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PubMed2001

Epileptic and non-epileptic seizures in multiple sclerosis.

Knowledge concerning the relationship between multiple sclerosis and epilepsy is reviewed. Epidemiological studies have established that epileptic seizures are more frequent in multiple sclerosis than predicted by chance. Partial epilepsies with focal seizures often with atypical symptoms and with or without secondary generalisation are the usual pattern. In the survey special emphasis is laid on the direct correlation between paroxysmal phenomena and plaques now demonstrable by modern imaging techniques. These images have shown that epileptic seizures can be caused by cortical and subcortical lesions and by their accompanying oedema. We extend the review to non-epileptic paroxysmal symptoms, such as tonic spasm, which may be confused with epileptic seizures. As far as they are supported by data, recommendations for diagnosis and therapy are given. Open questions are identified and issues for further research are suggested.

Anticonvulsants↗

PubMed1994

Neuro-ophthalmology of multiple sclerosis.

Neuro-ophthalmic manifestations are important in multiple sclerosis. Optic neuritis is a frequent harbinger of the disease, and is characterized by subacute painful visual loss, with disproportionate loss of color and contrast sensitivity, central or cecocentral scotoma, and an afferent pupillary defect. Visual recovery is the rule, but tests have been developed to detect most cases of recovered optic neuritis. Intraocular inflammation has come to be recognized as a frequent accompaniment of multiple sclerosis. Because of the predilection of multiple sclerosis for the infratentorial white matter, defects in eye movement control are common, particularly internuclear ophthalmoplegias and nystagmus.

Humans↗

PubMed1984

[Complement markers Bf and C4 in multiple sclerosis].

Some immunogenetic HLA markers are significantly correlated with multiple sclerosis, e.g.: the antigens B7, DR2, and the associations B7-DR2, A3-B7-DR2. In addition, the polymorphism of the allotypes Bf and C4 is also controlled by chromosome 6; a study of these markers is therefore of interest. The study of Bf and C4 in multiple sclerosis included a population of genotyped unrelated patients: 50 patients for Bf markers and 41 for C4A and C4B markers. This study revealed an over-representation of allotype S and homozygous BfSS in multiple sclerosis. BfSS homozygote was significantly more frequent in the B7 negative and/or DR2 negative patients, i.e. when the risk markers per se were absent. No correlation could be evidenced with the remittent or progressive character of the disease. These data, obtained from the study of C4, are still preliminary ones. The results found with the Bf markers confirm the existence of a genetic factor in multiple sclerosis and suggest that the susceptibility gene of the disease could be closer to locus Bf than to locus DR.

Chromosomes, Human, 6-12 and X↗

PubMed2006

Antibiotic use and risk of multiple sclerosis.

Some reports suggest that bacteria, including Chlamydophila pneumoniae, could be involved in the etiology of multiple sclerosis. If that is true, persons who used antibiotics active against these bacteria, compared with nonusers, might be at lower risk of multiple sclerosis. Using a 1993-2000 case-control study nested in the United Kingdom-based General Practice Research Database cohort, the authors identified 163 multiple sclerosis cases who were followed up for at least 3 years before their first symptoms (the index date). Up to 10 controls matched to the cases by age, sex, general practice, and time in the cohort were selected. Exposure to antibiotics was assessed through computerized medical records. Overall antibiotic use or use of antibiotics against C. pneumoniae was not associated with multiple sclerosis risk. However, use of penicillins in the 3 years before the index date decreased the risk of developing a first attack of multiple sclerosis (odds ratio=0.5, 95% confidence interval: 0.3, 0.9 for those who used penicillins for >or=15 days compared with no use). In conclusion, use of antibiotics active against C. pneumoniae was not associated with a decreased risk of short-term multiple sclerosis. The observed lower risk of multiple sclerosis for penicillin users needs to be confirmed in other populations.

Adult↗

PubMedDate not supplied

Migrant studies in multiple sclerosis.

