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Results for “SCLEROSIS, MULTIPLE”

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PubMed2003

Disease-modifying Therapies for Multiple Sclerosis.

Multiple sclerosis (MS) is likely an autoimmune disorder, although this remains unproven. Immunotherapeutic treatments have been shown to be helpful, especially in relapsing forms of the illness, but the treatments are incomplete, and many patients continue to worsen over time, even with standard therapy. Immunotherapies presently available appear to have their greatest effect when used early in the course of the illness. In relapsing-remitting multiple sclerosis (RRMS), there is overwhelming Class I data from large clinical trials that supports the use of interferon-beta-1a (IFNbeta-1a), interferon-beta-1b (IFNbeta-1b), and glatiramer acetate. Comparative data are limited, and results published in different trials support the idea that treatment outcomes with the various drugs are more similar than different. Decisions about treatment choice should be tailored to the needs of the individual patient. With the exception of a small number of patients with benign MS, all RRMS patients should be treated with one of the interferons or glatiramer acetate. There are Class I data consistent with the idea that higher dose or more frequent administration of interferon-beta (IFNbeta) is associated with better clinical outcome and reduced progression of changes on brain MRI scans. The duration of this effect is not clear, and higher dose with more frequent administration is associated with higher cost, more side effects, and greater production of interferon antibodies. Interferon antibodies possibly reduce efficacy of IFNbeta in RRMS and secondary progressive multiple sclerosis (SPMS). Clinically isolated syndromes (CIS) of demyelination in the central nervous system can be reliably diagnosed, and the risk of further episodes of demyelination is consistent with the diagnosis of RRMS stratified by use of brain MRI scans. Patients at high risk of developing RRMS after CIS achieve significant benefit after treatment with IFNbeta-1a, and initiation of therapy after CIS should be given strong consideration. There are no similar data for IFNbeta-1b or glatiramer acetate, but logic would dictate a similar response with these agents. In SPMS, there are Class I data that treatment with IFNbeta-1a or IFNbeta-1b has a significant effect on progression of brain MRI lesions, but clinical outcomes are less clearly affected. It is justifiable to treat SPMS patients with IFNbeta. Mitoxantrone may be effective in slowing progression of SPMS, and its risks are moderate. It should be used in patients with SPMS, but potential long-term risks must be discussed with the patient in detail. Results of treatment of SPMS in advanced cases (Extended Disability Status Score greater than 6.5, or restricted to wheelchair) is mostly unknown. These patients are at high risk of developing infections, especially if they use indwelling catheters, and the use of agents that induce immunosuppression may be risky. There are no effective therapies for primary progressive multiple sclerosis (PPMS). Although PPMS patients are frequently treated with one or more therapeutic agents, there is no medical justification for this now.

Journal Article↗

PubMed1999

Sensory-motor and genito-sphincter dysfunctions in multiple sclerosis.

Multiple sclerosis is a chronic demyeliniting disease of the central nervous system which is characterized by an extreme multiplicity of clinical features. Multiple sclerosis can have a profound impact on the quality of life of patients. The induced handicap varies from one patient to an other, and depends on the location of the demyeliniting lesions. Among the symptoms, sensory-motor disorders and genito-sphincter dysfunctions are some of the more disabling. Thus, up to 70% of patients suffer from urinary troubles, and 15 years after the onset of the illness, 50% of patients have difficulties for deambulation. A good knowledge of these pathologies is necessary to improve the management of patients suffering from multiple sclerosis.

Female Urogenital Diseases↗

PubMed1985

Immunosuppressive treatment of multiple sclerosis.

Multiple sclerosis is one of the most common causes of chronic neurologic disease in adults. Although the exact pathogenesis of multiple sclerosis is unknown, evidence suggests that it is an autoimmune disease. Recent studies have shown a possible significant beneficial effect of cyclophosphamide in the treatment of multiple sclerosis. This article will discuss the rationale of immunosuppressive therapy and identify nursing measures required in such a clinical trial.

Adrenocorticotropic Hormone↗

PubMed1996

Neuro-ophthalmology of multiple sclerosis.

