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Tophaceous gout of the lumbar spine mimicking infectious spondylodiscitis and epidural abscess: MR imaging findings
Journal of Clinical Neuroscience (2005) 12(1), 44–46 0967-5868/$ - see front matter ª 2004 Elsevier Ltd. All rights reserved. doi:10.1016/j.jocn.2004.03.020
Neuroradiology report
Tophaceous gout of the lumbar spine mimicking infectious spondylodiscitis and epidural abscess: MR imaging findings Pao-Sheng Yen1
MD,
Jui-Feng Lin2
MD,
Shin-Yuan Chen2,3
MD MSC,
Shinn-Zong Lin2 MD PHD
1 Department of Radiology, Buddhist Tzu-Chi General Hospital, Hualien, Taiwan, 2Department of Neurosurgery, Buddhist Tzu-Chi General Hospital, Hualien, Taiwan, 3Department of Neurosurgery, Wang-Fang Municipal Hospital/Taipei Medical University, Taipei, Taiwan
Summary We report a case of surgically proven tophaceous gout of the lumbar spine at the L5-S1 level that mimicked infectious spondylodiscitis and epidural abscess on magnetic resonance (MR) images in a 65-year-old woman. The spinal tophi were hypointense on T1weighted images; focally and strongly hyperintense on T2-weighted images; and heterogeneously, marginally enhancing on contrast-enhanced T1-weighted images. The aim of this report is to emphasize the importance of considering this disease entity in the differential diagnosis of an epidural mass in a patient with chronic back pain. ª 2004 Elsevier Ltd. All rights reserved. Keywords: spinal gout, epidural abscess, magnetic resonance imaging
INTRODUCTION Tophaceous gout affecting the axial skeleton is rare. It is caused by the abnormal deposition of monosodium urate crystals around joints and disc spaces. The spinal tophi can closely resemble infectious spondylodiscitis and epidural abscesses on magnetic resonance (MR) images. Thus, the preoperative diagnosis of spinal gout is difficult, especially in the absence of known hyperuricaemia or prior episodes of acute gouty arthritis. We report a case of spinal gout at the L5-S1 level in a 65-year-old woman who presented with chronic low back pain and radiculopathy. CASE REPORT A 65-year-old woman presented with 10-month history of progressive low-back pain, walking inability, and distal paraparesis. She was experiencing severe pain. On examination, she had no elevation of temperature or clinical signs of infection. Mild weakness (grade 4/5) of knee extension and foot-toe extension and moderate weakness (grade 3/5) of plantar flexion were present and slightly more prominent on the right side than on the left. Proprioception was intact. Sensation to light touch was decreased, and the patient complained of dysesthesia primarily on the right L5 and S1 dermatomes. Examination of the deep tendon reflexes revealed mildly reduced bilateral knee jerks and a markedly reduced right-sided ankle jerk. Results of straight-leg-raising tests were positive at 70 on both sides. All other findings were normal. No clinical signs of gout, such as joint inflammation or subcutaneous tophi, were observed. Laboratory results were remarkable for an elevated erythrocyte sedimentation rate (52 mm/h; normal, <20 mm/h). The patient's white blood cell count (6700/mm3 ) was normal. Routine radiographs of the lumbar spine showed spondylolysis of the pars interarticularis with spondylolisthesis of L5 on S1 and
Received 28 December 2003 Accepted 1 March 2004 Correspondence to: Shin-Yuan Chen, Department of Neurosurgery, Buddhist Tzu-Chi General Hospital, 707, Section 3, Chung-Yang Road, Hualien, Taiwan. Tel.: +886-3-856-1825x2151; Fax: +886-3-846-3164; E-mail: [email protected]
44
bony erosion at the inferior endplate of L5. A lumbar spine MR revealed an abnormal soft-tissue mass arising from the right posterior epidural space of L5-S1 with extension into the L5-S1 disc. This mass caused bony destruction of the right facet joint and bony erosion of the posterior aspect of the L5 inferior endplate. The soft tissue was isointense relative to the intervertebral disc on T1-weighted images and heterogeneous with foci of hyperintensity on T2-weighted images. After the intravenous administration of a gadolinium-based contrast agent, the mass demonstrated fairly homogeneous enhancement with foci of low signal intensity without enhancement (Fig. 1). With the impression of infectious spondylodiscitis with an epidural abscess, decompression laminectomy was performed. During the operation, a large, irregular, epidural mass was found to arise from the right L5-S1 facet joint with extension into the disc space. Obliteration of the lateral recess and encasement of the S1 nerve root were found. The mass had a cheesy and yellowish appearance. Pathological examination of the mass revealed fibrocartilaginous tissue with multinucleated giant cells and amorphous crystalline material (Fig. 2). No evidence of infection was found. The diagnosis of tophaceous gout was therefore established. After surgery, a rheumatologist examined the patient and found no evidence of gouty arthropathy. Serum urea, urate, and creatinine levels were all normal. The patient was discharged home and underwent regular follow-up in our outpatient department.
