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Multiple sclerosis is an autoimmune disease in which immune cells attack and destroy the protective myelin sheaths that surround nerve fibres, leading to neurological disturbances.
Fatigue is a burdensome symptom that is commonly encountered in people with neurological or non-neurological diseases, but it is poorly understood and lacks a common definition and conceptualization. This Review presents new a conceptual model of fatigue that is designed to improve communication between experts from different methodological and medical backgrounds.
Myelin damage in multiple sclerosis can be detected up to 7 years before symptoms, with early immune pathway activation and a 21-protein panel showing promise for presymptomatic diagnosis.
Autologous haematopoietic stem cell transplantation (AHSCT) offers effective therapy for people with multiple sclerosis (MS), according to new real-world data.
In the 2024 revisions of the McDonald criteria for diagnosis of multiple sclerosis (MS), dissemination in time is no longer required. This paradigm shift is the result of advances in understanding of MS and the development of other biomarkers, enabling earlier diagnosis and treatment that will ultimately improve long-term outcomes.
The 2024 revisions of the McDonald criteria for multiple sclerosis for the first time permit diagnosis in asymptomatic people with MRI findings suggestive of multiple sclerosis pathology. Although these changes promise opportunities for earlier treatment and improved clinical outcomes, they present a new risk in the form of overdiagnosis.
The 2024 revision of the McDonald criteria for diagnosis of multiple sclerosis marks a substantial departure from previous iterations, establishing a unified framework that integrates presentation, lesion topography and a flexible combination of paraclinical tools. This Clinical Outlook considers the major changes and their clinical implementation, and the implications of the new criteria.
Updates to the McDonald criteria for diagnosis of multiple sclerosis emphasize the value placed on recognizing the earliest manifestations of multiple sclerosis, providing new opportunity to advance understanding of the prodromal phase.
B cells that expand following infection with EBV can colonize the brain, where they recruit activated T cells that have potential to cause neuronal damage, thereby providing a mechanism to explain the link between EBV and increased MS risk.
