腰椎椎体后缘终板骨坏死症42例报告

目的探讨腰椎椎体后缘终板骨坏死症的发病机制和诊断治疗方法。方法42例患者，以腰腿痛症状为主，少数伴有间歇性跛行和马尾压迫症状，平均发病时间7．6年。X线检查发现下腰椎管内有一与椎体后缘相连的小骨块，CT扫描清晰显示椎体后缘有类圆形或多囊状骨质稀疏区，周边形成硬化带，后方骨质凸入椎管内，或压迫硬膜囊或压迫神经根。MRI显示对应椎间盘大都呈严重退变状态。本组全部行手术治疗，将凸入椎管内骨质切除和对应间隙的退变髓核摘除，短节段椎弓根螺钉系统内固定、椎体间植骨融合。术中完整切除的11例标本作组织病理学检查。结果术中肉眼所见，切除的凸入骨质为松质骨组织，周围硬化带为骨皮质。组织学所见病灶区为小梁骨和髓腔，表现为不同程度的骨坏死，无髓核组织成分充填于骨坏死区。术后所有患者均获随访，时间3月-7年，平均3.8年。38例腰腿痛症状消失，4例仍有轻度腰痛，2例伴有马尾功能障碍者大小便功能基本恢复正常。结论腰椎受异常应力或过度活动或其它一些尚不明的原因引起椎体终板后缘缺血性变性、坏死，引起腰痛。向后塌陷、增生的骨质凸入椎管压迫硬脊膜囊内马尾神经或腰神经根，导致神经根性症状。因此将本病命名为“腰椎椎体后缘终板骨坏死症”能比较准确地反映它的病理本质。     

腰椎后缘骨内软骨结节：附11例报告

作者分析了１１例腰椎后缘骨内软骨结节的临床，Ｘ线及ＣＴ表现，多为青壮年，主要症状为腰腿痛，均为单处发病。典型的Ｘ线表现为发病椎体后下缘有一骨质缺损，其后有一骨块突入椎管。ＣＴ扫描均见椎体后缘类圆型或多囊状骨质缺损，为典型的软骨结节（许莫氏结节）结节的骨性后壁凸入椎管构成侧位Ｘ线片上的骨块，作者认为腰椎后骨内软骨结节多形成于青少年时期，是由椎间盘组织经破裂的软骨终板突入椎体后缘的松质骨内所致。当症状     

终板破裂型椎间盘突出症的诊断与治疗

目的：探讨终板破裂型椎间盘突出症的发病机理和诊断治疗。方法：37例病人，以腰腿痛症状为主。CT或MRI扫描显示椎体后缘终板破裂压迫神经根。全部行手术治疗，摘除突出的椎间盘髓核，部分病例凿除破裂的终板。结果：术后37例病人全部获随访，时间6个月-4年，按JOA评分，术前13分，最终随访26分。结论：青少年时期腰椎受异常应力的作用引起椎体软骨终板破裂，破裂的软骨终板在髓核的作用下凸入椎管，导致本病的发生。手术治疗可获得满意的结果。     

终板破裂型椎间盘突出症的诊断与治疗

目的探讨终板破裂型椎间盘突出症的发病机理和诊断治疗.方法37例病人,以腰腿痛症状为主.CT或MRI扫描显示椎体后缘终板破裂压迫神经根.全部行手术治疗,摘除突出的椎间盘髓核,部分病例凿除破裂的终板.结果术后37例病人全部获随访,时间6个月～4年,按JOA评分,术前13分,最终随访26分.结论青少年时期腰椎受异常应力的作用引起椎体软骨终板破裂,破裂的软骨终板在髓核的作用下凸入椎管,导致了本病的发生.手术治疗可获得满意的结果.     

