Disorders of the spinal cord and cauda equina.
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Cauda Equina↗
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Subarachnoid haemorrhage due to cauda equina haemangiopericytoma.
A case of cauda equina haemangiopericytoma presenting with spinal subarachnoid haemorrhage is reported. The tumour had been asymptomatic until 2 weeks prior to presentation, and resulted in complete paraplegia below L3. The authors underline the uncommon association of spinal subarachnoid haemorrhage and cauda equina tumour and the rare finding of a cauda equina haemangiopericytoma.
Aged↗
MR of the cauda equina.
To define the anatomy of the cauda equina nerve roots by MR imaging, the lower spine of 14 normal volunteers was imaged using a high-field surface-coil technique. A total of 56 sagittal and 56 axial MR sections (eight selected slices from each case) were correlated with undistorted anatomic sections from cadaver spine specimens, and the visualization of the nerve roots was assessed. In addition, MR images of three patients with infiltrating or seeding tumors affecting the cauda equina were analyzed. Seventy-eight percent of the MR sections from normal cases clearly showed the anatomy of the cauda equina nerve roots. The nerve roots were fairly shown in 17% of the sections; and false findings (presumably caused by CSF pulsation) were observed in the remaining 5%. Coronal imaging provided excellent anatomic views of the nerve roots within the intervertebral foramina. Morphologic alterations in the pathologic cases were correctly shown when both T1- and T2-weighted imaging were used. In conclusion, MR proved efficient in viewing the cauda equina region.
Adult↗
Magnetic resonance imaging of arachnoid diverticula associated with cauda equina syndrome in ankylosing spondylitis.
Cauda equina syndrome is an uncommon complication of ankylosing spondylitis (AS), but results in significant morbidity in those patients affected. We report 2 patients who developed classical cauda equina syndrome, which was well visualized by magnetic resonance imaging. This technique allows accurate noninvasive diagnosis of this complication of AS.
Aged↗
[Metastatic Grawitz's tumor to the cauda equina: case report].
A case of Grawitz's tumor metastasizing to the cauda equina is presented. A 51-year-old male was hospitalized due to severe low back pain radiating to the left lower extremity. Neurological examination showed only hyporeflexia of the left patella reflex and positive Lasegue's sign. MRI showed intradural mass at the L4 level. Preoperatively, we diagnosed a cauda equina tumor. A laminectomy of both L3 and L4 was performed, and total removal of the cauda equina tumor was performed. Microscopically, the tumor cells were large, the appearance of the cytoplasm ranging from optically clear with sharply outlined boundaries, to deeply granular, with many transitional forms. These histological findings were typical findings of Grawitz's tumor, and were the same as those of this patient's renal tumor. Finally, we diagnosed Grawitz's tumor metastasizing to the cauda equina. Metastatic cauda equina tumor from outside the central nervous system is very rare and only 7 cases have been reported. This case is the first one of Grawitz's tumor spreading to the cauda equina.
Carcinoma, Renal Cell↗
[Cauda equina neurinoma associated with intracranial hypertension--case report].
A case of cauda equina neurinoma associated with intracranial hypertension is reported. A 59-year-old female with a history of disturbed orientation was admitted. A neurological examination upon admission revealed the disorientation and gait disturbance. Superficial sensation under L3 was impaired. A computed tomographic(CT) scan presented the enlargement of ventricles and the slightly poor description of cerebral sulci. Since the patient had a high fever up to 40.1 C, meningitis was suspected. Cerebrospinal fluid revealed that cell count was only 2/3, while the protein concentration was markedly elevated (389mg/dl). Froin reaction was extremely positive and fibrin was observed. Based upon these findings, the spinal tumor was considered. Plain lumber film showed the posterior scalloping of the L5 and S1 vertebral bodies. Gd-DTPA enhanced MRI showed a high signal intensity area at the cauda equina. Diagnosed as a cauda equina tumor, the total resection of the tumor was performed via laminectomy of L3-S1. The tumor was involved with nerve filaments at the cauda equina. The pathological diagnosis was neurinoma. After the operation, her symptoms improved and a CT scan revealed the reduction of the ventricular size. However, the protein concentration of cerebrospinal fluid did not normalized.