To re-evaluate how migrant studies contribute to our understanding of the epidemiology and aetiology of multiple sclerosis, we undertook a systematic review of all relevant studies published in English language journals, comparing rates of multiple sclerosis in migrant populations with those in the host country and in the country of origin. Interpretation of migrant studies is difficult. Migrants are seldom representative of the country of origin, tending to be younger, healthier and of higher socioeconomic status. Data quality may be poor, and lack of age-standardisation can mislead when rates are compared. Nevertheless, two consistent patterns can be discerned in these studies of the effect of migration on risk of multiple sclerosis. Migrants who move from an area where the disease is common to an area where it is rarer show a decrease in rate of disease. By contrast, people who migrate in the opposite direction tend to retain the low risk of their country of origin. Results from the few studies which have examined the effect of age at migration on risk of multiple sclerosis suggest that an individual's risk of the disease is largely established during the first two decades of life. Risk of multiple sclerosis can change rapidly between generations: although migrants from low risk countries to high risk countries retain their low risk, their children have a risk of multiple sclerosis that approaches that of the host country. Migrant studies add little to our understanding of the genetics of multiple sclerosis but they emphasise the importance of environmental factors. We discuss several possible interpretations of the patterns seen in migrant studies, including the hypothesis that multiple sclerosis is a sequel to delayed exposure to a common infectious agent. One candidate for such an infectious agent is Epstein-Barr virus.

Age Factors↗

PubMed2001

Assessing the risk of early multiple sclerosis in patients with clinically isolated syndromes: the role of a follow up MRI.

OBJECTIVES: With increasing evidence that permanent tissue damage occurs early in the course of multiple sclerosis, it is important that treatment trials include patients in the earliest stages of the disease. For many patients with multiple sclerosis the first presentation is a clinically isolated syndrome. Not all patients with a clinically isolated syndrome develop multiple sclerosis, however, and treatment of all such patients would be unwarranted. A single abnormal brain MRI identifies patients at a higher risk for the early development of multiple sclerosis, but current criteria are limited by either poor specificity (T2 lesions) or sensitivity (contrast enhancing lesions). The aim of the study was to assess the positive predictive value, sensitivity, and specificity of MRI indices for the development of multiple sclerosis after 1 year from two MRI examinations obtained 3 months apart. METHODS: MRI examinations were performed in 68 patients with a clinically isolated syndrome, with a clinical assessment after 1 year. RESULTS: Contrast enhancing lesions at both time points were the most predictive indices for developing multiple sclerosis (positive predictive value 70%) but had low sensitivity (39%). The combination of T2 lesions at baseline with new T2 lesions at follow up had the best overall positive predictive value (53%), sensitivity (83%), and specificity (76%). In patients with T2 lesions at baseline, the presence or absence of new T2 lesions at follow up significantly altered the risk of multiple sclerosis within 1 year (55% and 5% respectively, p<0.001). Multiple sclerosis also developed in 10% of patients with a normal baseline MRI. CONCLUSIONS: Serial imaging in patients with clinically isolated syndromes improved the positive predictive value, sensitivity, and specificity of MRI for the development of early multiple sclerosis and also identified patients at a lower risk of early multiple sclerosis than would have been expected from their abnormal baseline MRI. Selection of patients with clinically isolated syndromes for therapeutic intervention or clinical trials may benefit from serial MRI, to target those at greatest risk of early development of multiple sclerosis.

Adolescent↗

PubMed2005

Modulating processes within the central nervous system is central to therapeutic control of multiple sclerosis.

