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We present a case of spinal subarachnoid hemorrhage due to an ependymoma of the filum terminale in a 23-year-old male. Clinical signs indicating a spinal origin of the subarachnoid hemorrhage are discussed. Subarachnoid hemorrhages are only rarely caused by an intraspinal tumor, most of which are located in the cauda equina. Our findings in this case proved the value of MRI examination in tumors of the cauda equina.
Nerve root enhancement of the cauda equina occurs in Guillain-Barré syndrome (GBS), but the frequency, diagnostic value, and meaning of this finding is unknown. We prospectively obtained gadolinium-enhanced lumbosacral spine MRIs in 24 consecutive patients with acute GBS and blindly rated nerve root enhancement as absent, mild, or prominent. The MRIs were obtained 13 days, mean, after onset of symptoms (range 2 to 42 days). Twenty of 24 patients had cauda equina nerve root enhancement, which was mild in 6 and prominent in 14. Eighteen of 19 with "typical" GBS had enhancement, compared with 2 of 5 with a variant presentation. Sixty percent of patients with prominent enhancement had severe back or leg pain in contrast to 10% of patients with mild or no enhancement. The GBS disability grade (0 to 5 scale) was higher in patients with prominent enhancement, and significantly fewer patients with prominent nerve root enhancement could walk independently by 2 months. There was no relationship between nerve root enhancement and the timing of the MRI, CSF protein, any of several EMG abnormalities, duration of hospitalization, mean disability grade at 2 months, or the time required for patients to improve to grade 2. In two patients, the EMGs at 11 and 20 days, respectively, were normal except for slightly prolonged F-responses and neurogenic recruitment, but there were prominent nerve root enhancement and an elevated CSF protein. Enhancement of the cauda equina nerve roots with gadolinium on lumbosacral MRI is 83% sensitive of acute GBS and was present in 95% of typical cases. This finding may be useful when electrophysiologic abnormalities are equivocal. In addition, conspicuous nerve root enhancement correlates with pain, GBS disability grade, and duration of recovery.
OBJECTIVE: Isolated intramedullary spinal cord or cauda equina involvement by sarcoidosis is quite rare. We report three patients with intraspinal sarcoidosis and absent systemic manifestations of the disease. The clinical presentation, operative management, electrophysiologic studies, pathology, laboratory investigations, and current therapy are discussed with attention to the previous literature. METHODS: Two of the three patients had a preoperative diagnosis of a cervical intramedullary spinal cord tumor. The third patient had the preoperative diagnosis of an infectious process involving the cauda equina. Magnetic resonance imaging (MRI) with gadolinium did not suggest an inflammatory process. Intraoperative somatosensory evoked potential performed in two patients exhibited normal amplitudes, but a prolonged latency in seven out of eight extremities; with normal central conduction time suggesting a peripheral or radicular involvement. All three patients underwent laminectomy and biopsy of the intraspinal pathology. RESULTS: Pathologic examination demonstrated sarcoidosis in all three patients. Intraoperative observations, intramedullary nodules, and thickening of the meninges were inconsistent with neoplasm and limited the surgical procedure to a biopsy. Frozen sections performed at two of the operations revealed an inflammatory process that confirmed the intraoperative observations. Postoperatively, the diagnostic work-up for all patients was negative for systemic manifestations. CONCLUSIONS: Isolated intraspinal sarcoidosis is a rare process. The current management for intramedullary spinal cord or cauda equina sarcoidosis is prolonged corticosteroids. The surgeon should not attempt complete resection if this granulomatous process is suspected.
AIM OF THE STUDY: In patients with cauda equina or conus medullaris lesions, bilateral electromyographic (EMG) examination of the subcutaneous external anal sphincter (EAS) muscles has been suggested. In spite of its circular shape, EAS should be considered as two separate semicircular muscles. The aim of the present study was to test the hypothesis that information obtained by bilateral examination of the EAS muscle outweighs inconvenience due to additional needle insertions. PATIENTS AND METHODS: A group of 67 patients with clinical and radiological data supportive of cauda equina or conus medullaris lesion was studied. From the subcutaneous EAS muscles motor unit potentials (MUPs) were sampled by the standard concentric EMG needle electrode, and an advanced EMG system with template operated multi-MUP analysis. Severity of EMG abnormalities was determined, and compared in 48 pairs of the left/right subcutaneous EAS muscles. RESULTS: In 18 patients, bilateral EMG abnormalities were found, in five of them asymmetry of involvement was demonstrated. Unilateral MUP abnormalities were found in 22 patients. The sensitivity of unilateral EMG analysis was 57% and of bilateral examination, 83%. CONCLUSION: In patients with suspected cauda equina lesions, as a rule, bilateral EMG of the subcutaneous EAS muscle is recommended.
