Spinal epidural hematoma is a well known complication of spinal surgery. Clinically insignificant small epidural hematomas develop in most spinal surgeries following laminectomy. However, the incidence of clinically significant postoperative spinal epidural hematomas that result in neurological deficits is extremely rare. In this report, we present a 33-year-old female patient whose spinal surgery resulted in postoperative spinal epidural hematoma. She was diagnosed with lumbar disc disease and underwent hemipartial lumbar laminectomy and discectomy. After twelve hours postoperation, her neurologic status deteriorated and cauda equina syndrome with acute spinal epidural hematoma was identified. She was immediately treated with surgical decompression and evacuation of the hematoma. The incidence of epidural hematoma after spinal surgery is rare, but very serious complication. Spinal epidural hematomas can cause significant spinal cord and cauda equina compression, requiring surgical intervention. Once diagnosed, the patient should immediately undergo emergency surgical exploration and evacuation of the hematoma.
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.
Cauda equina compression; Intermittent claudication; Vascular endothelial growth factor; Angiogenesis
A case of cauda equina lesion as a result of recurrent adjacent segment degeneration (ASD) after multiple lumbar fusions is reported. ASD might be a consequence of biomechanical overload or simply a normal degenerative process. The reported clinical relevance of ASD is rather low. We describe an unusual case of cauda equina compression at L1–L2 in a patient who had undergone L2–L4 fusion 8 years previously and 2 decompression-fusion surgeries 16 years before.
Materials and methods
A 72-year-old man, who had two previous lumbar fusion–decompression procedures, underwent a third lumbar surgery in December 2000 to treat symptomatic spinal canal stenosis associated with L3–L4 pseudoarthrosis. After a symptom-free period of 8 years, the patient experienced low back pain radiating to both legs while standing, associated with saddle sensory disturbances and incontinence. Physical examination ruled out significant motor deficits. Plain radiographs showed solid fusion from L2 to L4, good spinal alignment, and low-grade L1–L2 retrolisthesis. Stainless steel pedicular instrumentation distorted magnetic resonance imaging, preventing adequate spinal canal evaluation. Electromyography demonstrated signs of cauda equina compression (bilateral L3–S2). CT myelography showed a stop at L1–L2, due to a severe spinal canal stenosis. L1–L2 decompression and fusion were performed.
After an uneventful surgery with no complications, the symptoms abated and incontinence recovered.
Even if the reported clinical relevance of ASD is very low, fused patients with a constitutional narrow spinal canal are at risk of developing severe neural compression at the level adjacent to the fusion.
Recurrent disease; Adjacent segment; Cauda equina; Degenerative changes; Narrow spinal canal
Cauda equina syndrome following decompression for spinal stenosis appears to occur more commonly than the literature suggests. A large series of spinal stenosis decompressions was reviewed. Based on these findings, a theory is put forth as to the cause of this complication. One hundred seventy-five cases of decompression for spinal stenosis done over a 2.5-year period were reviewed. Follow-up was 1year to 2 years and 4 months. There were 14 cases of postoperative urinary retention, for an incidence of 8%. Of those, five were ultimately diagnosed with cauda equina syndrome, for an incidence of 2.8%. Of the nine cases that were not diagnosed as cauda equina syndrome, five resolved spontaneously over 2 to 6 weeks. The remaining four were diagnosed as having mechanical urinary problems (e.g., prostate or prolapsed bladder) that required surgical treatment. Anal sphincter monitoring at the time of surgery was not predictive in those patients who developed cauda equina syndrome. All patients who developed cauda equina syndrome improved over 3 to 9 months, but none completely resolved. Three cases underwent further decompression with no apparent improvement. Cauda equina syndrome occurs in 2.8% of decompressions for spinal stenosis.
cauda equina syndrome; spinal stenosis; decompression; postoperative complications
Schwannoma is a relatively common benign spinal cord and/or cauda equina tumor; however, giant cauda equina schwannoma with extensive scalloping of the lumbar vertebral body is a rare pathology, and the treatment strategy, including the use of surgical procedures, is controversial. In this report, we present a rare case of a giant lumbar schwannoma of the cauda equina with extremely large scalloping of the vertebral body, and we discuss the surgical strategy we used to treat this pathology.
