Utilità della risonanza magnetica perfusionale nella diagnosi differenziale tra lesioni demielinizzanti e patologia multinfartuale

1997 ◽  
Vol 10 (2_suppl) ◽  
pp. 35-36
Author(s):  
C. Micheli ◽  
M. Gallucci ◽  
O. Gagliardo ◽  
G. Cardone ◽  
G. B. Minio Paluello ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Arrival Time ◽  
Demyelinating Disease ◽  
Risonanza Magnetica ◽  
Demyelinating Diseases ◽  
Vascular Lesions ◽  
Acquisition Time ◽  
Conventional Mri ◽  
Number Of Patients ◽  
The Difference

20 pts affected by chronic cerebrovascular disease (10) and demyelinating disease (10) were studied by means of conventional MRI and T2*-w dynamic scans (6 slices acquired in 2“, 60 dynamic scans obtained for each slice, total acquisition time ?120”) with the aim of evaluating wether different patterns could be defined between infarctions and demyelinations. 5 subjects were excluded for different reasons. Signal intensity (SI) and transit time (BPAT = Bolus Peak Arrival Time) values were calculated from ROIs positioned on affected and contralateral non affected areas in each pt. In the group affected by demyelinating diseases, data from pathological ROIs were not significantly different from the contralateral, although the basal value of the lesions started from more elevated levels. On the contrary, pts affected by vascular lesions showed significantly different values of SI between pathological ROIs and apparently normal contralateral brain (χ2 test, p<0.001). In two cases, asymmetry of the BPAT due to extracranial carotid stenosis were recorded. In conclusion, our experience encourages the use of perfusional studies with the aim of characterizing pathological processes. The difference recorded between the two groups could suggest wider use of the technique when differential diagnosis between the two pathological entities is not simply obtainable by standard MRI (i.e.: Multiple Sclerosis vs. autoimmune vasculitides). The limited number of patients enrolled in this study makes our results to be considered non definitive, although encouraging.

scholarly journals Multiple Sclerosis in Malaysia: Demographics, Clinical Features, and Neuroimaging Characteristics

2013 ◽  
Vol 2013 ◽  
pp. 1-10 ◽  
Author(s):  
S. Viswanathan ◽  
N. Rose ◽  
A. Masita ◽  
J. S. Dhaliwal ◽  
S. D. Puvanarajah ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Neuromyelitis Optica ◽  
Demyelinating Disease ◽  
Age At Onset ◽  
Positive Family History ◽  
Disease Onset ◽  
Demyelinating Diseases ◽  
Lesion Length ◽  
Relapsing Remitting ◽  
Spectrum Disorders

Background. Multiple sclerosis (MS) is an uncommon disease in multiracial Malaysia. Diagnosing patients with idiopathic inflammatory demyelinating diseases has been greatly aided by the evolution in diagnostic criterion, the identification of new biomarkers, and improved accessibility to neuroimaging in the country.Objectives. To investigate the spectrum of multiple sclerosis in Malaysia.Methods. Retrospective analysis with longitudinal follow-up of patients referred to a single tertiary medical center with neurology services in Malaysia.Results. Out of 245 patients with idiopathic inflammatory demyelinating disease, 104 patients had multiple sclerosis. Female to male ratio was 5 : 1. Mean age at onset was 28.6 ± 9.9 years. The Malays were the predominant racial group affected followed by the Chinese, Indians, and other indigenous groups. Subgroup analysis revealed more Chinese having neuromyelitis optica and its spectrum disorders rather than multiple sclerosis. Positive family history was reported in 5%. Optic neuritis and myelitis were the commonest presentations at onset of disease, and relapsing remitting course was the commonest disease pattern observed. Oligoclonal band positivity was 57.6%. At disease onset, 61.5% and 66.4% fulfilled the 2005 and 2010 McDonald’s criteria for dissemination in space. Mean cord lesion length was 1.86 ± 1.65 vertebral segments in the relapsing remitting group as opposed to 6.25 ± 5.18 vertebral segments in patients with neuromyelitis optica and its spectrum disorders.Conclusion. The spectrum of multiple sclerosis in Malaysia has changed over the years. Further advancement in diagnostic criteria will no doubt continue to contribute to the evolution of this disease here.

