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PubMed2003

The enigma of multiple sclerosis: inflammation and neurodegeneration cause heterogeneous dysfunction and damage.

PURPOSE OF REVIEW: The demyelinating disease multiple sclerosis has an autoimmune inflammatory component, which has dominated the description of multiple sclerosis. A degenerative component to multiple sclerosis was always apparent, but was underappreciated until recently. Recent work has brought axonal pathology and brain atrophy into new focus. The purpose of this review is to highlight the relative roles played by the inflammatory and degenerative processes in multiple sclerosis pathology. RECENT FINDINGS: In the past year reports have been published to show that early disability and disease progression correlate with axonal damage, and that brain atrophy resulting from axonal loss is a feature of early multiple sclerosis, and is not restricted to the secondary progressive forms of the disease. Inflammatory mediators (CD8 T cells and antibodies) are implicated in axonal damage, and treatment with steroids or anti-inflammatory therapies reduce brain atrophy, pointing to the involvement of the inflammatory response in the initiation of degeneration. Reduced regenerative capability also contributes to degeneration, and inflammatory responses are shown to inhibit the growth and migration of precursor cells for oligodendrocytes. SUMMARY: Oligodendrocyte precursors are abundant in multiple sclerosis lesions, but fail to remyelinate. Oligodendrocyte growth and regeneration are probably compromised by the action of growth inhibitory signals and lack of growth stimuli. Inflammatory cells and mediators induce axonal loss as well as demyelination. The degenerative response is therefore an integral and early component of multiple sclerosis.

Atrophy↗

PubMed1976

Optic neuritis in relation to multiple sclerosis.

Available estimates of the frequency with which a patient with optic neuritis develops multiple sclerosis range from as low as 13% to as high as 87%. In an effort to obtain a better estimate, a nation-wide study of optic neuritis was carried out in Israel. Patients who fulfilled strict diagnostic criteria of optic neuritis were identified and examined periodically. Between 1955 and 1964, 105 patients were found and on the basis of these, the average annual age-adjusted incidence of optic neuritis in Israel was 0.56 per 10(5) population compared to 1.2 per 10(5) cases of multiple sclerosis per year, i.e. optic neuritis was about half as frequent as multiple sclerosis each year. As with multiple sclerosis, optic neuritis was more common in European immigrants to Israel than Afro-Asian immigrants. During a follow-up interval which ranged from 3.3 to 15.6 years (mean 9.5 years), at least 27 of the 105 patients developed multiple sclerosis (28%). A life-table analysis showed that after 10 years 32.3 +/- 5.6% of patients with optic neuritis would develop multiple sclerosis and, after 14 years, about half would develop multiple sclerosis. Risk of dissemination was highest in those who were youngest when optic neuritis developed. Neither sex nor ethnic background influenced risk significantly. Results of the present study support earlier work using life-table methods carried out in Hawaii which also showed that between 29 and 39% of patients with optic neuritis will develop multiple sclerosis within 10 years of onset. The life-table method is a better predictor of prognosis than newer laboratory techniques such as spinal fluid studies of IgG, kappa-lambda light chain ratios and serum/CSF IgG ratios.

Adolescent↗

PubMed1995

Varicella zoster virus and multiple sclerosis in a Hutterite population.

There are similarities between multiple sclerosis and varicella. They are common in the same parts of the world and both are scarce in other areas. Immigration studies suggest the environmental cause of multiple sclerosis (MS) must be contracted prior to age 15 years and will usually remain dormant for years. At age 10 years varicella has occurred in greater than 95% of children living in the high-risk areas for both of these diseases. The varicella zoster virus (VZV) could be etiologically important in multiple sclerosis. The known host containment of the virus for decades with recrudescence and the variable cell-mediated immunity of the host, which can wax and wane without clinical manifestations, all lend themselves to the natural history of multiple sclerosis. A population-based study of the medical records of 5601 Hutterite Brethren was performed to determine the occurrence of multiple sclerosis, varicella, and herpes zoster. Compared to their matched non-Hutterite neighbors who acted as controls, these events were significantly less common among the Hutterites. Included in the study was an assessment of other common neurological diseases and "autoimmune" diseases among the Hutterites and the controls. There is evidence of a relationship between MS and VZV that may not be coincidental.

