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PubMed2006

Growth hormone and insulin growth factor-I levels in plasma and cerebrospinal fluid of patients with multiple sclerosis.

Multiple sclerosis (MS) has several clinically different forms. Whereas the illness progresses slowly in most of the patients, 10% have an aggressively progressive course with fatal outcome without signs of remyelination capability. The process of remyelination depends on numerous interactive factors, including the presence of various growth factors, the most important of which in the adult is insulin growth factor-I (IGF-I). On the other hand, the most powerful postnatal regulator of IGF-I is growth hormone (GH), which also acts as a neuroprotective and an antiapoptotic agent, and has direct influence on myelination. Levels of these growth factors have never been examined in the cerebrospinal fluid (CSF) of patients with MS. The levels of IGF-I and GH were measured in serum and CSF of 46 MS patients and compared with those of 49 patients with no evidence of demyelinating disease. The only positive finding was a deficiency of GH in the CSF of MS patients. The possible implications of those findings in the etiopathogenesis of MS will be discussed.

Adolescent↗

PubMed1996

Multiple sclerosis.

Multiple sclerosis is a chronic disease that begins in late adolescence or adulthood. It is highly variable in its expression and severity. It is believed to be autoimmune in nature. The cause is unknown; both genetic and environmental factors have been implicated in the pathogenesis. MS generally presents with the acute or subacute onset of neurologic abnormalities that may wax and wane over many years. Diagnosis is generally made by means of observation of the clinical course in conjunction with a neurologic examination and laboratory tests. These tests may include magnetic resonance imaging of the head and spine, lumbar puncture, and evoked potentials. Treatment is based on general supportive care, the use of corticosteroids for relapses, and symptomatic management of ongoing problems. The frequency of relapses can be reduced with interferon-beta (Betaseron). Copolymer 1 and interferon-beta la are being evaluated by the U.S. Food and Drug Administration for approval for use for reduction in the frequency of relapses in relapsing-remitting MS. Treatment of chronic progression is often attempted with immunosuppressive agents such as corticosteroids, azathioprine, and cyclophosphamide. Use of other agents is being investigated.

Adolescent↗

PubMed2000

Neurology. 4: Multiple sclerosis.

Multiple sclerosis (MS) is a chronic inflammatory demyelinating disease of the central nervous system (CNS) and a common cause of disability in young adults; it is most likely an autoimmune disease. Typically, MS initially follows a relapsing-remitting course, but most patients eventually develop secondary progressive MS, where there is progressive deterioration without relapses or remissions; in some patients, MS has a primary progressive course. The diagnosis of MS requires evidence of CNS lesions disseminated in time and place, as well as the exclusion of other likely causes of these lesions; the clinical history, neurological examination and investigations, such as magnetic resonance imaging of the brain and spinal cord, all have key roles in the diagnosis. Education and counselling of the patient and family members are essential for good patient management. Moderate to severe attacks of MS are best treated with intravenous infusions of high-dose methylprednisolone. Interferon beta reduces the frequency of attacks and the progression of disability in relapsing-remitting MS. Symptomatic therapy is important in the management of spasticity, pain, urinary problems and the other symptoms or complications of MS.

Adult↗

PubMed2002

Reproductive decision making in women with multiple sclerosis.

Multiple sclerosis (MS), the most common acquired neurological disorder of young adults, often strikes young women in their childbearing years. Despite the overlap of MS onset with the childbearing years of women, little is known about how women with MS make decisions about pregnancy and childbearing. In an effort to understand the process of decision making in these women, an exploratory descriptive qualitative study was undertaken; 15 pregnant women with MS were interviewed about their decisions to become pregnant and the factors that entered into their decision-making processes. Content analysis was used to identify and describe the fears and concerns of women with MS around the process of making decisions and about how the presence of MS had influenced that process. The unpredictability of MS and the effect that pregnancy might have on MS was a strong theme that emerged from the analysis. Although participants in this study had proceeded to become pregnant despite their fears related to the effect of pregnancy on the course of their MS, they continued to perceive their decision as risky. The diagnosis of MS affected their previous plans for number of children as well as spacing of pregnancies.

