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
Extractions: 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.
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
Extractions: 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!
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
Extractions: 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
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
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
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
Extractions: 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.
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
Extractions: 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
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
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
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
Extractions: Back to Program PNS Home 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.
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
Extractions: 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
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
Extractions: 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
[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
Extractions: 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;
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
Extractions: 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.
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
GBS Not Plasma Exchange or Corticosteroids. miller fisher syndrome ClinicalExternal ophthalmoplegia ± pupillary dysfunction; Ataxia; http://www.geocities.com/HotSprings/Spa/3960/gbs.html
Extractions: Classification Axonal Motor : Associated with Sensory Autonomic Cranial Nerve Syndromes: Associated with 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. Progression Course Prognosis Cerebrospinal Fluid (CSF) Few or no cells Variable features Motor, Sensory, or Autonomic involvement
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
Extractions: Sites d'informations 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...
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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
Extractions: 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
