British Journal of Radiology (2007) 80, 686-689
© 2007 British Institute of Radiology
doi: 10.1259/bjr/53147199
Acute spinal cord compression
D Butteriss, BSc, MBBS(Hons), FRCR
and
V Jayakrishnan, FRCR
Department of Neuroradiology, Regional Neurosciences Centre, Newcastle General Hospital, Westgate Road, Newcastle upon Tyne NE4 6BE, UK
Correspondence: Dr V Jayakrishnan, Department of Neuroradiology, Regional Neurosciences Centre, Newcastle General Hospital, Westgate Road, Newcastle upon Tyne NE4 6BE, UK. E-mail: vijay.jayakrishnan{at}nuth.nhs.uk
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Case report
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A 57-year-old man with a known diagnosis of metastatic prostate cancer presented to the neurosciences centre complaining of increasing bilateral lower limb weakness and sensory changes over a period of several weeks. There was also long-standing back pain. He had initially been managed with radical radiotherapy and hormonal manipulation with cyproterone acetate (Zoladex), but following disease progression had been changed to palliative chemotherapy with mitoxantrone and prednisolone. This had been terminated early following a significant pulmonary embolus and he was currently on symptomatic treatment only. Examination confirmed bilateral symmetrical reduced power and reflexes in both lower limbs, with altered sensation distal to the level of the upper abdomen. A presumptive diagnosis of spinal cord compression secondary to spinal metastases was made. MRI of the entire spine was performed. Selected sagittal (Figure 1
) and axial (Figure 2) images are shown.
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Figure 1. MidsagittalT2 weighted images of the (a) cervicothoracic and (b) thoracolumbar spine, together with corresponding (c) sagittal short tau inversion recovery (STIR) and (d) T1 weighted images of the cervicothoracic spine.
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- a) Is there evidence of metastatic spinal disease?
- b) Is there evidence of cord compression and, if so, at which level(s)?
- c) What is the cause of any cord compression?
MRI demonstrates areas of signal abnormality within multiple vertebral bodies consistent with bony metastatic disease. At T8 there is infiltration of the posterior elements by tumour, with an extradural soft tissue nodule present dorsal to the thecal sac. This is not, however, causing overt cord compression.
MRI also demonstrates an abnormal accumulation of extradural fat dorsal to the thoracic theca, between the T4 and T8/9 levels. This is isointense to normal fat on all sequences, including signal nulling on short tau inversion recovery (STIR) images. The maximum anteroposterior diameter of the fat is 12.29 mm. There is associated compression of the mid-thoracic cord, with effacement of the surrounding cerebrospinal fluid (CSF) and flattening of the cord itself. In the lumbar region, the abnormal extradural fat accumulation is more circumferential, resulting in compression and polygonal deformation of the thecal sac and crowding of the cauda equina roots.
This appearance is characteristic of spinal epidural lipomatosis (SEL). In the thoracic spine, the fat accumulation in the epidural space is contributing to cord compression produced by the extradural metastatic nodule.
The patient was treated with fractionated radiotherapy to T7–9 in an attempt to reduce the mass effect of the tumour and is an inpatient at a local hospice for palliative care.
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Discussion
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SEL is an uncommon condition characterized by an abnormal accumulation of normal fat in the extradural space, resulting in cord or cauda equina compression. It was first described in 1975 [1]. It is commonest in the thoracic region (58–61%), where fat deposition is predominantly posterior to the thecal sac, and is by definition greater than 7 mm thick in the anteroposterior dimension [2]. In the lumbar region, affected in 39–42% of cases, the fat deposition is circumferential, resulting in characteristic polygonal deformation of the thecal sac, caused by the persistent attachments of the meningovertebral ligaments. This is usually termed the "Y sign", although triangular and stellate appearances have also been described [3]. An MRI grading for the severity of lumbosacral SEL has been described [4] using ratios of the dural sac diameter to extradural fat diameter or extradural fat diameter to spinal canal diameter, suggesting that 2.1% of patients undergoing lumbosacral MRI had symptomatic severe extradural fat overgrowth.
The condition is most common in middle-aged men and usually presents with a long history of gradually worsening signs and symptoms including paraparesis, back pain and lower limb sensory changes. Other signs, such as radiculopathy, or bladder and bowel functional disturbance, are less common. The exact pattern varies depending on the position and severity of the neural compression [5].
MRI is the investigation of choice, demonstrating the extradural fat, which is isointense with subcutaneous fat on all sequences, and the degree and position of cord compression. Fat suppression techniques are useful to confirm the diagnosis and exclude other causes of cord compression with potentially similar appearances, such as epidural haematoma.
The aetiology of SEL is varied. Most cases are associated with raised circulating corticosteroid levels, either iatrogenic or, in Cushing's disease, endogenous. Local steroids from epidural injection have also been implicated. It may occur as a side effect of the use of other medications such as protease inhibitors or anti-androgens. Rarely, simple obesity is associated with SEL, and the condition may be truly idiopathic.
Treatment is directed against the causative agent when possible, with reduction of iatrogenic steroid doses, management of Cushing's disease and weight loss in the obese. In severe or refractory cases surgical decompression with multilevel laminectomy, debulking of the extradural fat and posterolateral fusion has a high success rate. There are reports of less-invasive endoscopic fat aspiration and of epidural steroid injection as treatment, which presumably induces local fat atrophy [6].
Received for publication September 1, 2005.
Revision received February 13, 2006.
Accepted for publication February 20, 2006.
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References
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- Lee M, Lekias J, Gubbay SS, Hurst PE. Spinal cord compression by extradural fat after renal transplantation. Med J Aust 1975;1:201–3.[Medline]
- Robertson SC, Traynelis VC, Follett KA, Menezes AH. Idiopathic spinal epidural lipomatosis. Neurosurgery 1997;41:68–75.[CrossRef][Medline]
- Geers C, Lecouvet FE, Behets C, Malghem J, Cosnard G, Lengele BG. Polygonal deformation of the dural sac in lumbar epidural lipomatosis: an anatomic explanation by the presence of meningovertebral ligaments. AJNR Am J Neuroradiol 2003;24:1276–82.[Abstract/Free Full Text]
- Borre DG, Borre GE, Aude F, Palmieri GN. Lumbosacral epidural lipomatosis: MRI grading. Eur Radiol 2003;13:1709–21.[CrossRef][Medline]
- Deogaonkar M, Goel A, Tingare K, Dahiwadkar H, Nagpal H. Extradural lipomatosis presenting with paraplegia. J Postgrad Med 1995;41:85–6.[Medline]
- Fassett DR, Schmidt MH. Spinal epidural lipomatosis: a review of its causes and recommendations for treatment. Neurosurg Focus 2004;16:1–3.[Medline]
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Case report
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