腰椎间盘突出合并马尾神经损伤的外科治疗

目的探讨腰椎间盘突出症伴马尾神经综合征的发病机制、治疗及预后。方法回顾性分析18例腰椎间盘突出症伴马尾神经综合征病例,均在出现症状7 d后行手术减压治疗。结果术后平均随访3.1年,所有患者腰痛全部恢复,下肢肌力部分恢复16例,未恢复2例,但括约肌功能障碍无明显改善。按Masato标准评价疗效：好转8例,差10例。结论腰椎间盘突出症伴马尾神经综合征是手术的绝对适应证,一经明确诊断必须尽早手术,以抢救神经功能。     

腰椎间盘手术致马尾神经综合征的影像学分析

目的：探讨腰椎间盘突出症围手术期产生马尾神经综合征原因。方法： 通过15例患者发病前后的脊髓造影、CT、MRI等影像学表现,结合临床的发病时间综合分析。结果：8例术后的急性马尾神经综合征是由于术中直接造成马尾损伤或血肿压迫;7例慢性发作的患者由于疤痕生椎管狭窄二度形成。结论：腰椎管犯狭窄是马尾神经综合征形成首要的发病基础,术中不完全减压、马尾神经的直接损伤、术后疤痕组织过度增生使狭窄椎管的再形成,麻醉、马尾神经粘连等是马尾神经综合征的重要的病理基础。     

下腰椎骨折合并马尾神经损伤的治疗观察

目的观察下腰椎骨折合并马尾神经损伤的手术治疗效果。方法本文总结了38例下腰椎骨折合并马尾神经损伤病例的临床治疗及随访结果，进行综合分析。结果急性不完全性马尾神经损伤者手术时机与其功能恢复的优良率有关；完全性损伤及陈旧性损伤功能恢复与手术时机无显著关系。结论手术治疗是下腰椎骨折合并马尾神经压迫、损伤的首选治疗措施，一旦出现马尾神经损伤症状应及早手术治疗。     

游离型腰椎间盘脱出症44例临床分析

目的：探讨游离型腰椎间盘脱出症合并马尾神经损伤的发病率,分析临床症状,体征与影像学检查的重要意义。方法：４４例病人全部做ＣＴ扫描,诊断可疑者进行脊髓造影ＣＴＭ检查,脑脊液的检验,并且与马尾神经肿瘤进行了严格的鉴别。结果：马尾神经功能完全恢复３３例不,完全恢复１１例。恢复所需时间１．５－２年,唯双下肢瘫痪及性功能障碍恢复所需时间较长并且功能不理想。     

腰椎间盘突出症合并马尾神经损伤(附26例报告)

方法：采用椎板切除及带蒂复合体回植成形髓核摘除术治疗腰椎间盘突出症合并马尾神经损伤２６例。结果：平均随访５年８个月，腰腿痛症状完全消失１４例，部分缓解１２例；马尾神经功能完全恢复８例，未恢复５例；下肢肌肉瘫痪的１８例中，肌力完全恢复１２例，未恢复２例。结论：本病预后与马尾神经损伤程度及手术减压是否彻底有关，马尾神经损伤程度与突出物大小、突出速度及病程长短有关。腰椎管狭窄是本病的前置因素，继发性、粘连性马尾神经炎是影响马尾神经功能恢复的重要原因。本病一旦确诊应尽早手术。带蒂复合体回植成形髓核摘除术优于全椎板切除术     

腰椎间盘突出症并马尾综合征26例治疗分析

目的:探讨腰椎间盘突出症并马尾综合征的手术疗效。方法:将26例采用全椎板切除,摘除脱出或游离椎管内的髓核组织,结果:经2～7年的随访,优3例,良8例,尚可10例,差5例,治疗效果大多不完全恢复。结论:腰椎间盘突出症并马尾综合症应尽早于术手术治疗,预后不如仅有神经根受累者效果好。     