Adult↗

PubMed2005

Immunology of multiple sclerosis.

Multiple sclerosis (MS) develops in young adults with a complex predisposing genetic trait and probably requires an inciting environmental insult such as a viral infection to trigger the disease. The activation of CD4+ autoreactive T cells and their differentiation into a Th1 phenotype are a crucial events in the initial steps, and these cells are probably also important players in the long-term evolution of the disease. Damage of the target tissue, the central nervous system, is, however, most likely mediated by other components of the immune system, such as antibodies, complement, CD8+ T cells, and factors produced by innate immune cells. Perturbations in immunomodulatory networks that include Th2 cells, regulatory CD4+ T cells, NK cells, and others may in part be responsible for the relapsing-remitting or chronic progressive nature of the disease. However, an important paradigmatic shift in the study of MS has occurred in the past decade. It is now clear that MS is not just a disease of the immune system, but that factors contributed by the central nervous system are equally important and must be considered in the future.

Autoantibodies↗

PubMedDate not supplied

An overview of assistive technology for persons with multiple sclerosis.

Multiple sclerosis (MS) is a progressive neurologic disease clinically characterized by episodes of focal disorder of the cranial nerves, spinal cord, and the brain. MS affects a significant number of young adults, and they most often face a future of progressive functional losses as more of their central nervous system and cranial nerves are affected. As the disease progresses, they have new impairments with accompanying limitations in activities, restrictions to their participation in life, and compromised quality of life. Assistive technology includes any item that is used to maintain or improve functional capabilities. The rehabilitation healthcare provider has many opportunities to intervene with assistive technologies to decrease activity limitations and participation restrictions. The purpose of this article is to (1) review the impairments and associated activity limitations and participations restrictions experienced by persons with MS, (2) provide an overview of high- and low-tech assistive technologies appropriate for persons with MS, (3) discuss funding opportunities for assistive technologies, (4) review current studies of assistive technology used for persons with MS and discuss future research directions, and (5) consider assistive technology as an intervention for disability prevention.

Activities of Daily Living↗

PubMed1994

[Sevoflurane anesthesia in a patient with multiple sclerosis].

Multiple sclerosis (MS) is a disorder of the nervous system in which myelin breakdown is a prominent feature. We report a 65-yr-old woman scheduled for femoral neck prosthetic replacement under sevoflurane anesthesia, who had been suffering from a progressive type of MS for 27 years. Previously she had a history of exacerbation of symptoms after caudal block done for sciatic neuralgia. Stress such as surgery, anesthesia, emotional distress and variable body temperature can exacerbate the disease. Spinal and epidural block are relatively contraindicated in MS. Thiopental was reported to worsen MS. But there is no evidence that any of the volatile anesthetic agents has a deleterious effect on MS. Sevoflurane can be used to induce anesthesia quickly. To avoid thiopental, we chose slow induction with sevoflurane (GOS). Anesthesia was maintained with GOS. It seems that intraoperative hypotension which resists to ephedrine administration is partly due to autonomic abnormality. Yet, there is no report of sevoflurane anesthesia in MS patient. We consider that in this case sevoflurane is a safe anesthetic because of its less effect on postopreative neurological symptoms than that of epidural block.

Aged↗

PubMed1998

[Promoting remyelination as a future therapeutic principle in multiple sclerosis?].

Multiple sclerosis (MS), the most common neurological autoimmune disorder diagnosed in young adults, is characterised by the repeated occurrence of demyelinating lesions within the central nervous system (CNS). Promotion of remyelination in the brain and spinal cord constitutes a potential strategy for therapeutic intervention in MS and other demyelinating diseases. Three different principles are known to promote remyelination in the CNS of different animal models: Application of growth factors, transplantation of myelin-forming cells and intravenous immunoglobulin (IVIg) therapy. However, the systemic application of growth factors could be limited by effects on unaffected tissue. For successful transplantation we still have the problem of homologous cells not tolerated by a immunological different organism. Currently the required combination of growth factors needed to cultivate human homologous cells is not known, so that cells suitable for transplantation are still not available. Nevertheless, there is increasing evidence for beneficial effects of IVIg therapy on the promotion of remyelination in humans. In this review we summarise recent findings on the regulation of myelin sheath development and oligodendrocyte differentiation, and discuss the presented strategies in the context of possible clinical application for the therapy of MS.

