Multiple Sclerosis (Contemporary Neurology Series)
Moses Rodriguez, Orhun H. Kantarci, Istvan Pirko
Format: PDF / Kindle (mobi) / ePub
This latest edition to the 'Contemporary Neurology Series' will fill one of the few remaining 'neurologic gaps' within the Series. 'Multiple Sclerosis,' written solely by Moses Rodriguez, Orhun Kantarci and Istvan Pirko of the Mayo Clinic in Rochester, MN will offer proven, effective treatments for specific presentations and symptoms of multiple sclerosis along with a pathophysiological explanation of why they work. It bridges a needed gap between overly simplistic therapy manuals and basic science texts that discuss human disease only insofar as it mimics what is observed in animal models of the disease in the laboratory. Additionally, it seeks to offer an efficient integrative approach to symptomatic treatment to avoid over-medication and side effects. It discusses the heterogeneous causes of the disease and the need to develop individualized treatments that address the basic pathophysiologic processes that characterize each patient's disease with the future goal of individualized medicine.
'Multiple Sclerosis' covers both the basic research aspects of MS: epidemiology, neuropathology, genetics, and immunology as well as the treatment options associated with the MS patient: sleep, steroids, pharma, neuropsychology, and growth factors (to name a few). 'Multiple Sclerosis' will focus on the medical treatment - drug treatment - of MS rather than on physical medicine and rehabilitation (not the author's strength). The authors will also make ample use of flow diagrams, bulleted points, and tables to help the reader better understand MS and its etiology and treatment.
products. The double-dose intramuscular interferon beta-1a study did not show a dose–response relationship, perhaps because the increased dose was given with the same frequency as the standard dose. The injectable immunomodulators offer incomplete evidence for efficacy in disability-based outcome measures. Many long-term extension studies suffer from several drawbacks, including open-label unblinded design, significant dropout rates, and lack of controls. Overall, these agents remain partially
devices has significant drawbacks: the high cost and unbearable discomfort associated with the electrical shock. The current generation of devices administers shock nonselectively to motor nerves. However, we have had success in rare, selected patients. Spasticity is a common problem in MS, especially in advanced disease. Some spasticity, especially in moderate-to-severe weakness, actually helps patients with supported gait and transfers. Overtreatment in this situation may increase weakness.
determine the specific cell types most likely to induce remyelination. Similar experiments have also been done in myelin-mutant models in which there is a defect in one of the myelin proteins;28,29 specifically, in the jimpy myelin mutant, which has a deficiency in proteolipid protein, and in the shiverer mouse mutant, which has a deficiency in myelin basic protein. Early classic experiments clearly demonstrated that adoptive transfer of progenitor glial cells induces remyelination in mouse-model
be defined clinically.1 The main problem with this definition is that it ignored subclinical disease activity, which is more common than clinical activity, and slowly worsening neurological function, such as in PPMS, when making a definite diagnosis of MS. Therefore, imaging changes (e.g., new nonenhancing or enhancing lesions that develop on magnetic resonance imaging [MRI]) did not play a role in the diagnosis of the disease. Until a second relapse occurred, most of these patients were
with irreversible neuronal loss mediated by either cytotoxic or hypertoxic mechanisms. Some patients have relapses, recover completely, and never develop permanent disability or even a progressive disease course29–31 (see discussion in Chapter 1). However, many pathological and MRI studies indicate that patients do have relapses and that cumulative neurological dysfunction eventually results in permanent abnormalities. Factors such as chemokines, cytokines, and changing receptors on target cells