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PubMed1999

Surgical outcome in patients with coexisting multiple sclerosis and spondylosis.

OBJECTIVES: Multiple sclerosis (MS) is a neuro-degenerative disease of unknown etiology which results in destruction of myelin. A variety of neurologic signs and symptoms are associated with MS and include myelopathy, extremity weakness, low back pain, sciatica and paresthesias. Many of these signs and symptoms are identical to those experienced by patients with spondylosis (e.g. spinal stenosis, disc herniations). The coexistence of MS with spondylosis can be problematic both for diagnosis and treatment. MATERIALS AND METHODS: During the period 1992 to 1996 we identified 7 patients with previously diagnosed MS who developed new syndromes which were thought to be related to a variety of degenerative spine conditions. The diagnosis of MS was based on standard clinical, immunological and neuroradiological criteria. RESULTS: Five of 7 patients demonstrated significant improvement after surgery. One patient experienced a transient MS exacerbation after surgery. CONCLUSIONS: From our series we concluded that surgery for degenerative spine conditions can be performed in a safe and effective manner in patients with coexisting multiple sclerosis.

Adult↗
PubMed1997

The controversy surrounding the pathogenesis of the multiple sclerosis lesion.

The main issues in multiple sclerosis research revolve around four fundamental questions. (1) What initiates the disease-that is, autoimmune T cells, a virus, or a toxin? (2) Is the inflammatory response primary to the development of demyelination, or is it a secondary response to injury? (3) Is the oligodendrocyte, the myelin-producing cell, the primary target? (4) How can myelin repair be promoted? This review focuses on the controversies revolving around these important questions. Although many investigators believe that T-cell receptors on CD4+ cells interact with myelin antigens to initiate an inflammatory cascade that leads to myelin destruction, others maintain that a viral agent may have a direct or indirect role in the pathogenesis of multiple sclerosis. The concept that the immune system contributes to the tissue destruction in multiple sclerosis is generally accepted; however, the debate about cause versus consequence of the pathologic process remains unresolved, as does the identification of the initial event or focus of the damage. Electron microscopic studies have disclosed evidence of remyelination (albeit often incomplete) in lesions of multiple sclerosis. Enhanced understanding of the factors limiting remyelination could help formulate strategies to promote repair. By innovative experimental design and application of available molecular techniques, the answers to these questions may provide insights on how to prevent or treat multiple sclerosis.

Animals↗
PubMed1999

Progress in determining the causes and treatment of multiple sclerosis.

The cause of multiple sclerosis remains unknown after more than a century of study. Unconfirmed work has once more indicated that a viral infection may be important in the aetiology of the disease, and there is considerable evidence for an important genetic influence on disease susceptibility. The clinical course is as variable as that of any disease in medicine. Studies using serial magnetic resonance imaging have helped to define the disease course and response to experimental therapies. Although the predominant pathological characteristic is myelin loss with preservation of axons, some studies recall classic descriptions that irreversible axonal destruction may occur, perhaps even in the early stages of the illness. There are now several, partially effective therapies for relapsing forms of multiple sclerosis and here I review progress in determining the timing and course of the illness and the steps that need to be taken to identify more effective treatments for this disease.

Animals↗
PubMed1997

Age at immigration to England of Asian and Caribbean immigrants and the risk of developing multiple sclerosis.

OBJECTIVES: Previous studies have shown that multiple sclerosis is very uncommon among Indian and Pakistani immigrants to England but that their children born in the United Kingdom, in the age groups available for study, have a similar risk of developing the disease as occurs in the general British population. The present study was to ascertain if these immigrants who enter England as children below the age of 15, have a higher risk of developing multiple sclerosis than those that enter after this age. METHODS: A search was made in Greater London, the West Midlands, Leicester, Bradford, Halifax, and Huddersfield to find ethnic Indian, Pakistani, and Bangladeshi immigrants to England with multiple sclerosis. During the course of the study some immigrants from the Caribbean with multiple sclerosis were also found. The population at risk by ethnic group and age at entry was not available from the 1991 Census but was available in the annual Labour Force Surveys. RESULTS: Indian and Pakistani immigrants who entered England younger than 15 had a higher risk of developing multiple sclerosis than those that entered after this age. Caribbean immigrants, who have a higher multiple sclerosis prevalence than Asian immigrants, did not show this difference. CONCLUSION: This study confirms previous studies which show that the environment during childhood is a major factor in determining the risk of developing multiple sclerosis.