A 42-year-old Japanese man presented to our department with complaints of a gait disturbance and muscle weakness in the left lower limb. His muscle strength in the proximal part of the left lower limb was grade 2 or 3/5, and he exhibited a mild urinary disturbance on the first visit. X-ray and computed tomography myelography of the lumbar spine showed an extremely large erosive lesion at the L3 vertebral body. Magnetic resonance imaging of the lumbar spine showed a large soft-tissue mass in the spinal canal at L2-L3 and the vertebral body at L3. A one-stage complete tumor resection and instrumented circumferential fusion were performed via a posterior approach, and a good outcome was achieved after the surgery.
We performed one-stage posterior surgery in a patient with a giant cauda equina schwannoma with extensive scalloping of the vertebral body, and a good post-operative outcome was achieved.
Giant cauda equina tumor; Posterior surgery; Scalloping lesion; Schwannoma; Transdural approach
This study is a prospective, clinical study assessing the efficacy of selective decompression of the level responsible in a two-level stenosis in accordance with the neurological findings defined by the gait load test with a treadmill.
To clarify the clinical features of multilevel lumbar spinal stenosis (LSS) regarding the neurological level responsible for the symptoms, neurogenic claudication, and outcomes of selective decompression.
Overview of Literature
Most spine surgeons have reported that multilevel compression of the cauda equina induces a more severe impairment of the nerve function than a single-level compression. However, the clinical effects of multilevel LSS on the cauda equine and nerve roots are unknown.
A total of 21 patients with lumbar spinal canal stenosis due to spondylosis and degenerative spondylolisthesis were selected. The level responsible for the symptoms in the two-level stenosis was determined from the neurological findings on the gait load test and functional diagnosis based on a selective nerve root block. All patients underwent a prospective, selective decompression at the level neurologically responsible only. The average follow-up period was 2.6 years (range, 1 to 6 years). The postsurgical outcome was defined using the Visual Analogue Scale (VAS) at the post-gait load test, 2 weeks after surgery, 3 months after surgery and at the last follow up.
Before surgery, the mean threshold distance and mean walking tolerance was 34.3 m and 113 m, respectively. All patients had neurogenic claudication and 19 of the patients had cauda equina syndrome, including hypesthesia in 11 cases, muscle weakness in 5 cases and radicular pain in 7 cases. Selective nerve blocks to determine the level responsible for the lumbosacral symptoms in 2 cases revealed a mean VAS score of 7.1, 2.61, 3.04, and 3.47 at the post-gait load test, 2 weeks after surgery, 3 months after surgery and at the last follow up, respectively. All subjects underwent surgery. After the operation, neurogenic claudication with or without cauda equna syndrome subsided in all patients.
The gait load test allows an objective and quantitative evaluation of the gait characteristics of patients with lumbar canal stenosis and is useful for determining the appropriate level for surgical treatment.
Gait load test; Neurogenic claudication; Lumbar canal stenosis
There is no validated gold-standard diagnostic support tool for LSS, and therefore an accurate diagnosis depends on clinical assessment. Assessment of the diagnostic value of the history of the patient requires an evaluation of the differences and overlap of symptoms of the radicular and cauda equina types; however, no tool is available for evaluation of the LSS category. We attempted to develop a self-administered, self-reported history questionnaire as a diagnostic support tool for LSS using a clinical epidemiological approach. The aim of the present study was to use this tool to assess the diagnostic value of the history of the patient for categorization of LSS.
The initial derivation study included 137 patients with LSS and 97 with lumbar disc herniation who successfully recovered following surgical treatment. The LSS patients were categorized into radicular and cauda equina types based on history, physical examinations, and MRI. Predictive factors for overlapping symptoms between the two types and for cauda equina symptoms in LSS were derived by univariate analysis. A self-administered, self-reported history questionnaire (SSHQ) was developed based on these findings. A prospective derivation study was then performed in a series of 115 patients with LSS who completed the SSHQ before surgery. All these patients recovered following surgical treatment. The sensitivity of the SSHQ was calculated and clinical prediction rules for LSS were developed. A validation study was subsequently performed on 250 outpatients who complained of lower back pain with or without leg symptoms. The sensitivity and specificity of the SSHQ were calculated, and the test-retest reliability over two weeks was investigated in 217 patients whose symptoms remained unchanged.
