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PubMed2005

[Gadolinium enhancement of the cauda equina following ischemia of the lumbar cord].

Enhancement of the cauda equina is a well-recognized finding, in particular in patients with inflammatory diseases of the peripheral nervous system. However, we report an unusual case of a woman with an ischemic lesion in the lumbar intumescence who developed enhancement of the cauda equina 18 days after disease onset. Seventy-six days after the onset of illness, contrast uptake was no longer detectable. Severe injury to the motor neurons in the lumbar intumescence was evident clinically and electromyographically. We propose that the enhancement of the cauda equina was due to blood-nerve barrier disruption during Wallerian degeneration following ischemic injury to the motor neurons of the lumbar cord.

Adult↗
PubMed1979

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↗
PubMed1994

Radiographic features of cauda equina syndrome complicating ankylosing spondylitis.

Cauda equina syndrome is an uncommon complication of ankylosing spondylitis. The characteristics of this disease, as shown by plain radiography, computed tomography and magnetic resonance imaging (MRI) in a 56-year-old man, are described. The MRI features are pathognomonic, allowing accurate noninvasive diagnosis of the disorder.

Cauda Equina↗
PubMed1994

Reversible motor and sensory neurophysiological abnormalities in cauda equina claudication.

A case of cauda equina claudication with canal stenosis is presented. Neurophysiological studies show reversible changes during symptomatic and asymptomatic phases. The somatosensory evoked potential from the tibial nerve was reduced in amplitude. Central motor conduction time (CMCT) after transcranial magnetic stimulation of the brain was reversibly prolonged in the symptomatic phase. Reversible CMCT changes have not been previously shown. The findings are discussed in the light of the pathophysiology of ischaemic nerve.

Cauda Equina↗
PubMed1996

A study of motor and sensory evoked potentials in chronic cauda equina compression of the dog.

Previous experimental studies have shown the effects of acute compression of the spinal cord and peripheral nerve roots. Recently, however, a few studies of chronic compression of the cauda equina in animal models have been reported. The purpose of this study was to determine the long-term electrophysiologic changes resulting from chronic compression of the cauda equina in dogs. An animal model of lumbar spinal stenosis was prepared according to Delamarter's method. Four experimental groups, each containing six dogs, were studied. One group underwent only laminectomy of the sixth and seventh lumbar vertebrae; these animals served as controls. In the three other groups, a laminectomy was performed and the cauda equina was constricted by 25%, 50%, and 75%, respectively, to produce chronic compression. Weekly neurologic examinations were carried out, and the neurologic deficits were graded using a modified Tarlov system. Sensory, and motor evoked potentials were recorded preoperatively, immediately after constriction, and at 2 weeks and 1, 2, and 3 months postoperatively. The animals in the control group showed no changes in sensory or motor evoked potentials. The dogs in which the cauda equina had been constricted by 25% showed no neurologic deficits and only mild changes in sensory and motor evoked potentials. The dogs in which the cauda equina had been constricted by 50% showed mild initial motor weakness, and major changes in the evoked potentials. The dogs in which the cauda equina had been constricted by 75% showed significant weakness, paralysis of the tail, and urinary incontinence; all dogs were partially recovered by the 3rd month, but all still showed neurogenic changes in the evoked potentials. Sensory and motor evoked potentials revealed neurologic abnormalities before the appearance of neurologic signs and symptoms. Constriction of more than 50% was the critical point that resulted in complete loss or reduction of the evoked potentials and in neurologic deficits. Dogs in which motor and sensory evoked potentials recovered also showed gradual disappearance of neurologic symptoms and signs. Recovery of motor evoked potentials in particular was associated with complete disappearance of neurologic symptoms and signs. For accurate prognosis in cases of chronic cauda equina compression, a combined diagnostic study of sensory and motor evoked potentials is recommended.

Analysis of Variance↗
PubMed1992

[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↗
PubMed2000

Lumbar herniated disc presenting with cauda equina syndrome. Long-term follow-up of four cases.

