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PubMed2003

Spinal cord compression due to tumoral idiopatic calcinosis.

STUDY DESIGN: A case of thoracic spinal cord compression due to tumoral calcinosis (TC) is reported. SETTING: Galiza, Spain. CASE REPORT: A 59-year-old man was admitted to our hospital with a 2-month history of gradual leg weakness and sensory deficit. The neurological examination revealed paraparesis with T12 sensory level. Magnetic resonance imaging (MRI) showed an extradural right posterolateral mass at T11-T12 level, resulting in a marked spinal cord compression. He underwent T11-T12 laminectomy and mass excision. Histological examination finally led to the diagnosis of TC. CONCLUSION: TC is an uncommon cause of mass lesions of the spine. Since there is no typical spine TC MRI appearance, the final diagnosis is done by histological studies. TC should be considered in differential diagnosis of spinal cord compression and constitutes a treatable cause of paraparesis.

Calcinosis↗
PubMedDate not supplied

[The effect of prolonged spinal cord compression on the extent of morphological changes in experimental spinal cord injury in rabbits].

The analysis of early spinal cord decompression influence on the extent of morphological and microvascular changes after traumatic cord injury was the subject of this study, carried out on Polish-breed rabbits divided into two groups. Microvascular changes were evaluated in the first group of 20 animals and morphological changes in the second group of 36 rabbits. The injury causing paraplegia was performed at D9-D10 level by Allen method modified. Every group was subdivided into 4 subgroups depending on the duration of cord compression 2, 4, 6 and 12 hours. Fragments of cord were taken for examination 12 hours after decompression, from sites 0.5, 1.0 and 1.5 cm distant from the injury level. Histopathological analysis was performed by light and electron microscopy and for the analysis of microcirculation with microangiography the Górkiewicz method was used. Great changes were found in nerve fibres, vascular endothelium and microcirculation. The most pronounced lesions were found in the subgroup with 6-hour compression, in the form of haemorrhage, central necrosis and oedema within and around axona as well as destruction of myelin sheaths. Early decompression (within 6 hours) can reduce the extent of morphological and vascular changes.

Animals↗
PubMed1995

Metastatic nasopharyngeal carcinoma with epidural spinal cord compression: report of an unusual and catastrophic event.

Nasopharyngeal carcinoma (NPC) with epidural metastasis of spinal cord has rarely been reported. We present an NPC patient with epidural spinal cord compression due to metastasis. In spite of emergent radiotherapy and large dose decadron treatment, this patient still had severe sequela of paraplegia and incontinence. The epidemiology, clinical findings, diagnosis, treatment and outcome of this metastatic epidural tumor compression were discussed.

Carcinoma, Squamous Cell↗
PubMed1989

Spinal cord compression in small cell lung cancer: a retrospective study of 610 patients.

The records of 610 consecutive patients with small cell lung cancer, treated on a common protocol in a multicentre trial, were reviewed and 24 (4%) cases of spinal cord compression identified. Five hundred patients had isotope bone scans performed at presentation, and in 131 (26%) there was abnormal isotope uptake in the spinal column; only 7% of these patients developed spinal cord compression. However, of the 24 patients who presented with back pain and had a positive bone scan affecting the spine, 36% developed cord compression. Cerebral metastases occurred at some stage in 19.5% of all patients and in 45% of patients with cord compression. The combination of cerebral metastases and a positive bone scan gave a 25% chance of developing spinal cord compression. There were two distinct forms of clinical presentation. Six patients (group A) presented with cord compression: All had back pain and positive bone scans, five out of six had sphincter disturbance, and median survival from cord compression was 30 weeks. Eighteen patients (group B) developed cord compression while on treatment: 28% had positive initial bone scans, 44% back pain and 61% sphincter disturbance, and median survival from cord compression was 4 weeks. Spinal cord compression is an important cause of morbidity and mortality in small cell lung cancer. We suggest that it may be possible to select patients who should receive radiotherapy to the spine to try to prevent the development of this complication.

Adult↗
PubMed1987

Spinal cord compression due to ethmoid adenocarcinoma.

Adenocarcinoma of the ethmoid sinus is a rare tumor which has been epidemiologically linked to woodworking in the furniture industry. It has a low propensity to metastasize and has not been previously reported to cause spinal cord compression. A symptomatic epidural spinal cord compression was confirmed on magnetic resonance imaging (MRI) scan in a former furniture worker with widely disseminated metastases. The clinical features of ethmoid sinus adenocarcinoma and neoplastic spinal cord compression, and the comparative value of MRI scanning in the neuroradiologic diagnosis of spinal cord compression are reviewed.

Adenocarcinoma↗
PubMed1984

[Spinal cord compression in multiple myeloma. Study of 10 cases].

