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Presented by
Jeramiah Yim, M.D., Stroke Fellow

History

A 58-year-old male experienced a progressive myelopathy over a two-year period, with rapid worsening over the month prior to admission. He reported the gradual onset of bilateral lower extremity weakness and stiffness. About four weeks prior to admission the weakness worsened, causing him to use a cane. For the week prior to admission, he was homebound, but able to ambulate.

Eight years ago he suffered an injury at work, where an 80-lb. box fell on his back. This apparently caused a lumbar fracture and a right foot drop, requiring laminectomy.

On physical examination he had normal strength and sensation in the upper extremities. He had increased tonus and 4/5 weakness in both lower extremities. There was patchy loss of light touch below the umbilicus, and decreased joint position sense in the distal lower extremities, but no clear-cut sensory level. Deep tendon reflexes were 4+ in the LEs, with unsustained clonus. Babinski's sign was present bilaterally. Romberg's test was positive. He could not perform tandem gait.

Diagnostic Procedures

Initial radiological studies included an MRI that suggested a spinal AVM. He therefore underwent spinal catheter angiography (Figure 1), and this demonstrated a dural arteriovenous fistula fed primarily by branches of the right T4 and T5 segmental arteries. The angiographic architecture of the malformation was used intraoperatively to guide treatment. The prominent venous loop (identified by "A") is also demonstrated in the intraoperative photograph (see Figure 2).

Hospital Course

The patient was evaluated for possible endovascular treatment of the lesion. It was thought that the small caliber of the feeding vessels made curative embolization less likely. Direct surgical treatment of the lesion was offered.

Surgical Procedure

Surgery was performed by Joshua Bederson, M.D. A T4 , T5 laminectomy was made. The T5 segmental feeding artery was seen entering the dura below the right T5 nerve root. A midline dural opening was made. The feeding artery entered directly into a fistula with the radiculomedulary vein at that level. Additional arterial supply from T4 and other rostral arteries was identified. The rostral supply entered the venous system within the subarachnoid space. The tense and turgid draining vein had compressed and distorted the adjacent spinal cord.

Figure 2 is an Intraoperative photograph showing the right T5 nerve root (A), the intradural feeding artery (B), and the draining vein (C). The venous loop (white arrow) corresponds to the loop seen angiographically in Figure 1 A.

The lesion was treated by coagulating the arteriovenous fistula and dividing the draining vein. With this maneuver the draining vein collapsed, and the cord was no longer compressed.

Postoperative Course

The patient tolerated the surgical procedure well and had an uneventful postoperative recovery, returning to home on the 7th postoperative day. He experienced an immediate improvement in stregnth, but remained hyperreflexic.

Figure 3 illustrates the Postoperative Right T5 injection showing absence of the arteriovenous fistula and no filling of the draining vein.

Discussion

This patient's progressive myelopathy was most likely due to ischemia of the spinal cord induced by venous hypertension. Transmission of arterial pressure directly into the venous system by the arteriovenous fistula limits normal perfusion of the spinal cord and causes symptoms. By obliterating the fistula, the venous system is relieved of the arterial pressure.

In some cases the fistula can be treated with endovascular techniques. In this patient the arterial supply could not be precisely cannulated for safe embolization. Direct surgical obliteration of the fistula was straightforward, aided in part by precise localization provided by the preoperative angiogram.

Further References

• Bederson JB: Pathophysiology and Animal Models of Dural Arteriovenous Malformations. In: Awad I and Barrow D, eds: Dural Arteriovenous Malformations. American Association of Neurological Surgeons Park Ridge, Illinois 1993, pages 23-34.
• Bederson JB, Weistler OD, Brustle O, Yasargil MG, Frick R, Roth P: Intracranial venous hypertension and the effects of venous outflow occlusion in a rat model of arteriovenous fistula. Neurosurgery 29:(3)341-350, 1991.
• Ullman J, Bederson J: Spinal Arteriovenous Malformations: Pathophysiology and Hemodynamics. In: Barrow, D, Awad, I, Eds, Spinal vascular Malformations. American Association of Neurological Surgeons, Park Ridge, Illinois, 1997.