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Results for “SCLEROSIS, MULTIPLE”

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PubMed2002

Early intervention with immunomodulatory agents in the treatment of multiple sclerosis.

Multiple sclerosis (MS) is a lifelong neurologic disease leading to moderate or severe disability in the majority of affected patients. Studies of the natural history of MS suggest that 90% of patients with relapsing-remitting MS eventually develop secondary progressive (SP) disease. Magnetic resonance imaging (MRI) studies have consistently shown a high frequency of new T2 lesions and new gadolinium enhancing lesions even in the absence of clinical relapse. Lesion burden on T2 MRI increases by 5% to 10% per year and both axonal transection and cerebral atrophy are present at the earliest stages of RR MS. A wealth of evidence suggests that MS is a disease process that is continuously active, and that irreversible damage occurs early in the disease. Despite knowledge of the natural history and the availability of treatments that reduce relapse rates, decrease the accumulation of disability, and decrease surrogate measures of disease activity, only 60% of eligible patients have been treated with immunomodulating agents. This paper reviews the available evidence suggesting that immunomodulatory therapy modifies the natural history of MS and presents an argument for early intervention in the treatment of MS.

Adjuvants, Immunologic↗

PubMedDate not supplied

Concerns about the future among older adults with multiple sclerosis.

Multiple sclerosis (MS) is a chronic, progressive neurological disease that causes demyelination of the central nervous system. Typically diagnosed in adulthood, it does not significantly reduce life expectancy. The goal of this exploratory study was to describe the health-related concerns and service needs of 27 older adults with MS, ages 55 to 81 years. Through in-depth interviews using a phenomenological approach, fear of the future was found to be a predominant concern among the participants. Within this fear, participants expressed particular concerns about experiencing further losses of mobility and independence, becoming a burden on caregivers, and having to move to a nursing home. The findings raise three major challenges for occupational therapists that include: (1) developing or modifying interventions that can enable older adults with MS to gain a sense of control over their future, (2) working with families affected by MS together with other disciplines such as psychology and social work, and (3) advocating for more and better community support options for persons with MS.

Activities of Daily Living↗

PubMed1997

Quantitation of lower physical activity in persons with multiple sclerosis.

Multiple sclerosis (MS) is a demyelinating disease of the central nervous system that often affects the motor system. We tested the hypothesis that physical activity was lower in a group of 17 MS patients (mean +/- SD; age = 46 +/- 6 yr, 11 females, 6 males) compared with 15 healthy sedentary control subjects (age = 44 +/- 7 yr, 9 females, 6 males). Physical activity was measured with a three-dimensional accelerometer and with an activity questionnaire for 7 d. Vector magnitude values from the accelerometer for the MS and sedentary control subjects were 121,027 +/- 59,336 and 185,892 +/- 60,566 arbitrary units/day, respectively (P = 0.01). Estimated energy expenditure values derived from the questionnaire were 35.9 +/- 3.0 and 36.2 +/- 4.1 Kcal.kg-1.d-1 (NS), respectively. Thus, when measured directly with an accelerometer, activity was lower in MS compared with sedentary control subjects. The data also suggest that the accelerometer was more sensitive than the questionnaire for detecting differences in activity between two relatively sedentary populations, including one with neurologic disease.

Activities of Daily Living↗

PubMed2002

[Brain atrophy and cognitive disorder in multiple sclerosis].

Multiple sclerosis (MS) is an autoimmune disease of the central nervous system causing severe disability via the progressive damage of white matter. Beyond physical signs cognitive dysfunction might be present as well. The aim of this study was to investigate the frequency and characteristics of brain atrophy and cognitive alterations. Significant cortical and subcortical atrophy was found on brain MRI of 30 MS patients included in this study comparing to healthy controls. Abnormal findings were detected in more than 60% of patients using a cognitive test battery. Generally, verbal abstraction, visuospatial orientation, attention, short-term memory was impaired and the psychomotor speed was decreased, even in the early stage of the disease. Depression-related complaints were found in 57% of this population. The Kurtzke scale, the atrophy of corpus callosum and widening of 3rd ventricle and Sylvian fissures were related to impaired cognitive performances. The authors would like to call attention to the early cognitive deficit and the need of treatment in MS.

