硬膜内腰椎间盘突出症术后炎症所致脊髓空洞伴中央管扩大。

NMC case report journal Pub Date : 2024-12-25 eCollection Date: 2024-01-01 DOI:10.2176/jns-nmc.2024-0165
Hiroki Hagizawa, Yu Moriguchi, Tomonori Yamada, Masafumi Kashii
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摘要

硬膜内腰椎间盘突出症(ILDH)是一种非常罕见的疾病,脑脊液(CSF)漏是术后并发症。据报道,髓圆锥中央管通过尾侧孔与蛛网膜下腔相通;然而,这种孔径从未在体内观察到过。在此,我们报告一例L1/2 ILDH合并术后脊髓粘连蛛网膜炎和脊髓空洞,其中被认为是尾端孔的通信被检测到。67岁女性主诉急性腰痛、右腿痛伴肌肉无力。磁共振成像(MRI)显示在L1/2水平的椎管内有一个大肿块。术中未见硬膜外腔碎片突出。因此,怀疑是ILDH,硬膜内检查显示肿胀的马尾和周围新生血管紧密粘附的突出碎片。术后症状改善1次;然而,3个月后,出现严重的双侧腿部肌肉无力和尿潴留。通过MRI诊断为术后脊髓空洞,并进行脊髓造影和后续计算机断层扫描。在给予非离子造影剂后,立即通过中央管勾画出圆锥和上圆锥的鼻窦,并能看到中央管与蛛网膜下腔的联系。经静脉-蛛网膜下腔分流术及硬脑膜成形术后症状改善。当髓圆锥周围粘连性蛛网膜炎导致脑脊液灌注受损时,原本因生长受阻的中央管重新开放,患者出现脊髓空洞。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

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Syringomyelia with Central Canal Enlargement Caused by Postoperative Inflammation after Surgery for Intradural Lumbar Disc Herniation.

Intradural lumbar disc herniation (ILDH) is a very rare condition, with cerebrospinal fluid (CSF) leakage as a postoperative complication. The central canal of the conus medullaris was reported to communicate with the subarachnoid space through a caudal aperture; however, this aperture has never been observed in vivo. Herein, we report a case of L1/2 ILDH with postoperative spinal adhesive arachnoiditis and syringomyelia in which the communication considered to be a caudal aperture was detected. A 67-year-old woman complained of acute lower back pain and right leg pain with muscle weakness. Magnetic resonance imaging (MRI) revealed a large mass in the spinal canal at the L1/2 level. Intraoperatively, no herniated fragments were found in the epidural space. Thus, ILDH was suspected, and an intradural examination revealed tightly adherent herniated fragments in the swollen cauda equina and surrounding neovascularization. Postoperatively, symptoms improved once; however, 3 months later, severe bilateral leg muscle weakness and urinary retention developed. She was diagnosed with postoperative syringomyelia by MRI, and myelography and follow-up computed tomography was performed. Immediately after the administration of nonionic contrast agents, the syrinx of conus and epiconus were delineated through the central canal, and the communication between the central canal and the subarachnoid space could be visualized. Symptoms improved after syringo-subarachnoid shunt and duroplasty. It is likely that when CSF perfusion was impaired because of adhesive arachnoiditis around the conus medullaris, the central canal, which had been obstructed with growth, reopened, and the patient presented with syringomyelia.

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