DOCSLIB.ORG

Acute Disseminated Encephalomyelitis, Transverse Myelitis, and Neuromyelitis Optica

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Acute Disseminated Encephalomyelitis, Transverse Myelitis, and Neuromyelitis Optica Review Article Address correspondence to Dr Brian G. Weinshenker, Department of Neurology, Acute Disseminated Mayo Clinic, 200 First St SW, Rochester, MN 55905, [email protected]. Encephalomyelitis, Relationship Disclosure: Dr Wingerchuk receives research support from Transverse Myelitis, and Alexion, Genentech, Genzyme Corporation, Guthy-Jackson Charitable Foundation, and Terumo BCT, Neuromyelitis Optica Inc. Dr Weinshenker serves on the data and safety Dean M. Wingerchuk, MD, MSc, FRCP(C), FAAN; monitoring board of Biogen Idec and Novartis and serves Brian G. Weinshenker, MD, FRCP(C), FAAN as a consultant regarding neuromyelitis optica therapeutics for Asahi Kasei ABSTRACT Medical Co, Ltd, Elan Corporation, and Novartis. Purpose of Review: This review defines current clinical criteria for diagnosis, Dr Weinshenker receives differential diagnosis, and clinical evaluation of acute disseminated encephalomy- royalties for licensed elitis, transverse myelitis, and neuromyelitis optica, and summarizes principles of technology for the diagnosis of neuromyelitis optica from treatment. RSR Limited, and receives Recent Findings: Consensus criteria for transverse myelitis and acute dissemi- research funding from nated encephalomyelitis have been proposed. A specific biomarker, aquaporin-4 Guthy-Jackson Charitable Foundation. autoantibody, has been discovered for neuromyelitis optica that allows for early and Unlabeled Use of accurate diagnosis even in the absence of cardinal findings of optic neuritis and myelitis. Products/Investigational The antibody is pathogenic and is facilitating an understanding of the pathophysiology Use Disclosure: Drs Wingerchuk and Weinshenker of neuromyelitis optica and development of antigen-specific treatments. discuss the unlabeled uses of Summary: Clinical and radiologic findings combined with serologic findings may corticosteroids and plasma permit classification of syndromes of transverse myelitis and acute disseminated exchange for the treatment of acute disseminated encephalomyelitis in ways that may predict risk of relapse, type of relapse, and encephalomyelitis, transverse prognosis. Treatment, especially to prevent relapse, is dependent on the specific myelitis, and neuromyelitis disease context in which syndromes such as transverse myelitis occur. optica; IV immunoglobulin for acute disseminated encephalomyelitis; and Continuum (Minneap Minn) 2013;19(4):944–967. azathioprine, mycophenolate mofetil, rituximab, mitoxantrone, methotrexate, and eculizumab for INTRODUCTION: SYNDROME their inflammatory characteristics and neuromyelitis optica. * 2013, American Academy VERSUS DISEASE overlapping pathology. of Neurology. The nosology of demyelinating dis- Distinction between syndromes eases of the CNS is complex. Multiple that reflect localization (eg, optic neu- sclerosis (MS) has been an umbrella ritis and transverse myelitis) and dis- term for recurrent inflammatory dis- ease entities (eg, ADEM, MS, and NMO) ease of the CNS after definable non- is now feasible. Distinction is important demyelinating mimics are excluded. because of the prognostic and treat- Acute disseminated encephalomyelitis ment implications of different disease (ADEM), transverse myelitis, and neu- entities. For example, transverse myeli- romyelitis optica (NMO) are inflamma- tis refers to a syndrome of acute or tory conditions that have not been subacute myelopathy accompanied by well distinguished from MS or its indicators of inflammation, either ra- presenting syndromes (termed ‘‘clini- diologically or based on spinal fluid. It cally isolated [demyelinating] syn- may occur as a stand-alone syndrome, a dromes’’) but are linked by their component of ADEM, a relapse of MS or tendency to relapse and remit and by NMO, or a nondemyelinating syndrome 944 www.ContinuumJournal.com August 2013 Copyright © American Academy of Neurology. Unauthorized reproduction of this article is prohibited. KEY POINTS such as an infectious myelitis or a cephalomyelitis. ADEM is also known h Distinguishing between granulomatous myelitis. If due to her- as postvaccinal encephalomyelitis syndromes (eg, optic pes virus infection, it is best treated with when it follows vaccination. Accord- neuritis and transverse antiviral treatment; if indicative