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A review of 158 cases of metastatic extradural spinal cord compression referred to three radiotherapy departments shows that the median survival time is less than 3 months, that recovery of motor and sphincter function is uncommon, and that low fraction (2-5) regimens have a similar clinical outcome to more protracted regimens.
We performed a randomised single blind trial of high-dose dexamethasone as an adjunct to radiotherapy in patients with metastatic spinal cord compression from solid tumours. After stratification for primary tumour and gait function, 57 patients were allocated randomly to treatment with either high-dose dexamethasone or no steroidal treatment. Dexamethasone was administered as a bolus of 96 mg intravenously, followed by 96 mg orally for 3 days and then tapered in 10 days. A successful treatment result defined as gait function after treatment was obtained in 81% of the patients treated with dexamethasone compared to 63% of the patients receiving no dexamethasone therapy. Six months after treatment, 59% of the patients in the dexamethasone group were still ambulatory compared to 33% in the no dexamethasone group. Life table analysis of patients surviving with gait function showed a significantly better course in patients treated with dexamethasone (P < 0.05). Median survival was identical in the two treatment groups. Similar results were found in subgroup analysis of 34 patients with breast cancer as the primary malignancy. Significant side-effects were reported in 3 (11%) of the patients receiving glucocorticoids, 2 of whom discontinued the treatment. We conclude that high-dose glucocorticoid therapy should be given as adjunct treatment in patients with metastatic epidural spinal cord compression.
OBJECTIVES: To provide an overview on the presentation, diagnosis, and treatment of metastatic epidural spinal cord compression (MESCC). DATA SOURCES: Published articles, book chapters, and research reports. CONCLUSIONS: MESCC is a common oncologic emergency that requires prompt recognition and emergency treatment to relieve pain and preserve neurologic function. The signs and symptoms of MESCC are easily detected and can be integral assessment components of the nursing care of any patient with a solid tumor. IMPLICATIONS FOR NURSING PRACTICE: Nurses can have a dramatic impact on preventing neurologic complications caused by this oncologic metastatic problem. When neurologic compromise is not prevented or reversed, nurses also can provide expert care to patients and families in the rehabilitation phase of MESCC.
Spinal cord compression as a consequence of mass lesions due to extramedullary hematopoiesis is a well-described but rare syndrome occurring in thalassemia and some other hematologic conditions. After low-dose radiotherapy alone, a rapid and durable response occurred in a patient with thalassemia. No side effects were encountered and the patient has been stable neurologically for over 7 years since treatment. The results of the current case, and those previously reported in which radiotherapy alone was given, suggest that low-dose radiotherapy should be considered as a primary treatment modality for the management of this syndrome, at least in patients with thalassemia.
The growth rate of a tumor, patterns of tumor growth and metastatic spread, and toxicity of therapy contribute to the type and severity of complications. Four common critical care complications resulting from compressive and invasive properties of tumors include spinal cord compression, malignant bowel obstruction, malignant ascites, and gastrointestinal bleeding. Knowledge of the clinical presentations of each of these complications provides a foundation for nursing assessment.
PURPOSE: To investigate prospectively the prognostic value of the time of developing motor deficits before radiation therapy (RT) for post-treatment functional outcome in metastatic spinal cord compression. METHODS AND MATERIALS: From November 1998 until October 1999, 57 patients were included. Two subgroups were formed according to the time of developing motor deficits before RT: 1-14 days (n = 29) and > 14 days (n = 28). Therapeutic effect on motor function was evaluated by an 8-point scale directly, 6, 12, and 24 weeks after RT. Patients with rapid deterioration of motor function within 48 h before RT (n = 14) were evaluated separately. RESULTS: Directly after RT, 26/28 patients (93%) of the group developing motor deficits > 14 days showed improvement of motor function, in comparison to 3/29 patients (10%) of the group 1-14 days (p < 0.001). Deterioration rates were 0% (> 14 days) and 45% (1-14 days). In patients with rapid deterioration of motor function within 48 h before RT, prognosis was poor (improvement 0%, no change 43%, deterioration 57%). Results were comparable 6, 12, and 24 weeks after RT. CONCLUSION: A slower development of motor deficits before RT predicts a better post-treatment functional outcome. In patients with rapid deterioration of motor function within 48 h before RT, prognosis was extraordinarily poor. These results support the findings of our preceding retrospective analysis.
