A 60-year-old woman, who was from a non-endemic area, presented with symptoms such as headache, short-term memory impairment, and mild consciousness disturbance. Her medical history included traumatic subarachnoid hemorrhage nine months before presentation, but her family history was unremarkable. The patient had a medical history of using cough suppressants, expectorants, anti-allergy agents, and corticosteroid nasal drops. About five years previously, pigeons had nested in the veranda of the patient’s home for a period of time.\nIn the neurological examination, her consciousness level was Glasgow Coma Scale E4V4M6 as disorientation was present, and the Babinski and Chaddock signs were positive on the left. Other neurological symptoms or signs were negative. Blood biochemical test findings revealed an elevated white blood cell count of 8900/µL (normal range = 3300‒8000/µL) and elevated C-reactive protein level of 0.05 ng/mL (normal 0‒0.14 ng/mL). In the cerebrospinal fluid (CSF) test, cell count was elevated (212/µL), with an increased monocyte predominance, a low glucose level of 48 mg/dL (normal range = 50–75 mg/dL), and a high protein level of 61 mg/dL (normal range = 10–40 mg/dL), suggestive of meningitis. Plain chest radiograph and CT were performed but were unremarkable. CSF analysis was sent for both acid-fast staining and tuberculosis culture, both of which were negative. Erythrocyte sedimentation rate (ESR) was not evaluated in this case.\nFor magnetic resonance imaging (MRI) examination, a 3-T MR system (Signa HDxt; GE Healthcare, Milwaukee, WI, USA) was used. In each clinical stage, the patient underwent serial examinations that included T2-weighted (T2W) images (TR/TE = 5800/84 ms) and gadolinium (Gd)-enhanced, spoiled gradient echo (GRE) T1-weighted (T1W) images (TR/TE = 7.12/3.15, flip angle [FA] = 13°) with Gadteridol 0.2 mL/kg.\nCerebral MRI examination was performed on admission. On T2W imaging, multiple poorly demarcated, variously sized, hyperintense lesions were observed from the periventricular to the deep white matter of the bilateral lateral ventricle, including in the right inferior horn, bilateral triangle, right anterior horn, and body of the ventricle. The right hippocampus, bilateral basal ganglia, and thalami, as well as the white matter in the bilateral temporal and occipital lobes were also affected ().\nOn Gd-enhanced three-dimensional (3D) GRE T1W imaging, multiple enhanced miliary foci, measuring up to 2 mm in size, were partially confluent along the subependyma and the deep white matter, indicating perivascular space involvement (). Some abnormal sulcal enhancement was detected along the pia mater of the parietal and occipital lobes, suggestive of meningitis. Similarly, in the right internal auditory canal and geniculate ganglion area of the facial nerve, faint enhancement was demonstrated. The ventricle was slightly enlarged and a CSF circulatory disorder was suspected. On 3D susceptibility-sensitive GRE T2* images, the bilateral thalami and triangles of the lateral ventricle showed linear hypointense changes, suspected to represent venous congestion ().\nAlthough cryptococcus antigen and CSF polymerase chain reaction for Mycobacterium tuberculosis complex were negative, the initial India ink staining gave an equivocal result. From these laboratory data and the suspicious history of possible exposure to a pigeon parasite, cryptococcal meningitis was suspected, and therefore antifungal agent administration was begun soon after admission. Serology was negative for various possibly causative viruses. At this stage, although the CSF laboratory data showed a tendency toward improvement, the patient’s symptoms did not improve.\nOn the 12th hospital day, a positive QuantiFERON (QTF) test result was obtained, and the possibility of brain tuberculoma or tuberculous meningitis was considered. Therefore, combined anti-TB drug and steroid therapy was started. MRI performed one month after initiation of the therapy revealed an increased number of hyperintense lesions in the lateral periventricular white matter, subcortical white matter, basal ganglia, and thalamus on T2W imaging (). The lateral ventricle was prominently enlarged, as compared with the corresponding images obtained at admission (). In contrast to T2W imaging, the number of enhancing miliary foci had decreased on post-contrast T1W imaging (). Furthermore, the patient’s cognitive function showed improvement, allowing hospital discharge, with her subsequent course continuing to be smooth.\nOn MRI obtained two months after discharge, the aforementioned hyperintense lesions on T2W imaging showed some improvement (), while the contrast-enhanced miliary foci showed significant improvement (). Hydrocephalus gradually worsened during the course after discharge, which was revealed on serial follow-up MRI studies. Because enlargement of the ventricle ceased, and clinical symptoms associated with hydrocephalus were not observed, treatment to prevent the enlargement of the ventricles was not performed.
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.