SEARCH · PubMed Health

Results for “SCLEROSIS, MULTIPLE”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

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

At least 1,675 records · Page 93Linked to original sources

PubMedDate not supplied

Multiple sclerosis and parkinsonism: a case report.

Multiple sclerosis (MS) is a well-known disease characterized by the distribution of plaques in the periventricular and subcortical white matter. Although plaques can also be found in the striatum, pallidum and thalamus, extrapyramidal symptoms are very rare in MS. However, the association of MS and parkinsonism is still a controversial topic as it has not been established whether these two conditions occur coincidentally or causally. In the literature, eleven cases of parkinsonism associated with MS have been described. Here, we report a patient with clinically definite MS and signs of parkinsonism. Our patient had slow progressive bradykinesia, static tremor and bradymimia that were not associated with exacerbation or progression of the MS. This rare and interesting association of multiple sclerosis with parkinsonism is discussed in the light of literature reports.

Brain↗

PubMed1983

Serum demyelinating factors in multiple sclerosis.

Sera from 21 patients with multiple sclerosis were applied to myelinated spinal cord cultures and evaluated for demyelinating activity. Samples were collected at various times when patients were on or off therapy with myelin basic protein or prednisone or both, and at various stages of disease. Five of 31 serum samples from 17 patients exhibited demyelinating activity when tested in a 40% concentration in tissue culture nutrient medium. Four of the 10 serum samples taken from patients with active or remitting multiple sclerosis (2 samples from the same patient) were demyelinative; 1 of 21 sera collected during stationary periods of disease was positive. There was no correlation between serum demyelinating activity and the presence or absence of treatment. Sera positive for demyelinating activity failed to inhibit myelin formation in initially unmyelinated cerebellar cultures.

Animals↗

PubMed1985

In vivo activated T lymphocytes in the peripheral blood and cerebrospinal fluid of patients with multiple sclerosis.

We found an increase in peripheral-blood lymphocytes bearing the T-cell-specific activation antigen Ta1 in 20 of 35 patients with progressive multiple sclerosis, 4 of 18 patients with stable or improving multiple sclerosis, 1 of 17 patients with other neurologic diseases, and 1 of 14 normal controls (P less than 0.0002, Fisher's exact test). No increases in two other markers of T-cell activation, T113 and the interleukin-2 receptor, were found. In the cerebrospinal fluid, patients with progressive multiple sclerosis (pleocytosis, 3.9 +/- 1.6 cells per cubic millimeter) had 42 +/- 3.0 per cent Ta1+ cells. In contrast, patients with other inflammatory central nervous system diseases (36 +/- 13 cells per cubic millimeter) had 9.6 +/- 1.8 per cent Ta1+ cells (P less than 0.01). In patients with other neurologic diseases without inflammation (0.7 +/- 0.16 cells per cubic millimeter), the percentage of Ta1+ cells was equivalent to that in patients with multiple sclerosis (39 +/- 5.4 per cent), although the absolute number was lower. There was a positive correlation between the presence of Ta1+ cells in the spinal fluid and blood of patients with other neurologic diseases, but not patients with multiple sclerosis. Less than 1 per cent of lymphocytes from the spinal fluid of patients with multiple sclerosis expressed interleukin-2 receptors, as compared with 9.8 per cent of cells from subjects with other inflammatory neurologic diseases (P less than 0.01). These results suggest that the T cells in the spinal fluid of patients with multiple sclerosis may be activated by a different mechanism or in a different temporal sequence from that in patients with other nervous system diseases. Furthermore, the increase in Ta1+ cells in the peripheral blood of patients with multiple sclerosis demonstrates systemic immune activation in the disease; monitoring such cells may provide an objective measure of abnormal immunologic activity.

Adolescent↗

PubMed1977

Neuropsychological aspects of multiple sclerosis.

