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This article reviews the radiologic examination of the canine cauda equina. The radiographic technique and interpretation of survey radiographs, radiographs with the spine in flexion and extension, tomography and contrast procedures, the diagnostic value and limits of these methods are discussed. The diseases which may cause cauda equina compression and the radiographic findings are described and illustrated.
Although saddle sensory deficit seems the most useful clinical sign in the diagnosis of a cauda equina or conus medullaris lesion, findings of previous studies were controversial. The aim of the present study was to try to resolve this issue. The data from the author's series of patients with clinical, electrodiagnostic and radiological findings compatible with a cauda equina lesion were reviewed. Of the 117 patients in the series, 11 (10 men) did not have a saddle sensory deficit. These 11 patients had less severe sacral dysfunction than the others, and none of them needed urgent surgical intervention. They all had electromyographic (EMG) signs of a significant motor fibre lesion, and in seven men the sacral (penilo-cavernosus) reflex was clinically abnormal. The study revealed normal saddle sensation in approximately 10% of patients with cauda equina or conus medullaris lesions. Dissociation between preserved touch sensation and abnormal EMG findings, as well as dissociation between preserved touch sensation and a non-elicitable penilo-cavernosus reflex might be explained by preservation of the thinner sensory nerve fibres, which are more resistant to compression. Although, saddle sensory loss seems to identify patients who might benefit from urgent spinal imaging and surgery, further diagnostic evaluation is also indicated in patients with normal saddle sensation, particularly due to the increased frequency of spinal tumours found in this subgroup.
An unusual, well demarcated, and encapsulated neoplasm of the cauda equina is presented. At first, the tumor was considered to be a variant of myxopapillary ependymoma, but the reaction for glial fibrillary acidic protein was negative. At the ultrastructural level, the neoplastic cells contained many small dense core vesicles, and the diagnosis of paraganglioma was established. The literature and histogenesis of paraganglioma of the cauda equina is reviewed.
We present two cases of cauda equina syndrome in ankylosing spondylitis. Cauda equina syndrome is a rare complication of ankylosing spondylitis, the pathogenesis of which is not well understood. The onset is insidious with pain and sensory symptoms; sphincter disturbances are common. After a period of increasing neurological symptoms, the condition tends to stabilize. The degree of nerve involvement is variable and can be accurately defined by electromyography. The diagnosis has to be confirmed by computed tomography (CT) or magnetic resonance imaging (MRI); myelography must be avoided. There is no specific treatment, except for pain control. The different clinical presentations and the role of new imaging techniques, CT and MRI, are demonstrated.
PURPOSE: To determine the incidence and treatment outcome of compression of the cauda equina by metastatic disease in patients with breast cancer. METHODS: A retrospective study of individuals diagnosed with breast cancer at a single institution during a 16-year period was undertaken. RESULTS: Of the 1,283 patients studied, 15 (1.2%) developed cauda equina syndrome from metastatic disease. The median survival was eight months; ten (67%) survived for at least six months. Among the evaluable patients, pain was completely relieved in eight of ten women; complete resolution of neurologic deficits was observed in five of nine patients. CONCLUSION: Metastatic breast cancer compression of the cauda equina and long-term survival of patients are infrequent occurrences. Beneficial responses can be mediated by radiotherapy.
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.
OBJECTIVE: Many investigators have reported satisfactory outcome in anterior lumbar interbody fusion (ALIF) performed for lumbar disc herniation or "multiply operated back" (MOB), but without comparing preoperative and postoperative dural tube area and cauda equina adhesion in magnetic resonance imaging (MRI). We conducted this study to determine these data in ALIF performed for lumbar disc herniation and MOB. METHODS: Thirty-two patients who underwent ALIF, involving 38 discs, were studied. In MRI obtained before and after surgery (interval 9-48 months, mean 19.2 months), cross-sectional areas of the lumbar dural tube were measured from axial T2-weighted images using a computer-linked digitizer. At 30 disc levels operated on, the cauda was identified in images; cauda equina adhesions were classified according to Matsui et al (grade I-III). Clinical improvement was scored. RESULTS: Bony union was observed in radiographs of all patients. Preoperative and postoperative cross-sectional areas of the lumbar dural tube were 1.32 +/- 0.4 and 1.87 +/- 0.5 cm, respectively, and expansion ratio was 1.43 +/- 0.4. Recovery did not correlate with expansion ratio. Positive correlation was noted between expansion ratio and disc height ratio. At 30 disc levels where cauda equina was identified, 22 represented grade I and 8 represented grade II. At three of the latter, prior surgery had been performed via a posterior approach. CONCLUSIONS: No significant difference was noted in occurrence of grade II adhesions between primary ALIF and ALIF performed for MOB. Dural tube expansion was accomplished even without exposure of the tube, and cauda equina adhesion was uncommon in primary ALIF.