Adolescent↗
PubMedDate not supplied

[Prevalence of multiple sclerosis in Colombia].

INTRODUCTION: Multiple sclerosis (MS) is the commonest demyelinating condition of the nervous system. It is characterized by numerous demyelinating areas or plaques of demyelination which are found dispersed throughout the nervous system. It has been shown that MS is less frequent in tropical regions than in subtropical regions. In Latin America particularly, there are some studies which show this phenomenon. However, in Colombia no studies of prevalence of MS have been done. OBJECTIVE: To determine the prevalence of multiple sclerosis in five provinces of Colombia (Antioquia, Caldas, Santander, Risaralda and Bolivar). PATIENTS AND METHODS: The capture-recapture method was used for two sources to determine the number of cases defined on the criteria of Poser et al seen between July 1995 and June 2000. RESULTS: The prevalence (cases of MS per 100,000 inhabitants) varied between 1.48 in Antioquia (95% CI 1.12; 1.78) and 4.98 in Risaralda (95% CI 3.52; 6.43). Seventy two percent were women. The regions included in this study represented 25% of the population of Colombia. CONCLUSIONS: There is a low prevalence of MS which is as expected in tropical areas. Persons with MS in these regions may be very useful in the study of other factors involved in the aetiology of MS (genetic). The capture-recapture method is an excellent tool for carrying out prevalence studies since it is cheap and requires little time.

Colombia↗
PubMed1999

EBV-induced expression and HLA-DR-restricted presentation by human B cells of alpha B-crystallin, a candidate autoantigen in multiple sclerosis.

The development of multiple sclerosis is most likely influenced by autoimmune responses to central nervous system myelin proteins as well as by infections with common viruses such as EBV and human herpesvirus-6. However, much remains to be established on how these factors interact. In this study, we show that upon EBV infection, human B cells start to express alpha B-crystallin, a small stress protein that was identified previously as an immunodominant Ag of CNS myelin in multiple sclerosis patients. EBV-induced expression of alpha B-crystallin in B cells leads to HLA-DR-restricted presentation of the protein and to activation of proinflammatory alpha B-crystallin-specific Th cells. While alpha B-crystallin is present in EBV-infected human B cells, the protein is absent from human lymphoid tissues under normal conditions. This is in sharp contrast to other stress proteins such as heat-shock protein (hsp)27 and hsp60 that are ubiquitously expressed in these tissues. In addition, the absence of alpha B-crystallin from lymphoid tissues in humans is unique as compared with other mammals. All other species examined, including rodents, sheep, and primates, showed constitutive expression of alpha B-crystallin in secondary lymphoid tissues and sometimes even in the thymus. Since constitutive lymphoid expression most likely results in immunologic tolerance, such a state of tolerance to alpha B-crystallin can be expected for all of these species, but not for humans. When taken together, our data provide evidence for a novel mechanism by which common viral infections can trigger myelin-directed autoimmunity in a way that is unique for humans.

Animals↗
PubMed1980

[Computed tomography in multiple sclerosis].

Sixty patients with multiple sclerosis were examined by computed tomography using an Acute 200 Pfizer apparatus (matrix: 256 X 256; sections: 8 mm thick). In 48 cases iodine contrast medium was injected prior to examination, and in 6 cases the examination was repeated after several months. Abnormal C.T. readings were found in three quarters of the patients; increased image density in 10 patients, reduced density in 10 other cases; isolated cerebral atrophy in 26 patients, associated in 10 other cases with increased or reduced density of the image. Increased densities were seen mainly during acute episodes, then tended to isodensities or low densities. Though these different images are not specific, their association, the absence of mass effect and the absence of correlation between their location and the clinical signs, are elements in favor of the diagnosis of multiple sclerosis. Regions of increased density probably represent active foci of demyelinization and their investigation could be of value during long-term follow-up of these patients.

Adult↗
PubMed1996

Multiple sclerosis: sunlight, diet, immunology and aetiology.