DISCUSSION Gout is a common metabolic disorder with well-defined clinical, biochemical, and radiological features. It is caused by hyperuricemia due to either increased production or decreased renal excretion of uric acid. It is a worldwide disease, with a prevalence of 0.2–0.4% and an annual incidence of about 0.01–0.015%.5 Typically, acute gout manifests with pain, swelling, and tenderness in the first metatarsophalangeal joint, tarsal joints, ankles, and knees. It may be monoarticular or oligoarticular. Histopathologically, the acute attack is caused by inflammation of the synovial membrane due to monosodium urate crystals in the synovial fluid. In the chronic phase of the disease, a soft-tissue mass of monosodium urate crystals forms in the articular cartilage, subchondral bone, synovial membrane, and periarticular tissues,
Tophaceous gout of the lumbar spine 45
Fig. 1 Images in a 65-year-old woman with 10-month history of progressive low-back pain, walking inability, and distal paraparesis. (A) Sagittal T1-weighted (516/29/1 [TR/TE/excitations]) MR image shows an isointense lesion in the L5-S1 disc and posterior epidural space. The lesion represents gouty tophi (arrowheads). Bony erosion of the inferior endplate of L5 is also present. (B) Sagittal T2-weighted (4500/90/1) MR image shows focal area of strong hyperintensity within the isointense lesion in the L5-S1 disc space (arrow). (C) Contrast-enhanced sagittal T1-weighted (516/29/1) MR image shows good heterogeneous enhancement of the gouty tophi with nonenhancing foci, which probably result from crystalline material (arrows). (D) Contrast-enhanced axial T1-weighted (516/29/ 1) MR image of L5-S1 shows good marginal enhancement of the disc space and epidural mass (arrowheads). Bony erosion of the right facet joint is also present.
Fig. 2 Photomicrographs of surgical specimens from the L5-S1 disc show amorphous material with a multinucleated giant cell reaction (arrowheads), a characteristic of gout (hematoxylin and eosin stain, 200).
ª 2004 Elsevier Ltd. All rights reserved.
leading to the formation of tophi. These deposits can be found in the subcutaneous tissues, tendons, bursae, or joint capsule, where they cause cartilaginous degeneration and erosion.11 Gouty involvement of the spine is rare. Gouty tophi may occur in the spine, including intervertebral disc spaces, ligament flavum, facet joints, lamina, pedicles, extradural soft tissues, and filum terminale. The cervical, thoracic, and lumbar spine are roughly equally affected.2;4;8;9;14 Radiographic features of spinal gout may include degenerative spondylosis; discovertebral erosions; bone destruction causing joint subluxation; spinal deformity; spontaneous fusion; and, occasionally, pathological fractures.7 Although MR imaging is now commonly used in the evaluation of back pain, the MR pattern of spinal gout is not well recognized because of the rarity of this disease. In previously reported cases, the MR features of spinal tophi appeared as homogeneous areas of intermediate-tolow signal intensity on T1-weighted images. On T2-weighted images, the signal intensity of the tophi varies from homogeneous hyperintensity to homogeneous hypointensity. This hyperintensity may result from a relative increase in the water content of the tophus and the relative homogeneity of local magnetic field within Journal of Clinical Neuroscience (2005) 12(1), 44–46
