[Metastatic spinal cord compression and spinal anesthesia].
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Anesthesia, Spinal↗
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Experimental analysis of the spinal cord compressed by spinal metastasis.
The purpose of the present study of experimental spinal metastasis, developed in rats by inoculation of tumor cells through the spinous process, was to find the factor that causes the initial damage to the cord in this disorder. In the early stage of paralysis, the degenerated posterior funiculus originated from a small hemorrhagic area in the posterior column of the involved cord. Using the scanning electron microscope, the hemorrhage was found to be from the intrinsic vein, resulting from the disturbance of venous drainage in the compressed portion. In the early stage of compression, extravasation of horseradish peroxidase was observed in the white matter, but histologic degeneration was not. A hemorrhage existed wherever degeneration of the funiculus was observed. Therefore, the trigger to induce the initial damage on the cord in spinal metastasis was not likely to be vasogenic edema, but instead the intrinsic venous hemorrhage.
Angiography↗
Long-term changes in spinal cord evoked potentials after compression spinal cord injury in the rat.
1. After traumatic spinal cord injury (SCI), histological and neurological consequences are developing for several days and even weeks. However, little is known about the dynamics of changes in spinal axonal conductivity. The aim of this study was to record and compare repeated spinal cord evoked potentials (SCEP) after SCI in the rat during a 4 weeks' interval. These recordings were used: (i) for studying the dynamics of functional changes in spinal axons after SCI, and (ii) to define the value of SCEP as an independent outcome parameter in SCI studies. 2. We have used two pairs of chronically implanted epidural electrodes for stimulation/recording. The electrodes were placed below and above the site of injury, respectively. Animals with implanted electrodes underwent spinal cord compression injury induced by epidural balloon inflation at Th8-Th9 level. There were five experimental groups of animals, including one control group (sham-operated, no injury), and four injury groups (different degrees of SCI). 3. After SCI, SCEP waveform was either significantly reduced or completely lost. Partial recovery of SCEPs was observed in all groups. The onset and extent of recovery clearly correlated with the severity of injury. There was good correlation between quantitated SCEP variables and the volumes of the compressing balloon. However, sensitivity of electropohysiological parameters was inferior compared to neurological and morphometric outcomes. 4. Our study shows for the first time, that the dynamics of axonal recovery depends on the degree of injury. After mild injury, recovery of signal is rapid. However, after severe injury, axonal conductivity can re-appear after as long as 2 weeks postinjury. In conclusion, SCEPs can be used as an independent parameter of outcome after SCI, but in general, the sensitivity of electrophysiological data were worse than standard morphological and neurological evaluations.
Animals↗
Spinal cord compression from spinal tuberculosis in a child.
Tuberculosis in children most frequently involves the pulmonary system. Spinal tuberculosis is very rare and insidious in children. We present a 1-year-old girl who was brought to our clinic with complaints of a bulge on her back and weakness in the feet. She was investigated with magnetic resonance imaging and at the thoracic level which revealed vertebral destruction and para- and perispinal abscess. Computed tomography of the lungs showed tuberculous lesions. The child's mother gave a post history of recovered lung tuberculosis. Due to appearance paraparesis secondary to vertebral destruction, we removed the abscess and infected bone and reconstruction was carried out with fibular allograft anteriorly. Tuberculosis bacilli were isolated from the postoperative biopsy culture. In this study, we evaluated the methods of diagnosis and treatment of spiral tuberculosis according to the studies and publications which have been done previously.
Epidural Abscess↗
Neuropathological changes and neurological function after spinal cord compression in the rat.