of a ingly, it is believed to be induced by myelitis) and disease relapse or harbinger of MS, an MS an immune reaction directed at a entities (multiple immunomodulatory treatment may be cross-reacting myelin antigen. Its sclerosis, neuromyelitis appropriate; if a relapse of NMO, an somewhat unique pathology of optica, and acute immunosuppressive drug, such as aza- perivenous ‘‘sleeves’’ of inflammation disseminated thioprine, would be appropriate, and demyelination has been recog- encephalomyelitis) whereas interferon-" or natalizumab nized for decades but has been re- is vital. Demyelinating may actually be deleterious. Noninfec- cently rediscovered and expanded.1 syndromes may be a component of different tious and noninflammatory disorders, Pathologically, ADEM can be distin- diseases and may such as arteriovenous fistula, may guished from fulminant acute MS, have vastly different produce syndromes suggestive of which is a major consideration in the prognoses depending transverse myelitis but would require differential diagnosis. Acute MS is on the disease context entirely different treatment. associated with confluent demyelin- (and may therefore ADEM, as currently defined, is char- ation and prominent macrophages require different acterized by acute encephalopathy but admixed with reactive astrocytes. treatment). frequently accompanied by optic neuri- When cases are identified based on h Although the proposed tis or transverse myelitis. NMO is the pathologic features, these features consensus criteria for first inflammatory demyelinating condi- seem to be associated with some of acute disseminated tion to be defined, in part, by a bio- the key clinical characteristics that have encephalomyelitis marker that is molding our evolving been identified in consensus clinical allows for recurrent or concept of this condition (an auto- diagnostic criteria (Table 3-12) to dis- multiphasic forms immune aquaporinopathy) and ex- tinguish ADEM from MSVin particular, of the disease, the panding the spectrum of the disease encephalopathy.1 Pathology has re- existence of relapsing to include nonYoptic nerve and spinal cently been proposed as the ‘‘refer- forms remains controversial. A cord syndromes and MRI-detected ence standard’’ to distinguish ADEM criterion standard brain lesions that, in the past, would from fulminant MS, although this has for distinguishing have excluded a diagnosis of NMO. not been widely debated and cannot acute disseminated Understanding of the distinction and be considered as generally accepted at encephalomyelitis 2 interrelationships of these syndromes the present time. Consensus criteria from multiple sclerosis has been facilitated by insights into the remain imperfect in distinguishing pa- has not been widely pathophysiology, informed by the neu- tients who, in the course of follow-up, accepted, although ropathology, and illustrated by ad- will remain free of future relapses. pathology has been vances in NMO over the past decade Furthermore, consensus criteria allow proposed. as outlined below. for recurrent and even multiphasic ADEM episodes with criteria that might ACUTE DISSEMINATED distinguish it from MS (ie, a new ENCEPHALOMYELITIS episode must also meet the criteria Although a number of definitions have for ADEM and not be those of an been proposed for ADEM, it remains a attack of MSVsee Table 3-1). Contro- poorly defined syndrome of symptom- versy persists about whether relapses atic diffuse or multifocal CNS inflam- may occur in ADEM and remain con- mation that is typically, if not always, a sistent with the diagnosis of ADEM, monophasic illness. ADEM has been especially in adult patients. historically regarded as the clinical The key clinical features required counterpart of the experimental dis- for a diagnosis of ADEM include ease experimental autoimmune en- diffuse encephalopathy but may also Continuum (Minneap Minn) 2013;19(4):944–967 www.ContinuumJournal.com 945 Copyright © American Academy of Neurology. Unauthorized reproduction of this article is prohibited. ADEM, Transverse Myelitis, and NMO a TABLE 3-1 International Pediatric Multiple Sclerosis Study Group Consensus Definitions b Monophasic Acute Disseminated Encephalomyelitis (ADEM) A first clinical event with a presumed inflammatory or demyelinating cause Acute or subacute onset that affects multifocal areas of the CNS Polysymptomatic and must include encephalopathy, including one or more of the following: Behavioral change (confusion, irritability) Alteration