Are we ready to redefine disease pathogenesis?

Η πολλαπλή σκλήρυνση παραδοσιακά θεωρείται μία χρόνια φλεγμονώδης απουμελινωτική νόσος της λευκής ουσίας του κεντρικού νευρικού συστήματος.  Πρόσφατη εργασία του Zivadinov, εν όψει των πολυάριθμων μελετών που εντοπίζουν πλέον φλεγμονώδεις εστίες στον φλοιό (φαιά ουσία) του εγκεφάλου των ασθενών, από την αρχή της νόσου, και χαρακτηρίζουν αυτές καλύτερο δείκτη αναπηρίας από τις εστίες της λευκής ουσίας, καταλήγει πως πρέπει να επαναπροσδιορίσουμε την παθογένεση της σκλήρυνσης, ως ασθένεια και της φαιάς ουσίας.

Advances in understanding gray matter pathology in multiple sclerosis

Although it has been shown that cortical lesions could occur secondary to WM damage in relation to Wallerian degeneration, [12] recent histopathological and MRI studies have demonstrated that cortical demyelination mainly occurs spatially distant from WM pathology.  [13,14] It has also been shown that highly inflammatory subpial cortical demyelination and adjacent meningeal inflammation can occur very early on in the disease. [15] Therefore, it is probable that GM could represent an important initial target of the MS disease process.

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There is mounting evidence that about 40% of patients with clinically isolated syndrome show cortical lesions on MRI. [9] These data were recently corroborated by histopathological findings. [15] On the other hand more than 80% of progressive MS patients present with cortical lesions in advanced stages of the disease. [15,17] Interesting, in progressive forms of MS, cortical demyelination in the cerebellum is almost universal, affecting over 38% of the entire cerebellar cortex on average. [19] The mechanisms responsible for triggering meningeal inflammation in MS patients are not yet elucidated, and they should be further investigated in relation to their role in initiating and perpetuating the disease process.  Determining the role of antigens, environmental and genetic factors for pathogenesis of cortical pathology in MS is critical.