View clinical trials related to Multiple Sclerosis.
Filter by:The current project will fill a knowledge gap in the follow-up of people with Multiple Sclerosis (MS) with mild and moderate disability levels, with the purpose to assess the adequacy of measurement tools for trunk control and balance, functions that are pre-requisites for optimal performance in everyday physical activities.
Participation in medical trials usually favors a particular demographic group. But there is limited research available to explain what trial attributes affect the completion of these specific demographic groups. This study will admit a wide range of data on the clinical trial experience of Multiple Sclerosis patients to determine which factors prevail in limiting a patient's ability to join or finish a trial. It will also try to analyze data from the perspective of different demographic groups to check for recurring trends which might yield insights for the sake of future Multiple Sclerosis patients.
In total, 27 patients with MS (Expanded Disability Status Scale (EDSS) score equal to or less than 5.5) were randomly assigned to either Telko plus conventional physical therapy (CPT) experimental group (n=14) or the CPT control group (n=13). All patients received 15-minute CPT, three times a week, for four weeks. The patients in the experimental group received 15-minute Telko at the end of each CPT session. The outcome measures used were the Berg Balance Scale (BBS), 6-Minute Walk Test (6MWT), and Timed Up and Go (TUG) assessment.
Multiple sclerosis (MS) is an autoimmune neurodegenerative disease characterized by demyelination and neurodegeneration of the central nervous system (CNS) . Current diagnostic criteria and management depend on MRI, clinical status, and oligoclonal immunoglobulin g bands . These markers often fail to predict relapse, progression and therapy response .There is an increased need to identify biomarkers for clinical endpoints . One of the hallmark features of MS is axonal damage which associated with brain and cervical atrophy.Nf levels indicate the extent of axonal damage. Neurofilaments are composed of four subunits: neurofilament light polypeptides (NfL) is the most abundant and soluble and it is highly sensitive to neurodegenerative processes . Chitinase 3-like 1 (CHI3L1) is expressed in astrocytes in the brain tissue of MS patients . CHI3L1 plays a role as prognostic biomarker in patients with MS. CHI3L1 cerebrospinal fluid levels were associated correlated with disease activity and neurological disability. Dendritic cells (DCs) are highly specialized antigen-presenting cells with a key role in activating and preventing CNS immune-mediated damage in MS . Dendritic cells express Human Leukocyte Antigen-antigen D Related (HLA-DR) . Plasmacytoid dendritic cells characterized by the expression of blood dendritic cells antigen-2 (BDCA-2) .Plasmacytoid dendritic cells are present in the cerebrospinal fluid (CSF), leptomeninges and demyelinating lesions of patients with MS . Plasmacytoid dendritic cells also exhibit up-regulation of chemokine (CCR7C) expression. It was demonstrated increased amounts of chemokine CCR7 in the CSF from MS patients during relapses .CCR7 controls migration and functional activity of regulatory T cells and plays an important role in the establishment of tolerance . Tolerogenic DCs (TolDCs) present an intermediate phenotype between immature dendritic cells (iDCs) and mature dendritic cells (mDCs) regarding costimulatory molecules, a pronounced shift toward anti-inflammatory . TolDCs exhibit tolerogenic molecules such as HLA-G and CD274 [programmed death-ligand 1 (PD-L1)] either in peripheral blood or in CSF. These characteristics lead to T cell clonal anergy and T cell unresponsiveness due to Ag presentation in the presence of low co-stimulation .We aim to investigate the role of NfL,(CHI3L1) and markers of plasmacytoid dendritic cells in MS.
The aim of the study is to analyze the effects of Nordic Walking and free walking in the clinical-functional, postural balance, motor control, muscular echographic quality, and gait analysis (pendulum gait mechanism), in people with Multiple Sclerosis.
