Physiological Relapse after Venous Sinus Stenting in Idiopathic Intracranial Hypertension and the Case for Pressure-Based Surveillance

Background: Dural venous sinus stenting (VSS) is an accepted treatment for idiopathic intracranial hypertension (IIH) in patients with confirmed transverse sinus stenosis and a haemodynamically significant trans-stenotic pressure gradient on catheter manometry. The procedure interrupts a venous hypertension feedback loop and produces reliable short-term symptomatic benefit. Current post-stenting follow-up protocols focus on imaging surveillance for stent-adjacent stenosis (SAS) and clinical review. They do not routinely incorporate lumbar puncture (LP) manometry to verify that intracranial pressure (ICP) remains controlled after the procedure. The consequence is a structural inability to detect the specific failure mode we describe here: physiological relapse—sustained ICP re-elevation behind a radiographically patent stent, in the absence of structural stent failure. Objective: To present three patients with medically refractory IIH who underwent technically successful VSS with documented initial improvement and subsequently relapsed with confirmed stent patency and elevated LP opening pressures—and to argue that routine post-stenting LP manometry is necessary to detect this pattern. In all three cases, stenosis was confirmed on pre-procedural imaging and a trans-stenotic gradient meeting the published threshold for intervention was documented on catheter manometry. Specific gradient values were not available in the data set; this is acknowledged as a principal limitation. Cases: A 33-year-old woman with systemic lupus erythematosus (SLE) and acetazolamide intolerance (Case 1), a 27-year-old woman with three priors failed lumboperitoneal shunts and IIH without papilloedema (Case 2), and a 39-year-old man with morbid obesity (BMI 57.1 kg/m², pre-stenting LP opening pressure 480 mmH₂O) (Case 3). All three experienced documented initial improvement following VSS. All three subsequently relapsed. Post-relapse imaging confirmed bilateral stent patency without thrombosis or SAS in every case. LP opening pressures at relapse, where measured, were above the diagnostic threshold despite patent venous outflow. Conclusion: These patients had the right diagnosis, the right imaging, the right gradients, and the right procedure. The stents are open. The intracranial pressure was not controlled. This is not a failure of patient selection or surgical technique—it is a failure of the post-stenting surveillance framework to ask the correct question. A patent stent does not guarantee controlled ICP. Serial LP opening