Adult↗

PubMed2007

Multiple sclerosis.

Multiple sclerosis (MS) is a demyelinating disease of the central nervous system that commonly leads to inflammatory and atrophic brain pathology, often causing cognitive impairment. MS-associated cognitive impairment was first described over a century ago. However, with the advent of standardized neuropsychological testing and quantitative brain imaging, the frequency, quality, and correlates of cognitive impairment are better understood. Dementia is rare in MS, although it is known to occur in 10 to 25% of patients. Our data suggest a frequency of 22% among clinic attendees. In addition to the cognitive impairments evident in MS dementia, changes in personality and social behavior also occur. For example, some patients develop euphoria sclerotica and marked deficiency in social empathy, conditions that in combination with executive dysfunction cause considerable hardship for patients and caregivers. These neuropsychiatric manifestations of MS dementia are correlated with magnetic resonance imaging indicators of brain atrophy, including ventricle enlargement, neocortical volume, and normalized whole brain volume. Recent developments in pharmacological treatment for disease progression and management of cognitive symptoms hold promise for patients suffering from the degenerative aspects of MS.

Atrophy↗

PubMed2001

Differential diagnosis in multiple sclerosis.

Multiple sclerosis can usually be diagnosed from a patient's history, clinical examination, cerebrospinal fluid (CSF) analysis, and observations from magnetic resonance imaging (MRI). However, sometimes, the classic clinical criteria, even when supported by MRI findings or by abnormalities of the CSF, may not be sufficiently specific. Many conditions can produce a multifocal central nervous system syndrome with a relapsing-remitting course in young adults. The rate of misdiagnosis is around 5%, indicating that 1 in 20 patients thought to have MS have instead a condition resembling MS. The need to reach diagnostic certainty is particularly important given the availability of treatments which may potentially prevent the progression of the disease. Therefore, the search for new methodological approaches which increase the sensitivity and specificity of the diagnosis is warranted. While waiting for the development of new techniques to facilitate an early and correct diagnosis, a correct approach to a suspect MS patient has to be underlined in order to reduce the risk of a misdiagnosis. In this paper, I illustrate the diagnostic work-up that the practicing physician should follow when first confronted by a patient suspected of having MS.

Diagnosis, Differential↗

PubMed2005

Antioxidants and polyunsaturated fatty acids in multiple sclerosis.

Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system (CNS). Oligodendrocyte damage and subsequent axonal demyelination is a hallmark of this disease. Different pathomechanisms, for example, immune-mediated inflammation, oxidative stress and excitotoxicity, are involved in the immunopathology of MS. The risk of developing MS is associated with increased dietary intake of saturated fatty acids. Polyunsaturated fatty acid (PUFA) and antioxidant deficiencies along with decreased cellular antioxidant defence mechanisms have been observed in MS patients. Furthermore, antioxidant and PUFA treatment in experimental allergic encephalomyelitis, an animal model of MS, decreased the clinical signs of disease. Low-molecular-weight antioxidants may support cellular antioxidant defences in various ways, including radical scavenging, interfering with gene transcription, protein expression, enzyme activity and by metal chelation. PUFAs may not only exert immunosuppressive actions through their incorporation in immune cells but also may affect cell function within the CNS. Both dietary antioxidants and PUFAs have the potential to diminish disease symptoms by targeting specific pathomechanisms and supporting recovery in MS.

Animals↗

PubMedDate not supplied

[Rationale for an early treatment of multiple sclerosis].