Twenty-six persons (five males and 21 females) with the neurological diagnosis of multiple sclerosis, and an equal number of control subjects matched on age, sex, and education were given a battery of tests designed to assess motor and intellectual functioning. Subjects in the multiple sclerosis group displayed marked deficits on all tests of motor skill except grip strength. Although verbal intelligence was not impaired in subjects with multiple sclerosis, these subjects performed more poorly than control subjects on two different tests of memory even though these tasks required minimal motor responsivity. Correlational analyses on the several motor and cognitive tasks revealed that correlations between motor and memory performance were consistently higher in persons with multiple sclerosis than in controls. These results suggest that whereas multiple sclerosis may not have mch effect on the utilization of stored verbal information, the processing and storage of new verbal material are disrupted by the disease to a degree that is paralleled by the extent of motor impairment. This finding is consistent with the view that the memory impairments observed are secondary to the primary motor deficit, but the alternative explanation that memory functions, like motor functions, are especially vulnerable to the demylination process of multiple sclerosis is equally viable at present.

Adult↗

PubMed1981

Coronavirus antibodies in sera from patients with multiple sclerosis and matched controls.

Sera from patients with multiple sclerosis and carefully matched controls were tested for antibodies to three strains of coronavirus. There was no significant difference in the levels of antibody in the patients vs the controls. We conclude that unless the strains of coronaviruses recently reported to have been isolated from patients with multiple sclerosis express important serological differences from those used in these studies, coronaviruses are not associated with the cause of multiple sclerosis.

Animals↗

PubMed1991

Association between tumor necrosis factor-alpha and disease progression in patients with multiple sclerosis.

BACKGROUND: Cachectin, or tumor necrosis factor-alpha (TNF-alpha), is a principal mediator of the inflammatory response and may be important in the pathogenesis and progression of multiple sclerosis, an inflammatory disease of the central nervous system. METHODS: In a 24-month prospective study, we used a sensitive enzyme-linked immunosorbent assay to determine levels of TNF-alpha in cerebrospinal fluid and serum in 32 patients with chronic progressive multiple sclerosis and in 20 with stable multiple sclerosis and 85 with other neurologic diseases. An attempt was made to relate TNF-alpha levels with the degree of disability of the patients with multiple sclerosis and with their neurologic deterioration during the 24 months of observation. RESULTS: High levels of TNF-alpha were found in the cerebrospinal fluid of 53 percent of the patients with chronic progressive multiple sclerosis and in none of those with stable multiple sclerosis (P less than 0.001). TNF-alpha was detected in the cerebrospinal fluid of 7 percent of the controls (P less than 0.01) with other neurologic disease. In patients with chronic progressive multiple sclerosis, mean TNF-alpha levels were significantly higher in the cerebrospinal fluid than in corresponding serum samples (52.41 vs. 11.88 U per milliliter; range, 2 to 178 vs. 2 to 39; P less than 0.001). In these patients, cerebrospinal fluid levels of TNF-alpha correlated with the degree of disability (r = 0.834, P less than 0.001) and the rate of neurologic deterioration (r = 0.741, P less than 0.001) before the start of the study. Cerebrospinal fluid levels also correlated with the increase in neurologic disability after 24 months of observation (r = 0.873, P less than 0.001). CONCLUSIONS: These data provide evidence of intrathecal synthesis of TNF-alpha in multiple sclerosis and suggest that the level of TNF-alpha in cerebrospinal fluid correlates with the severity and progression of the disease. Our results suggest that TNF-alpha may reflect histologic disease activity in multiple sclerosis and could be used to monitor outcomes or responses to therapy.

Adult↗

PubMed1999

The Fatigue Descriptive Scale (FDS): a useful tool to evaluate fatigue in multiple sclerosis.

