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Practice Guideline: Disease-Modifying Therapies for Adults with Multiple Sclerosis
Practice guideline: Disease-modifying therapies for adults with multiple sclerosis Report of the Guideline Development, Dissemination, and Implementation Subcommittee of the American Academy of Neurology Alexander Rae-Grant, MD1; Gregory S. Day, MD, MSc2; Ruth Ann Marrie, MD, PhD3; Alejandro Rabinstein, MD4; Bruce A.C. Cree, MD, PhD, MAS5; Gary S. Gronseth, MD6; Michael Haboubi, DO7; June Halper, MSN, APN-C, MSCN8; Jonathan P. Hosey, MD9; David E. Jones, MD10; Robert Lisak, MD11; Daniel Pelletier, MD12; Sonja Potrebic, MD, PhD13; Cynthia Sitcov14; Rick Sommers, LMSW15; Julie Stachowiak, PhD16; Thomas S.D. Getchius17; Shannon A. Merillat, MLIS18; Tamara Pringsheim, MD, MSc19 1. Department of Neurology, Cleveland Clinic, OH 2. Department of Neurology, Charles F. and Joanne Knight Alzheimer Disease Research Center, Washington University in St. Louis, MO 3. Departments of Medicine and Community Health Sciences, Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada 4. Department of Neurology, Mayo Clinic, Rochester, MN 5. UCSF Weill Institute for Neurosciences, Department of Neurology, University of California, San Francisco 6. Department of Neurology, Kansas University Medical Center, Kansas City 7. Department of Neurology, School of Medicine, University of Louisville, KY 8. Consortium of Multiple Sclerosis Centers, Hackensack, NJ 9. Department of Neuroscience, St. Luke’s University Health Network, Bethlehem, PA 10. Department of Neurology, School of Medicine, University of Virginia, Charlottesville 11. Consortium of Multiple Sclerosis Centers, Hackensack, NJ, and Department of Neurology, School of Medicine, Wayne State University, Detroit, MI 12. Department of Neurology, Keck School of Medicine, University of Southern California, Los Angeles 13. Neurology Department, Southern California Permanente Medical Group, Kaiser, Los Angeles 14. -
OLIGOCLONAL Igg BANDS in the CEREBROSPINAL FLUID of PORTUGUESE PATIENTS with MULTIPLE SCLEROSIS
Arq Neuropsiquiatr 2005;63(2-B):375-379 OLIGOCLONAL IgG BANDS IN THE CEREBROSPINAL FLUID OF PORTUGUESE PATIENTS WITH MULTIPLE SCLEROSIS Negative results indicate benign disease Maria José Sá1, Lucinda Sequeira2, Maria Edite Rio3, Edward J. Thompson4 ABSTRACT - We assessed the frequency of cerebrospinal fluid (CSF) restricted oligoclonal IgG bands (IgG- OCB) in Portuguese multiple sclerosis (MS) patients and its relationship with outcome. Paired CSF/serum samples of 406 patients with neurological disorders were submitted to isoelectric focusing with immunodetection of IgG. Ninety-two patients had definite MS; non-MS cases were assembled in groups inflammatory/infectious diseases (ID, n=141) and other/controls (OD, n=173). We found in the MS group: mean duration, 38.9 months; clinically isolated syndromes, 24%; relapsing/remitting course (RR), 65%; in RR patients the mean EDSS was 2.1 and the mean index of pro g ression was 0.31. Positive patterns significantly p redominated in MS (82.6%; ID, 40.4%; OD, 3.5%). The sensitivity and the specificity of positive IgG-OCB for MS diagnosis was 82.6% and 79.9%, respectively. The sole statistically significant difference in the MS g roup was the lower pro g ression index observed in negative cases. We conclude that the frequency of positive IgG-OCB patterns in our MS patients fits most values reported in the literature, and that negative results indicate benign disease. KEY WORDS: multiple sclerosis, CSF, oligoclonal bands, IgG, isoelectric focusing. Bandas oligoclonais da IgG no líquido céfalo-raquidiano de doentes portugueses com esclerose múltipla: resultados negativos indicam doença benigna RESUMO - Analisamos a frequência de bandas oligoclonais (BOC) restritas ao líquido céfalo-raquidiano (LCR) em doentes portugueses com esclerose múltipla (EM) e sua relação com a clínica. -