The key predictive factors for overlapping symptoms between the two categories of LSS were age > 50, lower-extremity pain or numbness, increased pain when walking, increased pain when standing, and relief of symptoms on bending forward (odds ratio ≥ 2, p < 0.05). The key predictive factors for cauda equina type symptoms were numbness around the buttocks, walking almost causes urination, a burning sensation around the buttocks, numbness in the soles of both feet, numbness in both legs, and numbness without pain (odds ratio ≥ 2, p < 0.05). The sensitivity and specificity of the SSHQ were 84% and 78%, respectively, in the validation data set. The area under the receiver operating characteristic curve was 0.797 in the derivation set and 0.782 in the validation data set. In the test-retest analysis, the intraclass correlation coefficient for the first and second tests was 85%.
A new self-administered, self-reported history questionnaire was developed successfully as a diagnostic support tool for LSS.
A retrospective study.
The aim of present study was to investigate imaging findings suggestive of cauda equina entrapment in thoracolumbar and lumbar burst fractures.
Overview of Literature
Burst fractures with cauda equina entrapment can cause neurologic deterioration during surgery. However, dural tears and cauda equina entrapment are very difficult to diagnose clinically or radiographically before surgery.
Twenty-three patients who underwent spinal surgery for thoracolumbar or lumbar burst fractures were enrolled in this study. In magnetic resonance imaging T2-weighted images of the transverse plane, we defined cauda equina notch sign (CENS) as a v-shaped image that entrapped cauda equina gathers between lamina fractures. We evaluated the fractured spine by using CENS and lamina fractures and the rate of available space for the spinal canal at the narrowest portion of the burst fracture level. We classified patients into entrapment group or non-entrapment group, based on whether cauda equina entrapment existed.
Lamina fractures were detected in 18 (78.3%) and CENS were detected in 6 (26.1%) of 23 burst-fracture patients. Cauda equina entrapment existed in all the patients with CENS. In addition, the rate of available space for the spinal canal increased according to logistic regression. The size of the retropulsed fragment in the spinal canal was the most reliable of all the factors, suggesting cauda equina entrapment.
CENS was the most predictable sign of cauda equina entrapment associated with burst fractures.
Burst fracture; Dural tear; Cauda equina entrapment; Lamina fracture; Magnetic resonance imaging
The timing of surgery in cauda equina syndrome due to prolapsed intervertebral disc remains controversial. Assessment of these patients requires magnetic resonance imaging (MRI), which is of limited availability outside normal working hours in the UK.
PATIENTS AND METHODS
We reviewed radiological results in all patients undergoing emergency MRI within our unit for suspected cauda equina syndrome over a 2-year period, and all subjects undergoing emergency lumbar discectomy for cauda equina syndrome within the same period. Outcome measures were: proportion of positive findings in symptomatic patients and proportion of patients referred with diagnostic MRI scans undergoing emergency surgery. We also assessed outcomes of patients having surgery for cauda equina syndrome in terms of improvement of pain, sensory and sphincter disturbance.
A total of 76 patients were transferred for assessment and ‘on-call’ MRI; 27 were subsequently operated upon. Only 5 proceeded to emergency discectomy that night (prior to next scheduled list). This may be due to delays in timing – from referral to acceptance, to arrival in the department, to diagnostic scan and to theatre. With the second group of patients, 43 had emergency discectomy for cauda equina syndrome during the study period. Of these, 6 patients had an out-of-hours MRI at our hospital for assessment (one patient living locally). Most surgically treated patients experienced improvement in their pain syndrome, with approximately two-thirds experiencing improvement in sensory and sphincter disturbance.
These data support a policy of advising MRI scan for cauda equina syndrome at the earliest opportunity within the next 24 h in the referring hospital, rather than emergency transfer for diagnostic imaging which has a relatively low yield in terms of patients operated on as an emergency.
