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).
Cauda equina; Disc herniation; Spinal stenosis; Spinal surgery; Sacral
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.
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.
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.
Giant spinal schwannoma of the cauda equine involving many nerve roots is rare, and ossification is usually not observed in the schwannoma. A 21-year-old man presented with a 12-month history of urinary dysfunction and numbness below the buttocks. Plain radiography showed scalloping of the posterior surface of the vertebral bodies from L4 to the sacrum, and magnetic resonance imaging and computed tomography revealed a giant cauda equina tumor with dystrophic calcification. The tumor was completely removed, with intraoperative neurophysiologic monitoring. Histopathologic examination showed that the tumor was a schwannoma. The patient's postoperative course was uneventful, with urinary function and numbness gradually improving. Although a giant schwannoma accompanied by dystrophic calcification is extremely rare, such a tumor can be removed safely and completely by meticulous dissection and careful neuromonitoring of the cauda equina spinal nerves involved in the tumor.
Giant schwannoma; Cauda equina; Complete excision; Calcification; Neuromonitoring
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
Although postoperative spinal epidural hematoma (SEH) is not uncommon, hematomas that require surgery are rare. Cauda equina syndrome (CES) may be associated with postoperative SEH. In these cases, early recognition and emergency decompression can prevent further damage and better neurologic recovery.
A 41-year-old man underwent two-level discectomy with insertion of an interspinous spacer at L3-4 and L4-5 because of low back pain and radiculopathy. Eight hours after the operation, the patient developed CES. MRI revealed SEH compressing posteriorly at the L3-4 level. On emergency decompression and hematoma evacuation, the interspinous spacer had obstructed the laminotomy site at L3-4 completely, blocking drainage to the drain. The patient experienced complete neurologic recovery by 2 months followup.
Many studies report risk factors for SEH. However, postoperative SEH can also be encountered in patients without these risks. One study reported a critical ratio (preoperative versus postoperative cross-sectional area) correlated with postoperative symptoms, especially in those with CES. The propensity to develop CES is likely dependent on a number of patient-specific factors.
Surgeons should be aware that patients without risk factors may develop acute CES. Wider laminotomy (larger than half of the device size) may help to prevent this complication when one uses the compressible type of device, especially in patients with relatively small lamina.
To determine the level of brain-derived neurotrophic factor (BDNF) in experimental dog model of severe acute cauda equina syndrome, which was induced by multiple cauda equina constrictions throughout the entire lumbar (L), sacral (S) and coccygeal (Co) spinal cord and their central processes of the dorsal root ganglia neurons. Adult male mongrel dogs were randomly divided into 2 groups. The experiment group (n=4) was subjected to multiple cauda equina constrictions. The control group (n=4) was subjected to cauda equina exposure without constrictions. Level of BDNF in the spinal cord and the dorsal root ganglion cells (L7, S1-S3) was assessed 48 hours after multiple constrictions by immunohistochemical and histopathological analyses. 48 hours after multiple constrictions of cauda equina, up-regulation of BDNF within lumbosacral (L7-S3) spinal cord and dorsal root ganglion was observed in experimental group as compared to control group. Our result suggests that BDNF might play a role in the inflammatory and neuropathic pain as a result of multiple cauda equina constrictions. Regulation of BDNF level could potentially provide a therapy for treating cauda equina syndrome.
Cauda equina syndrome (CES); dorsal root ganglion (DRG); brain-derived neurotrophic factor (BDNF); multiple cauda equina constrictions (MCEC); neurotrophic factors (NFs)
Cauda equina syndrome (CES) has been described in the literature as a clinical entity consisting of low back pain, bilateral leg pain with motor and sensory deficits, genitourinary dysfunction with overflow incontinence or retention, and faecal incontinence. CES has been recognised as a rare complication of spinal manipulative therapy, and is an absolute contraindication to this type of therapy. A case of CES that presented in an atypical manner is presented, highlighting the lack of leg symptomatology, but with the presence of painless urinary retention. A definition of CES as a condition presenting with bladder dysfunction and possible motor and/or sensory loss in the region of sacral and/or lumbar dermatomes is discussed. Evaluation of patients with lumbar disc pathology who are suspected of suffering from CES should include questioning regarding urinary difficulty and neurologic examination of the sacral plexus, including sensation; and may include advanced imaging such as contrast computerized tomography (CT) scan or magnetic resonance imaging (MRI). Immediate referral for consideration of decompression surgery is recommended for optimal recovery of neurologic function. Clinicians should be knowledgeable of the various forms CES can present in, and maintain a high index of suspicion for this condition in patients with suspected lumbar disc herniation or urinary dysfunction.