Cauda Equina↗
Cauda equina syndrome in patients undergoing manipulation of the lumbar spine.
Cauda equina syndrome has been implicated as a potential complication of spinal manipulation. A review of the literature from 1911 to 1989 revealed ten reported cases of cauda equina syndrome in patients undergoing manipulation without anesthesia. This article presents three new cases where a temporal association was found between the onset of cauda equina symptoms and lumbar manipulation. The type of manipulation administered and the relationship between the treatment and symptoms is reviewed. In each of these cases both the chiropractic practitioner and the emergency room physician failed to comprehend the nature of the problem and take appropriate action. As a consequence, the patients went untreated for several days. This may have led to residual symptomatology. It is concluded that patients who present with bowel or bladder disturbances, leg weakness, or rectal and genital sensory changes after manipulation, be recognized as experiencing a cauda equina syndrome.
Adult↗
Experimental nerve root compression. A model of acute, graded compression of the porcine cauda equina and an analysis of neural and vascular anatomy.
Nerve root compression has been suggested as one important pathogenetic factor in low-back pain syndromes and sciatica. The underlying pathophysiologic mechanisms are, however, incompletely known, partly because of the lack of experimental data on this topic. In the present study, a model for experimental compression of the porcine sacrococcygeal cauda equina is presented. The model consists of surgical exposure of the cauda equina and compression of the cauda equina toward the ventral aspect of the spinal canal by an inflatable balloon fixed to the spine. This compression system was shown to have a high accuracy in pressure transmission from the balloon to the cauda equina. The gross and microscopic neural anatomy and the vascular anatomy of the porcine cauda equina were analyzed with light microscopic and ink-perfusion techniques. The porcine cauda equina showed a close anatomic resemblance to the human lumbosacral cauda equina. The presented model offers unique possibilities for experimental studies on nerve root compression injury because of the easy surgical exposure and the sufficient length of the nerve roots. In separate studies, this model, along with investigations of solute transport to the nerve tissue and of impulse propagation, has been used to analyze the effects of acute, graded compression on blood flow and edema formation in the cauda equina. The porcine cauda equina would also be particularly suitable for chronic compression studies because any neurologic deficit acquired would be restricted to the tail.
Animals↗
Cauda equina syndrome complicating ankylosing spondylitis.
The cauda equina syndrome is an uncommon and poorly understood complication of ankylosing spondylitis. The clinical and radiologic findings in five patients with this syndrome are described. Typical findings include cutaneous sensory impairment of the lower limbs and perineum with sphincter disturbances. Motor impairment occurs less frequently, and associated pain is an inconstant feature. Enlargement of the caudal sac and dorsal arachnoid diverticula that erode the lamina and spinous processes are characteristic myelographic and computed tomographic findings. The pathogenesis of the cauda equina syndrome in ankylosing spondylitis remains unknown but may be due to demyelination, post-irradiation ischemia, or compression from spinal arachnoiditis.
Adult↗
Slowed motor conduction in lumbosacral nerve roots in cauda equina lesions: a new diagnostic technique.
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.
Adult↗
Angiotropic lymphoma (intravascular large cell lymphoma) presenting with cauda equina syndrome.
A 50-year-old man developed cauda equina syndrome of unknown etiology that was stable for 20 months. Two months prior to sudden death, he experienced new back pain, confusion, seizures, and multiple cranial nerve palsies. Neuropathologic examination revealed angiotropic lymphoma without parenchymal involvement or infarcts in the brain, spinal cord, and muscle. In addition, nerve roots in the cauda equina contained angiotropic lymphoma and infarcts of various ages. Angiotropic lymphoma should be considered as a cause of cauda equina syndrome and of disorders that affect the central and peripheral nervous systems concurrently.