OBJECTIVE: To study the changes of neural electrophysiology properties of cauda equina under double level compression and dynamic burdens, and to clarify the mechanisms of intermittent neurogenic claudication. METHODS: Thirty SD rats were divided into 5 groups (6 in each group). The laminectomy of L5 was performed in control group. In the experimental groups, the silicon sheets were inserted into the spinal canal of L4 and L6 to cause double level compression of cauda equina by 30%. Two hours after onset of compression, no dynamic burden was introduced in experimental group 1. Only high frequency stimulation(HFS) was introduced for 6 minutes in experimental group 2. Both HFS and additional increased compression were introduced for 6 minutes in experimental group 3. While only additional increased compression was introduced for 6 minutes in experimental group 4. After 6 minutes of dynamic burdens, all were returned to the status of static compression for another 30 minutes and then electrical examination was made. RESULTS: After 2 hours of compression, motor and sensory nerve conduction velocity (NCV) of all the four experimental groups decreased significantly (P < 0.05), but there was no significant difference between them. There was no significant change in the control group. There was no significant change of NCV in experimental group 1 during the last 30 minutes of experiment. NCV in the other three experimental groups decreased after introduction of dynamic burdens, especially in the experimental group 3. CONCLUSION: The above results showed that NCV of cauda equina decreased significantly under dynamic burdens during static compression. Two kinds of dynamic burdens introduced at the same time can cause more profound change than a single one.
This study was designed to test surgical techniques for reconstruction of an injured cauda equina. After transection of the intradural lumbar nerve root, end-to-end anastomosis was performed under surgical microscope in the dog. To preserve accurate adaptation of the transected nerve root, the root sheath and the funiculi were carefully sutured with a minimal number of stitches. Regenerated axons in the ventral root appeared distal from the suture at five weeks postoperatively, whereas those in the dorsal root appeared at seven weeks after anastomosis. The histogram and regrowth rate of the ventral root showed regenerative processes similar to those of peripheral nerves, though a little slower. The fact that an evoked potential from the sutured ventral root was recordable after stimulation of the sciatic nerve indicated restoration of nerve conduction. Although further experimental studies are required to develop adequate surgical techniques, microsurgical anastomosis of the transected cauda equina is potentially applicable for appropriate clinical cases of a cauda equina injury.
A primary epidermoid cyst of the cauda equina was diagnosed in an eleven-year-old boy. The patient had a previous two months history of lumbar pain with unilateral L 4 radicular pain. The diagnosis of an epidermoid cyst of the cauda equina, suspected by MRI, was confirmed by histology following surgery. Wide tumor resection, as complete as possible, was performed with minimum trauma. Presence of an epidermoid cyst in the filum terminale is a rare finding, few cases have been reported in the literature. However, surgical treatment and favorable post-operative course are similar to that observed in intraspinal localizations. MRI is helpful for the preoperative and differential diagnosis and for post-operative follow-up.
OBJECTIVE: To investigate the effects of cauda equina lesions on sexual function in men. METHODS: Sexual function was investigated in 46 men with long standing cauda equina/conus medullaris lesions. All had clinical and radiological findings supporting the diagnosis. The validated Slovene translation of the international index of erectile function (IIEF) was used. The responses were scored and sexual dysfunction categorised as absent, mild, moderate, or severe. The number of patients receiving help for sexual dysfunction was noted. Neurological examination of the trunk and lower limbs, electromyographic (EMG) evaluation of the sacral reflex, and quantitative EMG of the external anal sphincter muscles were done. RESULTS: Severe sexual dysfunction was reported by 35% of patients, moderate dysfunction by 24%, and slight dysfunction by 26%; normal sexual function was reported by 15%. Orgasmic function was slightly more impaired than erectile function, and sexual desire slightly less. The patients' age, but no findings on clinical neurological or EMG examination, correlated with sexual function. Only five men had received medical attention for sexual dysfunction. CONCLUSIONS: There is significant sexual impairment in men with lesions of the cauda equina or conus medullaris. This is poorly correlated with neurological and EMG findings and has received insufficient medical attention.
Three cases of sarcoidosis of the cauda equina are presented. In two there was no previous history suggestive of sarcoidosis and the presentation was one of a painful flaccid paralysis; in these the diagnosis was made after myelography and laminectomy with subsequent histology. The third patient had a previous diagnosis of lupus pernio and magnetic resonance imaging (MRI) was used to aid diagnosis. Only two previous cases have been reported of sarcoidosis presenting in the cauda equina with no other systemic manifestations. This is the first report of the use of MRI in sarcoidosis of the lower meninges.