BACKGROUND: Cauda equina syndrome is a relatively rare presenting symptom of lumbar herniated discs. Early operative decompression is advocated, but it may not always restore the bladder function. In such cases, knowing the long-term outcome of bladder or sphincter disturbances is quite useful in planning the management of these patients. METHODS: Hospital records of patients operated on for lumbar herniated discs were reviewed. Charts and imaging studies of those patients who presented with classic cauda equina syndrome were analyzed. RESULTS: There were 4 patients (2.8%) of 144 consecutive surgical series of lumbar disc herniation, whose presenting symptom was classic cauda equina syndrome. Postoperatively, the patients had been followed at the clinic for a mean period of 6.4 years. Certain characteristic findings were noted on patients' neurological and radiological examinations. Although the recovery process of bladder function was very slow, taking months to years, all four patients achieved almost normal voiding with no major impairment of daily activities. CONCLUSIONS: Even if short-term recovery of bladder function is poor after lumbar disc surgery for cauda equina syndrome, the long-term outcome is not necessarily so. We should follow up on these patients with such measures as intermittent self-catheterization and drug therapy, expecting slow but steady recovery of bladder and sphincter function.

Adult↗
PubMedDate not supplied

Cauda equina syndrome. Implications for the orthopaedic nurse in a clinical setting.

Cauda equina syndrome (CES) is a presentation of signs and symptoms that indicate nerve compression involving one or more of the nerve roots in the lumbar spine. The Clinical Nurse Specialist working in a general orthopaedic practice must become familiar with the presentation of CES to appropriately assess the patient and alert the physician. Prompt and accurate care of the patient is critical when cauda equina syndrome is suspected to minimize permanent nerve damage. This article describes the syndrome, its signs and symptoms, basic triage techniques, plan of care, and recovery for the patient with cauda equina syndrome.

Cauda Equina↗
PubMed1991

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↗
PubMed1990

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↗
PubMed2003

Non-Hodgkin's lymphoma involving the cauda equina and ocular cranial nerves: case reports and literature review.

Although rare, direct infiltration of the cauda equina by non-Hodgkin's lymphoma (NHL) must be considered as a potential cause of subacute onset paraplegia. We present two cases of lymphomatous involvement of the cauda equina presenting with subacute paraplegia, each associated with a palsy of an oculomotor nerve. We highlight the need to use gadolinium-enhanced magnetic resonance imaging (MRI) when investigating potential cauda equina lesions, since it is crucial in detecting and outlining the extent of disease. Differential diagnoses and treatment options for NHL involving the cauda equina are also discussed.

Abducens Nerve Diseases↗
PubMed2004

A rare case of metastatic renal cell carcinoma resembling a nerve sheath tumor of the cauda equina.

We present a rare case of solitary metastasis to the cauda equina from the kidney. The patient was a 68-year-old man with a two-year history of low back pain. His past medical history revealed a renal cell carcinoma diagnosed seven years earlier. His lumbosacral MR imaging showed a well-demarcated, intradural extramedullary mass at the L3 level. He underwent an L2-4 laminectomy. The operative findings of the tumor quite resembled that of a nerve sheath tumor. It did not infiltrate into the subarachnoid space and involved only one spinal nerve. Pathology of the tumor was a metastasis of the renal cell carcinoma. Only 10 cases with such a metastasis to the cauda equina have been reported in the English literature. We added the 11th and reviewed the literature with reference to tumor pathologies, clinical findings and route of metastasis to the cauda equina.

Aged↗
PubMed1998

[Radiogenic amyotrophy. Cauda equina lesion as a late radiation sequela].

PURPOSE: Course and pathophysiology of a typical syndrome after irradiation of the cauda equina were studied. PATIENTS AND MATERIALS: 7 patients with irradiation damage of the cauda equina were examined clinically and neurophysiologically. RESULTS: After a mean delay of 5 years and 6 months all patients developed an ascending lower motor neuron weakness of the legs without pain, in part accompanied with mild sensory and sphincter symptoms. Electromyography, evoked potentials and neurography were important for the differential diagnosis to tumor infiltration. The course was progredient. DISCUSSION: For a long time, the underlaying damage was thought to be in the anterior horn cell body. The course of the studied patients with additional sensory and vegetative symptoms implies for a direct bilateral damage of the cauda equina. A better term for the syndrome is "post-irradiation cauda-equina-syndrome".

Adult↗
PubMed2004

Primary primitive neuro-ectodermal tumor of cauda equina with intracranial seeding.

Primitive neuro-ectodermal tumor (PNET) of the cauda equina is a rare entity. 18 cases have been reported in the literature so far, including 4 cases with intracranial seeding. Moreover parenchymal involvement of brain has never been reported as a form of intracranial seeding from PNET of the cauda equina. A 31 year-old female patient, with PNET of cauda equina showing intracranial seeding 6 months after surgery, is presented in this report. To our knowledge, this is the first adult case of spinal cord PNET with parenchymal involvement of brain. The histopathological, clinical and radiological findings as well as treatment of the patient were evaluated.

