Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “MULTIPLE SCLEROSIS”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,189 records · Page 66Linked to original sources
PubMed2006

Increased frequency and broadened specificity of latent EBV nuclear antigen-1-specific T cells in multiple sclerosis.

Epidemiological studies consistently demonstrate that patients with multiple sclerosis are almost universally infected with Epstein-Barr virus (EBV) and that the risk of developing the disease increases with the level of EBV-specific antibody titers. The EBV-encoded nuclear antigen-1 (EBNA1) maintains the viral episome in replicating infected human B cells, and EBNA1-specific CD4+ T cells have been identified as a crucial part of the EBV-specific immune control in healthy individuals. We studied 20 untreated EBV seropositive patients with multiple sclerosis and 20 healthy EBV carriers matched demographically and for the expression of multiple sclerosis-associated HLA-DR alleles for their immunological control of EBV latency at the level of EBNA1-specific T cells. Using 51 overlapping peptides covering the C-terminal of EBNA1 domain of EBNA1 (amino acids 400-641), peptide-specific CD4+ memory T cells in patients with multiple sclerosis were found to be strikingly elevated in frequency, showed increased proliferative capacity and an enhanced interferon-gamma production. In contrast to EBNA1, T-cell responses to three other latent and three other lytic immunodominant EBV antigens and human cytomegalovirus (HCMV) epitopes did not differ between patients and controls, indicating a distinct role for EBNA1-specific T-cell responses in multiple sclerosis. CD4+ T cells from healthy virus carriers preferentially recognized multiple epitopes within the centre part of the C-terminal, whereas the stimulatory epitopes in multiple sclerosis patients covered the entire sequence of this domain of EBNA1. Quantification of EBV viral loads in peripheral blood mononuclear cells (PBMC) by real-time polymerase chain reaction (PCR) showed higher levels of EBV copy numbers in some patients with multiple sclerosis, although the overall difference in viral loads was not statistically significant compared with healthy virus carriers. We suggest that the accumulation of highly antigen-sensitive EBNA1-specific Th1 cells in multiple sclerosis is capable of sustaining autoimmunity by cross-recognition of autoantigens or by TCR-independent bystander mechanisms.

Adult↗
PubMed1971

Immunoglobulin M specific for measles and mumps in multiple sclerosis.

Sera from 43 patients with multiple sclerosis were tested by immunofluorescence. Sera from patients with active multiple sclerosis included four with measles virus-specific immunoglobulin M (measles IgM) and two with mumps virus-specific IgM (mumps IgM). In one case each mumps IgM and measles IgM seem to have persisted for two and a half years and three years respectively. In a comparable group of 43 patients with other nervous diseases measles IgM was found in only one serum, and among 43 normal patients no measles or mumps IgM was found.Herpes simplex virus-specific IgM (herpes simplex IgM) was distributed among all three groups. Anticellular IgM was also found, predominantly in active multiple sclerosis, and persisted in two sera for two and a half years.

Autoantibodies↗
PubMed1983

Schwann cell remyelination of demyelinated axons in spinal cord multiple sclerosis lesions.

To investigate remyelination in multiple sclerosis lesions, we immunostained spinal cord sections from patients with multiple sclerosis and neurological normal (control) patients with antisera to P0 protein, a major constituent of peripheral nervous system myelin, and myelin basic protein, which is found in both central and peripheral nervous system myelin. In sections from five of the eight patients with no clinical or pathological evidence of neurological disease, P0 immunostaining was confined to peripheral myelin sheaths in dorsal and ventral roots. They were intensely stained, and peripheral--central nervous system transition zones were clearly demarcated. Sections from the other three control patients contained a few P0-stained sheaths in the central nervous system near root entry zones or among marginal glia near the dorsal sulcus. Spinal cord sections from six of the ten patients with multiple sclerosis contained clusters of myelin sheaths immunostained by P0 antiserum. These regenerating sheaths of peripheral nervous system origin were most numerous in large lesions and were commonly located in central areas or peripherally near root entry zones. The sheaths were observed frequently in areas of active demyelination and appeared morphologically normal even when surrounded by debris-filled macrophages. Near margins of small inactive plaques were a few basic protein--stained oligodendroglia extending processes to thin basic protein--stained sheaths.(ABSTRACT TRUNCATED AT 250 WORDS)

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMedDate not supplied

[Erythrocyte complement receptor (C3b) expression in multiple sclerosis].

