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PubMedDate not supplied

Cauda equina syndrome with pagetic vertebral fusion. Clinical recovery under calcium-vitamin D supplementation plus clodronate after apparent failure of pamidronate and acquired resistance to etidronate.

A patient with an osteolytic L2-L3 pagetic block and pagetic lesions of L1 and the sacrum seen only as increased radionuclide activity became resistant to etidronate after the fifth course (5 mg/kg/d six months per year) and developed severe cauda equina syndrome (reduction in walking distance to 30 m and sphincter dysfunction) due primarily to vertebral hypertrophy. Five months after a ten-day course of intravenous pamidronate (22.5 mg/d), the clinical symptoms were unchanged, although the alkaline phosphatase level was down 50%. Oral clodronate (1,600 mg/day for six months per year) in combination with calcium and vitamin D supplementation dramatically improved the walking distance and sphincter disorders. Resolution of the neurological manifestations was complete after the second clodronate course. At last follow-up nine months after the fourth clodronate course, there was no evidence of a relapse and the alkaline phosphatase level was normal. The time course of events in this patient does not allow to affirm that pamidronate was ineffective and suggests that calcium and vitamin D supplementation improved mineralization of the pagetic block and enhanced the effect of bisphosphonate therapy.

Aged↗
PubMed2006

Cauda equina compression revealing brown tumor of the spine in a long-term hemodialysis patient.

Brown tumors, or osteoclastomas, are erosive bony lesions arising as a complication of hyperparathyroidism (HPT). In patients with end-stage renal disease (ESRD), brown tumors are classic skeletal manifestations usually seen in severe forms of secondary HPT. However, involvement of the spine is considered extremely rare. We report a long-term hemodialysis case, in which cauda equina compression developed due to a sacral brown tumor. A decompressive surgery and subtotal parathyroidectomy were indicated to preserve neurologic function, and to ensure remineralization of the lesion. This case illustrates that, though rare, brown tumors should be considered in uremic patients with neurological symptoms. Emergent decompressive surgery is required to remove pressure on neurological structures and to stabilize the spine.

Adult↗
PubMed1985

Diabetic Charcot spine as cauda equina syndrome: an unusual presentation.

Some 6% to 21% of Charcot joints occur in the spine. The underlying disease is usually tabes dorsalis, but diabetes mellitus is another etiology. Degeneration of spinal elements is accelerated and lumbar spinal stenosis with weakness may occur, as has been reported in tabetic arthropathy. The case presented is unusual in two respects: first, the Charcot spine was secondary to diabetic complications, which resulted in a compressive cauda equina syndrome; second, the patient presented with progressive paraparesis and bowel and bladder dysfunction but physical examination by several examiners revealed no clinically evident sensory abnormality. The patient had vague and inconsistent sensory complaints for several years preceding definitive workup, but the overall picture of his disease process only could be made following multiple laboratory, electrodiagnostic, microbiologic, and radiologic testing. The patient presented with subacute paraparesis, providing a wide differential diagnosis ranging from Guillain-Barré syndrome to spinal neoplasm. The physical, radiologic, laboratory, electrophysiologic, histologic/pathologic findings, treatment, and recovery status are included in this report.

Aged↗
PubMed1981

Arterial vascularization of the cauda equina.

UNLABELLED: Vascular injection of eleven perinates revealed that each lumbosacral spinal-nerve root received its intrinsic blood supply from both distal and proximal radicular arteries through which the blood flowed toward a mutual anastomosis in the proximal one-third of the root. Segmental arteries supplied the distal vessels while their proximal equivalents received blood from their respective anterior or dorsolateral spinal arteries, which derived their flow from the large, irregularly located medullary arteries. CLINICAL RELEVANCE: The region of relative hypovascularity formed below the conus by the combined areas of anastomoses in the cauda equina may provide an anatomical rationale for the suspected neuroischemic manifestations concurrent with degenerative changes in the lumbar spine.

Angiography↗
PubMed1992

[Lumbosacral instability. The cauda equina compression syndrome in dogs].

