Endovascular treatment of spinal arteriovenous lesions: beyond the dural fistula

Abstract

During the past few decades, there have been significant advances in the understanding of spinal vascular lesions, mainly because of the evolution of imaging technology and selective spinal angiography techniques. In this article, we discuss the classification, pathophysiology, and clinical manifestations of spinal vascular lesions other than DAVFs and provide a review of the endovascular approach to treat these lesions.

Fig 1.

A, A 31-year-old patient presenting with quadriparesis secondary to intramedullary hemorrhage seen as hyperintensity in a sagittal T1-weighted MR image (arrow). B−D, The spinal angiograms show an intramedullary AVM (arrow) with arterial feeders from the ASA (arrowheads), which, at this level, is supplied by the right vertebral artery (C and D) and the left ascending cervical artery from the thyrocervical trunk (B). E, The AVM is embolized with n-BCA (arrow) with a microcatheter positioned via the left ascending cervical artery into the ASA branch feeding the nidus. Postembolization angiogram shows no residual supply to the nidus from the left ascending cervical artery, while the supply to the ASA is preserved (arrowhead). F, Postembolization right vertebral artery angiogram shows residual nidus (<30% of the total AVM nidus) and preserved flow into the ASA (arrowhead).

Fig 2.

A, A 50-year-old patient with massive SAH (arrow), Hunt and Hess grade IV. B, Reconstructed image from a rotational angiogram shows an aneurysm (arrow) supplied by the ASA. The same arterial feeder supplies a pial AVM (block arrow) distal to the aneurysm. There is duplication of the ASA distally to the branch supplying the aneurysm and pial AVM. C, A Magic 1.2F microcatheter (Balt, Montmorency, France) is advanced over a Mirage 0.08-inch guidewire (ev3) into the ASA branch feeding the aneurysm and the pial AVM. D, Superselective angiography, with the microcatheter into the sulcal branch of the ASA, shows the aneurysm, the pial AVM, and the abnormal venous drainage of the pial AVM (arrows). E, The aneurysm and AVM are embolized with n-BCA, and the glue cast is shown on reformatted 3D CT images (arrow). The patient was temporarily weaker after the procedure, but motor function returned to baseline within a few days.

Fig 3.

A, Epidural AVM supplied by the left T7 intercostal artery (arrow). Note the venous drainage into dilated epidural veins (block arrow). B, Selective angiogram via a microcatheter placed into the arterial feeder shows no supply to the ASA or PSA. C, The AVM is embolized with n-BCA with the glue cast shown in the unsubtracted image.

Fig 4.

A, Angiogram of the left T10 intercostal artery shows a pial AVF supplied by the artery of Adamkiewicz (arrow). An aneurysm is seen at the level of the fistula (block arrow). B, Angiogram with a large FOV shows the extensive venous drainage into spinal perimedullary veins (arrows). C, A microcatheter was advanced to the arterial feeder just proximal to the aneurysm (arrow). The fistula and aneurysm are treated with n-BCA embolization (block arrow). D, The ASA remains patent after the embolization, while the fistula, aneurysm, and abnormal spinal perimedullary venous drainage are obliterated.

Fig 5.

A, A 69-year-old man with progressive bilateral lower extremity weakness. Sagittal T2-weighted MR image shows intramedullary edema in the lower thoracic spine and the conus medullaris (arrow) with flow voids surrounding the cauda equina and conus medullaris (arrowheads), consistent with venous hypertension. B, Catheter angiogram shows an AVF in the sacral region (block arrow), supplied by the iliolumbar arteries bilaterally (arrows). C, The arteriovenous shunt drains into the sacral epidural veins (arrowheads, B and C), which in turn communicate with dilated spinal veins (arrows), causing venous hypertension. D, This epidural AVF is embolized with Onyx with obliteration of the feeding arteries, the arteriovenous shunt, and epidural veins. There is no residual communication with the spinal veins. E, MR imaging of the lumbar spine obtained 7 months after the embolization shows marked improvement of the intramedullary edema and perimedullary flow voids, correlating with near-complete resolution of the patient's symptoms.

Fig 6.

A, Sagittal T2-weighted MR image in a 67-year-old patient with progressive bilateral leg weakness, gait instability, and tingling in both hands shows increased signal intensity in the spinal cord (arrows) and perimedullary flow voids, consistent with venous hypertension. B, Cerebral angiogram shows a dural AVF with venous drainage into the petrous, anterior medullary, and spinal perimedullary veins (arrows). C and D, The fistula is supplied by the meningo-hypophyseal trunk of the right internal carotid artery (arrow, C) and the petrous branch of the right MMA (arrow, D). E, A microcatheter is positioned in the MMA, just proximally to the fistula (arrow), and embolization is then performed with Onyx. F, The postembolization angiogram shows obliteration of the fistula.