The study was carried out in 121 patients with multiple sclerosis and a control group of 519 healthy individuals. In 13 cases of multiple sclerosis and 12 controls family studies were carried out. Complement receptors (C3bR) on the erythrocytes were demonstrated by the haemagglutination test using human IgG heat-aggregated and guinea pig serum which served as a source of complement. On the basis of haemagglutination intensity and results of radioimmunoassay three phenotypes of complement receptor were isolated: high HH(C3bRh/C3bRh) producing strong agglutination, medium HL (C3bRh/Cbl) producing weak agglutination, and low phenotype LL (C3bR1/Cbl) in which no visible agglutination of erythrocytes was noted. Considerable differences were observed in the distribution of these phenotypes between controls and multiple sclerosis patients in whom the low phenotype (C3bR1/C3bR1) was more frequent. Family studies of controls suggested presence of two codominant alleles C3bRh and C3bR1 with Mendelian inheritance while similar studies of multiple sclerosis patients it was found that e.g. a child with multiple sclerosis whose parents had high C3bR phenotypes, that it were homozygotes for the C3bRh gene, had low phenotype. On the other hand, the high phenotype was found in a child of a female multiple sclerosis patient with the low phenotype (C3bR1/C3bR1). These observations suggest that reduced expression of the complement receptor on the erythrocytes depends in multiple sclerosis on the disease process in the first place, and not on genetic factors.

Adult↗
PubMed2001

Effect of early interferon treatment on conversion to definite multiple sclerosis: a randomised study.

BACKGROUND: Interferon beta reduces activity in multiple sclerosis as measured clinically and by magnetic resonance imaging (MRI). We assessed the effect of interferon beta-1a on the occurrence of relapses in patients after first presentation with neurological events, who are at high risk of conversion to clinically definite multiple sclerosis. METHODS: Eligible patients had had a first episode of neurological dysfunction suggesting multiple sclerosis within the previous 3 months and had strongly suggestive brain MRI findings. Patients were randomly assigned interferon beta-1a 22 microg or placebo subcutaneously once weekly for 2 years. Neurological and clinical assessments were done every 6 months and brain MRI every 12 months. Analyses excluded one patient assigned placebo who received no study injections. FINDINGS: 241 (78%) of 308 randomised patients received study treatment for 2 years; 278 (90%) remained in the study until termination. 57 (85%) of 67 who stopped therapy did so after conversion to clinically definite multiple sclerosis. Fewer patients developed clinically definite multiple sclerosis in the interferon group than in the placebo group (52/154 [34%] vs 69/154 [45%]; p=0.047). The time at which 30% of patients had converted to clinically definite multiple sclerosis was 569 days in the interferon group and 252 in the placebo group (p=0.034). The annual relapse rates were 0.33 and 0.43 (p=0.045). The number of new T2-weighted MRI lesions and the increase in lesion burden were significantly lower with active treatment. INTERPRETATION: Interferon beta-1a treatment at an early stage of multiple sclerosis had significant positive effects on clinical and MRI outcomes.

Adolescent↗
PubMed2001

Prevalence of multiple sclerosis in Belgrade, Yugoslavia.

OBJECTIVES: To estimate the distribution of multiple sclerosis in the Belgrade population. METHODS: All persons who were affected and/or died from multiple sclerosis (Poser's criteria), with residence in the Belgrade region had been collected from January 1, 1985 to December 31, 1996. Prevalence was adjusted by direct method, using world population. RESULTS: From 1985 to 1996, 823 patients were suffering from multiple sclerosis. Sex ratio was 1:1.9. The mean age at onset was 32.2 +/- 9.8 years. A relapsing-remitting course of multiple sclerosis was reported in 50.7% patients, secondary progressive in 36.4%, patients, and primary progressive in 12.9% patients. On December 31, 1996, age-adjusted prevalence of multiple sclerosis in Belgrade was 41.5/100,000, 28.2/100,000 for males, and 54.1/100,000 for females. During the period studied, statistically highly significant increasing trend of multiple sclerosis prevalence was observed (P = 0.0001). CONCLUSIONS: According to findings presented in this study, Belgrade is an area with high prevalence of multiple sclerosis.

Adult↗
PubMed2005

Integrating cognitive function screening and assessment into the routine care of multiple sclerosis patients.