腰椎椎体终板后缘骨坏死病理演变过程的观察

目的：研究腰椎椎体终板后缘骨坏死的病理演变过程和Schmorl结节的形成机制。方法：对13例腰椎椎体终板后缘骨坏死症患者腰椎后路减压术中切除的完整病灶标本行组织病理学检查，观察不同年龄和不同阶段病变的组织学变化。结果：1例儿童和6例成人患者发病时间较短，其病灶的组织学特征表现为软骨终板明显增厚、变性，软骨终板下的骨组织坏死，部分坏死区为纤维组织替代，局部出现修复性新生骨。另6例成人患者发病时间较长，其病灶的组织学特征表现为软骨终板下的成熟骨组织。结论：腰椎椎体终板后缘先发生软骨终板下的骨组织坏死，然后出现修复性新生骨，新生的骨组织由于硬度较低，在压力的作用下发生塌陷，随着爬行替代的完成及骨骼的成熟，逐渐形成凸向椎管内的骨块，表明病变已发展至晚期，处于相对静止状态。腰椎椎体终板后缘骨坏死的病理演变过程实际上也是发生于腰椎椎体终板后缘Schmorl结节的形成过程。     

腰椎椎体后缘离断症

目的：对9例腰椎椎体后缘离断症进行回顾性分析。方法：所有病例均行X线片、CT扫描检查，其中2例行MRI检查，并对照症状体征进行诊断，手术加以证实。结果：病变主要见于L4、5椎体后上缘或下缘，典型的X线表现为病椎后角有一骨质缺损，其后有一骨块突入椎管；CT扫描均可见椎体后缘类园形或囊状骨质缺损，呈典型的许莫氏结节，椎体后缘突向椎管内的骨块与椎间盘髓核组织一起构成中央管或神经根管的狭窄，压迫马尾或神经根。结论：椎体后缘离断的征象可能是青少年时期椎体后缘环状骨骺陈旧性损伤及其继发改变的结果，X线片、CT、MRI检查具有诊断价值。     

腰椎椎体后缘离断合并椎间盘突出症

目的 分析腰椎椎体后缘离断合并椎间盘突出症的发病机理，探讨手术治疗方法。方法 回顾总结10例腰椎后缘离断合并椎间盘突出症患的临床表现、影像学资料及手术方法选择。结果 10例患中，6例表现为单侧腰腿痛，4例为双侧；4例合并间歇性跛行，其中2例伴有马尾神经受压。CT检查显示全部病例腰椎椎体后缘形成突向椎管内的骨块，其相应的椎体后角骨缺损区为椎间盘髓核组织，其中7例椎间盘突出物超过椎体后缘骨。10例均行手术切除突出的椎间盘组织，其中6例同时行离断骨块切除。全部病例经3～36个月随访取得满意效果。结论 本病发病机理主要还是由于青少年时期椎体后缘环状骨骺变异或损伤逐步引起椎间盘突出的继发改变，最终造成神经根和硬膜囊的压迫。椎体后缘骨块仅部分参与神经根压迫。椎管内神经根及硬膜囊的彻底减压才能达到满意效果。     

腰椎椎体后缘骨内软骨结节所致腰椎管狭窄症16例CT分析

目的　总结腰椎椎体后缘骨内软骨结节 (LPMN)所致腰椎管狭窄症临床、CT诊断及鉴别诊断 ,探讨有关的发病因素。方法　对经手术证实的 16例PLMN所致腰椎管狭窄症的临床表现、CT表现、手术方式进行回顾性分析总结。结果　典型的CT改变为 (1)椎体后上缘类圆形骨质缺损 ,边缘较致密硬化 ;(2 )缺损后方有一骨块突入椎管 ,(游离或部分与椎体相连 ) ;(3)硬膜囊及神经根受压 ,可伴有椎间盘突出。结论　CT检查能明确诊断腰椎椎体后缘骨内软骨结节 (LPMN)所致腰椎管狭窄症 ,并为制订治疗方案提供可靠依据。     