Radiologically Isolated Syndrome: a Review for Neuroradiologists
REVIEW ARTICLE Radiologically Isolated Syndrome: A Review for Neuroradiologists M. Hosseiny, S.D. Newsome, and D.M. Yousem ABSTRACT SUMMARY: Radiologically isolated syndrome refers to an entity in which white matter lesions fulfilling the criteria for multiple sclerosis occur in individuals without a history of a clinical demyelinating attack or alternative etiology. Since its introduction in 2009, the diagnostic criteria of radiologically isolated syndrome and its clinical relevance have been widely debated by neu- rologists and radiologists. The aim of the present study was to review the following: 1) historical evolution of radiologically iso- lated syndrome criteria, 2) clinical and imaging findings in adults and children with radiologically isolated syndrome, 3) imaging features of patients with radiologically isolated syndrome at high risk for conversion to MS, and 4) challenges and controversies for work-up, management, and therapeutic interventions of patients with radiologically isolated syndrome. ABBREVIATIONS: CIS ¼ clinically isolated syndrome; DIS ¼ dissemination in space; DIT ¼ dissemination in time; MAGNIMS ¼ Magnetic Resonance Imaging in MS; RIS ¼ radiologically isolated syndrome; RRMS ¼ relapsing-remitting multiple sclerosis; CADASIL ¼ cerebral autosomal dominant arteriopathy with sub- cortical infarcts and leukoencephalopathy; ADEM ¼ acute disseminated encephalomyelitis adiologically isolated syndrome (RIS) refers to an entity in patients are being evaluated for headache, trauma, or nonspecific Rwhich brain or spine MR -
Cerebrospinal Fluid Analysis in Multiple Sclerosis Diagnosis: an Update
View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by Archivio istituzionale della ricerca - Università di Palermo medicina Review Cerebrospinal Fluid Analysis in Multiple Sclerosis Diagnosis: An Update Bruna Lo Sasso 1, Luisa Agnello 1, Giulia Bivona 1 , Chiara Bellia 1 and Marcello Ciaccio 1,2,* 1 Institute of Clinical Biochemistry, Clinical Molecular Medicine and Laboratory Medicine, Department of Biomedicine, Neuroscience and Advanced Diagnostics, University of Palermo, 90100 Palermo, Italy; [email protected] (B.L.S.); [email protected] (L.A.); [email protected] (G.B.); [email protected] (C.B.) 2 Department Laboratory Medicine, University-Hospital, 90100 Palermo, Italy * Correspondence: [email protected]; Tel.: +39-091-23865701; Fax: +39-091-655-3275 Received: 25 March 2019; Accepted: 30 May 2019; Published: 4 June 2019 Abstract: Multiple sclerosis (MS) is an immune-mediated demyelinating disease of the central nervous system (CNS) with brain neurodegeneration. MS patients present heterogeneous clinical manifestations in which both genetic and environmental factors are involved. The diagnosis is very complex due to the high heterogeneity of the pathophysiology of the disease. The diagnostic criteria have been modified several times over the years. Basically, they include clinical symptoms, presence of typical lesions detected by magnetic resonance imaging (MRI), and laboratory findings. The analysis of cerebrospinal fluid (CSF) allows an evaluation of inflammatory processes circumscribed to the CNS and reflects changes in the immunological pattern due to the progression of the pathology, being fundamental in the diagnosis and monitoring of MS. The detection of the oligoclonal bands (OCBs) in both CSF and serum is recognized as the “gold standard” for laboratory diagnosis of MS, though presents analytical limitations. -
A Diffusion Tensor Magnetic Resonance Imaging Study of Brain Tissue from Patients with Migraine M a Rocca, B Colombo, M Inglese, M Codella, G Comi, M Filippi
