scholarly journals Magnetic resonance imaging in the diagnosis of multiple sclerosis cerebral foci

2001 ◽  
Vol XXXIII (3-4) ◽  
pp. 78-83
Author(s):  
M. M. Ibatullin ◽  
T. V. Matveeva ◽  
A. M. Anufriev
Keyword(s):  
Multiple Sclerosis ◽  
Demyelinating Disease ◽  
The United States ◽  
Pathological Feature ◽  
Subsequent Formation ◽  
Working Age ◽  
Autoimmune Processes ◽  
Subcortical Nuclei ◽  
Sclerotic Plaques

The close attention to the problem of multiple sclerosis (MS) is by no means accidental. The widespread prevalence of the disease, the young age of the patients, the low effectiveness of therapy and the high percentage of disability among people of the most working age cause extreme concern [3, 7, 19]. MS is the most common demyelinating disease of the nervous system, which is characterized by a polysymptomatic and recurrent course [1, 4, 5, 59]. According to R. Detd. et al. (1977) and S.M. Poser et al. (1983), MS occurs in 4-10% of cases in different countries, more often in the south of Russia, Israel, the United States, Europe and Latin America. The pathogenesis of the disease is not fully understood, in particular, the role of genetic factors and autoimmune processes in the mechanisms of MS development has not been fully determined [2, 55, 70]. The basis of the disease is the process of demyelination with the formation of disseminated dense sclerotic foci in the white matter of the brain [31, 33]. These foci, resembling gliosis scars, are the result of a local inflammatory process, accompanied by the destruction of the myelin sheaths and axons of nerve cells [28]. The pathological feature of MS is considered to be a violation of the blood-brain barrier. In the acute phase of the disease, the disintegration of oligodendrocytes, which make up the myelin sheath of axons, and the migration of activated immune cells to the focus of antigenic conflict (into microglia and astrocytes) occur. In this case, there is muff-like adhesion of endothelial cells and leukocytes around venules and along the pathways with the subsequent formation of dense sclerotic plaques [8, 16]. In some cases, remyelination occurs, and then re-disintegration with the formation of plaques. In postmortem examination, MS foci are most often detected near the anterior and posterior parts of the lateral ventricles, in the region of the semi-oval center, subcortical nuclei, trunk, cerebellum, in the spinal cord, and also in the optic nerves.

Review of neurological rehabilitation for Multiple Sclerosis in the British Military

2021 ◽  
pp. bmjmilitary-2021-001852
Author(s):  
Oliver O'Sullivan ◽  
L Allsopp ◽  
J Mitchell ◽  
L Price ◽  
K Tourle ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Armed Forces ◽  
Medical Rehabilitation ◽  
Neurological Rehabilitation ◽  
Patient Support ◽  
Rehabilitation Centre ◽  
Occupational Outcomes ◽  
British Military ◽  
Working Age

Multiple sclerosis (MS) is a progressive neurological disorder, classically presenting in working age adults, including those in the Armed Forces. The Defence Medical Rehabilitation Centre (DMRC) Stanford Hall offers vocationally focused neurorehabilitation services for service personnel (SP) with MS, with the goal to minimise disability, maximise independence and remain able to work.This paper has two aims. First, it briefly provides a clinical update of MS, focusing on pathology, presentation, diagnosis and management. Finally, it will describe the role of DMRC and data from the last decade in the management of MS.Our findings suggest not all SP with MS are being referred to DMRC, and some of those who do have significant delays, potentially impacting on patient support, symptom management and occupational outcomes. It is hoped that this paper will improve awareness and recognition of MS for Armed Forces personnel.

scholarly journals Myelin oligodendrocyte glycoprotein antibodies in pathologically proven multiple sclerosis: frequency, stability and clinicopathologic correlations

2007 ◽  
Vol 13 (1) ◽  
pp. 7-16 ◽  
Author(s):  
S J Pittock ◽  
M Reindl ◽  
S Achenbach ◽  
T Berger ◽  
W Bruck ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Western Blot ◽  
Demyelinating Disease ◽  
Clinical Course ◽  
Myelin Oligodendrocyte Glycoprotein ◽  
Poor Agreement ◽  
Predictive Role ◽  
Mog Antibodies ◽  
Serial Measurements

