Dural venous sinuses distortion and compression with supratentorial mass lesions: a mechanism for refractory intracranial hypertension?

OBJECTIVE To determine the effect of supratentorial intraparenchymal mass lesions of various volumes on dural venous sinuses structure and transluminal pressures. METHODS Three set of preparations were made using adult isolated head derived from fresh human cadaver. A supratentorial intraparenchymal balloon was introduced and inflated at various volumes and effect on dural venous sinuses was assessed by serial intravascular ultrasound, computed tomographic (CT), and magnetic resonance (MR) venograms. Contrast was injected through a catheter placed in sigmoid sinus for both CT and MR venograms. Serial trasluminal pressures were measured from middle part of superior sagittal sinus in another set of experiments. RESULTS At intraparenchymal balloon inflation of 90 cm(3), there was attenuation of contrast enhancement of superior sagittal sinus with compression visualized in posterior part of the sinus without any evidence of compression in the remaining sinus. At intraparenchymal balloon inflation of 180 and 210 cm(3), there was compression and obliteration of superior sagittal sinus throughout the length of the sinus. In the coronal sections, at intraparenchymal balloon inflations of 90 and 120 cm(3), compression and obliteration of the posterior part of superior sagittal sinus were visualized. In the axial images, basal veins were not visualized with intraparenchymal balloon inflation of 90 cm(3) or greater although straight sinus was visualized at all levels of inflation. Trasluminal pressure in the middle part of superior sagittal sinus demonstrated a mild increase from 0 cm H(2)O to 0.4 cm H(2)O and 0.5 cm H(2)O with inflation of balloon to volume of 150 and 180 cm(3), respectively. There was a rapid increase in transluminal pressure from 6.8 cm H(2)O to 25.6 cm H(2)O as the supratentorial mass lesion increased from 180 to 200 cm(3). CONCLUSIONS Our experiments identified distortion and segmental and global obliteration of dural venous sinuses secondary to supratentorial mass lesion and increase in transluminal pressure with large volume lesions. The secondary involvement of dural venous sinuses may represent a mechanism for refractory intracranial hypertension.