501 J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.74.4.501 on 1 April 2003. Downloaded from SHORT REPORT A diffusion tensor magnetic resonance imaging study of brain tissue from patients with migraine M A Rocca, B Colombo, M Inglese, M Codella, G Comi, M Filippi ............................................................................................................................. J Neurol Neurosurg Psychiatry 2003;74:501–503 PATIENTS AND METHODS Objective: To measure in vivo, using diffusion tensor mag- We studied 34 patients (31 women and three men; mean age netic resonance imaging (DT-MRI) the extent of pathologi- 35.2 years, range 18–55 years; mean duration of the disease cal damage of normal appearing brain tissue (NABT) from 13.6 years, range 1–40 years; mean number of episodes per patients with migraine. year 44.6, range 12–70) with migraine.10 All possible alterna- Methods: Dual echo and DT-MRI scans of the brain were tive diagnoses were carefully excluded.10 There were 28 acquired from 34 patients with migraine and 17 sex and patients affected by “migraine without aura” and six patients age matched healthy volunteers. Mean diffusivity (MD) affected by “migraine with aura”.10 Patients with hyper- and fractional anisotropy (FA) histograms of the NABT tension, hypercholesteraemia, diabetes mellitus, vascular/ were obtained from all subjects and the histograms’ peak heart diseases, and other major systemic and neurological heights and average NABT MD and FA measured. When conditions were excluded. At the time of the MRI assessment, present, average MD and FA values of T2 visible lesions 11 patients were treated with prophylactic drugs. Seventeen were also measured. -
New Insights Into Multiple Sclerosis Mechanisms: Lipids on the Track to Control Inflammation and Neurodegeneration
International Journal of Molecular Sciences Review New Insights into Multiple Sclerosis Mechanisms: Lipids on the Track to Control Inflammation and Neurodegeneration Maria Podbielska 1,2,* , Joan O’Keeffe 3 and Anna Pokryszko-Dragan 4 1 Department of Biochemistry & Molecular Biology, Medical University of South Carolina, Charleston, SC 29425, USA 2 Laboratory of Microbiome Immunobiology, Ludwik Hirszfeld Institute of Immunology & Experimental Therapy, Polish Academy of Sciences, 53-114 Wroclaw, Poland 3 Department of Analytical, Biopharmaceutical and Medical Sciences, School of Science & Computing, Galway-Mayo Institute of Technology, Galway, Ireland; [email protected] 4 Department of Neurology, Wroclaw Medical University, 50-556 Wroclaw, Poland; [email protected] * Correspondence: [email protected]; Tel.: +48-71-370-9912 Abstract: Multiple sclerosis (MS) is a central nervous system disease with complex pathogenesis, including two main processes: immune-mediated inflammatory demyelination and progressive degeneration with axonal loss. Despite recent progress in our understanding and management of MS, availability of sensitive and specific biomarkers for these both processes, as well as neuroprotec- tive therapeutic options targeted at progressive phase of disease, are still being sought. Given their abundance in the myelin sheath, lipids are believed to play a central role in underlying immunopatho- genesis in MS and seem to be a promising subject of investigation in this field. On the basis of our previous research and a review of the literature, we discuss the current understanding of lipid-related mechanisms involved in active relapse, remission, and progression of MS. These insights highlight Citation: Podbielska, M.; O’Keeffe, J.; potential usefulness of lipid markers in prediction or monitoring the course of MS, particularly in its Pokryszko-Dragan, A. -
Antibodies in Multiple Sclerosis Oligoclonal Bands Target Debris Ryan C
