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PubMed1997

Primary progressive multiple sclerosis.

Patients with multiple sclerosis who develop progressive disability from onset without relapses or remissions pose difficulties in diagnosis, monitoring of disease activity and treatment. There is a need to define the diagnostic criteria for this group more precisely and, in particular, to describe a comprehensive battery of investigations to exclude other conditions. The mechanisms underlying the development of disability and the role of MRI in monitoring disease activity in this clinical subgroup require elucidation, particularly in view of the lack of change on conventional imaging in the presence of continuing clinical deterioration. The prognosis is poor and there are currently no treatment trials for this form of the disease.

Disease Progression↗
PubMed1980

Problems in evaluating new treatments for multiple sclerosis.

There are multiple difficulties in evaluating new treatments for multiple sclerosis (MS). The clinical diagnosis is imprecise, and the correlation between lesion and clinical dysfunction is incomplete. The neurologic evaluation is complex and lacks full precision. The course of MS is complex and has limited predictability. There is no laboratory test that can be accepted now as compensating for the defects in diagnosis, lesion-symptom correlation, course, and neurologic evaluation. Because of these problems, which appear inherent in MS, there are limitations to the statistical methods that can be properly applied to trials of therapy. Most trials of definitive nature will require a random design. When improvement is seen in a trial of therapy, there may be difficulty in determining the mechanism.

Adrenocorticotropic Hormone↗
PubMed2004

Multiple sclerosis in children.

Multiple sclerosis can develop during childhood, even among children under 10 years of age, and the initial diagnosis can be difficult. A first demyelinating event in children may be an episode of monophasic acute disseminated encephalomyelitis or a first episode of a macrophage activation syndrome, angiitis affecting the central nervous system or MS. The risk of developing MS is lower if: the child is younger than 10 years old; onset is associated with severely altered consciousness; presentation is polysymptomatic; or there are large and poorly limited lesions of the white matter. MS in children probably has a slightly better outcome than MS in adults. Initial treatment mainly relies on methylprednisolone, and there is little information on the results of beta interferon treatment in children with MS.

Age Factors↗
PubMed2003

The diagnosis of primary progressive multiple sclerosis.

Primary progressive multiple sclerosis (PPMS) is a rather unique form of the more common relapsing inflammatory demyelinative disease. The absence of attacks that typify relapsing forms of MS imposes special challenges for diagnosis, but also provides an opportunity to study the pathogenesis of the more progressive aspects of the disease process in isolation of confounding transient clinical events. In this review, recent advances in diagnostic approaches are considered in relationship to baseline data from a large multinational study designed to better characterize and treat this clinical phenotype. PPMS subjects with cerebral spinal fluid (CSF) findings consistent with intrathecal immunoglobulin production may have a more tissue destructive disease process than those whose CSF lacks evidence of a B-cell immunopathogenic disease component.

Cerebrospinal Fluid Proteins↗
PubMed2006

Toward biomarkers in multiple sclerosis: new advances.

Multiple sclerosis is an autoimmune disease that commonly affects young adults. If initially characterized by acute relapses, it is later followed by only incomplete remission. Over years, progressive disability and irreversible deficit lead to chronic neurological deficits in the majority of patients. The clinical course is protracted and unpredictable, and no biological marker is useful in predicting the evolution of autoaggression and disability. It is difficult to diagnose and to monitor disease progression after the initial symptoms or even during the major clinical manifestations, and it is difficult to treat. In this review, the authors report recent advances in the field, focusing on the search of new antigens as a marker of the disease, in their relevance to the pathophysiology and diagnosis of the disease.

Biomarkers↗
PubMed2001

Immunogenetic heterogeneity of multiple sclerosis in Sardinia.

Multiple sclerosis (MS) predisposition is thought to be influenced by a complex, yet unclear interaction of genetic and environmental factors. Studying ethnically selected populations may reduce genetic and environmental heterogeneities and help clarify the underlying mechanisms of MS susceptibility. Sardinians kept a homogeneous genetic structure and have among the highest MS frequency rates worldwide. Interestingly, MS in Sardinia is linked to otherwise rare HLA alleles. In this light, recent findings from epidemiological and immunogenetic studies of Sardinian MS are presented. Results confirm that, likely due to significant genetic differences at a microgeographic level, even in this homogeneous population MS is immunogenetically heterogeneous and tends to preferentially cluster in some more archaic areas of the island.