MRI scan; Cauda equina syndrome; Discectomy; Back pain
Posterior epidural migration (PEM) of free disc fragments is rare, and reported PEM patients usually presented with radicular signs. An uncommon case involving a patient with cauda equina syndrome due to PEM of a lumbar disc fragment is reported with a review of the literature. The patient described in this report presented with an acute cauda equina syndrome resulting from disc fragment migration at the L3–L4 level that occurred after traction therapy for his lower back pain. The radiological characteristics of the disc fragment were the posterior epidural location and the ring enhancement. A fenestration was performed and histologically confirmed sequestered disc material was removed. An early postoperative examination revealed that motor, sensory, urological, and sexual functions had been recovered. At late follow-up, the patient was doing well after 18 months. Sequestered disc fragments may occasionally migrate to the posterior epidural space of the dural sac. Definite diagnosis of posteriorly located disc fragments is difficult because the radiological images of disc fragments may mimic those of other more common posterior epidural lesions.
Cauda equina syndrome Disc migration Lumbar disc Sequestered disc
Incidental or intentional durotomy causing cerebrospinal fluid (CSF) leakage, leading to the formation of a pseudomeningocele is a known complication in spinal surgery. Herniation of nerve roots into such a pseudomeningocele is very rare, but can occur up to years after initial durotomy and has been described to cause permanent neurologic deficit. However, cauda equina fiber herniation and entrapment into a pseudomeningocele has not been reported before. Here, we present a case of symptomatic transdural cauda equina herniation and incarceration into a pseudomeningocele, 3 months after extirpation of a lumbar Schwannoma. A 59-year-old man, who previously underwent intradural Schwannoma extirpation presented 3 months after surgery with back pain, sciatica and loss of bladder filling sensation caused by cauda equina fiber entrapment into a defect in the wall of a pseudomeningocele, diagnosed with magnetic resonance imaging. On re-operation, the pseudomeningocele was resected and the herniated and entrapped cauda fibers were released and replaced intradurally. The dura defect was closed and the patient recovered completely. In conclusion, CSF leakage can cause neurological deficit up to years after durotomy by transdural nerve root herniation and subsequent entrapment. Clinicians should be aware of the possibility of this potentially devastating complication. The present case also underlines the importance of meticulous dura closure in spinal surgery.
Pseudomeningocele; Dura defect; Nerve root entrapment
New techniques have been developed for the electrophysiological assessment of patients with suspected cauda equina lesions using transcutaneous spinal stimulation (500-1500 V: time constant 50 microseconds) to measure motor latencies to the external and sphincter and puborectalis muscles from L1 and L4 vertebral levels. These latencies represent motor conduction in the S3 and S4 motor roots of the cauda equina between these levels. Similarly motor latencies can be recorded from spinal stimulation to the anterior tibial muscles (L4 and L5 motor roots). Transrectal stimulation of the pudendal nerves is used to measure the pudendal nerve terminal motor latency. In 32 control subjects, matched for age and sex, mean motor latencies from L1 and L4 spinal stimulation were 5.5 +/- 0.4 ms and 4.4 +/- 0.4 ms (mean + SD). In the 10 patients with cauda equina disease including ependymoma, spinal stenosis, arachnoiditis and trauma, these latencies were 7.2 +/- 0.8 ms and 4.6 +/- 0.9 ms, a significant increase in the L1 latency. The L1/L4 latency ratios to the puborectalis muscle were 1.36 +/- 0.09 in control subjects and 1.72 +/- 0.13 in cauda equina patients. Pudendal nerve terminal motor latencies were normal in eight of the 10 patients with cauda equina disease. The single fibre EMG fibre density in the external and sphincter muscle (normal, 1.5 +/- 0.16) was increased in patients with cauda equina lesions (1.73 +/- 0.28), but was increased more than two standard deviations from the mean only in three patients. This increase in fibre density was not of diagnostic value since it was also found in two of the four patients with low back pain. Slowing of motor conduction in the cauda equina is thus a useful indication of damage to these intraspinal motor roots. These investigations can be used in the selection of patients for myelography, and to follow progress in patients managed conservatively.
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.
