The patient was a 12-year-old boy, with history of sputum-positive pulmonary tuberculosis for which he was already on anti-tubercular treatment for 3 months. He presented to us with an episode of generalized seizure which had been preceded by isolated right sixth nerve palsy, episodes of seizures and gradual onset, progressive quadriparesis over the past 1 month. On examination, he had postictal confusion. Fundus examination revealed papilledema. He had a grade 3–4/5 spastic quadriparesis.\nA magnetic resonance imaging (MRI) of the brain revealed multi-lobar tuberculomas of the brain with lesions in the brainstem and cerebellum []. MRI of the spine revealed cervical (C2–3, C7–D1), dorsal (D7, D10, D11–12) and lumbar (D12–L1 including conus medullaris), multiple homogeneous enhancing oval lesions []. Only a few lesions showed characteristic ring enhancement. Mantoux was positive (15 mm induration at 48 h) and tuberculosis-interferon-γ-release-assays (Quantiferon Tuberculosis Gold In-Tube) test were positive. Erythrocyte sedimentation rate (ESR) was 40 and serology for HIV was negative. The patient was continued anti-tubercular treatment and was supplemented with steroids for about a month. The boy showed gradual but definite clinical improvement by the time of discharge 7 days later. At 3 month follow-up, he was ambulant without support. Follow-up MRI of the brain and spine revealed reduction in the enhancement of the lesions with definite ring enhancing pattern now discernable [Figure –]. Complete resolution of lesions on the last follow-up at the 8th month of treatment was seen [Figure –] and clinically he was ambulant with improvement in his VIth nerve palsy. We decided to continue anti-tubercular treatment for 18 months and the end of which he was free from any neurological deficits and back to productive life.
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.