Elevated intracranial venous pressure as a universal mechanism in pseudotumor cerebri of varying etiologies.

Pseudotumor cerebri (PTC), or idiopathic intracranial hypertension, is a syndrome associated with multiple clinical conditions. We hypothesize that most if not all etiologies result in an increase in intracranial venous pressure as a final common pathway. We studied 10 patients with PTC. Five had dural venous outflow obstruction as demonstrated by venography, and the five remaining patients had normal venous anatomy. Pressure measurements, made during venography in eight patients, all showed elevated pressures. Pressure measurements in the superior sagittal sinus ranged from 13 to 24 mm Hg (mean, 16.6 mm HG). Patients with obstruction tended to have a high pressure gradient across the stenotic segment. Five patients with normal dural venous anatomy had elevated right atrial pressures (range, 6 to 22 mm Hg; mean, 11.8 mm Hg), which were transmitted up to the intracranial venous sinuses. Endovascular techniques, including angioplasty and infusion of thrombolytic agents in some cases, improved outlet obstruction from a hemodynamic perspective but were ineffective in consistently and reliably alleviating the clinical manifestations of PTC. Patients in both groups tended to respond well to conventional CSF diversion procedures. Our study suggests that elevated intracranial venous pressure may be a universal mechanism in PTC of different etiologies. This elevated venous pressure leads to elevation in CSF and intracranial pressure by resisting CSF absorption. Although the mechanism leading to venous hypertension in the presence of outflow obstruction is obvious, the etiology of increased intracranial and central systemic venous pressure in PTC remains obscure.