A 66-year-old woman was admitted with bilateral lower extremity weakness and voiding difficulty for 2 weeks. Paraparesis with muscle power of the right lower extremity was grade 2/5 and the left lower extremity was grade 1/5, impaired sensations below the L1 level and decreased strength in the anal sphincter tone. Lower extremity reflexes including knee jerk and ankle jerk were absent. No evident upper extremity motor or sensory deficit was seen. Magnetic resonance imaging (MRI) of the thoracolumbar showed about 1.2×1×4 cm sized intramedullary enhancing lesion with central necrosis on conus medullaris at T12-L1 levels. The lesions were isointense on T1-weighted images and hyperintense on T2-weighted images, which were associated with diffuse edema of spinal cord on T7-T11 level. We presumed that this abscess might be closely related with tuberculous abscess. However, in laboratory, sputum, Cerebrospinal fluid (CSF) cultures and Acid-Fast bacilli stains were negative. A cerebrospinal fluid study showed glucose levels 55 mg/dL, protein 100 mg/dL, and 50 lymphocytes/mm3. Initial C-reactive protein (CRP) was 24. On review of her previous medical history, she was treated for pulmonary tuberculosis, diagnosed six months earlier. And 1 month ago, pus was found in the right kidney due to her flank pain, which was proved to be tuberculosis after drainage. She was also treated by rifampin, ethambutol, pyrazinamide at other hospital. Chest simple X-ray showed that features of bilateral pulmonary tuberculosis with multiple patchy consolidations. We took brain MRI in order to differentiate the brain lesion. MRI findings of brain showed multiple abscesses at the cerebrum and cerebellum. Results of a Tb INF-r were positive. Initially, we planed surgical treatment, however, we postponed the surgery due to her poor general condition and refusal of her family. Under the diagnosis of multiple CNS tuberculomas on spinal cord and brain, the anti-tuberculous drugs were started with rifampicin 600 mg, isoniazid 300 mg, pyrizinamide 1000 mg, ethambutol 800 mg. At 2 month later after medication, the muscle power in the both lower limbs had improved to grade 4/5, and voiding was also recovered. After 3 months of medical treatment, she could walk by herself. Follow up lab of CRP was reduced from 24 to 0.9 at 2 month later. Normalization of CRP was seen at 3 months of medication for tberculosis. After 6 months, the MRI of spine showed the markedly decreased size of intramedullary nodule at T12-L1 levels, which meaned improvement of tuberculous abscess, though perilesional edema of conus medullaris still remain. And MRI of brain showed that marked improvement of multiple nodular enhancing lesions at both frontoparietal lobe, right thalamus and both cerebellar hemisphere. Finally, we concluded these lesions were due to tuberculosis though we did not have the pathologic confirmation.
A 48-year-old African American female presented with a one-month history of headaches and nausea. Her only significant past medical history was diabetes. Her social history was negative for such risk factors as a high-risk profession in the healthcare field, recent incarceration, known contact with persons diagnosed with active tuberculosis or recent travel to areas in which tuberculosis is endemic. Her physical exam was unremarkable, and she had no focal neurological deficits. She was afebrile and hemodynamically stable. She presented to an outside facility where she had a computerized tomography (CT) scan of her head performed, which showed a posterior fossa mass with moderate hydrocephalus. This was followed by a magnetic resonance imaging (MRI) of the brain with and without contrast, which revealed a large right cerebellar ring-enhancing mass (Figures -). The primary concern at that time was that this mass could possibly be a primary brain glioma like a high-grade astrocytoma or a medulloblastoma. The patient was transferred to another hospital for neurosurgical evaluation and excision of the mass. She underwent an exploratory posterior fossa craniectomy, cerebellar exploration and decompression, but no mass was identified at that time. Due to persistent headaches, she then had a repeat exploration of posterior fossa 15 days later, and identification and excision of the cerebellar mass occurred. Histopathology from the procedure revealed necrotizing granulomas (Figure ), and stains specific for acid fast bacilli and fungus were both negative. Subsequently, the brain tissue grew Mycobacterium tuberculosis. The patient reported no prior knowledge of having tuberculosis, nor did she endorse exposure to patients with active tuberculosis. She previously had purified protein derivative (PPD) tests for employment, which had been negative. She was not immunocompromised and had recently been tested negative for human immunodeficiency virus (HIV) six months prior.