Cognitive dysfunction, a common feature of multiple sclerosis (MS), frequently leads to impaired activities of daily living, social skills deficits, diminished social support, and unemployment. There is growing evidence indicating that cognitive impairment is amenable to the effects of medication and behavioral counseling. Unfortunately, routine neuropsychological testing is rare in MS clinics because screening is ineffective and testing strategies are often too cumbersome or expensive. Recent research supports the reliability of a brief screening test called the Multiple Sclerosis Neuropsychological Screening Questionnaire as well as a minimal neuropsychological battery called the Minimal Assessment of Cognitive Function in Multiple Sclerosis. Data indicate that the Multiple Sclerosis Neuropsychological Screening Questionnaire has excellent split-half and test-retest reliability, and that it predicts neuropsychological deficiency with good sensitivity and specificity. Recently acquired data also show that the Minimal Assessment of Cognitive Function in Multiple Sclerosis tests have good test-retest reliability, discriminate MS patients from normal controls, and predict unemployment in MS patients. Thus, these or similar methods should be employed for the routine monitoring of cognitive functioning of MS patients.

Adult↗
PubMed2001

[Genetic factors in multiple sclerosis].

GENERAL DATA: The clinical manifestations and neuropathological signs of multiple sclerosis have been recognized for more than one hundred years, but the cause remains unknown. EPIDEMIOLOGY: Multiple sclerosis is not evenly distributed throughout the world. There is an important north-south gradient in the northern hemisphere and inversely in the southern hemisphere; multiple sclerosis is more frequent in the higher altitudes. For a given latitude, there is a difference by ethnic origin. These observations indicate that multiple sclerosis is a multifactorial condition determined by both genetic and environmental factors. STRATEGIES OF GENETIC STUDIES: Progress in our knowledge of the human genome and statistical analysis techniques have made it possible to search for genetic factors in multiple sclerosis using two complementary approaches. The first is by anonymous screening and the second is to search for a candidate gene. The HLA locus is the only one with an identified predisposing effect for multiple sclerosis. It only accounts for 10 to 20% of the genetic predisposition for multiple sclerosis and many factors remain to be discovered.

Genetic Predisposition to Disease↗
PubMed1978

Decreased lymphocyte transformation to vaccinia virus in multiple sclerosis.

Lymphocyte transformation to vaccinia virus was measured in multiple sclerosis (MS) patients and normal controls. There was a significant reduction of lymphocyte transformation to vaccinia virus in multiple sclerosis patients compared with the control group. In addition, a positive correlation existed between the degree of disability of the multiple sclerosis patients and the extent of lymphocyte transformation in the presence of vaccinia virus. There was no correlation between cell-mediated immunity to vaccinia virus and either serum or cerebrospinal fluid (CSF) antibody levels to vaccinia in multiple sclerosis patients or controls, all of whom had been previously vaccinated. In conjunction with other studies, all of whom had been previously vaccinated. In conjunction with other studies that have demonstrated elevated antibody titers to vaccinia virus in the CSF of multiple sclerosis patients, these results support the possibility that vaccinia virus may play a role in the pathogenesis of multiple sclerosis.

Adolescent↗
PubMed1991

Anorectal sensory and motor function in neurogenic fecal incontinence. Comparison between multiple sclerosis and diabetes mellitus.

We measured anorectal sensory and motor function in 11 patients with multiple sclerosis and fecal incontinence, 11 continent patients with multiple sclerosis, 10 diabetics with fecal incontinence, and 12 healthy control subjects. The threshold volume at which patients with multiple sclerosis and fecal incontinence experienced rectal sensation was higher than that in healthy controls (42.7 +/- 6.2 mL vs. 13.3 +/- 2.8 mL; P less than 0.01) and was similar to that in incontinent diabetics (36.5 +/- 5.7 mL). Patients with multiple sclerosis and incontinent diabetics also showed increased thresholds of phasic external sphincter contraction compared with controls (P less than 0.05). Diabetics with incontinence had reduced resting and maximal voluntary anal sphincter pressures compared with controls (P less than 0.05), whereas patients with multiple sclerosis and incontinence showed only decreased maximal voluntary anal sphincter pressures (P less than 0.01 vs. controls and diabetics). Incontinent patients with multiple sclerosis also required smaller volumes of rectal distention to inhibit internal sphincter tone compared with diabetics and controls (P less than 0.01). Decreased maximal voluntary squeeze pressures were less severe in continent patients with multiple sclerosis than in incontinent patients with multiple sclerosis. We conclude that impaired function of the external anal sphincter and decreased volumes of rectal distention to inhibit the internal anal sphincter or both may contribute to fecal incontinence in multiple sclerosis. In addition, increased thresholds of conscious rectal sensation in some incontinent patients with multiple sclerosis and diabetes mellitus may contribute to fecal incontinence by impairing the recognition of impending defecation.

Adult↗
PubMed1995

Clinical and subclinical neurological involvement in children of conjugal multiple sclerosis patients.

