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Multiple sclerosis is a chronic and often disabling disease of the nervous system, affecting about 1 million people worldwide. Even though it has been known for over a hundred years, no cause or cure has yet been discovered-but now there is hope. New therapies have been shown to slow the disease progress in some patients, and the pace of discoveries about the cellular machinery of the brain and spinal cord has accelerated. This book presents a comprehensive overview of multiple sclerosis today, as researchers seek to understand its processes, develop therapies that will slow or halt the disease and perhaps repair damage, offer relief for specific symptoms, and improve the abilities of MS patients to function in their daily lives. The panel reviews existing knowledge and identifies key research questions, focusing on: Research strategies that have the greatest potential to understand the biological mechanisms of recovery and to translate findings into specific strategies for therapy. How people adapt to MS and the research needed to improve the lives of people with MS. Management of disease symptoms (cognitive impairment, depression, spasticity, vision problems, and others). The committee also discusses ways to build and financially support the MS research enterprise, including a look at challenges inherent in designing clinical trials. This book will be important to MS researchers, research funders, health care advocates for MS research and treatment, and interested patients and their families.
Intended for general neurologists as well as specialists in multiple sclerosis (MS) and imaging, this book provides comprehensive discussion of central nervous system (CNS) atrophy involving the brain and spinal cord, and both the chapter authors and topics have been selected to provide state-of-the-art reviews. Key issues covered in the book include pathogenesis and its mechanisms, technical aspects of MRI measurement, the relationship between CNS atrophy and other MRI metrics, clinical relevance, the association with neurobehavioral and genetic-immunologic components of MS, and the effects of disease-modifying therapies on tissue atrophy. Pros and cons of different technical approaches are discussed critically. Special attention is devoted to CNS atrophy as a clinically relevant biologic marker of the MS disease process.
This book provides cutting-edge information on the epidemiology, etiopathogenesis, clinical manifestations, diagnostic procedures and treatment approaches for the main white matter (WM) disorders of the central nervous system (CNS). WM lesions are associated with many neurological conditions, and with aging. The diagnostic work-up of neurological diseases characterized by the presence of these lesions has changed dramatically over the past few years. This is mainly due on the one hand to the discovery of specific pathogenetic factors in some of these conditions, and on the order to the optimized use of diagnostic tools. All of this has resulted in new diagnostic algorithms, and in the identification of new neurological conditions. The book offers neurologists essential guidance in the diagnosis and treatment of the most frequent WM conditions, promoting their correct and cost-saving diagnosis and management. By integrating neurological, laboratory and imaging concepts with the demands of accurate diagnosis, this reference guide provides a state-of-the-art overview of the current state of knowledge on these conditions, as well as practical guidelines for their diagnosis and treatment.
This thesis focuses on disease activity in clinically isolated syndrome (CIS) and newly diagnosed relapsing remitting multiple sclerosis (RRMS). The papers are based on data from 41 patients in a prospective longitudinal cohort study. All patients were untreated at baseline. Age- and sex-matched healthy controls (n=22) for blood and cerebrospinal fluid (CSF) samples were recruited from blood donors. Paper I evaluated the prognostic value of baseline levels of CXCL1, CXCL8, CXCL10, CXCL13, CCL22, neurofilament light chain (NFL), neurofilament heavy chain, glial fibrillary acidic protein, chitinase-3-like-1 (CHI3L1), matrix metalloproteinase-9 (MMP-9) and osteopontin in CSF in relation to disease activity during the first two years of follow-up. Disease activity was defined as clinical relapses, new T2 lesions in brain magnetic resonance imaging (MRI) and/or sustained Expanded Disability Status Scale (EDSS) progression. Absence of these three signs of disease activity was called no evidence of disease activity (NEDA-3). Logistic regression analysis showed that NFL in CSF was the best predictive marker of disease activity and correctly classified 93% of the patients with evidence of disease activity during two years of follow-up and 67% of those without. Paper II presented four year follow-up data from the cohort and also included brain volume data as well as serum levels of NFL. The correlation between NFL in CSF and serum was fairly strong (r=0.74, p<0.001). NFL in CSF was associated with new T2 lesions as well as with brain volume loss, whereas CHI3L1 in CSF was associated mainly with brain volume loss and CXCL1, CXCL10, CXCL13, CCL22 and MMP-9 in CSF were mainly associated with new T2 lesions. Taken together, paper I and II confirm and extend the knowledge of NFL as a useful biomarker in CIS and RRMS and suggests that NFL, rather than total brain volume loss, could be included in an expanded NEDA concept and used in clinical monitoring of disease activity/treatment effect. Although serum levels of NFL were correlated with the corresponding CSF levels, CSF-NFL showed a stronger association to subsequent disease activity (NEDA-3). Paper III addressed the patients´ self-reported Modified Fatigue Impact Scale (MFIS) scores in relation to other cohort study data. MFIS scores correlated with other self-assessment questionnaire data (Hospital Anxiety and Depression scale (HAD), Multiple Sclerosis Impact Scale 29 (MSIS-29) and Short Form 36 (SF-36) scores (Spearman´s rho 0.45-0.78, all p?0.01)) but not with EDSS ratings, number of T2 lesions, total brain volume or NFL levels, indicating that subjective fatigue scores are not well reflected by some commonly used and objectively measurable disease parameters. Paper IV focused on the complement factors C1q, C3, C3a and sC5b-9 in CSF and plasma. CSFC1q was significantly higher in patients than in controls at baseline. The subgroup of patients with ongoing relapse at baseline also had higher levels of CSF-C3a than controls. Baseline levels of CSF-C1q and CSF-C3a correlated significantly with several pro-inflammatory chemokines as well as with MMP-9, CHI3L1 and NFL in CSF. Baseline CSF-C3a also correlated significantly with the number of T2 lesions and Gadolinium enhancing lesions in brain MRI at baseline, as well as with the number of new T2 lesions during follow-up. This study indicates that the complement system is involved already at early stages of MS. It also suggests that especially CSF-C1q and CSF-C3a levels are associated with other neuroinflammatory and neurodegenerative markers and that CSF-C3a levels may carry some prognostic information.