Multiple sclerosis (MS) is a demyelinating disease of the central nervous system (CNS) of unknown etiology. Its pathological hallmark is the presence within the CNS of inflammatory infiltrates containing few autoreactive T cells and a multitude of pathogenic nonspecific lymphocytes. Based on that, various non-specific immunosuppressive agents have been tested with marginal benefits on the natural evolution of the disease and frequent short- and long-term adverse effects. Moreover, due to their unfavourable profile, these therapies have been usually limited to patients with progressive courses or high clinical activity. The recent approval of IFN beta and Copolymer 1, as therapies able to modify the disease course in relapsing-remitting and secondary progressive, as well as the available immunopathological and clinical data suggesting that the early treatment of MS with safe profile immunomodulatory drugs could be advantageous compared to late treatments, supports the 'putative' relevance of these new drugs in the early treatment of MS patients. However we must wait for the results of ongoing clinical trials to define if such an early treatment has substantial advantages compared to late treatment.

Adjuvants, Immunologic↗

PubMed1997

Therapeutic effects of alternating current pulsed electromagnetic fields in multiple sclerosis.

Multiple sclerosis is the third most common cause of severe disability in patients between the ages of 15 and 50 years. The cause of the disease and its pathogenesis remain unknown. The last 20 years have seen only meager advances in the development of effective treatments for the disease. No specific treatment modality can cure the disease or alter its long-term course and eventual outcome. Moreover, there are no agents or treatments that will restore premorbid neuronal function. A host of biological phenomena associated with the disease involving interactions among genetic, environmental, immunologic, and hormonal factors, cannot be explained on the basis of demyelination alone and therefore require refocusing attention on alternative explanations, one of which implicates the pineal gland as pivotal. The pineal gland functions as a magnetoreceptor organ. This biological property of the gland provided the impetus for the development of a novel and highly effective therapeutic modality, which involves transcranial applications of alternating current (AC) pulsed electromagnetic fields in the picotesla flux density. This review summarizes recent clinical work on the effects of transcranially applied pulsed electromagnetic fields for the symptomatic treatment of the disease.

Adult↗

PubMed1994

Natural history of multiple sclerosis.

Multiple sclerosis (MS) is the most common idiopathic inflammatory disease of the central nervous system. The distinction between MS and other benign or fulminant inflammatory demyelinating disorders is based on quantitative, rather than qualitative, differences in chronicity and severity. Primary progressive MS may differ from relapsing-remitting MS in MRI lesion frequency, immunogenetic profile, responsiveness to immunosuppressive treatment, and histology. In 60% of patients, MS begins as a relapsing-remitting disease and evolves secondarily into a progressive neurological illness. Life expectancy is not substantially altered in patients with MS, particularly in the early years of the illness. The rate of suicide has been reported to be increased sevenfold in MS patients. Up to 40% of patients with attacks severe enough to render them nonambulatory may not recover. At 15 years from MS onset, 50% of patients are disabled to the point at which they at least require a cane to walk a half block. Early age at onset, female sex, relapsing-remitting course at onset, and perhaps optic neuritis or sensory symptoms at onset and relatively few attacks in the first two years are associated with a favorable course.

Adult↗

PubMed2006

Abnormal hormonal control of gut hydrolytic enzymes causes autoimmune attack on the CNS by production of immune-mimic and adjuvant molecules: A comprehensive explanation for the induction of multiple sclerosis.

Multiple sclerosis (MS) is generally thought to be caused by an autoimmune attack on central nervous system (CNS) myelin. A microorganism containing a mimic of an immunogenic region of a myelin protein initiates the autoimmune process. However, no specific "MS" microorganism has been found. Recently a large number of normal human gut bacteria were found to possess different encephalitogenic mimics. A hypothesis is presented that the autoimmune process is started by abnormal proteolytic digestion of these bacteria. Sufficient quantities of the mimics are produced to be recognized by the immune system. Since proteolytic processes in the gut are strictly controlled, it is proposed that the MS process is triggered by abnormal hormonal control of gut proteolytic enzymes. It has previously been suggested that the recognition of CNS myelin antigens by activated MS immune cells is facilitated by proteolytic processing of myelin proteins. The CNS proteases are also under rigid control and these control processes are the same as is in the gut. Therefore, MS clinical activity is the result of improper hydrolytic degradation in the brain-gut axis caused by an abnormal hormonal variation.