COMMENTARY COMMENTARY Antibodies in multiple sclerosis oligoclonal bands target debris Ryan C. Wingera,b and Scott S. Zamvila,b,1 IgG oligoclonal bands (OCB) are detected in the of antibodies identified in CSF to OCB by studying cerebrospinal fluid (CSF) of more than 90% of multiple whole CSF IgG or recombinant antibodies constructed sclerosis (MS) patients and are considered the immu- from rearranged Ig heavy- and light-chain genes in nological hallmark that supports MS diagnosis. OCB individual B cells. are not unique to MS but are also observed in chronic Dornmair and coworkers used a combination of CNS infections, where they target their causative agents new biochemical, proteomic, and transcriptomic ap- (1–3). However, the target specificities of the IgG within proaches (4, 14) to examine the specificity of anti- OCB in MS have remained a mystery. Identification bodies in MS OCB. Disulfide-linked IgG heavy- (IgH) of those antigens recognized by OCB antibodies is and IgG light- (IgL) chain complexes were purified from thought to hold fundamental clues to the pathogenesis single OCB spots using affinity chromatography and of MS. In a recent PNAS publication, Brändle et al. (4) two-dimensional gel electrophoresis. Those antibody provide evidence that OCB in MS target ubiquitous (IgH2IgL2) complexes were then analyzed by mass intracellular antigens released in cellular debris. spectrometry to generate patient-specific Ig pepti- In 1942, Kabat et al. (5) established the diagnostic domes. In parallel, IgH and IgL genes, including the value of quantitative determinations of CSF gamma unique complementarity-determining region 3, from globulins in clinical neurology, and particularly in CSF B cells isolated from the corresponding patient MS. -
INFLAMMATORY/POST-INFECTIOUS ENCEPHALOMYELITIS L Bennetto, N Scolding I22
J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.2003.034256 on 20 February 2004. Downloaded from INFLAMMATORY/POST-INFECTIOUS ENCEPHALOMYELITIS L Bennetto, N Scolding i22 J Neurol Neurosurg Psychiatry 2004;75(Suppl I):i22–i28. doi: 10.1136/jnnp.2003.034256 ost-infectious and inflammatory encephalomyelitis are broadly represented by the syn- drome acute disseminated encephalomyelitis (ADEM). ADEM forms one of several Pcategories of primary inflammatory demyelinating disorders of the central nervous system. Others include multiple sclerosis (MS), acute transverse myelitis, and Devic’s disease. It should be remembered that these are syndromically defined diseases at present. There are no diagnos- tic tests presently available short of brain biopsy, but future advances may reveal diagnostic biological markers of disease and in so doing dramatically advance the pathophysiological and therapeutic understanding of these conditions. A wholesale change in classification and nomenclature may well follow. In the meantime clinicians must remain keenly appreciative of subtle shades of grey: ADEM, first MS relapse, or ultimately benign clinically isolated syn- drome? The answers are relevant to prognosis and, more recently, selection of the correct therapeutic strategy. c ACUTE DISSEMINATED ENCEPHALOMYELITIS ADEM is an inflammatory demyelinating disorder of the central nervous system that is usually monophasic, but a relapsing variant distinct from MS—multiphasic disseminated encephalomyelitis (MDEM) is well-described. ADEM is predominantly, though by no means copyright. exclusively, a disease of children and in particular infants. Historically it includes post- infectious encephalomyelitis and post-vaccination encephalomyelitis. While these two syndromes were distinguished by their precipitant it was realised that clinically and pathologically they were very similar. -
KIRA ÅKERLUND: Environmental and Lifestyle Factors in Multiple Sclerosis
