New Diagnostic Criteria for Multiple Sclerosis: Guidelines for Research Protocols
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Headache in Multiple Sclerosis from a Different Perspective: a Prospective Study
Volume 9 • Number 1 • March 2018 JOURNAL OF CLINICAL AND RESEARCHORIGINAL ARTICLEARTICLE EXPERIMENTAL INVESTIGATIONS Headache in Multiple Sclerosis from A Different Perspective: A Prospective Study Gökhan Özer¹, Ufuk Ergün², Levent Ertuğrul İnan³ 1 Sanko University Faculty of Medicine, Department of Neurology, Gaziantep, ABSTRACT Turkey Objective: It is known that patients with multiple sclerosis have a high incidence of headache. 2 Kırıkkale University School of Medicine, Kırıkkale, Turkey Although there is increasing evidence to suggest that periaqueductal gray matter (PAG) plays 3 Bozok University School of Medicine, a role in the pathophysiology of migraine headache, it is not known whether the type of Yozgat, Turkey headache may be a predictor of a MS relapse. Patients and Methods: The study enrolled 100 patients (68 females, 32 males) with clinically confirmed MS diagnosis established by McDonald diagnostic criteria. The type and duration of MS, MRI localization of lesions and cognitive status were recorded for all patients. Patients were questioned whether they experience headache during MS attacks. Results: Sixty-eight percent of the patients had headache and 32% of the patients were free of headache. Of the patients with headache, 16% had tension –type headache (TTH), 14% had migraine, 11% had primary stabbing headache (PSH), 8% had TTH+ migraine, 6% had PSH+ migraine, 6% had medication overuse headache , 2% had medication overuse headache + E-mail: [email protected] migraine, 2% had paroxysmal hemicrania, 1% had cervicogenic headache, 1% had chronic TTH, E-mail: [email protected] and 1% had unclassified headache. There was a statistically significant relationship between the E-mail: [email protected] presence of headache and MS relapse (p<0.001). -
Multiple Sclerosis Accepted: 15 May 2016 Receiving Tysabri
Iranian Journal Letter to Editor of Neurology Iran J Neurol 2016; 15(3): 175-176 Bacterial meningitis in a patient Received: 10 Mar 2016 with multiple sclerosis Accepted: 15 May 2016 receiving Tysabri Abdorreza Naser Moghadasi1, Soroor Advani2, Shiva Rahimi2 1 Multiple Sclerosis Research Center, Neuroscience Institute, Department of Neurology, Sina Hospital, Tehran University of Medical Sciences, Tehran, Iran 2 Department of Neurology, Sina Hospital, Tehran University of Medical Sciences, Tehran, Iran Keywords lesions (Figure 1-A) with no evidence of PML or Bacterial Meningitis; Multiple Sclerosis; Tysabri HSE encephalitis. Meningeal enhancement was seen after the injection of the contrast medium (Figure 1-B). The most important adverse effect of natalizumab is progressive multifocal leukoencephalopathy (PML).1 Apart from PML, there are reports of other cerebral infections including herpes simplex encephalitis (HSE)2,3 and cryptococcal meningitis4 in the literature. The patient was a 29-year-old woman, a known case of multiple sclerosis (MS) for at least 5 years. She was treated using natalizumab since 6 month before. She was under treatment with prednisolone 1 g daily for 5 days for optic neuritis, which was 2 weeks before the onset of symptoms of meningitis. Approximately three days before visiting the neurologist, a continuous headache in the left temporal lobe was developed. Figure 1. Periventricular lesions confirming the The patient was febrile at that time as well. diagnosis of multiple sclerosis (MS) in the FLAIR MRI Besides, two days before this, she had started view (A). Meningeal enhancement was seen after ciprofloxacin for treatment of a urinary gadolinium injection (B) tract infection. -
Demyelination: What Is It and Why Does It Happen?