Adult↗

PubMed2005

Applications of diffusion tensor MR imaging in multiple sclerosis.

Multiple sclerosis (MS) is an inflammatory demyelinating disease of the central nervous system that is the most common cause of nontraumatic disability in young adults in the United States. In recent years, magnetic resonance imaging (MRI) has been established as an important paraclinical tool in MS for the assessment of clinical diagnosis, natural history, and treatment effects. In MS studies, there are many advantages to having a sensitive and reliable in vivo method for investigating the specific pathological changes of white matter and its integrity during the disease process. As a consequence, in the past decade, the application of MRI to the study of MS has been explored from conventional MRI to new advanced quantitative techniques with greater pathological specificity and sensitivity. Diffusion tensor imaging (DTI) is one of the most promising techniques with regard to MS. It quantifies the amount of nonrandom water diffusion within tissues and provides unique in vivo information about the pathological processes that affect water diffusion as a result of brain microstructural damage. This review outlines the current state of the art and future direction of DTI and fiber tractography in the study of MS disease.

Body Water↗

PubMed1991

The pineal gland in multiple sclerosis.

Multiple sclerosis (MS) is a chronic demyelinating disease of unknown etiology. Clinical, neurochemical, and neuroradiological data implicate the pineal gland in the pathophysiology of MS. To investigate the relationship of MS to the pineal gland further, we surveyed the prevalence of pineal calcification (PC) on CT scan in a cohort of 29 MS patients (7 men, 22 women, mean age: 40.1 years, SD = 8.9) who were admitted consecutively to a neurological service for acute exacerbation of symptoms. For the purpose of comparison, we also surveyed the prevalence of choroid plexus calcification (CPC) in the sample. Twenty-one age and sex-matched neurological patients served as controls (5 men, 16 women, mean age: 37.0, SD = 9.2). PC was seen in 100% of MS patients, while 72.4% patients (N = 21) had CPC. In the control sample, PC was found in 42.8% (N = 9) and CPC in 28.5% (N = 6). Thus, the strikingly high prevalence of PC in MS provides indirect support for an association between MS and abnormalities of the pineal gland. Moreover, since pineal melatonin is involved in neuroimmunomodulation, we propose, for the first time, that abnormalities of pineal melatonin functions are implicated in the pathophysiology of the disease.

Adult↗

PubMed2000

HLA, molecular mimicry and multiple sclerosis.

Multiple sclerosis (MS) is an inflammatory demyelinating disease of the central nervous system in which an autoimmune response most probably contributes to pathogenesis. To date, the best characterized susceptibility-associated gene has been mapped to the HLA complex. The HLA-DRB1*1501 - DRB5*0101 - DQA1*0102 - DQB1*0602 haplotype is both associated and linked to MS in different ethnic groups. The locus within the HLA class II region encoding the MS-susceptibility gene is under intensive investigation. Epidemiological studies, however, have suggested that environmental antigens also play a critical role in MS pathogenesis. One of the ways a pathogen could trigger autoimmune disease is via immunological cross-reactivity or molecular mimicry. This concept argues that a microbial peptide with certain degree of homology to a self peptide can stimulate pathogenic self-reactive specific T cells to cause an autoimmune disease. Many microbial agents have regions of sequences that may serve as binding motifs for HLA-DR2. HLA genetics and molecular mimicry may therefore be intimately interlinked in the disease process. In the present review, we focus on the HLA association with MS and the role of microbial antigens in MS, with special reference to the molecular mimicry hypothesis.

Animals↗

PubMed1998

Myelin reactive T cells in the autoimmune pathogenesis of multiple sclerosis.

Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system (CNS) leading to demyelination. Although it is widely accepted that demyelination in MS results from an active inflammatory process, the cause of the inflammation is still not completely resolved. Findings in experimental autoimmune encephalomyelitis (EAE), an animal model of MS, and observations in human MS have led to the hypothesis that MS is an autoimmune disease mediated by autoreactive T cells with specificity for myelin antigens. The identity of the brain antigen(s) which is (are) the primary target(s) of the autoimmune process is not known, but current evidence indicates that myelin basic protein (MBP) is a likely candidate. In this paper we will overview some of the experimental evidence suggesting that MBP reactive T cells hold a central position in the pathogenesis of MS, and discuss some of the currently tested therapeutic strategies in MS which are directed towards the pathogenic MBP reactive T cells. Although there appears to be no direct correlation between anti-MBP T cell responses and clinical disease activity, some recent observations suggest that monitoring of anti-MBP T cell responses could be helpful to study immunological efficacy of experimental immunotherapies in MS.

Autoantibodies↗

PubMed2006

Neurogenesis in the adult spinal cord in an experimental model of multiple sclerosis.

Multiple sclerosis is an inflammatory disease of the central nervous system characterized by inflammation, demyelination, axonal degeneration and accumulation of neurological disability. Previously, we demonstrated that stem cells constitute a possible endogenous source for remyelination. We now addressed the question of whether neurogenesis can occur in neuroinflammatory lesions. We demonstrated that, in experimental autoimmune encephalomyelitis, induced in rats 1,1'-dioctadecyl-6,6'-di(4sulphopentyl)-3,3,3',3'tetramethylindocarbocyanin(DiI)-labelled ependymal cells not only proliferated but descendants migrated to the area of neuroinflammation and differentiated into cells expressing the neuronal markers beta-III-tubulin and NeuN. Furthermore, these cells were immunoreactive for bromodeoxyuridine and PCNA, markers for cells undergoing cell proliferation. Using the whole-cell patch-clamp technique on freshly isolated 1, DiI-labelled cells from spinal cord lesions we demonstrated the ability of these cells to fire overshooting action potentials similar to those of immature neurones. We thus provide the first evidence for the initiation of neurogenesis in neuroinflammatory lesions in the adult spinal cord.

Animals↗

PubMed2004

Refining the results of a whole-genome screen based on 4666 microsatellite markers for defining predisposition factors for multiple sclerosis.

Multiple sclerosis (MS) is a demyelinating disease of the central nervous system with a complex genetic background. In order to identify loci associated with the disease, we had performed a genome screen initially using 6000 microsatellite markers in pooled DNA samples of 198 MS patients and 198 controls. Here, we report on the detailed reanalysis of this set of data. Distinctive features of microsatellites genotyped in pooled DNA causing false-positive association or masking existing association were met by improved evaluation and refined correction factors in the statistical analyses. In order to assess potential errors introduced by DNA pooling and genotyping, we resurveyed the experiment in a subset of microsatellite markers using de novo-composed DNA pools. True MS associations of markers were verified via genotyping all individual DNA samples comprised in the pools. Microsatellites share characteristically superb information content but they do not lend themselves to automation in very large scale formats. Especially after DNA pooling many artifacts of individual marker systems require special attention and treatment. Therefore, in the near future comprehensive whole-genome screens may rather be performed by typing single nucleotide polymorphisms on chip-based platforms.

DNA Primers↗

PubMed1998

Increased reactivity to myelin oligodendrocyte glycoprotein peptides and epitope mapping in HLA DR2(15)+ multiple sclerosis.

Multiple sclerosis (MS) is a central nervous system-specific inflammatory and demyelinating disease where a myelin-directed autoimmune response is thought to be pathogenetically relevant. Myelin oligodendrocyte glycoprotein (MOG) is a surface-exposed minor myelin component that is a prime candidate autoantigen. We have investigated peripheral blood lymphocyte responses to synthetic 15-26 amino acids long overlapping MOG peptides in 20 MS patients and 14 healthy controls with the MS-associated HLA haplotype DR2(15). There were significantly increased responses, in terms of numbers of cells secreting IFN-gamma detected by Elispot in response to several MOG-derived peptides in the MS patients, but not the healthy controls. MOG peptide 63-87 evoked the strongest response, and the stimulatory property of this peptide was confirmed in additional DR2(15)+ MS patients where a peptide concentration-dependent proliferative response, which was inhibited by the addition of anti-HLA class II antibodies, was observed. This is the first work detailing putative immunodominant T cell epitopes of MOG in DR2(15)+ MS patients.