Historically considered to be an autoimmune demyelinating disease, multiple sclerosis is now recognized to be characterized by significant axonal and neuronal pathology. Addressing this neurodegenerative component of the disease is an important treatment objective, since axonal injury is believed to underlie the accumulation of disability and disease progression. The precise relationship between the inflammatory and neurodegenerative components in multiple sclerosis remains poorly elucidated, although neurodegeneration appears to be at least partially independent from neuroinflammation. The mechanisms underlying axonal injury appear complex and are likely to be multifactorial. Specific treatment strategies need to be developed that act within the central nervous system to prevent neurodegeneration and need to be provided from the earliest stages of disease. It is likely that immunomodulatory treatments acting purely in the periphery will provide only indirect and not direct neuroprotection. A promising approach is to enhance neuroprotective autoimmunity inside the brain, believed to be mediated, at least in part, by the release of neurotrophic factors within the nervous system from infiltrating immune cells. Such a beneficial process would be inhibited by a non-selective immunosuppressive strategy. In summary, treatments of multiple sclerosis should take into account the heterogeneous pathophysiology of the disease. The pathogenic process in the central nervous system itself should be the major focus in multiple sclerosis therapy in order to protect against demyelination and axonal loss and to promote remyelination and regeneration directly in the target tissue, independently of peripheral immune status. In conclusion, selective treatment strategies aimed at preventing axonal injury within the central nervous system are required to complement existing, peripherally acting treatments targeting the immune system.

Animals↗

PubMed1997

Multiple sclerosis: re-expression of a developmental gene in chronic lesions correlates with remyelination.

Central nervous system tissue from multiple sclerosis and non-multiple sclerosis subjects was studied for the expression of exon 2 myelin basic protein gene products at the protein and message levels by immunocytochemistry and in situ hybridization, respectively. The exon 2-encoded protein sequence is normally expressed during development (myelination) within the 21.5- and 20.2-kd isoforms of myelin basic protein and is downregulated in the adult central nervous system where the 18.5- and 17.2-kd isoforms predominate, the latter devoid of exon 2 owing to alternative splicing. Exon 2 myelin basic protein gene products were readily demonstrable in multiple sclerosis samples, the highest levels correlating with remyelination in chronic lesions while normal adult central nervous system and non-multiple sclerosis material showed very low levels and fetal human central nervous system tissue (a positive control) showed high levels. We conclude that recapitulation of ontogenetic events during myelin repair accounts for the increased expression of the exon 2-encoded protein sequence in the adult central nervous system during multiple sclerosis, an event that might underly the previously observed T-cell activation to this protein sequence during relapses.

Acute Disease↗

PubMed1993

The effect of corticosteroids for acute optic neuritis on the subsequent development of multiple sclerosis. The Optic Neuritis Study Group.

BACKGROUND: Optic neuritis is often the first clinical manifestation of multiple sclerosis, but little is known about the effect of corticosteroid treatment for optic neuritis on the subsequent risk of multiple sclerosis. METHODS: We conducted a multicenter study in which 389 patients with acute optic neuritis (and without known multiple sclerosis) were randomly assigned to receive intravenous methylprednisolone (250 mg every six hours) for 3 days followed by oral prednisone (1 mg per kilogram of body weight) for 11 days, oral prednisone (1 mg per kilogram) alone for 14 days, or placebo for 14 days. Neurologic status was assessed over a period of two to four years. The patients in the first group were hospitalized for three days; the others were treated as outpatients. RESULTS: Definite multiple sclerosis developed within the first two years in 7.5 percent of the intravenous-methyl-prednisolone group (134 patients), 14.7 percent of the oral-prednisone group (129 patients), and 16.7 percent of the placebo group (126 patients). The adjusted rate ratio for the development of definite multiple sclerosis within two years in the intravenous-methylprednisolone group was 0.34 (95 percent confidence interval, 0.16 to 0.74) as compared with the placebo group and 0.38 (95 percent confidence interval, 0.17 to 0.83) as compared with the oral-prednisone group. The beneficial effect of the intravenous-steroid regimen appeared to lessen after the first two years of follow-up. Signal abnormalities on magnetic resonance imaging (MRI) of the brain were a strong indication of risk for the development of definite multiple sclerosis (adjusted rate ratio in patients with three or more lesions, 5.53; 95 percent confidence interval, 2.41 to 12.66). The beneficial effect of treatment was most apparent in patients with abnormal MRI scans at entry. CONCLUSIONS: In patients with acute optic neuritis, treatment with a three-day course of high-dose intravenous methylprednisolone (followed by a short course of prednisone) reduces the rate of development of multiple sclerosis over a two-year period.