46 Yen et al.
the tophi. In comparison, the T2-weighted hypointensity may be caused by immobile protons in the tophi. Foci of low intensity can be seen on images obtained with all sequences; this appearance can be due to regions of calcifications, mature fibrous tissue, or hemosiderin deposition in the tophi. After gadolinium enhancement, the tophi show homogeneous or heterogeneous marginal enhancement. The enhancement of the tophi is thought to be the result of well-vascularized chronic, inflammatory fibrous tissue engendered by urate crystal deposition. The urate crystal itself, however, is not enhancing. In our patient, the tophi appeared as hypointensity on T1-weighted images and as foci of strong hyperintensity on T2-weighted images, with heterogeneous marginal enhancement. These findings are consistent with those previously reported.1;6;7 Clinically, the difficulty in diagnosis emerges when a patient with neurological symptoms presents with no history of gouty attacks or when the serum urate level is within the normal range. In fact, serum urate levels may be normal in 30% of patients with acute gouty attacks.10;12;13 However, on retrospective review of the MR images in our case, the following findings were useful in differentiating this condition from infectious spondylitis: (1) the association of spondylolisthesis due to bony erosion of the pars interarticularis and facet joint; (2) smooth bony erosion of the L5 inferior endplate rather than irregular destruction; and (3) normal bone-marrow signal intensity of the adjacent vertebrae, which is not commonly seen in infectious spondylitis. The key to correct diagnosis is careful history taking, analysis of imaging studies, or image-guided biopsy. Decompression surgery is probably the treatment of choice for acute neurological compromise and it is indicated when conservative treatment fails. However, medical treatment of spinal gout with steroids may be effective if the nature of the cord compression is acute intense inflammation, as in acute synovitis in a gouty attack affecting a peripheral joint.3 Current management recommendations for acute gout include the use of indomethacin and other nonsteroidal anti-inflammatory drugs, such as naproxen, ibuprofen, fenoprofen, and sulindac. Colchicine is no longer the drug of choice. Chronic gout can be managed effectively with probenecid, allopurinol, or both. Maintaining high fluid intake and the use of alkalinizing agents may limit the precipitation of uric acid and its sequelae.15
Journal of Clinical Neuroscience (2005) 12(1), 44–46
In conclusion, spinal gout should be included in the differential diagnosis of patients who present with back pain and an epidural mass. Careful history taking, analysis of imaging studies, or image-guide biopsy are helpful in correct diagnosis. Surgical decompression followed by optimization of pharmacological treatment almost always facilitates a good recovery from the neurological complications.