Adult↗
PubMed1997

Posterior vertebral body erosion by arachnoid diverticula in cauda equina syndrome: an unusual manifestation of ankylosing spondylitis.

Cauda equina syndrome is an uncommon complication of longstanding ankylosing spondylitis. It is associated with dorsal arachnoid diverticula, which may erode the lamina and spinous processes of the bony lumbosacral spine. We describe a patient who developed cauda equina syndrome associated with the unusual finding of erosion of the posterior aspect of 2 vertebral bodies by arachnoid diverticula. This was clearly revealed by magnetic resonance imaging of the spine.

Aged↗
PubMed2005

Postoperative cauda equina syndrome in patients undergoing single-level lumbar microdiscectomy. Report of two cases.

Cauda equina syndrome is a well-documented complication of uneventful lumbar microdiscectomy. In the vast majority of cases, no radiological explanation can be obtained. In this paper, the authors report two cases of postoperative cauda equina syndrome in patients undergoing single-level de novo lumbar microdiscectomy in which intraoperative electrophysiological monitoring was used. In both patients, the amplitudes of cortical and subcortical intraoperative somatosensory evoked potentials (SSEPs) abruptly decreased during discectomy and foraminotomy. In the first patient, a slow, partial improvement of SSEPs was observed before the end of the operation, whereas no improvement was observed in the second patient. In the first case, clinical findings consistent with cauda equina syndrome were seen immediately postoperatively, whereas in the second one the symptoms developed within 1.5 hours after the procedure. Postoperative magnetic resonance images obtained in both patients, and a lumbar myelogram obtained in the second one revealed no signs of conus medullaris or nerve root compression. Both patients showed marked improvement after an intense course of rehabilitation. The authors' findings support the proposition that intraoperative SSEP monitoring may be useful in predicting the development of cauda equina syndrome in patients undergoing lumbar microdiscectomy. Nevertheless, further prospective clinical studies are necessary for validation of these findings.

Adult↗
PubMed2006

[Bilateral papilledema as the manifestation of Schwannoma of the cauda equina].

PURPOSE: A case of schwannoma of the cauda equina in which the initial manifestation was visual loss, due to papilledema, is described. OBSERVATION: A 56-year-old man presented a history of 1 month of progressively blurred vision. On examination, visual acuity was 20/1,000 due to bilateral papilledema without spinal symptoms or neurological signs. Brain computed tomography demonstrated a nonobstructive hydrocephalus. He underwent a ventriculoperitoneal shunt without improvement. One month later, he complained of disturbance while walking associated with lower back pain. A lumbar puncture revealed an increased opening pressure. Analysis of the cerebrospinal fluid demonstrated an elevated protein level (6.8 g/l). Spinal magnetic resonance imaging showed a neurinoma of the cauda equina. We performed complete surgical resection and the histopathology diagnosis was schwannoma. Neurological dysfunctions resolved except visual acuity due to bilateral optic atrophy. DISCUSSION: The association of papilledema and spinal tumor is an unusual but well-known phenomenon. Several theories have been proposed to explain the development of increased intracranial pressure in such cases but the exact physiopathology remains unknown. CONCLUSION: Spinal cord tumor should be considered when acute papilledema associated with normal brain computed tomography and high cerebrospinal fluid protein levels are encountered. Spinal magnetic resonance imaging should then be performed.

Blindness↗
PubMed2006

Bowel dysfunction in patients with cauda equina lesions.

Despite their serious sequels on bowel function, lesions of the cauda equina have not been previously systematically studied in larger patient populations. This was the aim of the present report. From the registrars of a diagnostic and rehabilitation centres 67 patients with clinical, electrodiagnostic and radiological findings supportive of the cauda equina lesions were recruited. The Slovene versions of the standard questionnaires for anal incontinence and constipation were used. The responses were scored, impairments categorized and previous treatments noted. Neurological examination, electromyography (EMG) of lumbo-sacral myotomes, quantitative anal sphincter EMG and electromyographic evaluation of the sacral reflex were performed. Severe anal incontinence/constipation was reported by 18%/0%, moderate by 36%/33%, and slight by 28%/43% of our patients. Twenty-one per cent of patients wore pads continuously and 14% occasionally. More than half of the patients (60%) reported changes in their lifestyle due to anal incontinence. No patient had completely normal findings on neurological examination. Perianal sensory loss correlated (P < 0.05) with anal incontinence and gender with constipation (women > men). Only two patients had received medical attention for bowel dysfunction. Study thus demonstrated significant bowel impairment in patients with lesions of the cauda equina, which has received insufficient medical attention.

Adult↗