in consciousness (lethargy, coma) Postevent improvement clinically, on MRI, or both; residual deficits permitted No prior clinical episode consistent with demyelinating event No other etiologies apparent New or fluctuating symptoms, signs, or MRI findings occurring within 3 months of the inciting ADEM event permissible Brain MRI (T2-weighted) with focal or multifocal supratentorial or infratentorial lesions, often large (1 to 2 cm), predominantly involving white matter, but frequently present in gray matter (especially basal ganglia or thalamus), without evidence of previous destructive white matter changes; brain MRI showing a single large lesion (1 to 2 cm), predominantly affecting white matter also possible, although rare Spinal cord MRI may have confluent intramedullary
Load more

Recommended publications
  • Balo's Concentric Lesions with Concurrent Features of Schilder's
    Article / Autopsy Case Report Balo’s concentric lesions with concurrent features of Schilder’s disease in relapsing multiple sclerosis: neuropathological findings Maher Kurdia,b, David Ramsaya Kurdi M, Ramsay D. Balo’s concentric lesions with concurrent features of Schilder’s disease in relapsing multiple sclerosis: neuropathological findings. Autopsy Case Rep [Internet]. 2016;6(4):21-26. http://dx.doi.org/10.4322/acr.2016.058 ABSTRACT Atypical inflammatory demyelinating syndromes are rare neurological diseases that differ from multiple sclerosis (MS), owing to unusual clinicoradiological and pathological findings, and poor responses to treatment. The distinction between them and the criteria for their diagnoses are poorly defined due to the lack of advanced research studies. Balo’s concentric sclerosis (BCS) and Schilder’s disease (SD) are two of these syndromes and can present as monophasic or in association with chronic MS. Both variants are difficult to distinguish when they present in acute stages. We describe an autopsy case of middle-aged female with a chronic history of MS newly relapsed with atypical demyelinating lesions, which showed concurrent features of BCS and SD. We also describe the neuropathological findings, and discuss the overlapping features between these two variants. Keywords Multiple Sclerosis; Atypical Inflammatory Demyelination; Balo’s Concentric Sclerosis; Schilder’s Disease; Pathology CASE REPORT A 45-year-old woman presented in another treatment. Brain magnetic resonance imaging (MRI) hospital with a history of generalized tonic clonic with gadolinium contrast showed space-occupying seizure and acute confusion. She was admitted to lesions in the right and left frontal white matter, with the intensive care unit for close observation.
    [Show full text]
  • Para-Infectious and Post-Vaccinal Encephalomyelitis
    Postgrad Med J: first published as 10.1136/pgmj.45.524.392 on 1 June 1969. Downloaded from Postgrad. med. J. (June 1969) 45, 392-400. Para-infectious and post-vaccinal encephalomyelitis P. B. CROFT The Tottenham Group ofHospitals, London, N.15 Summary of neurological disorders following vaccinations of The incidence of encephalomyelitis in association all kinds (de Vries, 1960). with acute specific fevers and prophylactic inocula- The incidence of para-infectious and post-vaccinal tions is discussed. Available statistics are inaccurate, encephalomyelitis in Great Britain is difficult to but these conditions are of considerable importance estimate. It is certain that many cases are not -it is likely that there are about 400 cases ofmeasles notified to the Registrar General, whose published encephalitis in England and Wales in an epidemic figures must be an underestimate. In addition there year. is a lack of precise diagnostic criteria and this aspect The pathology of these neurological complications will be considered later. In the years 1964-66 the is discussed and emphasis placed on the distinction mean number of deaths registered annually in between typical perivenous demyelinating encepha- England and Wales as due to acute infectious litis, and the toxic type of encephalopathy which encephalitis was ninety-seven (Registrar General, occurs mainly in young children. 1967). During the same period the mean annual The clinical syndromes occurring in association number of deaths registered as due to the late effects with measles, chickenpox and German measles are of acute infectious encephalitis was seventy-four- considered. Although encephalitis is the most fre- this presumably includes patients with post-encepha-copyright.