The literature review includes a short anatomical description of the lumbosacral area, etiology, symptoms, diagnosis and therapy of CECS. Two hundred and twenty-seven large-breed dogs were examined clinically, neurologically and radiologically for diseases of the lumbosacral area. Radiological findings, such as dorsal dislocation of L7, spondylosis deformans, sloped craniodorsal contour of S1, sclerosis of the cranial plate of S1 as well as narrowing and increased density of the intervertebral foramen L7/S1 were compared with clinical and neurological results. In 15 dogs dorsal dislocation of L7 by 1 to 8 mm was found. An extended position proved to be more successful in demonstrating that finding than the flexed one. All other pathological changes were found either individually or in combination in patients with lumbosacral spondylolisthesis. One hundred and thirty-six dogs showed no sign of dorsal dislocation but all the other described changes. All detected changes have to be interpreted as instability of the lumbosacral area and resultant chronic and degenerative pathological processes. A definite correlation between spondylolisthesis of L7/S1 and compression of the cauda equina could not be found on plain radiography.

Animals↗
PubMed1999

Laser-assisted diskectomy performed by an internist resulting in cauda equina syndrome.

An internist performed percutaneous laser-assisted diskectomies (PLADs) on a patient with a sequestrated disc and stenosis. Subspecialists who perform PLADs should be trained in patient selection and lumbar diskectomy techniques. Chymopapain, percutaneous nucleotome-assisted diskectomy, and PLADs are alternatives to microdiskectomy for the management of lumbar disc herniations. PLADs were performed at the L4-5/L5-S1 levels in a 38-year-old woman with magnetic resonance (MR)-documented L4-5 stenosis and disc disease. After PLADs, she developed a subacute cauda equina syndrome. Two months later, a neurosurgeon performed an L4-5 coronal hemilaminectomy with diskectomy. Within 6 postoperative weeks, she was neurologically intact. Only specialists trained in the selection, neurodiagnostic, and surgical management of lumbar disc disease should perform PLADs.

Adult↗
PubMed1991

Diagnosis and treatment of cauda equina entrapment in the vertical lamina fracture of lumbar burst fractures.

Posterior dural lacerations associated with lumbar burst fractures are caused by impaction of the dural sac into the vertical lamina fracture. Neural elements may be extruded outside of the dura and become entrapped in the lamina fracture. This diagnosis must be made before surgery and is based on the patient's clinical presentation, the fracture pattern, and the radiographic findings. Entrapped neural elements can be successfully extracted from the lamina fracture by an opening laminoplasty of the posterior neural arch. Patients with lumbar burst fractures and radiographic evidence of posterior displacement of the neural elements in the lamina fracture should undergo posterior exploration of the spinal canal, extraction of cauda equina neural elements, and repair of the dural laceration before any spinal reduction maneuver.

Adult↗
PubMed1996

Posterior limbus vertebral lesions causing lumbosacral radiculopathy and the cauda equina syndrome.

This report reviews our experience with spinal decompression for posterior limbus vertebral lesions or osteocartilaginous vertebral corner defects in the lumbar spine in 29 children and young adults. There were 19 male and 10 female patients with a mean age of 16.5 years (range, 9 to 24 years). Twenty-four patients were involved with various athletic activities. Clinical presentation included low back pain with a variable degree of radiculopathy in 25 patients and a cauda equina syndrome in four. The level of the affected spinal area was L1-2 in one patient, L2-3 in one, L3-4 in seven, L4-5 in 17, and L5-S1 in three. The preoperative imaging workup showed lateralised "non-calcified' or 'calcified' limbus vertebral defects in 13 patients and centrally displaced lesions in 16 patients. All patients underwent posterior spinal decompression with a slightly extended laminotomy, except for three patients who had a subsequent posterolateral fusion. All of the patients consequently returned to practice their favourite preoperative sport and lifestyle, but five discontinued their previous sports. We suggest that patients with posterior limbus vertebral lesions require careful diagnosis and therapy that are different from those with an ordinary lumbar disc herniation.

Adolescent↗
PubMedDate not supplied

Association of cauda equina compression on magnetic resonance images and clinical signs in dogs with degenerative lumbosacral stenosis.

Magnetic resonance imaging (MRI) was used to examine the lumbosacral spine of 27 dogs with degenerative lumbosacral stenosis. Four normal dogs were also similarly imaged. Compression of the soft-tissue structures within the vertebral canal at the lumbosacral space was assessed in two ways: by measuring dorsoventral diameter on T1-weighted sagittal images and cross-sectional area on transverse images. The severity of the clinical signs was compared to the severity of cauda equina compression. No significant correlation was found. It is concluded that degree of compression as determined by MRI at time of presentation is independent of disease severity.