REFERENCES 1. Barrett K, Miller ML, Wilson JT. Tophaceous gout of the spine mimicking epidural infection: case report and review of the literature. Neurosurgery 2001; 48: 1170–1173. 2. Bonaldi VM, Duong H, Starr MR, Sarazin L, Richardson J. Tophaceous gout of the lumbar spine mimicking an epidural abscess: MR features. AJNR Am J Neuroradiol 1996; 17: 1949–1952. 3. Dhote R, Roux FX, Bachmeyer C, Tudoret L, Daumas-Duport C, Christoforov B. Extradural spinal tophaceous gout: evolution with medical treatment. Clin Exp Rheumatol 1997; 15: 421–423. 4. Fenton P, Young S, Prutis K. Gout of the spine. Two case reports and a review of the literature. J Bone Joint Surg Am 1995; 77: 767–771. 5. Hall AP, Barry PE, Dawber TR, McNamara PM. Epidemiology of gout and hyperuricemia; a long-term population study. Am J Med 1967; 42: 27–37. 6. Hsu CY, Shih TT, Huang KM, Chen PQ, Sheu JJ, Li YW. Tophaceous gout of the spine: MR imaging features. Clin Radiol 2002; 57: 919–925. 7. King KC, Nicholas C. Gouty arthropathy of the lumbar spine: a case report and review of the literature. Spine 1997; 22: 2309–2312. 8. Leaney BJ, Calvert JM. Tophaceous gout producing spinal cord compression: case report. J Neurosurg 1983; 58: 580–582. 9. Murshid WR, Moss TH, Ettles DF, Cummins BH. Tophaceous gout of the spine causing spinal cord compression. Br J Neurosurg 1994; 8: 751–754. 10. Paquette S, Lach B, Guiot B. Lumbar radiculopathy secondary to gouty tophi in the filum terminale in a patient without systemic gout: case report. Neurosurgery 2000; 46: 986–988. 11. Resnick D, Niwayama G. Gouty arthritis. In: Resnick D (ed) Diagnosis of Bone and Joint Disorders. Saunders, Philadelphia 1995; 1511–1555. 12. Van de Laar MA, Van Soesbergen RM, Matricali B. Tophaceous gout of the cervical spine without peripheral tophi. Arthritis Rheum 1987; 30: 237– 238. 13. Varga J, Giampaolo C, Goldenberg DL. Tophaceous gout of the spine in a patient with no peripheral tophi: case report and review of the literature. Arthritis Rheum 1985; 28: 1312–1315. 14. Yen HL, Cheng CH, Lin JW. Cervical myelopathy due to gouty tophi in the intervertebral disc space. Acta Neurochir (Wien) 2002; 144: 205–207. 15. Yu GH, Chen JY, Wu Y-JJ, Ho HH, Luo SF. Retrospective analysis of 822 gout patients. J Rheumatol ROC 1993; 10: 20–29.
ª 2004 Elsevier Ltd. All rights reserved.
Neuroradiology report
Tophaceous gout of the lumbar spine mimicking infectious spondylodiscitis and epidural abscess: MR imaging findings Pao-Sheng Yen1
MD,
Jui-Feng Lin2
MD,
Shin-Yuan Chen2,3
MD MSC,
Shinn-Zong Lin2 MD PHD
1 Department of Radiology, Buddhist Tzu-Chi General Hospital, Hualien, Taiwan, 2Department of Neurosurgery, Buddhist Tzu-Chi General Hospital, Hualien, Taiwan, 3Department of Neurosurgery, Wang-Fang Municipal Hospital/Taipei Medical University, Taipei, Taiwan
Summary We report a case of surgically proven tophaceous gout of the lumbar spine at the L5-S1 level that mimicked infectious spondylodiscitis and epidural abscess on magnetic resonance (MR) images in a 65-year-old woman. The spinal tophi were hypointense on T1weighted images; focally and strongly hyperintense on T2-weighted images; and heterogeneously, marginally enhancing on contrast-enhanced T1-weighted images. The aim of this report is to emphasize the importance of considering this disease entity in the differential diagnosis of an epidural mass in a patient with chronic back pain. ª 2004 Elsevier Ltd. All rights reserved. Keywords: spinal gout, epidural abscess, magnetic resonance imaging
INTRODUCTION Tophaceous gout affecting the axial skeleton is rare. It is caused by the abnormal deposition of monosodium urate crystals around joints and disc spaces. The spinal tophi can closely resemble infectious spondylodiscitis and epidural abscesses on magnetic resonance (MR) images. Thus, the preoperative diagnosis of spinal gout is difficult, especially in the absence of known hyperuricaemia or prior episodes of acute gouty arthritis. We report a case of spinal gout at the L5-S1 level in a 65-year-old woman who presented with chronic low back pain and radiculopathy. CASE REPORT A 65-year-old woman presented with 10-month history of progressive low-back pain, walking inability, and distal paraparesis. She was experiencing severe pain. On examination, she had no elevation of temperature or clinical signs of infection. Mild weakness (grade 4/5) of knee extension and foot-toe extension and moderate weakness (grade 3/5) of plantar flexion were present and