    [Show full text]
  • Sustained Efficacy of Natalizumab in the Treatment of Relapsing-Remitting Multiple Sclerosis Independent of Disease Activity
    Zurich Open Repository and Archive University of Zurich Main Library Strickhofstrasse 39 CH-8057 Zurich www.zora.uzh.ch Year: 2012 Sustained efficacy of natalizumab in the treatment of relapsing-remitting multiple sclerosis independent of disease activity and disability at baseline: real-life data from a Swiss cohort Kallweit, U ; Jelcic, I ; Braun, N ; Fischer, H ; Zörner, B ; Schreiner, B ; Sokolov, A A ; Martin, R ; Weller, M ; Linnebank, M Abstract: OBJECTIVES: Therapy for relapsing-remitting multiple sclerosis with natalizumab (Tysabri; Biogen Idec) has been shown to be effective in the reduction of the clinical relapse rate and disability progression. However, real-life longitudinal data, including years before baseline, are rare. METHODS: An observational single-center study was carried out. We analyzed data from 64 consecutive patients with multiple sclerosis. RESULTS: After 1 year of treatment (n = 64), score on the Expanded Disability Status Scale (EDSS) decreased by 0.47 points (P = 0.047) and the annualized relapse rate (ARR) decreased by 82% (P < 0.001). After 2 years (n = 41), EDSS score was still reduced by 0.28 (not significant) and ARR was reduced by 69% (P < 0.001). After 3 years (n = 23), EDSS score was reduced by 0.26 (not significant), and ARR was reduced by 77% (P < 0.001). Reduction of EDSS score andARRdid not depend on baseline ARR (1-2 vs >2) or EDSS score and was not biased by exceptional high disease activity or relapses around baseline. CONCLUSIONS: These real-life data reinforce that natalizumab is effective over years, reduces ARR, and stabilizes EDSS score independent of baseline ARR, baseline EDSS score, or baseline treatment.
    [Show full text]
  • Central Pain in the Face and Head
    P1: KWW/KKL P2: KWW/HCN QC: KWW/FLX T1: KWW GRBT050-128 Olesen- 2057G GRBT050-Olesen-v6.cls August 17, 2005 2:10 ••Chapter 128 ◗ Central Pain in the Face and Head J¨orgen Boivie and Kenneth L. Casey CENTRAL PAIN IN THE FACE AND HEAD Anesthesia dolorosa denotes pain in a region with de- creased sensibility after lesions in the CNS or peripheral International Headache Society (IHS) code and diag- nervous system (PNS). The term deafferentation pain is nosis: used for similar conditions, but it is more commonly used in patients with lesions of spinal nerves. 13.18.1 Central causes of facial pain 13.18.1 Anesthesia dolorosa (+ code to specify cause) 13.18.2 Central poststroke pain EPIDEMIOLOGY 13.18.3 Facial pain attributed to multiple sclerosis 13.18.4 Persistent idiopathic facial pain The prevalence of central pain varies depending on the un- 13.18.5 Burning mouth syndrome derlying disorder (Tables 128-1 and 128-2) (7,29). In the ab- 13.19 Other centrally mediated facial pain (+ code to sence of large scale epidemiologic studies, only estimates specify etiology) of central pain prevalence can be quoted. In the only prospective epidemiologic study of central Note that diagnosis with IHS codes 13.18.1, 13.18.4, and pain, 191 patients with central poststroke pain (CPSP) 13.18.5 may have peripheral causes. were followed for 12 months after stroke onset (1). Sixteen World Health Organization (WHO) code and diagnosis: (8.4%) developed central pain, an unexpectedly high inci- G 44.810 or G44.847.
    [Show full text]
  • Fingolimod (Gilenya)
    Clinical Policy: Fingolimod (Gilenya) Reference Number: HIM.PA.SP10 Effective Date: 05/17 Coding Implications Last Review Date: Revision Log Line of Business: Health Insurance Marketplace See Important Reminder at the end of this policy for important regulatory and legal information. Description Fingolimod (Gilenya®) is a sphingosine 1-phosphate receptor modulator. FDA approved indication Gilenya is indicated for the treatment of patients with relapsing forms of multiple sclerosis (MS) to reduce the frequency of clinical exacerbations and to delay the accumulation of physical disability. Policy/Criteria Provider must submit documentation (including office chart notes and lab results) supporting that member has met all approval criteria I. Initial Approval Criteria A. Multiple Sclerosis (must meet all): 1. Diagnosis of relapsing MS established by magnetic resonance imaging (MRI); 2. Prescribed by or in consultation with a neurologist; 3. Member will not use other disease modifying therapies for MS concurrently; 4. Dose does not exceed 0.5 mg per day (1 capsule per day). Approval duration: 6 months B. Other diagnoses/indications 1. Refer to HIM.PHAR.21 if diagnosis is NOT specifically listed under section III (Diagnoses/Indications for which coverage is NOT authorized). II. Continued Therapy A. Multiple Sclerosis (must meet all): 1. Currently receiving medication via Centene benefit or member has previously met initial approval criteria; 2. Documentation of positive response to therapy (e.g., improved or maintained disease control evidenced by increase in Expanded Disability Status Scale (EDSS) or reduction in relapses or MRI lesions); 3. Member is not using other disease modifying therapies for MS concurrently; 4. If request is for a dose increase, new dose does not exceed 0.5 mg per day (1 capsule per day).