As part of a series of experimental investigations of the effects of various pharmacological agents on the outcome of compressive spinal cord trauma in the rat, the time course of the cell changes in the cord at the site of and distal to the compression was studied at the light microscopic level. The degree of compression used with the present model results in a transient paraparesis that recovers almost completely over a period of 3 weeks as judged by the inclined plane technique. The most significant morphological findings were as follows. Initially (1 and 24 h after the impact) there was pronounced swelling and hemorrhage at the compression site, chiefly in the gray matter of the cord. On day 4 there was severe necrosis in the same region, with numerous macrophages and leukocytes. Rats killed after 21 days showed either minor residual signs of necrosis or essentially normal tissue architecture. Surprisingly, necrosis with delayed onset also developed in the dorsal columns, involving the pyramidal tracts. This necrosis was detected in animals killed after 9 and 21 days but not in those observed after 4 days or earlier. The longitudinal tracts of the white matter showed reduced staining in paraffin sections of the compression site. Epon sections revealed splits in the myelin sheaths and enlarged periaxonal spaces as early as 1 h after the impact. The alterations in the longitudinal tracts persisted throughout the 21-day observation period and extended down to L2-L4. There was gradual functional recovery, documented by the inclined plane test. Preinjury values were almost reached on day 21, although the cord still showed some morphological damage. In individual animals, no relation was found between degree of function as tested by inclined plane and extent of morphologic injury. Additional functional and morphological methods obviously are needed in future investigations of the effects of treatments on the outcome of compressive spinal cord injury.
Animals↗
Successful chemotherapeutic decompression of primary endodermal sinus tumor presenting with severe spinal cord compression.
Management of spinal cord compression from a primary paraspinal endodermal sinus tumor (EST) is described. A 17-month-old child presented for treatment with near-complete paraplegia secondary to spinal cord compression from a primary paraspinal EST. The child was treated with cisplatin-based chemotherapy without laminectomy or radiation therapy. Rapid resolution of symptoms was observed. The child had an excellent tumor response and complete neurologic recovery with no sequelae. Chemotherapy alone is an alternative to laminectomy or radiation therapy in the management of epidural cord compression from EST, even when the cord compression is severe.
Endodermal Sinus Tumor↗
Effect of acute spinal cord compression injury on regional spinal cord blood flow in primates.
Spinal cord blood flow (SCBF) was measured in 24 rhesus monkeys after injury to the cord produced by the inflatable circumferential extradural cuff technique. Measurement of regional blood flow in the white and gray matter of the cord in areas of 0.1 sq mm was achieved with the 14C-antipyrine autoradiographic technique and a scanning microscope photometer. After moderate cord injury (400 mm Hg pressure in the cuff maintained for 5 minutes), which produced paraplegia in 50% of animals and moderate to severe paresis in the other 50%, mean white matter SCBF was significantly decreased for up to 1 hour. White matter blood flow then rose to normal levels by 6 hours posttrauma and was significantly increased by 24 hours posttrauma. Gray matter SCBF was significantly decreased for the entire 24-hour period posttrauma. After severe cord injury (150 mm Hg pressure in the cuff maintained for 3 hours), which produced total paraplegia in almost all animals; SCBF in white and hours), which prodced total paraplegia in almost all animals, SCBF in white and gray matter was reduced to extremely low levels for 24 hours posttrauma. In addition, focal decreases in SCBF were seen in white and gray matter for considerable distances proximal and distal to the injury site. It is concluded that acute compression injury of the spinal cord is associated with long-lasting ischemia in the cord that increases in severity with the degree of injury.
Acute Disease↗
Primary extradural neoplasms causing spinal cord compression.
Thirteen patients presented primary extradural neoplasms compressing the spinal cord and/or roots in a four year period. Laminectomy and tumour excision or biopsy were carried out in twelve patients and transthoracic resection in the one remaining. Six tumours were benign; two were neurofibromata associated with von Recklinghausen's disease; two were osteochondromata; and there were single cases of cavernous haemangioma and aneurysmal bone cyst. All patients are alive and well; follow-up ranges between 1.3 an 8.5 years post-operation. Among the malignant neoplasms there were three malignant lymphomata, two Ewing's sarcoma and single instances of mesenchymal chondrosarcoma and chondrosarcoma of the classical type. Four patients are alive, having been followed up between 3.5 to 5 years.
Adolescent↗
[Radicular-spinal cord compression with spinal genesis in a female patient with achondroplasia].
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Achondroplasia↗
Malignant spinal-cord compression.