Acute Disease↗

PubMed2006

Serum 25-hydroxyvitamin D levels and risk of multiple sclerosis.

CONTEXT: Epidemiological and experimental evidence suggests that high levels of vitamin D, a potent immunomodulator, may decrease the risk of multiple sclerosis. There are no prospective studies addressing this hypothesis. OBJECTIVE: To examine whether levels of 25-hydroxyvitamin D are associated with risk of multiple sclerosis. DESIGN, SETTING, AND PARTICIPANTS: Prospective, nested case-control study among more than 7 million US military personnel who have serum samples stored in the Department of Defense Serum Repository. Multiple sclerosis cases were identified through Army and Navy physical disability databases for 1992 through 2004, and diagnoses were confirmed by medical record review. Each case (n = 257) was matched to 2 controls by age, sex, race/ethnicity, and dates of blood collection. Vitamin D status was estimated by averaging 25-hydroxyvitamin D levels of 2 or more serum samples collected before the date of initial multiple sclerosis symptoms. MAIN OUTCOME MEASURES: Odds ratios of multiple sclerosis associated with continuous or categorical levels (quantiles or a priori-defined categories) of serum 25-hydroxyvitamin D within each racial/ethnic group. RESULTS: Among whites (148 cases, 296 controls), the risk of multiple sclerosis significantly decreased with increasing levels of 25-hydroxyvitamin D (odds ratio [OR] for a 50-nmol/L increase in 25-hydroxyvitamin D, 0.59; 95% confidence interval, 0.36-0.97). In categorical analyses using the lowest quintile (<63.3 nmol/L) as the reference, the ORs for each subsequent quintile were 0.57, 0.57, 0.74, and 0.38 (P = .02 for trend across quintiles). Only the OR for the highest quintile, corresponding to 25-hydroxyvitamin D levels higher than 99.1 nmol/L, was significantly different from 1.00 (OR, 0.38; 95% confidence interval, 0.19-0.75; P = .006). The inverse relation with multiple sclerosis risk was particularly strong for 25-hydroxyvitamin D levels measured before age 20 years. Among blacks and Hispanics (109 cases, 218 controls), who had lower 25-hydroxyvitamin D levels than whites, no significant associations between vitamin D and multiple sclerosis risk were found. CONCLUSION: The results of our study suggest that high circulating levels of vitamin D are associated with a lower risk of multiple sclerosis.

Adolescent↗

PubMedDate not supplied

[Multiple sclerosis lesions simulating an expansive process on CT].

Patients with multiple sclerosis may present clinical data suggestive of cerebral tumor. It has been accepted that multiple sclerosis failed to show expansive signs in the computerized tomography (CT). However, since 1979 a total number of 13 patients have been reported to have expansive images at the CT. We report 3 cases with clinical symptoms suggesting a cerebral tumor associated with expansive signs at the CT. The subsequent follow-up of these patients confirmed the diagnosis of clinically defined multiple sclerosis. The management of these patients is difficult. Those patients with previous history suggestive of multiple sclerosis should be probably treated with steroids and followed with serial CT. If a clear recovery was not achieved in a relatively short term, a cerebral biopsy is recommended to rule out a neoplasm. When the clinical presentation begins with signs suggestive of a neoplasm, the cerebral biopsy is recommended.

Adult↗

PubMed1976

Direct leukocyte migration inhibition in multiple sclerosis--a possible assessment of activity.