Brain Neoplasms↗
Cauda equina syndrome after in situ arthrodesis for severe spondylolisthesis at the lumbosacral junction.
Relative stretching of the cauda equina over the posterosuperior border of the sacrum can be found in all patients who have Grade-III or IV spondylolisthesis at the lumbosacral junction. We identified twelve patients, all less than eighteen years old, who had cauda equina syndrome after in situ arthrodesis for Grade-III or IV lumbosacral spondylolisthesis. In all twelve patients, posterolateral arthrodesis had been done bilaterally through a midline or paraspinal muscle-splitting approach. Nothing in the operative reports suggested that the cauda equina had been directly injured during any of the procedures. Five of the twelve patients eventually recovered completely. The remaining seven patients had a permanent residual neurological deficit, manifested by complete or partial inability to control the bowel and bladder. If dysfunction of the root of the sacral nerve is noted preoperatively in a patient who has lumbosacral spondylolisthesis, decompression of the cauda equina concomitant with the arthrodesis should be considered. An acute cauda equina syndrome that follows a seemingly uneventful in situ arthrodesis for spondylolisthesis is best treated by an immediate decompression that includes resection of the posterosuperior rim of the dome of the sacrum and the adjacent intervertebral disc. In addition, posterior insertion of instrumentation and reduction of the lumbosacral spondylolisthesis should be considered.
Adolescent↗
1991 Volvo Award in experimental studies. Cauda equina syndrome: neurologic recovery following immediate, early, or late decompression.
An animal model of cauda equina syndrome was developed. Neurologic recovery was analyzed following immediate, early, and delayed decompression. Five experimental groups, each containing six dogs, were studied. Compression of the cauda equina was performed in all 30 dogs following an L6-7 laminectomy. The cauda equina was constricted by 75% in each group. The first group was constricted and immediately decompressed. The remaining groups were constricted for 1 hour, 6 hours, 24 hours, and 1 week, respectively, before being decompressed. Somatosensory evoked potentials were performed before and after surgery, before and immediately after decompression, and 6 weeks following decompression. Daily neurologic exams using the Tarlov grading scale were performed. At 6 weeks postdecompression, all dogs were killed, and the neural elements analyzed histologically. Following compression, all 30 dogs had significant lower extremity weakness, tail paralysis, and urinary incontinence. All dogs recovered significant motor function 6 weeks following decompression. The dogs with immediate decompression generally recovered neurologic function within 2-5 days. The dogs receiving 1-hour and 6-hour compression recovered within 5-7 days. The dogs receiving 24-hour compression remained paraparetic 5-7 days, with bladder dysfunction for 7-10 days and tail dysfunction persisting for 4 weeks. The dogs with compression for 1 week were paraparetic (Tarlov Grade 2 or 3) and incontinent during the duration of cauda equina compression. They recovered to walking by 1 week and Tarlov Grade 5 with bladder and tail control at the time of euthanasia. Immediately after compression, all five groups demonstrated at least 50% deterioration of the posterior tibial nerve evoked potential amplitudes.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Midline prolapse of a lumbar intervertebral disc with compression of the cauda equina.
Midline prolapse of a disc causing compression of the cauda equina is rare but needs urgent diagnosis and surgical treatment. The onset of bladder and rectal paralysis with saddle anaesthesia should be viewed with a high index of suspicion in a patient with backache and sciatica. Eight cases were seen over a period of five years, and they fell into three clinical groups. Group I patients presented with a sudden onset without any previous symptoms related to the back. Group II patients had a history of recurrent episodes of backache and sciatica, the latest episode resulting in involvement of the cauda equina. The group III patient was indistinguishable from one with a tumour as he presented with backache and sciatica slowly progressing to paralysis of the cauda equina. The prolapse was at the disc between L5 and S1 vertebrae in 50 per cent of the patients, most of whom did not have any limitation of straight leg raising. Urgent myelography and equally urgent removal of the disc within two weeks of the onset of the symptoms resulted in almost complete motor and bladder recovery within five months after the operation in most cases. However, recovery of sensation and sexual function was incomplete even four years after the operation.