Controversy exists regarding the pathogenic or predictive role of anti-myelin oligodendrocyte glycoprotein (MOG) antibodies in patients with multiple sclerosis (MS). Four immunopathological patterns (IP) have been recognized in early active MS lesions, suggesting heterogeneous pathogenic mechanisms. Whether MOG antibodies contribute to this pathological heterogeneity and potentially serve as biomarkers to identify specific pathological patterns is unknown. Here we report the frequencies of antibodies to human recombinant MOG (identified by Western blot and enzymelinked immunoabsorbent assay (ELISA)) in patients with pathologically proven demyelinating disease, and investigate whether antibody status is associated with clinical course, HLA-DR2 genotype, IP or treatment response to plasmapheresis. The biopsy cohort consisted of 72 patients: 12 pattern I, 43 pattern II and 17 pattern III. No association was found between MOG antibody status and conversion to clinically definite MS, DR-2 status, IP or response to plasmapheresis. There was poor agreement between Western blot and ELISA (kappa=0.07 for MOG IgM). Fluctuations in antibody seropositivity were seen for 3/4 patients tested serially by Western blot. This study does not support a pathologic pattern-specific role for MOG-antibodies. Variable MOG-antibody status on serial measurements, coupled with the lack of Western blot and ELISA correlations, raises concern regarding the use of MOG-antibody as an MS biomarker and underscores the need for methodological consensus.

Social Security Disability Application Experiences of People With Multiple Sclerosis in the United States

2007 ◽  
Vol 9 (4) ◽  
pp. 131-138 ◽  
Author(s):  
Lisa I. Iezzoni ◽  
Long Ngo ◽  
R. Philip Kinkel
Keyword(s):  
Multiple Sclerosis ◽  
Social Security ◽  
Disability Insurance ◽  
The United States ◽  
Legal Assistance ◽  
Income Support ◽  
Social Security Administration ◽  
The Social ◽  
Working Age ◽  
Social Security Disability

Studies suggest that more than half of working-age Americans with multiple sclerosis (MS) are unemployed because of their health. Many turn to public disability insurance for income support, applying through the Social Security Administration for either Social Security Disability Insurance (SSDI), which provides benefits to formerly employed people, or Supplemental Security Income (SSI), which supports impoverished individuals. Anecdotal reports suggest that many patients with MS face considerable problems when applying for federal disability benefits. To gather more systematic information about these experiences, we surveyed 983 working-age people with MS nationwide from May through November 2005. Most (60.2%) were unemployed; 36.4% had federal disability insurance, with 27.8% having SSDI alone. Almost one third (31.3%) had their initial SSDI application denied, and 31.9% used legal assistance when applying for this benefit. Although the time elapsed between SSDI application and approval was <12 months for 60.4% of applicants, 12–23 months passed for 19.8% and 24+ months for another 19.8%. Among people without SSDI, 15.4% had applied for this benefit at some time. Failure to meet disability criteria caused 60.3% of rejections, and inadequate documentation contributed to 32.1%. Neurologists must fully document the breadth of MS-related impairments in their patients' disability applications.

Multiple sclerosis attacks are associated with picornavirus infections

2004 ◽  
Vol 10 (2) ◽  
pp. 145-148 ◽  
Author(s):  
John D Kriesel ◽  
Andrea White ◽  
Frederick G Hayden ◽  
S L Spruance ◽  
Jack Petajan
Keyword(s):  
Multiple Sclerosis ◽  
At Risk ◽  
Demyelinating Disease ◽  
Respiratory Infections ◽  
Risk Period ◽  
Relapsing Remitting ◽  
The Central Nervous System ◽  
Upper Respiratory ◽  
Polymerase Chain

Multiple sclerosis (MS) is a chronic demyelinating disease of the central nervous system, which often follows a relapsing-remitting (RR) course with discrete attacks. MS attacks have been associated with upper respiratory infections (URIs), but the specific viruses responsible have not been identified. We studied a cohort of 16 RRMS patients experiencing URI and followed them for clinically identifiable attacks. The viral causes of 21 separate URIs were investigated using culture and polymerase chain reactio n (PCR) of nasal swab specimens, and by serology. Sibley’s ‘at-risk’ period for MS attacks, beginning two weeks before and continuing for five weeks after a URI, was used for the analysis. Seven of the nine (78%) URIs due to picornaviruses were associated with an MS attack during the at-risk period. By contrast, only two of 12 (17%) picornavirus-negative URIs were associated with an MS attack (P =0.01). The possible role of picornaviruses in the patho genesis of MS deserves further study.

Is There a Case for a Virus Aetiology in Multiple Sclerosis?

