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PubMed1980

On the role of sensitised T-lymphocytes in the pathogenesis of multiple sclerosis.

Peripheral blood lymphocytes from 24 out of 26 patients with clinically well-defined multiple sclerosis in remission showed sensitisation to multiple sclerosis brain extracts as assayed by enhancement of the early erythrocyte rosette test. Such an increase in the number of early rosettes was not found when the lymphocytes of multiple sclerosis patients were exposed to extracts of control brains. In contrast the sensitised cells were found in the circulation in only two of 11 patients with multiple sclerosis in acute relapse. The percentage of circulating T-lymphocytes which formed early rosettes was lower in the group of patients suffering a relapse than in patients in remission. A longitudinal study of one patient who was tested before, during and after a relapse revealed the disappearance from the blood of the sensitised T-cells during the relapse and their subsequent reappearance after recovery. Of 36 patients with other neurological diseases, two responded solely to multiple sclerosis brain, two responded to both multiple sclerosis and control brain, and three responded only to control brain. No healthy controls showed sensitisation to any brain extract.

Adult↗
PubMed1986

Breakdown of the blood-retinal barrier in multiple sclerosis measured by vitreous fluorophotometry.

Periphlebitis retinae in multiple sclerosis appears as transitory cellular infiltrations around veins in an otherwise normal retina. Similar cellular infiltrations have been found around veins in the central nervous system. In the present study the blood-retinal barrier has been investigated by vitreous fluorophotometry. Eight multiple sclerosis patients with actual periphlebitis retinae and 9 patients with previous but not active periphlebitis retinae were included in this study. Abnormal leakage of fluorescein was manifest in the group of multiple sclerosis patients with periphlebitis retinae. Permeability (1.8 +/- 0.2 X 10(-7) cm/sec; mean +/- SEM) but not in the control group as a whole permeability (1.3 +/- 0.1 X 10(-7) cm/sec; mean +/- SEM) compared to 17 normals (permeability 1.1 +/- 0.005). It is thus concluded that breakdown of the blood-retinal barrier may be transitory when connected with periphlebitis retinae in multiple sclerosis.

Adult↗
PubMed1976

Sex difference of multiple sclerosis in Japan.

Sex differences in the clinical course of multiple sclerosis were investigated in 947 patients with multiple sclerosis collected from all over Japan through the nationwide survey undertaken by the Multiple Sclerosis Research Committee of Japan from 1972 through 1973. A course of remissions and exacerbations, more frequent involvement of optic nerves, and more severe motor and visual disability were present in a higher proportion of women than men. These features corresponded to those which have been considered to characterize Oriental multiple sclerosis patients.

Adult↗
PubMed1993

Retinal periphlebitis in multiple sclerosis.

BACKGROUND: The ocular and visual manifestations of multiple sclerosis are varied. The most uncommon is sheathing of the veins, periphlebitis. METHODS: A 39-year-old white female presented with primary visual complaints of contrast problems on a computer terminal. The patient was lost to follow up for 4 years, however, upon return a clinical diagnosis of multiple sclerosis was confirmed. Six years after the initial presentation, ophthalmoscopic exam of both eyes revealed marked focal sheathing of the retinal veins in the periphery, and associated hemorrhages in the right eye. RESULTS: During follow-up, the left eye became further involved developing hemorrhages and a retinal hole, which was treated. The visual consequence of the multiple sclerosis as a result of further exacerbations were bilateral centrocecal scotomas and midly reduced visual acuity. CONCLUSIONS: Multiple sclerosis should be considered in the differential diagnosis of patients with retinal periphlebitis.

Adult↗
PubMed2003

[Proliferative retinal vasculitis and multiple sclerosis: a case report].

