Slide show: Spinal dural arteriovenous fistula
November 25th, 2009 by Administrator

The author: Professor Yasser Metwally


November 25, 2009 — Spinal dural arteriovenous fistula

Slide show 1. Spinal dural arteriovenous fistula

  • Review of literature

Spinal Dural AVFs, most common type of spinal vascular malformation constituting 80% of spinal AVMs [1]. There are three basic types of AVFs – extradural, dorsal intradural, and ventral intradural [3]. Dorsal intradural AVFs have been given a number of alternate names including long dorsal, angioma racemosum, dorsal extramedullary, angioma racemosum venosum, and Type I. The current literature supports use of term Type I [3]. Type I is further classified into subtypes A and B to designate AVMs with single or multiple feeding arteries, respectively [3]. These dural AVFs are malformations that most commonly occur in the thoracic region [1].

The dural AVFs consist of an abnormal communication between a radicular artery and a radicular vein within the dural sleeve of a nerve root [1]. The vein communicates with the coronal venous plexus along the surface of the spinal cord. The clinical manifestation of patients with this miscommunication is the insidious development of venous hypertension induced-progressive myelopathy [1]. Venous congestion produces progressive neurological deterioration that can manifest as sensory disturbances, paraparesis, and sphincter dysfunction [2,3]. The pathognomonic MR imaging studies is a pencil-like hyperintensity in the spinal cord on a T2-weighted image [2]. Aminoff and Logue detailed the clinical prognosis of 60 cases of dural AVFs [3]. Seven patients with acute onset symptoms had no progression of neurological dysfunction. The 53 other patients had symptom progression with acute neurological episodes, and lower extremity impairment. Within three years of developing impairment the patients became severely disabled [3]. This and similar outcomes has led to the rule that elimination of dural AVFs will halt the progressive neurological deterioration [1,3].

MR imaging findings of Type I AVMs include enlargement of the spinal cord, cord hypointensity on Tl-weighted images, central cord hyperintensity on T2-weighted images, scalloping of the surface of the cord on sagittal images, serpentine flow voids, and enhancement of the cord and dilated perimedullary veins after administration of gadopentetate dimeglumine. Hyperintensity of the cord on T2-weighted images is believed to be the most sensitive finding. In a review of 91 spinal vascular malformations, which included 31 Type I AVMs visualized by MR imaging, only increased hyperintensity in the center of the cord on T2-weighted images was seen in all cases. [6]

Increased T2 signal intensity is thought to result from cord edema. Isu et al, [7] studied two patients with Type I AVMs in the lumbar spine with MR imaging and angiography. They noted that the intramedullary high-signal-intensity changes on T2-weighted images corresponded with the level at which delay was seen in the venous drainage on spinal angiography. In both cases, the intramedullary high-intensity T2 signal disappeared after therapy, leading them to conclude that these MR imaging findings are caused by edema of the cord and are reversible. [7] Although high signal intensity on T2-weighted images is the most sensitive sign, it is nonspecific and can be seen in inflammatory, neoplastic, degenerative, demyelinating, and posttraumatic conditions. In the study by Gilbertson et al, no patient with a dural fistula had increased T2 signal abnormality as the only finding. [6]

The eliminations of dural AVFs can be performed through endovascular or surgical therapy. Endovascular therapy consists of embolization with liquid acrylic embolic material into the AVF and/or the proximal draining vein [1]. Surgical therapy involves microsurgical ligation of AVF draining vein and excision of affected dura [1]. Literature has supported the use of endovascular therapy as initial treatment with awareness of a 39% failure rate that should be followed up with definitive surgical therapy [1,5,8].


  1. Eskandar EN, Borges LF, et al. Spinal dural arteriovenous fistulas: Experience with endovascular and surgical therapy. J. Neurosurg (Spine 2) 96: 162-167, 2002.

  2. Kataoka H, Miyamoto S, et al. Venous congestion is a major cause of neurological deterioration in spinal arteriovenous malformations.

  3. Neurosurgery 48:1224-1230, 2001.

  4. Spetzler RF, Detwiler PW, et al. Modified classification of spinal cord vascular lesions. J. Neurosurg (Spine 2) 96:145-156, 2002.

  5. Doaa Abdulla: Venous disorders of the CNS. MS thesis, Ain Shams university school of medicine, Cairo, Egypt, 2005

  6. Gilbertson JR, Miller GM, Goldman MS, et al: Spinal dural arteriovenous fistulas: MR and myelographic findings. AJNR Am j Neuroradiol 16:2049-2057,1995

  7. Isu T, Iwasaki Y, Akino M, et al: Magnetic resonance imaging in cases of spinal dural arteriovenous malformation. Neurosurgery 24:919-923,1989

  8. Metwally, MYM: Textbook of neuroimaging, A CD-ROM publication, (Metwally, MYM editor) WEB-CD agency for electronic publication, version 10.4a October 2009 [Click to have a look at the home page]

  9. Arteriovenous Malformations/Fistulas of the Cervical Spinal Cord [full text]

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