Twenty-four patients with multiple sclerosis were evaluated and classified according to their clinical state. Specific migration inhibition studies were carried out on blood samples from each using myelin basic protein, an acid soluble protein fraction isolated from normal human CNS white matter, and multiple sclerosis myelin basic protein isolated from patients who had the disease, as the antigenic material. This test system employed selected media. Results were compared with those of normal controls and patients with other neurological disease states. Antigen concentration of 500 mu g/ml in serum free medium combined to produce the greatest inhibiting effect on leukocytes in patients with apparent multiple sclerosis and differentiated these patients from those in the other groups tested. Leukocytes in patients who had probable multiple sclerosis with partial impairment, signifying possible current activity of the disease, were especially inhibited as compared to the leukocytes from other groups tested against myelin antigen. Cerebrospinal fluid from affected patients when used as a media enhanced the test. This study suggests that migration inhibition of peripheral leukocytes using myelin protein may be useful in the diagnosis of patients with multiple sclerosis. There is additional evidence that the degree of leukocyte migration inhibition may reflect activity of the disease with its consequent implications on treatment and prognosis.

Antigens↗

PubMed1994

Erectile dysfunction in multiple sclerosis. Associated neurological and neurophysiological deficits, and treatment of the condition.

Forty-eight men with multiple sclerosis and erectile dysfunction were evaluated. Emphasis was placed on the neurological features and the relationship between impotence and the bladder dysfunction in multiple sclerosis. Erectile failure was invariably associated with pyramidal signs in the lower limbs and with urinary symptoms. All of the men with impotence and marked pyramidal dysfunction in their legs were found by cystometric studies to have bladder hyperreflexia. The severity of the urinary symptoms was related to the degree of pyramidal impairment in the lower limbs. The posterior tibial and the pudendal cortical evoked potentials were abnormal in most of the men with multiple sclerosis and erectile failure. However, recording the pudendal cortical responses in patients with multiple sclerosis and impotence provided no more information than the tibial cortical evoked potentials. The neurological examination findings together with the results of the neurophysiological and cystometric tests suggest that erectile dysfunction in multiple sclerosis is due to spinal lesions situated proximal to the sacral cord. The feasability of papaverine intracorporeal injection therapy for men with multiple sclerosis and impotence was assessed. Papaverine intracorporeal injections produced satisfactory erections in the majority of the impotent men. Erectile failure in patients with multiple sclerosis was successfully managed for up to 2 years, by intracorporeal self-injection therapy.

Adult↗

PubMed2005

Interferon-beta1b for multiple sclerosis.

Interferon-beta1b (Betaseron/Betaferon) was the first approved therapy for relapsing-remitting multiple sclerosis. The US Food and Drug Administration has expanded the indication to include relapsing forms of multiple sclerosis which encompasses secondary-progressive multiple sclerosis if relapses are present. In one scientifically sound head-to-head comparison (Independent Comparison of Interferon trial), interferon-beta1b was shown to be clinically superior to low-dose interferon-beta1a (Avonex). Current studies are underway to compare it with a double dosage of interferon-beta1b [corrected] as well as glatiramer acetate. Neutralizing antibodies are more likely to occur with interferon-beta1b, but their clinical significance has shown conflicting and confusing results making the utility of measuring neutralizing antibodies uncertain. Up to 12 years of follow-up data suggest that the drug remains effective on T2 magnetic resonance imaging burden of disease in those who stay on therapy. Initially, the major problem with interferon-beta1b was a lack of tolerability due to high incidents of skin reactions and influenza-like side effects. Patient adherence has improved dramatically with the introduction of autoinjectors and protocol changes including initial dose escalation, prophylactic ibuprofen or acetaminophen, evening administration of drug and an attentive nurse support system. Interferon-beta1b remains a first-line treatment for relapsing-remitting multiple sclerosis and relapsing forms of secondary-progressive multiple sclerosis based on robust efficacy data and a long-term safety profile.

Adjuvants, Immunologic↗

PubMed1988

Perivascular iron deposition and other vascular damage in multiple sclerosis.

