Radiography (2005) 11, 293e298
CASE REPORT
Malignant spinal cord compression A. Slocombe a, S. Boynes b,* a b
M.R.I. Department, Leeds General Infirmary, Great George Street, Leeds, United kingdom Division of Radiography, University of Bradford, 25 Trinity Road, Bradford, United Kingdom
Received 25 August 2004; accepted 25 April 2005 Available online 16 June 2005
KEYWORDS Metastatic; Spinal cord; Compression; M.R.I.
Abstract Back pain is a common affliction which usually does not require imaging. However there are instances when imaging is not only appropriate but essential and must be performed urgently. This article uses a case study to illustrate why patients presenting with back pain and loss of normal gait and sphincter control require urgent magnetic resonance imaging of the whole spine. ª 2005 The College of Radiographers. Published by Elsevier Ltd. All rights reserved.
Introduction In 1996, a survey of the prevalence of back pain in Great Britain, reported that 40% of adults had suffered from lower back pain in the previous year and just under half of these had visited a medical practitioner or specialist.1 The majority of patients with mechanical low back pain respond rapidly to conservative management2 and imaging is not routinely recommended.3 However pain, both local and radicular, is an early complaint in patients with spinal cord compression (SCC).4 If this pain is accompanied by clinical history suggesting infection, neoplasm, or is accompanied by features such as sphincter or gait disturbance, then diagnostic imaging is appropriate.3 Sphincter or gait disturbances are suggestive of malignant spinal cord compression, which requires prompt
* Corresponding author. E-mail address:
[email protected] (S. Boynes).
intervention to prevent permanent loss of neurological function. The most common causes of SCC are listed in Table 1. The most common cause of SCC is secondary to vertebral body metastases5 predominantly from primary tumours in the lungs, breast, colon and prostate.6,10 Metastatic SCC occurs in approximately 5% of all cancer patients, with the thoracic spine most commonly affected.7 It is thought that the thoracic spine is the most commonly affected spinal region due to the increased number of vertebrae present, although the site of the primary tumour may also be a factor.8 Carcinomas arising within the pelvic cavity, particularly carcinoma of the prostate, show a predilection for the lumbosacral region.10 Over 90% of bone metastatic lesions are found in red marrow, with 69% within the vertebrae.8 Metastatic spread is mainly by the venous system with the network of vertebral, epidural and perivertebral veins acting to transport the metastatic cells to the spinal bone marrow.10
1078-8174/$ - see front matter ª 2005 The College of Radiographers. Published by Elsevier Ltd. All rights reserved. doi:10.1016/j.radi.2005.04.007
294 Table 1
A. Slocombe, S. Boynes Causes of spinal cord compression
Degenerative e disc prolapse G canal stenosis Metastases Primary neoplasm e e.g. Meningioma Injury Abscess and infection Vascular-haematoma
Spinal metastases typically enlarge within the hypervascular marrow cavity and may later extend to involve cortical and trabecular bone. With progressive enlargement, the tumour mass may extend into the epidural space, with resultant compression of the spinal cord and/or nerve roots. Classical features of cord compression are a prodromal phase with central back pain at the level of disease. This is the initial symptom in 96% of patients and precedes the compressive phase by 5 days to 2 years.11 Symptoms of the compressive phase, which occur late in the natural history of SCC,6 include neurological deficits leading to: Bladder and bowel sphincter dysfunction causing urinary retention, constipation or incontinence. Loss of control over limbs and limb weakness often accompanied with saddle anaesthesia. Since back pain may be considered a nonspecific symptom of a number of spinal disorders, SCC is frequently diagnosed late in the progression of the disease.6,12 The following case report illustrates why prompt imaging of the whole spine with MRI is appropriate for patients with back pain accompanied by the clinically significant features of sphincter and/or gait disturbance.