    [Show full text]
  • Oral MS Disease-Modifying Therapies C21142-A
    Drug and Biologic Coverage Criteria Effective Date: 05/01/2019 Last P&T Approval/Version: 07/28/2021 Next Review Due By: 08/2022 Policy Number: C21142-A Oral MS Disease-Modifying Therapies PRODUCTS AFFECTED Mayzent (siponimod), Aubagio (teriflunomide), Gilenya (fingolimod), Mavenclad (cladribine), Tecfidera (dimethyl fumarate), Vumerity (diroximel fumarate), Bafiertam (monomethyl fumarate),dimethyl fumarate, Zeposia (ozanimod), Ponvory (ponesimod) COVERAGE POLICY Coverage for services, procedures, medical devices, and drugs are dependent upon benefit eligibility as outlined in the member's specific benefit plan. This Coverage Guideline must be read in its entirety to determine coverage eligibility, if any. This Coverage Guideline provides information related to coverage determinations only and does not imply that a service or treatment is clinically appropriate or inappropriate. The provider and the member are responsible for all decisions regarding the appropriateness of care. Providers should provide Molina Healthcare complete medical rationale when requesting any exceptions to these guidelines Documentation Requirements: Molina Healthcare reserves the right to require that additional documentation be made available as part of its coverage determination; quality improvement; and fraud; waste and abuse prevention processes. Documentation required may include, but is not limited to, patient records, test results and credentials of the provider ordering or performing a drug or service. Molina Healthcare may deny reimbursement or take additional appropriate action if the documentation provided does not support the initial determination that the drugs or services were medically necessary, not investigational or experimental, and otherwise within the scope of benefits afforded to the member, and/or the documentation demonstrates a pattern of billing or other practice that is inappropriate or excessive DIAGNOSIS: Multiple Sclerosis REQUIRED MEDICAL INFORMATION: A.
    [Show full text]
  • Caspr2 Antibodies in Patients with Thymomas
    View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by Elsevier - Publisher Connector MALIGNANCIES OF THE THYMUS Caspr2 Antibodies in Patients with Thymomas Angela Vincent, FRCPath,* and Sarosh R. Irani, MA* neuromuscular junction. Neuromyotonia (NMT) is due to Abstract: Myasthenia gravis is the best known autoimmune disease motor nerve hyperexcitability that leads to muscle fascicula- associated with thymomas, but other conditions can be found in tions and cramps. A proportion of patients have antibodies patients with thymic tumors, including some that affect the central that appear to be directed against brain tissue-derived volt- nervous system (CNS). We have become particularly interested in age-gated potassium channels (VGKCs) that control the ax- patients who have acquired neuromyotonia, the rare Morvan disease, onal membrane potential.4,5 VGKC antibody titers are rela- or limbic encephalitis. Neuromyotonia mainly involves the periph- tively low in NMT. eral nerves, Morvan disease affects both the peripheral nervous Morvan disease is a rare condition first described in system and CNS, and limbic encephalitis is specific to the CNS. 1876 but until recently hardly mentioned outside the French Many of these patients have voltage-gated potassium channel auto- literature.6 The patients exhibit NMT plus autonomic distur- antibodies. All three conditions can be associated with thymomas bance (such as excessive sweating, constipation, and cardiac and may respond to surgical removal of the underlying tumor
    [Show full text]
  • Vaccination and Demyelination: Is There a Link? Examples with Anti
    Vaccination and demyelination : Is there a link? Examples with anti-hepatitis B and papillomavirus vaccines Julie Mouchet Le Moal To cite this version: Julie Mouchet Le Moal. Vaccination and demyelination : Is there a link? Examples with anti-hepatitis B and papillomavirus vaccines. Human health and pathology. Université de Bordeaux, 2019. English. NNT : 2019BORD0015. tel-02134582 HAL Id: tel-02134582 https://tel.archives-ouvertes.fr/tel-02134582 Submitted on 20 May 2019 HAL is a multi-disciplinary open access L’archive ouverte pluridisciplinaire HAL, est archive for the deposit and dissemination of sci- destinée au dépôt et à la diffusion de documents entific research documents, whether they are pub- scientifiques de niveau recherche, publiés ou non, lished or not. The documents may come from émanant des établissements d’enseignement et de teaching and research institutions in France or recherche français ou étrangers, des laboratoires abroad, or from public or private research centers. publics ou privés. THÈSE PRÉSENTÉE POUR OBTENIR LE GRADE DE DOCTEUR DE L’UNIVERSITÉ DE BORDEAUX ÉCOLE DOCTORALE : Sociétés, Politique, Santé Publique (SP2) SPÉCIALITÉ : Pharmacologie option Pharmaco-épidémiologie, Pharmacovigilance Par Julie MOUCHET LE MOAL VACCINATION ET RISQUE DE DEMYELINISATION : EXISTE-T-IL UN LIEN ? EXEMPLES DES VACCINS ANTI-HEPATITE B ET ANTI-PAPILLOMAVIRUS Sous la direction de : Monsieur le Professeur Bernard Bégaud Soutenue publiquement le 29 Janvier 2019 Composition du jury Président : Christophe TZOURIO, Professeur des Universités