Evidence of damage to cerebral vein walls was sought in 70 cases of multiple sclerosis. Seventy control cases were also examined. The multiple sclerosis cases showed venous intramural fibrinoid deposition (7%), recent haemorrhages (17%), old haemorrhages revealed by haemosiderin deposition (30%), thrombosis (6%) and thickened veins (19%). In all, 41% of all multiple sclerosis cases showed some evidence of vein damage. Occasional control cases showed haemosiderin deposition in the brain but, unlike the multiple sclerosis cases, these were diffuse and almost entirely related to coexistent cardiovascular or cerebrovascular disease. Haemosiderin deposition was common in the substantia nigra and other pigmented nuclei in all cases. It is concluded that the cerebral vein wall in multiple sclerosis is subject to chronic inflammatory damage, which promotes haemorrhage and increased permeability, and constitutes a form of vasculitis.

Cerebral Hemorrhage↗

PubMed2003

Multiple sclerosis and glutamate.

Experimental autoimmune encephalomyelitis reproduces in rodents the features of multiple sclerosis, an immune-mediated, disabling disorder of the human nervous system. No adequate therapy is available for multiple sclerosis, despite anti-inflammatory, immunosuppressive, and immunomodulatory measures. Increasingly glutamate is implicated in the pathogenesis of neurodegenerative diseases. Here we (1) review changes in the glutamatergic system in multiple sclerosis and (2) reveal the effects of glutamate AMPA antagonists in acute and chronic rodent models of multiple sclerosis. Administration of structurally diverse competitive and non-competitive AMPA antagonists reduces neurologic disability in rodents subjected to acute experimental autoimmune encephalomyelitis. In addition, AMPA antagonists are active in both the adoptive transfer and in chronic models of experimental autoimmune encephalomyelitis in rats and mice and affect both the acute and chronic relapsing phases. Moreover, short-term therapy with AMPA antagonists leads to sustained benefit well into the progressive phases. These results imply that therapeutic strategies for multiple sclerosis should be complemented by glutamate AMPA antagonists to reduce neurologic disability.

Animals↗

PubMed1998

Clinical relapses and disease activity on magnetic resonance imaging associated with viral upper respiratory tract infections in multiple sclerosis.

BACKGROUND: Although the risk of clinical attacks of multiple sclerosis seems to be significantly increased with viral upper respiratory tract infections (URTI), serological evidence for the reported association remains controversial. In addition, although MRI is six to 10 times more sensitive than clinical exacerbations in indexing disease activity, any possible association between URTI and MRI activity has yet to be investigated. OBJECTIVES: To examine the relation between URTI and disease activity, in multiple sclerosis patients participating in a placebo controlled trial of interferon beta-1a, as indexed both by clinical exacerbation rate and by the number and volume of gadolinium-diethylenetriaminepentaacetic acid (Gd-DTPA) enhancing lesions on MRI. "At risk" periods were defined around symptomatic URTI, with or without serological confirmation. RESULTS: The relative risk of clinical relapse for serologically unconfirmed symptomatic URTI was 2.1 (p=0.004). Raised antiviral antibody titres conferred a relative risk of multiple sclerosis exacerbations that was 3.4 times higher than the "not at risk" periods (annual attack rates of 5.7 v 1.6, respectively, p=0.006). There was no definite relation between the number or the volume of active lesions on MRI and either symptomatic or serologically defined at risk periods. CONCLUSIONS: These results confirm the previously reported association between viral infections and multiple sclerosis exacerbations and indicate that the relative risk may be even higher when viral infection is serologically confirmed. However, the results, perhaps because of the confounding effects of interferon beta-1a, do not provide convincing evidence of increased blood-brain barrier breakdown or inflammation during periods of virally induced immune stimulation.

Adult↗

PubMed1993

Bipolar affective disorder prior to the onset of multiple sclerosis.

The frequent association of affective disorder and multiple sclerosis raises important aetiological and clinical considerations. Reported here are seven patients who presented with symptoms of multiple sclerosis and who had a preceding history of bipolar affective disorder. The hypothesis that bipolar illness may be the initial manifestation of multiple sclerosis is discussed with reference to relevant clinical and epidemiological research on the topic.

Adult↗