McAlpine's Multiple Sclerosis - Hardcover

Compston PhD MBBS FRCP, Alastair; Ebers MD FRCP(C), George; Lassmann MD, Hans; Matthews DM BM Bch FRCP, Bryan; Wekerle PhD MD, Hartmut

Hardcover

ISBN 10: 0443050082 ISBN 13: 9780443050084

Publisher: Churchill Livingstone, 1998

Synopsis

The book describes in detail the genetics, neurobiology, pathophysiology, and experimental modelling of multiple sclerosis. Though written to be read as a whole, each chapter can also be read separately. The text is written in a highly readable style, andis extensively illustrated in colour.

This new classic work on Multiple Sclerosis charts the progress that has been and is being made in understanding this difficult disease. This book has its origins in the work written by Douglas McAlpine, Nigel Compston, and Charles Lumsden in 1955 but not one word survives from that edition or the previous edition of McAlpines Multiple Sclerosis published in 1992.

This edition describes in more detail than before the genetics, neurobiology, pathophysiology, and experimental modelling of multiple sclerosis. The emphasis is always on clinical, epidemiological and therapeutic aspects of the disease. Each chapter is well illustrated, including a full colour section.

new edition of the classic book on the subject

four new authors, all internationally known authorities from UK, Canada, Germany & Austria

much more on imaging and investigations than 2E

new chapter on neurobiology and glial development

much better illustrated than 2E

very well referenced

totally rewritten, except for chapters 2 & 3 on symptoms and diagnosis, which have been revised

About this title

About the Authors

Alastair Compston, PhD is Emeritus Professor of Neurology in the Division of Clinical Neurosciences at the University of Cambridge. Compston's research focuses on the clinical science of human demyelinating disease including the discovery of genetic risk factors for multiple sclerosis and the introduction of alemtuzumab. Compston was formerly Professor of Neurology at the University of Wales, president of the European Neurological Society and the Association of British Neurologists, and editor of the journal Brain. Compston's work has been recognised by prizes including the Charcot Award; the K-J Zülch Prize; the World Federation of Neurology Medal; the John Dystel Prize; the Richard and Mary Cave Award of the Multiple Sclerosis Society of Great Britain; the Hughlings Jackson Medal; the Galen Medal; and the Association of British Neurologists Medal. Compston was elected a Fellow of the Royal Society (FRS) in 2016and appointed Commander of the Order of the British Empire (CBE) in the 2016 New Year Honours.

Hans Lassmann, MD, PhD, is a professor for neuroimmunology (ret.) and a research associate at the Center for Brain Research at the Medical University of Vienna, Austria.

Reviews

Multiple sclerosis was first described about 160 years ago by Jean Martin Charcot. Since then, it has become one of the most common conditions faced by clinical neurologists and one of the most intriguing puzzles for neuroscientists. Multiple sclerosis is a relatively frequent disease in Western countries, mainly affecting young people and causing, in many of them, severe and irreversible disability during the 10 to 15 years after onset. Despite its frequency, the causes and pathogenesis of multiple sclerosis remain uncertain, our understanding of its natural evolution is still in its infancy, and our ability to alter its course is limited.

Nevertheless, as a result of three factors, we have recently been witnessing major advances in our understanding of the dynamics of the disease. First, flourishing activity in the basic sciences, such as genetics, immunology, and immunopathology, has helped to elucidate the mechanisms responsible for neurologic damage and repair related to multiple sclerosis. Second, the development and intensive clinical application of sophisticated magnetic resonance imaging technology have helped to show in vivo how the complex and heterogeneous pathological features of the disease progress to cause acute and permanent disability. Third, the availability of treatment that is able to modify, albeit only slightly, the evolution of multiple sclerosis is providing information about the mechanisms of the disease and is also attracting attention from individual neuroscientists and research support from both public and private institutions.

The history of multiple sclerosis is also the history of the many authoritative reviews of the topic. The first chapter of this history was written by W.A. Hammond in 1871, and the latest is the third edition of the classic McAlpine's Multiple Sclerosis by Alastair Compston and colleagues, published in 1998. The principal merit of this book is the clear and coherent approach of the six authors, who are the world's leading figures in the field, to describing and interpreting the many complex and variable aspects of multiple sclerosis. The book does not attempt to be a comprehensive work on multiple sclerosis, as has been the declared intent since the first edition was published in 1985, but rather, it emphasizes what is considered by the authors to be relevant to the understanding of the mechanisms and dynamics of the disease and what still needs to be further clarified.

