author: Takashi Yamamura
November 18, 2022
Multiple sclerosis is an inflammatory demyelinating disease of the CNS, showing various clinical manifestations depending on the site, nature, and extent of the inflammatory lesions. In practice, multiple sclerosis is classified into clinical subtypes—relapsing-remitting, primary progressive, and secondary progressive—on the basis of the patient’s clinical course. Since the turn of the century, the precise distinction between relapsing-remitting and secondary progressive multiple sclerosis has become important, because secondary progressive disease does not respond to most disease-modifying drugs approved for relapsing-remitting disease (although disability progression in people with secondary progressive multiple sclerosis can be slowed with siponimod). However, the boundary between relapsing-remitting and secondary progressive disease is often unclear, and diagnosis of secondary progressive multiple sclerosis tends to be delayed because progression typically takes place silently without accompanying relapses (referred to as progression independent of relapse) in these patients.
Furthermore, it has become obvious that the traditional multiple sclerosis subtypes do not represent the biological heterogeneity of patients, as shown by their heterogeneous microglia gene expression profiles.
Research has explored how to group patients with multiple sclerosis according to objective markers that might represent radiological, immunological, or neurodegenerative processes. Taken together, in their Personal View in The Lancet Neurology, Tanja Kuhlmann and colleagues have good reasons to propose the need for a new mechanism-driven framework to define multiple sclerosis progression.
Although the goal is distant and many obstacles might arise (such as reaching a consensus between physicians, academia, and stakeholders), the time seems right to launch initiatives to reframe the classification of multiple sclerosis subtypes.
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