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Table of Contents    
Year : 2022  |  Volume : 70  |  Issue : 4  |  Page : 1714-1716

Spinal Tophus Mimicking, a Migration Disc with Acute Sciatica

1 Section of Neurosurgery, Department of Surgery, Ditmanson Medical Foundation, Chia-Yi Christian Hospital, Chia-Yi City 600; Department of Biotechnology, Asia University, Taichung City 41354; Department of Neurological Surgery, Tri-Service General Hospital, National Defense Medical Center, Taipei 114, Taiwan
2 Department of Neurological Surgery, Tri-Service General Hospital, National Defense Medical Center, Taipei 114; Division of Neurosurgery, Department of Surgery, Sijhih Cathay General Hospital, New Taipei City 22174; Department of Medicine, School of Medicine, Fu Jen Catholic University, New Taipei City 24205, Taiwan

Date of Submission09-Jul-2019
Date of Decision20-Dec-2019
Date of Acceptance15-May-2021
Date of Web Publication30-Aug-2022

Correspondence Address:
Cheng-Ta Hsieh
Division of Neurosurgery, Department of Surgery, Sijhih Cathay General Hospital, No. 2, Ln. 59, Jiancheng Rd., Xizhi Dist., New Taipei City 22174
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0028-3886.355145

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How to cite this article:
Sun JM, Hsieh CT. Spinal Tophus Mimicking, a Migration Disc with Acute Sciatica. Neurol India 2022;70:1714-6

How to cite this URL:
Sun JM, Hsieh CT. Spinal Tophus Mimicking, a Migration Disc with Acute Sciatica. Neurol India [serial online] 2022 [cited 2022 Oct 2];70:1714-6. Available from: https://www.neurologyindia.com/text.asp?2022/70/4/1714/355145


Gout is a common metabolic disorder characterized by the deposition of monosodium urate crystals in joints and periarticular connective tissue. In gout, most tophi, also known as tophaceous gouts, induce inflammatory arthritis and typically affect the peripheral joints including the knee, ankle, elbow, wrist, and hand.[1] However, a spinal tophus mimicking a migration disc has rarely been reported.[2] We report the case of a patient with a spinal tophus in the lumbar spine, presenting with acute sciatica, followed by literature review.

A 66-year-old man began experiencing acute lower back pain radiating to the left leg 1 week prior to presentation. He had peripheral gout arthritis for 1 year and presented with multiple tophi deposits over his hands and toes. Although he was taking allopurinol, the symptoms of gout arthritis recurred occasionally. He had undergone laminectomy and discectomy in the L4–5 vertebrae 2 years before admission. Physical examination at admission revealed radicular pain distributed along the left L3–5 nerves. The left straight leg raise test sign was positive. Muscle strength and deep tendon reflexes were normal. No joint swelling and tenderness were found over the knee, ankles, or toes, except for the deposition of the tophi in the hands and feet. Laboratory examination revealed a white blood cell count of 9320/μL and the uric acid level was 12.1 mg/dL.

Radiography of lumbosacral spine indicated a narrowing disc space and grade I spondylolisthesis at the L4–5 level [Figure 1]. Magnetic resonance imaging (MRI) revealed severe spinal stenosis at the L4–5 vertebrae and one mass lesion at the left L3–4 vertebrae [Figure 2]a. The mass lesion appeared hypointense in both T1- and T2-weighted images [Figure 2]b and [Figure 2]c. Compared with the images [Figure 2]d obtained 2 years before current admission, the current results revealed that the ruptured disc had migrated upward to the left L3–4, compressing the neural foramen, were highly suspected. The patient subsequently received laminectomy; the mass at the L3–4 vertebrae was removed, followed by posterior spinal fixation and open transforaminal lumbar interbody fusion at the L3–4 and L4–5 levels.
Figure 1: Preoperative lateral radiograph of the lumbar spine exhibiting mild spondylolisthesis at the L4–5 level