Multiple sclerosis and other demyelinating diseases

2011 ◽  
Author(s):  
Alastair Compston
Keyword(s):  
Multiple Sclerosis ◽  
Demyelinating Disease ◽  
Past History ◽  
Central Pontine Myelinolysis ◽  
Clinical Manifestations ◽  
Nerve Impulse ◽  
Demyelinating Diseases ◽  
Clinical Neurology ◽  
Disease Heterogeneity ◽  
Axonal Dysfunction

The oligodendrocyte–myelin unit subserves saltatory conduction of the nerve impulse in the healthy central nervous system. At one time, many disease processes were thought exclusively to target the structure and function of myelin. Therefore, they were designated ‘demyelinating diseases’. But recent analyses, based mainly on pathological and imaging studies, (re)emphasize that axons are also directly involved in these disorders during both the acute and chronic phases. Another ambiguity is the extent to which these are inflammatory conditions. Here, distinctions should be made between inflammation, as a generic process, and autoimmunity in which rather a specific set of aetiological and mechanistic conditions pertain. And there are differences between disorders that are driven primarily by immune processes and those in which inflammation occurs in response to pre-existing tissue damage.With these provisos, the pathological processes of demyelination and associated axonal dysfunction often account for episodic neurological symptoms and signs referable to white matter tracts of the brain, optic nerves, or spinal cord when these occur in young people. This is the clinical context in which the possibility of ‘demyelinating disease’ is usually considered by physicians and, increasingly, the informed patient. Neurologists will, with appropriate cautions, also be prepared to diagnose demyelinating disease in older patients presenting with progressive symptoms implicating these same pathways even when there is no suggestive past history. Both in its typical and atypical forms multiple sclerosis remains by far the commonest demyelinating disease. But acute disseminated encephalomyelitis, the leucodystrophies, and central pontine myelinolysis also need to be considered in particular circumstances; and multiple sclerosis itself has a differential diagnosis in which the relapsing-remitting course is mimicked by conditions not associated with direct injury to the axon–glial unit. Since our understanding of the cause, pathogenesis and features of demyelinating disease remains incomplete, classification combines aspects of the aetiology, clinical features, pathology, and laboratory components. Whether the designation ‘multiple sclerosis’ encapsulates one or more conditions is now much debated. We anticipate that a major part of future studies in demyelinating disease will be further to resolve this question of disease heterogeneity leading to a new taxonomy based on mechanisms rather than clinical empiricism. But, for now, the variable ages of onset, unpredictable clinical course, protean clinical manifestations, and non-specific laboratory investigations continue to make demyelinating disease one of the more challenging diagnostic areas in clinical neurology.

scholarly journals Anti-Myelin Oligodendrocyte Glycoprotein and Human Leukocyte Antigens as Markers in Pediatric and Adolescent Multiple Sclerosis: on Diagnosis, Clinical Phenotypes, and Therapeutic Responses

2018 ◽  
Vol 2018 ◽  
pp. 1-9 ◽  
Author(s):  
Maria P. Gontika ◽  
Maria C. Anagnostouli
Keyword(s):  
Multiple Sclerosis ◽  
Early Onset ◽  
Demyelinating Disease ◽  
Age Of Onset ◽  
Genetic Locus ◽  
Human Leukocyte ◽  
Myelin Oligodendrocyte Glycoprotein ◽  
Demyelinating Diseases ◽  
Disease Course ◽  
Clinical Phenotypes

Early-onset (pediatric and adolescent) multiple sclerosis (MS) is a well-established demyelinating disease that accounts for approximately 3-5% of all MS cases. Thus, identifying potential biomarkers that can reflect the pathogenic mechanisms, disease course and prognosis, and therapeutic response in such patients is of paramount importance. Myelin oligodendrocyte glycoprotein (MOG) has been regarded as a putative autoantigen and autoantibody target in patients with demyelinating diseases for almost three decades. However, recent studies have suggested that antibodies against MOG represent a distinct clinical entity of dominantly humoral profile, with a range of clinical phenotypes closely related to the age of onset, specific patterns of disease course, and responses to treatment. Furthermore, the major histocompatibility complex (MHC)—which has been regarded as the “gold standard” for attributing genetic burden in adult MS since the early 1970s—has also emerged as the primary genetic locus in early-onset MS, particularly with regard to the human leukocyte antigen (HLA) alleles DRB1⁎1501 and DRB1⁎0401. Recent studies have investigated the potential interactions among HLA, MOG, and environmental factors, demonstrating that early-onset MS is characterized by genetic, immunogenetic, immunological, and familial trait correlations. In this paper, we review recent evidence regarding HLA-genotyping and MOG antibodies—the two most important candidate biomarkers for early-onset MS—as well as their potential application in the diagnosis and treatment of MS.

