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Idiopathic intracranial hypertension (IIH), or perhaps more accurately chronic intracranial venous hypertension syndrome (CIVHS),1 is a disabling condition often resulting in severe pressure headaches, visual symptoms, and tinnitus. In the last decade, venous sinus stenting (VSS) has emerged as a safe and effective treatment for patients with IIH with associated venous sinus stenosis and a documented trans-stenosis pressure gradient (TSPG). While meta-analyses of small retrospective series have demonstrated low rates of retreatment with high rates of headache and visual improvement,2–4 some recent studies have revealed that many patients (as high as 60%) develop symptom recurrence after VSS.5 There are very few published articles that provide neurointerventionists with recommendations regarding the selection and treatment of IIH patients6 and essentially no evidence-based recommendations are available regarding the specifics of stent construct lengths or sizes. Further, questions remain about the pathophysiologic mechanism at play and why recurrent stenosis develops. Experience gained from a high-volume VSS practice has provided important insights into these phenomena. Herein I propose a unifying theory that explains the pathophysiology of de novo and recurrent venous sinus stenosis in IIH patients, with attention given to how this may impact stent construct size and length.
Unifying theory summary
The proposed theory is centered around four core principles: (1) elevations in intracranial pressure (ICP) have a diffuse impact on venous sinuses and their calibers; (2) there is variability in susceptibility to ICP-mediated stenosis in different regions of the sinuses, with the lateral transverse sinus being most susceptible and the torcula being resistant; (3) venous sinus stenosis is mediated through a positive feedback loop resulting in upstream venous congestion and elevated intramural venous pressures; and (4) recurrent stenosis occurs after stenting due to the effect of ongoing ICP elevations on susceptible regions of the sinuses in the setting of lower intramural venous …
Contributors The author is the sole contributor to the article and is responsible for its contents.
Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.
Competing interests None declared.
Patient consent for publication Not required.
Provenance and peer review Not commissioned; externally peer reviewed.
Data availability statement No additional data are available.
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