OBJECTIVE AND IMPORTANCE: Tumoral calcinosis is a rare disorder of unknown origin. Tumoral calcinosis involving the spine is extremely rare. This is the first case of tumoral calcinosis localized in the dura mater of the lumbar spine. CLINICAL PRESENTATION: This 55-year-old male patient presented with tumoral calcinosis of the lumbar meninges. T1-weighted, sagittal magnetic resonance imaging scans of the lumbar spine revealed a round mass of slightly increased intensity with high-intensity margins, located posterior to the cauda equina at the L4-L5 level. The cauda equina was severely compressed anteriorly. T2-weighted scans revealed that the mass was composed of a high-intensity area with low-intensity margins. T1-weighted magnetic resonance imaging scans obtained after intravenous gadolinium administration revealed some enhancement at the margins. INTERVENTION: The mass lesion was totally resected. Three years after surgery, no recurrence was observed in follow-up magnetic resonance imaging scans. CONCLUSION: Although tumoral calcinosis is a rare cause of mass lesions of the lumbar spine, it should be considered in differential diagnoses. If the lesion can be totally resected, the prognosis should be good, similar to that for general tumoral calcinosis.
A 54-year-old man with a history of partially dissected epidermoid cyst in the left cerebellopontine angle suffered from a slowly progressive dysesthesia and weakness in the lower extremities and trunk. Neurological examination revealed segmental muscular weakness and sensory disturbance in those regions, giving rise to the possibility of monoradiculopathy multiplex, as well as loss of tendon reflexes, dysuria and right facial nerve palsy. Electrophysiological studies indicated irregular motor axonopathy or neuronopathy and interruption of more central sensory pathways than the lumbosacral spinal nerve roots with spared peripheral sensory nerves. Although MRI demonstrated enhanced lesions in the cauda equina and lumbosacral leptomeninges, CSF cytology or a cauda equina biopsy showed no malignancy. His symptoms gradually progressed and he died 15 months after the onset. The autopsy failed to reveal any tumors in the general systemic internal organs. Histopathology demonstrated meningeal carcinomatosis with squamous-type carcinoma cells scattered in the cerebrospinal leptomeninges, and perineurium in almost all the spinal and cranial nerve roots, causing severe axonal degeneration. The dorsal root ganglions escaped tumor cell invasion. Absence of the malignant tumors in the systemic organs and the history of the operated epidermoid cyst indicate that the tumor may be the cause of the meningeal carcinomatosis in this case. Meningeal carcinomatosis almost always shows rapid progression and extremely poor prognosis with several month survival in general, and little attention has been paid that it can exhibit symptoms and signs of segmental involvement in the lumbosacral regions. Our present case prompts us to bear in mind that patients with this condition can survive fairly long, and raises the possibility that a careful neurological examination with segmental involvement will reveal such a feature more frequently than considered so far in this condition.
A case of chondrosarcoma of the spine in a 15-year-old female patient has been described. The tumor was localized within the body of S1 and it partially involved the left wing of the ilium. The radiological condition corresponded with the so-called "ivory vertebra". The symptoms of compression of the cauda equina took the lead. Surgical decompression of the cauda equina was performed and an attempt of resection of the tumor was undertaken but it failed because of extension of the process. The further course of the disease, in spite of radiotherapy, was exceptionally malignant and within several months, the process became generalized.
The cases of four patients with intermittent claudication due to compression of the cauda equina are reported. The cause of this syndrome is considered to be a compression of the cauda equina by a thickening of the ligamentum flavum. The clinical, neuro-radiological and surgical characteristics are discussed.
The tethered spinal cord syndrome is more often encountered in children, but does also occur in adults. Its clinical spectrum comprises low back pain, neurological deficits such as distal motor weakness and trophic and sensory disturbances in the legs, urological symptoms and such musculoskeletal signs as scoliosis or foot deformities. In addition, cutaneous lesions or subcutaneous lipomas in the lumbosacral region may be indirect signs of an intraspinal pathology. This consists in a tight, thickened and sometimes shortened filum terminale, an intraspinal lipoma, intradural scar formation or other lesions that lead to conus fixation. The common mechanism of injury of these types of pathologies is an impairment of longitudinal movement of the spinal cord, especially the conus medullaris, which subsequently leads to chronic local ischemia. Diagnosis is most readily achieved by magnetic resonance imaging. Treatment is aimed at the restoration of cord mobility by means of microsurgical release of the conus, the cauda equina and the filum terminale with the aid of cauda equina neuromonitoring. Further progression can be effectively halted; in fact almost half of the patient actually improve. Therefore, every patients presenting with the clinical diagnosis of tethered cord syndrome should be offered specialized surgical treatment.
Although most workers who sustain lower back can be managed without surgery, a carefully selected subset of patients benefit from operative intervention. When evaluating these patients, care must be taken to identify surgical emergencies, including patients with cauda equina syndrome and progressive neurologic deficits and patients with cauda equina syndrome and progressive neurologic deficits and patients with certain historical red flags that should prompt further evaluation. Conditions that may benefit from surgery include lumbar disc herniations, discogenic back pain, spinal stenosis, and spondylolisthesis. This article reviews the indications for surgery in injured workers and expected postoperative outcomes.
