Tuberculous meningitis (tuberculosis meningitis) is mostly caused by hematogenous dissemination of tuberculosis bacteria from the primary lesion. Most of the patients have low to moderate fever or even high fever, but relatively few symptoms of tuberculosis toxicity such as malaise, nausea, night sweats, intermittent headache in the early stage, and then become persistent headache and gradually worsen. The main neurological sign is meningeal irritation, the nodular brain is most obvious with skull base lesions, cranial nerve damage can occur, damage to the abducens nerve and oculogyric nerve can appear in the early stage, pupillary changes and facial nerve palsy are also common. Cerebrospinal fluid tests are extremely important in the diagnosis of nodular encephalopathy. The cytologic changes in nodular brain have a certain pattern: the cytology is characterized by predominantly neutrophils with a certain number of small lymphocytes, lymphocytes, plasma cells, and mononuclear phagocytes. Cerebrospinal fluid biochemistry can be characterized as “two low and one high”, i.e., low sugar, low chloride, and high protein, with a marked increase in cerebrospinal fluid protein content closely associated with cerebral nerve damage in the nodal brain. For various reasons, the detection rate of cerebrospinal fluid antacid bacilli is low, and the detection rate can be improved by centrifugal and floating concentration methods or by film smears after 24 hours of resting. Positive polymerase chain reaction for Mycobacterium tuberculosis DNA and adenosine deaminase can be used as early diagnostic indicators of tuberculous meningitis. The cerebrospinal fluid changes in tuberculosis and cryptococcal meningitis are very similar, and cryptococcal testing should be performed routinely. Because of the lack of symptoms of tuberculosis toxicity in tuberculous meningitis and the low rate of positive cerebrospinal fluid for antacid bacilli, the early cell count can be low and the cytologic changes atypical, which can be easily misdiagnosed as viral encephalitis, and misdiagnosed as septic encephalitis because of the high cell count, and easily misdiagnosed as epidemic encephalomyelitis in winter and spring when the onset of the disease is acute. In addition to timely review of cerebrospinal fluid cytology and parallel pathogenic testing, clinical observation of cranial nerve damage and active search for primary lesions, such as tuberculosis, should be emphasized to achieve early diagnosis and treatment when the diagnosis is not clear. Therefore, clinical attention should be paid to the following points: 1. Clinical fever, headache, meningeal irritation, cranial nerve damage, and cerebrospinal fluid examination with the phenomenon of “two low and one high” should be highly suspected of tuberculosis; 2. Early treatment is the key to reduce the death rate of tuberculosis; 3. The dose of isoniazid can be (12-20) mg/kg/d) in the whole course of the combination, and the amount should be sufficient, and the course of treatment can be 1.5 to 2 years; 4.