腰椎椎体后缘离断症

作者诊治了１３例腰椎椎体后缘离断症，其主要症状为腰腿痛与间歇性跛行，少数发生马尾压迫综合征。１３例共有１４个腰椎椎体的后缘形成突向椎管内的骨块，８个与椎体相连，６个与椎体分离，与其相对应的椎体后角骨缺损区内为椎间盘髓核组织；８个椎体后角的病损构成７例患者中央管或神经根管狭窄的主要原因，另６个椎体后角病损较小，仅部分参与神经根压迫；病变主要见于Ｌ４，５及Ｓ１椎体后上缘或下缘。作者认为成人中所见椎体后缘离断的征象很可能是青少年时期椎体后缘环状骨骺变异或陈旧性损伤及其继发改变的结果。     

对腰椎Schmorl结节形成的探讨

目的：探讨腰椎Schmorl结节的形成及其与下腰痛和椎间盘变的关系。方法：12个腰椎Schmorl结节来自10例严重下腰痛伴或不伴坐骨神经痛患者。均行腰椎X线摄片和CT扫描，并将术中完整切除的12个Schmorl结节病灶标本组织学检查，结果：CT扫描发现Schmorl结节形成区软骨终板下有一类圆形、多囊状骨密度不规则区，边缘通常硬化，呈骨坏死改变。组织学检查发现，在CT片上显示的骨密度不规则区实际上是骨坏死区，骨坏死区表面的软骨终板通常完整，软骨下髓腔内脂肪细胞消失，大量纤维组织增生和缺血性纤维软骨形成，小梁骨内骨细胞消失或死亡，形成空骨陷窝，结论：X线片显示的经典Schmorl结节实际上是椎体软骨终板下的片状骨坏死,灶软骨终板通常是完整的，有无髓核突出与Schmorl结节形成无关。     

Lumbar spinal stenosis. Radiographic diagnosis with special reference to transverse axial tomography.

Spinal stenosis due to malalignment and/or hypertrophy of the bony margins of the spinal canal is a recognized cause of cauda equina compression and nerve root entrapment. The plain lumbosacral spine roentgenograms reveal the number of lumbar vertebrae, their alignment, their interpedicular distances, the height of the intervertebral disk spaces and the presence of osteophyte formation. It correlates poorly with encroachment on the spinal canal. The transverse axial tomogram directly demonstrates a cross-section of the spinal canal and will show abnormal areas of bone encroachment usually arising from hypertrophied lamina and articular processes. These narrow the posterior portion of the spinal canal and encroach on the lateral recesses. This examination does not demonstrate soft tissue hypertrophy and the stenosis may be even greater than what is apparent due to the bony encroachment. The myelogram expresses how the narrowed spinal canal affects the dural sac and its contained cauda equina. Not infrequently there is an associated herniated disk.     

A case of traumatic spinal subarachnoid hematoma causing compression of the cauda equina]

A case of traumatic spinal subarachnoid hematoma causing compression of the cauda equina is reported here. The patient, a 76 year-old woman, who had fallen down by accident 1 month before, was admitted to our hospital presenting lumbar pain radiating into her right thigh, monoplegia of the right leg and urinary incontinence. Myelography and metrizamide CT demonstrated a filling defect mimicking intradural extramedullary tumor at the level of L1 and L2. Magnetic resonance imagings (MRI) revealed a subacute or chronic hematoma compressing the conus medullaris and the cauda equina. Operation was performed and an old hematoma, which occupied most of the spinal subarachnoid space and compressed the conus and cauda equina from right to left, was removed. No definite bleeding point was detected and no traumatic change was seen on the cord. Neither tumor nor abnormal vessel was detected. After surgery, the symptoms improved partially. On a review of the literature, we found only 4 cases of traumatic spinal subarachnoid hematoma, all of which occupied the cervical or thoracic portion of the spine. Our case is the first report, except for the cases following lumbar spinal tap, of traumatic spinal subarachnoid hematoma causing compression of the cauda equina. Though usually blood in CSF diffuses immediately, a clot may be formed when a large amount of bleeding obstructs the spinal canal. In our case, furthermore, deformity and narrowing of the spinal canal had preceded for many years, following lumbar vertebral compressed fracture related with osteoporosis. This might have promoted the process of canal obstruction and clot formation.(ABSTRACT TRUNCATED AT 250 WORDS)     

Lumbar posterior marginal node (LPMN) in adults. Report of fifteen cases.