Demyelination: What Is It and Why Does It Happen? • Causes • Symptoms • Types • MS and Demyelination • Treatment and Diagnosis • Vaccines • Takeaway What is demyelination? Nerves send and receive messages from every part of your body and process them in your brain. Nerves allow you to speak, see, feel, and think. Many nerves are coated in myelin. Myelin is an insulating material. When it’s worn away or damaged, nerves can deteriorate, causing problems in the brain and throughout the body. Damage to myelin around nerves is called demyelination. Nerves Nerves are made up of neurons. Neurons are composed of a cell body, dendrites, and an axon. The axon sends messages from one neuron to the next. The axon also connects neurons to other cells, such as muscle cells. Some axons are extremely short. Others are 3 feet long. Some axons are covered in myelin. Myelin protects the axons and helps carry axon messages as quickly as possible. Myelin Myelin is made of membrane layers that cover an axon. This is similar to the idea of an electrical wire with coating to protect the metal underneath. Myelin allows a nerve signal to travel faster. In unmyelinated neurons, a signal can travel along the nerves at about 1 meter per second. In a myelinated neuron, the signal can travel 100 meters per second. Certain diseases can damage myelin. Demyelination slows down messages sent along axons and causes the axon to deteriorate. Depending upon the location of the damage, axon loss can cause problems with feeling, moving, seeing, hearing, and thinking clearly. CAUSES Causes of demyelination Inflammation is the most common cause of myelin damage. -
Acute Disseminated Encephalomyelitis Or Multiple Sclerosis: Can the Initial Presentation Help in Establishing a Correct Diagnosi
636 REVIEW Acute disseminated encephalomyelitis or multiple sclerosis: can the initial presentation help in establishing a correct Arch Dis Child: first published as on 20 May 2005. Downloaded from diagnosis? R C Dale, J A Branson ............................................................................................................................... Arch Dis Child 2005;90:636–639. doi: 10.1136/adc.2004.062935 The differential diagnosis of CNS white matter disease is and MS cases must manifest disseminated disease of the CNS (more than one clinical or broad, and can be divided into vascular, metabolic, radiological site). Diseases isolated to specific infective, or inflammatory aetiologies. Isolated areas of the CNS (isolated optic neuritis, trans- inflammatory disorders of the CNS are often associated verse myelitis, and brain stem dysfunction) are considered distinct from both ADEM and MS with demyelination, and the two terms (inflammatory and (clinically and prognostically), and will not be demyelinating) are often used in conjunction. When the discussed in this review.89 disease is monophasic, the term acute disseminated 1 DEMOGRAPHICS encephalomyelitis (ADEM) is used. ADEM typically occurs Monophasic ADEM is more common in children, as a post-infectious phenomenon, and by definition, must whereas MS is more common in adults. Between be an isolated (monophasic) episode. If a relapse occurs 2.7% and 4.4% of MS presentations occur in children less than 16 years of age.8 Mikaeloff et al shortly after the ADEM presentation in association with a showed a mean age of 7.1 years and 12.0 years in further infection or steroid withdrawal, the term MDEM paediatric ADEM and MS patients respectively.8 (multiphasic disseminated encephalomyelitis) is used. -
Updated Criteria for Diagnosing Multiple Sclerosis
r e v i e w a r t i c l e Updated criteria for diagnosing Multiple Sclerosis or in the case of progressive MS, a slow or step- Key take home messages wise progression of disability over a period of • The diagnostic criteria for MS have at least six months been recently updated • and objective clinical evidence of lesions in • These criteria should only be applied two or more distinct sites in the white matter to populations in whom MS is of the central nervous system common and patients who present • with no more satisfactory explanation. Peter Brex with typical symptoms for which no The Schumacher criteria were purely clinical, MB BS, MD, FRCP is a Consultant Neurologist at King’s College Hospital better explanation can be found although investigations were encouraged (blood, NHS Foundation Trust. He trained in • All patients with suspected MS should urine, chest X-ray, CSF analysis) to exclude London and was appointed to his current have an MRI brain scan; spinal cord alternative conditions. role in 2005. He specialises in multiple imaging is not mandatory Over the next few years modifications to the sclerosis, with a particular interest in early 2,3 prognostic markers and the management • Unmatched oligoclonal bands in the Schumacher criteria were published but in 1983 of MS during pregnancy. CSF can be used as a substitute for the Schumacher criteria were replaced by criteria demonstrating dissemination in time, developed by a committee chaired by Charles allowing an earlier diagnosis than was Poser (1923 – 2010).4 The Poser criteria incorpor- previously possible ated laboratory and clinical tests developed in the previous decade to support the diagnosis with ‘paraclinical evidence’ of lesions. -