slightly more prominent on the right side than on the left. Proprioception was intact. Sensation to light touch was decreased, and the patient complained of dysesthesia primarily on the right L5 and S1 dermatomes. Examination of the deep tendon reflexes revealed mildly reduced bilateral knee jerks and a markedly reduced right-sided ankle jerk. Results of straight-leg-raising tests were positive at 70 on both sides. All other findings were normal. No clinical signs of gout, such as joint inflammation or subcutaneous tophi, were observed. Laboratory results were remarkable for an elevated erythrocyte sedimentation rate (52 mm/h; normal, <20 mm/h). The patient's white blood cell count (6700/mm3 ) was normal. Routine radiographs of the lumbar spine showed spondylolysis of the pars interarticularis with spondylolisthesis of L5 on S1 and
Received 28 December 2003 Accepted 1 March 2004 Correspondence to: Shin-Yuan Chen, Department of Neurosurgery, Buddhist Tzu-Chi General Hospital, 707, Section 3, Chung-Yang Road, Hualien, Taiwan. Tel.: +886-3-856-1825x2151; Fax: +886-3-846-3164; E-mail: [email protected]
44
bony erosion at the inferior endplate of L5. A lumbar spine MR revealed an abnormal soft-tissue mass arising from the right posterior epidural space of L5-S1 with extension into the L5-S1 disc. This mass caused bony destruction of the right facet joint and bony erosion of the posterior aspect of the L5 inferior endplate. The soft tissue was isointense relative to the intervertebral disc on T1-weighted images and heterogeneous with foci of hyperintensity on T2-weighted images. After the intravenous administration of a gadolinium-based contrast agent, the mass demonstrated fairly homogeneous enhancement with foci of low signal intensity without enhancement (Fig. 1). With the impression of infectious spondylodiscitis with an epidural abscess, decompression laminectomy was performed. During the operation, a large, irregular, epidural mass was found to arise from the right L5-S1 facet joint with extension into the disc space. Obliteration of the lateral recess and encasement of the S1 nerve root were found. The mass had a cheesy and yellowish appearance. Pathological examination of the mass revealed fibrocartilaginous tissue with multinucleated giant cells and amorphous crystalline material (Fig. 2). No evidence of infection was found. The diagnosis of tophaceous gout was therefore established. After surgery, a rheumatologist examined the patient and found no evidence of gouty arthropathy. Serum urea, urate, and creatinine levels were all normal. The patient was discharged home and underwent regular follow-up in our outpatient department.
DISCUSSION Gout is a common metabolic disorder with well-defined clinical, biochemical, and radiological features. It is caused by hyperuricemia due to either increased production or decreased renal excretion of uric acid. It is a worldwide disease, with a prevalence of 0.2–0.4% and an annual incidence of about 0.01–0.015%.5 Typically, acute gout manifests with pain, swelling, and tenderness in the first metatarsophalangeal joint, tarsal joints, ankles, and knees. It may be monoarticular or oligoarticular. Histopathologically, the acute attack is caused by inflammation of the synovial membrane due to monosodium urate crystals in the synovial fluid. In the chronic phase of the disease, a soft-tissue mass of monosodium urate crystals forms in the articular cartilage, subchondral bone, synovial membrane, and periarticular tissues,
Tophaceous gout of the lumbar spine 45
Fig. 1 Images in a 65-year-old woman with 10-month history of progressive low-back pain, walking inability, and distal paraparesis. (A) Sagittal T1-weighted (516/29/1 [TR/TE/excitations]) MR image shows an isointense lesion in the L5-S1 disc and posterior epidural space. The lesion represents gouty tophi (arrowheads). Bony erosion of the inferior endplate of L5 is also present. (B) Sagittal T2-weighted (4500/90/1) MR image shows focal area of strong hyperintensity within the isointense lesion in the L5-S1 disc space (arrow). (C) Contrast-enhanced sagittal T1-weighted (516/29/1) MR image shows good heterogeneous enhancement of the gouty tophi with nonenhancing foci, which probably result from crystalline material (arrows). (D) Contrast-enhanced axial T1-weighted (516/29/ 1) MR image of L5-S1 shows good marginal enhancement of the disc space and epidural mass (arrowheads). Bony erosion of the right facet joint is also present.
