A female child, three years old, 16 kg, had complaints of vomiting, weakness, and convulsion-like tremor at the right angle of the mouth a week before the admission. After a week in hospital care, the patient was discharged. A week later, the patient's head tilted to the right while talking, and the patient was less active than before. Therefore, the patient was admitted to the hospital again to be evaluated with brain magnetic resonance imaging (MRI) and brain tissue biopsy.
The patient was diagnosed with tuberculoma based on first brain MRI, brain tissue biopsy and got regimens of anti-tuberculosis therapy. A week after the patient got the anti-tuberculosis therapy, the patient's condition worsened. The patient was consulted to the pediatric neurologist with general weakness, altered consciousness, and hand tremor.
The patient was admitted with fever (39  C), Glasgow Coma Scale (GCS) was 7 (E2V2M3); pupils were asymmetric with slow response to the light, tetraparesis (the motoric strength were 1 of 5), increasing physiological reflexes; positive Babinsky with clonus, spastic, and hand tremorShe had high transaminases enzyme without proof of cytomegalovirus (CMV), HSV-1, HSV-2 syphilis, and tuberculosis infection.
First brain MRI (two weeks before admission) (Figure 1), showed hypointense lesion and hyperintense spots in T1W1, which became hyperintense dominance on T2W1 with perifocal edema. The size of the lesion is 7,8 x 8,1 x 7,9 cm in the corpus callosum and frontal lobe bilateral (with right dominance). The lesion adheres to the falx cerebri and bilateral lateral ventricle with compression to the anterior horn of the bilateral lateral ventricle. Another smaller lesion with the same characteristics was found in the left parietal lobe that adheres to the falx cerebri with multiple nodules. These nodules are hyperintense after contrast introduction and located in the left frontal, bilateral parietal, and left temporal lobes. This condition suggests glioblastoma with a differential diagnosis of necrotizing toxoplasma encephalitis.
The brain tissue biopsy showed a gemicytocytic cell adjacent to the edematous loose neutrophil stromal. A few parts of the tissue consisted of extensive necrotic tissue, which forms caseous necrosis with lymphocyte, macrophage, and epithelioid-like cell infiltration. The conclusion was a chronic inflammation in brain tuberculosis. The biopsy specimen was sent for a second opinion. The result showed a necrotic mass and inflammatory cells, suggesting an inflammatory process without malignancy or tuberculosis.
The patient was still treated with anti-tuberculosis, corticosteroid, anti-convulsant, antipyretic, 20% mannitol for high intracranial pressure management.
On the 3rd day of the hospitalization, the GCS was improved (E4V2M3). The second brain MRI was done (Figure 2). The lesions found in the subcortical and juxtacortical of the bilateral fronto-temporo-parietal, right occipital, bilateral parieto-occipital lobes, and bilateral head of the caudate nucleus, in the part of the putamen and the bilateral of globus pallidus without mass effect. This lesion was followed by an early subacute of hemorrhage component in the lesion of bilateral head of caudate nucleus with cortical laminar necrosis at the frontal and bilateral of parietal lobes. Spinal MRI was normal.
Several viral (adenovirus, coronavirus 229E, coronavirus HKU1, coronavirus NL63, coronavirus OC43, SARS-CoV-2, Human Metapneumovirus, Human Rhinovirus/Enterovirus, Influenza A and B, Parainfluenza 1 to 4, Respiratory Syncytial Virus) and bacterial infection (Bordatella parapertussis, Bordatella pertussis, Chlamydia pneumoniae, and Mycoplasma pneumoniae) were excluded by real time-polymerase chain reaction (RT-PCR) examination. The results of cerebrospinal fluid (CSF) examination are clear fluid, 100% mononuclear cells, leukocyte 2 cells/mm3, protein 3 mg/dL, glucose 59 mg/dL, negative Nonne test, positive Pandy test, negative of tuberculosis (Gene Xpert and fast acid bacilli examination) and negative of bacterial culture.
The second MRI showed hemorrhage and necrosis, which were inappropriate with the resolution of tuberculoma; then, the diagnosis ANEC was considered. The anti-tuberculosis therapy was stopped after two weeks. The intravenous (IV) acyclovir was started with consideration of HSV infection as an etiology of ANEC. The patient had 300 mg (dosis perkgBB berapa) of intravenous acyclovir three times a day for 21 days, 375 mg of methylprednisolone IV once a day for five days, and immunoglobulin IV 0,4 gram/kg BW/day for five days.
On the second week of hospitalization, patient's GCS was improved to 11 (E4V2M3), motor strength was increased to 3 of 5. The third brain MRI was done (Figure 3), which showed an extension of the lesion in the subcortical and juxtacortical of the bilateral fronto-temporo-parietal, right occipital, bilateral parieto-occipital lobes, the trunk of the corpus callosum, bilateral head of the caudate nucleus, part of the putamen and bilateral of the globus pallidus. These lesions were followed by the relatively stable early subacute of the hemorrhage component at the lesion, located at the bilateral head of the caudate nucleus, part of the putamen, and bilateral globus pallidus. There was also the addition of cortical laminar necrosis in the frontal and bilateral parietal lobes. On the third week of hospitalization, the clinical condition remained.
Examination of serum showed the negativity of anti-Histoplasma, aspergillus, autoimmune panel for encephalitis, and Ab MOG. The patient showed improvement with GCS 13 (E4V4M5) and slight tetraparesis after five months of discharge.