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. -
And Multiple Sclerosis Particular Problem, I Wish to Make the Follow
524 Maters arising prolong the lives of those suffering, thereby Most of these problems are not taken into 6 Poser C, Paty D, Scheinberg L, et al. New J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.55.6.524-b on 1 June 1992. Downloaded from providing the necessity for self-action by the consideration in Sibley's article. diagnostic criteria for multiple sclerosis. Ann patient. It is germane to point out that the "scien- Neurol 1983;13:227-31. Perhaps when we advise patients and tific" evidence of epidemiology and biostatis- families who face difficult decisions, we tics overlooks the fact that such studies can at Sibley et al reply: would be better to heed the available evi- best only be estimates within a cohort and dence about who will do well and who will do cannot be generalised; epidemiological stud- We age- and sex-matched MS patients with badly rather than withholding recommenda- ies are most useful in providing aetiological healthy controls solely to establish the degree tions because unduly cautious statisticians clues but cannot be used to deny possible of accident-proneness of MS patients. It choose to neglect the downside effects of causal relationships.2 As was pointed out by probably needs to be clearly restated that the their theoretical arguments. Neurologists are Schoenberg, "Statistical significance (or lack patients were used as their own controls in an especially favourable position to under- thereof) does not equal biological when they were not "at risk". stand the misery that accompanies chronic, significance". Physical trauma had no positive influence overwhelming brain damage. -
Neurodegeneration and Neuroprotection in Multiple Sclerosis and Other Neurodegenerative Diseases ⁎ Suhayl Dhib-Jalbut , Douglas L
Journal of Neuroimmunology 176 (2006) 198–215 www.elsevier.com/locate/jneuroim Conference report Neurodegeneration and neuroprotection in multiple sclerosis and other neurodegenerative diseases ⁎ Suhayl Dhib-Jalbut , Douglas L. Arnold, Don W. Cleveland, Mark Fisher, Robert M. Friedlander, M. Maral Mouradian, Serge Przedborski, Bruce D. Trapp, Tony Wyss-Coray, V. Wee Yong UMDNJ-Robert Wood Johnson Medical School, New Brunswick, NJ, United States McGill University, Montreal, Quebec, Canada UCSD, San Diego, CA, United States University of Massachusetts, Worcester, MA, United States Harvard Medical School, Boston, MA, United States Columbia University, New York, NY, United States The Cleveland Clinic, Cleveland, OH, United States Stanford University, Paolo Alto, CA, United States University of Calgary, Calgary, Alberta, Canada Received 3 March 2006; accepted 6 March 2006 Abstract Multiple sclerosis is considered a disease of myelin destruction; Parkinson's disease (PD), one of dopaminergic neuron depletion; ALS, a disease of motor neuron death; and Alzheimer's, a disease of plaques and tangles. Although these disorders differ in important ways, they also have common pathogenic features, including inflammation, genetic mutations, inappropriate protein aggregates (e.g., Lewy bodies, amyloid plaques), and biochemical defects leading to apoptosis, such as oxidative stress and mitochondrial dysfunction. In most disorders, it remains uncertain whether inflammation and protein aggregation are neurotoxic or neuroprotective. Elucidating the mechanisms -
Multiple Sclerosis (MS) What Do I Need to Know?
I’m Caring for a Veteran with Multiple Sclerosis (MS) What Do I Need to Know? Physical and Mental Changes to Expect Symptoms of multiple sclerosis (MS) can vary greatly from Veteran to Veteran and from time to time in the same person. For instance, one person with MS may experience abnormal fatigue and another person may have severe vision problems. While one person with MS may have loss of balance, muscle coordination or tremors — making walking and everyday tasks difficult to perform — another person may have slurred speech and memory issues. Some Facts These problems may be permanent or may come and go. Depression is frequently experienced by MS patients and can have a significant What is Multiple Sclerosis? impact on quality of life. Multiple sclerosis (MS) is an Physical changes may include: visual disturbances; difficulty in unpredictable, often disabling controlling strength and movements; impaired coordination and balance; disease of the central nervous numbness; tingling; sensitivity to heat and cold; bladder control problems; system that interrupts the flow of urinary tract infections; mild to severe fatigue and weakness information within the brain and between the brain and the body Mental changes may include: problems with memory and concentration and stops people from moving. Emotional changes may include: mood swings, ranging from depression Symptoms range from numbness to euphoria and tingling to blindness and paralysis. The progress, severity, and specific symptoms of MS in any one What Does This Mean for Me? person cannot yet be predicted. MS affects not only the Veterans with the illness, but also family members Treatment may include: and friends. -
(Pre-Allison & Millar) Ipsen Criteria: 1939-48, Boston, MA
