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PubMed1999

Nutritional supply to the cauda equina in lumbar adhesive arachnoiditis in rats.

Laminectomy-induced cauda equina adhesion has been proved by rat experiments and postoperative serial MRI in humans. A degenerative change of the cauda equina has been proved when cauda equina adhesion has been prolonged. Since it has not been reported how the nutritional supply is changed in such a condition, we evaluated the glucose supply to the adhered cauda equina in rats. Wistar rats were divided into the following three groups: the control group which received no operation, the laminectomy group which underwent L5-L6 laminectomy only, and the koalin group which received 5 mg of kaolin on the dorsal extradural space following L5-L6 laminectomy. Based on 3H-methyl-glucose uptake study, we analyzed (1) glucose transport from the intraneural vessels to the nerve tissue, and (2) glucose transport from the cerebrospinal fluid to the nerve tissue. We evaluated the relation between the severity of cauda equina adhesion and 3H uptake into the cauda equina. Cauda equina adhesion was observed in 2 of 12 rats in the control group, in 3 of 12 rats in the laminectomy group, and in 18 of 20 rats in the kaolin group. In the 3H-methyl-glucose uptake study, at 12 weeks the glucose transport to the cauda equina from the vessels increased by 44%, and that from the cerebrospinal fluid decreased by 64% in the kaolin group compared with the control group. In the condition of complete cauda equina adhesion, the glucose transport to the cauda equina from the vessels increased by 53% and that from the cerebrospinal fluid remarkably decreased by 72% compared with the normal cauda equina. Considering the greater nutritional importance of the cerebrospinal fluid in the cauda equina, it is most likely that the impairment of nutritional supply to adhered cauda equina may lead to eventual neural degeneration.

Animal Nutritional Physiological Phenomena↗
PubMed1990

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↗
PubMed1996

Lumboperitoneal shunt for cauda equina syndrome in ankylosing spondylitis.

Cauda equina syndrome is a rare complication in the late stage of ankylosing spondylitis, for which approximately 60 cases have been reported in the literature. The cause of the syndrome is unclear, and there is no effective treatment. Recently lumboperitoneal shunt was reported to have been effective in two patients. In our study, we performed lumboperitoneal shunt in a patient and evaluated the condition after the operation compared with that preoperatively. Some alleviation of neurologic symptoms was observed for 6 months after operation. Histopathologic examination of the dural diverticulum revealed a residual change after old inflammation. Lumboperitoneal shunt was an effective surgical treatment for cauda equina syndrome in this patient with ankylosing spondylitis, but its effects were not extreme. Arachnoiditis is suggested to be involved in the pathogenesis of cauda equina syndrome.

Cauda Equina↗
PubMed1999

Plexiform neurofibroma of the cauda equina. Case report.

Plexiform neurofibroma of the cauda equina has been reported only twice previously. The authors report the first pediatric patient in whom such a tumor has been found. A 4-year-old boy presented with low-back pain that radiated bilaterally into the L-4 and L-5 dermatomes. A dermal sinus noted at the midthoracic level was surrounded by a hemangiomatous lesion. Magnetic resonance imaging confirmed the presence of the dermal sinus and revealed a well-defined lumbosacral mass that showed heterogeneous intensity with irregular enhancement. Intraoperatively, a solid mass, which engulfed the entire cauda equina, could not be dissected from the roots. The dermal sinus tract, however, was excised from the thoracic spine. The patient underwent radiotherapy to control the tumor and relieve his pain. Plexiform neurofibromas of the cauda equina are characterized by an insidious and progressive clinical course. The tumor mass may engulf all the roots of the cauda equina. No plexiform neurofibroma of the cauda equina has been reported to be associated with neurofibromatosis Type 1. The authors assume that the thoracic-level dermal sinus observed in this child was an incidental finding.

Cauda Equina↗
PubMed2003

Autonomic and motor neuron death is progressive and parallel in a lumbosacral ventral root avulsion model of cauda equina injury.

