CSF disease - Management of intracranial hypertension - Ep.2/2

Idiopathic Intracranial Hypertension

This compelling session opened with a diagnostic challenge. Prof. Vincent displayed a diffusion-weighted MRI of a patient and asked junior colleague Dr. Marin Carlos to identify the abnormality. The correct observation: diffusion restriction in the optic nerves and chiasm, a subtle but urgent radiological finding indicating optic nerve ischemia. The case was one of Idiopathic Intracranial Hypertension (IIH) with impending vision loss, and Prof. Vincent emphasized that this constitutes a neuro ophthalmological emergency requiring urgent venous sinus stenting.

In my own clinical practice, I’ve certainly encountered IIH patients with worsening vision and papilledema, but until now I had never considered diffusion restriction in the optic apparatus as a radiological emergency. For me, venous stenting has always been an elective procedure, a last resort following failed conservative treatment, not a primary or urgent intervention. This session made me question whether I should reconsider the timing of stenting in select high-risk cases.

Prof. Vincent and Dr. Anne Ducros introduced the concept of a pathophysiological vicious cycle in IIH: a metabolic, hormonal or a hemodynamic trigger elevates intracranial pressure, which causes venous sinus compression leading to stenosis, leading to venous hypertension, which in turn exacerbates intracranial pressure, creating a self-sustaining loop. The logic of venous sinus stenting is to break this cycle by decompressing the venous system and improving CSF absorption.

Dr. Adnan Siddiqui added that GLP-1 agonists, used in diabetes and weight loss, may become one of the main line therapies in IIH management, further highlighting the metabolic dimension of the disease.

Although this theory is gaining traction, I believe that stenting, while impactful, is not necessarily curative for all patients. Yet, I’ve personally seen dramatic, sustained responses in every patient I’ve treated with venous sinus stenting for IIH. My longest follow-up is 2 years, and none of those patients have had recurrent symptoms or needed retreatment, strong anecdotal support for stenting as a long-term solution.

Despite this success, I still advocate for structured selection criteria. I do not offer stenting as a primary therapy. I reserve it for patients who fulfil all three of the following:

1. Clear clinical features of IIH, including progressive papilledema.
2. Failure of best medical therapy, including 1000–1250 mg acetazolamide daily and dedicated or failed weight loss.
3. Angiographic confirmation of venous sinus stenosis with a trans-stenosis pressure gradient >8 mm Hg.

Until robust data becomes available, this remains my working protocol. That’s why I’m excited by the upcoming DIVE-IIN trial (Direct Intracranial Venous Stenting Evaluation in Patients with Idiopathic Intracranial Hypertension in Early Phase), proposed by Dr. Vincent. With two arms, early stenting vs. delayed stenting after medical failure, it could provide the level 1A evidence we need to define optimal timing of intervention.

The session concluded with a pre-recorded case of venous hypertension due to a congenital dural AV fistula in a young patient. Prof. Vincent used advanced tools like the ARTERIA SmartGUIDE 0.014” steerable microwire to navigate sharply angled venous pathways and emphasized strategies like the pressure cooker technique for achieving durable occlusion. In my own setup, I haven’t yet had the opportunity to use steerable microwires, but I’m closely watching for their market availability.

This session reshaped my approach in multiple ways, from recognizing optic nerve ischemia as an emergency, to redefining the role and timing of stenting, and to anticipating how device evolution will enhance therapeutic precision. As we await data from trials like DIVE-IIN, it’s clear that IIH management is moving from stenting as a cautious rescue therapy toward personalized, physiology-driven decision-making.