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Figure 2: Preoperative magnetic resonance images of the lumbar spine. (a) Sagittal view of a T2-weighted image exhibiting considerably herniated disc at the L4–5 level and a mass (white arrow) at the L3–4 level. Axial view of the L3–4 level exhibiting the mass (white arrow) at the left L3–4 foraminal region and appearing as low-intensity signals in (b) T1- and (c) T2-weighted imaged. (d) Axial view of a T2-weighted image 2 years before the current admission revealing no mass lesion at the L3–4 level

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During surgery, the patient was administered general anesthesia and placed in the prone position. A posterior midline incision, extending along the previous surgical scar, was made from L3 to L5 under fluoroscopy. During this laminectomy, deposits of whitish chalky material were found in the synovial joint of the bilateral L3–4 and L4–5 facets. A soft mass with whitish chalky material was also found in the left L3–4 neural foreman, which formed a mass that compressed the thecal sac and nerve roots [Figure 3]a. After complete removal of these whitish chalky materials, transforaminal lumbar interbody fusion followed by posterior instrumentation was performed, all under fluoroscopy [Figure 3]b. Previous neurological deficits of the patient gradually recovered postoperatively.
Figure 3: (a) Whitish chalky mass (black arrow) removed intraoperatively. (b) Intraoperative lateral radiograph showing interbody fusion cages and posterior fixation system at the L3–4 and L4–5 levels

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Histological examination of the whitish chalky mass revealed that the deposits were of amphophilic material with needle-shaped slits of urate crystals, which were surrounded by foreign-body giant-cell reaction [Figure 4]. Bone erosion and focal granulation tissue formation were also present. Finally, the pathological finding confirmed the diagnosis of the spinal tophi.
Figure 4: Histological examination revealing the deposits of amphophilic material with needle-shaped slits of urate crystals, surrounded by the foreign-body giant-cell reaction

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Gout is a common inflammatory arthritis disorder worldwide. The prevalence of gout ranges from 0.2% to 0.4% in the Western population but it is higher in Taiwan.[3] In a national population study, the prevalence of gout in Taiwan was 6.24% and the incidence of approximately 2.74 per 1,000 person-years.[4] The deposition of tophi mostly occurs in the distal joints of the appendicular skeleton and soft tissues, such as in the first metatarsophalangeal joint.[3] However, tophi involving in the spine are rare and only approximately 150 cases of spinal gout have been reported.[2] According to a few systematic reviews,[2],[5],[6] men are more likely to develop spinal gout than are women. The median patient age is 58.9 years (range, 17–87 years).[2] Majority of the spinal gout cases have occurred in the lumbar spine.[2],[5],[6] Most patients with spinal gouts have reported a history of gout or hyperuricemia, a risk factor for gout.[2]

The low solubility of monosodium urate crystals, low temperature of the affected area, and low blood perfusion are the main reasons for the development of the tophi deposits in the distal extremities.[7] However, the pathogenesis of the spinal tophi remains unclear. The degenerative diseases of the spine, tissue necrosis, or previous spinal injury may be the predisposing factors for monosodium urate crystal deposition.[2],[5] Spinal tophi are frequently found at the facet articulation; however, they may also be present in the ligamentum flavum, pedicle, lamina, epidural soft tissue, intradural space, vertebral body, or disc space.[2],[5],[8] Depending on the location of the tophi and compressed neural structures, the symptoms of patients with spinal gout vary from back pain, radiculopathy, motor weakness, bladder dysfunction, or quadriparesis.[6] Although patients most commonly have a prior history of gout or hyperuricemia, spinal involvement can be the initial symptom of systemic gout despite normouricemia blood level.[9]