INTRODUCTION: Retinal periphlebitis can precede the neurological effects of multiple sclerosis and reveal the disease. Although these occurrences of vasculitis are noted in 10% - 35% of multiple sclerosis patients, proliferative retinopathy is, on the contrary, an exceptional complication. CASE REPORT: We report the case of a 28-year-old woman who presented bilateral, proliferative, retinal vasculitis complicated with recurrent vitreous hemorrhages occurring with multiple sclerosis. Initially, there was a unilateral, central venous thrombosis in a particularly ischemic and proliferative form. After a neurological, biological and radiological check-up, the diagnosis of multiple sclerosis was pronounced and treatment with Interferon was started. A pan-retinal laser photocoagulation and vitrectomy with proliferative membrane peeling were performed. After a follow-up of 2.5 years, a bilateral epiretinal membrane on the macula with a chronic macular edema persisted, with visual acuity limited to 0.2 Parinaud 4 in the right eye and 0.5 Parinaud 2 in the left eye. DISCUSSION: This case shows that the diagnosis of multiple sclerosis must be established in cases of ischemic retinal vasculitis, especially as the literature does not seem to report a correlation between the retinal vascular affect and how far multiple sclerosis has progressed. Moreover, the visual prognosis of these proliferative lesions remains uncertain. CONCLUSION: Multiple sclerosis can be revealed initially, although exceptionally, by bilateral, proliferative and severe retinal vasculitis complicated with recurrent vitreous hemorrhages and tractional retinal detachment.

Adrenal Cortex Hormones↗
PubMed2003

Cost-utility of interferon beta1b in the treatment of patients with active relapsing-remitting or secondary progressive multiple sclerosis.

Economic evaluations of treatments for multiple sclerosis have focused either on relapsing-remitting or secondary progressive disease. None has addressed specifically the question of how treatments affect disease progression from diagnoses to severe disability; however, in both clinical and economic terms this is one of the key questions. This study therefore created a disease model that includes both relapsing and progressive multiple sclerosis and covers the full range of disease severity. In addition, the issue of covariates influencing the cost per QALY and the uncertainty in the estimates is addressed. The model is based on our earlier approach using a Markov model, where disease progression is measured as functional disability (EDSS), costs and utilities associated with different disability levels, and outcome expressed as QALY. Treatment is based on a subgroup of patients with active disease in two placebo-controlled clinical trials and open-label extensions with interferon-beta(1b) in relapsing-remitting or secondary progressive multiple sclerosis, and natural history data are used for the extrapolation beyond the trials. Disease progression (transition probabilities) was estimated using a probit model controlling for differences in patient and disease characteristics, and costs and utilities for different disability levels are taken from large population-based observational studies. Results are presented for Sweden and compared to the United Kingdom. When treatment is given for 36 months (adjusted for compliance) and no further effect is included, the cost per QALY is EURO 7800 (direct, indirect, and informal care costs included, discounted at 3%) over 10 years. The total number of QALYs increases from 3.45 in the no-treatment group to 3.64 in the treatment group. When treatment is prolonged to 54 months, the cost per QALY is EURO 38,700. Using the full range of costs and utilities, the probability that the cost per QALY over a 20-year time-frame is below EURO 50,000 for patients starting treatment at EDSS 3.0 is 80%. In view of the progression of MS over many years models are required to estimate the cost-effectiveness of new treatments. The model proposed here allows estimating disease progression, costs, and QALYs for patients with different characteristics and types of MS, and it can be adapted to different countries. It can hence be used to assess the cost-effectiveness of a defined intervention, such as interferon-beta(1b).

Journal Article↗
PubMed2001

Size-selective neuronal changes in the anterior optic pathways suggest a differential susceptibility to injury in multiple sclerosis.