Adolescent↗

PubMed1976

Measles antibodies as related to HL-A types in multiple sclerosis.

One hundred thirty-six patients with multiple sclerosis and several control groups were studied for measles antibodies using several different antigens. Measles antibodies were higher in the multiple sclerosis population, but siblings also had higher titers than matched and random controls. The elevation in antibody titers (complement fixation) was found in female multiple sclerosis patients and male patients with HL-A types 3, 7, and W-18. Male patients not carrying these HL-A antigens had, as a group, relatively normal antibody levels. These data confirm a familial factor in elevated measles antibody titers. We suggest that HL-A antigens are linked to one of the factors that determines measles antibody titers in multiple sclerosis patients.

Age Factors↗

PubMed1998

Use of corticosteroids in multiple sclerosis by consultant neurologists in the United Kingdom.

OBJECTIVES: To survey the use of corticosteroids in multiple sclerosis as recommended by United Kingdom consultant neurologists. METHODS: A postal questionnaire covering the use of corticosteroids for acute multiple sclerosis relapse and chronic progressive multiple sclerosis with regard to frequency of use, type of corticosteroid, and dosage regime was sent to all members of the Association of British Neurologists with a United Kingdom address. RESULTS: Two hundred and twelve United Kingdom consultant neurologists replied to the survey (74% response rate). Eighty six per cent indicated that they prescribed corticosteroids in more than one quarter of acute multiple sclerosis relapses seen. Intravenous methylprednisolone was recommended at some time by 99% of consultant neurologists, the most popular regime being 1g daily for 3 days (74%; 154/ 208). Over one half (53%; 109/206) never recommended a subsequent tapering course of oral corticosteroids; of those that did, 25% (24/96) recommended a tapering course lasting more than 1 month. Eighty eight per cent (1811206) of prescribers of intravenous methylprednisolone were able to offer the course as a day case on the ward; 7% (151206) at an outpatient clinic; and 5% (111206) at home. Almost three quarters of neurologists recommended oral corticosteroids for some acute relapses, although the most popular response was for occasional use only (48%; 1011212). Forty five per cent (961211) at least occasionally recommended steroids for patients with chronic multiple sclerosis not experiencing an acute relapse. CONCLUSIONS: Although the vast majority of consultant neurologists would prescribe intravenous methylprednisolone for acute multiple sclerosis relapse at some time, the use of corticosteroids for multiple sclerosis was otherwise variable. There seemed to be little consensus about the use of oral steroids in acute relapse, the prescribing of a tapering course of oral steroids after intravenous methylprednisolone, or the utility of steroids in chronic multiple sclerosis. Variability of prescribing recommendations probably reflects a lack of clear evidence in the face of a wide range of clinical situations, variable access, and timing of access to neurologists in the acute phase of relapse and pressure on neurologists to treat in an otherwise "hopeless" situation. Large multicentred trials are needed to consider these issues.

Administration, Oral↗

PubMed1994

Genetic disorders that masquerade as multiple sclerosis.

There are many genetic disorders that have signs and symptoms suggestive of multiple sclerosis and that may easily be overlooked in the evaluation of both adult and pediatric multiple sclerosis patients. The recognition of a genetic disorder as the cause of a patient's "multiple sclerosis" phenotype has important implications not only for the patient, but often also for others in the patient's family who may be at risk for the same disease. We present here a review of single gene disorders that can masquerade as multiple sclerosis. For each disorder, the major clinical and biochemical characteristics are discussed, together with the appropriate testing to screen for and confirm the diagnosis. In addition, guidelines are presented for when to suspect an underlying genetic condition in a patient with a diagnosis of definite or probable multiple sclerosis. The great variety of genetic disorders that can masquerade as multiple sclerosis and the many implications of a genetic diagnosis underscore the importance of recognizing genocopies of multiple sclerosis.

Diagnosis, Differential↗

PubMed1985

Increased prevalence and titer of Epstein-Barr virus antibodies in patients with multiple sclerosis.

