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 5-year-old boy presented with fever for 12 days, progressive motor weakness in lower limbs for 9 days, and retention of urine and constipation for 6 days. The patient was treated elsewhere for fever for three days. However, on the fourth day of the illness, the child developed progressive symmetrical lower limb weakness causing difficulty in standing, sitting, and turning from side to side. Over the next three days, he developed retention of urine and constipation, hence was referred to our hospital for further management.\nThere was no history of headache, vomiting, altered sensorium, cranial nerve or sensory deficit, recent immunization, and head or spine trauma. The patient had no tuberculosis (TB) in the past nor TB contact.\nAt admission, his pulse rate was 88/min, respiratory rate was 32/min, and blood pressure was 90/60 mm of Hg. Bacillus Calmette Guerine vaccine scar was seen. Spine palpation revealed no tenderness or deformity. His weight (16kg) and height (106cm) both were between the 10th and 25th centiles for his age and sex. His higher mental functions, cranial nerves, and sensory examination were normal, and papilledema was absent. Tone, power, and reflexes of both upper limbs were normal. Both lower limbs had hypotonia, power grade 2/5, and exaggerated (3+) deep tendon reflexes. Abdominal and cremasteric reflexes were absent and plantar reflexes were extensor bilaterally. Meningeal signs were absent. The patient had mild firm hepatomegaly (2cm) and a palpable distended urinary bladder. Respiratory and cardiovascular system examination was normal.\nHis initial investigations showed iron deficiency anemia and elevated Erythrocyte sedimentation rate (25 mm at 1h), a negative Mantoux test, normal chest radiograph, and gastric aspirate negative for acid-fast bacilli. Enzyme-linked immunosorbent assay was negative for human immunodeficiency virus infection. MRI of dorsal spine (P + C) showed a well-defined oval T2 hypointense ring-enhancing lesion (4.5 × 2.5 mm) in the thoracic cord at D4-D5 level, with mild perilesional edema from D3 to D5 level suggestive of IMT []. MRI of brain revealed few tiny T2/fluid attenuation inversion recovery (FLAIR) hyperintense enhancing foci in left frontal white matter and subependymal region of the left ventricle. Minimal focal subcortical white matter edema was observed in right frontal lobe suggestive of tuberculoma [].\nThe patient was started on ATT regime containing two months of Isoniazid (H), Rifampicin (R), pyrazinamide (Z) and Ethambutol (E) followed by 7 months of Isoniazid (H), Rifampicin (R) and Ethambutol (E) therapy (2HRZE +7HRE) with steroids for four weeks. Parenteral dexamethasone was given for two days followed by oral prednisolone for a total of four weeks. He showed clinical improvement in three days and had complete clinical recovery by nine days. Meanwhile, family screening for TB detected sputum positive for pulmonary TB in father. His father was enrolled and started on standard ATT, the younger sibling was started on isoniazid prophylaxis as per Revised National Tuberculosis Control Program guidelines. On follow-up, the patient was found to be compliant with ATT and clinically well without adverse effects.