Injuries to the cauda equina of the spinal cord result in autonomic and motor neuron dysfunction. We developed a rodent lumbosacral ventral root avulsion injury model of cauda equina injury to investigate the lesion effect in the spinal cord. We studied the retrograde effects of a unilateral L5-S2 ventral root avulsion on efferent preganglionic parasympathetic neurons (PPNs) and pelvic motoneurons in the L6 and S1 segments at 1, 2, 4, and 6 weeks postoperatively in the adult male rat. We used Fluoro-Gold-prelabeling techniques, immunohistochemistry, and quantitative stereologic analysis to show an injury-induced progressive and parallel death of PPNs and motoneurons. At 6 weeks after injury, only 22% of PPNs and 16% of motoneurons remained. Furthermore, of the neurons that survived at 6 weeks, the soma volume was reduced by 25% in PPNs and 50% in motoneurons. Choline acetyltransferase (ChAT) protein was expressed in only 30% of PPNs, but 80% of motoneurons remaining at 1 week postoperatively, suggesting early differential effects between these two neuronal types. However, all remaining PPNs and motoneurons were ChAT positive at 4 weeks postoperatively. Nuclear condensation and cleaved caspase-3 were detected in axotomized PPNs and motoneurons, suggesting apoptosis as a contributing mechanism of the neural death. We conclude that lumbosacral ventral root avulsions progressively deplete autonomic and motor neurons. The findings suggest that early neuroprotection will be an important consideration in future attempts of treating acute cauda equina injuries.

Animals↗
PubMed2001

Cauda equina syndrome.

Single or double-level compression of the lumbosacral nerve roots located in the dural sac results in a polyradicular symptomatology clinically diagnosed as cauda equina syndrome. The cauda equina nerve roots provide the sensory and motor innervation of most of the lower extremities, the pelvic floor and the sphincters. Therefore, in a fully developed cauda equina syndrome, multiple signs of sensory disorders may appear. These disorders include low-back pain, saddle anesthesia, bilateral sciatica, then motor weakness of the lower extremities or chronic paraplegia and, bladder dysfunction. Multiple etiologies can cause the cauda equina syndrome. Among them, non-neoplastic compressive etiologies such as herniated lumbosacral discs and spinal stenosis and spinal neoplasms play a significant role in the development of the cauda equina syndrome. Non-compressive etiologies of the cauda equina syndrome include ischemic insults, inflammatory conditions, spinal arachnoiditis and other infectious etiologies. The use of canine, porcine and rat models mimicking the cauda equina syndrome enabled discovery of the effects of the compression on nerve root neural and vascular anatomy, the impairment of impulse propagation and the changes of the neurotransmitters in the spinal cord after compression of cauda equina. The involvement of intrinsic spinal cord neurons in the compression-induced cauda equina syndrome includes anterograde, retrograde and transneuronal degeneration in the lumbosacral segments. Prominent changes of NADPH diaphorase exhibiting, Fos-like immunoreactive and heat shock protein HSP72 were detected in the lumbosacral segments in a short-and long-lasting compression of the cauda equina in the dog. Developments in the diagnosis and treatment of patients with back pain, sciatica and with a herniated lumbar disc are mentioned, including many treatment options available.

Animals↗
PubMed1997

Lumbar spinal canal stenosis examined electrophysiologically in a rat model of chronic cauda equina compression.

STUDY DESIGN: A model of chronic cauda equina compression with conductive stress was studied electrophysiologically. OBJECTIVE: To analyze the pathophysiology arising from chronic compression electrophysiologically. SUMMARY OF BACKGROUND DATA: This rat model of cauda equina compression that is chronic, not acute, has been reported elsewhere. METHODS: A stainless steel wire and plate were fastened to the spine at L5 of 8 rats 3 weeks old. One year later, the ascending and descending nerve action potentials were recorded and the conduction velocities (CVs) were measured. Electrophysiologic changes after high-frequency stimulation (HFS) were observed. RESULTS: The waveform of the ascending cauda equina action potential at the cauda equina had three peaks, and that at the conus medullaris had a peak followed by a broad wave. The waveform of the descending nerve action potential had two peaks. The mean ascending and descending CVs of the treated rats were slower (P < 0.001) than those of the control rats. In the control rats, the mean CV and mean amplitude after HFS decreased slightly and returned to normal within 30 seconds, and the waveform was unchanged. In treated rats, the mean CV decreased after HFS but returned to normal within 10 minutes. The mean amplitude decreased after HFS and did not return to normal within 10 minutes. The waveform was unchanged. CONCLUSIONS: Because the differences between treated and control rats in amplitude (and CVs) were greater before HFS than after HFS, we concluded that treated rats had disturbance of the blood flow in vessels around the nerves of the cauda equina with histologic damage. In human patients, such disturbance may be one cause of intermittent claudication.

Action Potentials↗
PubMed1997

Postlaminectomy adhesion of the cauda equina. Changes of postoperative vascular permeability of the equina in rats.

