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.     

Cauda equina syndrome: a complication of lumbar discectomy

Six cases of acute postdiscectomy cauda equina syndrome (C.E.S.) following lumbar discectomy were reviewed retrospectively in a series of 2842 lumbar discectomies over a ten-year period. Five cases had coexisting bony spinal stenosis at the level of the disc protrusion. The bony spinal stenosis was not decompressed at the time of discectomy. Inadequate decompression played a role in the neurologic deterioration postoperation. The cause of the sixth case is unknown. Bowel and bladder recovery was good when the cauda equina decompressed early; sensory recovery was universally good, and motor recovery was poor if a severe deficit had developed before decompression. Careful review of the preoperative myelogram to rule out spinal stenosis and decompression of bony stenosis at discectomy are recommended for prevention of postoperative C.E.S. Urgent decompression of postoperative C.E.S. is advisable if compression of the cauda equina is confirmed radiographically.     

胸腰椎骨折椎管狭窄与神经功能的关系

对106例连续性胸腰椎爆裂骨折进行回顾性研究,探讨椎管狭窄与神经功能的关系。按自行设计的改良Frankel法将神经功能分六级,将椎管分脊髓圆锥段和马尾神经段,用直线回归相关法分析椎管狭窄与神经损伤程度之间的关系,用等级相关法分析椎管狭窄与发生神经损伤可能性之间的关系。结果表明:无论在脊髓圆锥段或马尾神经段,椎管狭窄与神经损伤程度、损伤可能性之间均存在相关性(r或r_s=0.38～0.90,P<0.05),且脊髓圆锥段的相关程度较高;相同程度椎骨狭窄致神经危害性在脊髓圆锥段较大。发生神经损伤的最小椎管狭窄在脊髓圆锥段为38％,在马尾神经段为63％(?)认为胸腰椎骨折椎管狭窄是神经损伤的主要因素,X-CT扫描可较好地预测神经损伤程度和损伤可能性。     

Acute cauda equina syndrome caused by a gas-containing prolapsed intervertebral disk

Gas production as a part of disk degeneration can occur, but it rarely causes clinical nerve compression syndromes. A rare case of gaseous degeneration in a prolapsed lumbar intervertebral disk causing acute cauda equina syndrome is described. Radiologic features and intraoperative findings are reported. A 78-year-old woman with severe lumbar canal stenosis had acute cauda equina syndrome. Magnetic resonance imaging revealed a large disk protrusion, and she underwent an urgent operation for this. Surgery confirmed the severe lumbar canal stenosis, but the disk prolapse contained gas that had caused the nerve compression.     

腰椎退变性滑脱症(附24例手术报告)

1981～1989年我科对24例有马尾神经症状的腰椎退变性滑脱症进行手术治疗。腰椎退变性滑脱症老年人发病率高,其病理是继发性椎管,侧隐窝狭窄,小关节增生,黄韧带肥厚,椎间盘退变突出等改变,造成对神经根或马尾神经的压迫,临床表现似腰椎间盘突出症。作者根据病因不同采用三种术式。细致操作,充分减压,解除压迫因素是手术和疗效的关键。     

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.     

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。     

Degenerative spondylolisthesis.

Degenerative spondylolisthesis is one important type of spinal stenosis. The spinal canal stenosis varies in degree. This is the result of anterior slipping of the whole vertebra, usually L4 on L5. The clinical picture is not greatly different from that observed in the other types of lumbar canal stenosis. The surgical management involves decompression of the cauda equina by laminectomy. Often this is associated with arthrectomy to decompress the nerve roots. Extensive excision of the neural arch may result in further spinal instability for which spinal fusion is generally advisable.     

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     

The neurological outcome following surgery for spinal fractures

Sixty consecutive patients with spinal injuries and encroachment upon the spinal canal of greater than 20% were assessed for neurological outcome. The patients were divided into two groups, those undergoing posterior surgery alone, and those undergoing anterior surgery for formal decompression with or without anterior or posterior instrumentation. In those patients undergoing posterior surgery, an improvement rate in the neurological function of 83% was noted in patients with incomplete lesions, whereas an 88% improvement rate was found in those undergoing the anterior procedure. There was no statistical difference in outcome between these two groups. Positive correlations were found between the level of injury and Frankel grades. The cord lesions tended to demonstrate more severe neurological deficit, whereas the cauda equina lesions were associated with a lesser severity of neurologic deficit. A component of dislocation to the injury also resulted in a more severe neurological deficit. There was no apparent difference between the degree of bony encroachment of the spinal canal and the initial Frankel grade, nor was there a clear difference between those patients undergoing anterior versus posterior surgery.     