Multiple sclerosis remains a pathophysiologic enigma. The epidemiology has recently been reexamined and appears to lend credence to a greater genetic basis than previously believed. Neuro-ophthalmologic signs and symptoms in multiple sclerosis are extremely common and often present to the eye care practitioner. Although diagnostic methodology is progressing, treatment of multiple sclerosis is currently undergoing a revolution.

Animals↗

PubMed2000

The overactive bladder in multiple sclerosis.

Multiple sclerosis is a common neurologic disorder that often affects the genitourinary system. One of the most common symptoms of multiple sclerosis is the hyperactive bladder. These patients will have symptoms that may affect their lifestyle, such as urinary incontinence, urgency, and frequency. They may also suffer from debilitating urinary tract symptoms, such as frequent or recurrent urinary tract infections and also on occasion, damage to the upper urinary tract. Fortunately, the neurogenic bladder dysfunction associated with multiple sclerosis can be treated with a reasonable chance of success. With proper treatment, related symptoms may be brought under control, allowing the physician to concentrate on the more debilitating aspects of this disease.

Humans↗

PubMed2003

Validity and reliability of the MSQLI in cognitively impaired patients with multiple sclerosis.

Multiple sclerosis (MS) has important effects on quality of life but it is unknown how cognitive impairment affects the ability to assess or report this. Our objective was to determine whether cognitive impairment negatively affects the construct validity and the reliability of the Multiple Sclerosis Quality of Life Inventory (MSQLI). A neuropsychological test battery and the Multiple Sclerosis Functional Composite (MSFC) were administered to a sample of 136 patients referred for cognitive testing by their neurologists. Age, sex, education and ethnicity-adjusted T scores were calculated for each cognitive variable. Cognitive impairment was defined as any T score less than the fifth percentile. The MSQLI was administered prior to neuropsychological testing and readministered one to four weeks later: Correlations between the MSFC and the SF-36 were determined and compared between the cognitively impaired and unimpaired groups as the main test of construct validity. Test-retest and internal consistency reliability of each of the scales were compared for the impaired and unimpaired groups. Seventy-six (56%) patients were cognitively impaired. Construct validity and internal consistency reliability did not differ between the cognitively impaired and unimpaired groups. Test retest reliability was lower for the bladder and vision scales in the impaired group, but remained acceptable for the bladder scale (r > 0.7). Cognitive impairment, a common MS manifestation, does not appear to reduce the reliability or validity of the MSQLI as a patient self-report measure of health status and quality of life.

Adult↗

PubMedDate not supplied

MSRV pol sequence copy number as a potential marker of multiple sclerosis.

Multiple sclerosis (MS) is a neurological disease in which demyelination in the brain and spinal cord is observed. The causal influence of bacterial/viral infections and genetic/immune factors in the etiology of multiple sclerosis is suggested. Multiple sclerosis-related retrovirus (MSRV) is one of the potential agents, which can lead to development of the disease. The aim of cytogenetic studies was assessment of MSRV pol sequence copy number in patients with MS compared to normal individuals. Cytogenetic slides with interphase nuclei and extended chromatin fibers were prepared from peripheral blood of 16 patients with MS and 10 healthy individuals. Fluorescence in situ hybridization (FISH) with biotinylated product of polymerase chain reaction was used in order to analyze MSRV pol sequence copy number in the examined material. Detection of MSRV pol probe was carried out by immunological reaction with avidin-fluorescein and biotinylated anti-avidin. MSRV pol sequence copy number was significantly greater in MS patients than in normal individuals. Using FISH technique to extended chromatin fibers, it was observed that MSRV pol exists as tandem repeats on various chromosomes. The increased number of MSRV pol sequence has been found on chromatin fibers of MS patients as compared to healthy controls.

Adult↗

PubMed2003

[Multiple stimulation of T lymphocytes in the pathogenesis of multiple sclerosis].

