MILLER FISHER SYNDROME STRAINS OF C. JEJUNI LPS INDUCE NMJ BLOCK. Goodyear CS, Plomp JJ, O'Hanlon GM, Morrison I, Veitch J, Conner J, Molenaar PC

    53. Dr Hugh J Willison
    ganglioside antibodies in the postinfectious paralytic neuropathy termed GuillainBarre syndrome (GBS) and the GBS variant termed miller fisher syndrome (MFS
    http://www.gla.ac.uk/departments/neurology/hjwillisonhome.htm
    Dr Hugh J Willison, MBBS, PhD, FRCP. Reader in Neurology Research Profile of Neuroimmunology Group Laboratory Site Neuroimmunology Laboratories Department of Neurology, Ground Floor Neurology Block Southern General Hospital 1345 Govan Road, Glasgow, G51 4TF, Scotland Group Leader Dr. Hugh Willison h.j.willison@ucdf.gla.ac.uk ; Tel: 44 141 201 2464/2474; Fax: +44 141 201 2993. The Neuroimmunology Group is concerned with understanding the pathogenesis of autoimmune neuropathies and developing novel therapies, using a wide variety of approaches, techniques and collaborations. The particular emphasis is on the role of anti-ganglioside antibodies in the post-infectious paralytic neuropathy termed Guillain Barre syndrome (GBS) and the GBS variant termed Miller Fisher syndrome (MFS). GBS has an incidence of 1-2:100,000 (500-1000 UK case per year), very high health care costs, substantial morbidity, and a mortality of 5-10%. Considerable evidence indicates that GBS is an autoimmune disease in which immune responses directed at peripheral nerve myelin or axonal antigens cause the nerve to fail and thereby produce paralysis and other neurological deficits. An important group of nerve antigens are the family of glycolipids termed gangliosides. The Neuroimmunology Group

    54. [Home]
    13, Pinchoff B, Slavin M, Rosenstein D,. Hyman R. Divergence paralysis as theinitial sign of miller fisher syndrome. Am J Ophthalmol 1986; 101741742.
    http://coopereyecare.com/vergence(7)_dir/vergence(7)_8.htm
    Home i Landry 0. Note sur la paralysie ascendante aigue. Gazette Hebdomadaire Guillain G, Band JA, Strohl A. Sur un syndrome de radiculonévrite avec hyperalbuminosie du liquide cdphalorachidien sans reaction cellulaire. Remarques sur les caractères cliniques et graphiques des reflexes tendineux. Bull Mém Soc Med Hop Paris. Masson et Cie Ropper AH, Wijdocks EFM, Truax BT. Guillain-Barré syndrome: Contemporary Neurology Series. Philadelphia: FA Davis Co, Feldon SE, Stark L, Lehman SL, Hoyt WE Oculomotor effects of intermittent conduction block in myasthenia gravis and Guillain-Barré syndrome. Arch Neurol Schor CM. Fixation disparity: a steady-state error of disparity induced vergence. Am J Optom Physiol Opt. North RV, Henson DB. Adaptation to prism-induced heterophoria in subjects with abnormal binocular vision or asthenopia. Am J Optom Physiol Opt North RV, Henson DB. Effect of orthoptics upon the ability of patients to adapt to prism-induced heterophoria. Am J Optom Physiol Opt Kertesz AE, Kertesz J. Wide-field fusional stimulation in strabismus. Am J Optom Physiol Opt 1986;

    55. Autoantibody Testing In Neuropathy
    Suspected miller fisher syndrome or other forms of acute ophthalmoplegiabelieved to be neuropathic in origin Order antiGQ1b antibodies.
    http://neuroland.com/nm/autoab_neuro.htm
    Neuroland
    Neurology information
    Click on the brain to index page