Case report A 59-year-old female patient presented at the Accident & Emergency Department with a history of leg weakness and 24 h loss of urinary control. Prior to admission, she complained of back pain for a 3-month period that had become progressively worse, and was now described as severe, she was otherwise pain free. The patient had also been unable to stand for 3 days preceding admission. Following neurological assessment a spinal disc protrusion was suspected of causing SCC and after discussion with the on-call neuroradiologist an urgent MRI of the lumbar spine was requested. At
the time of admission the patient’s medical records were unavailable. The radiographer reviewed the completed MRI Screening Questionnaire for MR compatibility and safety with the patient. It became evident that the patient had had gynaecological surgery for carcinoma of the cervix 2 years earlier. The radiographer thus became suspicious of the possibility of metastatic spread from the carcinoma of the cervix being responsible for the patient’s neurological symptoms. Consequently a large field of view was selected to image the lumbar spine by the radiographer to show the largest number of vertebrae possible in case of metastasis at a vertebral level remote from the sensory level. Following review of the lumbar spine images displaying pathology the radiographer contacted the radiologist to confirm the requirement for imaging the full spine and the necessity for administering contrast. It later transpired that the patient had a past history of adenocarcinoma of the cervix for which she had undergone hysterectomy approximately 2 years earlier. Histology at the time reported that the carcinoma was probably metastatic, even though pelvic lymph nodes appeared disease-free. Patients with SCC are often in severe pain and find it difficult to lie flat for any length of time. The patient was made as comfortable as possible before commencing the examination and whilst this patient did not require analgesia it is commonly required to enable the patient to remain still. A routine imaging protocol to demonstrate SCC would normally include T2 weighted sagittal imaging of the length of the spinal cord demonstrating a low signal intensity cord surrounded by high signal from CSF. This is complimented by a T1 weighted sequence planned in the same plane where low signal CSF surrounds intermediate signal from the cord. T1-weighted sequences are generally the most useful for the detection of vertebral body metastases. The increased cellularity of malignant lesions results in areas of low signal intensity on T1-weighted images, which may be contrasted with the expected high signal intensity from normal fatty marrow within the vertebrae.13 Images acquired in the sagittal plane permit visualisation of a large section of the spine, facilitating demonstration of the length of the spinal cord and are able to depict the relationship of nerve roots to foramina and the cephalocaudad extent of herniated disc material.14 T2-weighted axial images are then acquired through suspicious lesions or compressive areas demonstrated on the sagittal images. The axial plane is the optimal plane to assess compression of the spinal cord15
Malignant spinal cord compression with lesions in the paravertebral region and intervertebral foramina being easier to detect.8 Sagittal images with a small field of view (FOV) were not acquired in this case because of the time factor as the patient was distressed, however, the use of a small FOV targeted to sites of abnormality would increase image resolution and thereby optimise delineation of the expanding tumour mass and its relationship to critical anatomical structures. Contrast enhancement is not routinely used for SCC from suspected metastatic deposits as the lesion may become isointense with surrounding bone marrow and therefore difficult to visualise, unless fat suppression is used. Contrast enhancement has been shown not to improve the detection of tumours within the extradural space.16 In such cases, tumour involvement is predicted on the basis of marrow and epidural fat infiltration.17 However, T1-weighted Gadolinium-enhanced images can more effectively depict the soft tissue extent of a metastatic lesion, although this is often clearly seen on the more rapidly acquired T2weighted images. If an intramedullary deposit is suspected contrast enhancement is required and the lesion will be demonstrated as an enhancing mass.8 Fig. 1 is a sagittal T2-weighted image demonstrating a largely intermediate-to-low signal intensity mass protruding from the posterior aspect of the T7 vertebral body, with associated thecal sac invasion and spinal cord compression. Focal areas of high signal intensity within the mass are
Figure 1 spine.
T2 weighted TSE sagittal cervico-thoracic
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Figure 2 spine.
T1 weighted SE sagittal cervico-thoracic
suggestive of haemorrhage. There is no significant paraspinal mass. On T1 weighted images bone marrow fat normally produces high signal that gives a bright appearance on the image. Fig. 2 is a sagittal T1-weighted image demonstrating abnormal hypointense signal from the bone marrow at the level of T7. The appearance of the vertebral discs is significant in determining the likely aetiology of SCC. The normal appearance of the discs suggests that the cause of the SCC is not due to a degenerative or infective cause. Signal from CSF anterior to the spinal cord at the level of T7 is absent suggesting cord impingement. These changes are indicative of metastatic tumour replacing normal fatty marrow. On a T2 weighted TSE axial image, (Fig. 3), the vertebral body displays a homogeneous intermediate signal intensity. The expected low signal intensity of the cortical margin of the vertebral body is no longer well demarcated, and an invasive mass, originating from within the vertebral body has encircled the spinal cord, with resultant compression. These appearances demonstrate focal cord compression at T7 from a suspected metastatic deposit, which appears isolated. There is no evidence of an associated paraspinal mass. The lesion is unlikely to be intramedullary tumour as there is no expansion of the spinal cord.18 Following this examination, the patient was placed on steroid therapy and decompression surgery recommended as the most effective
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Figure 3
T2 weighted TSE axial.