Ten cases of multiple myeloma with spinal cord compression are reported. The compression was located in the thoracic spine in 9 cases and in the cervical spine in 1 case. It led to the discovery of the myeloma in 4 cases. Three patients suffered, during several months, from local pain aggravated by activity and from slight and slowly progressive neurologic symptoms resembling intermittent claudication. At the time of diagnosis, sphincter dysfunction was observed only in patients with low thoracic cord compressions. In 4 cases, lesions were first treated by radiotherapy which did not produce regression of the compression. Tumor excision surgery was carried out seven times, once after failure of radiotherapy. In 6 cases an definite and steady regression of the neurological symptoms was achieved. Survival varied from 10 months to 7.5 years after identification of spinal cord compression. Survival was equal to or more than 3 years in 4 patients and will probably reach 3 years in another. Thus spinal cord compression is not by itself a sign indicating a poor short term prognosis in multiple myeloma. It should be treated by excision surgery, then by chemotherapy as in multiple myeloma at other sites.

Aged↗
PubMedDate not supplied

Spinal cord compression: an oncologic emergency associated with metastatic cancer: evaluation and management for the home health clinician.

Spinal cord compression is an oncologic emergency that needs to be identified, evaluated, and treated promptly for favorable patient outcomes. Although there are nonmalignant types of spinal cord compression, this article focuses on patients presenting with metastatic cancer. Home care clinicians should be knowledgeable with current assessment strategies aimed at recognizing this potentially debilitating condition. Using an assessment tool could assist clinicians with early detection of spinal cord compression, which could improve the overall quality of life.

Breast Neoplasms↗
PubMed2006

Neuronal loss and expression of neurotrophic factors in a model of rat chronic compressive spinal cord injury.

STUDY DESIGN: An experimental animal study about neuronal loss and the expression of neurotrophic factors in the chronic compressive spinal cords. OBJECTIVES: To investigate neuronal loss and the expression of neurotrophic factors in the chronic compressive spinal cords of rats, and to evaluate effects of decompressive procedures for the neuronal loss. SUMMARY OF BACKGROUND DATA: Chronic compression of spinal cords induces the loss of motor neurons in the anterior horn. However, the precise mechanism of this neuronal loss is not still understood completely. Furthermore, it is uncertain whether decompressive procedures prevent this neuronal loss or not. METHODS: A thin expanding polymer sheet was implanted microsurgically underneath T7 laminae of rats. After 6, 9, 12, and 15 weeks, the thoracic spinal cord was harvested and examined histopathologically. The expression of neurotrophic factors, including NGF, BDNF, NT-3, GDNF, CNTF, and VEGF, was analyzed using semiquantitative RT-PCR, enzyme immunoassay, and immunohistochemistry. Decompressive surgery was performed through the removal of T7 laminae and the compression materials 6, 9, and 12 weeks after starting compression. Three weeks later, respectively, the neuronal loss in the anterior horn was estimated. RESULTS: The spinal cords were progressively flattened by the expanding of the implanted polymer sheet, and the number of motor neurons in the anterior horn decreased, especially from 6 to 9 weeks after starting compression. Semiquantitative RT-PCR analysis showed that the expression of NGF and BDNF mRNAs was decreased significantly in the spinal cords of 12-week compression group compared with the 6-week compression group and that NGF mRNA expression was up-regulated significantly in the 6-week compression group relative to the 6-week control group. Any changes of expression of other neurotrophic factors were not significant. Since BDNF, not NGF, has been known to be one of the powerful survival factors for spinal motoneurons, we investigated the levels of BDNF protein in the compressive spinal cords using enzyme immunoassay and immunohistochemistry. We demonstrated the level of BDNF protein in the compressive spinal cords was increased 6 weeks after compression but declined after 12 weeks. The decompressive procedure in the 6 weeks after compression prevented neuronal loss, but the same procedure in the 9 or 12 weeks was ineffective. CONCLUSIONS: From the point of view of neuronal loss, decompressive surgery at an earlier stage, when compensatory mechanisms including the up-regulation of BDNF might be still effective, could provide better therapeutic results against chronic mechanical compressive spinal cord lesions.

Animals↗
PubMed2001

[Spinal cord compression caused by extramedullary hematopoiesis foci in the course of thalassemia].

