A 54-year-old female patient was admitted to the hospital for 14 days, complaining of fever, headache, nausea, and vomiting. The temperature at the time of admission was 38.5 C. History taking revealed that the patient had undergone a lumbar puncture some days ago in a hospital. The lumbar pressure was 120 mmH2O, white blood cell count was 281x106/L, the cerebrospinal fluid protein was 1139 mg/L, cerebrospinal fluid glucose 2.50 mmol/L, and cerebrospinal fluid chloride was 117.8 mmol/L ( Table 1 ). The lady tested positive for serum tuberculosis infection T cell, and a diagnosis of tuberculous meningitis was made. The patient experienced intermittent limb twitching daily to the present admission, accompanied by loss of consciousness. In addition, the patient confessed to having a history of "diabetes" for about half a month. Physical examination was conducted upon admission. The patient had a positive result for the neck resistance test, and the head MRI showed lacunar infarction in the left basal ganglia. A Chest CT scan revealed multiple nodules in both lungs ( Figure 1 ). Organ function tests relating to the liver and kidney returned typical results. The sodium and chloride ion levels were 124.4mmol/L and 92.2mmol/L, respectively. Both HIV antibody and syphilis monitoring tests were negative. A diagnosis of tuberculous meningitis was made, and the patient was given antituberculosis drug therapy comprising isoniazid, rifampicin, and pyrazinamide. Re-examining the lumbar puncture on the second day of admission showed a lumbar pressure of 150 mmH2O, white blood cell count was 44x106/L, the cerebrospinal fluid protein was 636 mg/L, cerebrospinal fluid glucose was 5.84 mmol/L, and cerebrospinal fluid chloride was 111.8 mmol/L ( Table 1 ). Cerebrospinal fluid cytology was suggestive of mixed cell response. No abnormalities were seen regarding cryptococcal capsular antigen and acid-fast staining tests, cerebrospinal fluid mNGS (metagenomics next generation sequencing), culture and Gene Xpert MTB/RIF. Similarly, there were no pathogenic microorganisms found in the cerebrospinal fluid. The EEG results showed slowed brain wave frequencies during the awake period, and moderately slow waves (3-5 Hz) appeared intermittently in each lead. After instituting anti-tuberculosis treatment, the clinical symptoms improved rapidly; the headache resolved, but nausea and vomiting occasionally occurred ( Figure 2 ). One week after admission, the lumbar puncture was repeated, giving the following results: lumbar pressure was 75 mmH2O, white blood cell count was 42x106/L, cerebrospinal fluid protein was 651 mg/L, cerebrospinal fluid glucose was 6.30 mmol/L, and cerebrospinal fluid chloride was 110.9 mmol/L ( Table 1 ). Re-examination of the cerebrospinal fluid mNGS found no pathogenic microorganisms. Two weeks after admission, the patient had no headache and was discharged from the hospital on oral antituberculosis drugs. However, one week after being discharged from the hospital, the patient was re-admitted to the hospital, complaining of persistent nausea and vomiting. A re-examination of the lumbar puncture showed that the pressure was 100 mmH2O, the number of white blood cells was 23x106/L, cerebrospinal fluid protein 504 mg/L, and cerebrospinal fluid chloride was 108.1mmol/L. Blood sodium and chloride ions was 128.5 mmol/L and 90.9 mmol/L, respectively ( Table 1 ). A re-examination of the head MRI showed no typical APS imaging features ( Figure 3 ). The serum AQP4 antibody test (Cytometric Bead Array method) was 1:100, while the fundus examination, visual examination, evoked potential, and spinal cord magnetic resonance was negative. Besides, anti-MOG, anti-GFAP, anti-NMDA, anti-IgG4 antibodies, and autoantibodies were all negative, leading to a definite diagnosis of NMOSD. At the same time, antituberculosis drugs were discontinued. After instituting pulse therapy using 1000 mg of methylprednisolone, nausea and vomiting reduced rapidly. Six days later, the patient was discharged on oral treatment with prednisone. Three months later, the patient's clinical symptoms did not recur. In addition, five months later, the patient developed blurred vision in one eye during the follow-up. VEP showed prolonged P100 latency and decreased P100 amplitude. The visual field test indicated a superior and temporal visual field defect, AQP4-Ab testing was reviewed, which titer was 1:10. Lumbar pressure 90 mmH2O, white blood cell count was 1x107/L, cerebrospinal fluid protein was 312 mg/L, cerebrospinal fluid glucose 6.10 mmol/L, and cerebrospinal fluid chloride was 124.7mmol/L. Therefore, the possibility of optic neuritis was clinically considered, and mycophenolate mofetil was given. The patient's vision recovered rapidly in a short time after the treatment.