scholarly journals Loss of HDAC11 ameliorates clinical symptoms in a multiple sclerosis mouse model

2018 ◽  
Vol 1 (5) ◽  
pp. e201800039 ◽  
Author(s):  
Lei Sun ◽  
Elphine Telles ◽  
Molly Karl ◽  
Fengdong Cheng ◽  
Noreen Luetteke ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Mouse Model ◽  
Experimental Autoimmune Encephalomyelitis ◽  
Immune Cell ◽  
Demyelinating Disease ◽  
Demyelinating Diseases ◽  
Clinical Severity ◽  
Autoimmune Encephalomyelitis ◽  
Immune Mediated ◽  
Experimental Autoimmune

Multiple sclerosis (MS) is a chronic, immune-mediated, demyelinating disease of the central nervous system (CNS). There is no known cure for MS, and currently available drugs for managing this disease are only effective early on and have many adverse side effects. Results from recent studies suggest that histone deacetylase (HDAC) inhibitors may be useful for the treatment of autoimmune and inflammatory diseases such as MS. However, the underlying mechanisms by which HDACs influence immune-mediated diseases such as MS are unclear. More importantly, the question of which specific HDAC(s) are suitable drug targets for the potential treatment of MS remains unanswered. Here, we investigate the functional role of HDAC11 in experimental autoimmune encephalomyelitis, a mouse model for MS. Our results indicate that the loss of HDAC11 in KO mice significantly reduces clinical severity and demyelination of the spinal cord in the post-acute phase of experimental autoimmune encephalomyelitis. The absence of HDAC11 leads to reduced immune cell infiltration into the CNS and decreased monocytes and myeloid DCs in the chronic progressive phase of the disease. Mechanistically, HDAC11 controls the expression of the pro-inflammatory chemokine C–C motif ligand 2 (CCL2) gene by enabling the binding of PU.1 transcription factor to the CCL2 promoter. Our results reveal a novel pathophysiological function for HDAC11 in CNS demyelinating diseases, and warrant further investigations into the potential use of HDAC11-specific inhibitors for the treatment of chronic progressive MS.

111 Epileptic seizures in multiple sclerosis

2018 ◽  
Vol 89 (6) ◽  
pp. A44.1-A44
Author(s):  
Stephen Walsh ◽  
Joel Corbett ◽  
K Meng Tan ◽  
Simon Broadley
Keyword(s):  
Multiple Sclerosis ◽  
Demyelinating Disease ◽  
Age Of Onset ◽  
Case Reports ◽  
Case Series ◽  
Clinical Information ◽  
Epileptic Seizures ◽  
Disease Course ◽  
Number Of Patients ◽  
Significant Difference

IntroductionEpileptic seizures have been described in association with multiple sclerosis (MS) in both anecdotal case reports and case series. The recent identification of specific antibodies to myelin oligodendrocyte glycoprotein (MOG) protein in a small number of patients with demyelinating disease which may resemble neuromyelitis optica or acute disseminated encephalopathy, which may involve seizures, raises the possibility that anti-MOG antibody related demyelination may account for the association of epilepsy with MS.MethodsWe have undertaken a retrospective review of cases of MS diagnosed at the Gold Coast MS clinic over a 10 year period. All cases were systematically asked if they had ever had an epileptic seizure either via a patient completed questionnaire or at a clinic visit. Demographic and clinical information were also recorded. These data have been analysed using descriptive statistics and appropriate tests for significant differences between those with epilepsy and those without.Results428 cases with complete data were identified. Those with a history of epilepsy were slightly younger (median (range); 44.5 (27–64) years vs 4715–88 years), but this difference was not statistically significantly different. The gender ratio was the same for both groups (9/12 (75%) for those with epilepsy and 326/416 (78%)). There was no significant difference in age of onset, disease course, relapse frequency or level of disability. Although numbers are small, seizure appear to occur most frequently earlier in the disease course and are rarely an ongoing issue.ConclusionThese data support earlier work indicating that epilepsy occurs in people with MS who are younger. This fits with the notion that seizures arise in the context of the inflammatory stage of multiple sclerosis rather than the degenerative phase. Further work needs to be undertaken to assess any association with anti-MOG antibodies and epileptic seizures in demyelinating disease.