Multiple Sclerosis is a T-cell mediated autoimmune disease leading to demyelination of central nervous system. The precise mechanism by which auto-reactive T cells are activated and tolerance to self-antigens is broken are not fully understood. The dysregulation of costimulatory signals between T cell and antigen presenting cell is taken into consideration in this process. Among many costimulatory molecules presented on activated T cells CD40L and CD28 are of special interest. These molecules are involved in the positive regulation of T cell activation. Contrary to them CTLA-4, the another costimulatory molecule presented on activated T cells down-regulates activation. In this review the role of modification of costimulatory signals on the development and course of EAE, the animal model for multiple sclerosis as well as clinical data documenting the dysregulation of costimulation in Multiple Sclerosis are presented.

Antigens, CD↗

PubMed1995

Relationship between lower urinary tract abnormalities and disease-related parameters in multiple sclerosis.

Multiple sclerosis affects the lower urinary tract in many patients. The relationship between lower urinary tract abnormalities and disease-related parameters of multiple sclerosis is not well described. We screened urologically and neurologically 212 patients according to a standard protocol. Micturition complaints were noted in 52% of the patients and urodynamic abnormalities were found in 64%. A statistical correlation was found between detrusor hyperactivity and detrusor hypoactivity with disease-related parameters, that is disease duration, disability status, myelin basic protein concentration in the cerebrospinal fluid and neurophysiological investigations. No relationship was found between detrusor hypersensibility or detrusor hyposensibility and the aforementioned disease-related parameters. In 1 patient upper urinary tract abnormalities were noted in combination with urodynamic abnormalities. We conclude that lower urinary tract abnormalities can be found in every patient with multiple sclerosis unrelated to the state of the disease. Severe upper urinary tract abnormalities are rare.

Adolescent↗

PubMed2004

[Involvement of the peripheral nervous system in multiple sclerosis].

Multiple sclerosis is a demyelinating disease limited to the central nervous system, but the literature has provided recurring evidence which raises the question of associated peripheral nervous system abnormalities. The prevalence of peripheral neuropathy during multiple sclerosis remains controversial without prospective study. Nevertheless, some data have reported well documented case reports describing the co-occurrence of multiple sclerosis and radiculopathy or mononeuropathy or polyneuropathy in the same patients. By contrast, more frequent subtle nerve abnormalities may be found by using electrophysiological and neuropathological examinations. Some hypotheses have been proposed by Waxman to decipher the electrophysiological and neuropathological findings. The mechanisms for demyelinating disease and peripheral nerve pathophysiology may imply the antigenic properties or the presence of diffusing factors between peripheral nervous system and central nervous system myelin and the molecular plasticity of myelinated fibers.

Antigens↗

PubMed2004

[Sodium channels and multiple sclerosis].

Multiple Sclerosis is a chronic demyelinating disease of the central nervous system of undetermined etiology. Damage of myelinated fibers leads to block of conduction of impulses. In myelinated axons sodium channels are expressed at high density and they play a very important role in the conduction of nervous impulse. In myelinated fibers affected by Multiple Sclerosis substantial variations of sodium channels pattern occurs. These variations can help to explain pathophysiological and clinical aspects of Multiple Sclerosis and open a new way to approach and, probably, treat this disease.

Humans↗

PubMed1996

Genetic epidemiology of multiple sclerosis.

Multiple sclerosis appears to be a complex trait determined by genes and environmental factors. This hypothesis is increasingly supported by genetic epidemiological studies of large populations. Well ascertained studies of adoptees and half siblings indicate that familial aggregation is genetic. These results have important implications for the nature of environmental factors influencing susceptibility to multiple sclerosis. These appear to act at a population level and probably exert an influence on risk that matches or exceeds that from any single genetic locus. The identification of susceptibility genes in multiple sclerosis will be difficult.

Canada↗

PubMedDate not supplied

Hyperreactivity to myelin basic protein in multiple sclerosis.

Multiple sclerosis patients, control patients with other neurological diseases, and normal volunteers were assayed in a short-term 51chromium release assay for cell-mediated cytotoxicity against lymphocyte targets coated with myelin basic protein. Multiple sclerosis patients, compared to the other two groups, were hyperreactive to myelin basic protein, both before and after in vitro boost with additional myelin basic protein. The boost served to augment the difference between multiple sclerosis patients and controls.

Cytotoxicity, Immunologic↗

PubMed2002

The diagnosis of multiple sclerosis.

