Stenoses in Idiopathic Intracranial Hypertension: 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.¹ 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.¹ 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.² 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,³ 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.⁴ This indicates that 140 mL/min bypasses the dominant outflow stenosis via the collateral vessels,⁴ 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 al⁵ modeled the relationship between ICP and the formation and reabsorption of CSF showing that,

where R_out is the resistance of CSF outflow, FR_CSF is the formation rate of CSF, and P_SS is the sagittal sinus pressure. In a report by King et al³ in which they studied 21 patients with IIH, a mean CSF pressure of 27 mm Hg and sagittal sinus pressure of 22 mm Hg gave a CSF-superior sagittal sinus (SSS) gradient of 5 mm Hg, which is in the normal range (2–6 mm Hg). Rearranging Davson’s equation, we find that the CSF-SSS pressure gradient is equal to the product of the CSF rate of production and the resistance to flow across the arachnoid granulations, ie,

Malm et al⁶ used a technique of constant flow to measure FR_CSF and showed it to be normal in this condition. If the gradient and the rate of formation are normal, then the R_out must also be normal in IIH. Therefore, the elevated venous pressure is the sole variable effecting the elevation in CSF pressure despite itself being secondary to the elevated CSF pressure. This finding indicates that a feedback loop must exist in which both the CSF and venous pressures are cause and effect. It follows that this condition could be treated by attacking either side of the feedback loop (ie, reducing the CSF pressure with placement of a shunt or stent into an overly compliant transverse sinus will break the loop). Thus, I believe that the assertion by Rohr et al¹ that placement of a stent should not be offered to patients who have IIH and collapsible stenoses is not necessarily correct. The only proviso is that the stent must support all of the compliant sections of the venous system or the stenosis will recur (well documented by the authors in patient 1). Ultimately, whether the front-line treatment of IIH associated with collapsible venous outflow is stent placement or shunt insertion will depend on the relative morbidity of these procedures and their long-term rates of success.