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Abstract

Objective
To investigate characteristics of the internal cerebral veins (ICVs) and their main tributaries and the deep medullary veins (DMVs) in patients with relapsing-remitting MS (RRMS) with enhanced T2*-weighted angiography imaging (ESWAN).

Methods
Fifty-three RRMS patients and 53 normal controls underwent conventional MRI and ESWAN. ESWAN venograms were created by performing minimum intensity projections of the phase images, and the resulting venograms were used to observe characteristic vascular changes, including scores of the ICVs and their main tributaries and manifestations of the DMVs. Two experienced radiologists analysed all data.

Results
Patients showed decreased mean scores of the ICVs and their main tributaries compared with controls. The mean score in acute patients was higher than in stable patients. Furthermore, the DMVs diminished and shortened in 48 patients with longer disease duration, whereas the DMVs increased and elongated in 5 patients with shorter disease duration. The penetrating veins were well defined in 30 active lesions, whereas the veins were ill defined in 69 non-active lesions. Interestingly, well-defined penetrating veins were shown in 15 non-active lesions in the stable patients.

Conclusions
Enhanced T2*-weighted MR angiography can detect cerebral vein characteristics in relapsing-remitting MS patients, which may provide important information on the pathogenesis of MS.
Key Points
• Enhanced T 2 * -weighted magnetic resonance angiography (ESWAN) provides new insights into multiple sclerosis
• ESWAN venograms clearly demonstrate the internal cerebral and deep medullary veins
• The internal cerebral veins exhibit abnormalities in patients with relapsing-remitting MS
• Deep medullary veins exhibit different manifestations in patients with different disease duration

Several vascular dysfunction mechanisms may exist. Firstly, there may be reduced blood oxygen utilization from chronically damaged
brain tissue that leads to decreased levels of oxygen extraction [18]. Secondly, MS patients are at higher risk of ischaemic stroke, which might involve endothelial dysfunction secondary to inflammatory disease activity [29]. Alterations in endothelial function have been reported in MS [30–32]. Wakefield et al. demonstrated fibrin deposition and vessel thrombosis in the absence of cellular infiltration in three acute cases of MS, suggesting that the thrombosis of small veins and capillaries could represent an ischaemic basis for disease [33]. Thirdly, MS patients have global cerebral hypoperfusion, which might predispose them to ischaemic stroke development. Using dynamic susceptibility contrast-enhanced MRI, Law and colleagues found that cerebral blood flow (CBF) was markedly decreased and that the mean transit time was prolonged throughout the NAWM in 17 RRMS patients compared with 17 control subjects [14]. Finally, several studies have suggested that the pathogenesis of MS might be the consequence of CCSVI, which has proved controversial [34–36]. It could be hypothesised that decreased venous outflow from the brain parenchyma to the periphery might lead to increased intracranial pressure and subsequent venous stasis, especially in the small vein vasculature. However, the exact pathogenesis of this process remains unknown