Fig. 2 Photomicrographs of surgical specimens from the L5-S1 disc show amorphous material with a multinucleated giant cell reaction (arrowheads), a characteristic of gout (hematoxylin and eosin stain, 200).
ª 2004 Elsevier Ltd. All rights reserved.
leading to the formation of tophi. These deposits can be found in the subcutaneous tissues, tendons, bursae, or joint capsule, where they cause cartilaginous degeneration and erosion.11 Gouty involvement of the spine is rare. Gouty tophi may occur in the spine, including intervertebral disc spaces, ligament flavum, facet joints, lamina, pedicles, extradural soft tissues, and filum terminale. The cervical, thoracic, and lumbar spine are roughly equally affected.2;4;8;9;14 Radiographic features of spinal gout may include degenerative spondylosis; discovertebral erosions; bone destruction causing joint subluxation; spinal deformity; spontaneous fusion; and, occasionally, pathological fractures.7 Although MR imaging is now commonly used in the evaluation of back pain, the MR pattern of spinal gout is not well recognized because of the rarity of this disease. In previously reported cases, the MR features of spinal tophi appeared as homogeneous areas of intermediate-tolow signal intensity on T1-weighted images. On T2-weighted images, the signal intensity of the tophi varies from homogeneous hyperintensity to homogeneous hypointensity. This hyperintensity may result from a relative increase in the water content of the tophus and the relative homogeneity of local magnetic field within Journal of Clinical Neuroscience (2005) 12(1), 44–46
46 Yen et al.
the tophi. In comparison, the T2-weighted hypointensity may be caused by immobile protons in the tophi. Foci of low intensity can be seen on images obtained with all sequences; this appearance can be due to regions of calcifications, mature fibrous tissue, or hemosiderin deposition in the tophi. After gadolinium enhancement, the tophi show homogeneous or heterogeneous marginal enhancement. The enhancement of the tophi is thought to be the result of well-vascularized chronic, inflammatory fibrous tissue engendered by urate crystal deposition. The urate crystal itself, however, is not enhancing. In our patient, the tophi appeared as hypointensity on T1-weighted images and as foci of strong hyperintensity on T2-weighted images, with heterogeneous marginal enhancement. These findings are consistent with those previously reported.1;6;7 Clinically, the difficulty in diagnosis emerges when a patient with neurological symptoms presents with no history of gouty attacks or when the serum urate level is within the normal range. In fact, serum urate levels may be normal in 30% of patients with acute gouty attacks.10;12;13 However, on retrospective review of the MR images in our case, the following findings were useful in differentiating this condition from infectious spondylitis: (1) the association of spondylolisthesis due to bony erosion of the pars interarticularis and facet joint; (2) smooth bony erosion of the L5 inferior endplate rather than irregular destruction; and (3) normal bone-marrow signal intensity of the adjacent vertebrae, which is not commonly seen in infectious spondylitis. The key to correct diagnosis is careful history taking, analysis of imaging studies, or image-guided biopsy. Decompression surgery is probably the treatment of choice for acute neurological compromise and it is indicated when conservative treatment fails. However, medical treatment of spinal gout with steroids may be effective if the nature of the cord compression is acute intense inflammation, as in acute synovitis in a gouty attack affecting a peripheral joint.3 Current management recommendations for acute gout include the use of indomethacin and other nonsteroidal anti-inflammatory drugs, such as naproxen, ibuprofen, fenoprofen, and sulindac. Colchicine is no longer the drug of choice. Chronic gout can be managed effectively with probenecid, allopurinol, or both. Maintaining high fluid intake and the use of alkalinizing agents may limit the precipitation of uric acid and its sequelae.15
Journal of Clinical Neuroscience (2005) 12(1), 44–46
In conclusion, spinal gout should be included in the differential diagnosis of patients who present with back pain and an epidural mass. Careful history taking, analysis of imaging studies, or image-guide biopsy are helpful in correct diagnosis. Surgical decompression followed by optimization of pharmacological treatment almost always facilitates a good recovery from the neurological complications.