Autoimmune Diseases↗

PubMed2000

IgG allotypes and subclasses in Norwegian patients with multiple sclerosis.

Multiple sclerosis (MS) is a multifactorial disease in which genetic and environmental factors apparently have a major influence on the susceptibility and course of the disease. In the present study we have investigated the genetic basis and subclass levels of IgG in MS. Hundred and thirty-six Norwegian patients with MS and 92 controls were genotyped for IgG allotypes of the GM and KM systems. IgG and IgG subclasses were quantified in sera from 115 MS patients and 20 controls. Neither GM nor KM allo-, haplo- or genotypes were significantly correlated with susceptibility, severity or course of the disease. The G1M (3) (3), G2M (23) (23) and G3M (5) (5) allotypes were significantly correlated with high serum levels of IgG3, whereas high IgG2 levels were correlated with G1M (3) (3) and G2M (23) (23) in both patients and controls. Serum levels of IgG subclasses were not significantly correlated with course or severity of the disease. The results indicate no major role for IgG allotypes or IgG subclass levels in the pathogenesis of MS.

Female↗

PubMed2004

[Determination of autoantibody for myelin antigens in the serum of patients HLA-DQB1*0602 with multiple sclerosis].

Multiple sclerosis (MS) is a chronic inflammatory demyelinating disease of the human central nervous system (CNS) mediated by autoimmune Th1 lymphocytes. We determined the serum levels of autoantibodies for myelin basic protein (MBP), proteolipid (PLP) and myelin oligodendrocyte glycoprotein sequence MOG 92-106 in a group of 54 healthy individuals and 26 MS patients expressing or not HLA-DQB1*0602. Regardless expression of the susceptibility allele DQB1*0602, MS patients presented marked (p<0.0001) IgG antibody production for MBP and MOG92-106. Yet, significant (p<0.0001) IgA antibody levels were mainly observed for PLP and MOG antigens. Our results suggest that other HLA class II alleles may be conferring susceptibility to MS in this population and influencing the pattern of immune recognition of encephalitogen antigens. Furthermore, distinct IgG and/or IgA autoantibody production may be contributing to the control or maintenance of the CNS inflammatory reaction.

Adolescent↗

PubMed2005

Multiple sclerosis.

Multiple sclerosis (MS) is a complex genetic disease associated with inflammation in the central nervous system (CNS) white matter and is thought to be mediated by autoimmune processes. Clonal expansion of B cells, their antibody products, and T cells, hallmarks of inflammation in the CNS, are found in MS. The association of the disease with major histocompatibility complex genes, the inflammatory white matter infiltrates, similarities with animal models, and the observation that MS can be treated with immunomodulatory and immunosuppressive therapies support the hypothesis that autoimmunity plays a major role in the disease pathology. This review discusses the immunopathology of MS with particular focus given to regulatory T cells and the role of B cells and antibodies, immunomodulatory therapeutics, and finally new directions in MS research, particularly new methods to define the molecular pathology of human disease with high-throughput examination of germline DNA haplotypes, RNA expression, and protein structures that will allow the generation of a new series of hypotheses that can be tested to develop better understandings and therapies for this disease.

Animals↗

PubMed1996

Newer versus older treatments for relapsing-remitting multiple sclerosis.

Multiple sclerosis (MS) is a chronic disease with an unpredictable clinical course and several distinct clinical patterns. Recent developments in immunology, molecular biology and genetics have improved our understanding of the pathophysiology of MS. Further, advances in trial methodology, including the availability of magnetic resonance imaging (MRI) as a surrogate outcome measure, have led to the identification of several new therapeutic options for relapsing-remitting (RR) MS. These therapies include corticosteroids, recombinant interferon-beta-1b (rIFN beta-1b), recombinant interferon-beta-1a (rIFN beta-1a) and copolymer-1 (Cop-1). Corticosteroids have been shown to accelerate the recovery from acute exacerbations, but there are still conflicting data on their effect on outcome and long term course. rIFN beta-1b, rIFN beta-1a and Cop-1 all effectively alter the natural history of RR-MS. These 3 agents all decrease the relapse rate by approximately one-third, but differ in their adverse effect profiles and administration regimens. Further trials are required to define the optimal treatment of RR-MS.