Although fatigue is common among multiple sclerosis (MS) patients, evaluation of this symptom is difficult due to the subjectivity and variability of the complaint. We proposed the Fatigue Descriptive Scale (FDS) as a tool to evaluate the severity and quality of fatigue in a group of patients suffering from MS. As a way to demonstrate the usefulness of this scale we applied the FDS in a group of 155 patients (105 women and 50 men) with clinically-definite multiple sclerosis, as outlined according to Poser's criteria. Age was 36.2 +/- 11.1 years (range 12-62) and time of evolution was 8.3 +/- 9.4 years (range 1-44). The Fatigue Severity Scale (FSS) was also used. Descriptive statistics techniques and techniques for nonparametric distribution (Spearman Rank, Kruskal-Wallis ANOVA) were used. One hundred and eighteen patients reported fatigue (73 spontaneously, 45 when questioned). All descriptions of fatigue were ranked according to FDS categories. Eighty-five patients defined the symptom as fatigue with exercise, 26 as asthenia and seven as the worsening of other symptoms. Fatigue by itself produced limited or disrupted activity in 78 patients; work-related functions were limited in 48 patients; social relations were limited in 29 patients; and self-care difficult for one patient. Fifty-six patients suffered fatigue daily. FDS score was 4.9 +/- 3.9 (range 0-13). FSS was 3.1 +/- 1.7 (range 0.2-6.6). FDS and FSS of Krupp were highly correlated (R = 0.87, p < 0.001). Therefore, in comparison with other scales, the FDS shows remarkable usefulness in classifying, periodicity, and severity of fatigue in MS patients. The high correlation with the FSS implies that it is a valid method to measure the severity of fatigue, as was demonstrated in our paper proposing the FDS. The importance of this new scale is its ability to inform the clinicians in a very quick, easy, and at the same time complete way, how severe the fatigue really is and how it affects the patient.

Adolescent↗

PubMed1991

Quantitative MRI changes in gadolinium-DTPA enhancement after high-dose intravenous methylprednisolone in multiple sclerosis.

In 12 patients with definite multiple sclerosis who received a total of 21 courses of high-dose (1 gram daily for 10 consecutive days) intravenous methylprednisolone, we performed MRI of the brain with and without gadolinium-DTPA before and after treatment. On the initial MRI, there was a total of 98 enhancing lesions, 93 of which were also represented on the unenhanced images. After treatment, 13 patients improved clinically, and 78 of the lesions lost enhancement but remained visible on the unenhanced images. There were six new enhancing lesions on the second MRI. Thus, the blood-brain-barrier integrity improved after high-dose IV methylprednisolone, which correlated well with the clinical improvement. The lesions remaining visible on the unenhanced images indicate an incomplete histologic recovery at the time of the second scan, and also demonstrate that unenhanced MRI alone is not sufficient to monitor disease activity in the short term in multiple sclerosis.

Adult↗

PubMed1991

Multiple sclerosis and affective disorders.

Affective disorders occurring in association with multiple sclerosis have been attributed both to the psychosocial impact of a chronic disabling illness and to the structural lesions of cerebral demyelination. A review of research evidence suggests that while there is a correlation between chronic depressive symptoms and both progressive disability and lack of social support, acute major depressive and manic episodes may be psychiatric manifestations of demyelinating lesions and may be the initial presenting symptoms of multiple sclerosis. Anti-inflammatory agents may be required in the management of acute psychiatric symptoms despite the fact that these agents have a propensity to precipitate psychotic episodes. Two case reports are presented to illustrate the clinical challenge of distinguishing between organic and functional affective illness in patients with multiple sclerosis. The interplay between biological and psychological aspects of multiple sclerosis in precipitating affective disorders is discussed, with implications for patient assessment and management.

Adult↗

PubMed1996

Distinct patterns of multiple sclerosis pathology indicates heterogeneity on pathogenesis.