Fourteen dogs were used in this study. A plastic balloon inflated to 10 mmHg was placed under the lamina of the 7th lumbar vertebra for 1 week. OP-1206-cyclodextrin clathrate (OP-1206-CD: prostaglandin E1 derivate) was administered orally. The blood vessels of the second or third sacral nerve root were identified using a specially designed surgical microscope equipped with a video camera. The diameter of the blood vessels was measured on video-recordings every 15 minutes until 90 minutes after the administration of the PGE1 derivate.
We observed seven arteries and seven veins. The diameter and blood flow of the arteries was significantly increased compared with the veins at both 60 and 75 minutes after administration of the PGE1 derivate (p < 0.05). Blood flow velocity did not change over 90 minutes in either the arteries or veins.
The PGE1 derivate improved blood flow in the arteries but did not induce blood stasis in the veins. Our results suggest that the PGE1 derivate might be a potential therapeutic agent, as it improved blood flow in the nerve roots in a canine model of chronic cauda equina compression.
In animal models of degenerative lumbar disease, inducible nitric oxide synthase (iNOS) is expressed in macrophages and Schwann cells following compression of the cauda equina. We previously reported that NO metabolites (nitrite plus nitrate: [NOx]) in the cerebrospinal fluid (CSF) correlate with postoperative pain relief in patients with degenerative lumbar disease and with neurologic recovery rate postoperatively or after conservative treatment in patients with spinal cord injury. The objective of the present study was to examine the relationship between [NOx] and neurologic severity, and recovery in degenerative cervical and lumbar diseases. Two hundred fifty-seven cases, including 85 patients with cervical compression myelopathy (CCM), 25 with cervical disc herniation (CDH), 70 with lumbar canal stenosis (LCS), and 77 with lumbar disc herniation (LDH), were examined. The CSF [NOx] was measured using the Griess method. Severity of neurologic impairment and clinical recovery was assessed using the Japanese Orthopedic Association score and Hirabayashi’s method. [NOx] in CCM and LCS, but not CDH and LDH groups, was significantly higher than that in controls, and correlated with postoperative recovery rates, but not with preoperative neurologic severity. [NOx] significantly correlated with neurologic recovery following surgery for CCM and LCS.
Nitric oxide; Degenerative cervical diseases; Degenerative lumbar diseases; Cerebrospinal fluid; Neurologic severity; Neurologic recovery
Existing studies on micro-endoscopic lumbar discectomy report similar outcomes to those of open and microdiscectomy and conflicting results on complications. We designed a randomised controlled trial to investigate the hypothesis of different outcomes and complications obtainable with the three techniques. 240 patients aged 18–65 years affected by posterior lumbar disc herniation and symptoms lasting over 6 weeks of conservative management were randomised to micro-endoscopic (group 1), micro (group 2) or open (group 3) discectomy. Exclusion criteria were less than 6 weeks of pain duration, cauda equina compromise, foraminal or extra-foraminal herniations, spinal stenosis, malignancy, previous spinal surgery, spinal deformity, concurrent infection and rheumatic disease. Surgery and follow-up were made at a single Institution. A biomedical researcher independently collected and reviewed the data. ODI, back and leg VAS and SF-36 were the outcome measures used preoperatively, postoperatively and at 6-, 12- and 24-month follow-up. 212/240 (91%) patients completed the 24-month follow-up period. VAS back and leg, ODI and SF36 scores showed clinically and statistically significant improvements within groups without significant difference among groups throughout follow-up. Dural tears, root injuries and recurrent herniations were significantly more common in group 1. Wound infections were similar in group 2 and 3, but did not affect patients in group 1. Overall costs were significantly higher in group 1 and lower in group 3. In conclusion, outcome measures are equivalent 2 years following lumbar discectomy with micro-endoscopy, microscopy or open technique, but severe complications are more likely and costs higher with micro-endoscopy.