Female↗
PubMed2002

Current concepts in multiple sclerosis: Part II.

Multiple sclerosis (MS) is a complex and challenging autoimmune disease of the central nervous system, affecting approximately 0.1% of the US population. Evidence to date suggests that viral infection triggers autoimmune attack against nerve cells in genetically-susceptible individuals. Neurologic deficits then appear, typically with a variable course and episodes of remission. Partial treatment success has been obtained with immunomodulating agents, such as interferon-beta and intravenous immunoglobulins. Current research is directed at elucidating potential viral causes of MS, as well as the interaction of host genes with the immunopathogenic mechanisms involved in MS. In the future, it may be possible to vaccinate susceptible individuals against MS, as well as refine immunomodulation therapy for the treatment of MS.

Adjuvants, Immunologic↗
PubMed2000

A multiple course trial of desferrioxamine in chronic progressive multiple sclerosis.

Chronic progressive multiple sclerosis (MS) is a debilitating disease that is often refractory to treatment. We have previously published a pilot study using a single 2-week course of the iron chelating drug, desferrioxamine (DFO), as a candidate drug for treatment of this form of MS. In this study, we gave 9 patients up to 8 courses of this regimen over 2 years. The patients tolerated the medication well. During the study, 1 patient improved, 3 remained stable, and 5 worsened by 0.5 on the Kurtzke expanded disability status scale (EDSS). These results suggest that, while the drug is well tolerated, no effect on disease progression can be identified at this dosage level. A more continuous dosage schedule could be studied as a candidate for treatment in this disease process.

Adult↗
PubMedDate not supplied

Nursing at a specialist diagnostic clinic for multiple sclerosis.

People with multiple sclerosis (MS) need support, information, education and guidance in order to adapt effectively to the impact of the disease (Sheridan, 1997). The care received at the time of diagnosis is central to this adaptation process as the information given and received may impact on the person with MS for the rest of his/her life. In order to achieve effective coping strategies, the person with MS needs to develop a collaborative relationship with the team of healthcare professionals. At the National Hospital for Neurology and Neurosurgery (NHNN), University College London Hospital (UCLH), the MS team believes that the foundations of this relationship should be cemented at the diagnostic stage. This article describes a diagnostic model that facilitates accurate timely diagnosis of MS and the role of the MS nurse in providing expert clinical assessment, guidance, support and education in order to help the patient adjust to the disease.

Humans↗
PubMed1999

The genetics of multiple sclerosis. A review.

Multiple sclerosis (MS) is characterized by chronic inflammation and demyelination in the central nervous system (CNS). Although the etiology of MS is unknown, both genetic and environmental contributions to the pathogenesis are inferred from epidemiologic studies. Geographic distributions and epidemics of MS and data from migration studies provide evidence for some, thus far unidentified, environmental effects. The co-occurrence of MS with high and low frequencies in ethnic groups often sharing an environment, the increased recurrence rate in families, and the high concordance rate among identical twins point to inheritable determinants of susceptibility. Based on the autoimmune hypothesis of demyelination, genetic studies sought associations between MS and polymorphic alleles of candidate genes which regulate either the immune response or myelin production. The most consistent finding in case-control studies was the association with the major histocompatibility complex (MHC) (also called human leukocyte antigen--HLA) class II, DR15, DQ6, Dw2 haplotype. Studies on other gene products encoded within or close to the MHC complex on chromosome 6p21.3 (e.g., HLA DP, complement components, transporter proteins, tumor necrosis factor, and myelin-oligodendrocyte glycoprotein) resulted in conflicting observations in different patient populations. The potential contribution of polymorphic alleles within the genes of the T-cell receptor alpha beta chains, immunoglobulins, cytokines, and oligodendrocyte growth factors or their receptors to MS susceptibility either remains equivocal or is rejected. Studies on families with multiple affected members have revealed that MS is a complex trait, that the contribution of individual genes to susceptibility is probably small, and that differences are possible between familial and sporadic forms. The development of molecular and computer technologies have facilitated the performance of comprehensive genomic scans in multiplex families, which have confirmed the possible linkage of multiple loci to susceptibility, each with a minor contribution. Several provisional sites were reported, but only 6p21 (MHC complex), 5p14, and 17q22 were positive in more than one study. The British update demonstrated segregation among regions of interest depending on DR15 sharing, and excluded a gene of major effect from 95%, and one with a moderate effect from 65% of the genome. The extended study by the US collaboration group revealed that the MHC linkage was limited to families segregating HLA DR2 alleles, which suggested that linkage to the MHC is related to the HLA DR2 association, and that sporadic and familial MS share at least one common susceptibility marker. Further identification of MS susceptibility loci may involve additional family sets, more polymorphic markers, and the exploration of telomeric chromosomal regions. Data from these studies may further elucidate pathogenic mechanisms of MS.