Multiple sclerosis is more common in temperate latitudes, and migration studies indicate the involvement of an aetiological environmental factor in pre-pubertal life; the precise nature of this factor has never been identified and may perhaps have been overlooked. Here we suggest a simple explanation for the latitude gradient of multiple sclerosis, i.e. that it can be explained by the immunosuppressant effects of sunlight mediated via suppression of the secretion of the immunostimulatory neurohormone melatonin from the pineal gland. The effects of dietary fatty acids in multiple sclerosis also indicate the involvement of anti-inflammatory eicosanoids in its pathogenesis. We further suggest that the exceptions to the latitude gradient (e.g. Japan), which have previously been attributed to genetic factors, may in fact have a dietary basis. Since sunlight also influences the metabolism of fatty acids in the retina, it may also influence the development of retrobulbar optic neuritis-a common antecedent of multiple sclerosis. We suggest a re-examination of the epidemiology of multiple sclerosis based on an understanding of the immunological consequences of illumination of the retina by sunlight.

Autoimmunity↗
PubMedDate not supplied

Multiple sclerosis and oral care.

Multiple sclerosis is a complex neurological condition affecting sensory and motor nerve transmission. Its progression and symptoms are unpredictable and vary from person to person as well as over time. Common early symptoms include visual disturbances, facial pain or trigeminal neuralgia and paraesthesia or numbness of feet, legs, hands and arms. These, plus symptoms of spasticity, spasms, tremor, fatigue, depression and progressive disability, impact on the individual's ability to maintain oral health, cope with dental treatment and access dental services. Also, many of the medications used in the symptomatic management of the condition have the potential to cause dry mouth and associated oral disease. There is no cure for multiple sclerosis, and treatment focuses on prevention of disability and maintenance of quality of life. Increasingly a multi-disciplinary team approach is used where the individual, if appropriate his/her carer, and the specialist nurse are key figures. The dental team plays an essential role in ensuring that oral health impacts positively on general health.

Adult↗
PubMed1989

Measles virus-polypeptide specificity of the cytotoxic T-lymphocyte response in multiple sclerosis.

Some patients with multiple sclerosis (MS) have been shown previously to have a reduced capacity to generate measles virus (MV)-specific cytotoxic T-lymphocytes (CTLs). The mechanism of this reduction is not understood. Possibilities include sequestration of MV-CTLs within the central nervous system (CNS), abnormalities in regulation of this response (e.g., suppression), a defect in the T-cell repertoire of MS patients and a defect in the induction or maintenance of the CTL response to MV. To examine these possibilities, the CTL response to three purified polypeptides of MV (hemagglutinin (HA), fusion (F), and nucleocapsid (NC] was studied in eight healthy controls and 14 patients with multiple sclerosis. A defect in the response to two polypeptides of the virus (HA and NC) was found in the MS patients with reduced MV-CTL response. The response to F was also reduced but to a lesser extent. Limiting dilution analysis of the MV polypeptide-specific CTL response indicated that suppression is an unlikely cause for the reduction in CTL activity. The lymphoproliferative response to MV, HA, F, and NC was comparable in three MS patients and three controls examined. Together, the results of these studies indicate that the reduced MV-CTL response in MS patients was not due to a defect in the T-cell repertoire or sequestration due to cross-reactivity with a single myelin antigen. More likely mechanisms include abnormalities in the induction or maintenance of the MV-CTL response or sequestration within the CNS due to recognition of MV antigens.

Capsid↗
PubMed2000

Evaluation of the apo-1/Fas promoter mva I polymorphism in multiple sclerosis.

The pathogenesis of multiple sclerosis is under strong genetic control involving several or more genes each of modest effect. Whilst the mechanisms underlying the pathogenesis of MS remain unknown, it has been hypothesised that either decreased apoptosis of autoreactive T cells in the CNS, or increased apoptosis of oligodendrocytes may play an important role. The Apo-1/Fas antigen (CD95), the gene for which is located in a chromosomal region showing linkage in MS genome screens, is a critical inducer of apoptosis and studies have shown aberrant expression of this molecule in MS, correlating with a decrease in T cell apoptosis or increase in CNS tissue damage. This study investigated an Mva I polymorphism in the Apo-1/Fas promoter region in a group of 124 Australian patients with relapsing-remitting MS and in 183 normal controls. Whilst there were increases in the Mva I*2 allele in MS individuals overall (59% vs 52%, P not corrected=0.08), and in HLA-DRB1*1501 negative MS patients (62% vs 55%), these were not significantly different from controls. Interactions were investigated between the Mva I alleles and T cell receptor beta chain variable region (TCRBV) germline polymorphisms, with a trend in MS individuals towards a decrease of the Mva I*1 allele when combined with the TCRBV3S1*2 allele (Relative Risk=0.25, P=0.067), and with the TCRBV8S1*1 allele (Relative Risk=0.44, P=0.12). Overall, the findings of this study indicate a possible effect of the Apo-1/Fas promoter Mva I polymorphism in MS susceptibility, which needs to be confirmed in further studies. Multiple Sclerosis (2000) 6 14 - 18

Alleles↗
PubMed1996

Transient increase in symptoms associated with cytokine release in patients with multiple sclerosis.