Axonal damage is found in both acute and chronic lesions of multiple sclerosis. Direct axon counting in post-mortem tissue has suggested that smaller axons might have a greater susceptibility to damage, but methodological limitations have precluded unequivocal interpretation. However, as neuronal and axonal sizes are linked and neuronal changes would be expected with retrograde or transsynaptic degeneration following axon injury, we hypothesized that an alternative strategy for studying this phenomenon would be to define multiple sclerosis-associated changes in neurones. To test this hypothesis, we measured both axonal loss and neuronal size changes in the anterior optic pathway [including the optic nerve (ON), optic tract (OT) and lateral geniculate nucleus] of the brains of eight patients who died with multiple sclerosis and in eight control brains. The ONs and OTs in brains from the multiple sclerosis patients showed a trend to smaller mean cross-sectional areas (ON, multiple sclerosis = 6.84 mm(2), controls = 9.25 mm(2); and OT, multiple sclerosis = 6.45 mm(2), controls = 7.94 mm(2), P = 0.08) and had reduced axonal densities (ON, multiple sclerosis = 1.1 x 10(5)/mm(2), controls = 1.7 x 10(5)/mm(2); and OT, multiple sclerosis = 1.4 x 10(5)/mm(2), controls = 1.8 x 10(5)/mm(2), P = 0.006). Estimated total axonal counts were reduced by 32 (OT)-45% (ON) in the patients relative to controls (ON, multiple sclerosis = 8.1 x 10(5) axons, controls = 14.8 x10(5), P = 0.05; and OT, multiple sclerosis = 9.1 x 10(5), controls = 13.3 x 10(5), P = 0.02). The size distributions of the magnocellular cells in the lateral geniculate nucleus were similar for the two groups, but in multiple sclerosis brains the parvocellular cells were significantly smaller (mean sizes: multiple sclerosis = 226 microm(2), controls = 230 microm(2), P < 0.001) and had a larger variation in size, suggesting a greater proportion of atrophic neurones. Axon loss in the optic nerves of multiple sclerosis patients correlated strongly with measures of increased dispersion of cell sizes in the parvocellular layer (r = 0.8, P < 0.04). These data demonstrate that both atrophy and decreased density contribute to the substantial axonal loss in the anterior visual pathway of these patients. This appears related to a relatively selective atrophy of the smaller neurones of the parvocellular layer in the lateral geniculate nucleus, supporting the hypothesis that smaller axons may be preferentially susceptible to injury in multiple sclerosis.

Adult↗
PubMed1999

Human herpesvirus 6 is latent in peripheral blood of patients with relapsing-remitting multiple sclerosis.

Studies of the association between HHV-6 and multiple sclerosis are hindered by the difficulty in discriminating between latent and active infection. A follow up study was undertaken of patients with multiple sclerosis, searching peripheral blood mononuclear cells for molecular markers associated with HHV-6 latency and lytic replication. The results show that HHV-6 is latent and did not support systemic infection in patients with multiple sclerosis. Likewise, patients with multiple sclerosis did not show any evidence of active infection with other human herpesviruses HHV-7 and HHV-8.

Adolescent↗
PubMed2003

Altered expression patterns of group I and II metabotropic glutamate receptors in multiple sclerosis.

Recent evidence supports a role for glutamate receptors in the pathophysiology of multiple sclerosis. In the present study, we have focused specifically on the expression of metabotropic glutamate receptors (mGluRs) in multiple sclerosis brain tissue. The expression of group I (mGluR1alpha and mGluR5) and group II (mGluR2/3) mGluRs was studied using immunohistochemistry in tissue from 12 multiple sclerosis cases and seven non-neurological controls. The expression patterns of both group I and II mGluRs in multiple sclerosis tissue differed significantly from those in control tissue. Strong mGluR1alpha immunoreactivity was observed in axons of the subcortical white matter, particularly in the centre of actively demyelinating lesions and in the borders of chronic active lesions. mGluR1alpha axonal immunopositivity was also found in normal appearing multiple sclerosis white matter, but axons in control white matter were generally negative. mGluR1alpha axonal labelling was associated with the presence of non-phosphorylated neurofilaments and beta-amyloid precursor protein, which are sensitive markers for axonal injury and disturbed axonal transport. Changes in mGluR immunoreactivity were also observed in glia. A diffuse increase in the expression of mGluR5 and mGluR2/3 was detected in reactive astrocytes in multiple sclerosis lesions. However, only a subpopulation of reactive astroglial cells expressed mGluR1alpha. In addition, labelling with antibodies to mGluR2/3 and, to a lesser extent labelling with antibodies to mGluR1alpha, was detected in a population of cells of the microglial/macrophage lineage that displayed a macrophage-like morphology. Our data suggest that mGluRs, like ionotropic glutamate receptors, play a role in the complex processes that are associated with the progressive brain damage in multiple sclerosis, including both glial activation and pathological changes in axons.

