Abstract

Traditionally, multiple sclerosis has been viewed as a disease predominantly affecting white matter. However, this view has lately been subject to numerous changes, as new evidence of anatomical and histological changes as well as of molecular targets within the grey matter has arisen. This advance was driven mainly by novel imaging techniques, however, these have not yet been implemented in routine clinical practice. The changes in the grey matter are related to physical and cognitive disability seen in individuals with multiple sclerosis. Furthermore, damage to several grey matter structures can be associated with impairment of specific functions. Therefore, we conclude that grey matter damage - global and regional - has the potential to become a marker of disease activity, complementary to the currently used magnetic resonance markers (global brain atrophy and T2 hyperintense lesions). Furthermore, it may improve the prediction of the future disease course and response to therapy in individual patients and may also become a reliable additional surrogate marker of treatment effect.

Highlights

  • Multiple sclerosis has been viewed as a disease predominantly affecting white matter

  • The aim of this review is to summarise the current knowledge of the grey matter (GM) damage in Multiple sclerosis (MS) and of its clinical implications

  • Assessing grey matter pathology Both GM atrophy [11,34,38,41,42,44,48] and GM lesions [29,30,31,32,49,50,51,52] were demonstrated in cerebral cortex and deep GM structures using magnetic resonance imaging (MRI) supported by histological studies [32,53,54,55,56]

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Summary

41 RRMS 16 HC

Cortical atrophy was found in cognitively impaired but not in cognitively preserved patients, and was correlated with a poorer performance on tests of verbal memory, attention, and verbal fluency. Decrease in cortical volume was significantly higher in cognitively deteriorating than in stable or improving patients (-43 ml vs. -18 ml)

62 RR MS 16 SP MS 1 PP MS 16 HC crosssectional crosssectional
Conclusions
Weiner HL
Findings
16. Barkhof F
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