scholarly journals Myelin oligodendrocyte glycoprotein antibody-associated disease: an immunopathological study

Brain ◽  
2020 ◽  
Vol 143 (5) ◽  
pp. 1431-1446 ◽  
Author(s):  
Yoshiki Takai ◽  
Tatsuro Misu ◽  
Kimihiko Kaneko ◽  
Norio Chihara ◽  
Koichi Narikawa ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Humoral Immunity ◽  
Demyelinating Disease ◽  
Myelin Oligodendrocyte Glycoprotein ◽  
Demyelinating Diseases ◽  
Perivascular Spaces ◽  
Clinical Diagnoses ◽  
Demyelinating Lesions ◽  
Oligoclonal Igg ◽  
Aqp4 Antibody

Abstract Conformation-sensitive antibodies against myelin oligodendrocyte glycoprotein (MOG) are detectable in patients with optic neuritis, myelitis, opticomyelitis, acute or multiphasic disseminated encephalomyelitis (ADEM/MDEM) and brainstem/cerebral cortical encephalitis, but are rarely detected in patients with prototypic multiple sclerosis. So far, there has been no systematic study on the pathological relationship between demyelinating lesions and cellular/humoral immunity in MOG antibody-associated disease. Furthermore, it is unclear whether the pathomechanisms of MOG antibody-mediated demyelination are similar to the demyelination patterns of multiple sclerosis, neuromyelitis optica spectrum disorders (NMOSD) with AQP4 antibody, or ADEM. In this study, we immunohistochemically analysed biopsied brain tissues from 11 patients with MOG antibody-associated disease and other inflammatory demyelinating diseases. Patient median onset age was 29 years (range 9–64), and the median interval from attack to biopsy was 1 month (range 0.5–96). The clinical diagnoses were ADEM (n = 2), MDEM (n = 1), multiple brain lesions without encephalopathy (n = 3), leukoencephalopathy (n = 3) and cortical encephalitis (n = 2). All these cases had multiple/extensive lesions on MRI and were oligoclonal IgG band-negative. Most demyelinating lesions in 10 of 11 cases showed a perivenous demyelinating pattern previously reported in ADEM (153/167 lesions) and a fusion pattern (11/167 lesions) mainly in the cortico-medullary junctions and white matter, and only three lesions in two cases showed confluent demyelinated plaques. In addition, 60 of 167 demyelinating lesions (mainly in the early phase) showed MOG-dominant myelin loss, but relatively preserved oligodendrocytes, which were distinct from those of AQP4 antibody-positive NMOSD exhibiting myelin-associated glycoprotein-dominant oligodendrogliopathy. In MOG antibody-associated diseases, MOG-laden macrophages were found in the perivascular spaces and demyelinating lesions, and infiltrated cells were abundant surrounding multiple blood vessels in and around the demyelinating lesions, mainly consisting of macrophages (CD68; 1814 ± 1188 cells/mm2), B cells (CD20; 468 ± 817 cells/mm2), and T cells (CD3; 2286 ± 1951 cells/mm2), with CD4-dominance (CD4+ versus CD8+; 1281 ± 1196 cells/mm2 versus 851 ± 762 cells/mm2, P &lt; 0.01). Humoral immunity, evidenced by perivascular deposits of activated complements and immunoglobulins, was occasionally observed in some MOG antibody-associated demyelinating lesions, and the frequency was much lower than that in AQP4 antibody-positive NMOSD. Subpial lesions with perivenous demyelination were observed in both ADEM and cortical encephalitis. Our study suggests that ADEM-like perivenous inflammatory demyelination with MOG-dominant myelin loss is a characteristic finding of MOG antibody-associated disease regardless of whether the diagnostic criteria of ADEM are met. These pathological features are clearly different from those of multiple sclerosis and AQP4 antibody-positive NMOSD, suggesting an independent autoimmune demyelinating disease entity.

scholarly journals State-of-the-Art Review: Demyelinating Diseases in Indonesia

2021 ◽  
Vol 2021 ◽  
pp. 1-15
Author(s):  
Hana Larassati ◽  
Riwanti Estiasari ◽  
Reyhan E. Yunus ◽  
Paul M. Parizel
Keyword(s):  
Multiple Sclerosis ◽  
Demyelinating Disease ◽  
State Of The Art ◽  
Acute Disseminated Encephalomyelitis ◽  
Demyelinating Diseases ◽  
Diagnostic Process ◽  
Imaging Features ◽  
Indonesian Population ◽  
The Central Nervous System ◽  
Medical Advances