BACKGROUND: Extramedullary haematopoiesis is a physiological response to chronic anemia, observed frequently during homozygous thalassemia. It is usually asymptomatic but can be manifested by compression of adjacent organs, particularly the spinal cord. CASE REPORT: A 44-year-old woman diagnosed with thalassaemia intermedia, was admitted for difficulties to walk and sphincter disturbances. Neurologic examination suggested spinal cord compression, which is confirmed by dorso-lumbar resonance magnetic imaging. The histology obtained by laminectomy led to the diagnosis of extramedullary hematopoiesis related to thalassemia. A radiotherapy enabled with good outcome. DISCUSSION: Spinal cord compressions by extramedullary hematopoiesis during thalassemia are uncommon (75 cases in the literature) but can induce severe sequelae if the diagnostic is not rapidly obtained. Magnetic resonance imaging is the gold standard allowing precise diagnosis and spreading of extramedullary hematopoiesis. Radiotherapy and more recently hydroxyurea are the first line treatment. CONCLUSION: This observation recalls that extramedullary hematopoiesis is a differential diagnostic of spinal cord compression in patients with thalassemia. A screening of paravertebral localization of extramedullary hematopoiesis should be performed in high risk thalassemic patients.

Adult↗
PubMed2004

Morphologic change and astrocyte response to unilateral spinal cord compression in rabbits.

In myelopathy, unilateral compression of the spinal cord in cases of disc herniation would be expected to produce Brown-Séquard syndrome. However, a transverse lesion syndrome occurs in most clinical cases. In order to reveal the mechanism by which unilateral compression induces transverse damage to the spinal cord, damage of the gray and white matter in each half of the spinal cord were evaluated quantitatively to determine the density of GFAP-positive astrocytes. The cervical spinal cord in rabbits was unilaterally compressed with a small screw. The area of each half of the damaged cord and the density of GFAP-positive astrocytes of the compressed and contralateral halves were investigated one week after the surgery. No apparent paralysis was observed during the period of observation. As the compression increased, the area of the compressed half of the spinal cord decreased significantly compared to the contralateral half. The densities of GFAP-positive astrocytes in the gray matter and the anterior funiculus increased significantly in the compressed half. There were no significant differences in the densities at the lateral and dorsal funiculi between the compressed and contralateral halves. The tissue damage in the gray matter of the compressed half was markedly higher. No significant difference between the two halves in damage was seen in the lateral funiculus, where in the lateral pyramidal and the dorsal spinocerebellar tracts are found. These findings provide evidence of the mechanistic basis for the spinal cord damage that leads to transverse lesion syndrome in unilateral compression myelopathy.

Animals↗
PubMed1979

[Solitary vertebral osteochondroma with spinal cord compression (author's transl)].

Solitary vertebral osteochondromas with spinal cord compression are very rare. Here we report a case of an osteochondroma of the 5th cervical vertebra protruding into the spinal canal. The therapeutic approach is discussed in relation to the natural evolution and the favourable prognosis of these lesions. The usefullness of the C.T. scan is shown both in diagnosis and post-operative follow-up.

Adult↗
PubMed1996

Nonfunctioning malignant paraganglioma of the posterior mediastinum with spinal cord compression. A case report.

STUDY DESIGN: Case report and review of the literature. OBJECTIVE: To present a case with an uncommon nonfunctioning malignant paraganglioma of the posterior mediastinum with compression of the spinal cord. An update survey is given with respect to diagnostic, histopathologic, and therapeutic aspects of paragangliomas. SUMMARY OF BACKGROUND DATA: Paragangliomas in the posterior mediastinum are uncommon and rarely may produce spinal cord compression. To illustrate the low incidence, only two cases of paraganglioma of the posterior mediastinum were reported by the Mayo Clinic, Rochester, Minnesota, during a 40-year period. METHOD: Case report and review of the literature. RESULT: The diagnosis was made by modern imaging techniques (computed tomography, magnetic resonance imaging, and metaiodobenzylguanidine scan) and verified by computed tomography guided per thoracic puncture. A wide local resection was performed; the patient is disease-free 1 year after surgery. CONCLUSION: The uncertainty of prognosis and possibility of local recurrence of paragangliomas even after a long period emphasizes the importance of wide local surgical resection with or without adjuvant therapy and makes long-term follow-up and continued surveillance of the patient mandatory.

Female↗
PubMed2001

Radiation-induced myelopathy in long-term surviving metastatic spinal cord compression patients after hypofractionated radiotherapy: a clinical and magnetic resonance imaging analysis.