low back pain; disc herniation; cauda equina syndrome; cauda equina compression; bladder dysfunction
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
A prospective longitudinal inception cohort study of 33 patients undergoing surgery for cauda equina syndrome (CES) due to a herniated lumbar disc. To determine what factors influence spine and urinary outcome measures at 3 months and 1 year in CES specifically with regard to the timing of onset of symptoms and the timing of surgical decompression. CES consists of signs and symptoms caused by compression of lumbar and sacral nerve roots. Controversy exists regarding the relative importance of timing of surgery as a prognostic factor influencing outcome. Post-operative outcome was assessed at 3 months and 1 year using the Oswestry Disability Index (ODI), Visual Analogue Scale (VAS) scores for leg and back pain and an incontinence questionnaire. Statistical analysis was used to determine the association between pre-operative variables and these post-operative outcomes with a specific emphasis on the timing of surgery. Surgery was performed on 12 (36%) patients within 48 h of the onset of symptoms including seven patients (21%) who underwent surgery within 24 h. Follow up was achieved in 27 (82%) and 25 (76%) patients at 3 and 12 months, respectively. There was no statistically significant difference in outcome between three groups of patients with respect to length of time from symptom onset to surgery- <24, 24–48 and >48 h. A significantly better outcome was found in patients who were continent of urine at presentation compared with those who were incontinent. The duration of symptoms prior to surgery does not appear to influence the outcome. This finding has significant implications for the medico-legal sequelae of this condition. The data suggests that the severity of bladder dysfunction at the time of surgery is the dominant factor in recovery of bladder function.
Cauda equina syndrome; Surgical outcome; Timing; Herniated nucleus pulposus
Disturbance of autonomic function is an unusual feature of compression of the cauda equina. A 61 year old man who had complete occlusion of the lumbar spinal canal with compression of the cauda equina from a large centrally prolapsed disc, had spontaneous priapism, precipitated by walking and relieved by resting. This symptom was comparable to claudication by compression of cauda equina. It subsided completely after surgical removal of a prolapsed L4-5 disc.
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
Sacral fractures are rare but severe injuries. They are often associated with neurological impairment and pelvic instability. We present a case of a 28-year-old woman who sustained an H-type fracture of the sacrum with complete cauda equina syndrome treated with cauda equina decompression and pelvic percutaneous stabilization with an iliosacral screw. Two years after she underwent screw removal, but complained of back and nape pain after the operation. A lumbosacral MRI showed the presence of a lytic lesion involving the S1 and S2 bodies that was judged to be a pseudomeningocele leaning against the sacral screw hole and cerebrospinal fluid fistulas through this. To our knowledge, this is the first case of such a complication after sacral screw removal to be reported.
Pseudomeningocele; Cerebrospinal fluid fistulas; Sacral fracture; Complication
Sacral nerve stimulation (SNS) is an effective treatment for bladder and bowel dysfunction, and also has a role in the treatment of chronic pelvic pain. We report two cases of intractable pain associated with cauda equina syndrome (CES) that were treated successfully by SNS. The first patient suffered from intractable pelvic pain with urinary incontinence and fecal incontinence after surgery for a herniated lumbar disc. The second patient underwent surgery for treatment of a burst fracture and developed intractable pelvic area pain, right leg pain, excessive urinary frequency, urinary incontinence, voiding difficulty and constipation one year after surgery. A SNS trial was performed on both patients. Both patients' pain was significantly improved and urinary symptoms were much relieved. Neuromodulation of the sacral nerves is an effective treatment for idiopathic urinary frequency, urgency, and urge incontinence. Sacral neuromodulation has also been used to control various forms of pelvic pain. Although the mechanism of action of neuromodulation remains unexplained, numerous clinical success reports suggest that it is a therapy with efficacy and durability. From the results of our research, we believe that SNS can be a safe and effective option for the treatment of intractable pelvic pain with incomplete CES.
Sacral Plexus; Neuromodulator; Pain; Cauda Equina
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
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
We report here on a case of a 23-year-old male who received en block spondylectomy for a vertebral Ewing's sarcoma at our hospital. Nine days after surgery, he presented with severe back pain and motor weakness of the lower extremities. Based on the physical examination and the computed tomography scan, he was diagnosed with acute cauda equina syndrome that was caused by compression from an epidural hematoma. His neurological functions recovered after emergency evacuation of the hematoma. This case showed that extensive surgery for a malignant vertebral tumor has a potential risk of delayed epidural hematoma and acute cauda equina syndrome and this should be treated with emergency evacuation.