腰椎间盘突出症合并马尾神经综合征的临床研究

目的通常认为腰椎间盘突出症患者如果并发马尾神经综合征,一经诊断应立即手术。即使早期手术,临床中仍发现有部分患者膀胱功能无法恢复,对此类患者膀胱及括约肌功能恢复程度的判断对于手术方案的制定尤为重要。方法对本院148例因患腰椎间盘突出症行手术治疗的患者进行回顾性研究,并对其中4例（2．7％）合并典型马尾神经综合征的患者进行长期随访（5个月-9年,平均6．1年）,随访内容主要包括二便功能及下肢放射性疼痛症状恢复情况。结果下肢放射性疼痛症状恢复较快,二便功能恢复较为缓慢。但经过数年的随访,全部4例患者二便功能基本恢复,生活能够自理,结果较满意。结论腰椎间盘突出症并发马尾神经综合征患者经手术减压后二便功能近期恢复不满意,经长期非手术治疗后能够有较满意的恢复情况。     

腰椎间盘手术损伤神经的原因分析及预防

1　临床资料本组手术病例共 2 2 2例 ,其中并发　神经损伤 4例 ,发生率为 1.8% (4/ 2 2 2 ) ,　详见附表病　　例　　介　　绍性别年龄突出水平及类型损伤原因临床表现随访结果男 46岁 L4 - 5右侧型左侧侧隐窝减压时咬骨钳撕破硬膜吸引头吸出马尾神经下肢不全瘫足下垂一年后恢复女 52岁 L4 - 5中央型因突出物巨大神经根挤压变薄 ,误认为纤维环切开损伤。右小腿外侧麻木 ,大拇趾无力一年半基本恢复女 38岁 L5- S1 中央型髓核钳挤压马尾神经双下肢感觉障碍足下垂二年后好转女 52岁 L5- S1 偏左侧型 髓核钳挤压误伤神经术后左足下垂趾不能背…     

腰椎间盘突出症合并马尾神经损伤

方法；采用椎板切除及带蒂复合体回植成形髓核摘除术治疗腰椎间盘突出症合并马尾神经损伤２６例。结果：平均随访５年８个月，腰腿痛症状完全消失１４例，部分缓解１２例，马尾神经功能完全恢复８例，未恢复５例；下肢肌肉瘫痪的１８例中，肌力完全恢复１２例，示恢复２例，结论；本病预后与马尾神经损伤程度及手术减压是否彻底有关，马尾神经损伤程度与突出物大小，突出速度及病程长短有关。腰椎管狭窄是本病的前置因素，继发性，粘     

腰椎间盘术后并发急性马尾综合征

目的：探讨腰椎间盘术后并发急性马尾综合征的原因。方法：结合5例患者发病前后的MRI、CT和脊髓造影，手术时间，手术方法和随访结果综合分析。结果：术后磁共振检查不能发现引起急性马尾综合征的原因，而且在再次手术中也不能证实。术前5例患者都存在腰椎管狭窄，再次扩大减压术后2例完全恢复，3例有程度不同的后遗症状。后遗症状与再次手术减压的时间没有明显的联系。结论：相对的椎管狭窄和术后水肿反应引起静脉回流障碍，静脉淤血，引起马尾神经缺血，可能是引起腰椎问盘突出术后发生急性马尾综合征的原因。采用术后48h内再次手术扩大减压治疗。     

Synovial cysts and the lithotomy position causing cauda equina syndrome

We describe a case of cauda equina syndrome caused by synovial cysts and the lithotomy position. A transurethral resection of the prostate was performed under spinal anesthesia in the lithotomy position. We believe that this is the first case report of facet joint synovial cysts and the lithotomy position causing ischemic neurologic injury to the cauda equina. Other etiologies such as needle trauma, neurotoxicity, hematoma, and abscess were not evident. We believe that positioning the patient in the lithotomy position narrowed the cross-sectional area of the spinal canal in a patient with a coexisting critically stenosed lumbar spinal canal. The resultant mechanical pressure caused an ischemic compression injury to the cauda equina.     