Arachnoiditis ossificans is uncommon and has been reported to occur in areas surrounding the brain stem, the spinal cord, and the cauda equina. Predisposing etiologic factors include vascular anomalies, spinal anesthetics, and meningitis. This report adds a case of arachnoiditis ossificans about the cauda equina occurring after septic complications following laminectomy. Surgical excision of the ossific tissue resulted in clinical improvement.
The role of peripheral parasympathetic and sympathetic pathways was explored in erectile responses elicited by hypothalamic medial preoptic area (MPOA) stimulation in adult male anesthetized rats. Under control conditions, MPOA stimulation reliably elicited erectile responses evidenced by an increase of the intracavernous pressure-to-blood pressure ratio. The erectile response was abolished by 1) acute bilateral section of cavernous or pelvic nerves or cauda equina and 2) chronic lesions of pelvic nerves or cauda equina. Acute section of the hypogastric nerve did not significantly decrease the erectile response. The erectile response was significantly depressed after acute or chronic sections of the paravertebral sympathetic chain at the L4-L5 level or chemical sympathectomy with 6-hydroxydopamine. The decrease due to acute sympathetic chain lesion was reversed by bilateral ligation of the external iliac arteries. Accordingly MPOA stimulation elicits erectile responses via 1) activation of the parasympathetic outflow conveyed by the pelvic and cavernous nerves and 2) activation of neural fibers conveyed by the sympathetic pathways. We propose that sympathetic fibers running in the paravertebral sympathetic chain are responsible for vasoconstriction of nonpenile areas to divert blood to the penis, allowing the dramatic increase of penile arterial inflow required for erection.
A cauda equina syndrome in association with ankylosing spondylitis is well recorded. We report the occurrence of an upper limb radiculopathy which progressed to a cauda equina syndrome in association with ankylosing spondylitis.
Thirty-one children under the age of 13 years with spinal cord and cauda equina compression are presented. Some of these cases are used to illustrate the problems encountered in the early recognition of compressive lesions involving the spinal cord and cauda equina in the paediatric age group.
The complications of surgical treatment for lumbar disc herniation (LDH) are important to know, but hard to measure because of their low incidence and varied pattern. Using data from the National Hospital Discharge Survey, which codes discharges and procedures according to the ICD-9-CM, we assessed acute complication rates for 3,289 surgically treated LDH patients and 4,025 nonoperative LDH patients, identifying complications from codiagnoses. The complication rates were significantly correlated with the postoperative length of stay and with the risk factors of obesity, hypertension, and diabetes. We found fewer instances of thrombophlebitis (0.3/1,000) and slightly lower mortality (0.9/1,000) than previously reported. Although the frequency of the cauda equina syndrome in the literature approximates our findings of 5/1,000, our data did not allow correction for the fraction of preexistent cauda equina syndromes. Our any-complication-rate is 3.7%. Even though LDH surgery is relatively safe, its complications should not be overlooked.
This is a presentation of 3 patients who manifested with the clinical syndrome of anterior spinal cord injury at the lumbar level. A combined injury of conus medullaris and cauda equina in this particular level of the cord between T12 to L2 spines makes clinical assessment difficult leading to a false diagnosis of "cauda equina injury". Careful studies of the ventral cord of the conus medullaris are needed to confirm a contusion, hematomyelia or compression. Basis for theoretical presence of lumbar anterior cord syndrome as well as clinical diagnosis are discussed.
A cauda equina schwannoma presented solely with rectal pain. The tumor was found to have infarcted and hemorrhaged. A discussion of rectal pain is included, and it is speculated that some forms of rectal pain, especially those classified as proctalgia fugax or rectal neuralgia, may be due to cauda equina tumors.
Hereditary paraganglioma of the head and neck is associated with germline mutations in the SDHD gene, which encodes a mitochondrial respiratory chain protein. Paragangliomas of the central nervous system are very rare, occur almost exclusively in the cauda equina of the spinal cord and are considered non-familial. In the present study, we screened 22 apparently sporadic paragangliomas of the cauda equina for SDHD mutations. One spinal paraganglioma and similar cerebellar tumours that developed 22 years later in the same patient contained a missense mutation at codon 12 (GGT-->AGT, Gly-->Ser) and a silent mutation at codon 68 (AGC-->AGT, Ser-->Ser). There was no family history of paragangliomas but DNA from white blood cells of this patient showed the same sequence alterations, indicating the presence of a germline mutation. All other cases of spinal paraganglioma had the wild-type SDHD sequence, except one case with a silent mutation at codon 68 (AGC-->AGT, Ser-->Ser). This is the first observation indicating that inherited SDHD mutations may occasionally cause the development of paragangliomas in the central nervous system.