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).     

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.     

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.     

Posterior lumbar interbody fusion

This paper reports the posterior lumbar interbody fusion (PLIF) that has been performed on fourteen patients. It includes 6 cases of spondylolytic spondylolisthesis, 3 cases of degenerative spondylolisthesis, 2 cases of postoperative recurrence of lumbar disc protrusion, 2 cases of unstable prolapse of intervertebral disc, 1 cases of consequent spinal canal stenosis after lumbar lamina fusion. As a result 92 per cent of the operations are successful. The method of operation and it's modification are reported in detail. The indication of operation and the evaluative criteria of interbody bone union discussed. The intact of lumbar posterior structures, the condition of bone grating bed, the quality and disperse of bone graft are main factors that influencing bone union. Bleeding from venous plexus of spinal canal and from vertebral cancellous bone, injury of lumbosacral nerve root and cauda equina are the main surgical complications that should be stressed.     

Spinal stenosis: assessment of motor function,VEGF expression and angiogenesis in an experimental model in the rat

Reduction of blood flow in compressed nerve roots is considered as one important mechanism of induction of neurogenic intermittent claudication in lumbar spinal canal stenosis. Vascular endothelial growth factor (VEGF) is a potent stimulator of angiogenesis, and is increased in expression in hypoxic conditions. The objective of this study was to examine if cauda equina compression affects motor function and induces expression of VEGF and angiogenesis. The cauda equina was compressed by placing a piece of silicone rubber into the L5 epidural space. Walking duration was examined by rota-rod testing. The compressed parts of the cauda equina and L5 dorsal root ganglion (DRG) were removed at 3, 7, 14, or 28 days after surgery, and processed for immunohistochemistry for VEGF and Factor VIII (marker for vascular endothelial cells). Numbers of VEGF-immunoreactive (IR) cells and vascular density were examined. Walking duration was decreased after induction of cauda equina compression. The number of VEGF-IR cells in the cauda equina and DRG was significantly increased at 3, 14, and 28 days after cauda equina compression, compared with sham-operated rats (P < 0.05). Vascular density in the cauda equina was not increased at any of the time points examined. Cauda equina compression decreased walking duration, and induced VEGF expression in nerve roots and DRG.     

Myeloscopic study on lumbar spinal canal stenosis with special reference to intermittent claudication

Twenty-five cases of lumbar spinal canal stenosis were investigated by dynamic myeloscopy to explain the pathophysiologic mechanism of intermittent claudication, one of the characteristic signs of the disorder. Myeloscopic examination revealed that, in accordance with postural alteration, the diameter of blood vessels on the cauda equinae showed significant changes in many patients in the stenosis group, but showed no changes in control group. In this series, it was suggested that the microcirculatory disturbance of vessels on cauda equinae might play an important role in the development of intermittent claudication.     

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.     

Prognostic factors associated with the surgical indication for lumbar spinal stenosis patients less responsive to conservative treatments: An investigator-initiated observational cohort study

Background

A few cohort studies have determined which patients with lumbar spinal stenosis are likely to need surgery because of the deterioration of symptoms. However, there are still insufficient data regarding the management of lumbar spinal stenosis due to lack of prognostic factors associated with the need for surgery. The purpose of this study was to identify the prognostic factors associated with the need for surgical treatment in patients with lumbar spinal stenosis.

Evaluation of circulatory compromise in the leg in lumbar spinal canal stenosis

To evaluate whether hemoglobin oxygen saturation and hemoglobin concentration of the leg are useful indicators for circulatory compromise in patients with lumbar spinal canal stenosis, we investigated the changes in the indices during level gait using reflectance spectrophotometry. Thirty-three patients with lumbar spinal stenosis were studied. Preoperatively, the hemoglobin oxygen saturation was greater in the 33 patients than in the control subjects. The indices increased in the control subjects more than those in the patients. Postoperatively, the increases in hemoglobin oxygen saturation were greater in the patients with lumbar spinal canal stenosis than before decompression and the hemoglobin concentration tended to approximate that in the control subjects. The results suggest these indices might be useful for monitoring disease severity in patients with lumber spinal canal stenosis. In addition to stenotic ischemia in the spinal canal, it is thought that the neurogenic intermittent claudication is secondarily caused by circulatory failure in the lower extremities attributable to the autonomic nervous dysfunction.     

Urodynamic evaluation of patients with spinal stenosis

Spinal stenosis, which may be congenital/developmental or acquired in origin, is a narrowing of the spinal canal, nerve root canals, or intervertebral foramina. Compression of the spinal cord or nerve roots may lead to structural neuronal damage, neuronal ischemia or edema, and axonal transport block. The most frequent symptom in patients with spinal stenosis is back pain and some have classic neurogenic claudication. We have performed urodynamic evaluations in 2 patients with combined cervical and lumbar spinal stenosis. A girl with achondroplastic dwarfism had urgency incontinence and detrusor hyperreflexia. An adult man with acquired degenerative spinal stenosis had difficulty voiding and findings compatible with the cauda equina syndrome.     

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.     

Primary liposarcoma of the lumbar spine

BackgroundWe describe a rare case of the cauda equina syndrome caused by a primary pleomorphic liposarcoma of the lumbar spine.Case reportA 35-year-old man presented a 2-month history of back pain and slowly progressive weakness of lower limbs without sphincter dysfunction. It had a laminectomy for a supposed disc herniation three years previously. A diagnosis of recurrence hernia or fibrosis was discussed.ResultsMagnetic Resonance Imaging (MRI) and CT scan of the lumbar vertebral column shows diffuse involvement of L4/L5 vertebral bodies, and an intradural lesion surrounding the nerve roots of cauda equina. The tumor occupied almost the whole width of the spinal canal. The diagnosis of plasmocytoma or metastasis was advocated and the patient was managed by an extended posterior approach in emergency. Histopathological findings revealed a pleomorphic liposarcoma. The patient received a course of radiotherapy and unfortunately he died at 3 months follow-up.ConclusionIn spite of his unusual location in the spine, pleomorphic liposarcoma should be considered in the differential diagnosis of primary spinal tumors.     