    [Show full text]
  • Neurosyphilis Presenting with Myelitis-Case Series and Literature Review
    Neurosyphilis presenting with myelitis-Case series and literature review Yali Wu Capital Medical University Aliated Beijing Ditan Hospital https://orcid.org/0000-0002-9737-6439 Wenqing Wu ( [email protected] ) https://orcid.org/0000-0001-7428-5529 Case report Keywords: Syphilis, Neurosyphilis, Spinal cord, Magnetic resonance imaging Posted Date: April 5th, 2019 DOI: https://doi.org/10.21203/rs.2.1849/v1 License: This work is licensed under a Creative Commons Attribution 4.0 International License. Read Full License Version of Record: A version of this preprint was published at Journal of Infection and Chemotherapy on February 1st, 2020. See the published version at https://doi.org/10.1016/j.jiac.2019.09.007. Page 1/9 Abstract Background Neurosyphilis is a great imitator because of its various clinical symptoms. Syphilitic myelitis is extremely rare manifestation of neurosyphilis and often misdiagnosed. However, a small amount of literature in the past described its clinical manifestations and imaging features, and there was no relevant data on the prognosis, especially the long-term prognosis. In this paper, 4 syphilis myelitis patients admitted to our hospital between July 2012 and July 2017 were retrospectively reviewed. In the 4 patients, 2 were females, and 2 were males. We present our experiences with syphilitic myelitis, discuss the characteristics, treatment and prognosis. Case presentation The diagnosis criteria were applied: (1) diagnosis of myelitis established by two experienced neurologist based on symptoms and longitudinally extensive transverse myelitis (LETM) at the cervical and thoracic levels mimicked neuromyelitis optic (NMO) on magnetic resonance imaging (MRI) ; (2) Neurosyphilis (NS) was diagnosed by positive treponema pallidum particle assay (TPPA) and toluidine red untreated serum test (TRUST) in the serum and CSF; (3) negative human immunodeciency virus (HIV).
    [Show full text]
  • Clinical and MRI Clues and Pitfalls in the Diagnosis and Differential Diagnosis of Multiple Sclerosis
    Clinical and MRI clues and pitfalls in the diagnosis and differential diagnosis of Multiple Sclerosis Aksel Siva, M.D. MS Clinic & Department Of Neurology Istanbul University Cerrahpaşa School of Medicine [email protected] MSParis2017 - 7th Joint ECTRIMS - ACTRIMS Meeting, 25 - 28 October 2017 Disclosure • Received research grants to my department from The Scientific and Technological Research Council Of Turkey - Health Sciences Research Grants numbers : 109S070 and 112S052.; and also unrestricted research grants from Merck-Serono and Novartis to our Clinical Neuroimmunology Unit • Honoraria or consultation fees and/or travel and registration coverage for attending several national or international congresses or symposia, from Merck Serono, Biogen Idec/Gen Pharma of Turkey, Novartis, Genzyme, Roche and Teva. • Educational presentations at programmes & symposia prepared by Excemed internationally and at national meetings and symposia sponsored by Bayer- Schering AG; Merck-Serono;. Novartis, Genzyme and Teva-Turkey; Biogen Idec/Gen Pharma of Turkey Introduction… • The incidence and prevalence rates of MS are increasing, so are the number of misdiagnosed cases as MS! • One major source of misdiagnosis is misinterpretation of nonspecific clinical and imaging findings and misapplication of MRI diagnostic criteria resulting in an overdiagnosis of MS! • The differential diagnosis of MS includes the MS spectrum and related disorders that covers subclinical & clinical MS phenotypes, MS variants and inflammatory astrocytopathies, as well as other Ab-associated atypical inflammatory-demyelinating syndromes • There are a number of systemic diseases in which either the clinical or MRI findings or both may mimic MS, which further cause confusion! Related publication *Siva A. Common Clinical and Imaging Conditions Misdiagnosed as Multiple Sclerosis.
