Multiple sclerosis : clinical and laboratory research
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Myelin oligodendrocyte glycoprotein (MOG) antibody disease is a rare autoimmune disorder with antibodies against the MOG predominantly involving the optic nerve and spinal cord leading to vision loss and paralysis. When MOG antibody disease involves the brain, the phenotype is similar to acute disseminated encephalomyelitis (ADEM). In this review, we discuss MOG-positive cases presenting with encephalitis, encephalopathy, or ADEM-like presentation based on recently published series.
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Randomized Controlled Trial Multicenter Study
Efficacy and safety of ozanimod in multiple sclerosis: Dose-blinded extension of a randomized phase II study.
Ozanimod, an oral immunomodulator, selectively targets sphingosine 1-phosphate receptors 1 and 5. ⋯ Ozanimod demonstrated sustained efficacy in participants continuing treatment up to 2 years and reached similar efficacy in participants who switched from placebo; no unexpected safety signals emerged.
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To explore resting-state (RS) functional connectivity (FC) of the main sensory/motor networks of patients with neuromyelitis optica spectrum disorders (NMOSDs), clinically isolated optic neuritis (ON), and myelitis. ⋯ Sensory and motor RSN abnormalities occur in NMOSD. Loss of function within disease-target networks may elicit cross-modal plasticity across sensory networks potentially preserving clinical function.
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Randomized Controlled Trial
Efficacy of Cladribine Tablets in high disease activity subgroups of patients with relapsing multiple sclerosis: A post hoc analysis of the CLARITY study.
In the CLARITY (CLAdRIbine Tablets treating multiple sclerosis orallY) study, Cladribine Tablets significantly improved clinical and magnetic resonance imaging (MRI) outcomes (vs placebo) in patients with relapsing-remitting multiple sclerosis. ⋯ Patients with HDA showed clinical and MRI responses to Cladribine Tablets 3.5 mg/kg that were generally better than, or at least comparable with, the outcomes seen in the overall CLARITY population.
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Monitoring neuronal injury remains one key challenge in early relapsing-remitting multiple sclerosis (RRMS) patients. Upon axonal damage, neurofilament - a major component of the neuro-axonal cytoskeleton - is released into the cerebrospinal fluid (CSF) and subsequently peripheral blood. ⋯ sNfL indicates acute inflammation as demonstrated by correlation with Gd+ lesions. It is a promising biomarker for neuro-axonal damage in early multiple sclerosis (MS) patients, since higher baseline sNfL levels predicted future brain atrophy within 2 years.