Various imaging modalities, including plain radiography, MRI, and computed tomography (CT), or positron emission tomography, have been used to investigate spinal tophi; however, the diagnostic dilemma remains.[2],[5] Since monosodium urate crystals are not radiographically opaque, spinal gout radiography is nonspecific and varied and it mostly reveals the degenerative changes or erosion in the spine.[8] In addition, CT may offer more features including the facet joint erosion with well-defined sclerotic margins or even calcified monosodium urate crystal depositions.[2],[3] Moreover, most spinal tophi appear have low-to-intermediate T1-signal intensity and heterogeneous T2-signal intensity, depending on the degree of its hydration and classification.[10] However, all these images are nonspecific and cannot definitely exclude the other spinal mass pathologies, such as abscesses, neoplasms, or disc fragments.[2],[10] In our case, the spinal abscesses and neoplasms were ruled out based on previous MRI and laboratory study results; however, the ruptured disc fragment with upward migration could not be confirmed since the patient presented symptoms of acute sciatica. Recent studies have demonstrated that dual-energy CT may possibly reveal uric acid crystal deposition in the spinal facet joints and provide diagnostic clues for the lower back pain in patients with hyperuricemia or history of gout.[2],[10],[11]

Treatment of the spinal tophi depends on the clinical presentation and the associated neural structure compressed by the tophi. Surgical intervention is performed for two main reasons: Firstly, most spinal tophi causing the neural structure compression require decompression surgery such as laminectomy or foraminotomy.[1],[2],[5],[6] Secondly, spinal tophi are hard to distinguish from other spinal masses such as neoplasms, abscesses, and disc fragments.[7],[8] Spinal tophi are most commonly diagnosed through histological examination after surgical intervention. Biopsy or aspiration may be performed to confirm spinal tophi when the patient either is asymptomatic or has low-back pain. Posterior spinal fixation is recommended if an unstable spine exists. In general, the surgical outcomes for spinal tophi are favorable like those in the present case.[2]

In conclusion, spinal tophi may develop in patients with a history of gout or hyperuricemia. Moreover, in our patient with gout and acute sciatica, a spinal tophus mimicked a ruptured disc. Finally, the possibility of spinal tophi should be considered during differential diagnosis for spinal mass lesions.

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Conflicts of interest

There are no conflicts of interest.

  References Top

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;77:767-71.  Back to cited text no. 1
Toprover M, Krasnokutsky S, Pillinger MH. Gout in the spine: Imaging, diagnosis, and outcomes. Curr Rheumatol Rep 2015;17:70.  Back to cited text no. 2
Ragab G, Elshahaly M, Bardin T. Gout: An old disease in new perspective-A review. J Adv Res 2017;8:495-511.  Back to cited text no. 3
Kuo CF, Grainge MJ, See LC, Yu KH, Luo SF, Zhang W, et al. Epidemiology and management of gout in Taiwan: A nationwide population study. Arthritis Res Ther 2015;17:13.  Back to cited text no. 4
Draganescu M, Leventhal LJ. Spinal gout: Case report and review of the literature. J Clin Rheumatol 2004;10:74-9.  Back to cited text no. 5
Elgafy H, Liu X, Herron J. Spinal gout: A review with case illustration. World J Orthop 2016;7:766-75.  Back to cited text no. 6
Lam HY, Cheung KY, Law SW, Fung KY. Crystal arthropathy of the lumbar spine: A report of 4 cases. J Orthop Surg (Hong Kong) 2007;15:94-101.  Back to cited text no. 7
Yoon JW, Park KB, Park H, Kang DH, Lee CH, Hwang SH, et al. Tophaceous gout of the spine causing neural compression. Korean J Spine 2013;10:185-8.  Back to cited text no. 8
Lorente R, Lorente A. Low back pain may be the initial symptom of systemic gout despite normouricemia blood level. Ann Spine Res 2018;1:1002.  Back to cited text no. 9
Chowalloor PV, Siew TK, Keen HI. Imaging in gout: A review of the recent developments. Ther Adv Musculoskelet Dis 2014;6:131-43.  Back to cited text no. 10
Parikh P, Butendieck R, Kransdorf M, Calamia K. Detection of lumbar facet joint gouty arthritis using dual-energy computed tomography. J Rheumatol 2010;37:2190-1.  Back to cited text no. 11


  [Figure 1], [Figure 2], [Figure 3], [Figure 4]


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