    Search NeuroLand

    Neuro disease
    Notes ...
    Neuro Med
    Autoantibody testing in Neuropathy Initial evaluation of Neuropathy: history, examination and electrodiagnostic studies to define the neuropathy symmetric vs. asymmetric sensory vs. motor axonal or demyelinating and if conduction block is present If the etiology for the PN is not apparent, check a serum SPEP and IFE for monoclonal protein Urine testing for a paraprotein is done in some cases, particularly patients with primarily small-fiber sensory or autonomic involvement. Sensory or sensorimotor PN Demyelinating neuropathy with IgM gammopathy: particularly if there is prolonged distal latencies, anti-MAG testing is performed. Early in the course, these patients have sensory greater than motor deficits that are primarily distal. Most patients with positive anti-MAG will have an IgM monoclonal protein. Pure sensory syndromes (Ganglionopathy): Especially if asymmetric, rapidly progressive, sensory loss involving proprioception.

    56. Untitled
    Kato T, Kurita K, Arawaka S, Hosoya T, Yuki N, Shikama Y, Yamaguchi K, Sasaki H.Cranial nerve enhancement on threedimensional MRI in miller fisher syndrome.
    http://www.dokkyomed.ac.jp/dep-m/neuro/jap/caserepo-e.html
    1) Hayashi H, Park-Matsumoto Y-C, Yuki N, Itoh T, Amakawa T, Muneyuki T. A case of recurrent Guillain-Barre syndrome preceded by different infections. J Neurol 1993;240:196-197.
    2) Suzuki T, Obara Y, Yuki N. Fisher's syndrome, anti-GQ1b antibody, and HLA-B39 antigen. Am J Ophthalmol 1994;118:119.
    3) Sugita K, Ishii M, Takanashi J, Niimi H, Yuki N. Guillain-Barre syndrome associated with IgM anti-GM1 antibody following Campylobacter jejuni enteritis. Eur J Pediatr 1994;153:181-183.
    4) Takano H, Yuki N. Fisher's syndrome associated with chickenpox and anti-GQ1b antibody. J Neurol 1995;242:255-256.
    5) Kanzaki A, Yabuki S, Yuki N. Bickerstaff's brainstem encephalitis associated with cytomegalovirus infection. J Neurol Neurosurg Psychiatry 1995;58:260-261.
    6) Nagaoka U, Kato T, Kurita K, Arawaka S, Hosoya T, Yuki N, Shikama Y, Yamaguchi K, Sasaki H. Cranial nerve enhancement on three-dimensional MRI in Miller Fisher syndrome. Neurology 1996;47:1601-1602.
    7) Wicklein E.M, Pfeiffer G, Yuki N, Hartard C, Kunze K. Prominent sensory ataxia in Guillain-Barre syndrome associated with IgG anti-GD1b antibody. J Neurol Sci 1997;151:227-229.
    8) Kikuchi M, Tagawa Y, Iwamoto H, Hoshino H, Yuki N.Bickerstaff's brainstem encephalitis associated with IgG anti-GQ1b antibody subsequent to Mycoplasma pneumoniae infection: Favorable response to immunoadsorption therapy. J Chil Neurol 1997;12:403-405.

    57. GBS
    Not Plasma Exchange or Corticosteroids. miller fisher syndrome ClinicalExternal ophthalmoplegia ± pupillary dysfunction; Ataxia;
    http://www.geocities.com/HotSprings/Spa/3960/gbs.html
    Acute Immune Polyneuropathies
    Acute Motor Neuropathy
    Acute Sensory Neuropathy

    Classification

    Differential diagnosis of acute motor dysfunction
    ...
    Treatment of GBS-like syndromes

    Classification
    • Demyelinating (± 2° axonal loss)
        Motor + Sensory: Motor
      Axonal
        Motor + Sensory
          GBS-like syndrome Vasculitis
        Motor : Associated with
          Campylobacter jejuni prodrome Serum IgG vs GM1 ganglioside
        Sensory Autonomic
      Cranial Nerve Syndromes: Associated with
        Campylobacter jejuni prodrome Serum IgG vs GQ1b ganglioside Miller-Fisher Bickerstaff's Brainstem encephalitis
      Acute immune neuropathies: General principles Acute immune neuropathies have several features in common as well as those that vary and are distinctive for a particular syndrome. Some features suggest a different diagnosis among the causes of acute motor dysfunction . Principles regarding which treatment to use are somewhat subjective.
      • Common features
          Prodrome
            50% of patients in 2 weeks prior to disease onset
          Progression
            Average: 5 to 10 days Spectrum: 2 to 28 days
          Course
            Usually monophasic Rare relapses
          Prognosis
            Recovery in most
          Cerebrospinal Fluid (CSF)
            Few or no cells Variable features
              Motor, Sensory, or Autonomic involvement