Magnetic resonance (MR) imaging and spectroscopy are powerful tools for demonstrating and monitoring pathological processes of the brain and spinal cord. Multiple sclerosis (MS), a common and as yet incurable disease of the brain and spinal cord, is being studied intensively using these techniques. They perform a major role in facilitating the diagnosis, understanding the mechanisms of symptoms, and monitoring the effect of new treatments. Written by experts in the field, this extensively illustrated text provides a comprehensive review of the benefits and limitations of MR in the study of MS. Coverage ranges through the contributions of MR, the variety of techniques available, diagnosis and differential diagnosis, MR as a predictor of the clinical course, MR views of pathophysiology, and finally monitoring new treatment efficacy.
Quantitative Magnetic Resonance Imaging is a 'go-to' reference for methods and applications of quantitative magnetic resonance imaging, with specific sections on Relaxometry, Perfusion, and Diffusion. Each section will start with an explanation of the basic techniques for mapping the tissue property in question, including a description of the challenges that arise when using these basic approaches. For properties which can be measured in multiple ways, each of these basic methods will be described in separate chapters. Following the basics, a chapter in each section presents more advanced and recently proposed techniques for quantitative tissue property mapping, with a concluding chapter on clinical applications. The reader will learn: - The basic physics behind tissue property mapping - How to implement basic pulse sequences for the quantitative measurement of tissue properties - The strengths and limitations to the basic and more rapid methods for mapping the magnetic relaxation properties T1, T2, and T2* - The pros and cons for different approaches to mapping perfusion - The methods of Diffusion-weighted imaging and how this approach can be used to generate diffusion tensor - maps and more complex representations of diffusion - How flow, magneto-electric tissue property, fat fraction, exchange, elastography, and temperature mapping are performed - How fast imaging approaches including parallel imaging, compressed sensing, and Magnetic Resonance - Fingerprinting can be used to accelerate or improve tissue property mapping schemes - How tissue property mapping is used clinically in different organs - Structured to cater for MRI researchers and graduate students with a wide variety of backgrounds - Explains basic methods for quantitatively measuring tissue properties with MRI - including T1, T2, perfusion, diffusion, fat and iron fraction, elastography, flow, susceptibility - enabling the implementation of pulse sequences to perform measurements - Shows the limitations of the techniques and explains the challenges to the clinical adoption of these traditional methods, presenting the latest research in rapid quantitative imaging which has the possibility to tackle these challenges - Each section contains a chapter explaining the basics of novel ideas for quantitative mapping, such as compressed sensing and Magnetic Resonance Fingerprinting-based approaches
Presenting the novel concept of white matter dementia, this unique book offers hope for a better understanding and treatment of dementia.
This is the latest edition of the classic book on the subject of multiple sclerosis. An international group of authors has been involved in updating this edition which features more information on imaging and investigations, and a new chapter on neurobiology and glial development.
Dear Readers, If you are engaged in the treatment of patients with MS (pwMS), this e-book’s aim is to offer novel insights to improve on an understanding of one of the major problems of pwMS: fatigue. Although there is increasing research into fatigue and its impact on MS, this collection of ten articles supports a better understanding of fatigue in MS patients. It explores pathophysiological concepts, provoking mechanisms, objective measurements, personality interactions, pharmacological and non-pharmacological interventions and summarizes clinical management. It is written by neurologists, psychologists, scientists and therapists and addresses this group of people, who deal with pwMS in private, clinical, rehabilitation or scientific settings. Its aim is to communicate high-quality information, knowledge and experience on MS to healthcare professionals, while providing global support for the international MS community.
"Why are there no effective treatments for my condition? Why do researchers exclude patients with primary progressive multiple sclerosis from enrolling in clinical trials? Please let me know if you hear of studies that I might be allowed to enter or treatments that I could try for my condition. " Thus, in recent years, the sad lament of the patient with primary progressive MS (PPMS). This variant, often in the guise of a chronic progressive myelopathy or, less commonly, progressive cerebellar or bulbar dysfunction, usually responds poorly to corticosteroids and rarely seems to benefit to a significant degree from intensive immunosuppressive treatments. In recent years, most randomized clin ical trials have excluded PPMS patients on two counts. Clinical worsening devel ops slowly in PPMS and may not be recognized during the course of a 2-or 3-year trial even in untreated control patients. This factor alone adds to the potential for a type 2 error or, at the very least, inflates the sample size and duration of the trial. In addition, there is mounting evidence that progressive axonal degeneration and neuronal loss (rather than active, recurrent inflammation) may be important components of the pathology in this form of the disease. Although contemporary trials are evaluating whether PPMS patients may benefit from treatment with the ~-interferons and glatiramer acetate, preliminary, uncontrolled clinical experi ence suggests that the results may not be dramatic.