PMC9479640_01
(a) Sagittal view of T2-weighted magnetic resonance imaging (MRI) of the spinal cord shows a diffuse high signal intensity from Th5 to Th11 (arrowheads) and multiple flow voids in the subarachnoid space (arrows). (b) Preoperative spinal angiography from the left L2 segmental artery reveals a spinal epidural fistula supplied from the dorsal somatic branch (long arrow) through retrocorporeal anastomosis (short arrow). The shunt forms a venous pouch and cranially drains through the posterior spinal vein (arrowheads). (c) The fusion image of MRI and maximum intensity projection shows the shunt point located in the lateral epidural space (asterisk). (d) NBCA injected from the microcatheter infiltrates into the shunt points and upper part of the venous pouch. (e) Postoperative angiography shows complete obliteration of the shunts with remnant venous congestion.
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F1
Th5-Th11 and multiple flow voids on the back of the region, indicating venous congestion and perimedullary venous ectasia [Figure 1a]. The conus medullaris ended at the L1 vertebral level. The left Th8 segmental artery injection demonstrated delayed spinal venous drainage in the anterior spinal artery, while the left L2 segmental artery injection revealed a SEAVF with perimedullary venous drainage. The shunt was supplied from the left dorsal somatic branch through the retrocorporeal anastomosis and was located in the contralateral ventral epidural space with a venous pouch [Figures 1b and c]. Intradural venous reflux through the posterior spinal vein was observed from the lower edge of the venous pouch at the L2 vertebral level [Figure 1b]. The NBCA infiltrated the upper part of the venous pouch through the shunt point and control angiography revealed complete shunt obliteration [Figures 1d and e].
Potentials in the upper row show baseline records. Potentials in the lower row were recorded at the end of the procedures. (a) Motor evoked potentials (MEPs) from both lower extremities and the anal MEP were monitored at the first treatment. The amplitude and latency of the MEPs from the lower extremities were stable during the embolization of the shunt. The anal MEP was not recorded. (b) The bilateral anterior tibial nerve SEP at the first treatment shows no changes throughout the treatment. The BCR was not recordable throughout the procedure. (c) The anal MEP was observed at the 1.5-year follow-up angiography. The mean amplitude was 8.8 muV, and the mean latency was approximately 80 ms. (d) The BCR was observed at the 1.5-year follow-up angiography. The mean amplitude was 294.9 muV and the mean latency was approximately 50 ms. APB: Abductor pollicis brevis, TA: Tibialis anterior, AH: Abductor hallucis, MEP: Motor evoked potential, SEP: Somatosensory evoked potential, BCR: Bulbocavernosus reflex.
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F2
Anal MEP/BCR monitoring revealed no potential during the procedure and no changes in other MEPs and SEPs were observed after treatment [Figures 2a and b]. Aminoff-Logue scale gait, micturition, and bowel scores were 4, 1, and 1. Anal MEP/BCR monitoring revealed potentials that were not observed during the follow-up angiography [Figures 2c and d; mean latencies and average amplitudes of anal MEP and BCR, approximately 60 ms and 50 ms and 9.5 muV and 295 muV, respectively].
(a) The follow-up magnetic resonance imaging shows the disappearance of the spinal cord congestion. (b) The follow-up spinal angiography demonstrates no recurrence of the shunts and improved venous flow of the spinal cord.
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F3
The angiography showed persistent shunt occlusion and improved venous drainage of the spinal cord, while MRI confirmed a normal spinal cord without edema [Figures 3a and b].