Patient was 15 years old, female, previously healthy, eutrophic, with a history of a month of tremor in the right hand.
On physical examination, the patient was wet, Glasgow 15, with no signs of meningeal irritation and mild, intentional tremor.
The evaluation of cranial nerves and eye fundus was normal.
Magnetic resonance imaging (MRI) with gadolinium showed a nodular image of expansive aspect with intense reinforcement after contrast administration, located at the level of the left mesencephalon.
It measured 10 x 11 mm in diameter, surrounded by perilesional edema with mild mass effect.
A complete blood count was performed: leukocytes 5,100 cells/ mm3 (neutrophils 63% and lymphocytes 33%), hemoglobin 12 g/dl, platelets 480,000 cells/mm3.
Proteinogram: total proteins 6.5 g/dl; albumin 3 g/dl; α1, α2 and β globulins normal.
A stereotactic biopsy was performed and treatment with dexamethasone 0.6 mg/kg/day was initiated.
Serology for HIV, toxoplasmosis and Chagas were performed within the etiological study, which were negative.
A PPD was non-reactive, the patient had BCG vaccination scar.
A chest X-ray showed a bilateral interstitial-alveolar pattern.
The sputum smear was positive for Mycobacterium tuberculosis.
Stereotactic biopsy was performed with the diagnosis of TBC with pulmonary and CNS involvement (tuberculoma), and treatment with isoniazid, rifampicin, pyrazinamide and dnisamide was initiated with concomitant treatment with isoniazid.
At the end of the second week of treatment, with good clinical evolution and negative direct sputum tests, the patient was discharged.
After one month of treatment with the confirmation of isoniazid-sensitive M. tuberculosis and rifampicin, etambu bag was discontinued and progressive withdrawal of corticosteroid treatment was indicated.
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At week 8 of treatment, the patient consulted for a sudden decrease in left eye vision and diplopia.
Pathological examination revealed an anisocoria due to dilatation of the left pupil with normal eye fundus.
Neurological examination revealed vigilance, oriented person, time and space.
There was limitation in the upper look and convergence, mydriatic pupils (left cranial nerve III and IV complex) and central right facial paralysis.
Muscle strength was decreased in the right hemibody (hemiparesis) and homolateral dysmetria.
A new MRI showed progression of brain injury.
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Because of clinical worsening and CNS imaging, a stereotactic biopsy was performed to rule out other associated pathologies.
The pathological anatomy study reported an edematous nervous parenchyma accompanied by reactive gliosis compatible with an inflammatory process.
No granulomas were observed.
SAP, Ziehl Neelsen stains and immunohistochemistry for toxoplasmosis were negative.
Bacterial cultures and mycobacteria were negative.
Treatment with methylprednisone was added initially at 2 mg/kg/day for two weeks and then 1 mg/kg/day, with the diagnosis of a paradoxical reaction in a patient with medication.
In the second week of corticosteroid therapy, a slight decrease in right hemiparesis was observed on clinical examination, with a slight tremor when performing rapid eye movements, continuing with the rest of neurological disorders.
One month after starting treatment, a control MRI scan showed a decrease in volume and contrast enhancement of the left lateral mesencephalic lesion, with resolution of the right frontal lesions.
A total of two months of methylprednisone 1 mg/kg/day was completed.
By improving the images and neurological manifestations, the scheduled dose reduction was started until it was discontinued.