Animals↗
PubMed2004

Intradural spinal metastasis of renal clear cell carcinoma causing cauda equina syndrome.

Metastasis of renal clear cell carcinoma to the spinal cord are quite rare. Intradural localization causing a cauda equina syndrome has been previously reported only in two cases. The present report details the clinical, surgical and neuroradiological findings of a third case requiring emergency surgery, and presents data available from a brief review of cases reported in the literature. From the data available in the literature, we suggest that cerebral and spinal MRI and PET imaging should be widely performed in the staging of patients treated for renal clear cell carcinoma, in order to early detect CNS involvement.

Adenocarcinoma, Clear Cell↗
PubMed1995

Intradural tumors of the cauda equina: a single institution review of clinical characteristics.

A retrospective review of 106 cases of intradural tumors of the cauda equina are presented, subdivided into 5 groups according to their histological characteristics. For each group the clinical course and long-term postoperative results were analyzed: it emerged that differential diagnosis between neurinomas, meningiomas or non-tumoral lesions is not possible based on clinical findings alone and that neuroradiological diagnosis is more accurate when MRI is employed. Long-term prognosis was always favorable with the exception of the group of ependymomas. Nevertheless, early diagnosis in the latter group of tumors gives excellent results because prognosis is apparently directly correlated to the length of preoperative clinical history.

Adolescent↗
PubMed2005

Persistent cauda equina syndrome with no identifiable facilitating condition after an uneventful single spinal administration of 0.5% hyperbaric bupivacaine.

We diagnosed cauda equina syndrome 15 h after uneventful single spinal administration of 0.5% hyperbaric bupivacaine 12.5 mg through a 27-gauge pencil-point type needle. No preexisting neurologic disorder was recorded. There was no pain or paresthesia during needle placement or drug injection. The sensory levels were bilateral, symmetric, and caudal to T8. Resolution of most of the symptoms occurred within a few days but some foot drop persisted for 2 yr after the procedure. Bupivacaine neurotoxicity is suggested by the absence of any other identifiable cause for this neurologic deficit.

Aged↗
PubMed1998

Effects of lidocaine on nucleus pulposus-induced nerve root injury. A neurophysiologic and histologic study of the pig cauda equina.

STUDY DESIGN: Application of autologous nucleus pulposus on nerve roots and treatment with local application of lidocaine in the pig. OBJECTIVES: Studies of the effects of lidocaine on nucleus pulposus-exposed nerve roots. SUMMARY OF BACKGROUND DATA: Nerve root infiltration may improve radicular symptoms beyond the pharmacologic duration of local anesthetics, but the mechanisms for this effect are not known. METHODS: Nucleus pulposus was harvested from a lumbar disc and placed onto the sacrococcygeal cauda equina in pigs. In Series 1, early lidocaine treatment of nucleus pulposus-induced nerve root injury, pigs received 2% lidocaine (n = 5) or saline (n = 5) before and after surgery. Nerve conduction velocity and histologic appearance were studied after 3 days. In Series 2, delayed lidocaine treatment of nucleus pulposus-induced nerve root injury, after 7 days 2% lidocaine was administered epidurally to nucleus pulposus-exposed (n = 4) and -nonexposed (n = 4) nerve roots. Nerve conduction velocity, muscle action potentials, and histologic appearance were assessed. RESULTS: In Series 1, early treatment with lidocaine limited the reduction in nerve conduction velocity. The epidural inflammation was less in lidocaine treated animals. In Series 2, nerve conduction velocity was lower in nucleus pulposus-exposed animals than in nonexposed animals. The initial reduction of nerve conduction velocity and muscle action potential was similar between the groups, but the recovery of muscle action potential was slower and less complete in nucleus pulposus-exposed nerve roots. There was minimal histologic nerve injury in both series and in both protocols. CONCLUSIONS: Early treatment with lidocaine may reduce nucleus pulposus-induced nerve root injury. Lidocaine induced a delayed recovery in nerve roots exposed to nucleus pulposus. Further studies are needed to clarify the therapeutic effects of nerve root infiltration and the pathophysiology of nucleus pulposus-induced nerve root injury.