approach to relieving the cord compression and associated symptoms. Radiotherapy was considered but there was concern that this may cause swelling of the cord, exacerbating the problem. Two days following the MRI examination the patient underwent spinal decompression surgery with bone biopsy, the result of which confirmed a lesion with areas of necrosis and haemorrhage. A metastatic lesion was not confirmed, histology was considered abnormal but non-specific in appearance. Six months following surgery the patient remains chair bound and is clinically depressed. She has not regained the use of her legs, her bladder is atonic and permanent catheterisation is required. However, she does retain bowel function. The patient’s home required modification so that she could return to live with her husband who has been trained in her care.
Discussion In cases of malignant spinal cord compression, patient outcome is related to the degree of neurological deficit at the start of the treatment. If patients are diagnosed and treated while they are still ambulant and in control of bladder and anal sphincters, they are more likely to retain neurological function.11 Irreversible loss of function will result if the compression is not relieved promptly.11 Malignant SCC is thus considered an oncological emergency and should be treated within 24 h of the onset of major neurological symptoms.12
In an audit of patients with malignant SCC, Levack et al. demonstrated that there was a mean delay of 66 days from patients presenting to a health care professional and a comprehensive syndrome definitively being diagnosed and documented.6 At the time of diagnosis four out of five patients were unable to walk without assistance; thus 80% of patients were considered to have a poor prognosis. Approximately 60% of these patients were known to have a history of a primary cancer at the initial onset of symptoms.6 Clinically determined sites of pain and sensory level localisation are unreliable and cannot be depended upon to establish diagnosis and plan treatment.6 Patients are often clinically diagnosed with a suspected compromised vertebral level that is subsequently found to be inaccurate by MRI examination. Clinical examination and MRI findings often vary by as much as four vertebral levels below and two vertebral levels above the suspected sensory level.19 Jamieson et al. argued that high thoracic or cervical cord compression may mimic disease from the lumbar spine,20 thereby supporting the strategy of whole spine imaging in cases of malignant SCC. This approach provides accurate lesion detection, even in cases where lesions exist at multiple vertebral levels. Multiple levels of compression are not uncommon, with approximately 25% of patients presenting with disease at two or more levels, and frequently in more than one spinal region.19,21 The accuracy and non-invasive nature of MRI22 and its ability to image the whole spine and surrounding soft tissue has established it as the
Malignant spinal cord compression imaging modality of choice in the evaluation of malignant SCC.8 In comparison, other imaging modalities play a limited role in facilitating the prompt and accurate diagnosis of this pathological condition and only when MRI is contraindicated should other techniques be employed.8 While plain radiographs can depict bony destruction suggestive of metastatic disease with erosion of vertebral bodies and associated fractures and collapse, research suggests that this imaging technique demonstrates only one third of all cases of malignant SCC,19 and inaccurately depicts the vertebral level in approximately 80% of these.6 CT may demonstrate vertebral bone and soft tissue disease extending into the spinal canal and the relationship of tumour to the spinal cord. Mutidetector CT permits reconstruction of images in the sagittal and coronal planes permitting the full extent of disease to be depicted.8 CT with mylography can demonstrate paravertebral lesions growing into the spinal canal, bony lesions and herniated discs but this increases the invasiveness of the examination.9 Bone scintigraphy remains the most cost effective imaging modality for diagnosing bone metastases although MRI is more sensitive and specific.13
Conclusion Malignant SCC is a common sequel to cancer and must be considered for patients with a history of malignant disease who present with low back and/ or nerve root pain. Early diagnosis and appropriate treatment is essential to reduce the risk of permanent disability. Failure to treat in a timely fashion has the potential to impair, suddenly and drastically, the quality of life, not only of a patient with malignant disease but also that of their relatives and carers.22 Patients who lose mobility and bladder or bowel control require 24 h nursing care and for those nursed at home, this puts an immense burden on the family. SCC is, without doubt, one of the most devastating complications of cancer.7 MRI has proven itself as the imaging modality of choice, due to its ability to accurately demonstrate the site and aetiology of cord compression and assist with treatment planning. Alternative investigations may have a role in the care pathway, but they can be misleading and waste valuable time. Therefore, high-risk patients should proceed directly to MRI and the whole spine to ensure metastases at different levels in the spine are not missed.
