A previously healthy 10-year-old girl presented to our emergency department with a history of back pain, fever, and night sweats for 4-month duration associated with progressive walking difficulty and back deformity over the last 2 months. Physical examination revealed middle back swelling with kyphotic (gibbus) deformity. Neurological examination revealed grade 4/5 motor weakness in both lower extremities with normal deep tendon reflexes and sensations. There was no evidence of cranial nerve involvement, meningeal irritation, or cerebellar dysfunction. Laboratory tests showed a normal complete blood count, elevated C-reactive protein of 81 mg/dl, and erythrocyte sedimentation rate of 111 mm/h. Serology testing for HIV was negative. Her Mantoux test was positive of 25 mm although there was no history suggestive of tuberculosis in the family. Chest X-ray was normal; however, spine X-ray demonstrated destruction of the thoracic vertebra (T11) body and inferior end plate of the T10 vertebra with loss of disk spaces between T10, T11, and T12 (). The contrasted magnetic resonance imaging (MRI) of her spine showed kyphotic destruction of thoracic vertebrae T10, T11, and T12 with abnormal high signal on T2 and low signal on T1 in addition to a large heterogeneous multiloculated prevertabral and paraspinal abscess extending from T7 through T12 with a peripheral thick wall that had low T2 and high T1 signal with intense enhancement. These are associated with an epidural collection and retropulsed collapsed T11, which result in complete attenuation of the anterior subarachnoid spaces and compression of the distal cord (). She underwent open surgical drainage of the paravertebral abscess and posterior spine fixation from T6 to L2 with pedicle screws. During surgery, a massive purulent fluid was discharged, and biopsy from the bone and soft tissue was taken and sent for microbiological examination and cultures including Mycobacterium tuberculosis. Both acid-fast staining and mycobacterial polymerase chain reaction were negative. Histopathology examination revealed caseating granulomatous inflammation consistent with tuberculosis. Based on radiological and histopathological findings, Pott's disease was highly suspected; therefore, the decision was made to start the patient on four anti-TB drug therapy of isoniazid, rifampicin, pyrazinamide, and ethambutol) while waiting for the final result of the mycobacterial culture. Ophthalmology team was consulted for baseline eye examination before starting ethambutol, and incidentally, bilateral papilledema was detected during fundus examination. Consequently, MRI of the brain showed multiple brain lesions in the left cerebellar hemisphere, left superior temporal gyrus, and right occipital lobe (). The lesions show a ring enhancement with a hypointense center mildly surrounded by a hyperintense area, most likely represent vasogenic edema which is highly suggestive of brain tuberculomas. There was no leptomeningeal enhancement suggestive of meningitis. After four weeks, her tissue culture grew Mycobacterium tuberculosis. The patient was treated with four antituberculous drug regimen for 2-month duration, followed by additional 10 months of isoniazid and rifampicin. Oral prednisone was given initially at a dose of 2 mg/kg/day for 4 weeks and tapped gradually over the next 6 weeks. In a three-year follow-up, the patient had normal neurological examination, and her brain MRI showed complete resolution of the tuberculomas.
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.