The patient was a 12-year-old boy, with history of sputum-positive pulmonary tuberculosis for which he was already on anti-tubercular treatment for 3 months. He presented to us with an episode of generalized seizure which had been preceded by isolated right sixth nerve palsy, episodes of seizures and gradual onset, progressive quadriparesis over the past 1 month. On examination, he had postictal confusion. Fundus examination revealed papilledema. He had a grade 3–4/5 spastic quadriparesis.\nA magnetic resonance imaging (MRI) of the brain revealed multi-lobar tuberculomas of the brain with lesions in the brainstem and cerebellum []. MRI of the spine revealed cervical (C2–3, C7–D1), dorsal (D7, D10, D11–12) and lumbar (D12–L1 including conus medullaris), multiple homogeneous enhancing oval lesions []. Only a few lesions showed characteristic ring enhancement. Mantoux was positive (15 mm induration at 48 h) and tuberculosis-interferon-γ-release-assays (Quantiferon Tuberculosis Gold In-Tube) test were positive. Erythrocyte sedimentation rate (ESR) was 40 and serology for HIV was negative. The patient was continued anti-tubercular treatment and was supplemented with steroids for about a month. The boy showed gradual but definite clinical improvement by the time of discharge 7 days later. At 3 month follow-up, he was ambulant without support. Follow-up MRI of the brain and spine revealed reduction in the enhancement of the lesions with definite ring enhancing pattern now discernable [Figure –]. Complete resolution of lesions on the last follow-up at the 8th month of treatment was seen [Figure –] and clinically he was ambulant with improvement in his VIth nerve palsy. We decided to continue anti-tubercular treatment for 18 months and the end of which he was free from any neurological deficits and back to productive life.
A 79-year-old African American male patient with a past medical history of prostate cancer presented with progressive weakness, headache, and confusion. Brain MRI with gadolinium contrast showed a 41 × 33 × 41 mm left frontal lesion at the surface of the left lateral ventricle with vasogenic edema and midline shift (). A stereotactic biopsy of the lesion presented the possibility of a non-caseating granuloma. Metastatic prostate cancer was ruled out. The free and total prostate specific antigen (PSA) level was within the normal limit. The patient had immigrated from Liberia but denied any constitutional symptoms such as fever, cough, night sweats, or weight loss. Quantiferon gold test was positive but active pulmonary tuberculosis was ruled out with chest imaging. The basic metabolic panel was unremarkable; complete blood count showed lymphocytosis only. HIV antibodies were negative. Subsequently, we proceeded with a lumbar puncture. Histoplasma, blastomycosis, and HIV antibodies in cerebrospinal fluid were negative. Serum Cryptococcus antigen, Bartonella Hensale, and Bartonella Quintana IgM and IgG and rapid plasma reagin (RPR) tests were negative. Bone marrow acid-fast bacteria (AFB) stain and culture, C-ANCA, and P-ANCA were negative. 1, 25 OH, 25 Oh vitamin D3, and angiotensin-converting enzyme level were within normal limits. He underwent a left-sided frontal open brain biopsy, and pathology results were compatible with non-caseous granulomatous inflammation (). Fungus tissue culture, sputum, and blood cultures were negative. He was empirically started on anti-tuberculous treatment with Ethambutol, Isoniazid (INH), Rifampin, Pyrazinamide, Pyridoxine, and dexamethasone. We were unable to achieve significant clinical improvement two weeks after anti-tuberculous treatment. Considering the possible diagnosis of neurosarcoidosis, methylprednisolone 1 g daily treatment was initiated for three days and gradually tapered. Later on, after six weeks, the culture of the brain biopsy result came positive for tuberculosis. Anti-tuberculosis (TB) medications were re-initiated, to be continued for 18 months. After two months of treatment, the control MRI brain with gadolinium contrast showed near resolution of the midline shift and a decrease in the left frontal lobe and bilateral parietal lobes edema ().