ANNALES UNIVERSITATIS TURKUENSIS UNIVERSITATIS ANNALES D 1465 D Kira Åkerlund Kira ENVIRONMENTAL AND LIFESTYLE FACTORS IN MULTIPLE SCLEROSIS With Emphasis on Vitamin D, EBV Infection, Smoking and Cancer Risk Kira Åkerlund Painosalama Oy, Turku, Finland 2020 Finland Turku, Oy, Painosalama ISBN 978-951-29-7962-2 (PRINT) – ISBN 978-951-29-7963-9 (PDF) TURUN YLIOPISTON JULKAISUJA ANNALES UNIVERSITATIS TURKUENSIS ISSN 0355-9483 (Print) SARJA - SER. D OSA - TOM. 1465 | MEDICA - ODONTOLOGICA | TURKU 2020 ISSN 2343-3213 (Online) ENVIRONMENTAL AND LIFESTYLE FACTORS IN MULTIPLE SCLEROSIS With Emphasis on Vitamin D, EBV Infection, Smoking and Cancer Risk Kira Åkerlund TURUN YLIOPISTON JULKAISUJA – ANNALES UNIVERSITATIS TURKUENSIS SARJA - SER. D OSA – TOM. 1465 | MEDICA – ODONTOLOGICA | TURKU 2020 University of Turku Faculty of Medicine Department of Neurology Doctoral Programme in Clinical Research Division of Clinical Neurosciences Turku University Hospital Supervised by Docent Merja Soilu-Hänninen Division of Clinical Neurosciences Turku University Hospital Turku, Finland Reviewed by Docent Mikko Kallela Docent Markus Färkkilä Helsinki University Hospital University of Helsinki Department of Neurology Helsinki, Finland University of Helsinki Helsinki, Finland Opponent Professor Anne Remes Unit of Clinical Neuroscience Neurology, University of Oulu Oulu, Finland The originality of this publication has been checked in accordance with the University of Turku quality assurance system using the Turnitin OriginalityCheck service. ISBN 978-951-29-7962-2 (PRINT) ISBN 978-951-29-7963-9 (PDF) ISSN 0355-9483 (Print) ISSN 2343-3213 (Online) Painosalama Oy, Turku, Finland 2020 To Rita, Viktor and Finn 3 UNIVERSITY OF TURKU Faculty of Medicine Department of Neurology KIRA ÅKERLUND: Environmental and lifestyle factors in multiple sclerosis with emphasis on vitamin D, EBV infection, smoking and cancer risk Doctoral Dissertation, 155 pp. -
Increased Tissue Pressure Induces Demyelinated Lesions and Necroses in the Brain
American Journal of Neuroscience Original Research Paper Increased Tissue Pressure Induces Demyelinated Lesions and Necroses in the Brain 1Helmut Barz, 2Ulrich Barz and 3Almut Schreiber 1Department of Neuropathology, Dietrich-Bonhoeffer Hospital Neubrandenburg, Mecklenburg-West-Pomerania, Germany 2Martin-Luther-Universität Halle-Wittenberg, Halle, Saxony-Anhalt, Germany 3Consultant Occupational Health Physician, Institut Für Arbeits-und Sozialhygiene, Aktiengesellschaft, Dresden, Saxony, Germany Article history Abstract: A general brain edema increases the size of the brain tissue and Received: 08-12-2014 stretches the elastic neuronal and glial fibers. Myelinated fibers are more Revised: 20-01-2015 elastic than unmyelinated fibers. The stretching of the neuronal fibers leads Accepted: 12-03-2015 particular in regions of the white matter or areas surrounded by myelinated fiber tracts to an increased tissue pressure. This physical principle can be Corresponding Author: Helmut Barz the reason for demyelination and tissue necrosis. The higher the tissue Department of Neuropathology, pressure, the lower the blood perfusion. We support the pressure-hypothesis Dietrich-Bonhoeffer Hospital by comparison with well-known pressure related pathologies of the nervous Neubrandenburg, Mecklenburg- system and other organs. One convincing example is the central pontine West-Pomerania, Germany myelinolysis. A general or local tissue edema may lead especially in the Email: [email protected] periventricular and the deep white matter, but also in the cerebellum, the brain stem and the spinal cord to the formation of hypoxemic lesions. In consequence, this could result in diseases like leukoaraiosis, Binswanger encephalopathy, idiopathic intracranial hypertension and Multiple Sclerosis (MS). In cases of brain tissue swelling, capsula-like structures may lead to a rapid increase in tissue pressure within the enclosed areas. -
