A total of 24 patients with non-TBM who were admitted to our Department of Neurology from January 2017 to June 2021 and diagnosed with early cerebrospinal fluid changes consistent with the characteristics of TBM were selected. The non-TBM patients included 12 males and 12 females, aged 21-78 years old, with an average of 48.13 +- 14.6 years old. The patients included 2 cases of Liszt's meningitis, 2 cases of Brucella infection in the CNS, 4 cases of Varicella zoster virus encephalitis, 2 cases of human herpes simplex virus type 1, 2 cases of lupus encephalopathy, 2 cases of anti-NMDAR receptor encephalitis, 2 cases of meningeal carcinomatosis, 5 cases of cryptococcal meningitis, 2 cases of CNS sarcoidosis, and a case of invasive Rhizopus oryzae infection (Table 1).
All patients in the group had acute onset. There were 5 cases of upper respiratory tract infection, fever (9 cases), headache (6 cases), mental symptom (5 cases), cognitive disorder (6 cases), meningeal irritation (9 cases), and epilepsy (6 cases). The changes of consciousness content and (or) consciousness level occurred in 16 patients during admission, which was as follows: confusion (8 cases), apathy (1 case), delirium (2 cases), deep coma (1 case), light coma (2 cases), and somnolence (2 cases); 11 cases were transferred to ICU during hospitalization. More details are shown in Table 1.
For cerebrospinal fluid, all patients underwent lumbar puncture and cerebrospinal fluid examination in our hospital. The leukocyte count was increased (>8 x 106/L), and the median value is 124.0 x 106/L (89.0 x 106/L and 490.5 x 106/L); total protein increased (>450 mg/L), and the median value is 1300 mg/L (1009.5 mg/L and 2314.5 mg/L); glucose decreased (<3.66 mmol/L), and the median value is 1.345 mmol/L (1.045 mmol/L and 2.478 mmol/L); and chloride decreased (<120 mmol/L), and the average value is 111.7 +- 5.2 mmol/L. More detailed results of the patients are shown in Table 2.
All patients were tested for NGS in cerebrospinal fluid, and the pathogen types and copy sequences are shown in Table 2. Eight patients were diagnosed with anti-NMDAR encephalitis, meningeal carcinomatosis, lupus encephalopathy, and CNS sarcoidosis. Anti-NMDAR encephalitis and lupus encephalopathy were confirmed by antibody test results. Meningeal carcinomatosis was confirmed by cerebrospinal fluid cytology, and the CNS sarcoidosis met the clinical diagnostic criteria. Video EEG results show that except 6 who were examined during hospitalization, other patients showed an extensive moderate or above abnormality.
All the patients were examined by cranial MRI. A total of 10 patients had abnormal findings on cranial MRI, including 2 cases of anti-NMDA encephalitis. The two patients showed abnormal signals in the unilateral temporal lobe, hippocampus, and another limbic system. One case of meningeal carcinomatosis showed enhancement of pia mater by enhanced MRI. Two cases of meningococcal disease showed meningeal enhancement and basal ganglia infarction. Two cases of VZV encephalitis showed diffuse brain parenchymal lesion accompanied by cranial nerve enhancement. Two cases of HSV1 encephalitis showed abnormal signals in the right hippocampus and insula. One case of Liszt's encephalitis suggested brainstem damage (Figure 1).
All patients were treated according to diagnosis, and partial patients were treated with immunosuppressive therapy (glucocorticoid and intravenous immunoglobulin 0.4 g kg/d treatment for 5 days). None of the patients had any adverse reactions. Six-month follow-up showed that 9 patients died (5 cases of cryptococcal meningitis, 2 cases of meningeal carcinomatosis, 1 case of Rhizopus oryzae infection, and 1 case of severe VZV encephalitis). 15 cases had a good prognosis without obvious sequelae.