Lumbar disc herniation; Discectomy; Microdiscectomy; Micro-endoscopic discectomy
Typically situated posterolateral in the spinal canal, intraspinal facet cysts often cause radicular symptoms. Rarely, the midline location of these synovial or ganglion cysts may cause thecal sac compression leading to neurogenic claudication or cauda equina syndrome. This article summarizes the clinical presentation, radiographic appearance, and management of three intraspinal, midline facet cysts. Three patients with symptomatic midline intraspinal facet cysts were retrospectively reviewed. Documented clinical visits, operative notes, histopathology reports, and imaging findings were investigated for each patient. One patient presented with neurogenic claudication while two patients developed partial, subacute cauda equina syndrome. All 3 patients initially responded favorably to lumbar decompression and midline cyst resection; however, one patient required surgical stabilization 8 mo later. Following the three case presentations, we performed a thorough literature search in order to identify articles describing intraspinal cystic lesions in lateral or midline locations. Midline intraspinal facet cysts represent an uncommon cause of lumbar stenosis and thecal sac compression. Such entities should enter the differential diagnosis of midline posterior cystic lesions. Midline cysts causing thecal sac compression respond favorably to lumbar surgical decompression and cyst resection. Though laminectomy is a commonly performed operation, stabilization may be required in cases of spondylolisthesis or instability.
Midline; Synovial; Ganglion; Intraspinal; Cyst; Neurogenic; Claudication; Laminectomy; Facet
We report the case of a patient with metastatic hormone refractory prostate cancer in whom “indirect” cauda equina syndrome developed concurrent with multilevel spinal cord compression (SCC). Three months after his first positive bone scan, a 65-year-old otherwise healthy man presented with severe back pain, bilateral lower extremity paresthesias, leg weakness and urinary retention. Magnetic resonance imaging (MRI) showed a dural-based mass causing SCC at the T9, T10 and T11 vertebrae, with a normal cauda equina. He received corticosteroids and palliative external beam radiotherapy, resulting in good pain control and gradual improvement in his neurological symptoms. He did well for 8 months, at which time his residual bilateral leg weakness abruptly worsened and he experienced numbness, paresthesias, urinary incontinence and constipation. Repeat MRI showed progression of epidural metastatic disease compressing the spinal cord or thecal sac at 7 thoracic vertebral levels. The cauda equina was also distorted and flattened without evidence of direct solid tumour impingement. We hypothesized that the etiology was increased intrathecal pressure due to disrupted cerebrospinal fluid flow resulting from multiple levels of upstream thecal sac compression. It is essential to image the entire spinal cord and cauda equina when patients with metastatic bone disease present with neurological symptoms to institute correct treatment and preserve function and mobility.
Background and purpose
Cauda equina syndrome (CES) is a severe complication of lumbar spinal disorders; it results from compression of the nerve roots of the cauda equina. The purpose of this study was to evaluate the clinical usefulness of a classification scheme of CES based on factors including clinical symptoms, imaging signs, and electrophysiological findings.
The records of 39 patients with CES were divided into 4 groups based on clinical features as follows. Group 1 (preclinical): low back pain with only bulbocavernosus reflex and ischiocavernosus reflex abnormalities. Group 2 (early): saddle sensory disturbance and bilateral sciatica. Group 3 (middle): saddle sensory disturbance, bowel or bladder dysfunction, motor weakness of the lower extremity, and reduced sexual function. Group 4 (late): absence of saddle sensation and sexual function in addition to uncontrolled bowel function. The outcome including radiographic and electrophysiological findings was compared between groups.
The main clinical manifestations of CES included bilateral saddle sensory disturbance, and bowel, bladder, and sexual dysfunction. The clinical symptoms of patients with multiple-segment canal stenosis identified radiographically were more severe than those of patients with single-segment stenosis. BCR and ICR improved in groups 1 and 2 after surgery, but no change was noted for groups 3 and 4.
We conclude that bilateral radiculopathy or sciatica are early stages of CES and indicate a high risk of development of advanced CES. Electrophysiological abnormalities and reduced saddle sensation are indices of early diagnosis. Patients at the preclinical and early stages have better functional recovery than patients in later stages after surgical decompression.
To report a case of Cauda Equina syndrome with the completion of the paralysis after the reduction of a L4L5 dislocation due to a herniated disc. Although several articles have described a post-traumatic disc herniation in the cervical spinal canal, this is not well known in the lumbar region. A 30-year-old man was admitted to the emergency room with blunt trauma to the chest and abdomen with multiple contusions plus a dislocation of L4-L5 with an incomplete neurological injury. After an emergency open reduction and instrumentation of the dislocation, the patient developed a complete cauda equina syndrome that has resulted from an additional compression of the dural sac by a herniated disc. In a dislocation of the lumbar spine, MRI study is mandatory to check the state of the spinal canal prior to surgical reduction. A posterior approach is sufficient for reduction of the vertebral displacement, however an intra-canal exploration for bony or disc material should be systematically done.
