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A well-recognized feature of the jugular and vertebral venous systems in the neck is the way in which they respond to changes in body orientation: during upright position the vertebral plexus takes over nearly all of the jugular venous outflow,5 suggesting that a great deal of adaptability and autoregulation also exist in the venous neck drainage system. The interesting correlation between jugular venous obstruction and demyelinating disease found by Zamboni et al.1,2,8 recently, has therefore come as a surprise because the cerebral venous system appears, at least in theory, to cope quite well with low flow. Neck surgeons have for a long time occluded the jugular veins during radical neck surgery to treat cancer and they have largely succeeded without seeing significant hemodynamic changes of the intracranial pressure doing each side’s ligation in stages. Uneventful outcomes exist even in cases of simultaneous bilateral jugular ligation.9 To the best of the authors’ knowledge there are no reports of clinical or neuroimaging findings resembling those of demyelinating disease after those procedures. Similarly, we have not seen imaging changes resembling MS in patients suffering jugular thrombosis from central lines inserted in intensive care unit (ICU) patients. Put simply, the vertebral venous system appears to compensate efficiently for impaired flow in the jugular veins.


If we follow the venous system caudally, parallel to the jugular system, the drainage of the posterior neck and cervical spine takes place through a complex and rich vertebral plexus that eventually proceeds to the brachiocephalic veins, one on each side. These large trunks converge into the superior vena cava (SVC). The azygos vein joins the superior vena cava before the latter reaches the right atrium.10 The upper third of the thoracic spine drainage is through the superior intercostal veins that flow into the azygos and left hemiazygos in 75% of cases. In the remainder the superior intercostal veins end in the brachiocephalic trunks. The mid, lower thoracic and lumbosacral spine venous drainage is largely shared by the lumbar, azygos, and sacral veins. Hence, the azygos system is a back up venous route for the vena cava arrangement,11 in cases of vena cava obstruction. It would be surprising if insufficiency of a collateral system such as the azygos were enough to alter the well-adjusted spinal venous homeostasis and produce the spinal manifestations of MS.

In well-documented cases of venous hypertension created by the presence of a high flow lesion such as dural Arteriovenous (AV) fistula, any spinal cord lesions present on MRI have very different characteristics from a demyelinating plaque. The former feature is a significant edematous swelling involving the whole segment of the spinal cord and not a single lesion in the posterior columns.

We embrace the challenge of understanding better the relationship between chronic venous insufficiency and MS through future studies. While Zamboni et al.’s theory is assessed, the least we can do is to remain prudent, understanding that angioplasty or stenting of the jugular and/or azygos veins cannot be considered safe or well-known therapies. If ongoing research proves there is a role for venous intervention in MS, certainly research for devices better suited for veins will also be necessary.