This report concerns 15 adults (nine men and six women) who experienced lumbar and sciatic pain associated with an unusual defect of the edges of the vertebral bodies together with a small bony ridge protruding into the spinal canal. This lesion was well demonstrated by computed tomography and easily differentiated from the posterior longitudinal ligament or herniated disc calcifications, as well as from posterior degenerative ridge osteophytes. This lesion looked like the so-called lumbar posterior marginal node. First described in adolescents, this entity was considered as a traumatic fracture of the posterior ring apophysis. Recently, identical cases were noted in young adults in the absence of previous trauma, which were a particular type of marginal cartilaginous node. In the cases reported here, the computed tomographic scans suggested several mechanisms of formation of the vertebral lesion: a variant of marginal cartilaginous nodes; traumatic avulsion; avulsion related to disc herniation; and fusion of the avulsed bony fragment with the vertebral body.     

The effect of Lipo prostaglandin E1 on cauda equina blood flow in patients with lumbar spinal canal stenosis: myeloscopic observation.

STUDY DESIGN: Myeloscopic examination was performed to observe the cauda equina in patients with lumbar spinal canal stenosis before and after treatment with Lipo prostaglandin E1, a strong peripheral vasodilator. OBJECTIVES: The purpose of this study was to clarify the effects of Lipo prostaglandin E1 on blood flow in the cauda equina in patients with lumbar spinal canal stenosis. SETTING: Japan, Kagoshima METHODS: We performed myeloscopic observations of morphological changes in blood vessels running along the cauda equina in 11 patients with lumbar spinal canal stenosis before and after treatment with Lipo prostaglandin E1. RESULTS: In six of these patients, dilation of the running blood vessels was observed immediately after administration. In all of the patients who exhibited a dilation of vessels on the surface of the cauda equina, intermittent claudication and lower extremity pain and/or numbness lessened immediately after examination. However, none of the patients who exhibited no morphological changes in the vessels along the cauda equina after administration of Lipo prostaglandin E1 experienced any improvement of symptoms at the time of examination. CONCLUSION: Results of this study suggest that Lipo prostaglandin E1 may enhance blood flow in the cauda equina and improve clinical symptoms in some patients with lumbar spinal stenosis.     

Ganglioneuroblastoma of the cauda equina

A 39-year-old lady presented with low back pain and neurogenic claudication. Magnetic resonance imagining revealed an intradural neoplasm in the cauda equina region. The patient underwent lumbar laminectomy and total excision of the neoplasm. Biopsy showed it to be a ganglioneuroblastoma, which is rare in the spinal canal and so far does not appear to have been reported in the region of the cauda equina. Its management is discussed.     

Assessment of lumbar spinal canal stenosis by magnetic resonance phlebography

 There is evidence to suggest that cauda equina intermittent claudication is caused by local circulatory disturbances in the cauda equina as well as compression of the cauda equina. We evaluated the role of magnetic resonance phlebography (MRP) in identifying circulatory disturbances of the vertebral venous system in patients with lumbar spinal canal stenosis. Extensive filling defects of the anterior internal vertebral venous plexus were evident in patients with lumbar spinal canal stenosis (n = 53), whereas only milder abnormalities were noted in patients with other lumbar diseases (n = 16) and none in normal subjects (n = 13). The extent of the defect on MRP correlated with the time at which intermittent claudication appeared. In patients with lumbar spinal canal stenosis, extensive defects of the internal vertebral venous plexus on MRP were noted in the neutral spine position, but the defect diminished with anterior flexion of the spine. This phenomenon correlated closely with the time at which intermittent claudication appeared. Our results highlight the importance of MRP for assessing the underlying mechanism of cauda equina intermittent claudication in patients with lumbar spinal canal stenosis and suggest that congestive venous ischemia is involved in the development of intermittent claudication in these patients. Received: January 16, 2002 / Accepted: August 5, 2002 Offprint requests to: M. Manaka