This study examines morphological changes of the blood-brain barrier (BBB) after spinal cord compression. The lowest thoracic segment (T13) of female guinea pigs was injured and the BBB was tested from 7 days to 5.5 months postinjury using intravenously injected horseradish peroxidase (HRP) as a tracer. Tracer leakage in the injured segment was verified with the light microscope and the fine structure of capillaries was examined. Diffuse tissue staining was observed at T13 up to 2 weeks following injury. A leaky BBB correlated with expected changes in the fine structure of endothelial cell junctions. These were predominantly nonoverlapping cell junctions which, in many instances, were separated by clefts between adjacent cells. At early survival times, numerous capillary profiles with juxtaposed astrocyte foot processes were noted in addition to altered cell associations. Complete sealing of the BBB against interstitial HRP leakage was not observed until 17 days postinjury. After the first week, some of the endothelial cells were contacted by macrophages, processes of perivascular microglia, and processes of swollen and degenerating astrocytes. Perivascular spaces varied in extent and contained amorphous deposits of extracellular materials in addition to supernumerary layers of basal lamina. The early changes were followed by profound tissue restructuring due to loss of both neurons and glia. At longer survival times the BBB to HRP repaired. Endothelial cells formed complex overlapping junctions with zonulae occludentes. Most of the capillaries in the injured segment were no longer in direct contact with astrocyte foot processes, although reactive astrocytes constituted the predominant cell type in the remaining gray matter. Substantial expansion of perivascular spaces was evident. The cytoplasm of endothelial cells had numerous pinocytotic vesicles. Perivascular spaces contained layers of assembled collagen arranged perpendicularly to each other in addition to amorphous matrix materials. The findings suggest that decoupling of astrocyte foot processes from endothelial cell surfaces does not prevent reformation of tight junctions. It remains to be examined what effects the larger perivascular spaces, extracellular matrix deposits, and changes of cell associations may have on transport systems and ionic buffering. The data are relevant for estimating an opportune time for application of barrier-impermeable drugs to the lesion area.
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Between 1971 and 1988, 20 patients with previously undiagnosed non-Hodgkin's lymphoma (NHL), of intermediate or high grade histology presented with extradural spinal cord compression. All had decompressive surgery. The first treatment after surgery was chemotherapy in nine and radiotherapy in 11 patients. At presentation 15% were ambulant and this improved to 55% after surgery; urinary continence improved from 30 to 80%. Mobility and sphincter control remained unchanged, regardless of subsequent therapy. Chemotherapy as the initial treatment modality after surgery, either alone or in combination with radiotherapy, did not jeopardise functional outcome. Mobility after surgery was an independent prognostic factor for survival, when corrected for age and stage at presentation (P = 0.04). The treatment of intermediate and high grade NHL presenting with spinal cord compression should be based on histology, extent of disease and age, as with other sites of presentation, but should also take into consideration the prognostic importance of post-surgical mobility.
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Explore the source record for details and available documents.
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In a patient with advanced Hodgkin's disease (HD) associated with generalized pruritus, an unexpected relief of itching was found to be an early sign of spinal cord compression. Following irradiation of an extradural mass at the Th II level, itching recurred. Although the mechanisms bringing about itching in HD are unknown, the relief and recurrence of the symptom in our patient are in line with a peripheral origin of pruritus in the disease. Spontaneous relief of pruritus in HD despite other signs of active disease should prompt a neurological examination, since early recognition and treatment of spinal cord compression in lymphoma are important to avoid residual neurological disability.
OBJECTIVE: To describe three cases with false localising levels illustrating the difficulty in clinical diagnosis of spinal cord compression. PATIENTS AND METHODS: Three patients (aged 53, 55 and 57 years) developed acute (in one) and subacute (in two) spinal cord syndrome with paraparesis, bladder symptoms and sensory levels suggesting lower thoracic or higher lumbar involvement. Imaging at suspected levels was normal. Follow-up investigations after a significant delay showed compression at higher levels (up to 11 segments). Diagnoses were surgically verified. In one patient who died, post mortem investigation discloseed a caudally situated artery of Adamkiewicz and absent vicarious vessels at T7-T8 that are usually present in such cases. CONCLUSIONS: The well known but rare phenomenon of false localizing sensory levels in spinal cord syndromes should be kept in mind. Its causes can lie in remote higher levels of compressive lesion or in vascular compromise due to variants of the blood supply.