STUDY DESIGN: The authors evaluated the vascular permeability changes of the cauda equina after lumbar laminectomy in rats. OBJECTIVES: To clarify the early vascular responses in postlaminectomy adhesive arachnoiditis. SUMMARY OF BACKGROUND DATA: Laminectomy-induced cauda equina adhesion has been visualized by postoperative serial magnetic resonance imaging in humans. In laminectomized rats, fibrinous exudation was apparent among the adhered cauda equina. To date, there has been no report of substantial changes in vascular permeability in the cauda equina after lumbar laminectomy. METHODS: Wistar rats laminectomized from L5-L6 were used for four studies; 1) Evans blue albumin tracer study; 2) horseradish peroxidase tracer study; 3) lanthanum tracer study; and 4) fluoroscein isothiocyanate-dextran (molecular weights: 20K, 70K, and 150K) tracer study. Untreated rats were used as controls. RESULTS: 1) In the laminectomized (L5-L6) area, the cauda equina tended to conglomerate from 3 hours after surgery; this was relatively resolved by 6 weeks. Extravascular leakage of Evans blue albumin in the cauda equina appeared at 3 hours after surgery and reached a plateau at 24 hours; it mostly disappeared by 6 weeks. At 24 hours after surgery, the extent of Evans blue albumin extravasation was seen in one or more levels adjacent to the laminectomized area. Evans blue albumin leakage and cauda equina adhesion started to appear in nearly a same phase after laminectomy, followed by a plateau of vascular permeability facilitating complete cauda equina adhesion by 24 hours after surgery. The restoration of Evans blue albumin leakage was noted 1 week after surgery, and tended to precede recovery of the cauda equina adhesion; 2) in the laminectomy group, Horseradish peroxidase penetrated from the lumen to the extracellular space beyond the basal laminae of the endothelial cells. Numerous horseradish peroxidase-labeled vesicles in the endothelial cells were found; 3) There was a significant increase in lanthanum distribution in the endothelial cytoplasm at the laminectomized levels. Lanthanum filled the interendothelial clefts beyond the tight junction, but did not penetrate through the perivascular basal laminae; 4) Fluoroscein isothiocyanate-dextran (20K, 70K, 150K) permeability increased in the laminectomy group, but there was no difference in extravasation of fluoroscein isothiocyanate-dextran, irrespective of the molecular weight. CONCLUSION: Laminectomy consistently induced an increase in vascular permeability in the cauda equina, an increase of vesicular transport in the endothelial cell, and opening of the tight junction early after laminectomy, suggesting breakdown of the blood nerve barrier in the cauda equina. The accelerated permeability may enhance cauda equina adhesion.

Animals↗
PubMedDate not supplied

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↗
PubMed1996

MRI demonstration of arachnoiditis in cauda equina syndrome of ankylosing spondylitis.

The cauda equina syndrome is a rare but well-recognised complication of longstanding ankylosing spondylitis, usually presenting when the joint disease is quiescent. The clinical and radiological findings in a patient with only a 3-year history, in whom the onset of joint and neurological symptoms was apparently simultaneous, are presented. MRI revealed characteristic expansion of the lumbar spinal canal with scalloping of the pedicles, laminae and spinous processes, related to numerous posterior dural diverticula. The quantity and extent of such diverticula are unusual. We demonstrated adherence of individual nerve roots to the arachnoid surface of these diverticula and to each other. In a second patient, with a much longer history of both ankylosing spondylitis and cauda equina syndrome, MRI again showed florid, multilocular dural ectasia, marked irregularity and thickening of nerves, and adherence to the dural diverticula. These cases provide evidence for the role of arachnoiditis in the pathogenesis of the cauda equina syndrome of ankylosing spondylitis.

Aged↗
PubMed1985

Intradural cyst with compression of the cauda equina in ankylosing spondylitis.

A cauda equina syndrome complicating long-standing ankylosing spondylitis was found to be due to a large multiloculated cyst. This differed from posterior dural diverticula identified in similar cases in that the cyst filled the lumbar canal with erosion of the upper lumbar vertebral bodies and chronic inflammatory changes were evident in the cyst wall. Cauda equina compromise in ankylosing spondylitis has several possible mechanisms including fibrosis following arachnoiditis, root damage by dural diverticula, and direct compression by arachnoid cyst.

Aged↗
PubMed2000

Medical realities of cauda equina syndrome secondary to lumbar disc herniation.