Demyelinating diseases are more common in Indonesia than previously believed. However, it is still a challenge for a country such as Indonesia to implement the scientific medical advances, especially in the diagnostic process of demyelinating diseases, to achieve the best possible outcome for these groups of patients, within the constraints of what is socially, technologically, economically, and logistically achievable. In this review, we address the 4 major classes of demyelinating disease: multiple sclerosis (MS), neuromyelitis optica (NMO), anti-MOG-associated encephalomyelitis (MOG-EM), and acute disseminated encephalomyelitis (ADEM), and discuss their prevalence, demographics, clinical diagnosis workup, and imaging features in the Indonesian population, as well as the challenges we face in their diagnosis and therapeutic approach. We hope that this overview will lead to a better awareness of the spectrum of demyelinating diseases of the central nervous system in Indonesia.

scholarly journals Old Dog Encephalitis and Demyelinating Diseases in Man

1975 ◽  
Vol 12 (3) ◽  
pp. 220-226 ◽  
Author(s):  
J. M. Adams ◽  
W. J. Brown ◽  
H. D. Snow ◽  
S. D. Lincoln ◽  
A. W. Sears ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Neuromyelitis Optica ◽  
Plasma Cells ◽  
Demyelinating Disease ◽  
Subacute Sclerosing Panencephalitis ◽  
Fluorescent Antibody ◽  
Optic Tract ◽  
Demyelinating Diseases ◽  
Relationship Of ◽  
Perivascular Infiltration

Pathologic findings in mature dogs with old dog encephalitis were compared with the findings in multiple sclerosis, subacute sclerosing panencephalitis and neuromyelitis optica in man. Fluorescent antibody studies in animal and human tissues were compared. Optic neuritis in dogs with chronic distemper shows changes similar to those in the optic tract of human patients with severe demyelinating disease. The pathologic changes in multiple sclerosis, such as perivascular infiltration with lymphocytes, plasma cells and demyelination are similar to those seen in old dog encephalitis. Demyelination in old dog encephalitis is usually diffuse. The findings strongly support a possible relationship of old dog encephalitis to multiple sclerosis, subacute sclerosing panencephalitis, and neuromyelitis optica.

scholarly journals Radiologically Definite Multiple Sclerosis (RDMS) as a New Terminology in Demyelinating Disease

2013 ◽  
Vol 2 (4) ◽  
pp. 187-188
Author(s):  
Sadegh Izadi
Keyword(s):  
Multiple Sclerosis ◽  
Demyelinating Disease ◽  
Neurological Diseases ◽  
Neurological Symptoms ◽  
Demyelinating Diseases ◽  
Mri Findings ◽  
Disease Modifying Drugs ◽  
Definite Multiple Sclerosis ◽  
Disease Modifying ◽  
Symptoms And Signs