Fourteen patients with multiple sclerosis were treated with the humanized monoclonal antibody CAMPATH-1H which targets the CD52 antigen present on all lymphocytes and some monocytes; four also received anti-CD4 antibody. Lymphopaenia developed rapidly and was sustained for at least 1 year. In 12 patients, the first infusion of antibody was characterized by significant exacerbation or re- awakening of pre-existing symptoms lasting several hours. These clinical effects of antibody treatment correlated with increased levels of circulating cytokines. Peak levels of tumour necrosis factor (TNF)-alpha and interferon (IFN)-gamma occurred at 2 h, whereas the rise in interleukin-6 (IL-6) was significantly delayed and peaked at 4 h after starting antibody treatment. There was a decline in CH50, indicating complement activation. The neurological symptoms could not be attributed directly to pyrexia and were not provoked (in one patient) by an artificial rise in temperature. In the remaining two patients, a single pre-treatment with intravenous methylprednisolone (500 mg) prevented both the transient increase in neurological symptoms and the cytokine release. Our results, involving 14 intensively studied patients treated with humanized monoclonal antibodies, suggested that soluble immune mediators contribute to symptom production in multiple sclerosis; the mechanism remains uncertain but, on the available evidence, we favour the interpretation that cytokines directly affect conduction through partially demyelinated pathways.

Adult↗
PubMed1994

Multiple sclerosis.

Differences in the risk of multiple sclerosis depending on racial background, and the high clinical concordance rates in monozygotic compared with dizygotic twins, have stimulated attempts to identify and locate genes that confer susceptibility to the disease. The risk of multiple sclerosis is increased from 1 in 800 in northern European Caucasians to 1 in 3 in the monozygotic co-twins of affected individuals, with intermediate rates for siblings, offspring and more distant relatives. Concordance rates in monozygotic and dizygotic co-twins of affected individuals rise to 35% and 15%, respectively when magnetic resonance imaging is used to supplement clinical evidence for disease status. The increased recurrence risk in relatives of patients with multiple sclerosis is consistent with a model in which more than one gene contributes to susceptibility. Population studies have demonstrated an association with the class 2 major histocompatibility complex (MHC) phenotypes DR15 and DQw6 and their corresponding genotypes DRB1.1501, DRB5.0101 and DQA1.0102, DQB2.0602. An extensive search, using population studies, for other polymorphic alleles involved in restriction of the immune response may have yielded an additional candidate gene in the VH2-5 immunoglobulin heavy-chain variable region. Identity by descent analysis of candidate genes encoded within the alpha-chain of the T-cell receptor and the gene for myelin basic protein has failed to demonstrate linkage; paradoxically, this is also true for the MHC class 2 region, despite the population association. However, studies involving a large number of sibling pairs have reported a bias in the distribution of T-cell receptor beta-chain variable region haplotype sharing, favouring linkage. This becomes more marked when stratification is made for the presence of DR2 in both affected siblings, suggesting an interaction between genetic polymorphisms encoded within the MHC and T-cell receptor genes, as expected from their known functional co-operation in antigen presentation. The same is true for the immunoglobulin heavy chain, providing provisional evidence for linkage to a gene encoded within the immunoglobulin heavy-chain variable region in families reported from the UK. Taken together, these findings demonstrate the importance of family studies in elucidating the genetic basis of multiple sclerosis, and confirm that several genes are involved, one or more of which regulates genetic restriction of the immune response. The contribution made by the susceptibility genes that have provisionally been identified, occurring in isolation or together, can account for only a proportion of the increased risk of multiple sclerosis implicated by family studies.(ABSTRACT TRUNCATED AT 250 WORDS)

Genes↗
PubMed1998

The prevalence of multiple sclerosis in the Leeds Health Authority.