Malignant spinal-cord compression (MSCC) is a common complication of cancer and has a substantial negative effect on quality of life and survival. Despite widespread availability of good diagnostic technology, studies indicate that most patients are diagnosed only after they become unable to walk. We review the epidemiology, pathophysiology, and clinical features of MSCC. Clinical trials have informed the optimum management of MSCC, and we review the role of corticosteroids, radiotherapy, and surgery in the management of patients. We also emphasise advances in radiation delivery and the results of a randomised trial that supported aggressive debulking in patients with MSCC.
Combined Modality Therapy↗
Final results of a prospective study of the prognostic value of the time to develop motor deficits before irradiation in metastatic spinal cord compression.
PURPOSE: Metastatic spinal cord compression often requires urgent treatment selection, which could be facilitated by strong prognostic factors. Because only the type of primary tumor and pretreatment ambulatory status are known as prognostic factors for functional outcome, we investigated the prognostic value of the time of motor deficit development before radiotherapy (RT). METHODS AND MATERIALS: Ninety-eight patients were included between November 1998 and April 2000. Three subgroups were formed, according to time of motor deficit development before RT: 1-7 days (n = 31), 8-14 days (n = 31), and >14 days (n = 36). Ambulatory rates and motor function were evaluated for < or =24 weeks after RT. In a multivariate analysis, all three prognostic factors and radiation parameters were included. RESULTS: In the >14-day subgroup, improvement occurred significantly (p < 0.001) more often than in the other subgroups (86% vs. 29% and 10%) and the posttreatment ambulatory rate was significantly higher (86% vs. 55% and 35%, p = 0.026). Multivariate analysis revealed the time of development of motor deficits before RT to be the strongest prognostic factor. CONCLUSION: Functional outcome is significantly better with slower development of motor deficits before RT. This new, independent, prognostic factor must be considered in future trials aiming to define an optimal RT schedule.
Adult↗
[A case of posttraumatic spinal pseudomeningocele which caused spinal cord compression 20 years after injury].
We reported an extremely rare case of posttraumatic spinal pseudomeningocele which caused spinal cord compression 20 years after getting injury, and demonstrated that sequelae of an injury may occur many years after the original wound. A 39-year-old man, who got left cervical root avulsion due to a traffic accident when he was 17 years old, began to complain of progressive muscle atrophy and weakness of left lower extremity 1 year ago. Myelography demonstrated pseudomeningocele at left C6-C8 level, and MRI and CT myelography revealed that the pseudomeningocele extends through the intervertebral foramen and compresses the spinal cord to the right side in the spinal canal. Bilateral functional compression of spinal cord dorsal and lateral column was also verified with SEP and MEP electrophysiologically.
Accidents, Traffic↗
Spinal cord compression produced by osteomyelitis mimicking spinal epidural metastasis.
Spinal cord compression is a common neurological emergency. The causes of spinal cord compression may include primary or (more frequently) metastatic tumor, infections, trauma, and vertebral or intervertebral disc disease. In most instances the underlying etiology is known or easily ascertained. We present here three recent cases in which patients presented with spinal cord compression and lytic bone lesions suggesting metastatic cancer. In these cases, vertebral osteomyelitis was found to be the cause.
Adult↗
Synaptic blockade plays a major role in the neural disturbance of experimental spinal cord compression.
We analyzed dynamic processes of neural excitation propagation in the experimentally compressed spinal cord using a high-speed optical recording system. Transverse slices of the juvenile rat cervical spinal cord were stained with a voltage-sensitive dye (di-4-ANEPPS). Two components were identified in the depolarizing optical responses to dorsal root electrical stimulation: a fast component of short duration corresponding to pre-synaptic excitation and a slow component of long duration corresponding to post-synaptic excitation. In the directly compressed dorsal horn, the slow component was attenuated more (attenuated to 37.4 +/- 9.1% of the control) than the fast component (to 70.5 +/- 14.9%) (p < 0.01) at 400 msec after stimulation. Depolarizing optical responses to compression and to chemical synaptic blockade were similar. There was a regional difference between white matter (attenuated to 86.2 +/- 10.5%) and gray matter (to 72.6 +/- 10.4%) (p < 0.03) in compression-induced changes of the fast components; neural activity in the white matter was resistant to compression, especially in the dorsal root entry zone. Depolarizing optical signals in the region adjacent to the directly compressed site were also attenuated; the fast component was attenuated to 77.6 +/- 10.4% and the slow component to 31.8 +/- 11.3% of the control signals (p < 0.01). Spinal cord dysfunction induced by purely mechanical compression without tissue destruction was virtually restored with early decompression. We suggest that a disturbance of synaptic transmission plays an important role in the pathophysiological mechanisms of spinal cord compression, at least under in vitro experimental conditions of juvenile rats.
