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Tumor

Metastatic Epidural Bony Tumor Causing Spinal Cord Compression

A Case Report

Yamashita, Kazuo; Aoki, Yasuaki; Hiroshima, Kazuo

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Clinical Orthopaedics and Related Research: July 1996 - Volume 328 - Issue - p 231-235
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Abstract

The causes of spinal cord compression from a metastatic tumor often include pressure from an epidural soft tissue tumor mass, spinal angulation after vertebral collapse, vertebral dislocation after pathologic fracture, or, rarely, pressure from an intradural metastasis.1,5 Spinal cord compression caused by an epidural bony tumor expanding from a vertebral metastasis into the spinal canal is rare as well. The authors treated a patient with breast cancer in whom this condition developed. The patient did not respond to radiotherapy, but subsequent neurologic improvement was achieved with surgical decompression.

CASE REPORT

In April 1994, a 58-year-old woman underwent standard radical mastectomy followed by hormonal therapy for invasive ductal carcinoma of the breast. The presence of a metastasis at T8 was already diagnosed radiographically at the time of diagnosis of the breast cancer. In August, the patient experienced back pain. On September 23, the patient experienced sudden weakness of the lower extremities and was admitted to the hospital. A bone scintigram revealed focal areas of increased tracer uptake in the T8 vertebra and left sixth and tenth ribs. Forty grays of irradiation was delivered to the area. The back pain lessened, but the patient could not walk and had difficulty urinating.

Radiographs of the thoracic spine showed osteoblastic changes and collapses of the T6 and T8 vertebral bodies (Fig 1). On October 31, magnetic resonance imaging (MRI) of the thoracic spine was performed. A sagittal T1 weighted MRI demonstrated low signal intensity in the collapsed vertebral body and lamina of T8 (Fig 2). A sagittal T2 weighted MRI demonstrated high signal intensity in the same vertebral body and lamina as well as an epidural spinal cord compression at the level of T8 (Fig 3). Axial T2 weighted MRI of T8 revealed an epidural mass of high signal intensity, contiguous with the left lamina and pedicle, that compressed the spinal cord laterally (Fig 4). These MRI findings indicated the persistent compression of the spinal cord by an epidural tumor mass that did not respond to radiotherapy. On November 10, computed tomography (CT) of the thoracic spine was performed. Computed tomography of T8 demonstrated a fracture of the vertebral body with a small fragment in the anterior spinal canal. A large bony mass expanding from the left lamina and pedicle into the spinal canal was observed as well (Fig 5). The bony mass on CT corresponded to the epidural mass of high signal intensity, compressing the spinal cord, as identified on axial T2 weighted MRI.

On November 11, the patient was transferred to the Department of Orthopaedics. Physical examination disclosed sensory deficity in the trunk and lower extremities, weakness of the lower extremities (Grade ⅘ on the right and Grade ⅖ to ⅗ on the left, as determined by manual muscle testing), and exaggerated deep tendon reflexes in the lower extremities. Ankle clonus and Babinski's sign were present bilaterally.

On November 16, the patient underwent posterior decompression of the spinal cord. A total laminectomy of T8 and a partial laminectomy of T7 were performed. No epidural soft tissue tumor mass was found, although a bony mass expanding from the medial wall of the left pedicle of T8 with compression of the dural sac was identified. The left pedicle of T8 was ground down, and the bony mass was reflected and removed along with the superior facet. The bony mass did not adhere to the dura. Finally, spinal fixation with posterior instrumentation was performed at T5-T10. Pathologic examination of the bony mass disclosed the presence of thick, disorganized bony trabeculae and clusters of tumor cells with glandular formation within the marrow space (Fig 6).

The patient experienced no postoperative complications. One week after surgery, the patient was able to ambulate using a handcart, and the difficulty on urination resolved. In February 1995, the patient was discharged from the hospital and was able to walk with the aid of a cane. The muscle strength of her lower extremities returned, reaching a Grade 5/5 on the right side and a Grade 4/5 on the left. Minimal numbness of the legs remained. By July 1995, the patient was able to walk without aid.

DISCUSSION

Epidural spinal cord compression from a metastatic tumor is most often due to pressure from an epidural soft tissue tumor mass and rarely is secondary to an epidural bony tumor mass expanding from a vertebral metastasis into the spinal canal. In the current study, the authors reported the case of a patient with breast cancer in whom spinal cord compression developed, caused by an epidural bony tumor expanding from a vertebral metastasis, as demonstrated by CT. In reviewing the literature, the authors found 6 similar cases2,4,7,8: 5 involving patients with prostate cancer and 1 involving a patient with breast cancer.

