A 5-year-old boy presented with fever for 12 days, progressive motor weakness in lower limbs for 9 days, and retention of urine and constipation for 6 days. The patient was treated elsewhere for fever for three days. However, on the fourth day of the illness, the child developed progressive symmetrical lower limb weakness causing difficulty in standing, sitting, and turning from side to side. Over the next three days, he developed retention of urine and constipation, hence was referred to our hospital for further management.\nThere was no history of headache, vomiting, altered sensorium, cranial nerve or sensory deficit, recent immunization, and head or spine trauma. The patient had no tuberculosis (TB) in the past nor TB contact.\nAt admission, his pulse rate was 88/min, respiratory rate was 32/min, and blood pressure was 90/60 mm of Hg. Bacillus Calmette Guerine vaccine scar was seen. Spine palpation revealed no tenderness or deformity. His weight (16kg) and height (106cm) both were between the 10th and 25th centiles for his age and sex. His higher mental functions, cranial nerves, and sensory examination were normal, and papilledema was absent. Tone, power, and reflexes of both upper limbs were normal. Both lower limbs had hypotonia, power grade 2/5, and exaggerated (3+) deep tendon reflexes. Abdominal and cremasteric reflexes were absent and plantar reflexes were extensor bilaterally. Meningeal signs were absent. The patient had mild firm hepatomegaly (2cm) and a palpable distended urinary bladder. Respiratory and cardiovascular system examination was normal.\nHis initial investigations showed iron deficiency anemia and elevated Erythrocyte sedimentation rate (25 mm at 1h), a negative Mantoux test, normal chest radiograph, and gastric aspirate negative for acid-fast bacilli. Enzyme-linked immunosorbent assay was negative for human immunodeficiency virus infection. MRI of dorsal spine (P + C) showed a well-defined oval T2 hypointense ring-enhancing lesion (4.5 × 2.5 mm) in the thoracic cord at D4-D5 level, with mild perilesional edema from D3 to D5 level suggestive of IMT []. MRI of brain revealed few tiny T2/fluid attenuation inversion recovery (FLAIR) hyperintense enhancing foci in left frontal white matter and subependymal region of the left ventricle. Minimal focal subcortical white matter edema was observed in right frontal lobe suggestive of tuberculoma [].\nThe patient was started on ATT regime containing two months of Isoniazid (H), Rifampicin (R), pyrazinamide (Z) and Ethambutol (E) followed by 7 months of Isoniazid (H), Rifampicin (R) and Ethambutol (E) therapy (2HRZE +7HRE) with steroids for four weeks. Parenteral dexamethasone was given for two days followed by oral prednisolone for a total of four weeks. He showed clinical improvement in three days and had complete clinical recovery by nine days. Meanwhile, family screening for TB detected sputum positive for pulmonary TB in father. His father was enrolled and started on standard ATT, the younger sibling was started on isoniazid prophylaxis as per Revised National Tuberculosis Control Program guidelines. On follow-up, the patient was found to be compliant with ATT and clinically well without adverse effects.
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.