Therapeutic Mechanism of Action (Moas) in MS: Targeting T- and B-Cells to Reset the Immune System Learning Objectives
Therapeutic Mechanism of Action (MOAs) in MS: Targeting T- and B-cells to Reset the Immune System Learning Objectives • Explore emergent concepts in the management of MS, focusing on targeting T- and B-cells including: – Risks associated with continuous immunosuppression – Action on the inflammatory activity in the CNS compartment • Review the benefit/risk strategies in selecting therapy for MS patients while assessing treatment regimens that carry acceptable or diminished risk of disease progression • Identify strategies that simplify patient dosing and side effects to: – Increase treatment compliance – Improve patients’ quality of life – Slow disease progression Treatment: Immunomodulation Type BBB CNS Systemic immune T Tc Treg Te reg compartment Tc Tc Tc Treg Te Te APC Tc Tc Te Te B Bi Bi Bi Bi B APC, antigen presenting cells; B, B lymphocytes; BBB, blood-brain barrier; Bi, inflammatory B cells; CNS, central nervous system; Tc, T lymphocytes; Te, encephalitogenic T cells; Treg, regulatory T cells. Figure is reproduced with permission from 1. Wiendl H, Kieseier B. Nat Rev Neurol. 2013;9:125-126. Treatment: General Immunosuppression Type BBB CNS Systemic immune compartment Te Tc Treg Te APC Tc Tc Te B Bi Bi B APC, antigen presenting cells; B, B lymphocytes; BBB, blood-brain barrier; Bi, inflammatory B cells; CNS, central nervous system; Tc, T lymphocytes; Te, encephalitogenic T cells; Treg, regulatory T cells. Figure is reproduced with permission from 1. Wiendl H, Kieseier B. Nat Rev Neurol. 2013;9:125-126. 1. Wiendl H, Kieseier B. Nat Rev Neurol. 2013;9:125-126; 2. Cohen JA et al. N Engl J Med. -
Acute Disseminated Encephalomyelitis: Treatment Guidelines
[Downloaded free from http://www.annalsofian.org on Monday, February 06, 2012, IP: 115.113.56.227] || Click here to download free Android application for this journal S60 Acute disseminated encephalomyelitis: Treatment guidelines Alexander M., J. M. K. Murthy1 Department of Neurological Sciences, Christian Medical College, Vellore, 1The Institute of Neurological Sciences, CARE Hospital, Hyderabad, India For correspondence: Dr. Alexander Mathew, Professor of Neurology, Department of Neurological Sciences, Christian Medical College, Vellore, Tamil Nadu, India Annals of Indian Academy of Neurology 2011;14:60-4 Introduction of intracranial space occupying lesion, with tumefactive demyelinating lesions.[ 13-17] Acute disseminated encephalomyelitis (ADEM) is a monophasic, postinfectious or postvaccineal acute infl ammatory Certain clinical presentations may be specifi c with certain demyelinating disorder of central nervous system (CNS).[1,2] The infections: cerebellar ataxia for varicella infection, myelitis pathophysiology involves transient autoimmune response for mumps, myeloradiculopathy for Semple antirabies vaccination, and explosive onset with seizures and mild directed at myelin or other self-antigens, possibly by molecular [18,19] mimicry or by nonspecifi c activation of autoreactive T-cell pyramidal dysfunction for rubella. Acute hemorrhagic clones.[3] Histologically, ADEM is characterized by perivenous leukoencephalitis and acute necrotizing hemorrhagic leukoencephalitis of Weston Hurst represent the hyperacute, demyelination and infi ltration of vessel wall and perivascular [20] spaces by lymphocytes, plasma cells, and monocytes.[4] fulminant form of postinfectious demyelination. Diagnosis The annual incidence of ADEM is reported to be 0.4–0.8 per 100,000 and the disease more commonly affects children Cerebrospinal fl uid (CSF) is abnormal in about two-thirds and young adults, probably related to the high frequency of of patients and shows a moderate pleocytosis with raised exanthematous and other infections and vaccination in this age proteins.