The patient reported in the current study as well as the 6 patients reported previously had radiographically diagnosed osteoblastic vertebral metastases. None of the latter 6 patients had radiographic evidence of vertebral collapse or spinal instability. Although the patient reported in the current study had vertebral collapses, the fracture fragment in the anterior spinal canal was too small to have caused the spinal cord compression. The patient underwent MRI for detection of the spinal cord compression. Magnetic resonance imaging did not reveal the presence of bony elements contained in the epidural mass causing spinal cord compression, although it did make possible the localization of spinal cord compression. The bony elements contained in the epidural mass were demonstrable by CT only. In centers in which MRI is available, it is the diagnostic procedure of choice for patients with suspected metastatic spinal cord compression, because it is noninvasive, it is superior to myelography in the detection of bone metastases, and it affords easy imaging of the entire spine and spinal cord.6 However, MRI has the disadvantage of being relatively insensitive in demonstrating calcified deposits in bone tumors.9 In cases of spinal cord compression such as that presented in the current study, this insensitivity in the detection of bony elements within the epidural tumor may delay surgical intervention. Therefore, CT should be used for patients who have radiographically diagnosed osteoblastic vertebral metastases and epidural spinal cord compression diagnosed by MRI.

The optimal treatment of metastatic epidural spinal cord compression is controversial regarding indications for radiotherapy or surgery. In general, radiotherapy is appropriate for most patients. Surgery is reserved for patients with an unknown histologic diagnosis, a highly radioresistant primary tumor, spinal instability, a deteriorating course despite ongoing radiotherapy, or postradiation disease relapse.3,5 Unlike the cases of metastatic epidural spinal cord compression reported in the literature, the current case involved the presence of bony elements contained in an epidural tumor, which caused spinal cord compression. Theoretically, the patient's spinal cord compression due to the osseous cause was unresponsive to radiotherapy; therefore, the spinal cord compression became an absolute indication for surgical decompression.

F1-36
Fig 1:
. Radiograph of the thoracic spine showing osteoblastic changes and collapses of the T6 and T8 vertebral bodies.
F2-36
Fig 2:
. Sagittal T1 weighted MRI (TR 500 ms, TE 15 ms) of the thoracic spine demonstrating low signal intensity in the collapsed vertebral body and lamina of T8.
F3-36
Fig 3:
. Sagittal T2 weighted MRI (TR 5000 ms, TE 90 ms) of the thoracic spine demonstrating high signal intensity in the collapsed vertebral body and lamina of T8 as well as an epidural spinal cord compression at the level of T8.
F4-36
Fig 4:
. Axial T2 weighted MRI (TR 4500 ms, TE 103 ms) of T8 revealing an epidural mass of high signal intensity (arrow) contiguous with the left lamina and pedicle that is compressing the spinal cord (asterisk) laterally.
F5-36
Fig 5:
. Computed tomography of T8 demonstrating a fracture of the vertebral body with a small fragment in the anterior spinal canal and a large bony mass (arrow) expanding from the left lamina and pedicle into the spinal canal.
F6-36
Fig 6:
. Pathologic section of the bony mass expanding from the vertebral metastasis, disclosing the thick, disorganized bony trabeculae and clusters of tumor cells with glandular formation within the marrow space (Decalcified, hematoxylin and eosin; original magnification ×40).

References

1. Constans JP, de Divitiis E, Donzelli R, et al: Spinal metastases with neurological manifestations: Review of 600 cases. J Neurosurg 59:111-118, 1983.
2. Hirschfeld A, Beutler W, Seigle J, Manz H: Spinal epidural compression secondary to osteoblastic metastatic vertebral expansion. Neurosurgery 23 662-665, 1988.
3. Hoskin PJ: Radiotherapy in the Management of Bone Metastases. In Rubens RD, Fogelman I (eds). Bone Metastases: Diagnosis and Treatment. London, Springer-Verlag 171-185, 1991.
4. Hove B, Gyldensted C: Spiculated vertebral metastases from prostatic carcinoma: Report of first two cases. Neuroradiology 32:337-339, 1990.
5. Nielsen OS, Munro AJ, Tannock IF: Bone metastases: Pathophysiology and management policy. J Clin Oncol 9:509-524, 1991.
6. Richards MA: Magnetic Resonance Imaging. In Rubens RD, Fogelman I (eds). Bone Metastases: Diagnosis and Treatment. London. Springer-Verlag 83-97, 1991.
7. Wada E, Yamamoto T, Furuno M, et al: Spinal cord compression secondary to osteoblastic metastases. Spine 18:1380-1381, 1993.
8. Yamashita K, Ueda T, Komatsubara Y, et al: Epidural compression of the spinal cord caused by vertebral osteoblastic metastasis of prostate carcinoma: A case report. Clin Orthop 291:138-141, 1993.
9. Zimmer WD, Berquist TH, McLeod RA, et al: Bone tumors: Magnetic resonance imaging versus computed tomography. Radiology 155:709-718, 1985.

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SECTION II

ORIGINAL ARTICLES

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