A 71-year-old male with a past medical history of cervical spinal fusion surgery, C5 nerve palsy, lumbar spinal decompression surgery, and non-Hodgkin lymphoma status post chemotherapy with R-CHOP therapy (rituximab, cyclophosphamide, doxorubicin hydrochloride, vincristine sulfate, and prednisone) presented to his primary care physician with concerns of chronic recurrent right hip and lower back pain which acutely worsened. The patient also acknowledged new-onset progressive numbness of his right thigh with associated intermittent, sharp muscle spasms. However, the patient denied recent urinary or bowel incontinence and speech or vision changes.
The patient's physical exam was unremarkable aside from poor coordination, hyperalgesia of the bilateral lower extremities, moderate tenderness to palpation of the lumbar spine at L1-L2 level, a positive bilateral straight leg test, and an unsteady tandem gait. Skin examination also revealed a violaceous plaque noted on the patient's anterior right thigh just above the knee. An initial lumbar magnetic resonance imaging (MRI) with contrast was completed and revealed moderate multilevel lumbar spondylotic changes with facet joint degeneration without evidence of destructive osseous lesions or intradural masses. Given these relatively benign physical exam and radiographic findings, the patient was diagnosed with lumbar radiculopathy and treated with analgesics and a fluoroscopy-guided lumbar transforaminal epidural (LTFE).
Despite initial treatment, the patient's pain progressively worsened, therefore, he was scheduled for a repeat lumbar MRI to elucidate the etiology of his pain and worsening motor weakness. Repeat lumbar MRI with and without contrast was completed two months after he initially became symptomatic. It showed an abnormal focal increased T2 signal and a rounded area of enhancement within the right posterior aspect of the distal thoracic cord at the T11 level. The etiology of this new lesion was unclear and a thoracic MRI with and without contrast was completed and showed a pathologic cord signal with expansion and abnormal enhancement involving T7-T12 (Figures 1 and 2). The differential diagnoses at this time included transverse myelitis, recurrent lymphoma, cord infarction, or neoplasm.
The patient was admitted to the hospital for further evaluation and management. Upon hospital admission, the patient was afebrile with normal vital signs. Initial lab work revealed a white blood count of 6.3 x 103/mm3, hemoglobin of 9.6 g/dL, platelets of 277 x 103/mm3, neutrophils at 53%, and lymphocytes at 33%. Inflammatory markers revealed an erythrocyte sedimentation rate of 104 mm/hr and c-reactive protein of 4.0 mg/L. The patient's HIV test was negative. Cerebrospinal fluid analysis was completed to rule out the possibility of lymphomatous meningitis. CSF analysis revealed a clear, colorless sample with lymphocytic pleocytosis and elevated protein. Atypical lymphocytes were noted, but no evidence of lymphoma was observed on flow cytometry. Microscopic testing of the cerebrospinal fluid for acid fast bacteria, fungi, mycobacterium, and cryptococcus neoformans were negative. The patient's TB spot test also was negative.
F-18 fluorodeoxyglucose (FDG) PET/CT imaging divulged a linear focus of mildly accentuated FDG activity from the middle of the T10 to the middle of the T11 vertebral body, correlating with the signal abnormality noted in prior imaging studies. Biopsy of the lesion was subsequently performed to establish a histopathological diagnosis. The biopsy disclosed an area of necrosis surrounded by pale histiocytes consistent with necrotizing granulomatous inflammation. Given the imaging and histopathological findings, the suspicion was that the lesion represented spinal tuberculosis. However, initial special stains of the biopsy specimen for microorganisms, including Ziehl-Neelsen and Grocott methenamine silver stains, were negative. Additional stains of the biopsy specimen for microorganisms, including the Fite stain for acid fast bacilli and periodic Acid-Schiff for fungi, were completed and revealed rare acid-fast bacilli identified on Fite stain, thus confirming the suspected diagnosis of intramedullary spinal tuberculoma.
The patient was initiated on an anti-tuberculous pharmacotherapy regimen of rifampin 600 mg/day, isoniazid 300 mg/day, pyrazinamide 1500 mg/day, and ethambutol 1200 mg/day (RIPE therapy), supplemented with adjuvant pyridoxine 50 mg/day. He was continued on RIPE treatment for two months followed by 10 months of continuation therapy with rifampin and isoniazid alone. Pharmacotherapy was supplemented with analgesics, physical therapy, and occupational therapy. The patient was followed on a monthly basis in the outpatient setting throughout treatment. After completing 12 months of pharmacotherapy, a repeat thoracic MRI with and without contrast was done, which revealed slight improvement in the T2 hyperintense signal within the thoracic spinal cord adjacent to the focal areas of enhancement at T8 - T9 and T10 - T11. These focal areas of enhancement did not appear to have changed significantly and no new areas of enhancement or abnormal signal were observed to suggest disease progression. Over the next two years he had persistent radicular pain, but his disability significantly improved from initial presentation. He is alive without recurrence of disease and has had significant improvement in his gait and mobility, now ambulating with a cane.