This case report describes a paraganglioma of the cauda equina in a 63 year old woman. Very few examples of paraganglioma have been recorded in this site. Histologically these neoplasms may have considerable similarity with ependymoma, the most common neoplasm of the lower spinal cord, and the diagnosis can be easily missed unless special techniques are employed. The clinical and pathological data obtained from this and the other reported examples suggests that paragangliomas of the cauda equina are benign, slowly growing neoplasms. In contrast to ependymomas and to paragangliomas elsewhere, they are well circumscribed, amenable to complete resection and have an excellent prognosis.
Primary primitive neuroectodermal tumours of the cauda equina are rare. We report a case and review the literature.
A 49-year-old woman developed paraplegia 26 hours after appendectomy under epidural and general anesthesia. Systolic blood pressure fell to 85 mmHg for 25 minutes after epidural anesthesia, which was performed at the level of the L1/2 intravertebral space. Neurological examination revealed paraplegia and superficial sensory impairment below the level of the L 1 spinal cord. The bladder was atonic by cystometry. MRI showed gadolinium enhancement of the cauda equina extending over a long period (3 months) and spinal cord infarction. The infarction was at the level of 10th thoracic spinal vertebra to conus and was limited to the gray matter of the spinal cord. We consider that the reason for spinal cord infarction was prolonged hypotension of the patient, who was diabetic, hypertensive and hypercoagulopathic. The blood supply to the gray matter is mainly from the central artery which is derived from the anterior spinal artery, and the gray matter is particularly vulnerable to hypotension. Our hypotheses concerning gadolinium enhancement of the cauda equina are the following: 1) enhancement of the cauda equina was seen due to collateral formation after spinal cord infarction, and 2) long-term enhancement of the cauda equina was observed due to an ischemic lesion involving a large area.
Facet joint cysts are commonest at the L4-L5 level and are associated with facet joint degeneration and type III (degenerative) spondylolisthesis. It is extremely rare for facet joint cysts to cause symptomatic cauda equina compression. Three elderly patients presented to us with significant cauda equina compression caused by facet joint cysts. One presented with classic symptoms and signs of a cauda equina syndrome, a second with bilateral lower limb neurologic loss associated with uncontrolled epilepsy, and the third with bilateral leg symptoms as well as an upper limb tremor and fasciculation. The diagnosis was easily made after magnetic resonance scanning in two patients, although in one patient, it was significantly delayed because of his confounding neurologic picture. Lumbar spine surgery (decompression and cyst resection) was successful in resolving symptoms in all three, even though two patients had significant neurologic compromise before surgery. The occurrence of facet joint cysts in older patients can be associated with other degenerative neurologic conditions, and the diagnosis might not be apparent early. We suggest that in older patients who have a mixed picture of central and peripheral neurologic compromise, this diagnosis should be considered and investigation of the whole of the spine, not just the brain and spinal cord, should be undertaken.
Acute lumbosacral fracture-dislocation is an unusual injury. A delayed cauda equina injury accompanying the fracture-dislocation is seldom encountered. We report a cauda equina lesion complicating an acute lumbosacral fracture-dislocation 3 weeks postinjury. The patient had been trapped in a knee-elbow position under an overturned vehicle. Symptoms were relieved following posterior decompression and fusion from L5 to S1.
Adequate electrophysiological techniques to monitor function of the cauda equina have been proposed for surgery in patients with lumbosacral lipoma or myeloschisis. Motor fibers were identified by electrical stimulation in the operating field with bipolar rectangular impulses of 200 mu sec duration at 2 Hz under 5 mA and compound muscle action potentials (CMAPs) recorded from the leg and anal muscles. By recording CMAPs from the tibialis anterior, the biceps femoris, the gastrocnemius, and the external anal sphincter muscles, all of the roots from the fourth lumbar to the fourth sacral segment were continuously monitored. To spare recording channels, recordings were obtained from the right versus the left side. In our institute, 5 patients have undergone lumbosacral surgery while using this monitoring system, and the results indicated that there was no postoperative neurological exacerbation in any of the cases. According to a combination of the CMAPs produced by stimulation, the segment of the stimulated motor root could be identified electrophysiologically. Monitoring of somatosensory evoked potentials was not performed because this would have required too much time and would have prolonged surgery. However, some sensory fibers, which appeared to be posterior roots of the cauda equina on intraoperative inspection, could be identified indirectly with CMAPs recording because of current spreading from the stimulation to motor fibers.