Multiple sclerosis is an inflammatory demyelinating disease of the central nervous system. The hallmark of its pathology is the demyelinated plaque with reactive glial scar formation. However, a detailed analysis of the patterns of demyelination, oligodendroglia cell pathology and the reaction of other tissue components suggests that the pathogenesis of myelin destruction in this disease may be heterogeneous. In this review we present a new classification scheme of lesional activity on the basis of the molecular composition of myelin degradation products in macrophages. When these criteria are used, different patterns of demyelination can be distinguished, including demyelination with relative preservation of oligodendrocytes, myelin destruction with concomitant and complete destruction of oligodendrocytes or primary destruction or disturbance of myelinating cells with secondary demyelination. Furthermore, in some cases a primary selective demyelination may be followed by a secondary oligodendrocyte loss in the established lesions. Finally, some extraordinarily severe conditions may result in destructive lesions with loss of myelin, oligodendrocytes, axons and astrocytes. This heterogeneity of plaque pathology is discussed in the context of recent experimental models of inflammatory demyelination, which show that different immunological pathways may lead to the formation of demyelinated plaques that reveal the diverse structural aspects described above. Our data indicate, that the demyelinated plaques of multiple sclerosis may reflect a common pathological end point of a variety of different immunological mechanisms of myelin destruction in this disease.

Animals↗

PubMed1998

Cerebrospinal fluid and serum nitric oxide metabolites in patients with multiple sclerosis.

Nitric oxide is hypothesised to play a role in the immunopathogenesis of multiple sclerosis. Raised cerebrospinal fluid and serum levels of the nitric oxide metabolites nitrate and nitrite have been described in patients with multiple sclerosis. Cerebrospinal fluid and serum nitrate and nitrite were measured in patients with multiple sclerosis, inflammatory and non-inflammatory neurological diseases, and correlated with the albumin quotient, an index of blood-brain-barrier dysfunction. Patients undergoing diagnostic lumbar and vene puncture were prospectively recruited, clinical data were obtained from the hospital records, and the CSF and serum nitrate and nitrite levels were measured by the nitrate reductase and Griess reaction methods. Nitrate and nitrite, were raised in the CSF and serum of patients with multiple sclerosis and other inflammatory neurological diseases compared to patients with non-inflammatory neurological disorders (median nitrate and nitrite: cerebrospinal fluid = 10.3 microM vs 15.4 microM vs 6.6 microM, P < 0.001, and serum = 49.0 microM vs 46.4 microM vs 38.8 microM, P = 0.02, respectively). CSF nitrate and nitrite levels correlated with the albumin quotient (n = 59, r = 0.42, P < 0.001). This study provides further evidence for a role of nitric oxide in the immunopathogenesis of multiple sclerosis and supports a role for nitric oxide as a possible mediator of inflammatory blood-brain-barrier dysfunction.

Adult↗

PubMed2000

Acute disseminated encephalomyelitis, multiphasic disseminated encephalomyelitis and multiple sclerosis in children.

Forty-eight children with disseminated demyelination of the CNS, 28 with acute disseminated encephalomyelitis (ADEM), seven with multiphasic disseminated encephalomyelitis (MDEM) and 13 with multiple sclerosis were studied for a mean follow-up period of 5.64 years. The presentation findings of the ADEM/MDEM group were compared with those of the multiple sclerosis group. The following findings were more commonly seen in ADEM/MDEM presentation compared with the multiple sclerosis presentations: predemyelinating infectious disease (74 versus 38%, P: < 0.05); polysymptomatic presentation (91 versus 38%, P: < 0.002); pyramidal signs (71 versus 23%, P: < 0.01); encephalopathy (69 versus 15%, P: < 0.002); and bilateral optic neuritis (23 versus 8%, not significant). Seizures occurred only in the ADEM/MDEM group (17 versus 0%, not significant). Unilateral optic neuritis occurred only in the multiple sclerosis patients (23 versus 0%, P: < 0.01). There were no differences in the frequencies of transverse myelitis, brainstem involvement, cerebellar signs and sensory disturbance between the two groups. ADEM/MDEM patients were more likely to have blood leucocytosis (64 versus 22%, P: < 0.05), CSF lymphocytosis (64 versus 42%, not significant) and CSF protein elevation (60 versus 33%, not significant). Patients presenting with multiple sclerosis were more likely to have intrathecal synthesis of oligoclonal bands on presentation (64 versus 29%, not significant). MRI showed that subcortical white matter lesions were almost universal in both groups, though periventricular lesions were more common in multiple sclerosis (92 versus 44%, P: < 0.01). By contrast, in ADEM/MDEM there was absolute and relative periventricular sparing in 56 and 78% of patients, respectively. Follow-up MRI revealed complete or partial lesion resolution in 90% and no new lesions in the ADEM/MDEM group. All of the multiple sclerosis patients had new lesions on repeat MRI (five during relapse and six during asymptomatic convalescent phases). The outcome in the ADEM patients was mixed; 57% of patients made a complete recovery. The mean follow-up for the 35 ADEM/MDEM patients was 5.78 years (range 1.0-15.4 years). Eight of the 13 multiple sclerosis patients relapsed within the first year; 11 had a relapsing-remitting course, one a primary progressive course and one a secondary progressive course. These differences in the presentation of ADEM/MDEM compared with multiple sclerosis may help in the prognosis given to families regarding the possibility of later development of multiple sclerosis.

