Stenoses in idiopathic intracranial hypertension: to stent or not to stent?

or Not To Stent? I read with great interest the paper entitled “Reversibility of Venous Sinus Obstruction in Idiopathic Intracranial Hypertension” recently published in the American Journal of Neuroradiology by Rohr et al. This paper presents the case histories of 3 patients with idiopathic intracranial hypertension (IIH) and venous outflow stenoses. The first patient had an initial resolution of her symptoms after insertion of a stent into the transverse sinus, but the symptoms recurred and a restenosis was noted just upstream from the stent. This patient was later treated with insertion of a shunt tube. In the second and third cases, the patients were treated with insertion of a shunt, with the venous stenoses in the second patient improving after the insertion. On the basis of these cases, the authors suggest that the elevated venous pressure in IIH is caused by the collapse of the sinuses. They go on to assert that insertion of a stent should be reserved for fixed stenoses and should not be used for dynamic stenoses. This suggestion is proposed because, logically, if the raised pressure in the CSF has caused the collapse of the venous sinus, then the elevated venous pressure cannot also be the cause of the raised CSF pressure. I wish to discuss whether the cause-and-effect relationship, as outlined, is the only one possible given the data as presented. Most patients with IIH have morphologic stenoses in the venous outflow. Many of these stenoses reduce the outflow by more than 70% in area and would be deemed significant if found on the arterial side of the vascular tree. Direct manometry has shown the pressure gradients across these stenoses to average 24 mm Hg, which would also suggest that these stenoses were significant by the usual criteria. Finally, I have measured the arterial inflow and venous outflow in 21 patients with IIH and stenoses and found, on average, a 13% reduction in the sagittal sinus outflow as a percentage of the inflow in IIH. This indicates that 140 mL/min bypasses the dominant outflow stenosis via the collateral vessels, again suggesting significance. Can we reconcile the apparent significant nature of the stenoses with the fact that they occur secondary to the CSF pressure? Intracranial pressure (ICP) is dependent on a balance between the production and reabsorption of CSF. Davson et al modeled the relationship between ICP and the formation and reabsorption of CSF showing that,