Chromosomes, Human, Pair 6↗
PubMed1981

Suppressor cell activity in multiple sclerosis.

Patients with multiple sclerosis and matched controls were tested for lymphocyte stimulation response and induction of suppressor cell activity in response to concanavalin A (Con A) and antigens from axolemma or myelin. Of 17 stable patients, 6 failed to have a suppressor cell response activated by one of these brain cell antigens. Among the patients who lacked these suppressor responses, five had lymphocyte stimulation responses to the same antigens. All matched controls except for one had suppressor cell responses to these antigens and none responded with a positive cellular immune reaction. We found no difference in lymphoproliferative responses to Con A in patients and controls. The level of suppressor cell activity induced by Con A in the stable MS patients varied but did not differ significantly from that of controls.

Antigens↗
PubMed1997

Outcome measures in multiple sclerosis clinical trials.

Multiple sclerosis remains incurable. The urgency of this problem, together with the need to test an ever increasing number of promising therapeutic agents emerging from animal studies, has renewed interest in both the application and the development of efficient outcome measures for treatment trials. The selection and usage of instruments used to detect outcomes is probably the most important issue in treatment trial design. Thus, familiarity with them is essential not only for researchers, but also for clinicians who wish to interpret trial results critically. This chapter begins with a discussion of the properties of an ideal outcome instrument, then reviews the strengths and limitations of existing clinical, radiological and laboratory outcome measures. With this knowledge, the current consensus regarding appropriate outcome measure selection, as well as recommendations and future perspectives in trial design, are discussed.

Biomarkers↗
PubMed1977

Latitude, migration, and the prevalence of multiple sclerosis.

Prevalence of multiple sclerosis (MS) was determined in three groups of Caucasians in King and Pierce Counties (Washington) and in Los Angeles County (California): natives (born in study state), migrants from high-risk states (North), and migrants from low risk states (South). A diagnosis of definite or probable MS (excluding migrants with onset before migration) was established in 1816 of the persons found. The prevalence in Los Angeles County natives and in migrants from the South to either Los Angeles County or King-Pierce Counties were relatively low, while prevalence in King-Pierce Counties among natives and migrants from the North were high. The prevalence in migrants from the North to Los Angeles was intermediate. The results suggest that some degree of protection is provided to migrants by residence in low-prevalence areas, either early or later in life.

California↗
PubMed1986

Multiple sclerosis: neuroimmunologic puzzle.

Multiple sclerosis (MS), a chronic disease with a relapsing and remitting course, is the most common neuroimmunologic condition in the United States. The hallmarks of the disease are focal demyelination and inflammation within the central nervous system (CNS). Because histopathologic changes can be identified only at autopsy, attention has been directed at formulating standardized clinical and laboratory procedures to aid in MS diagnosis. Currently, there are no MS-specific clinical or laboratory tests, but detection of abnormality in cerebrospinal fluid (CSF) IgG is important in supporting clinical evidence of disease. A number of other immunologic abnormalities have been recognized in MS, including the presence of T- and B-lymphocytes within the CNS and alterations in circulating suppressor T-lymphocytes. These findings have been interpreted as indicating disturbed immunoregulation associated with a chronic autoimmune response within the CNS. Evidence implicates viral infection in the pathogenesis of MS but the cause of the disease remains unknown.

