Intracranial Masses with Perilesional Edema: Differential Diagnosis with Perfusion CT.

Perilesional edema (PE) is commonly observed in association with an intracranial mass. PE is thought to be determined by vasogenic effects in the cerebral parenchyma surrounding the mass due to the loss or absence of the blood-brain barrier (BBB) inside the lesion. Alterations in capillary permeability induce extrusion of fluids into the extravascular space around the mass. On Computed Tomography (CT) PE corresponds to an area of low density for the increased water content, outside the margins of the lesion. It is difficult to differentiate PE from areas of parenchymal compressive ischemia and sometimes the two events could be associated. A solitary mass with PE is more commonly discovered on a non-enhanced computed tomography (NECT) study performed for the onset of stable or rapidly progressive neurological symptoms. In such cases, a supplementary CT scan with contrast (CECT) is generally indicated to complete the baseline imaging before MRI. Contrast enhancement is generally present in a mass with PE and it is not specific for differential diagnosis. Perfusion computed tomography (PCT) requires a few minutes in addition to the time needed for CECT. PCT may give information on regional microvascular density, permeability and blood flow, thus it may play a role when tumoral neo-angiogenesis or non-neoplastic altered haemodynamics are suspected. We therefore investigated the utility of PCT in the differential diagnosis of the intracranial solitary masses with PE.

Phase-contrast MR angiography of intracranial dural arteriovenous fistulae.

MRI and phase-contrast MR angiography (PC MRA) were obtained in 13 patients with angiographically confirmed intracranial dural arteriovenous fistulae (DAVF). Three- and two-dimensional PC MRA was obtained with low (6-20 cm/s) and high (> 40 cm/s) velocity encoding along the three main body axes. MRI showed focal or diffuse signal abnormalities in the brain parenchyma in six patients, dilated cortical veins in seven, venous pouches in four with type IV DAVF and enlargement of the superior ophthalmic vein in three patients with DAVF of the cavernous sinus. However, it showed none of the fistula sites and did not allow reliable identification of feeding arteries. 3D PC MRA enabled identification of the fistula and enlarged feeding arteries in six cases each. Stenosis or occlusion of the dural sinuses was detected in six of eight cases on 3D PC MRA with low velocity encoding. In six patients with type II DAVF phase reconstruction of 2D PC MRA demonstrated flow reversal in the dural sinuses or superior ophthalmic vein.