We report the occurrence of clinically definite multiple sclerosis in an offspring of a couple with conjugal multiple sclerosis. Extensive investigation of all members of this family, which includes two additional asymptomatic children, eliminated the possibility of alternative neurological diagnoses. All family members were studied with magnetic resonance imaging (MRI), evoked potentials, and human leukocyte antigen (HLA) typing. An asymptomatic child had subtle white matter abnormalities on MRI, suggesting subclinical neurological involvement. This study documents the third case of multiple sclerosis in the child of conjugal multiple sclerosis patients and provides the first report of MRI lesions in an asymptomatic offspring of the same parents. Neurodiagnostic and immunogenetic investigations of such rare family clusters may contribute to the elucidation of the pathogenesis of multiple sclerosis.

Adolescent↗
PubMed2005

Cortical demyelination and diffuse white matter injury in multiple sclerosis.

Focal demyelinated plaques in white matter, which are the hallmark of multiple sclerosis pathology, only partially explain the patient's clinical deficits. We thus analysed global brain pathology in multiple sclerosis, focusing on the normal-appearing white matter (NAWM) and the cortex. Autopsy tissue from 52 multiple sclerosis patients (acute, relapsing-remitting, primary and secondary progressive multiple sclerosis) and from 30 controls was analysed using quantitative morphological techniques. New and active focal inflammatory demyelinating lesions in the white matter were mainly present in patients with acute and relapsing multiple sclerosis, while diffuse injury of the NAWM and cortical demyelination were characteristic hallmarks of primary and secondary progressive multiple sclerosis. Cortical demyelination and injury of the NAWM, reflected by diffuse axonal injury with profound microglia activation, occurred on the background of a global inflammatory response in the whole brain and meninges. There was only a marginal correlation between focal lesion load in the white matter and diffuse white matter injury, or cortical pathology, respectively. Our data suggest that multiple sclerosis starts as a focal inflammatory disease of the CNS, which gives rise to circumscribed demyelinated plaques in the white matter. With chronicity, diffuse inflammation accumulates throughout the whole brain, and is associated with slowly progressive axonal injury in the NAWM and cortical demyelination.

Acute Disease↗
PubMed2004

Certification of multiple sclerosis nurses: an international perspective.

The Multiple Sclerosis Nursing International Certification Board was formed as a special initiative of the International Organization of Multiple Sclerosis Nurses (IOMSN). The aim was to develop a certification examination for MS nursing practice. This certification should achieve the vision of the IOMSN and unite MS nurses worldwide through standard practices. Such practices are based on common knowledge and skills, and tasks that encourage the best outcome for the nurse-patient collaborative relationship. Certification allows recognition of an individual nurse's skill level, establishes a standard for all nurses treating patients with MS, improves patient care, and also benefits the neurological community. The Multiple Sclerosis Certified Nurse is revolutionary, as certification is an international effort to enhance and standardize MS care and develop MS nurse professionalism across borders.

Certification↗
PubMed1998

[New therapeutic agents in the management of multiple sclerosis].

THERAPEUTIC ADVANCES: Several effective therapies for multiple sclerosis capable of modifying the disease course in certain patients are now available in France. INTERFERONS: Interferon beta-1b and interferon beta-1a have been given specific marketing approval in France for ambulatory patients with active relapsing-remitting multiple sclerosis. Interferon beta-1b has been shown to have a beneficial effect in progressive multiple sclerosis. COPAXONE: This drug has a temporary authorization in France for ambulatory patients with relapsing-remitting multiple sclerosis who cannot tolerate interferon. PERSPECTIVES: Other promising therapeutic options (mitoxantrone, intravenous immunoglobulins, drug associations) are under evaluation.

Adjuvants, Immunologic↗
PubMed1984

Disability rating scales in multiple sclerosis.

The International Federation of Multiple Sclerosis Societies has been attempting to define a Minimal Data Set for multiple sclerosis following the tripartite scheme of the World Health Organization, with one rating scheme for neurologic signs, one for physical disabilities, and one for the societal impact of the disease. Current recommendations are the Disability Status Scale or the Expanded DSS plus Functional Systems for the first, Incapacity Status Scale of 16 items for the second, and Environmental Status Scale of 7 items for the third. All are graded in an ordinal (rank) scale from 0 (normal) with larger numbers for greater involvement. ISS scores range from 0-4 and ESS from 0-5 for each item. The only part of this scheme useful for measurement in clinical trials is the (E)DSS + FS. The DSS ranges from 0-10; EDSS subdivides each DSS grade 1-9 into two. FS are pyramidal, cerebellar, brain stem, sensory, bowel and bladder, visual, cerebral, or other; all save the last are graded 0-5 or 0-6. The DSS correlates well with both frequency and severity of involvement in all FS, which in turn represent a coded standard neurologic examination.