Animals↗
PubMed2003

Future immunotherapies in multiple sclerosis.

Immunotherapy of multiple sclerosis (MS) will continue to benefit from an increasing understanding of this disease. This knowledge results in newly defined targets for novel therapies. In this article the development of future immunotherapies will be discussed by classifying the approaches into three main types: (1) antigen-specific therapies; (2) agents with a defined target in pathogenic steps of the MS lesion; and (3) therapies with broad immunomodulatory activity. Success in developing new immunotherapies depends on understanding the underlying complexity and heterogeneity of the disease. The current practice of employing a single therapy across a heterogeneous group of MS patients is in part a likely reason for their modest efficacy. The mechanism of action of a single agent may target the appropriate defect in one individual but not others. The therapy of MS in the future will most likely use a combination of agents that are directed at the underlying disease state and stage in the individual patient.

Adjuvants, Immunologic↗
PubMed2004

Beta 2-adrenoceptor involvement in inflammatory demyelination and axonal degeneration in multiple sclerosis.

Relapses of multiple sclerosis (MS) are considered to be the clinical expression of acute T-cell-mediated inflammatory demyelinating lesions disseminated in the CNS, whereas disease progression seems to result from widespread axonal degeneration. The pathophysiology of both disease components is incompletely understood. Astrocytes in MS lack beta(2)-adrenoceptors, which via cAMP-mediated processes inhibit the expression of major histocompatibility (MHC) class II molecules and stimulate glycogenolysis in normal conditions. In a pro-inflammatory CNS environment this beta(2)-adrenoceptor defect might allow astrocytes to transform into facultative antigen-presenting cells that can initiate the inflammatory cascade. The same receptor defect might impair astrocytic glycogenolysis, which normally generates lactate that is transported to axons as an energy source. Failure of axonal energy metabolism might result in axonal degeneration through mechanisms that involve intra-axonal accumulation of Ca(2+) ions and mitochondrial dysfunction. If this hypothesis is correct, therapies designed to elevate cAMP levels in astrocytes should reduce or prevent both relapses and progression of MS.

Astrocytes↗
PubMed2006

Limited impact of the summer heat wave in France (2003) on hospital admissions and relapses for multiple sclerosis.

Patients with multiple sclerosis (MS) often report worsening of symptoms with increased environmental temperature. The aim of this paper was to determine whether or not the heat wave of the summer of 2003 in France was responsible for an increase in hospital admissions and relapses in MS patients. MS patients who were hospitalized between January 1,2000 and December 31,2003 were identified, and we established which patients were suffering relapses. Hospitalization and relapse seasonality were examined and analyzed according to ambient temperature variations. We did not observe a greater number of hospital admissions and relapses during the summer of 2003 compared to the previous 3 years. Results showed that MS hospitalizations display a significant trough in the winter season, especially in December, but no significant peak season or month was observed. There was no statistically significant correlation between mean ambient temperature and the number of admissions and relapses. The adverse symptoms associated with high temperatures that are usually observed in MS patients may require rapid rises in ambient temperate or in internal body temperature.

France↗
PubMed1992

Life expectancy in patients attending multiple sclerosis clinics.

One multiple sclerosis (MS) is diagnosed, important considerations often include life expectancy and the availability of life insurance. We designed a study specifically to examine life expectancy among MS clinic patients and analyzed the data using standard actuarial methods, both including and excluding suicides. The data show that severe MS disability, as measured by an Expanded Disability Status Score (EDSS) of greater than or equal to 7.5, is a major risk factor for death with case fatality ratios for this group of patients approaching 4 times the rate for controls. Conversely, excluding deaths by suicide, case fatality ratios for those with mild and moderate disability (EDSS less than or equal to 7.0) approach 1.4 times and 1.6 times for age- and sex-matched comparison groups. Life tables indicate that the overall life expectancy for MS is only about 6 to 7 years less than that for the "insured" population without MS.

Adolescent↗