1995 ◽  
Vol 40 (2) ◽  
pp. 55-62 ◽  
Author(s):  
Bernard E. Souberbielle ◽  
Paul W.S. Szawlowski ◽  
William C. Russell
Keyword(s):  
Multiple Sclerosis ◽  
Demyelinating Disease ◽  
Autoimmune Response ◽  
Aggressive Approach ◽  
Shetland Islands ◽  
North East ◽  
High Prevalence ◽  
Specific Virus ◽  
Very High

Multiple Sclerosis (MS) is a devastating demyelinating disease with a very high prevalence in North-East Scotland and in the Orkney and Shetland Islands. MS appears to be a multifactorial disorder with environmental and genetic elements and it has been proposed that these, in tandem, provoke an autoimmune response giving rise to the disease. Although there is no direct evidence of a specific virus being involved in MS, there are nevertheless grounds for suspecting a viral association. This review discusses these aspects of MS and suggests that a more aggressive approach to unravelling the role of viruses is needed.

scholarly journals A Review of Vascular Disease Risk Factors and Multiple Sclerosis

US Neurology ◽  
2017 ◽  
Vol 13 (02) ◽  
pp. 90
Author(s):  
Meena R Kannan ◽  
Vijayshree Yadav ◽  
◽  
Keyword(s):  
Risk Factors ◽  
Multiple Sclerosis ◽  
Vascular Disease ◽  
Type Ii Diabetes ◽  
Demyelinating Disease ◽  
Disease Risk ◽  
Current Knowledge ◽  
Type Ii Diabetes Mellitus ◽  
The Central Nervous System

Multiple sclerosis (MS) is the most common demyelinating disease of the central nervous system and the most common non-traumatic cause of disability in young adults. Recent research shows that vascular disease risk factors (VDRFs) such as obesity, smoking, hyperlipidemia, hypertension, type II diabetes mellitus, and metabolic syndrome, can influence MS on its onset, disease activity, progression, and resultant disability. This review evaluates the current knowledge on the role of VDRFs on outcomes among people with MS (PwMS) and shows that while VDRF prevalence may or may not be higher among PwMS compared with the general population, its presence can influence MS in myriad ways. Management of VDRFs through early detection and treatment may be a promising approach to improving outcomes in PwMS.

Role of Gut Microbiota in Multiple Sclerosis and Potential Therapeutic Implications

2021 ◽  
Vol 19 ◽  
Author(s):  
Xu Wang ◽  
Zhen Liang ◽  
Shengnan Wang ◽  
Di Ma ◽  
Mingqin Zhu ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Gut Microbiota ◽  
Demyelinating Disease ◽  
Inflammatory Diseases ◽  
Intestinal Barrier ◽  
Autoimmune Response ◽  
Therapeutic Implications ◽  
The Central Nervous System ◽  
Underlying Mechanisms

: The role of gut microbiota in health and diseases has been receiving increased attention recently. Emerging evidence from previous studies on the gut-microbiota-brain axis highlighted the importance of gut microbiota in neurological disorders. Multiple sclerosis (MS) is a chronic, inflammatory, demyelinating disease of the central nervous system (CNS) resulting from T-cell-driven, myelin-directed autoimmunity. The dysbiosis of gut microbiota in MS patients has been reported in published research studies, indicating that gut microbiota plays an important role in the pathogenesis of MS. Gut microbiota has also been reported to influence the initiation of disease and severity of experimental autoimmune encephalomyelitis, which is the animal model of MS. However, the underlying mechanisms of gut microbiota involvement in the pathogenesis of MS remain unclear. Therefore, in this review, we summerized the potential mechanisms for gut microbiota involvement in the pathogenesis of MS, including increasing the permeability of the intestinal barrier, initiating an autoimmune response, disrupting the blood-brain barrier integrity, and contributing to chronic inflammation. The possibility for gut microbiota as a target for MS therapy has also been discussed. This review provides new insight into understanding the role of gut microbiota in neurological and inflammatory diseases.

scholarly journals Overcoming the inhibitory microenvironment surrounding oligodendrocyte progenitor cells following experimental demyelination

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Darpan Saraswat ◽  
Hani J. Shayya ◽  
Jessie J. Polanco ◽  
Ajai Tripathi ◽  
R. Ross Welliver ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Progenitor Cells ◽  
Demyelinating Disease ◽  
Heparan Sulfate Proteoglycans ◽  
Oligodendrocyte Progenitor Cells ◽  
Subsequent Generation ◽  
Oligodendrocyte Progenitor ◽  
Demyelinating Lesions ◽  
Experimental Demyelination

