Spinal Gout Presenting with Acute Paraplegia: A Case Report and Literature-Based Diagnostic Framework

Background: Spinal gout is an uncommon manifestation of chronic hyperuricemia caused by the deposition of monosodium urate (MSU) crystals within axial skeletal structures. Although gout predominantly involves peripheral joints, axial deposition within the ligamentum flavum, facet joints, and epidural space can lead to spinal cord compression and severe neurological impairment. Because clinical and radiological features mimic spinal neoplasms, epidural abscesses, and degenerative disorders, diagnostic delays are common. Case Presentation: A 58-year-old man with an 8-year history of poorly controlled hyperuricemia and essential hypertension presented with progressive lower-limb weakness, severe thoracic back pain, lower-body numbness below the T10 dermatome, and acute urinary retention over two weeks. Neurological examination revealed flaccid paraplegia (Medical Research Council grade 0/5 in both lower extremities), complete loss of pinprick and light touch sensation below T10, absent deep tendon reflexes, and loss of anal sphincter tone, corresponding to American Spinal Injury Association (ASIA) Impairment Scale Grade A. Serum uric acid was elevated at 9.5 mg/dL, alongside mildly elevated inflammatory markers. Magnetic resonance imaging (MRI) revealed a posterior extradural mass from T9 to T12 with severe cord compression centered at the T11–T12 level. Multi-sequence MRI demonstrated T1 iso/hypointensity, T2 heterogeneous hypointensity, thick peripheral rim enhancement on post-contrast T1-weighted sequences, and no restricted diffusion on DWI. Emergency decompressive laminectomy was performed, revealing a chalky white mass compressing the dural sac. Histopathological evaluation confirmed monosodium urate crystal deposits surrounded by granulomatous inflammation and multinucleated foreign-body giant cells. Postoperatively, the patient was initiated on treat-to-target urate-lowering therapy with allopurinol alongside short-term colchicine prophylaxis. At the 6-month follow-up, lower-limb motor strength recovered to grade 4/5, cutaneous sensation was restored, voluntary sphincter control was regained (ASIA Impairment Scale Grade D), and serum uric acid was normalized to 5.2 mg/dL. Conclusions: Spinal gout should be considered in the differential diagnosis of acute spinal cord compression, even in patients without active peripheral tophi. Prompt surgical decompression combined with long-term urate-lowering therapy is essential to facilitate neurological recovery and prevent disease recurrence.