Normal Pressure Hydrocephalus Caused by a Spinal Neurinoma at the Cauda Equina Level: A Case Report

Neurinomas are common space-occupying lesions located in the spinal canal. Many reports concerning their clinical characteristics, diagnoses, treatments, and operative results have been published. Some case reports have discussed spinal neurinomas located at the cauda equina level. However, there is little information on their natural history. Here, we report a case of spinal neurinoma located at the cauda equina level, which caused normal pressure hydrocephalus (NPH). All symptoms resulting from the NPH were resolved by tumor removal. These findings suggested that if a spinal neurinoma located at the cauda equina level causes symptoms due to NPH, then removal of the tumor should be considered, when appropriate removal procedures are possible.     

腰椎椎体后缘终板骨坏死症

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：21例病人,以腰腿痛症状为主,少数伴有间隙性跛行和马尾压迫症状,平均发病时间4．5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缺损,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。本组病人全部行手术治疗,将凸入椎管内骨质凿除和对应突入的椎间盘摘除,部分病人行手术节段的植骨融合和内固定。结果：术中肉眼所见,切除的凸入骨质都与纤维环边缘相连在一起,骨缺损区为纤维软骨组织和骨性组织所充填。术后21例病人均获随访,时间6个月－3年,平均18个月。18例腰腿痛症状消失,3例有轻度腰痛,3例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缺血性变性、坏死,终板内形成骨软骨性坏死缺损区（Schmorl结节）,终板缺损区四周骨软骨组织在压力作用下增生、硬化。向后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,导致了本病的发生。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。     

氟骨症性椎管狭窄症的手术治疗

１９８７～１９９０年手术治疗氟骨症性椎管狭窄症１００例。包括颈椎９例，胸椎８例，腰、骶椎８３例。术后随访１～４年，复查结果：临床治愈９３例（９３％）：显效３例（３％）、有效３例（３％）、无效１例（１％）。手术原则是彻底减压，因氟骨症具有椎骨及其骨周组织严重退变、异化和骨化的临床病理特点，故在胸、腰椎减压术后，一般不影响其稳定性，在颈椎施行双开式或单开式椎管扩大加植骨融合术，则可收减压、稳定及防止或减少椎板间隙瘢痕狭窄的效果。     

Arteries and veins of the lumbar nerve roots and cauda equina.

An abundant vascular system supplies the nerve roots, within the cauda equina, in the spinal canal and in the nerve root tunnels. The arterial supply of nervous tissue, as noted by previous observers, is "just adequate for its minimal needs." The veins of the area are classified into 3 groups, those of the spinal canal within the extradural space, those of the nerve roots themselves (radicular veins) and those which drain the bony skeleton. These thin-walled venous channels are a source of serious bleeding both at operation and in the postoperative period. Elsewhere in this symposium, emphasis has been placed on the way in which spinal stenosis and pressure on nerves cause the complex group of symptoms. Pressure on arteries, veins and capillaries can impair nerve conduction, with changes in sensation and loss of motor power in one or both limbs. If the pressure is prolonged, irreversible changes take place in the substance of the nerve roots. Recovery of sensation and of motor power following adequate surgical decompression will then be incomplete.     

Vasodilative effects of prostaglandin E<Subscript>1</Subscript> derivate on arteries of nerve roots in a canine model of a chronically compressed cauda equina

Background  

Reduction of blood flow is important in the induction of neurogenic intermittent claudication (NIC) in lumbar spinal canal stenosis. PGE₁ improves the mean walking distance in patients with NIC type cauda equina compression. PGE₁ derivate might be effective in dilating blood vessels and improving blood flow in nerve roots with chronically compressed cauda equina. The aim of this study was to assess whether PGE₁ derivate has vasodilatory effects on both arteries and veins in a canine model of chronic cauda equina compression.     

