• Max Nedelmann, Manfred Kaps, and Wibke Mueller-Forell.
• Department of Neurology, Justus Liebig University Giessen, Am Steg 14, 35385, Giessen, Germany. max.nedelmann@neuro.med.uni-giessen.de
• J. Neurol. 2009 Jun 1; 256 (6): 964-9.

AbstractThe pathophysiology of elevated intracranial pressure in idiopathic intracranial hypertension (IIH) is unclear. Cerebral venous outflow obstruction and elevated intracranial venous pressure may play an etiological role. We examined jugular valve insufficiency as a potential factor contributing to intracranial hypertension. Jugular venous valve function was assessed bilaterally by duplex sonography in 20 consecutive patients with diagnosis of IIH and in 20 healthy controls matched for age, gender and body mass index. Diagnosis of valvular insufficiency was based on reflux duration during a controlled Valsalva maneuver. Intracranial venous outflow was evaluated in 11 patients (MR venography in 10, digital subtraction angiography (DSA) in two cases). As a principle result, valvular insufficiency was significantly more frequent in patients with IIH (70 vs. 30%; p < 0.05). This finding was associated with irregular leaflet structures on B-mode imaging (p < 0.01). Bilateral insufficiency was more frequent in the patient group which, however, was not significant (p = 0.08). In addition, sinovenous outflow obstruction was found in five of six patients that had undergone contrast-enhanced MR venography and DSA. The detection rate was inferior in phase-contrast MR imaging (one of five patients). In conclusion, this study gives evidence that valvular insufficiency may play a causal role in IIH. Obesity is a major risk factor for the disease and weight reduction leads to improvement of symptoms. Possibly, increased intra-abdominal pressure is transmitted into the intracranial venous system, causing intracranial hypertension. Jugular valve insufficiency may facilitate pressure transmission. As transverse sinus stenosis was a concomitant finding, these factors may be complementary.

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