The prevalence and titer of serum antibodies to several Epstein-Barr virus (EBV) antigens were compared among patients with multiple sclerosis, healthy siblings of multiple sclerosis patients, patients with other neurological diseases, and healthy non-blood-related subjects. Serum-cerebrospinal fluid (serum-CSF) pairs were available on a selected number of multiple sclerosis and control subjects. An increased antibody response to EBV antigens was noted rather consistently in the sera of the multiple sclerosis group in comparison with the control groups. A greater number of reduced ratios of serum:CSF IgG antibody to EBV-capsid antigen and antibody to EBV-early antigen components than to adenovirus, a reference or control virus, were found in the multiple sclerosis group. Reduced ratios of these EBV antibodies were detected more frequently or showed a trend in this direction in multiple sclerosis patients compared with the group with other neurological diseases. Our findings extend the results of an earlier report and strengthen the association between EBV and multiple sclerosis.

Adenoviruses, Human↗

PubMed2004

[Immunomodulatory therapy in multiple sclerosis].

During the past decade, several disease-modifying agents have been established and have become available for the treatment of multiple sclerosis. The disease-modifying agents could be grouped into immunomodulatory and immunosuppressive therapies altering the long-term course of multiple sclerosis. Therapy is now available for relapsing-remitting, secondary progressive and progressive-relapsing multiple sclerosis. Different disease-modifying agents became also available for the treatment of relapsing-remitting multiple sclerosis in Hungary which makes the therapeutic decision difficult. This overview might help to give an answer for different questions in the management of multiple sclerosis: Which agent to choose? When to initiate the therapy? Which dose to apply? Are the drugs safe? How long to treat the patients with immunomodulatory drugs? We give a review from the literature to assess the efficacy of disease-modifying therapies and to compare the data from phase three trials of interferon beta1b, two preparations of interferon beta1a or glatiramer acetate for the treatment of multiple sclerosis. We analyzed the efficacy and safety of these agents on physical, inflammatory and cognitive measures of disease activity. Comparison of study results indicated similar effects of immunomodulatory agents on relapse-related and inflammatory measures in relapsing multiple sclerosis. Interferon beta1a slowed the progression of disability in relapsing multiple sclerosis. One interferon beta1a preparation (intramuscularly injected) demonstrated efficacy in slowing progression of cognitive dysfunction. The interferons reduced relapses at early phase of secondary progressive multiple sclerosis, but their efficacy have not yet been proven in the later phase of secondary progressive multiple sclerosis without relapses. Mitoxantrone demonstrated efficacy in slowing the progression of disability in secondary progressive multiple sclerosis. All of the disease modifying agents are safe and tolerable, if the indication is correct and the patients are strictly controlled.

Adjuvants, Immunologic↗

PubMed2001

Developing a disease-specific quality of life measure for people with multiple sclerosis.

OBJECTIVES: To develop a patient-completed disease-specific measure of quality of life in multiple sclerosis and to validate the measure in a community-based population of people with multiple sclerosis. METHODS: The items in the scale were selected in focus group sessions of people with multiple sclerosis. The initial scale included 25 items and was tested in subgroups of 150 people from a population register of people with multiple sclerosis in Leeds. Following further developmental phases, a restructured 16-item scale was tested on a random sample of 200 people with multiple sclerosis from the population register, stratified according to disease course. This led to a final eight-item unidimensional scale, the Leeds Multiple Sclerosis Quality of Life (LMSQoL) scale. RESULTS: After initial development a 16-item scale was found to be both reliable and valid. Cronbach's alpha for the 16-item scale was 0.86. The test-retest correlation was 0.74, using a two-week retest interval. However, convergent validity with the General Well Being Index was 0.67 and with the SF-36 Physical Function Scale was 0.68. This suggested that the scale straddled these two concepts and was confirmed by fit of the data to the Rasch measurement model. This revealed the potential for a reduced eight-item version of the scale. The eight-item scale had a closer association to well-being (0.83) than to physical function (0.39), had good internal consistency (0.79) and test-retest reliability (0.85). There were virtually no floor or ceiling effects for the scale. CONCLUSIONS: The study presents a disease-specific measure of quality of life in multiple sclerosis, the Leeds Multiple Sclerosis Quality of Life (LMSQoL) scale. The instrument is brief, easy to use and practical to administer in clinic or as a postal questionnaire. It measures a construct related to well-being, and provides an important adjunct to the measurement of outcome in multiple sclerosis.