Many neuropsychiatric abnormalities associated with multiple sclerosis (MS). These may be broadly divided into 2 categories: disorders of mood, affect,and behavior and abnormalities affecting cognition. With respect to the former, theepidemiology, phenomenology, and theories of etiology are described for the syndromes ofdepression, bipolar disorder, euphoria, pathological laughing and crying, and psychosisattributable to MS. Finally,treatment pertaining to all these disorders is reviewed, with the observation thattranslational research has been found wanting when it comes to providing algorithms toguide clinicians. Guidelines derived from general psychiatry still largely apply, althoughthey may not always be most effective in patients with neurologic disorders. The importance of future research addressing this imbalance is emphasized, forneuropsychiatric sequel add significantly to the morbidity associated with MS.(1) The evolution of the neuropsychiatry of multiple sclerosis(MS), with a set sequence of events unfoldingoverthecourseofacenturyormore,providesahistoricalparadigmforotherneurologicdisorders .Accordingtotheparadigm,aclinically astute neurologist, whom posterity will treat kindly,first describes the neurologic (and occasionally, the psycho-logical) signs and symptomsthat cometo define the disorder. Over succeeding decades, the diagnostic criteria arerefined by further observation supplemented by data fromnew technologies. Mental state changes either pass with littlenoticeoraremissed.Acoupleofgenerationslatercomes belated recognition of prominent abnormalities in mentation-neuropsychiatryredux. . Invariably, the data reveal major psychiatric problems integral to the disease, and then, with fewexceptions, clinical research stops. Few double-blind,placebo-controlled treatment trials in neuropsychiatry provide an evidence-based approach to treating the newly discernedbehaviouralabnormalities. ThelifetimeprevalenceofmajordepressioninMS isapproximately 50% (2). A meta-analysis suggests that this is higherthan in other neurologic disorders (3) and, depending on thereferencepoint,is3to10 timestherateinthegeneral population (4). While the basic phenomenology of the MS depressive syndrome overlaps with that found in primarydepression, certain symptoms are more typical, while othersoccur less commonly. Thus, irritability, discouragement, andasenseoffrustration aremorelikelytoaccompanylowmoodthan are feelings of guilt and poor self-esteem (5). It is alsoimportanttorememberthatsymptomssuchasinsomnia,poorappetite,anddifficultieswithconcentrati onandmemorymaybe equally attributable to depression or to MS. Depression is an important reason for so many MS patients'thoughtsofself-harm:suicidalintentoccursinapproximately30% of MS patients and is linked to the presence and severityof depression and social isolation (
Investigating the effects of hydroxyvitamin D3 on clinical, radiologic and immunomodulatory markers in MS patients: A randomized, clinical trial- a pilot study
Multi-center observational study to assess the short-term response of multiple sclerosis (MS) patients initiated on Ozanimod with respect to fatigue. Patterns of brain changes on brain magnetic resonance imaging (MRI) that might modulate the effect of Ozanimod treatment on fatigue will also be assessed.
A limited number of studies on microRNA expression variation in immune cells have been reported in relapsing-remitting multiple sclerosis (RRMS). These studies have been performed mostly on a small scale and on whole blood mononuclear cells (PBMC). In a number of cases, RRMS progresses to a severe secondary neurodegenerative form. In this context, it is important to look for biomarkers that could indicate the pathogenic activity of certain immune cell subpopulations.
This is a prospective non interventional study including patients with Relapsing-Remitting Multiple Sclerosis (RRMS) or with Neuromyelitis Optica Spectrum Disorders (NMOSD) and healthy subjects, who are enrolled within the routinely programmed clinical examinations at the IRCCS Neuromed (Pozzilli, Italy), IRCCS Polyclinic Hospital San Martino (Genoa, Italy) and Sant'Andrea Hospital - University of Rome La Sapienza (Rome, Italy). Specifically, the study investigates how ozanimod may contrast neurodegenerative mechanisms triggered by both arms of the adaptive immune response (T and B cells) and by their suboptimal regulation in MS. Overall, the project aims at assessing by in vitro experiments (there will be no patients on treatment with ozanimod and the drug will be only used in vitro): AIM1: ozanimod ability to modulate the synaptotoxic effect of T-cells derived from patients with MS relapse in a MS-chimeric ex-vivo model and to identify possible mediators (IRCCS Neuromed-Pozzilli, in collaboration with Synaptic Immunopathology Laboratory Dep. Systems Medicine, Tor Vergata University of Rome); AIM2: ozanimod ability to reduce the cytokine-mediated breakdown of the BBB and the migration of the here studied immune cells through ex vivo models of BBB (IRCCS Polyclinic Hospital San Martino); AIM3: ozanimod ability to affect the migration properties of Epstein Barr virus (EBV) infected B cells in MS (Sant'Andrea Hospital); AIM4: ozanimod ability to modulate the number and/or function of regulatory T cells (Treg), a lymphocyte population playing a key role in the control of pathogenic adaptive immune responses (Treg Cell Laboratory, Università degli Studi di Napoli "Federico II", Naples, Italy, receiving blood samples from Neuromed Hospital and Sant'Andrea Hospital; not recruiting unit). The work of the four labs is conceptually and operationally integrated: the labs at IRCCS Neuromed-Pozzilli/Tor Vergata University (Aim1) and at Polyclinic Hospital San Martino (Aim2) will investigate the effects of ozanimod on well-known mechanisms of damage in MS, inflammatory synaptopathy and BBB damage and immune cell migration. The lab at Sant'Andrea Hospital (Aim3), will verify whether B cells infected by different EBV genotypes are involved in BBB migration, and how ozanimod may interfere with this mechanism. The Treg Cell Laboratory (Aim4) will investigate whether ozanimod can also act "upstream" of these mechanisms by regulating the adaptive immune response.