Early criteria (pre-Allison & Millar) Ipsen criteria: 1939-48, Boston, MA USA1 - Probable MS o Those cases with records presenting convincing evidence - Possible MS o Those cases whose evidence was more doubtful. Ipsen acknowledges these allocations are fairly arbitrary but also notes that absolutely certainty of diagnosis is impossible except by autopsy, a limitation we are similarly affected by even today. Westlund & Kurland: 1951, Winnipeg, MT Canada & New Orleans, LA USA2 Diagnostic groupings as follows, with no explicit requirements for each, rather deferring to the discretion of the examining neurologist: - Certain MS - Probable MS - Possible MS o In this class, the changes for and against MS were considered approximately even - Doubtful, unlikely or definitely-not MS2 Sutherland criteria: 1954, Northern Scotland3 - Probable MS o This category for patients in whom the history, the results of clinical examination and, where available, hospital investigations, indicated that the diagnosis of MS was beyond reasonable doubt. - Possible MS o Patients in whom a diagnosis of MS appears justifiable but in which the diagnosis could not be established beyond reasonable doubt; o This group also included patients who did not wish to be examined or could not be seen – review of hospital records for these patients suggested a diagnosis of MS - Rejected cases o Patients found to be suffering from a disease other than MS Allison & Millar Criteria and variants Allison & Millar criteria: 1954, Northern Ireland4 - Early disseminated sclerosis: 1) this category for patients with little in the way of symptomatic presentation but with a recent history consistent with disease onset, i.e. optic neuritis, ophthalmoplegia (double vision), vertigo, sensory problems like pins & needles or numbness, or motor problems like weakness. -
Pediatric MS and Other Demyelinating Disorders in Childhood Current Understanding, Diagnosis and Management 24
Pediatric MS and other demyelinating disorders in childhood Current understanding, diagnosis and management 24 Contents Pediatric MS from the perspective of both the 4 child and the family Biological reasons why children develop MS 4 Genetic and environmental risk factors for 5 pediatric MS Clinical features and outcome 6 Cognition and mood 6 MRI features 7 Conventional first-line treatment and general 7 management Escalation and emerging treatments 9 Defining MS in childhood and differentiating it 9 from mimics Acute disseminated encephalomyelitis (ADEM) 10 Acute transverse myelitis (ATM) 10 Optic neuritis 11 Neuromyelitis optica (NMO) 11 Acquired demyelinating syndrome (ADS) 12 References and further reading 13 Contributors The articles summarised in this publication are taken from a 2016 Neurology journal supplement, written by the International Pediatric MS Study Group. We gratefully acknowledge the editorial contribution of Dr Rosalind Kalb. Funders Associazione Italiana Sclerosi Multipla, Deutsche Multiple Sklerose Gesellschaft Bundesverband, MS Cure Fund, National MS Society (USA), Schweizerische Multiple Sklerose Gesellschaft/Société suisse de la Sclérose en plaques, Scleroseforeningen, Stichting MS Research. 34 Pediatric MS and other demyelinating disorders in childhood: Current understanding, diagnosis and management The understanding of multiple sclerosis (MS) and other demyelinating disorders in childhood has advanced considerably in the last ten years. This publication accompanies a series of articles written by subject experts that highlight the advances, unanswered questions and new challenges in understanding, diagnosis and management. It provides a short summary of the key points from each article, and a list of resources and further reading where you can find links to the full articles, all of which are available open access (free). -
Nayakphd2018.Pdf
This work is protected by copyright and other intellectual property rights and duplication or sale of all or part is not permitted, except that material may be duplicated by you for research, private study, criticism/review or educational purposes. Electronic or print copies are for your own personal, non- commercial use and shall not be passed to any other individual. No quotation may be published without proper acknowledgement. For any other use, or to quote extensively from the work, permission must be obtained from the copyright holder/s. 1 2 3 Structure and function of the visual pathway in demyelinating optic neuropathy Devaki Nayak Thesis submitted for degree of PhD June 2018 Keele University 4 Acknowledgments I take this opportunity to thank Professor Hawkins for all the help and advice that he provided me over the entire duration of work. I would like to thank the team at Keele Multiple Sclerosis Research Group for their help, friendship and humor throughout the period of research. I once again thank Professor Hawkins for guiding an Ophthalmologist to explore the world of MS in Neurology. I would like to thank Professor Peter Jones for his valuable input on statistical methodology and Professor Richard Strange for his weekly input on statistics from the very first recruitment into this project. I specially want to thank Dr. Ramachandran who spent considerable amount of time in guiding the project and helping with meetings with Professor Jones. I am also thankful to Janice Guildford who helped me with knowledge of existent database in the Keele Multiple Sclerosis Research Group.