Adult↗

PubMed2002

A multigenerational family with multiple sclerosis.

We report a family with 15 individuals affected with multiple sclerosis present in three and possibly four generations. The segregation of multiple sclerosis within this pedigree is consistent with an autosomal dominant mode of inheritance with reduced penetrance. The clinical characteristics of the affected individuals are indistinguishable from those seen in sporadic multiple sclerosis with respect to sex ratio, age at onset, onset symptom, MRI and clinical course. Eleven of 14 cases (78.6%) were positive for the known multiple sclerosis-associated major histocompatibility complex (MHC) Class II HLA DRB1*15 allele. Parametric linkage analysis gave a non-significant LOD score of 0.31 (theta; = 0.33) for the DRB1 gene. However, among 11 affected children with at least one DRB1*15 bearing parent, all 11 out of 11 received at least one copy of this known susceptibility allele. A transmission disequilibrium test analysis was significant for the DRB1*15 allele within this single family; P = 0.0054. The inheritance pattern in this family suggests the presence of a single major locus responsible for multiple sclerosis susceptibility, with DRB1 acting as an important modifier. This family could be an important resource for the identification of a multiple sclerosis susceptibility gene.

Adolescent↗

PubMedDate not supplied

[A review of the epidemiology of multiple sclerosis in Mexico].

OBJECTIVE: To review the epidemiological information on multiple sclerosis in Mexico. DEVELOPMENT AND CONCLUSIONS: The results of the few epidemiological studies on multiple sclerosis show a prevalence of 1.5/100,000 inhabitants, a figure which is not in concordance with studies carried out by institutions, which indicates an increase in the frequency of new cases. This information is not necessarily due to a true increase in prevalence. Possibly this increase is related to improved methodology for clinical and paraclinical diagnosis, especially the use of magnetic resonance. There is a need for descriptive and analytical epidemiological studies to obtain precise data on this. At present, the Mexican Group for the study of Multiple Sclerosis and The Mexican Association for the study of Multiple Sclerosis are using a questionnaire designed and validated for Mexico in order to determine the clinical characteristics and the prevalence of multiple sclerosis. The results will be available in the near future to improve knowledge regarding the epidemiology of this disorder and its economic impact on the Mexican health systems.

Humans↗

PubMed2000

Acute aphasia in multiple sclerosis.

Acute aphasia is rare in multiple sclerosis. We describe 3 patients with multiple sclerosis who had acute exacerbations presenting as aphasias. One patient had a mixed transcortical aphasia, 1 had a transcortical motor aphasia, and 1 had a Broca aphasia. Magnetic resonance imaging scans of the brain with contrast enhancement revealed new white matter lesions in the left hemisphere in all 3 patients. Two of the 3 patients had a good response to treatment with methylprednisolone sodium succinate. Arch Neurol. 2000;57:1207-1209

Acute Disease↗

PubMed2005

Early B-cell Factor gene association with multiple sclerosis in the Spanish population.

