A previously healthy 10-year-old girl presented to our emergency department with a history of back pain, fever, and night sweats for 4-month duration associated with progressive walking difficulty and back deformity over the last 2 months. Physical examination revealed middle back swelling with kyphotic (gibbus) deformity. Neurological examination revealed grade 4/5 motor weakness in both lower extremities with normal deep tendon reflexes and sensations. There was no evidence of cranial nerve involvement, meningeal irritation, or cerebellar dysfunction. Laboratory tests showed a normal complete blood count, elevated C-reactive protein of 81 mg/dl, and erythrocyte sedimentation rate of 111 mm/h. Serology testing for HIV was negative. Her Mantoux test was positive of 25 mm although there was no history suggestive of tuberculosis in the family. Chest X-ray was normal; however, spine X-ray demonstrated destruction of the thoracic vertebra (T11) body and inferior end plate of the T10 vertebra with loss of disk spaces between T10, T11, and T12 (). The contrasted magnetic resonance imaging (MRI) of her spine showed kyphotic destruction of thoracic vertebrae T10, T11, and T12 with abnormal high signal on T2 and low signal on T1 in addition to a large heterogeneous multiloculated prevertabral and paraspinal abscess extending from T7 through T12 with a peripheral thick wall that had low T2 and high T1 signal with intense enhancement. These are associated with an epidural collection and retropulsed collapsed T11, which result in complete attenuation of the anterior subarachnoid spaces and compression of the distal cord (). She underwent open surgical drainage of the paravertebral abscess and posterior spine fixation from T6 to L2 with pedicle screws. During surgery, a massive purulent fluid was discharged, and biopsy from the bone and soft tissue was taken and sent for microbiological examination and cultures including Mycobacterium tuberculosis. Both acid-fast staining and mycobacterial polymerase chain reaction were negative. Histopathology examination revealed caseating granulomatous inflammation consistent with tuberculosis. Based on radiological and histopathological findings, Pott's disease was highly suspected; therefore, the decision was made to start the patient on four anti-TB drug therapy of isoniazid, rifampicin, pyrazinamide, and ethambutol) while waiting for the final result of the mycobacterial culture. Ophthalmology team was consulted for baseline eye examination before starting ethambutol, and incidentally, bilateral papilledema was detected during fundus examination. Consequently, MRI of the brain showed multiple brain lesions in the left cerebellar hemisphere, left superior temporal gyrus, and right occipital lobe (). The lesions show a ring enhancement with a hypointense center mildly surrounded by a hyperintense area, most likely represent vasogenic edema which is highly suggestive of brain tuberculomas. There was no leptomeningeal enhancement suggestive of meningitis. After four weeks, her tissue culture grew Mycobacterium tuberculosis. The patient was treated with four antituberculous drug regimen for 2-month duration, followed by additional 10 months of isoniazid and rifampicin. Oral prednisone was given initially at a dose of 2 mg/kg/day for 4 weeks and tapped gradually over the next 6 weeks. In a three-year follow-up, the patient had normal neurological examination, and her brain MRI showed complete resolution of the tuberculomas.
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 ().