REFERENCES 1. Barrett K, Miller ML, Wilson JT. Tophaceous gout of the spine mimicking epidural infection: case report and review of the literature. Neurosurgery 2001; 48: 1170–1173. 2. Bonaldi VM, Duong H, Starr MR, Sarazin L, Richardson J. Tophaceous gout of the lumbar spine mimicking an epidural abscess: MR features. AJNR Am J Neuroradiol 1996; 17: 1949–1952. 3. Dhote R, Roux FX, Bachmeyer C, Tudoret L, Daumas-Duport C, Christoforov B. Extradural spinal tophaceous gout: evolution with medical treatment. Clin Exp Rheumatol 1997; 15: 421–423. 4. Fenton P, Young S, Prutis K. Gout of the spine. Two case reports and a review of the literature. J Bone Joint Surg Am 1995; 77: 767–771. 5. Hall AP, Barry PE, Dawber TR, McNamara PM. Epidemiology of gout and hyperuricemia; a long-term population study. Am J Med 1967; 42: 27–37. 6. Hsu CY, Shih TT, Huang KM, Chen PQ, Sheu JJ, Li YW. Tophaceous gout of the spine: MR imaging features. Clin Radiol 2002; 57: 919–925. 7. King KC, Nicholas C. Gouty arthropathy of the lumbar spine: a case report and review of the literature. Spine 1997; 22: 2309–2312. 8. Leaney BJ, Calvert JM. Tophaceous gout producing spinal cord compression: case report. J Neurosurg 1983; 58: 580–582. 9. Murshid WR, Moss TH, Ettles DF, Cummins BH. Tophaceous gout of the spine causing spinal cord compression. Br J Neurosurg 1994; 8: 751–754. 10. Paquette S, Lach B, Guiot B. Lumbar radiculopathy secondary to gouty tophi in the filum terminale in a patient without systemic gout: case report. Neurosurgery 2000; 46: 986–988. 11. Resnick D, Niwayama G. Gouty arthritis. In: Resnick D (ed) Diagnosis of Bone and Joint Disorders. Saunders, Philadelphia 1995; 1511–1555. 12. Van de Laar MA, Van Soesbergen RM, Matricali B. Tophaceous gout of the cervical spine without peripheral tophi. Arthritis Rheum 1987; 30: 237– 238. 13. Varga J, Giampaolo C, Goldenberg DL. Tophaceous gout of the spine in a patient with no peripheral tophi: case report and review of the literature. Arthritis Rheum 1985; 28: 1312–1315. 14. Yen HL, Cheng CH, Lin JW. Cervical myelopathy due to gouty tophi in the intervertebral disc space. Acta Neurochir (Wien) 2002; 144: 205–207. 15. Yu GH, Chen JY, Wu Y-JJ, Ho HH, Luo SF. Retrospective analysis of 822 gout patients. J Rheumatol ROC 1993; 10: 20–29.
ª 2004 Elsevier Ltd. All rights reserved.