Multiple sclerosis (MS) is an inflammatory and neurodegenerative disease of the central nervous system, in which several environmental factors act against the background of a complex, polygenetic trait. Pathologically, MS is characterized by T-cell-mediated inflammation and neuro-axonal damage that lead to tissue loss. While the former may be associated with functional deficits (commonly referred to as relapses) during early, relapsing phases of the disease, the latter is thought to be the morphological correlate of sustained disability characterizing more advanced stages of the disease. Exact mechanisms leading to degeneration of neurons and axons in MS, however, are far less well understood.

Furthermore, disease subtypes as well as individual disease phenotypes are characterized by significant clinical and pathological heterogeneity. The most commonly accepted in vivo surrogate marker to monitor disease activity to date is magnetic resonance imaging (MRI). With the introduction of the McDonald criteria, MRI has also become vital in MS diagnosis. Proving dissemination in space and time radiologically instead of clinically has led to earlier diagnoses or increased sensitivity of the new criteria. However, MRI findings associated with MS are largely unspecific as regards the underlying pathology. Advanced MRI sequences with potentially increased specificity for distinct pathological features—such as magnetization transfer (MTR) in case of de- and re-myelination or diffusion tensor imaging (DTI) in case of demyelination and/or axonal loss—are costly, time consuming, and not yet routinely available in many clinical settings.