Epidural hematoma; Ewing's sarcoma; Spine; En block spondylectomy
Community-acquired methicillin-resistant Staphylococcus aureus (CA-MRSA) is responsible for a broad range of infections. We report the case of a 46-year-old gentleman with a history of untreated, uncomplicated Hepatitis C who presented with a 2-month history of back pain and was found to have abscesses in his psoas and right paraspinal muscles with subsequent lumbar spine osteomyelitis. Despite drainage and appropriate antibiotic management the patient's clinical condition deteriorated and he developed new upper extremity weakness and sensory deficits on physical exam. Repeat imaging showed new, severe compression of the spinal cord and cauda equina from C1 to the sacrum by a spinal epidural abscess. After surgical intervention and continued medical therapy, the patient recovered completely. This case illustrates a case of CA-MRSA pyomyositis that progressed to lumbar osteomyelitis and a spinal epidural abscess extending the entire length of the spinal canal.
Air injected into the epidural space may spread along the nerves of the paravertebral space. Depending on the location of the air, neurologic complications such as multiradicular syndrome, lumbar root compression, and even paraplegia may occur. However, cases of motor weakness caused by air bubbles after caudal epidural injection are rare. A 44-year-old female patient received a caudal epidural injection after an air-acceptance test. Four hours later, she complained of motor weakness in the right lower extremity and numbness of the S1 dermatome. Magnetic resonance imaging showed no anomalies other than an air bubble measuring 13 mm in length and 0.337 ml in volume positioned near the right S1 root. Her symptoms completely regressed within 48 hours.
caudal epidural block; complications; epidural air; epidural injection
A 55-year-old obese man (body mass index, 31.6 kg/m2) presented radiating pain and motor weakness in the left leg. Magnetic resonance imaging showed an epidural mass posterior to the L5 vertebral body, which was isosignal to subcutaneous fat and it asymmetrically compressed the left side of the cauda equina and the exiting left L5 nerve root on the axial T1 weighted images. Severe arthritis of the left facet joint and edema of the bone marrow regarding the left pedicle were also found. As far as we know, there have been no reports concerning a solitary epidural lipoma combined with ipsilateral facet arthorsis causing lumbar radiculopathy. Solitary epidural lipoma with ipsilateral facet arthritis causing lumbar radiculopathy was removed after the failure of conservative treatment. After decompression, the neurologic deficit was relieved. At a 2 year follow-up, motor weakness had completely recovered and the patient was satisfied with the result. We recommend that a solitary epidural lipoma causing neurologic deficit should be excised at the time of diagnosis.
Solitary epidural lipoma; Posterior facet; Ipsilateral arthritis; Lumbar radiculopathy
Sparing of sensation in sacral dermatomes and of sphincter control was found in eight out of fourteen cases of severe cauda equina compression from massive central lumbar disc prolapse. Although the triangular shape of the lumbar spinal canal may be one factor for this it was found from a necropsy model that the increase in linear strain on the stretched roots of the cauda equina is least in the more centrally placed lower sacral roots. It is argued that the lower tension in these roots is determined by Young's Modulus.
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
Ependymomas presenting with intratumoural and/or subarachnoid haemorrhages are seen rarely. These haemorrhages are mostly due to anticoagulation, epidural analgesia or pregnancy. A 62-year-old male farmer with cauda equina syndrome after a work-related trauma is presented. He was admitted to our hospital with paraparesis, faecal incontinance and sensory loss below the level of the lumbar-2 dermatome. Magnetic resonance imaging of the spine displayed an intradural mass lesion at the level of the first lumbar vertebrae. The lesion was excised totally via dorsal midline approach. Histopathologic examination revealed grade-3 ependymoma with intratumoural haemorrhage. The patient’s symptoms were relieved completely on postoperative day 7. The patient was given information about periodical examination for recurrence and discharged on the third postoperative week. Asymptomatic spinal lesions should be considered for operation whenever detected because of unpredicted complications.
Cauda equina syndrome; Ependymoma; Filum terminale; Intratumoural haemorrhage; Spinal cord tumours; Spinal trauma
Intervertebral intradural lumbar disc herniation (ILDH) is a quite rare pathology, and isolated intradural lumbar disc herniation is even more rare. Magnetic resonance imaging (MRI) may not be able to reveal ILDHs, especially if MRI findings show an intact lumbar disc annulus and posterior longitudinal ligament. Here, we present an exceedingly rare case of an isolated IDLH that we initially misidentified as a spinal intradural tumor, in a 54-year-old man hospitalized with a 2-month history of back pain and right sciatica. Neurologic examination revealed a positive straight leg raise test on the right side, but he presented no other sensory, motor, or sphincter disturbances. A gadolinium-enhanced MRI revealed what we believed to be an intradural extramedullary tumor compressing the cauda equina leftward in the thecal sac, at the L2 vertebral level. The patient underwent total L2 laminectomy, and we extirpated the intradural mass under microscopic guidance. Histologic examination of the mass revealed a degenerated nucleus pulposus.
Intradural disc herniation; Spinal intradural tumor; Magnetic resonance imaging