Animals↗
Symptoms and signs in metastatic spinal cord compression: a study of progression from first symptom until diagnosis in 153 patients.
The symptoms in metastatic compression of the spinal cord or cauda equine are described after a systematic recording of the sequence of symptoms in 153 patients. Radicular pain was predominant in patients with metastases located in the lumbar area, while the severity of motor symptoms was positively correlated with thoracic metastases. The most common initial symptom was radicular pain, followed, with decreasing frequency, by motor weakness, sensory complaints and bladder dysfunction. The progression of motor weakness influenced the probability of establishing the diagnosis of spinal cord compression by stepwise marked increased probability when patients lost gait function or progressed into total paralysis.
Adult↗
[Diagnosis and interdisciplinary therapy of spinal cord compression caused by spinal metastases].
Metastatic tumours of the bone system occur up to 60% in the spinal cord. The epidural spinal cord compression is also found by metastatic tumour, so patients with metastatic disease in this localisation carry a poor prognosis. From 1986 to 1988 35 patients with symptomatic spine metastasis are operated upon. 43% of these patients recover their capability of walking. 90% from the operated collective show a reduction of pain. The primary tumour is first found from cancer of the lung and second from the kidneys. The most common localisation of metastatic tumour is the thoracic spine. The ratio from male to female is 2:1. If the risk of operation and differential therapy is discussed, the decompression and tumour resection will be the first. The concept for postoperative mobilisation and therapy concludes the stabilisation of spinal cord with internal fixation. Treatment of metastatic tumours takes aim at the improvement of life quality.
Adenocarcinoma↗
Managing malignant spinal cord compression.
BACKGROUND: Spinal malignancy can present as low back pain and accounts for most cases of spinal cord compression (SCC). OBJECTIVE: To assist the clinician in the diagnosis of malignant SCC and to increase awareness of various treatment modalities. A clinical approach for the workup of patients with 'metastatic carcinoma of unknown primary' is also outlined. DISCUSSION: It is important to diagnose SCC early and initiate urgent treatment to obtain optimum patient outcomes. Further management includes workup for the primary tumour source if unknown.
Combined Modality Therapy↗
Malignant spinal cord compression in cancer patients may be mimicked by a primary spinal cord tumour.
Although it is quite rare, second primary neoplasms in cancer patients may present with the signs and symptoms of malignant spinal cord compression. Primary spinal cord tumours in the cancer patients may be deceptive and considered as the recurrent first cancer. Therefore, it should be precisely differentiated and appropriately managed. We report such a case of intramedullary ependymoma of the cervical spinal cord mimicking metatstatic recurrent lymphoma and causing cord compression. A 50-year-old man developed intramedullary ependymoma of the cervical spinal cord 1.5 years following chemoradiation for Waldeyer's ring lymphoma. He presented with a 2-month history of neck pain, progressive upper- and lower-extremity numbness and weakness, and bowel and bladder dysfunction. Magnetic resonance imaging revealed an intramedullary expansive lesion extending from C4 to C6 levels of the cervical spinal cord. The clinical and radiological findings were suggestive of malignant process. A comprehensive investigation failed to detect another site of disease. He underwent operation, and the tumour was subtotally resected. The patient's neurological deficits improved subsequently. The development of the intramedullary ependymoma following treating lymphoma has not been reported. We describe the clinical, radiological and pathological findings of this case and review the literature.
Cervical Vertebrae↗