Multiple sclerosis is a clinical diagnosis and as such requires the integration of historical information with neurological examination and relevant laboratory and paraclinical tools, such as magnetic resonance imaging. A recent revision of the diagnostic guidelines for multiple sclerosis has been published that formalizes the use of magnetic resonance imaging information along with the clinical picture. These new guidelines should provide for the earlier and easier diagnosis of multiple sclerosis, useful for both clinical trials and neurological practice.

Central Nervous System↗

PubMed1999

[Evolution and surveillance of multiple sclerosis].

Multiple sclerosis is a highly complex disease due to the great diversity of symptoms and signs from disseminated demyelinating CNS lesions which lead to different levels of handicap, and to the different types of evolution (exacerbations or slow progression). Most of the patients with multiple sclerosis have a normal longevity. The main concern is the accumulation of disabilities. In order to follow accurately the progression of these disabilities, specific scales, especially EDSS, have been validated allowing more uniformity in method of collecting data from multiple sclerosis.

Central Nervous System↗

PubMed1989

MHC-restricted autoantigen-reactive T cell clones in multiple sclerosis.

Multiple sclerosis is a demyelinating disease of the central nervous system with genetic, viral and autoimmune characteristics. Myelin basic protein (MBP) is a suspected target autoantigen since it induces experimental autoimmune encephalomyelitis, an animal model closely resembling multiple sclerosis. The disease is mediated by Class II restricted, MBP-reactive T cells possessing the T helper/inducer phenotype. In the present study, we have isolated MBP-reactive T cell clones from the peripheral blood of a chronic progressive multiple sclerosis patient. The clones displayed blastogenic memory responses when rechallenged with the autoantigen and irradiated autologous lymphocytes. MBP recognition by the autoantigen-reactive T lymphocytes was restricted by major histocompatibility complex Class II antigens. Both CD4+8- and CD4-8+ MBP-reactive T cell clones were obtained.

Antigens, Differentiation, T-Lymphocyte↗

PubMed1997

Phosphodiesterase type IV inhibitors in the treatment of multiple sclerosis.

Multiple sclerosis is an autoimmune disease with inflammatory lesions localized to the white matter of the central nervous system. Early on, the disease is characterized by episodes of exacerbations and remissions. During exacerbations there is an acute inflammatory infiltrate characterized by the presence of mononuclear cells, monocytes, and T lymphocytes. These cells produce proinflammatory cytokines that have been implicated in the amplification of the inflammatory response as well as in the damage of oligodendrocytes. The inflammation ultimately results in loss of myelin and oligodendrocyte cell death (demyelination). Thus therapies aimed at preventing the inflammatory response may have a beneficial effect on the course of the disease. One such therapy is treatment with inhibitors of phosphodiesterase type IV. These drugs have proven to be extremely effective in the prevention and treatment of experimental allergic encephalomyelitis, the animal model for multiple sclerosis. These experiments, as well as other data discussed here, provide a rationale for the treatment of multiple sclerosis with inhibitors of phosphodiesterase type IV.

Animals↗

PubMed2002

An expert system for the evaluation of EDSS in multiple sclerosis.

Multiple sclerosis is a disease of unknown aetiology. Despite several advances in therapy in recent years, some problems such as the prognostic criteria are imperfectly understood. Several experimental trials of therapy in multiple sclerosis are in course in order to discover a successful treatment. Most of these research studies use a clinical rating scale named Expanded Disability Status Scale (EDSS) as an evaluation tool for the effects of drugs. This scale is defined by a set of rules written in English which provide a numerical quantification of the neurological examination. Although EDSS has been widely used for almost 20 years, its application still depends on the interpretation of the neurologist who performs the neurological examination, and many applications of the scale performed by different neurologist on the same patient can give different results. This is a serious problem for international trials because they lack of a reliable measure of the effects of drugs. Here, we present an expert system for the automatic evaluation of EDSS in multiple sclerosis, which has been developed to overcome this problem. The expert system exploits an explicit representation of EDSS rules, it is able to explain its conclusions and it provides a revision tool to support the user if no satisfying solution can be reached. Using this expert system, clinical trials based on EDSS can benefit of a more reliable evaluation tool providing more valuable results.

Disability Evaluation↗