AbstractChronic demyelination in the human CNS is characterized by an inhibitory microenvironment that impairs recruitment and differentiation of oligodendrocyte progenitor cells (OPCs) leading to failed remyelination and axonal atrophy. By network-based transcriptomics, we identified sulfatase 2 (Sulf2) mRNA in activated human primary OPCs. Sulf2, an extracellular endosulfatase, modulates the signaling microenvironment by editing the pattern of sulfation on heparan sulfate proteoglycans. We found that Sulf2 was increased in demyelinating lesions in multiple sclerosis and was actively secreted by human OPCs. In experimental demyelination, elevated OPC Sulf1/2 expression directly impaired progenitor recruitment and subsequent generation of oligodendrocytes thereby limiting remyelination. Sulf1/2 potentiates the inhibitory microenvironment by promoting BMP and WNT signaling in OPCs. Importantly, pharmacological sulfatase inhibition using PI-88 accelerated oligodendrocyte recruitment and remyelination by blocking OPC-expressed sulfatases. Our findings define an important inhibitory role of Sulf1/2 and highlight the potential for modulation of the heparanome in the treatment of chronic demyelinating disease.

scholarly journals Overcoming the inhibitory microenvironment surrounding oligodendrocyte progenitor cells following demyelination

2020 ◽  
Author(s):  
Darpan Saraswat ◽  
Hani J. Shayya ◽  
Jessie J. Polanco ◽  
Ajai Tripathi ◽  
R. Ross Welliver ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Progenitor Cells ◽  
Demyelinating Disease ◽  
Heparan Sulfate Proteoglycans ◽  
Oligodendrocyte Progenitor Cells ◽  
Subsequent Generation ◽  
Oligodendrocyte Progenitor ◽  
Demyelinating Lesions ◽  
Experimental Demyelination

Chronic demyelination in the human CNS is characterized by an inhibitory microenvironment that impairs recruitment and differentiation of oligodendrocyte progenitor cells (OPCs) leading to failed remyelination and axonal atrophy. By network-based transcriptomics, we identified sulfatase 2 (Sulf2) mRNA in activated human primary OPCs. Sulf2, an extracellular endosulfatase, modulates the signaling microenvironment by editing the pattern of sulfation on heparan sulfate proteoglycans. We found that Sulf2 was increased in demyelinating lesions in multiple sclerosis and was actively secreted by human OPCs. In experimental demyelination, elevated OPC Sulf1/2 expression directly impaired progenitor recruitment and subsequent generation of oligodendrocytes thereby limiting remyelination. Sulf1/2 potentiates the inhibitory microenvironment by promoting BMP and WNT signaling in OPCs. Importantly, pharmacological sulfatase inhibition using PI-88 accelerated oligodendrocyte recruitment and remyelination by blocking OPC-expressed sulfatases. Our findings define an important inhibitory role of Sulf1/2 and highlight the potential for modulation of the heparanome in the treatment of chronic demyelinating disease.

Multiple Sclerosis: A Systemic Review of Drugs and Therapeutics

2017 ◽  
Vol 1 (3) ◽  
pp. 01-03
Author(s):  
Theodore Eric
Keyword(s):  
Multiple Sclerosis ◽  
Demyelinating Disease ◽  
Disease Process ◽  
The United States ◽  
Systemic Review ◽  
Patient Response ◽  
Relapsing Remitting ◽  
The Central Nervous System ◽  
Individual Patient Response ◽  
Phase Ii And Iii

Multiple sclerosis (MS) is a chronic inflammatory autoimmune demyelinating disease of the central nervous system. It affects approximately 400,000 people in the United States and onset is usually during young adulthood. There are four clinical forms of MS, of which relapsing remitting type is the most common. As the etiology of MS is unknown, finding a cure will remain challenging. The main mechanism of injury appears to be inflammation and 8 agents are now FDA approved to help control MS. These agents for relapsing forms of MS target different parts of the immune system, with the end goal of decreasing and avoiding further inflammation. No agents are FDA approved for the primary progressive version of MS. FDA approved agents include four preparations of interferon β (Avonex, Rebif, Betaseron and Extavia), glatiramer acetate (Copaxone), mitoxantrone (Novantrone), natalizumab (Tysabri) and fingolimod (Gilenya). There are several drug undergoing phase II and III trials. The heterogeneity of the MS disease process, individual patient response, and medication toxicities continue to challenge the treating physician.

Sign in / Sign up

Export Citation Format

Share Document