BACKGROUND AND PURPOSE: Hypofractionated radiotherapy is often administered in metastatic spinal cord compression (MSCC), but no studies have been published on the incidence of radiation-induced myelopathy (RIM) in long-term surviving patients. Our report addresses this topic. PATIENTS AND METHODS: Of 465 consecutive MSCC patients submitted to radiotherapy between 1988 and 1997, 13 live patients (seven females, six males, median age 69 years, median follow-up 69 months) surviving for 2 years or more were retrospectively reviewed to evaluate RIM. All patients underwent radiotherapy. Eight patients underwent a short-course regimen of 8 Gy, with 7 days rest, and then another 8 Gy. Five patients underwent a split-course regimen of 5 Gy x 3, 4 days rest, and then 3 Gy x 5. Only one patient also underwent laminectomy. Full neurological examination and magnetic resonance imaging (MRI) were performed. RESULTS: Of 12 patients submitted to radiotherapy alone, 11 were ambulant (eight without support and three with support) with good bladder function. In nine of these 11 patients, MRI was negative; in one case MRI evidenced an in-field relapse 30 months after the end of radiotherapy, and in the other, two new MSCC foci outside the irradiated spine. In the remaining patient RIM was suspected at 18 months after radiotherapy when the patient became paraplegic and cystoplegic, and magnetic resonance images evidenced an ischemic injury in the irradiated area. The only patient treated with surgery plus postoperative radiotherapy worsened and remained paraparetic. Magnetic resonance images showed cord atrophy at the surgical level, explained as an ischemic necrosis due to surgery injury. CONCLUSIONS: On the grounds of our data regarding RIM in long-term surviving MSCC patients, we believe that a hypofractionated radiotherapy regimen can be used for the majority of patients. For a minority of patients, more protracted radiation regimens could be considered.

Aged↗
PubMed1986

[Spinal cord compression caused by dorsal disk hernia. Complication of Scheuermann's disease].

Association of Scheuermann's disease with a thoracic herniated disc compressing the spinal cord is rare but is clearly demonstrated in the case reported here. This confirms the non-fortuitous nature of this association also suggested by the analysis of published cases. The interest of spinal cord angiography and of surgery through a postero-lateral approach are emphasized.

Humans↗
PubMed2003

[Spinal cord compression caused by hematoma related to neuroaxial anesthesia in Spain].

OBJECTIVES: Spinal cord compression from a hematoma is a rare serious complication of neuroaxial anesthesia. Our objective was to investigate cases reported and published by Spanish authors. MATERIAL AND METHODS: Cases of spinal cord compression related to neuroaxial hematomas (epidural, subarachnoid, or both) reported at congreses and meetings in Spain or published in Medline-indexed journals from 1989 through December 2002 were reviewed. The clinical characteristics, risk factors, treatments, and outcomes were described for each case. RESULTS: Since 1996, when the first cases were reported, 20 cases in all have appeared: 8 related to sub-arachnoid anesthesia, 8 to epidural anesthesia, 1 to a combination, and 1 to diagnostic lumbar puncture. In 2 cases, the neuroaxial technique used was poorly defined. Factors that might have caused the complication could be identified in 11 cases, among which there were 7 cases of anesthetic puncture or manipulation of an epidural catheter during a period of hemorrhagic risk because of antithrombotic therapy. The hematoma was evacuated surgically in 11 cases, and medical treatment was provided in 9 cases. The neurologic outcome was satisfactory in 14 cases. CONCLUSIONS: The number of compressive spinal hematomas reported or published by Spanish authors is fairly high, and there are cases related to both sub-arachnoid and epidural anesthesia. Nonsurgical treatment was provided in 45% of the cases and the outcome was satisfactory in 70%. Risk factors were identified in over half of the reported cases.

Adult↗
PubMed1988

Comparison of soluble dexamethasone sodium phosphate with free dexamethasone and indomethacin in treatment of experimental neoplastic spinal cord compression.

In an experimental rat model of neoplastic spinal cord compression, the in vivo effect of steroidal and nonsteroidal anti-inflammatory agents on the water content, prostaglandin E2 (PGE2) production, and specific gravity of the compressed cord segments were assessed, as well as the effect on the course of the disease. Paraplegic animals presented a consistent increase in the water content, PGE2 synthesis, and specific gravity in the compressed cord segments. The effect of treatment given on onset of paraplegia with either dexamethasone sodium phosphate (Dex-p; 10 mg/kg twice daily), or free dexamethasone (F-dex; 8.25 mg/kg twice daily) or indomethacin (10 mg/kg twice daily), was evaluated after 30 hours of therapy. Both F-dex and indomethacin eliminated spinal cord edema but varied in the rate of inhibitory effect on PGE2 production (dexamethasone less than indomethacin). Dexamethasone sodium phosphate failed to reduce spinal cord edema and PGE2 synthesis, but specific gravity changes were corrected by each of the administered agents. Evaluation of the effect of treatment on the course of the disease required dose reduction by 50% for Dex-p and F-dex, and to 25% for indomethacin, to avoid lethal toxicity. Treatment was started on appearance of the first sign of neurologic dysfunction (Grade 1) and continued to paraplegia (Grade 5). In the saline-treated rats, the mean time interval between Grades 1 and 5 was 2.7 +/- 0.3 days. Free dexamethasone, Dex-p, and indomethacin significantly prolonged this interval by 57%, 54%, and 48% respectively (P less than 0.005). The three agents differed in their ability to control the increases in water content and in PGE2 production, but proved almost equally effective in the prompt control of the specific gravity changes.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