A 58-year-old man presented with a fever (39.8 C), headache, and confusion for 1 week. He has no previous history of other illnesses or medication use. A neurological examination demonstrated neck stiffness, positive Kernig's sign, and motor power grade 4 in both lower extremities. Blood routine examination, C-reactive protein, and procalcitonin were in the normal range. The cerebrospinal fluid (CSF) sample displayed normal open pressure (110 mmH2O), slightly elevated nucleated cells of 80/ul (normal range: 0-10/ul), significantly elevated protein of 158.71 mg/L (normal range: 15-45 mg/dL), and decreased glucose level of 2.15 mmol/L (blood glucose: 7.29 mmol/L). Brain magnetic resonance imaging (MRI) revealed abnormal leptomeningeal enhancement in the brainstem (Figures 1C, D). In addition, brain MRI showed the high signal intensity of the corpus callosum on T2 sequence MRI (Figure 1A) and diffusion-weighted MRI (Figure 1B). Possible tuberculous meningoencephalitis was diagnosed and anti-tuberculosis therapy was started with oral isoniazid, rifampicin, pyrazinamide, and ethambutol.
A few days after admission, acute delirium and urinary retention developed. A repeated lumber puncture showed high open pressure (250 mmH2O), normal nucleated cells, significantly elevated protein (119.13 mg/L), and decreased glucose level (2.65 mmol/L).
On the 13th day after admission, the patient's condition deteriorated again, with light coma (remaining light reflex and responding to pain) and epilepsy. The neurological examination revealed motor power grade 0 in both lower extremities, tendon areflexia, and limited bilateral abduction. Second-generation sequencing (BGI platform, China) for CSF in this patient revealed no abnormalities. We sent an autoimmune encephalitis panel and demyelinating antibody panel including serum and CSF samples, and the anti-GFAP antibody was positive (1:10) in the serum and CSF analysis (Figure 2). Subsequently, anti-tuberculosis therapy was discontinued and the patient was treated with intravenous 500 mg methylprednisolone per day for 5 days, 240 mg per day for 5 days, 120 mg per day for 5 days, and followed by a slow tapering dose of prednisone over half year. Additionally, the patient received oral immune suppressants (mycophenolate mofetil 500 mg twice daily) for 6 months.
On the fifth day after intravenous methylprednisolone, the patient's consciousness and motor power improved significantly. After completing glucocorticoid pulse therapy, all symptoms of the patient disappeared except urinary retention, and a repeat brain MRI revealed the lesion in the corpus callosum and abnormal leptomeningeal enhancement in the brainstem disappeared (Figures 1F-H). In addition, the spine MRI showed no T2 hyperintensities throughout the cervical spinal cord and thoracic spinal cord (Figure 1E). For urinary retention, we give oral vitamins B1 and B12, and acupuncture and moxibustion rehabilitation training. At follow-up 1 year after symptom onset, the urinary retention of our patient partly improved, and the patient remained clinically stable and had no relapse.