BACKGROUND: The etiology of multiple sclerosis (MS) is at present not fully elucidated, although it is considered to result from the interaction of environmental and genetic susceptibility factors. In this work we aimed at testing the Early B-cell Factor (EBF1) gene as a functional and positional candidate risk factor for this neurological disease. Axonal damage is a hallmark for multiple sclerosis clinical disability and EBF plays an evolutionarily conserved role in the expression of proteins essential for axonal pathfinding. Failure of B-cell differentiation was found in EBF-deficient mice and involvement of B-lymphocytes in MS has been suggested from their presence in cerebrospinal fluid and lesions of patients. METHODS: The role of the EBF1 gene in multiple sclerosis susceptibility was analyzed by performing a case-control study with 356 multiple sclerosis patients and 540 ethnically matched controls comparing the EBF1 polymorphism rs1368297 and the microsatellite D5S2038. RESULTS: Significant association of an EBF1-intronic polymorphism (rs1368297, A vs. T: p = 0.02; OR = 1.26 and AA vs. [TA+TT]: p = 0.02; OR = 1.39) was discovered. This association was even stronger after stratification for the well-established risk factor of multiple sclerosis in the Major Histocompatibility Complex, DRB1*1501 (AA vs. [TA+TT]: p = 0.005; OR = 1.78). A trend for association in the case-control study of another EBF1 marker, the allele 5 of the very informative microsatellite D5S2038, was corroborated by Transmission Disequilibrium Test of 53 trios (p = 0.03). CONCLUSION: Our data support EBF1 gene association with MS pathogenesis in the Spanish white population. Two genetic markers within the EBF1 gene have been found associated with this neurological disease, indicative either of their causative role or that of some other polymorphism in linkage disequilibrium with them.

Chromosome Mapping↗

PubMed2000

Multiple sclerosis simulating a mass lesion.

The cases of two young women with a homonymous hemianopia are described. Both women had a progressively enlarging mass lesion that was seen with neuroimaging studies. One patient had neurologic deterioration despite intravenous corticosteroid treatment. In each case, results of a stereotactic biopsy showed demyelination that was consistent with multiple sclerosis. Multiple sclerosis infrequently presents as a mass lesion. The atypical clinical and radiographic features of large demyelinating plaques may lead to an erroneous diagnosis of a brain tumor, infection, or demyelination from other causes.

Adult↗

PubMed1981

The significance of abnormal immune responses in patients with multiple sclerosis.

Early diagnosis of multiple sclerosis (MS) may be assisted by tests for the abnormal immune responses of the central nervous system (CNS) including oligoclonal IgG bands in the cerebrospinal fluid (CSF), increased CNS IgG synthesis, increased CNS antibody synthesis against multiple viruses and increased numbers of enlarged lymphoid cells in the CSF. Alterations in immunological responses are important in the pathogenesis of MS. Further studies are needed, however, to identify the antigen(s) and/or antibodies responsible for oligoclonal IgG in the CSF of MS patients. Also, the cause(s) for the other immunological abnormalities with diagnostic importance need to be identified. The increased synthesis of antibodies against multiple unrelated viruses suggests generalized alteration in the immune regulatory system. The etiology of MS might be multifactorial involving abnormal immunological responses, possibly precipitated by infectious agents acquired during childhood by genetically susceptible individuals. The immunological responses including alterations in myelin basic protein concentration, antimyelin antibody and immune complex activities in CSF, and in vitro stimulation, suppression and migration inhibition of blood lymphocytes appear to correlate with stage of MS and severity of CNS damage. Some of the tests may become useful in estimating the prognosis of the disease. Longitudinal studies are needed to clarify the sensitivity of the diagnostic and prognostic immunological tests and etiological significance of these abnormalities in MS.

Antibodies, Viral↗

PubMed1996

Cognitive therapy for multiple sclerosis: a preliminary study.

BACKGROUND: Drug treatments for multiple sclerosis are expensive, may cause side effects, and do not have demonstrated efficacy for cognitive deficits associated with this disease. OBJECTIVE: To test the effectiveness of a multimodal cognitive therapy on cognitive and physical measures known to be affected in multiple sclerosis. DESIGN: Quasi-experimental wait-list control. SETTING: Alternative medicine clinic. PATIENTS: 27 persons with clinically definite multiple sclerosis. INTERVENTION: Multimodal cognitive therapy. MAIN OUTCOME MEASURES: Neuropsychological measures of verbal learning and memory, abstraction, vocabulary, and information processing speed; Beck Depression Inventory; tactile sensitivity of the hands; grip strength; and visual acuity. MAIN RESULTS: 12 of 14 patients in the therapy group and 10 of 13 patients in the control group completed 24 weeks of treatment and all assessments. Patients who received therapy showed significantly greater improvement in verbal learning, verbal abstraction, depression, and some measures of grip strength and tactile sensitivity than did patients in the untreated control group. The groups did not differ in the magnitude of change on vocabulary, information processing speed, or visual acuity. CONCLUSION: Cognitive therapy appears to be a promising treatment for ameliorating some symptoms of multiple sclerosis. A larger study with a randomized design and additional outcome measures is warranted.

