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 65-year-old female visited the emergency department, complaining about headache, paraplegia, numbness of both legs, and urinary incontinence for one week. She had a history of kidney transplantation because of a stage 5 chronic kidney disease. She was also diagnosed with active pulmonary TB two weeks ago and started taking the combination of antituberculosis medication (isoniazid, ethambutol, rifabutin, and pyridoxine). Neurologic examination revealed only a trace or a flicker of movement on both lower extremities and impaired sensations below T10 level, while the motor and sensory functions of upper extremities were normal. The anal sphincter tone was decreased, and the deep tendon reflexes were absent on both lower limbs.\nThe spine magnetic resonance imaging (MRI) showed a round, well-defined, intramedullary-enhancing lesion (7×6×14mm in size) at T9-T10 levels with high signal change of spinal cord at T5-L1 levels (). Surgical resection was performed to decompress the spinal cord. There was a noted greyish, well-demarcated, firm mass that was radically removed. Consistent with tuberculosis, the histopathologic examination showed noncaseating, granulomatous inflammation. A few acid-fast bacilli were detected in granuloma (), and the neurologic deficit was not fully recovered right after the resection. After surgery, patient complains of persistent headache, so we took brain MRI in order to differentiate the brain lesion and it revealed multiple rim-enhancing nodular lesions which were suggestive of tuberculomas (). Anti-tuberculosis medications were persisted with rehabilitation program.