Out of hours magnetic resonance imaging for suspected cauda equina syndrome: lessons from a comparative study across two centres

BackgroundCauda equina syndrome, a rare but disabling spinal surgical emergency, requires prompt investigation, ideally using magnetic resonance imaging as patients may require decompressive surgery. Out of hours access to magnetic resonance imaging is only routinely available in major trauma centres and neurosurgical units. Patients in regional hospitals with suspected cauda equina syndrome may require transfer for diagnostic imaging. We retrospectively studied the proportion of patients referred with suspected cauda equina syndrome who required out of hours transfer for magnetic resonance imaging and decompressive surgery.Materials ands methodsRetrospective cohort study of patients referred using online referral platforms with suspected acute cauda equina syndrome and transferred out of hours between 6pm to 8am on weekdays and all day on weekends to two of the largest neurosurgical units in the UK in Birmingham and Cambridge.ResultsA total of 441 patients were referred across both sites with a suspicion of acute cauda equina syndrome; 339 patients were transferred for diagnostic scans and only 16 of them (4.7%) were positive for cauda equina compression, necessitating prompt decompressive surgery. Of the patients with negative magnetic resonance scans, 50% had their discharge or transfer back to referring hospitals delayed by more than 24 hours.ConclusionsOver 95% of patients who were transferred for imaging did not undergo emergency decompression. The authors propose a greater role for the provision of out of hours magnetic resonance imaging in all hospitals admitting emergency patients to streamline management.     

A study of motor and sensory evoked potentials in chronic cauda equina compression of the dog

Previous experimental studies have shown the effects of acute compression of the spinal cord and peripheral nerve roots. Recently, however, a few studies of chronic compression of the cauda equina in animal models have been reported. The purpose of this study was to determine the long-term electrophysiologic changes resulting from chronic compression of the cauda equina in dogs. An animal model of lumbar spinal stenosis was prepared according to Delamarter's method. Four experimental groups, each containing six dogs, were studied. One group underwent only laminectomy of the sixth and seventh lumbar vertbrae; these animals served as controls. In the three other groups, a laminectomy was performed and the cauda equina was constricted by 25%, 50%, and 75%, respectively, to produce chronic compression. Weekly neurologic examinations were carried out, and the neurologic deficits were graded using a modified Tarlov system. Sensory, and motor evoked potentials were recorded preoperatively, immediately after constriction, and at 2 weeks and 1, 2, and 3 months postoperatively. The animals in the control group showed no changes in sensory or motor evoked potentials. The dogs in which the cauda equina had been constricted by 25% showed no neurologic deficits and only mild changes in sensory and motor evoked potentials. The dogs in which the cauda equina had been constricted by 50% showed mild initial motor weakness, and major changes in the evoked potentials. The dogs in which the cauda equina had been constricted by 75% showed significant weakness, paralysis of the tail, and urinary incontinence; all dogs were partially recovered by the 3rd month, but all still showed neurogenic changes in the evoked potentials. Sensory and motor evoked potentials revealed neurologic abnormalities before the appearance of neurologic signs and symptoms. Constriction of more than 50% was the critical point that resulted in complete loss or reduction of the evoked potentials and in neurologic deficits. Dogs in which motor and sensory evoked potentials recovered also showed gradual disappearance of neurologic symptoms and signs. Recovery of motor evoked potentials in particular was associated with complete disappearance of neurologic symptoms and signs. For accurate prognosis in cases of chronic cauda equina compression, a combined diagnostic study of sensory and motor evoked potentials is recommended.     

腰椎间盘巨大突出和马尾综合征

本文通过对腰椎间盘突出引起的马尾综合征７６例的临床分析，将本病症分为典型与非典型两种类型。诊断上主要依据病史与理学检查。非典型者比较多见。持久的双侧坐骨神经痛提示有马尾神经损害，鞍区的感觉变化与肛门反射有重要价值．脊髓造影和脊柱ＣＴ扫描检查可明确诊断。马尾综合征一旦确诊，应及早采取手术减压。本组病例在半个月内手术者大多效果满意，急性发病者预后差。持久的下肢麻痛与肛周感觉减退，可作为重要的预测指标。引起本病症的机理尚不清楚。过伸位脊柱损伤、巨大突出物的持久压迫、椎管狭窄与局限性蛛网膜炎的发生均是造成马尾神经损害的重要因素。     

Cauda equina syndrome after in situ arthrodesis for severe spondylolisthesis at the lumbosacral junction