OBJECTIVES: To determine the prevalence of multiple sclerosis in the Leeds Health District. METHODS: Multiple sources of case ascertainment were used-namely, neurology departments, hospital episode statistics, general practitioners, the Leeds branch of the Multiple Sclerosis Society, the West Yorkshire Multiple Sclerosis Therapy Centre, community physiotherapists and occupational therapists, the Leeds Wheelchair Centre, and the Young Disabled Unit. Data collection was from retrospective analysis of hospital and primary care case records. A population based incidence register was established by prospectively registering all new patients with diagnoses of multiple sclerosis. RESULTS: On prevalence day, 30 April 1996, 712 people with multiple sclerosis were identified living in Leeds (population 732,061), giving a prevalence of 97/10(5). The prevalence for definite and probable multiple sclerosis was 84/10(5), and for suspected multiple sclerosis it was 13/10(5). The sex ratio of prevalent people with multiple sclerosis was 2.79 to 1 women to men. The mean age of prevalent cases was 51 years, the mean age at symptom onset was 34 years, and the mean duration of disease was 16 years. Forty cases were prospectively reported as incident cases from 1 November 1995 to 1 February 1996. CONCLUSIONS: The prevalence of multiple sclerosis in Leeds was found to be similar to that in the south of the United Kingdom but lower than that in Scotland. There is no evidence of a latitudinal gradient of increasing prevalence of multiple sclerosis from the south to the north of England.

Adult↗
PubMed1981

Concurrence of multiple sclerosis and primary intracranial neoplasms.

The concurrence of multiple sclerosis and primary intracranial neoplasms is uncommon. The literature contains 20 cases of multiple sclerosis associated with gliomas and nine cases with non-gliomatous neoplasms. This report describes a protoplasmic astrocytoma and arteriovenous malformation found incidentally at autopsy of a 63-year-old woman with a 25-year history of multiple sclerosis. This is the first demonstrated association of multiple sclerosis with an arteriovenous malformation. Although neoplastic transformation of reactive glial cells in multiple sclerosis plaques has been proposed as the source of gliomas, the association of multiple sclerosis with astrocytoma and arteriovenous malformation in the present case is considered to be coincidental. Gliomas reported in association with multiple sclerosis are more frequently (30%) multicentric than are uncomplicated gliomas.

Astrocytoma↗
PubMed2003

[Therapy of day time fatigue in patients with multiple sclerosis].

Fatigue is the most common symptom of multiple sclerosis. 75%-90% of patients with multiple sclerosis report having fatigue, and 50%-60% describe it as the worst symptom of their disease. Fatigue is significantly associated with reduced quality of life and is also a major reason for unemployment, especially for patients with otherwise minor disability. The mechanisms underlying abnormal levels of fatigue in multiple sclerosis are poorly understood. To date, drug treatment has been only partially successful in alleviating fatigue, and effects vary widely from patient to patient. Amantadine and modafinil showed to be effective in the treatment of fatigue in some studies. Non-pharmacological management of fatigue in multiple sclerosis includes inpatient rehabilitation and endurance training. There is also evidence, that pulsing electromagnetic fields may improve fatigue associated with multiple sclerosis. This paper summarizes the recent literature on pathophysiology, diagnosis and therapy of the most common symptom of multiple sclerosis.

Central Nervous System Stimulants↗
PubMed2003

Early clinical predictors and progression of irreversible disability in multiple sclerosis: an amnesic process.

Prognosis of multiple sclerosis is highly variable. Clinical variables have been identified that are assessable early in the disease and are predictors of the time from the disease onset to the onset of irreversible disability. Our objective was to determine if these clinical variables still have an effect after the first stages of disability have been reached. We determined the dates of disease onset and assignment of scores of irreversible disability in 1844 patients with multiple sclerosis. We used three scores on the Kurtzke Disability Status Scale as benchmarks of disability accumulation: 4 (limited walking but without aid); 6 (walking with unilateral aid); and 7 (wheelchair bound). We used Kaplan-Meier analyses and Cox regression models to determine the influence of the clinical variables on the time to disability onset. Median times from onset of multiple sclerosis to assignment of a score of 4, 6 and 7 were significantly influenced by gender, age, symptoms and course (relapsing-remitting or progressive) at onset of the disease, degree of recovery from the first relapse, time to a second neurological episode, and the number of relapses in the first 5 years of the disease. Similarly, times from onset of multiple sclerosis to a score of 6 and 7 were influenced by time to a score of 4. In contrast, none of the variables substantially affected the time from a score of 4 to a score of 6 or 7, or from a score of 6 to a score of 7. Early assessable clinical variables significantly influence the time from the onset of multiple sclerosis to the assignment of a disability score of 4, but not the subsequent progression of irreversible disability.

Adolescent↗