Adult↗
PubMed1980

Bilateral epileptiform discharges in multiple sclerosis.

A case of multiple sclerosis is presented here with bilateral epileptiform discharges which were associated with acute demyelination. The abnormality changed to slow wave activity with the passage of time and as the acute phase of demyelination was over.

Brain↗
PubMed1993

[The diagnostic value of nuclear magnetic resonance tomography, multimodal evoked potentials and cerebrospinal fluid examination in multiple sclerosis].

Seventy patients with multiple sclerosis (according to Poser's criteria) were clinically assessed and examined with MRI, multimodal evoked potentials (VEP, AEP, SSEP) and CSF analysis (transformed lymphocytes, IgG-Index, oligoclonal banding). In relation to the clinical criteria of McAlpine 40 patients had possible, 16 patients probable and 14 patients definite MS. 81% of the patients (73% possible MS, 94% probable MS, 93% definite MS) had multiple white matter lesions detected by MRI, 79% (78% possible MS, 94% probable MS, 64% definite MS) had an abnormal CSF profile and 67% (60% possible MS, 75% probable MS, 79% definite MS) abnormal results in multimodal EP testing. Of the patients who experienced only one attack (n = 40) 78% had multiple lesions on MRI, 88% had abnormal CSF-findings and 60% had pathologic EPs. Patients with two or more attacks showed in 87% multiple lesions on MRI, in 77% abnormal EPs and in 70% abnormal CSF findings. The number of abnormal MRI and EPs increases with the duration of the disease. 13 patients with a normal MRI were discussed separately. MRI is the most sensitive method in detecting the spatial pattern of disseminated lesions. To monitor the dissemination over time a careful clinical follow-up is still mandatory.

Adolescent↗
PubMed1997

A cytotoxic factor for glial cells: a new avenue of research for multiple sclerosis?

A novel retrovirus, provisionally called Multiple Sclerosis RetroVirus (MSRV), was recently described in multiple sclerosis (MS). We report here that monocyte/macrophage culture supernatants from MS patients containing reverse transcriptase activity secrete a cytotoxin which induces death of primary mouse cortical glial cells. This cytotoxin, which was also found in MS cerebrospinal fluid, specifically causes death of mouse immortalized astrocytes and oligodendrocytes in vitro and seems to be associated to MSRV-specific RNA. This toxic factor, called gliotoxin, is present only in active cases of MS and is a stable glycosylated protein of 17 kDa, in CSF as well as in monocyte/macrophage culture supernatants. Since this gliotoxin is highly toxic for glial cells, it may represent an initial pathogenic factor, leading to the neuropathological features of MS, like blood brain barrier disruption and demyelination.

Animals↗
PubMedDate not supplied

Stabilizing suspension procedure involving multiple tendon transfers in a patient with multiple sclerosis.

Patients afflicted with multiple sclerosis develop weaknesses of the lower extremity resulting in drop foot, making ambulation very difficult. A review of the literature by the authors failed to reveal any cases or manuscripts discussing the podiatric management of patients with this disease. This manuscript offers a review of the disease, common principles regarding tendon transfers, a case report, and unique surgical approach consisting of a stabilizing suspension procedure involving multiple tendon transfers. At 1 year following correction, the patient was pleased with the results and ambulatory status.

Adult↗
PubMed2001

A study of tremor in multiple sclerosis.