Adolescent↗

PubMed2000

A meta-analysis of methylprednisolone in recovery from multiple sclerosis exacerbations.

Despite recent advances in multiple sclerosis treatment, patients experience relapses for which standard treatment remains glucocorticosteroids (GCS). However, there is limited information comparing doses or routes of administration for different GCS types or the benefit of GCS compared to natural recovery. Currently, high dose (HD) methylprednisolone (MP) is the preferred therapy. We conducted meta-analyses of published studies assessing MP at different doses and in comparison to other steroid products or no treatment. Relevant studies were identified through predetermined processes and five articles met the inclusion criteria. Three studies compared HD MP to placebo; two studies compared the effect of HD MP and low dose (LD) MP; only one accepted report compared HD MP to another GCS. This report could not be included in a meta-analysis. The meta-analysis of HD MP vsplacebo studies indicated a mean treatment difference of 0.76 in Expanded Disability Status Score (EDSS) changes from baseline. The meta-analysis of HD and LD MP demonstrated no difference in EDSS change. Despite these rather obvious findings, these meta-analyses have been valuable in identifying further research questions. We recommend studies to determine optimum benefit related to dosage, timing for starting therapy and the most appropriate GCS type. Given the advances in MS therapeutics, these studies will have to include patients on additional disease modifying therapy. Multiple Sclerosis (2000) 6 267 - 273

Disability Evaluation↗

PubMed1997

[Physical trauma and multiple sclerosis].

Without a more detailed knowledge of etiology and pathogenesis of multiple sclerosis final conclusions regarding an association between physical trauma and the onset or course of multiple sclerosis cannot be drawn. Only a few prospective studies which are appropriately designed to prove a putative correlation have been published. A critical review of these studies and some case reports, in the light of the current pathophysiological concepts of multiple sclerosis, does not indicate a causal relationship between physical trauma and onset of multiple sclerosis or exacerbations.

Central Nervous System↗

PubMed2003

Multiple sclerosis: severity and progression rate in African Americans compared with whites.

OBJECTIVE: Although epidemiology indicates that multiple sclerosis is more common among whites than African Americans, the course of disease may be more aggressive among African Americans. This study examines disease course in a large multiple sclerosis clinic population. DESIGN: A case-controlled, retrospective record review compared the severity of multiple sclerosis for African Americans and for whites. Because the baseline demographics of the two groups differed, we performed analyses of multiple subgroups in an attempt to control for various characteristics. RESULTS: Consistent evidence of more disability in African Americans compared with whites was found, although subgroups were often too small to establish statistical significance. African Americans had a higher mean Expanded Disability Status Scale score than whites in a subgroup selected to minimize differences in access to care and disease perceptions. African Americans reported limb weakness as a presenting symptom of multiple sclerosis more frequently than did whites. When patients were followed at our multiple sclerosis center, rates of disease progression were nearly identical. CONCLUSIONS: More African Americans than whites experience pyramidal system involvement early in multiple sclerosis, leading to greater disability as measured by the ambulation-sensitive Expanded Disability Status Scale. Once patients have moderate difficulty walking, the rate of progression is the same for both groups, albeit occurring at a later age for whites than for African Americans.

