A 49-year-old man had headache and fever for 1 month.Neurologic examination showed cognitive dysfunction: recent memory loss, dyscalculia, and disorientation. Muscle stretch reflexes were increased with Babinski signs. Sensory and cerebellar function were normal without meningeal signs. T2-weighted MRI revealed hyperintense signal areas in the internal capsules, globus pallidus, and subcortical white matter regions (A). Normal flow void appearance was not seen in the superior sagittal sinus (A, arrow).Diffusion-weighted imaging also disclosed diffuse hyperintensity in the subcortical white matter. In addition, T1-weighted MRI showed abnormal flow void sign in the cerebellum with gadolinium enhancement (B). Brain MR angiography suggested arteriovenous shunts. Arterial phase of the right external carotid arteriogram indicated dural arteriovenous fistula in the straight and transverse sinus (C). The venous phase of arteriogram demonstrated prominent venous collaterals and congestion in the great vein of Galen, inferior sagittal, and straight sinus (D). The internal carotid angiogram did not define the superior sagittal,transverse, and sigmoid sinus obviously. These images strongly support that perturbation of the venous outflow and sinus thrombosis could induce diffuse brain edema or infarction. Dural arteriovenous fistula occasionally causes a unique distribution of MRI lesions mimicking acute leukoencephalopathy.
补充病史:A 67-year-old woman had in her medical history an operation for an acoustic neurinoma on the right. She presented with a rapid cognitive decline.The T2-weighted images (first two rows) show a diffuse signal increase in the deep white matter of both cerebral hemispheres.Abnormal flow voids are visible on the cerebral surface and in the brain parenchyma, especially in the temporal lobes and in the posterior fossa.The T1-weighted images after contrast (third and fourth rows) show extensive enhancement of cortical and parenchymal veins
公布DSA:
Angiography of the patient presented in Fig. 101.2. Selective injection of the external carotid artery (first row, left) shows hypertrophy of the superficial temporal artery and middle meningeal artery. Immediate enhancement of the superior sagittal sinus is seen, suggesting the presence of a DAVF. Selective internal carotid artery injection (first row, right; middle row, left) shows filling of the artery of the falx cerebri through a (hypertrophied) ophthalmic artery (first row, right).There is early enhancement of the superior sagittal sinus, consistent with a DAVF.There is slow passage of contrast through the brain parenchyma because of venous congestion, resulting in a late parenchymal and venous phase.This is also illustrated by the poor visibility of peripheral arteries in the early phase (middle row, left) and by the “pseudo-phlebitic” aspect of the brain parenchyma in a later phase of the angiogram (middle row, right).After treatment by both an endovascular approach (selective glue injections in external carotid branches feeding the arteriovenous fistula) and by direct placement of coils in the superior sagittal sinus (third row, left; middle row, right), there is a marked reduction in the size of external carotid artery branches.The internal carotid artery injection after treatment shows abnormal drainage of the brain due to occlusion of the superior sagittal sinus (third row, right).The brain is no longer using the superior sagittal sinus for its drainage.However the transit time of contrast is much shorter.The cognitive symptoms of the patient have disappeared almost completely