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SNIS 8th annual meeting oral abstracts
O-034 Criteria for assessment of endovasal techniques for idiopathic intracranial hypertension (IIH)
  1. A Mironov
  1. Department of Radiology, Creighton University Medical Center, Omaha, Nebraska, USA


Purpose The debate about the effect of venous sinus outflow improvement in IIH—does it simply mitigate a consequence of primary raised intracranial pressure, or does it address the cause of raised intracranial pressure itself remains controversial. With reference to this question, we present the evaluation of endovascular manomentry and treatment in 12 patients with refractory IIH.

Materials and Methods All patients (11 f, 1 m; 16 to 34-year-old; BMI kg/m2: 20–85) were referred with history of progressive headache, visual disturbance, or change of personality. They underwent MRI, MRV, catheter phlebography, and manometry of dural sinuses (pullback pressure measurement in multiple locations between the sagittal sinus and superior vena cava). In 6 cases, percutaneous angioplasties of dural sinuses with compliant balloons (4 and 4.5 mm) were considered.

Results The opening lumbar CSF pressure has been elevated in all patients between 30 cm 120 cm H2O. The venography (MRV, conventional) revealed subtle stenotic lesions of lateral sinuses in all cases. Regarding the gradients across the sinus stenosis (AG), the cases were divided in 3 groups: I. AG up to 15 mm Hg—6 cases (4, 6, 7, 8, 9, 12 mm); II. AG up to 30 mm Hg—4 cases (21, 25, 26, 30 mm); III. Ag above 30 mm Hg—2 cases (50, 35 mm). Angioplasties were performed for patients in II and III group. In 4 cases (JV/jugular vein pressure 8, 10, 12, 16 mm Hg) there was a durable dramatic improvement with resolving of symptoms. In 2 cases (JV pressure 22 and 24 mm Hg) there was transitory improvement.

Conclusion The consideration for balloon angioplasty was predicated on the notion that venous outflow obstruction plays some part in the etiology of symptoms and signs in patients with IIH. Those with considerable durable improvement included cases with distinct elevated AG (50, 35, 25, 21 mm Hg) and moderate elevation of JV pressure (8, 10, 12, 16 mm). These with lack of clinical efficacy included cases with elevated AG (26, 30 mm Hg), but also with distinct JV pressure (22, 24 mm Hg). All of the treated patients had AG above 21 mm Hg, but only those with JV pressure below 16 mm Hg responded extremely well. The group I was considered for medical therapy, because AG below 15 mm Hg seems not predictable for successful treatment. Perhaps some cases of IIH are exacerbated by a coexistent effect of pre-existent anatomic narrowing of the lateral sinuses with elevated across gradients, and perfusion improvement breaks the iterative cycle. The lack of clinical response after angioplasty (or stenting) reflects probably on the both: the lack of exposed AG, and the elevation of JV pressure due to central venous pressure elevation. Alternatively, IIH may include two populations: one truly idiopathic (with central venous pressure elevation, without associated sinus flow obstruction, not responding to angioplasty), and the other with additional exacerbated IIH by preexistent venous outflow obstruction (responding to angioplasty). This would have clear implications for clinical management.

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