Multiple sclerosis (MS) is a chronic neuroinflammatory and neurodegenerative disease.
1 Despite the availability of multiple treatment options, many patients live with disability or experience progressive symptoms that limit their quality of life and longevity. Even if pathobiological causes of disability accrual and disease progression are not completely understood, individual lesion-type patterns might account for clinical and prognostic variability.
2-4 After the acute phase of inflammatory demyelination at lesion onset, chronic lesions can show different pathological and repair outcomes, namely “chronic active/slowly expanding/smoldering,” “chronic inactive,” and, when repair is successful, “remyelinated.”
5,6 As personalized treatment paradigms emerge, imaging the distribution of different lesion types within individuals may prove critical.