In this light, section 4, which provides a comprehensive, thoughtful, and up-to-date overview of the current state of knowledge of the pathogenesis of multiple sclerosis, can be considered the heart of the book. All the evidence, both in support of and against a given hypothesis, is clearly and comprehensively discussed, and the areas of uncertainty that are ripe for future research are indicated.

Inflammation is one of the earliest events in the evolution of multiple sclerosis, and it starts with the migration of activated T lymphocytes into the central nervous system. Inflammation is maintained by the interaction of the activated lymphocytes with antigen-presenting cells in the central nervous system through the release of proinflammatory cytokines. These cytokines increase the permeability of the blood-brain barrier and recruit secondary effector cells and humoral factors, which can lead to varying degrees of damage to the myelin sheath and death of oligodendrocytes. In the meantime, however, several other mechanisms down-regulate the process. These mechanisms include apoptosis of lymphocytes, release of antiinflammatory cytokines, and systemic endocrine responses. Progressive and irreversible loss of myelin is the result of the variable and complex interplay between the number of dead oligodendrocytes and oligodendrocyte progenitor cells and the ability of the remaining oligodendrocytes to promote remyelination. The pathologic progression of the disease is completed by astroglia reaction and axonal loss, which can occur through wallerian degeneration or loss of nerve cells.

Each of those events is expressed clinically. Acute symptoms are due to the blocking of nerve conduction, which, in turn, results from the opening of the blood-brain barrier, inflammation, and demyelination. Recovery from acute symptoms is the result of down-regulation of the inflammatory process, the ability to remyelinate, and the restoration of conduction through the insertion of new sodium channels into the demyelinated axolemma. Persistent and severe demyelination and, more important, axon depletion are the most likely causes of irreversible and severe disability.

From this brief description of the pathogenesis of multiple sclerosis, it will be clear that many aspects of the disease are still poorly understood. These range from the definition of the cause of multiple sclerosis to the role of individual pathogenetic mechanisms in determining persistent demyelination and axonal loss in the various phenotypes of the disease and, in these same phenotypes, during the various clinical phases. One illustration of the degree to which multiple sclerosis remains a mystery is our lack of understanding of the contributions of remyelination and astroglia reaction to the evolution of the disease. Although it may seem that remyelination is beneficial and gliosis harmful, there is evidence that remyelinated lesions can become targets for new waves of demyelination, and the gliotic ensheathment of the demyelinated axons may favor the restoration of nerve conduction.

The multidisciplinary and coherent nature of McAlpine's Multiple Sclerosis is shown in its other sections. An example is the second section of the book, entitled "Genetic Epidemiology," in which the usual approach of listing the evidence for a genetic or an environmental origin of the disease has been replaced by a thoughtful and up-to-date description of the complex interplay between environmental triggers and genetic susceptibility. Another example is the first section, entitled "The Story of Multiple Sclerosis," which is not merely a list of names and dates, but also an elegant and informative chapter about the history of our comprehension of the disease, providing readers with the necessary background for understanding the present state of knowledge of the disease.

We are facing rapid changes in our understanding of multiple sclerosis. Nevertheless, the principles and much of the detailed information in this book are likely to have lasting value. McAlpine's Multiple Sclerosis will appeal to a broad spectrum of neuroscientists and health care professionals, regardless of the stage of their involvement in the field. For those experienced in the study of multiple sclerosis or in the management of the disease, it constitutes a valuable summary of the state of the art. For residents and students interested in multiple sclerosis, it is a valuable cornerstone from which they can start to build their future professional lives. The moderate optimism that permeates the book is well summarized in the last sentence of the preface by Compston: "We chart systematic and steady progress in understanding this difficult disease... but the final solution to the problem must wait for another edition."

Reviewed by Massimo Filippi, M.D.
Copyright © 1999 Massachusetts Medical Society. All rights reserved. The New England Journal of Medicine is a registered trademark of the MMS.

Edition details

• Publisher: Churchill Livingstone
• Publication date: 1998
• Language: English
• ISBN 10: 0443050082
• ISBN 13: 9780443050084
• Binding: Hardcover
• Edition number: 3
• Number of pages: 700