Adult↗
[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)
Aged↗
Spinal nerve root compression. Nutrition and function of the porcine cauda equina compressed in vivo.
A model for experimental studies of acute, graded compression of the cauda equina in pigs was presented (Olmarker et al. 1991a). Detailed analyses of the neural and vascular anatomy demonstrated a close resemblance to the human cauda equina. There were structural and vascular differences between spinal nerve roots and peripheral nerves that could contribute to differences in compression susceptibility between these two parts of the nervous system. The pressure transmission from the balloon to the nerve roots showed to have a high accuracy. The occlusion-pressures for the arterioles, capillaries and venules of the cauda equina were determined (Olmarker et al. 1989a). Arteriolar blood flow was stopped at a pressure close to the mean arterial blood pressure. Capillary blood flow was found to be dependent upon flow in the connected venules. The blood flow in some venules was found to be stopped at 5-10 mm Hg. However, venular occlusion pressures ranged from 5 to 60 mm Hg. Compression up to 200 mm Hg for 2 hours did not induce a "no-reflow" phenomenon when the compression was ended. However, a transient hyperemia was noted at all pressure/time relations studied, indicating nutritional deficit in the compressed segment during compression. Signs of edema were seen in nerve roots exposed to compression for 2 hours at either 50 or 200 mm Hg. The nutritional supply to the cauda equina was found to be impaired at low pressure levels (less than 10 mm Hg; Olmarker et al. 1990a). Diffusion from adjacent tissues with a better nutritional supply, including the cerebrospinal fluid, could thus not compensate completely for compression-induced effects on the transport of nutrients. However, a certain nutritional supply to the compressed segment was present even at 200 mm Hg compression. There were more pronounced effects on the nutritional supply induced by a rapid (0.05-0.1 sec.) than a slow (20 sec.) compression onset rate. Nutritional impairment was noted both within and outside the compressed nerve segment. An increase in vascular permeability was induced by compression at 50 mm Hg for 2 minutes (Olmarker et al. 1989b). The magnitude of this permeability increase was dependent on both the magnitude and the duration of compression. The permeability increase was more pronounced for the rapid than for the slow compression onset rate at all pressure/time relations studied. Reduction of muscle action potential (MAP) amplitude in tail muscles, after stimulation cranial to the compression zone, was induced by compression at 100 and 200 mm Hg for 2 hours (Olmarker et al. 1990b).(ABSTRACT TRUNCATED AT 400 WORDS)
Acute Disease↗
Hydrocephalus and cavernoma of the cauda equina.
The association of a tumor of the cauda equina and hydrocephalus is unusual. We report a case of hydrocephalus with normal pressure associated with an equally rare affliction, a cavernous angioma of the cauda equina, which regressed after surgical ablation. The physiological mechanism involved is discussed.
Aged↗
Aggressive oncocytic neuroendocrine tumour ('oncocytic paraganglioma') of the cauda equina.
An oncocytic neuroendocrine tumour ('oncocytic paraganglioma') of the cauda equina is reported. The tumour was predominantly intradural, with extension into and destruction of surrounding vertebral bone. The tumour had an organoid pattern, and the tumour cells had abundant non-argyrophilic eosinophilic cytoplasm. Immunocytochemical stains for neurone-specific enolase, S-100 protein, keratin and carcinoembryonic antigen were positive, but stains for glial fibrillary acidic protein were negative. On ultrastructural examination, there were numerous mitochondria and scattered 200 nm dense-core membrane-bound granules, that rarely clustered in small aggregates. Intermediate filaments were focally arranged in long compact bundles. The histogenesis of tumours reported as cauda equina paragangliomas is discussed.
Actin Cytoskeleton↗