Dear editor Multiple sclerosis (MS) is the most common inflammatory demyelinating disease of the central nervous system. MS is characterized by dissemination in time and place. Dissemination can be clinically (clinically definite multiple sclerosis) or radiologically by magnetic resonance imaging (MRI). Correct diagnosis of MS needs dissemination both in time and in place and also exclusion of all other neurological diseases that can mimic MS. Clinically, dissemination in time is defined as two episodes of neurological symptoms occurrence, separated at least one month apart, and dissemination in place is characterized as the presence of symptoms or signs in at least two different parts of central nervous system (CNS) (e.g. visual, sensory, motor, etc.). Radiologically dissemination in space (DIS) was defined as the presence of clinically silent lesions in T2-weighted MRI in two of four locations including juxtacortical, preventricular, infratentorial, and spinal cord and dissemination in time (DIT) as the presence of simultaneous gadolinium enhancing and non enhancing lesions in MRI [1,2]. There are some terminologies which are frequently used in patients with demyelinating disorders including clinically definite MS (CDMS), clinically isolated syndrome (CIS) and radiologically isolated syndrome (RIS) [1-3]. CDMS is defined as two attacks of neurological symptoms in two different neurological systems (e.g. optic neuritis and myelitis) separated and apart for at least one month [1]. Radiologically isolated syndrome (RIS) was used in persons with MRI findings suggestive of MS without typical symptoms and signs [3].CIS is defined as the first episode of neurological symptoms and signs suggestive of MS. The onset of MS in 85% of patients presents as CIS. This terminology is widely used in clinical practice. By definition, CIS is always clinically isolated in time. Around 50-70% of patients with CIS have white matter lesions in brain or spinal MRI. On the other hand, CIS usually represents a wide clinical spectrum of diseases of CNS and can be present in a multitude of clinical manifestation [1, 2].At present time, MRI is the most important tool for diagnosis of MS in patients with CIS and the application of MRI for diagnosis of MS has been increased during the past few years [4]. Today, the diagnosis of MS is possible very earlier than before due to the wide integration of MRI in McDonalds’ criteria (2010). MacDonald’s criteria mostly rely on MRI findings to facilitate the early diagnosis of MS [1, 4]. By using the new MacDonald’s criteria some patients who presented with CIS can be diagnosed as MS if MRI fulfills dissemination in time and space. For patients who fulfill the criteria of both DIT and DIS, the term of CDMS is used; but for patients who have had one attack of neurological symptoms and fulfill DIT and DIS radiologically (by MRI) there is no appropriate terminology and all of them are classified as CIS [2, 4]. We know that this terminology is somewhat ambiguous, because CIS may be the first presentation of many neurological diseases including demyelinating diseases, inflammatory diseases such as vasculitis or non-inflammatory non-demyelinating diseases like vascular lesions [2].We recommend the term of radiologically definite MS (RDMS) for patients who have had one attack of neurological symptoms and fulfill DIT and DIS radiologically by MRI. Because many neurologists are not completely familiar with the term CIS and some are confused about it, we need an appropriate terminology to use in every day’s clinical practice. Also, early diagnosis of MS in patients with CIS is very important. Because early treatment of patients with CIS by disease modifying drugs including Beta-Interferon can delay turning into CDMS and also decreases brain atrophy and new brain lesions. All current disease modifying drugs have been shown to be effective in treating CIS [5]. But it is clear that all patients with CIS do not require these treatments and only those patients who show dissemination in time and space by MRI should be treated by these agents [2, 6].In conclusion, radiologicaly definite MS (RDMS) is the recommended terminology for patients who have one attack of neurological symptoms and radiologically fulfill DIT and DIS criteria and these patients should be treated by disease modifying agents as well.

How similar are commonly combined criteria for EDSS progression in multiple sclerosis?

2006 ◽  
Vol 12 (6) ◽  
pp. 782-786 ◽  
Author(s):  
J J Kragt ◽  
J M Nielsen ◽  
F AH van der Linden ◽  
B MJ Uitdehaag ◽  
C H Polman
Keyword(s):  
Multiple Sclerosis ◽  
Neurological Impairment ◽  
Point Change ◽  
Perceived Disability ◽  
Number Of Patients ◽  
Sum Score ◽  
Disability Status ◽  
Edss Score ◽  
The Difference ◽  
Quantitative Scoring

Introduction Measuring disease progression is an important aspect of multiple sclerosis (MS) clinical trials. Commonly applied disability endpoints include time to clinically meaningful Expanded Disability Status Scale (EDSS) change, or the number of patients in whom such a change has occurred. Typically, clinically meaningful EDSS change has been defined as a change of 1.0 point on Kurtzke’s EDSS in patients with an entry EDSS score of 5.5 or lower, or 0.5 point in patients with a higher EDSS score. Our goal was to evaluate whether these changes can be considered as similar. Therefore, we compared EDSS changes to corresponding changes in the Guy’s Neurological Disability Scale (GNDS), which is a measure of patient perceived disability, and the Multiple Sclerosis Functional Composite (MSFC), which is an examination-based quantitative scoring of neurological impairment. Methods From a large longitudinal database, we selected two groups of patients with a clinically meaningful change in EDSS score according to the usual criteria: patients with EDSS change]/1.0 for baseline EDSS 5/5.5 and patients with EDSS change]/0.5 for baseline EDSS]/6.0. We compared changes in GNDS sum score and in MSFC score between both groups. Results In the group with baseline EDSS]/6.0, GNDS and MSFC changes were higher than in patients with baseline EDSS 5/5.5. The difference in change was 1.00 (95% confidence interval (CI): / 0.35 to 2.36) for the GNDS and 0.412 (95% CI: 0.300-0.525) for the MSFC. Conclusion Our results indicate that a 0.5 point EDSS change in patients with baseline EDSS / 6.0 cannot be considered equal to a 1.0 point change in patients with baseline EDSS 5/5.5.

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