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References 1. Office for National Statistics Social Survey Division. The prevalence of back pain in Great Britain 1998 e a report on research for the Department of Health using the ONS Omnibus Survey. London: The Stationery Office; 1999. 2. McNally EG, Wilson DJ, Ostlere SJ. Limited magnetic resonance imaging in low back pain instead of plain radiographs: experience with first 1000 cases. Clin Radiol 2001;56:922e5. 3. The Royal College of Radiologists. Making the best use of a department of clinical radiology, guidelines for doctors. 5th ed. London: The Royal College of Radiologists; 2003. 4. Axford J, editor. Neurological disease, Medicine. London: Blackwell Science; 1996. p. 6.81e2 [Chapter 6]. 5. Baines MJ. Spinal cord compression e a personal and palliative care perspective. Clin Oncol 2002;14:135e8. 6. Levack P, Graham J, Collie D, et al. Don’t wait for a sensory level e listen to the symptoms: a prospective audit of the delays in diagnosis of malignant cord compression. Clin Oncol 2002;14:472e80. 7. Rades D, Black M, Bremer M, Wildfang I, Karstens JH, Heidenreich F. Prognostic significance of the time of developing motor deficit before radiation therapy in metastatic spinal cord compression: one-year results of prospective trial. Int J Radiat Oncol Biol Phys 2000;48: 1403e8. 8. Husband JE, Reznek RH. Metastatic effects on the nervous system. In: MacVicar D, editor. Imaging in oncology. 2nd ed. London: Taylor & Francis; 2004. p. 1085e109 [Chapter 43]. 9. Souhami RL, Tannock I, Hohenberger P, Horiot JC. Spinal metastatic disease. In: Siegal T, Siegal T, Brada M, editors. Oxford textbook of oncology. 2nd ed. Oxford: Oxford University Press; 2002. p. 977e93 [Chapter 5.5]. 10. Stoker DJ, Saifuddin A. Bone tumours (2): malignant lesions. In: Grainer RG, Allison DJ, Adam A, Dixon AK, editors. Diagnostic radiology a textbook of medical imaging. 4th ed. London: Churchill Livingstone; 2001. p. 1869e75 [Chapter 80]. 11. Tannock RLS, Hohenberger P, Horiot JC, editors. Oxford textbook of oncology. 2nd ed. Oxford: Oxford University Press; 2002. 12. Husband DJ. Malignant spinal cord compression; prospective study of delays in referral and treatment. BMJ 1998; 317:18e21. 13. Runge VM. Thoracic spine. Clinical MRI. London: W B Saunders Company; 2002. p. 157e61 [Chapter 7]. 14. Czervionke LF, Daniels DL. Degenerative disease of the spine. In: Atlas SW, editor. Magnetic resonance imaging of the brain and spine. New York: Raven Press; 1991. p. 795e864 [Chapter 22]. 15. Stevens JM, Rich PM. The imaging of spinal pathology. In: Grainer RG, Allison DJ, Adam A, Dixon AK, editors. Diagnostic radiology a textbook of medical imaging. 4th ed. London: Churchill Livingstone; 2001. p. 2429e61 [Chapter 102]. 16. Sze G, Twohig M. Neoplastic disease of the Spine & Spinal Cord. In: Atlas SW, editor. Magnetic resonance imaging of the brain and spine. New York: Raven Press; 1991. p. 921e 65 [Chapter 24]. 17. Najem ES, Bazan III C, Jinkins JR. Thoracic spine. In: Stark DD, Bradley Jr WG, editors. 3rd ed. Magnetic resonance imaging, vol. III St. Louis: Mosby; 1999. p. 1851e82 [Chapter 86]. 18. Keoller KK, Osenblum RS, Morrison AL. Neoplasms of the spinal cord and filum terminale: radiologicepathologic correlation. Radiographics 2000;20:1721e49.
298 19. Husband DJ, Grant KA, Romaniuk CS. MRI in the diagnosis and treatment of suspected malignant spinal cord compression. Br J Radiol 2001;74:15e23. 20. Jamieson DRS, Teasdale E, Willison HJ. Lesson of the week: false localising signs in the spinal cord. BMJ 1996;12:243e4.
A. Slocombe, S. Boynes 21. Chamberlin MC, Kormanik PA. Epidural spinal cord compression: a single institution’s retrospective experience. Neuro-oncol 1999 Apr;1(2):120e3. 22. Hardy JR, Huddart R. Spinal cord compression e what are the treatment standards. Clin Oncol 2002;14:132e4.