A case of the spinal subdural hematoma formation following ventriculoperitoneal shunting for von Recklinghausen's disease associated with aqueductal stenosis

Von Recklinghausen's disease associated with hydrocephalus due to non-tumoral aqueductal stenosis is rare. Furthermore the formation of subdural hematoma within the spinal canal is also a very rare complication of ventriculoperitoneal shunt. We presented a case of spinal subdural hematoma formation following ventriculoperitoneal shunting for von Recklinghausen's disease associated with aqueductal stenosis. A 10-year-old girl with von Recklinghausen's disease was referred to our hospital for gait disturbance during the previous 8 months. Magnetic resonance imaging (MRI) revealed hydrocephalus due to non-tumoral aqueductal stenosis, and ventriculoperitoneal shunt was instituted. Three months later, the patient developed lumbar pain and paraplegia. MRI revealed subdural hematoma in the lumbosacral spinal canal, and bilateral intracranial subdural hematoma were shown on computerized tomography (CT) scans. Subdural hematoma in the lumbosacral spinal canal was evacuated by laminectomy. Improvement of her neurological deficit was obtained postoperatively, and intracranial subdural hematomas disappeared spontaneously. Spinal subdural hematoma is assumed to be formed by the migratory movement of intracranial subdural hematoma under the influence of gravity. A characteristic finding of MRI is that such a subdural hematoma in the lumbosacral canal is located around the cauda equina.     

Pathophysiology,clinical presentation,natural history,and review of the SPORT trials

Lumbar spinal stenosis is a combination of intervertebral disk degeneration (leading to loss of normal disk height), facet joint hypertrophy, ligamentum flavum hypertrophy/infolding, and osteophyte formation that results in narrowing of the spinal canal and compression of the lumbo-sacral nerve roots. This mechanical compression presents in patients as neurogenic claudication and resultant back and leg pain. Spinal stenosis is most commonly seen in the elderly population secondary to the normal aging of the lumbar spine. However, some patients may be predisposed to its effects due to congenitally narrowed canal secondary to short pedicles. The literature describes a variable natural history with a general worsening over time. Recently, more has been learned about the natural history of lumbar spinal stenosis with the addition of the Spine Patient Outcomes Research Trial (SPORT) to the literature.     

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.     

Clinical aspects of the narrow spinal canal

Not infrequently the lumbosacral root-compression syndrome is due to stenosis of the lumbal spinal canal. The clinical symptoms, usually emerging in the middle-aged, may be characterized by either simple radicular pain with or without neurological deficit or by exercise-dependent transient functional disturbance of the cauda equina, namely, the so-called neurogenic intermittent claudication (NIC). In most cases, NIC is due to mechanical compression of the cauda fibers as a result of extension of the patient's lumbar spine. In some patients, exercise-induced ischemic radiculopathy is assumed to be the main factor. Differential diagnosis must take into account true intermittent claudication, certain rare myopathies (if the exercise-dependent pain is the main feature), and certain transient disturbances in spinal cord function (if a motor and/or sensory deficit arises during the NIC attack).     

Lumbar sympathectomy increases blood flow in a dog model of chronic cauda equina compression

OBJECTIVE: This study was designed to assess changes in blood flow of the dog cauda equina after lumbar sympathectomy using an experimental chronic cauda compression model. METHODS: The cauda equina was compressed at 10 mm Hg with a plastic balloon in all animals (n = 12). One week later, bilateral lumbar sympathectomy was carried out in the LSX group (n = 7), and vessels of the cauda equina were thereafter observed for 90 minutes using a specially designed microscope supplied with a video camera. Five animals did not undergo sympathectomy and were used as controls. The volume of blood flow was calculated from two parameters: velocity (mm/s) and diameter (microm) of a vessel observed in each animal. RESULTS: The increment in vessel diameter in the LSX group was pronounced at 30 and 45 minutes after sympathectomy compared with the control group (P < 0.05). Blood flow in the LSX group was increased at 30 minutes depending on dilation of the vessel diameter compared with the control group (P < 0.05). The velocity in the observed vessels remained unchanged throughout the measurements. CONCLUSIONS: These data suggest that lumbar sympathectomy could induce an increase in blood flow of the compressed cauda equina. As lumbar sympathetic block increases blood flow not only in the lower limbs but also in the cauda equina, it might be evaluated for a conservative treatment of intermittent claudication due to lumbar spinal canal stenosis.