One hundred patients with definite multiple sclerosis, who were randomly selected from a multiple sclerosis unit in London, were examined in order to study the prevalence, subtypes, clinical features and associated disability of tremor in this population. There were 35 males and 65 females with an average age of 47 years and an average disease duration of 18.8 years. The mean tremor duration was 13 years, with a median latency of 11 years from disease onset to appearance of tremor. Tremor was reported in 37 patients but was detected in 58. Tremor affected the arms (56%), legs (10%), head (9%) and trunk (7%). There were no examples of face, tongue or jaw tremor. All the patients had action tremor, either postural or kinetic (including intention). Rest, Holmes' ('rubral') and primary orthostatic tremors were not encountered. Tremor severity ranged from minimal in 27%, to mild in 16% and moderate or severe in 15% of cases. Tremor severity correlated with the degree of dysarthria, dysmetria and dysdiadochokinesia but not with grip strength. In order to determine the clinical characteristics of these tremors, the action tremors of the upper limbs were subclassified according to the predominant site and state of tremulous activity. Of the 50 patients with tremor in the right arm, 32% had distal postural tremor, 36% had distal postural and kinetic tremor, 16% had proximal postural and kinetic tremor; 4% had proximal and distal postural and kinetic tremor and 12% isolated intention tremor. Twenty-seven percent of the overall study population had tremor-related disability and 10% had incapacitating tremor. Patients with abnormal tremor (severity grade >1/10) were more likely than those without tremor to be wheelchair dependent and have a worse Expanded Disability Systems Score, but Barthel activities of daily living indices and cognitive scores were comparable in the two groups.

Activities of Daily Living↗
PubMedDate not supplied

Multiple sclerosis and brain tumor: a diagnostic challenge.

Multiple sclerosis may present as a lesion indistinguishable clinically and radiologically from brain tumor. A case of multiple sclerosis is reported with clinical and radiologic features of a brain tumor. A brain biopsy was later undertaken that provided pathological confirmation of the diagnosis of this demyelinating disease. This case report in conjunction with those in the literature indicate that conservative treatment with steroid therapy and serial computed tomography should establish the diagnosis of multiple sclerosis without the need for surgical intervention.

Adrenocorticotropic Hormone↗
PubMed1988

The site of the lesion causing deafness in multiple sclerosis.

A patient with multiple sclerosis who developed sequential hearing loss, first on the right, with recovery is discussed. Magnetic resonance imaging demonstrated lesions in the VIII nerve root entry zones which were thought to be responsible for the hearing loss.

Deafness↗
PubMed2002

A longitudinal study of abnormalities on MRI and disability from multiple sclerosis.

BACKGROUND: In patients with isolated syndromes that are clinically suggestive of multiple sclerosis, such as optic neuritis or brain-stem or spinal cord syndromes, the presence of lesions as determined by T2-weighted magnetic resonance imaging (MRI) of the brain increases the likelihood that multiple sclerosis will develop. We sought to determine the relation between early lesion volume, changes in volume, and long-term disability. METHODS: Seventy-one patients in a serial MRI study of patients with isolated syndromes were reassessed after a mean of 14.1 years. Disability was measured with the use of Kurtzke's Expanded Disability Status Scale (EDSS; possible range, 0 to 10, with a higher score indicating a greater degree of disability). RESULTS: Clinically definite multiple sclerosis developed in 44 of the 50 patients (88 percent) with abnormal results on MRI at presentation and in 4 of 21 patients (19 percent) with normal results on MRI. The median EDSS score at follow-up for those with multiple sclerosis was 3.25 (range, 0 to 10); 31 percent had an EDSS score of 6 or more (including three patients whose deaths were due to multiple sclerosis). The EDSS score at 14 years correlated moderately with lesion volume on MRI at 5 years (r=0.60) and with the increase in lesion volume over the first 5 years (r=0.61). CONCLUSIONS: In patients who first present with isolated syndromes suggestive of multiple sclerosis, the increases in the volume of the lesions seen on magnetic resonance imaging of the brain in the first five years correlate with the degree of long-term disability from multiple sclerosis. This relation is only moderate, so the volume of the lesions alone may not be an adequate basis for decisions about the use of disease-modifying treatment.

Adolescent↗