Adjuvants, Immunologic↗

PubMed1987

In vivo labeling of blood T cells: rapid traffic into cerebrospinal fluid in multiple sclerosis.

Multiple sclerosis (MS) is an inflammatory disease of the central nervous system (CNS). In MS patients being treated with anti-T11, a murine monoclonal antibody which recognizes the sheep red blood cell receptor, it was found that peripheral blood T cells were labeled in vivo by the antibody. Furthermore, anti-T11 did not lyse cells or enter the cerebrospinal fluid (CSF). In CSF specimens obtained by serial lumbar punctures from patients with progressive MS who received five daily infusions of anti-T11, 70 +/- 12% of the T cells had mouse antibody bound to their surface by 72 to 96 hours. No in vivo staining of CSF T cells was observed in patients infused with anti-T4, a murine monoclonal antibody that was not found to label T cells in vivo. These results demonstrate that there is rapid movement of lymphocytes from the peripheral blood to the CNS in patients with progressive MS. This rapid trafficking of T cells suggests that the ongoing pathological process within the CNS may be closely linked to the peripheral immune system and may have implications for the monitoring and treatment of MS.

Antibodies, Monoclonal↗

PubMed1998

Urinary tract infections may trigger relapse in multiple sclerosis.

Multiple Sclerosis (MS), a demyelinating disease of the central nervous system, is the most common neurological disease affecting young adults in North America and, in the majority of cases, is associated with accumulating disability. Urinary tract dysfunction affects up to 90% of the MS population, and urinary tract infections are encountered in up to 74% of the tested population. Viral infections have previously been shown to trigger acute exacerbation and it is our experience that urinary tract infection also commonly precedes relapse, and, when recurrent, is associated with neurologic progression. We present three case studies from our MS Clinic where recurrent UTI was associated with acute exacerbation and neurologic progression refractory to intravenous steroid treatment. Interferons, protein signaling molecules, have recently been found to play a role in acute exacerbation and disease progression in individuals with MS. Viral infections induce interferon release which may activate T cells to produce gamma-interferon. Interferon-gamma precipitates relapse and stimulates production of tumour necrosis factor-alpha, a cytokine directly toxic to oligodendrocytes. Bacterial infections similarly induce interferon release and may activate immune pathways that result in MS exacerbation and neurologic progression.

Acute Disease↗

PubMed2000

Immunological markers in multiple sclerosis.

Multiple sclerosis (MS) is characterized by the presence in the central nervous system (CNS) of perivascular inflammatory infiltrates containing, among others, autoreactive T cells and activated macrophages. These observations indicate that MS is a T cell-mediated CNS-confined chronic inflammatory demyelinating disease in which the ultimate effector cell is the activated macrophage. The inflammatory process, leading to patchy demyelination and axonal loss, is mainly sustained by pro-inflammatory cytokines that, along with chemokines, adhesion molecules and metalloproteases, modulate at different levels the pathogenic process underlying MS. Due to their central role in MS pathogenesis, "inflammatory" molecules might represent suitable peripheral markers of disease (disease-trait) and/or disease activity (state-trait). However, reliable disease-trait or state-trait immunological markers for MS have not yet been identified. The intrinsic characteristics of these molecules (i.e. autocrine/paracrine activity, short half-life, redundancy) may in part explain their inconsistency as disease markers. Additionally, the unreliability of methodologies and the lack of careful patient stratification can also, at least in part, account for the unsatisfactory results so far obtained.

Biomarkers↗