Priapism as a feature of claudication of the cauda equina

A case is reported of a man 60 years of age with degenerative stenosis of the lumbar canal at the L3–4 level and lumbar arachnoiditis, whose symptoms of claudication of the cauda equina were accompanied by uncomfortable involuntary erections. All symptoms were relieved by surgical decompression.     

Cauda equina syndrome as a postoperative complication in five patients operated for lumbar disc herniation

STUDY DESIGN: A retrospective analysis of records and radiographs in five patients who developed acute cauda equina syndrome after surgery for lumbar disc herniation. OBJECTIVES: To postulate as a possible pathophysiologic mechanism the venous congestion caused by preexisting spinal stenosis and to present a management plan: extended decompression within 48 hours. SUMMARY OF BACKGROUND DATA: Cauda equina syndrome is reported as a sequela in 0.2%-1% of the surgeries for lumbar disc herniation. There is, however, no consensus on the possible pathophysiologic mechanism to the complication or to its management. METHODS: Preoperative investigations consisted of magnetic resonance imaging, or myelography and computed tomography. There was a good correlation between clinical appearance and radiographic findings in all patients. When the complication became apparent in four of the patients, they were investigated with magnetic resonance imaging and reoperated on within 48 hours with wide decompressions. RESULTS: The index operation was reported uneventful in all patients. Postoperative magnetic resonance imaging did not show the cause of the cauda equina syndrome, nor could this be established at the reoperation. Before surgery, all five patients had preexisting narrowing of the spinal canal. In no case was the lumbosacral disc the index level. Two patients recovered fully, whereas the other three experienced varying degrees of residual symptoms. There was no correlation between the end result and the delay until secondary decompression. CONCLUSION: Relative spinal stenosis may contribute to the development of cauda equina syndrome after surgery for lumbar disc herniation. A venous congestion can be triggered by postoperative edema, leading to nerve root ischemia. The treatment of choice seems to be extended decompression within 48 hours.     

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)     

Cauda equina lesions as a complication of spinal surgery

Although the most common aetiology of cauda equina lesions is lumbar intervertebral disc herniation, iatrogenic lesions may also be the cause. The aim of this study was to identify and present patients in whom cauda equina lesions occurred after spinal surgery. From the author’s series of patients with cauda equina lesions, those with the appearance of sacral symptoms after spinal surgery were identified. To demonstrate lesions more objectively, electrodiagnostic studies were performed in addition to history and clinical examination. Imaging studies were also reviewed. Of 69 patients from the series, 11 patients in whom a cauda equina lesion developed after spinal surgery were identified. The aetiology comprised surgery for herniated intervertebral disc in 5 (4 performed by a single surgeon), spinal stenosis surgery in 4, and postoperative lumbar epidural haematoma in 2 patients (each performed by a different surgeon). Proportion of spinal surgeries with this complication varied from 0 to 6.6‰ in different centres. Patients with iatrogenic cauda equina lesion were significantly older (p < 0.001), and reported more severe urinary, but similar bowel and sexual symptoms compared to other patients in the series. In conclusion the study identified spinal surgery as the cause of approximately 15% of cauda equina lesions. More than a third of lesions developed after procedures performed by a single surgeon. Most of the remaining lesions could probably be avoided by better surgical technique (e.g. the use of a high-speed drill instead of a Kerrison rongeur in patients with severe spinal stenosis), or prevented by closer postoperative monitoring (e.g. in patients with postoperative lumbar epidural haematoma).     

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。     

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.     

Redundant nerve roots in patients with degenerative lumbar spinal stenosis

Extensive fundamental and clinical investigations have been performed concerning redundant nerve roots (RNR) and the pathogenesis of cauda equina claudication (CEC) in degenerative lumbar canal stenosis (DLCS). These investigations consisted of (1) anatomic observations on RNR in 117 fixed cadaveric specimens, (2) myelographic study in 117 patients with or without DLCS, (3) operative observation on neural elements with special reference to the cauda equina in 56 DLCS patients (including a postoperative follow-up), and (4) electrophysiologic tests using spinal cord action potential recording under walking load preoperatively and intraoperative measurement of nerve conduction velocity of RNR. The RNR have neuronal losses resulting from a longer duration stenosis that suggests a sort of friction neuritis. Complicated factors contribute to the pathogenesis of CEC and the development of root gripping, such as the magnitude of RNR, the extent of the stenosis, a narrowed sac, age-dependent axial shortening of the spinal canal, and dynamic or postural factors. In cases with severe RNR, satisfactory operative results can be obtained only after thorough decompression with dural incision.     

Neurogenic claudication without spinal stenosis arising as a result of lumbar epidural varices

Neurogenic claudication is most frequently observed in patients with degenerative lumbar spinal stenosis. We describe a patient with lumbar epidural varices secondary to obstruction of the inferior vena cava by pathological lymph nodes presenting with this syndrome. Following a diagnosis of follicular lymphoma, successful chemotherapy led to the resolution of the varices and the symptoms of neurogenic claudication. The lumbar epidural venous plexus may have an important role in the pathogenesis of spinal stenosis. Although rare, epidural venous engorgement can induce neurogenic claudication without spinal stenosis. Further investigations should be directed at identifying an underlying cause.