A 46-year-old male was admitted to our institute due to a history of progressive paraparesis for 2 weeks. Eight months earlier, he experienced severe left buttock pain radiating to left leg for 2 weeks. He was admitted to other private hospital and underwent discectomy L5-S1. Five months later, he suffered from right leg pain and urinary retention. He went back to the same private hospital and underwent revised surgery with spinal fusion L5-S1. Two weeks before hospitalization, he developed progressive paraparesis and constipation. He was unable to walk more than about 100 m. The patient went to another private hospital and was transferred to Prasat Neurological Institute for further investigation and proper treatment after performing MRI of the lumbosacral and thoracic spine. The neurological examination revealed the evidence of spastic paraparesis (muscle strength 3/5) and the lack of pinprick sensation below T10 level, impairment of proprioception, hyperreflexia, and presence of Babinski's sign in the lower extremities. The previous series of MRI of the lumbosacral and thoracic spine were retrospectively reviewed and revealed spinal canal stenosis and bilateral lateral recesses stenosis at L5-S1 level due to moderate diffuse annular disc bulging with moderate enlargement of facet joints and thickening of the ligamentum flavum []. There was an abnormal hyperintense T2 signal with patchy enhancement representing spinal cord congestion extending from the conus medullaris to the level of T4 with subtle perimedullary flow voids along ventral and dorsal cord surfaces [Figures and ]. Magnetic resonance (MR) myelography also showed “worm-like” appearance of the area from thoracic level to the conus medullaris []. MR angiography (MRA) of the thoracolumbar spine demonstrated early opacification of perimedullary venous plexus along anterior and posterior surfaces of spinal cord []. Furthermore, there was a curvilinear flow void, probably the dilated vein of the filum terminale, running from lower lumbar level to the conus medullaris []. Spinal angiography demonstrated SDAVF at the level of L5-S1, probably located on the left S1 nerve root sleeve, which is supplied by the left lateral sacral artery (LSA) originating from the internal iliac artery with venous drainage through the dilated radicular vein into the dilated vein of the filum terminale [Figure and ]. The artery of Adamkiewicz arose from the left L2 lumbar artery and left T9 intercostal artery. Transarterial embolization with N-butyl-cyanoacrylate (NBCA) through the left LSA was successfully performed with NBCA filling across the fistula into the proximal draining vein []. The patient had gradually improved until being the ability to walk independently 3 months later. His bowel and bladder controls had completely regained. Six months after the embolization, follow-up MRI of the thoracolumbar spine also confirmed completely regression of spinal cord congestion [].
A 33-year-old male presented with a 2-year history of pain in the lumbosacral spine with progressive lower-limb weakness, urinary frequency, and incontinence. Symptoms intensified after exercise and prolonged standing. Lumbar spine MRI demonstrated a tethered cord at the L3 level, a filum terminale lipoma, and edema in the spinal cord. It also showed tortuous veins on the posterior surface of the spinal cord (Figures ).\nThe neurological examination revealed bilateral hip-joint flexion weakness (grade 4 according to modified Medical Research Council system), plantar flexion weakness (grade 3 according to modified Medical Research Council system), and reduced sensation in the S2–S3 dermatomes. The Babinski and Rossolimo signs were present bilaterally. Based on the clinical and radiological signs, a SDAVF was suspected. A DSA confirmed the SDAVF at the S2-S3 level, in the dura supplied by lateral sacral arteries and branches from the internal iliac arteries. Tortuous draining veins were present on the posterior surface of the entire spinal cord and terminated intracranially (Figures ).\nThe patient underwent three endovascular embolizations, each with a different agent. First, embolization was performed with Onyx™ 18, administered in two microcatheters. This treatment resulted in an occlusion of the fistula. The patient significantly improved, but due to poor penetration of the draining vein, after a few weeks, the fistula recanalized and symptoms returned.\nA second embolization was performed 4 months later. The vascular access to the fistula was more complicated. A 25% Phil™ injection was feasible only through the small sacral branches of the left internal iliac artery. This procedure achieved a significant reduction of flow through the fistula. Eighteen months later embolization of the fistula was attempted with diluted glue. Despite good occlusion of the fistula observed in a DSA, the tortuous vessels remained visible in the follow-up MRI (Figures ). The symptoms persisted, and the patient was qualified for surgical treatment.\nThe goal of surgery was to occlude the draining vein and the arterial feeder and to reduce the lipoma. With a median incision, the sacral canal was opened on the right side. The dura was thick, and there were multiple vessels filled with embolic agents. There was one large, bright-red vessel extradurally and one intradurally at the S2-S3 level. A clip was placed upon the arterialized vein intradurally for a couple of minutes. After that, the vessel changed color and the tension decreased. Both intra- and extradural vessels were coagulated. Afterwards, the lipoma was visualized and partially removed. The dura was sutured in a watertight fashion, and the wound was closed in layers.\nThe postoperative course was uneventful, and a few days later, the patient was discharged. After 6 months, a follow up MRI showed the absence of tortuous vessels on the posterior surface of the spinal cord and a significant reduction in the myelopathic changes (Figure ). On follow-up, the patient considerably improved, with no incontinence, some urinary frequency and mild weakness (grade 4 according to modified Medical Research Council system).