Cauda equine; Herniated disc; Lumbar dislocation; MRI; Reduction
A retrospective review of medical records and
imaging studies. To investigate characteristic clinical features and surgical outcomes of spinal cord tumors (SCTs) of the thoracolumbar junction (TLJ). The spinal cord transitions to the cauda equina in the TLJ. The TLJ contains the upper and lower motor neurons of the spinal cord and cauda equina. As a result, the clinical features of lesions in the TLJ vary, and these anatomical characteristics may affect surgical outcome.
Materials and Methods
diagnosis, clinical features, neurological signs, and surgical outcomes were investigated in 76 patients surgically treated at our institute for SCTs arising from T11 to L2. The patients were divided into epiconus (T11-12, n = 18) and conus groups (L1-2, n = 58).
Patients in the
epiconus group had hyperactive deep tendon reflexes (DTRs), while those in the conus group had hypoactive DTRs (p < 0.05). Nine patients were misdiagnosed with intervertebral disc diseases (IVDs) before correct diagnoses were made. It was impossible to definitively determine the exact cause of symptoms in four patients who had both SCTs and IVDs.
Among SCTs of the TLJ, the
epiconus group displayed upper motor neuron syndrome and the conus group displayed lower motor neuron syndrome. SCTs of the TLJ were frequently misdiagnosed as IVDs due to symptomatic similarities. SCTs of the TLJ should be included in differential diagnosis of back and leg pain, and it is highly recommended that routine lumbar magnetic resonance imaging include the TLJ.
Spinal cord neoplasms; thoracolumbar junction; conus medullaris; cauda equina
Lumbar spinal stenosis (LSS) is the leading cause of morbidity and mortality worldwide. LSS pathology is associated with secondary injury caused by inflammation, oxidative damage and cell death. Apart from laminectomy, pharmacological therapy targeting secondary injury is limited. Statins are FDA-approved cholesterol-lowering drug. They also show pleiotropic anti-inflammatory, antioxidant and neuroprotective effects. To investigate the therapeutic efficacy of simvastatin in restoring normal locomotor function after cauda equina compression (CEC) in a rat model of LSS, CEC injury was induced in rats by implanting silicone gels into the epidural spaces of L4 and L6. Experimental group was treated with simvastatin (5 mg/kg body weight), while the injured (vehicle) and sham operated (sham) groups received vehicle solution. Locomotor function in terms of latency on rotarod was measured for 49 days and the threshold of pain was determined for 14 days. Rats were sacrificed on day 3 and 14 and the spinal cord and cauda equina fibers were extracted and studied by histology, immunofluorescence, electron microscopy (EM) and TUNEL assay. Simvastatin aided locomotor functional recovery and enhanced the threshold of pain after the CEC. Cellular Infiltration and demyelination decreased in the spinal cord from the simvastatin group. EM revealed enhanced myelination of cauda equina in the simvastatin group. TUNEL assay showed significantly decreased number of apoptotic neurons in spinal cord from the simvastatin group compared to the vehicle group. Simvastatin hastens the locomotor functional recovery and reduces pain after CEC. These outcomes are mediated through the neuroprotective and anti-inflammatory properties of simvastatin. The data indicate that simvastatin may be a promising drug candidate for LSS treatment in humans.