Adult↗

PubMed1985

The acute deafness of definite multiple sclerosis: BAEP patterns.

Of 705 patients with or suspected of multiple sclerosis who underwent evoked potential recording during a 5 year period, 12 patients with definite multiple sclerosis experienced an acute hearing loss during a relapse of the demyelinating disease. Hearing loss was unilateral in all of the 12 cases but one; tinnitus was associated with hearing loss in 9 of the 12 patients. Deafness is an unfrequent symptom in the course of multiple sclerosis, being estimated to be no more than 3% in large series of multiple sclerosis. Brain-stem auditory evoked potentials were recorded in all 12 patients, during the relapse with acute hearing loss in 4 of them, after the relapse with hearing loss in the 8 others. During the relapse with hearing loss, BAEP abnormalities were present ipsilateral to the hearing loss in all 4 patients, wave I being absent in 2 of them. BAEPs were drastically improved when recorded after the relapse with hearing loss in 2 of the 3 patients in whom repeated records were made. BAEPs were abnormal on the side of the previous hearing loss in 5 out of the 8 patients recorded after the relapse with hearing loss. Clinical and BAEP data suggest that, in accordance with the anatomical organization of the auditory pathways, the lesion causing unilateral hearing loss in multiple sclerosis could be situated in the cochlear nerve or close to its entry zone in the brain-stem. However, dissociation between unilateral hearing loss and a normal peak I and I-III interval may occur.

Acoustic Stimulation↗

PubMed1997

Reduced bone mass and fat-free mass in women with multiple sclerosis: effects of ambulatory status and glucocorticoid Use.

Multiple sclerosis (MS) is associated with reduced bone mass and vitamin D deficiency. The underlying pathophysiology of the bone disease is uncertain, however, acute and long-term glucocorticoid use, progressive immobilization, vitamin D deficiency, and possibly skeletal muscle atrophy are likely to be determinants. The aims of this study were to determine (a) whether multiple sclerosis is associated with reduced fat-free mass and (b) whether in patients with multiple sclerosis, ambulation ability or glucocorticoid use is associated with bone mass and/or fat-free mass. Seventy-one female patients with MS were compared with 71 healthy, age-matched female controls. Total body bone mineral content (TBBMC, kg), fat mass (FM, kg), and fat-free mass (FFM, kg) were measured using dual X-ray absorptiometry. Disability status was graded according to the Kurtzke Expanded Disability Status Scale (EDSS) as ambulatory, with or without aide (EDSS score of 0 to 6.5), or predominantly wheelchair bound (EDSS score > 6.5). The patients with MS, when compared to age-comparable controls, had deficits in TBBMC ( approximately 8%, -0.3 +/- 0.1 SD, P < 0.04) and FFM ( approximately 5%, -0.3 +/- 0.1 SD, P < 0.01). Both TBBMC and FFM were negatively associated with EDSS score (r = 0.33, P < 0.01, and r = 0.41, P < 0.01, respectively). Patients with MS who were nonambulatory had even greater deficits in TBBMC and FFM as compared with age-matched controls (-0.6 +/- 0.1 SD, P < 0.01, and -0.6 +/- 0. 1 SD, P < 0.01, respectively). By contrast, as compared with age-comparable controls, ambulatory patients with MS had no deficits in bone mass or soft tissue mass. When compared with ambulatory patients with MS, nonambulatory patients with MS had deficits in TBBMC and FFM (P < 0.01 and P < 0.01, respectively). The difference in TBBMC was largely caused by the difference in fat-free mass, whereas the difference in FFM was largely caused by the difference in glucocorticoid use based on analysis of covariance. We conclude that in patients with multiple sclerosis, physical disuse is the main determinant for the reduction in bone mass. Glucocorticoid treatment is the major determinant of the reduction in fat-free mass and thus also contributes to the reduction in bone mass.

Adipose Tissue↗