SUMMARY Evidence of damage to cerebral vein walls was sought in 70 cases of multiple sclerosis. Seventy control cases were also examined. The multiple sclerosis cases showed venous intramural fibrinoid deposition (7%), recent haemorrhages (17%), old haemorrhages revealed by haemosiderin deposition (30%), thrombosis (6%) and thickened veins (19%). In all, 41% of all multiple sclerosis cases showed some evidence of vein damage. Occasional control cases showed haemosiderin deposition in the brain but, unlike the multiple sclerosis cases, these were diffuse and almost entirely related to coexistent cardiovascular or cerebrovascular disease. Haemosiderin deposition was common in the substantia nigra and other pigmented nuclei in all cases. It is concluded that the cerebral vein wall in multiple sclerosis is subject to chronic inflammatory damage, which promotes haemorrhage and increased permeability, and constitutes a form of vasculitis.Involvement of the cerebral venous system in multiple sclerosis has been recognised for many years. In particular, plaques are centred on small veins or venulesl and extend outwards therefrom along branch veins as Dawson's fingers.2 3 The veins in acute cases are usually the site of a lymphocyte-plasma cell infiltrate, which varies in intensity between modest to moderately severe. Chronic cases show less perivenular infiltration, which is often absent in the inactive or "burnt-out" case.48 In some active acute cases of multiple sclerosis the vein walls themselves are heavily infiltrated with inflammatory cells, but without infiltration of the adventitia and perivascular tissues. Chronic plaques often contain vein walls thickened by collagen.9 Although these processes are nonspecific, they do indicate that the vein wall is implicated in the inflammatory process, and is thereby damaged and thickened, partly analogous to the thickening in endarteritis obliterans in arteries passing through foci of chronic inflammation. Nevertheless, it could be held that the vein wall is merely acting as a conduit for inflammatory cells but, if so, it

No abstract

No abstract