    58. Le Portail De L'oeil Et De La Vision
    the spinal cord.. Postganglionic Horner's Syndrome. The Universityof Illinois at Chicago. miller fisher syndrome. In 1956, C Miller
    http://www.ophtalmologiefr.com/thematique/medicale/oculomoteurs.html
    Sites d'informations
    • American Orthoptic Journal The American Orthoptic Journal was founded in 1950 by the American Orthoptic Council. It is the official journal of The American Association of Certified Orthoptists....
    • Eye Movement Simulation Application This is the original neurological eye simulator that was developed and placed on the web in 1997. It simulates interactive eye motion and allows various neurological pathologies to be simulated...
    • Eye Movements Normally, both eyes are aimed at the same target. When the target is far away, the eyes move conjugately: that is, the right and left eyes move the same amount in the same direction...
    Nystagmus, Pathologic
    • Nystagmus Information Page Nystagmus is an eye condition characterised by rapid, jerky eye movements. It is a symptom which should always be investigated by a specialist as it can be a result of other disorders.
    • American Nystagmus Network Nystagmus is an involuntary eye movement which usually results in some degree of visual loss. The degree and direction of eye movement, amount of visual loss and resulting impairment...
    • Nystagmus Over thirty years later, a wealth of information is available and continually being published on the oscillations (undulating movements) of the eyes known as nystagmus...

    59. Guillain-Barre Syndrome - Everybody - Guillain-Barre Syndrome
    The risk is that while it suppresses the abnormal immune response, treatmentcan also affect normal immune functions. miller fisher syndrome.
    http://www.everybody.co.nz/docsd_h/GBS.html
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    60. MEDLINEplus: Guillain-Barre Syndrome
    Control and Prevention); miller fisher syndrome (National Instituteof Neurological Disorders and Stroke). Treatment Plasmapheresis and
    http://www.nlm.nih.gov/medlineplus/guillainbarresyndrome.html
    Skip navigation
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    Guillain-Barre Syndrome
    Contents of this page:
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    Autoimmune Diseases (General)

    Paralysis
    Peripheral Nerve Disorders Brain and Nervous System From the National Institutes of Health
  • Guillain-Barrè Syndrome (National Institute of Neurological Disorders and Stroke) Also available in: Spanish
  • General/Overviews
  • Guillain-Barre Syndrome (Mayo Foundation for Medical Education and Research)
  • Anatomy/Physiology
  • Understanding the Immune System (National Cancer Institute) Also available in: Spanish
  • Coping
  • Coping With Autoimmunity (American Autoimmune Related Diseases Association)
  • Diagnosis/Symptoms
  • Electromyography and Nerve Conduction Velocities (Muscular Dystrophy Association) Spinal Tap (Lumbar Puncture) (Mayo Foundation for Medical Education and Research)
  • Specific Conditions/Aspects
  • Campylobacter: Low-Profile Bug Is Food Poisoning Leader (Food and Drug Administration) Chronic Inflammatory Demyelinating Polyneuropathy (CIDP) (National Institute of Neurological Disorders and Stroke) Guillain-Barre Syndrome (GBS) and Influenza Vaccine (Centers for Disease Control and Prevention) Miller Fisher Syndrome (National Institute of Neurological Disorders and Stroke)
  • Treatment
  • Plasmapheresis and Autoimmune Disease (Muscular Dystrophy Association)
  • Directories
  • Find a Neurologist (American Academy of Neurology)
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