Disability Evaluation↗
PubMed2005

Intense immunosuppression followed by autologous stem cell transplantation in severe multiple sclerosis.

Aggressive forms of multiple sclerosis (MS) represent a limited group of demyelinating diseases that rapidly progress to severe disability. Currently available therapies are poorly effective against these clinical entities. Recently, it has been demonstrated that intense immunosuppression followed by autologous haematopoietic stem cell transplantation (AHSCT) can affect the clinical course of individuals with severe MS and completely abrogate the inflammatory activity detected by MRI. We report the result of the Italian phase 2 GITMO study, a multicentre study in which 21 MS patients, who were rapidly deteriorating and not responding to the usual therapeutic strategies, were treated with this procedure. The clinical effect of the treatment is long lasting, with a striking abrogation of inflammation detected by MRI findings. These results support a role for intense immunosuppression followed by ASCT as treatment in rapidly evolving MS cases unresponsive to conventional therapies.

Adult↗
PubMed2003

Antimyelin antibodies as a predictor of clinically definite multiple sclerosis after a first demyelinating event.

BACKGROUND: Most patients with multiple sclerosis initially present with a clinically isolated syndrome. Despite the fact that clinically definite multiple sclerosis will develop in up to 80 percent of these patients, the course of the disease is unpredictable at its onset and requires long-term observation or repeated magnetic resonance imaging (MRI). We investigated whether the presence of serum antibodies against myelin oligodendrocyte glycoprotein (MOG) and myelin basic protein (MBP) in patients with a clinically isolated syndrome predicts the interval to conversion to clinically definite multiple sclerosis. METHODS: A total of 103 patients with a clinically isolated syndrome, positive findings on cerebral MRI, and oligoclonal bands in the cerebrospinal fluid were studied. At base line, serum samples were collected to test for anti-MOG and anti-MBP antibodies with Western blot analysis, and the lesions detected by cerebral MRI were quantified. Neurologic examinations for relapse or disease progression (defined as conversion to clinically definite multiple sclerosis) were performed at base line and subsequently every three months. RESULTS: Patients with anti-MOG and anti-MBP antibodies had relapses more often and earlier than patients without these antibodies. Only 9 of 39 antibody-seronegative patients (23 percent) had a relapse, and the mean (+/-SD) time to relapse was 45.1+/-13.7 months. In contrast, 21 of 22 patients (95 percent) with antibodies against both MOG and MBP had a relapse within a mean of 7.5+/-4.4 months, and 35 of 42 patients (83 percent) with only anti-MOG antibodies had a relapse within 14.6+/-9.6 months (P<0.001 for both comparisons with antibody-seronegative patients). The adjusted hazard ratio for the development of clinically definite multiple sclerosis was 76.5 (95 percent confidence interval, 20.6 to 284.6) among the patients who were seropositive for both antibodies and 31.6 (95 percent confidence interval, 9.5 to 104.5) among the patients who were seropositive only for anti-MOG antibodies, as compared with the seronegative patients. CONCLUSIONS: Analysis of antibodies against MOG and MBP in patients with a clinically isolated syndrome is a rapid, inexpensive, and precise method for the prediction of early conversion to clinically definite multiple sclerosis. This finding may be important for the counseling and care of patients with a first demyelinating event suggestive of multiple sclerosis.

Adolescent↗
PubMed1996

A study of oligoclonal band negative multiple sclerosis.

OBJECTIVES: To determine whether oligoclonal band (OCB) negative multiple sclerosis is a reliable diagnosis and, if so, whether it has a distinctive prognosis. METHODS: Retrospective and matched prospective comparison of the clinical and laboratory features of patients with clinical definite multiple sclerosis with and without intrathecal synthesis of oligoclonal IgG. RESULTS: Thirty four patients were identified with apparent OCB negative clinically definite multiple sclerosis. The results of oligoclonal banding proved to have been equivocal in 14 of 34; the clinical diagnosis of multiple sclerosis was questionable in 8 of 34. The remaining 12 patients with "true" OCB negative multiple sclerosis were significantly less disabled than matched OCB positive controls. Re-examination of CSF-serum pairs from six OCB negative patients showed that three remained OCB negative while three showed evidence of intrathecal synthesis of OCBs. CONCLUSIONS: OCB negative clinically definite multiple sclerosis is rare and should be diagnosed with caution; in unequivocal cases it seems to have a relatively benign prognosis.

Adult↗