Anesthetics, Local↗
PubMed1988

[Venous pressure in the vertebral venous plexus and its role in cauda equina claudication].

The venous pressure in the ascending lumbar vein was measured by catheter and pressure transducer to document venous stasis in degenerative lumbar spinal canal stenosis. Measurement of the pressure in the ascending lumbar vein at rest revealed a progressive rise of the mean pressure from the control group to the lumbar intervertebral disc herniation group, and the lumbar spinal canal stenosis (LSCS) group in ascending order. Pressure curve tracings showed a plateau accompanying increased abdominal pressure during the Valsalva maneuver. Phase 3 was defined as the recovery period of decreasing pressure which began with the release of abdominal compression and terminated with the return to the initial pressure. The duration of phase 3 was prolonged in LSCS (p less than 0.01). It followed that the prolonged phase 3 documented the existence of venous stasis and its extent in LSCS. It is conceivable that increased venous pressure in the lumbar vertebral venous plexus participates in the pathogenesis of cauda equina claudication in LSCS.

Adolescent↗
PubMed1990

Cauda equina neurinoma associated with normal pressure hydrocephalus--case report.

A 45-year-old male was hospitalized because of gait disturbance, urinary incontinence, and memory disturbance. A computed tomographic (CT) scan revealed dilatation of the cerebral ventricles, and a metrizamide CT scan showed reflux into all ventricles. Cerebrospinal fluid obtained at the time of metrizamide CT was highly xanthochromic. Myelograms demonstrated a tumor between the inferior portion of the fifth lumbar vertebra and that of the second sacral vertebra. After removal of a spinal tumor involving nerve fibers at the cauda equina, his symptoms disappeared and the spinal fluid protein normalized. Three months after surgery, a CT scan revealed reduction of cerebral ventricular size. There are 10 reported cases of spinal tumors resulting in normal pressure hydrocephalus. All these and present cases involved protein in the spinal fluid, which might have been the cause of the hydrocephalus.

Cauda Equina↗
PubMed2005

November 2004: intradural mass of the cauda equina in a woman in her early 60s.

November 2004. A 63-year-old woman presented with slowly aggravating lower back pain and recent urinary urge incontinence. MRI revealed a sharply-delineated, partly cystic intradural mass with inhomogenous contrast-enhancement and ectatic vessels at the upper pole. An ependymoma was suspected, and the tumor was resected in toto. Histologically, at first glance, the tumor strongly resembled an ependymoma, showing a monomorphic cellular pattern, perivascular pseudorosettes and ependymal canal-like structures. However, the finding of a delicate collagen capsule, compartmentation of tumor cells into zellballen and the presence of ganglionic cells were untypical. These features were indicative of a paraganglioma with a gangliocytic component. Immunoreactivity of the tumor cells for neuroendocrine antigens, the detection of GFAP-positive sustentacular cells and the ultrastructural confirmation of neurosecretory granules substantiated this diagnosis. The clinical, radiological and morphological similarity between ependymomas, which are far more common in the cauda equina region than paragangliomas, has led to substantial diagnostic confusion in the past.

Cauda Equina↗
PubMed1998

Cauda equina syndrome after incidental total spinal anesthesia with 2% lidocaine.

A 77 year-old male presented for a right popliteal distal vein bypass graft procedure with continuous epidural anesthesia and light general endotracheal anesthesia. After the uneventful placement of the epidural needle and catheter at the L2-L3 interspace, fentanyl 150 microg and a total of 72 ml of preservative-free 2% lidocaine with epinephrine was continually injected through the epidural catheter for the duration of the more than 5 hour procedure. At the end of the procedure, it was noted that the patient had developed total spinal anesthesia, and his pupils were fixed and dilated. Further examination confirmed that the catheter tip was placed in the subarachnoid space. The patient was unable to turn or sit up by himself for over 1 month. Over a 12-month period, he improved to walking with a quad cane, but he required self-catheterization. Although numerous factors were considered, neurotoxicity of 2% lidocaine solution has been discussed as the potential cause. We were unable to find any other factors that could have caused the cauda equina syndrome.

Aged↗