Relative stretching of the cauda equina over the posterosuperior border of the sacrum can be found in all patients who have Grade-III or IV spondylolisthesis at the lumbosacral junction. We identified twelve patients, all less than eighteen years old, who had cauda equina syndrome after in situ arthrodesis for Grade-III or IV lumbosacral spondylolisthesis. In all twelve patients, posterolateral arthrodesis had been done bilaterally through a midline or paraspinal muscle-splitting approach. Nothing in the operative reports suggested that the cauda equina had been directly injured during any of the procedures. Five of the twelve patients eventually recovered completely. The remaining seven patients had a permanent residual neurological deficit, manifested by complete or partial inability to control the bowel and bladder. If dysfunction of the root of the sacral nerve is noted preoperatively in a patient who has lumbosacral spondylolisthesis, decompression of the cauda equina concomitant with the arthrodesis should be considered. An acute cauda equina syndrome that follows a seemingly uneventful in situ arthrodesis for spondylolisthesis is best treated by an immediate decompression that includes resection of the posterosuperior rim of the dome of the sacrum and the adjacent intervertebral disc. In addition, posterior insertion of instrumentation and reduction of the lumbosacral spondylolisthesis should be considered.     

Two-stage decompression for combined epiconus and cauda equina syndrome due to multilevel spinal canal stenosis of the thoracolumbar spine: a case report

INTRODUCTION: A case of combined epiconus and cauda equina syndrome due to multilevel spinal canal stenosis of the thoracolumbar spine is reported. METHODS: A 76-year-old man with multilevel spinal canal stenosis of the thoracolumbar spine (Th11-12, L2-S) who showed symptoms of epiconus syndrome was reported. First, we performed anterior decompression and fusion at the thoracolumbar junction (decompression: Th11-12, fusion: Th10-L2), which ameliorated his symptom partially. However, he presented cauda equina symptoms. Then, he underwent posterior spinal decompression (L3-5) and fusion (Th12-L5). RESULTS: After anterior decompression, several symptoms disappeared. However, motor and sensory disturbance below L4 and bladder-bowel disturbance remained. We then performed a secondary operation. At three years' follow-up, he was able to walk with the aid of a cane. CONCLUSIONS: Combined epiconus and cauda equina syndrome due to multilevel spinal canal stenosis was treated by combined two-stage anterior and posterior decompression. In this case, multilevel decompression via anterior and posterior approaches was necessary to relieve the symptoms.     

Posterior epidural migration of an extruded free fragment from a lumbar disc herniation

The majority of symptomatic lumbar disc herniations are located in a posterolateral position with resultant nerve root compression. Although caudal, rostral and lateral migrations of disc fragments are common, posterior epidural migration of an extruded free fragment from a lumbar disc herniation is a rare occurrence and sometimes may cause a dural sac compression with cauda equina syndrome. This retrospective case report describes a 63-year-old man with intractable lower back pain and cauda equina syndrome. Emergency magnetic resonance imaging (MRI) revealed a posterior epidural soft tissue compressing the dural sac. The lesion was hypointense on T1-weighted images, hyperintense on T2-weighted images and showed rim enhancement after intravenous injection of gadolinium. A laminectomy at L3 was performed and the extruded disc fragment was removed with dural sac decompression. Postoperatively the patient's radicular symptoms completely resolved. At the 2-year follow-up visit, the patient had recovered full motor, sensory and urinary functions. MRI is the modality of choice in the evaluation of an extruded free disc fragment and a cauda equina compression. In such cases a wide decompressive laminectomy is recommended. Received: 13 November 2000; Accepted: 4 December 2000     

Neuropathic bladder in ankylosing spondylitis with spinal diverticula

Cauda equina type of syndrome with neuropathic bladder is a rare but known complication of long-standing ankylosing spondylitis. From 1968 until now, diverticula from the subarachnoid space eroding into the bodies of the lumbosacral vertebrae have been reported in 46 cases of ankylosing spondylitis with cauda equina syndrome and neuropathic bladder. We report 3 cases of neuropathic bladder and ankylosing spondylitis with cauda equina symptoms. In 1 of the 3 patients, these rarely encountered spinal diverticula were demonstrated by computerized tomography (CT) scan. The etiology of these diverticula and their treatment are reviewed.