STUDY DESIGN: An analysis of 44 cauda equina syndrome cases. OBJECTIVES: To determine the neurologic outcome of cauda equina syndrome cases, in light of the significant medical implications of this disorder. SUMMARY OF BACKGROUND DATA: Cauda equina syndrome from lumbar disc herniation accounts for up to 1% of all disc herniations. Most of the literature supports surgery within 24 hours as a means of improving the outcome. METHODS: A retrospective chi 2 analysis was performed of 44 patients surgically treated for lumbar disc herniation who initially sought treatment for cauda equina syndrome. RESULTS: In 20 patients, diagnosis was made and surgery performed within 48 hours of the cauda equina syndrome onset, including 18 patients (90%) who underwent surgery within 24 hours. In 24 patients, surgery was performed more than 48 hours after the onset of cauda equina syndrome, with a mean delay of 9 days, including 17 patients (71%) with a mean delay of 3.7 days. Causes for delay were patient-related in 4 cases (17%) and physician-related in 20 cases (83%). According to chi 2 analysis, a greater chance of persistent bladder/sphincter problem (P = 0.008), persistent severe motor deficit (P = 0.006), persistent pain (P = 0.025), and sexual dysfunction (P = 0.006) existed with delayed surgery. CONCLUSION: The data strongly support the management of cauda equina syndrome from lumbar disc herniation as a diagnostic and surgical emergency.

Adult↗
PubMed2003

Utility of intraoperative ultrasound for tumors of the cauda equina.

STUDY DESIGN: A retrospective chart review of patients with tumors of the cauda equina was performed. OBJECTIVES: To assess the role of intraoperative ultrasound for detecting tumor migration and modifying the approach to cauda equina tumors. SUMMARY OF BACKGROUND DATA: Rostral migration of cauda equina tumors relative to preoperative imaging is well described. The utility of intraoperative ultrasound to identify tumor migration and to modify the surgical approach was analyzed. METHODS: The medical records of nine consecutive patients undergoing biopsy or resection of a cauda equina tumor diagnosed by magnetic resonance imaging at the authors' institution from January 1994 through December 2000 were reviewed. Four patients with tumors of the cauda equina underwent transdural sonography of the intraspinal compartment after initial laminectomy and before durotomy. RESULTS: In three patients, the findings on intraoperative ultrasound showed rostral migration of the lesion with respect to the preoperative magnetic resonance imaging, necessitating additional laminectomy and modifying the site of durotomy. One tumor had migrated rostrally one full bony vertebral segment, whereas two tumors each had migrated one half of a bony vertebral segment. Pathology examination in the three patients whose lesions had migrated rostrally demonstrated a schwannoma in every case. In one patient, intraoperative ultrasound showed no lesion migration with respect to the preoperative magnetic resonance imaging, and no modifications to the surgical approach were needed. Pathology examination of this patient demonstrated an ependymoma. CONCLUSIONS: Intraoperative ultrasound was useful in documenting rostral migration of cauda equina tumors, and facilitated appropriate laminectomy and durotomy. The technique may be particularly valuable for schwannomas of the cauda equina, which seem to have a greater potential for rostral migration.

Adenocarcinoma↗
PubMed1990

[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↗
PubMed2004

Experimental spinal stenosis: relationship between degree of cauda equina compression, neuropathology, and pain.

STUDY DESIGN: An analysis of pathologic changes after different degrees of cauda equina compression. OBJECTIVES: To explore the association between the degree of the cauda equina compression and the extent of pathologic change, expression of tumor necrosis factor (TNF-alpha), and neuropathic pain. To compare with distal nerve compression injury. SUMMARY OF BACKGROUND DATA: Compression of the cauda equina reduces blood flow in compressed nerve roots and causes TNF-alpha expression and neuropathological change. In peripheral nerve, expression of TNF-alpha in Schwann cells is associated with primary demyelination without pain while TNF-alpha expression by macrophages is associated with axonal (Wallerian) degeneration and pain. METHODS: Two square-shaped pieces of silicon were placed into the fourth and sixth epidural space in rats. Various sized silicon was used in each group (mild, moderate, and strong compression groups), while no silicon was used in the sham-operated group. Mechanical allodynia was determined by the von Frey test. Comparisons of the number of TNF-alpha- and apoptosis-positive cells were made using immunohistochemistry. RESULTS: There was no significant mechanical allodynia observed in any group. Some nerve roots showed demyelination following mild cauda equina compression. Axonal degeneration was observed in the moderate and strong cauda equina compression groups. TNF-alpha-immunoreactive cells were increased in all compression groups. Apoptosis of dorsal root ganglion cells was less than apoptosis in the spinal cord. CONCLUSION: Mild cauda equina compression induces TNF-alpha expression and demyelination. Moderate and strong cauda equina compression induces TNF-alpha expression and degeneration associated with macrophage invasion. Neither demyelination nor degeneration in the cauda equina induced mechanical allodynia. Nerve lesions proximal to the dorsal root ganglion do not produce significant mechanical allodynia. Dorsal root ganglion apoptosis may be important for pain.

Animals↗