Adult↗

PubMed2001

Matrix metalloproteinases and their tissue inhibitors as markers of disease subtype and response to interferon-beta therapy in relapsing and secondary-progressive multiple sclerosis patients.

Matrix metalloproteinases (MMPs) have recently been implicated in the pathogenesis of multiple sclerosis. Their suggested role includes the disruption of the blood-brain barrier, immune cell transmigration into the central nervous system, and myelin degradation. The present study characterized the mRNA level of a wide spectrum of MMPs and tissue inhibitors of metalloproteinases (TIMPs) expressed by peripheral blood leukocytes from relapsing-remitting (n = 16) and secondary-progressive (n = 12) multiple sclerosis patients. The expression of the same MMPs and TIMPs was evaluated also in a prospective 12-month follow-up of 6 patients randomly chosen from each of the 2 groups during interferon beta-1a treatment. Reverse transcription-polymerase chain reaction assessment demonstrated elevated levels of MT1-MMP and MMP-7 mRNA levels in both groups of patients, and no significant differences in MMP-9 levels, compared with healthy controls. Divergent expression of MMP-2 between relapsing-remitting and secondary-progressive patients compared with controls was observed. Interferon-beta treatment was associated with significant suppression of MMP-9 and MMP-7 mRNA in relapsing-remitting patients, though no significant changes were observed in the secondary-progressive group. These results contribute to the understanding of the IFN-beta-mediated immunomodulatory and therapeutic effects in multiple sclerosis patients and also support evidence for distinct immune mechanism(s) underlying relapsing-remitting versus secondary-progressive multiple sclerosis. The study also suggests that MMPs may be considered as potential biomarkers for response to treatment as well as targets for immunotherapy in multiple sclerosis.

Adjuvants, Immunologic↗

PubMed2002

Growth dynamics of meningiomas in patients with multiple sclerosis treated with interferon: report of two cases.

BACKGROUND: Although multiple sclerosis (MS) is a common disease of the central nervous system, the association of intraparenchymal tumour has been rarely reported and the potential relationship between intracranial meningioma and MS has not been seriously analysed. This report addresses the association of multiple sclerosis and intracranial meningioma and discusses the effect of interferon treatment on tumour progression. CLINICAL PRESENTATION: We report two cases with multiple sclerosis, who developed meningioma four and twenty years after the diagnosis of MS was made. Neither patient had a history of meningioma initially and both were being treated interferon when the meningioma was progressed. FINDINGS: Histological examination of two cases revealed meningothelial meningioma. The first patient's KI67 level was 2.5% and was positive for the progesterone and estrogen receptor. Chromosomal analysis showed some abnormalities. In the second case, mild atypical change by presence of nuclear enlargement and rare mitotic figures were noted and PCNA, KI67 levels were less than 2%. CONCLUSIONS: We reported the association of multiple sclerosis and intracranial meningioma and observed the progression of the meningiomas during interferon treatment. Although, we cannot exclude the coincidence between the two diseases we discussed suspicious relationship between the interferon treatment and the tumour progression.

Adjuvants, Immunologic↗

PubMed1995

[Pathogenesis and therapy of multiple sclerosis. The role of cytokines].

Multiple sclerosis (MS) is probably caused by multiple factors, but there is evidence that an autoimmunological process is relevant for the pathogenesis. Cytokines can operate in different ways in MS and the animal model "experimental allergic encephalomyelitis (EAE). "Interferon gamma (IFN-gamma), tumor necrosis factor-alpha (TNF-alpha), TNF-beta, interleukin-1 (IL-1) and IL-2 are important inflammation mediators within the MS plaque, whereas IFN-alpha, IFN-beta, transforming-growth-factor-beta (TGF-beta) and IL-10 exert mainly immunosuppressive functions. Application of these anti-inflammatory cytokines and the selective block of pro-inflammatory cytokines are promising new therapeutic strategies with fewer side effects than the commonly used cytostatic drugs.

Animals↗