Adult↗

PubMed2002

Bayesian approach to searching for susceptibility genes: Gc2 and EsD1 alleles and multiple sclerosis.

Multiple sclerosis (MS) is one of the most common causes of neurological disability in early adulthood. The current literature is interested in identifying biological or DNA markers associated with genetic susceptibility to MS. The aim of this study is to investigate, by means of Bayesian statistical inference, whether the presence of Gc2 (Gc = group-specific component) and/or EsD1 (EsD = esterase D) alleles affects MS susceptibility. Gc and EsD are two classical genetic markers, being the first a serum protein polymorphism, the latter an isoenzyme polymorphism. The interest of the proposed statistical approach of searching for MS susceptibility genes relies on the analysis of two different functions, one function being inferred from our results on 56 unrelated patients from central Italy affected by MS, the other one from Italian and worldwide epidemiological data. The graphical analysis suggests that MS susceptibility is influenced by both Gc2 and EsD1 alleles; and EsD1 allele is more informative than Gc2. These results point out the advantages of the Bayesian approach in searching for susceptibility genes. Furthermore, the significant association between the considered alleles and the susceptibility to MS suggests possible hypotheses about the pathogenesis of the disease.

Bayes Theorem↗

PubMed2006

Retinal ganglion cell loss induced by acute optic neuritis in a relapsing model of multiple sclerosis.

Multiple sclerosis (MS) and its animal model experimental autoimmune encephalomyelitis (EAE) are marked by inflammatory demyelinating lesions throughout the central nervous system, including optic nerve. Neuronal loss also occurs in MS and EAE lesions, but it is not known whether neuronal loss occurs secondary to inflammation, or as a primary process. In the current study, the relationship of inflammation to retinal ganglion cell (RGC) loss during acute optic neuritis is examined. RGCs were labelled with Flourogold, and EAE was induced in SJL/J mice by immunization with proteolipid protein peptide 139-151 (PLP). At various time points, RGCs were counted and optic nerves were examined for inflammatory cell infiltrates. No optic neuritis was detected prior to day 9 following immunization. Incidence of optic neuritis was 30% at day 9 and increased to over 70% by day 11, remaining high through day 18. In contrast, no RGC loss was detected in eyes with optic neuritis until day 14. A 43.1% reduction in RGC numbers at day 14 increased to 50.8% by day 18. No RGC loss occurred in eyes without optic neuritis. The fact that inflammation precedes RGC loss suggests that neuronal loss during optic neuritis occurs secondary to the inflammatory process.

Animals↗

PubMed1994

Clinical scoring methods for multiple sclerosis.

Multiple sclerosis (MS) clinical rating scales are used to classify the degree of neurological dysfunction and to plan treatment measures. In clinical trials, rating scales are used to monitor clinical course and response to experimental therapies. Selection of the appropriate clinical rating scale is determined by the nature of the research question (e.g., disability, impairment, handicap). The Expanded Disability Status Scale (EDSS, an impairment scale) has been the most widely used clinical rating method in natural history studies and clinical trials. The EDSS has the advantage of familiarity, yet is difficult to use consistently between evaluators. In the mid and higher ranges, the EDSS is relatively insensitive to clinical changes that do not impair gait. Evaluator unblinding may invalidate the clinical assessment of response to treatment. Additional work is needed to develop clinical and laboratory (imaging) measures of MS disease activity that will be objective, reliable, sensitive, responsive, and valid. Recent comparative studies have demonstrated that serial magnetic resonance imaging (MRI) studies are 7- to 10-fold more sensitive than clinical methods in detecting subclinical evidence of apparent MS disease activity. Widespread acceptance of MRI as a primary trial outcome measure awaits the results of studies designed to determine whether MRI findings accurately reflect irreversible pathological changes and predict future disability.

Clinical Trials as Topic↗