A 4-year-old girl presented with a history of multiple episodes of seizures since the last one and half years. The seizures were varying in semiology:initially multifocal with secondary generalization and later tonic seizures with frequency gradually increasing from once every 6 months to once every 2 weeks. There was no fever, vomiting or headache. On examination, she had papilloedema and brisk deep tendon reflexes. Weight was 13 kg (<15th centile) and blood pressure 110/70. Other systems were normal. There was no focal neurological deficit.
On investigation, haemogram, chest X-ray was normal. Computed tomography (CT) scan brain showed evidence of a large conglomerate ring enhancing focal lesion in the parafalcine frontal cortices mainly on the left side with extensive white matter hypodensity in both frontal lobes (Fig. 1). Small tuberculomas were also seen in the left occipital lobe and left lateral inferior cerebellum, tegmentum of pons and right temporal lobe. 
Magnetic resonance imaging (MRI) brain showed a 5.7 x 3.9 x 4.8 cm-sized heterogeneously hyperintense peripherally enhancing conglomerate lesion involving the left frontal parafalcine region crossing onto the midline and right parafalcine frontal lobe, extending into the genu of the corpus callosum and showing patchy restricted diffusion. The lesion showed extensive perilesional vasogenic oedema (Fig. 2) with multiple ring and disc enhancing lesions seen in the bilateral cerebral and cerebellar parenchyma and in the right hemipons. Magnetic resonance spectroscopy revealed lactate double peak and diffuse reduction in all the metabolite peaks suggestive of tuberculoma. The Mantoux test was negative. 
Patient was started on i.v. dexamethasone, which was given for 5 days, and subsequently lumbar puncture was done. Cerebrospinal fluid (CSF) examination was normal. CSF Gene Xpert revealed no Mycobacterium tuberculosis complex, and TB MGIT was negative for Acid Fast Bacilli. Antitubercular treatment (ATT) with isoniazid (10 mg/kg/day), rifampicin (10 mg/kg/day), ethambutol (20 mg/kg/day) and pyrazinamide (35 mg/kg/day) along with oral prednisolone at 2 mg/kg/day was started on Day 5 of hospitalization. The child improved, seizures stopped and the papilloedema gradually disappeared.
A neurosurgical opinion for biopsy of lesion was taken, but in view of classical MRI findings, it was deferred.
Follow-up MRI brain after 8 months of treatment showed a mild reduction in the size of the lesion to 4 x 4 x 2.3 cm with mild perilesional vasogenic oedema. The ring enhancing lesions in the bilateral cerebral hemispheres were still present. However, the cerebellar and pontine lesions had disappeared (Fig. 3). Child is on regular follow-up.