    [Show full text]
  • Post-COVID-19 Acute Disseminated Encephalomyelitis in a 17-Month-Old
    Prepublication Release Post-COVID-19 Acute Disseminated Encephalomyelitis in a 17-Month-Old Loren A. McLendon, MD, Chethan K. Rao, DO, MS, Cintia Carla Da Hora, MD, Florinda Islamovic, MD, Fernando N. Galan, MD DOI: 10.1542/peds.2020-049678 Journal: Pediatrics Article Type: Case Report Citation: McLendon LA, Rao CK, Da Hora CC, Islamovic F, Galan FN. Post-COVID-19 acute disseminated encephalomyelitis in a 17-month-old. Pediatrics. 2021; doi: 10.1542/peds.2020- 049678 This is a prepublication version of an article that has undergone peer review and been accepted for publication but is not the final version of record. This paper may be cited using the DOI and date of access. This paper may contain information that has errors in facts, figures, and statements, and will be corrected in the final published version. The journal is providing an early version of this article to expedite access to this information. The American Academy of Pediatrics, the editors, and authors are not responsible for inaccurate information and data described in this version. Downloaded from©202 www.aappublications.org/news1 American Academy by of guest Pediatrics on September 27, 2021 Prepublication Release Post-COVID-19 Acute Disseminated Encephalomyelitis in a 17-month-old a,b Loren A. McLendon, MD, a,b Chethan K. Rao, DO, MS, c Cintia Carla Da Hora, MD, c Florinda Islamovic, MD, b Fernando N. Galan, MD Affiliations: a Mayo Clinic College of Medical Science Florida, Division of Child and Adolescent Neurology, Jacksonville, Florida b Nemours Children Specialty Clinic, Division of Neurology, Jacksonville, Florida c University of Florida College of Medicine Jacksonville, Division of Pediatrics, Jacksonville, Florida Corresponding Author: Fernando N.
    [Show full text]
  • Multiple Sclerosis Research: Diagnostics, Disease-Modifying
    S14 Journal of Neuroscience Nursing Multiple Sclerosis Research: Diagnostics, Disease-Modifying Treatments, and Emerging Therapies Kathleen Costello ABSTRACT Multiple sclerosis (MS) is a complex disease that affects the central nervous system. It is believed to be an immune mediated disease, and although the etiology remains unknown, it is believed to occur from a combination of genetic risk factors and environmental risk factors. There is no single diagnostic test for MS, and diagnostic criteria have been developed to aid the provider in making an accurate and timely diagnosis. Once a diagnosis of MS is made, treatments directed toward the inflammatory immune response should be initiated. Currently, there are 10 treatments for MS: four interferon beta products; one glatiramer acetate; one monoclonal antibodyVnatalizumab; three oral treatmentsVfingolimod, teriflunomide, and dimethyl fumarate; and one immunosuppressant agentVmitoxantrone. Each of these agents has a different administration and different risks and side effects. Numerous agents are in late stage development, and it is possible that several more agents, all with different mechanisms of action, will become available over the next several years. Keywords: alemtuzumab, daclizumab, dimethyl fumarate, disease modifying treatment, fingolimod, glatiramer acetate, interferon beta, laquinimod, MCDONALD Criteria, multiple sclerosis, natalizumab, teriflunomide ultiple sclerosis (MS) is a chronic disease of the disease from onset, known as primary progres- of the central nervous system
    [Show full text]