Spinal stenosis; Simvastatin; Cauda equina; Demyelination; g-ratio
Extramedullary hematopoiesis (EMH) is occasionally reported in idiopathic myelofibrosis and is generally found in the liver, spleen, and lymph nodes several years after diagnosis. Myelofibrosis presenting as spinal cord compression, resulting from EMH tissue is very rare. A 39-yr-old man presented with back pain, subjective weakness and numbness in both legs. Sagittal magnetic resonance imaging showed multiple anterior epidural mass extending from L4 to S1 with compression of cauda equina and nerve root. The patient underwent gross total removal of the mass via L4, 5, and S1 laminectomy. Histological analysis showed islands of myelopoietic cells surrounded by fatty tissue, consistent with EMH, and bone marrow biopsy performed after surgery revealed hypercellular marrow and megakaryocytic hyperplasia and focal fibrosis. The final diagnosis was chronic idiopathic myelofibrosis leading to EMH in the lumbar spinal canal. Since there were no abnormal hematological findings except mild myelofibrosis, additional treatment such as radiothepary was not administered postoperatively for fear of radiotoxicity. On 6 month follow-up examination, the patient remained clinically stable without recurrence. This is the first case of chronic idiopathic myelofibrosis due to EMH tissue in the lumbar spinal canal in Korea.
Hematopoiesis, Extramedullary; Myelofibrosis; Spinal Canal
techniques permit the separate analysis of the response from cauda
equina roots and the spinal potential that is probably generated by the
activation of dorsal horn cells. To improve the functional assessment
of focal lesions of the lumbosacral cord, lower limb somatosensory
evoked potentials (SEPs) were measured by multisegmental stimulation.
peroneal and tibial nerves SEPs were recorded in 14 patients in whom
MRI demonstrated compressive cord damage ranging from T9 to L1 levels.
SEPs were recorded in each patient at the lumbar level (cauda equina
response), lower thoracic level (spinal response), and from the scalp
in spinal response occurred in 50% and 70% of tibial and common
peroneal nerve SEPs respectively; these findings were well explained by
the radiological compression level, involving in most of the patients
lumbar rather than sacral myelomeres. The SEPs were often more
effective than the clinical examination in showing the actual extension
recording of spinal SEPs after multisegmental lower limb stimulation
proved useful in assessing cord dysfunction and determining the cord
levels mainly involved by the compression.
We report a case of a 44-year-old patient with paralysis of the left leg who had a thoracic epidural catheterization after general anesthesia for abdominal surgery. Sensory losses below T10 and motor weakness of the left leg occurred after the surgery. Magnetic resonance image study demonstrated a well-defined intramedullary linear high signal intensity lesion on T2-weighted image and low-signal intensity on T1-weighted image in the spinal cord between T9 and L1 vertebral level, and enhancements of the spinal cord below T8 vertebra and in the cauda equina. Electrodiagnostic examination revealed lumbosacral polyradiculopathy affecting nerve roots below L4 level on left side. We suggest that the intrinsic spinal cord lesion and nerve root lesion can be caused by an epidural catheterization with subsequent local anesthetic injection.
Spinal cord injuries; Epidural analgesia; Paralysis
To present a case of cauda equina syndrome (CES) caused by chronic inflammatory demyelinating polyneuropathy (CIDP) which seemed clinically similar to Charcot-Marie-Tooth disease type1 (CMT1). CIDP is an immune-mediated polyneuropathy, either progressive or relapsing-remitting. It is a non-hereditary disorder characterized by symmetrical motor and sensory deficits. Rarely, spinal nerve roots can be involved, leading to CES by hypertrophic cauda equina. A 34-year-old man presented with low back pain, radicular pain, bilateral lower-extremity weakness, urinary incontinence, and constipation. He had had musculoskeletal deformities, such as hammertoes and pes cavus, since age 10. Lumbar spine magnetic resonance imaging showed diffuse thickening of the cauda equina. Electrophysiological testing showed increased distal latency, conduction blocks, temporal dispersion, and severe nerve conduction velocity slowing (3 m/s). We were not able to find genetic mutations at the PMP 22, MPZ, PRX, and EGR2 genes. The pathologic findings of the sural nerve biopsy revealed thinly myelinated nerve fibers with Schwann cells proliferation. We performed a decompressive laminectomy, intravenous IgG (IV-IgG) and oral steroid. At 1 week after surgery, most of his symptoms showed marked improvements except foot deformities. There was no relapse or aggravation of disease for 3 years. We diagnosed the case as an early-onset CIDP with cauda equine syndrome, whose initial clinical findings were similar to those of CMT1, and successfully managed with decompressive laminectomy, IV-IgG and oral steroid.
Cauda equina syndrome; Chronic inflammatory demyelinating polyneuropathy; Charcot-Marie-Tooth disease; Laminectomy