Cysticercosis, also known as porcine cysticercosis, is a disease caused by the larvae (cysticercus) of the pork tapeworm parasitizing the human body, with cerebral cysticercosis being the most serious. 50%-70% of patients with cysticercosis may have central nervous system involvement. This disease is one of the more common parasitic diseases in China. The incidence is higher in northeast, north, northwest and southwest China. Etiology and pathogenesis: Humans can be the final host of pork tapeworm, causing intestinal tapeworm disease. It can also be its intermediate host, causing cysticercosis. When the eggs are excreted in the feces, they are already mature and contain six larvae. When people eat food containing eggs, the eggshells are digested by the duodenal fluid and the six larvae overflow into the intestinal wall, enter the veins and lymphatic vessels and are sent to the whole body, where they develop into cysticercus and are parasitized in different parts of the body, with brain, muscle and subcutaneous tissue being common. There are three modes of infection: 1. intrinsic self-infection; 2. exogenous self-infection; 3. exogenous allogeneic infection. Cysticerci (cysticercus) are ovoid, milky white and translucent, generally about the size of a soybean, with a head node that turns inward from the cyst wall. Cysticerci cause local inflammatory reactions in tissues, initially neutrophil and eosinophil infiltration, followed by plasma cell and lymphocyte dominance, fibroblast proliferation, and larvae are wrapped to form their own cysts. The disease often fluctuates due to the different developmental processes and death sequences of cysts. During the period of live cysts, there are usually no clinical symptoms, but after the regression and death of cysts, they cause obvious inflammatory reactions. Clinical manifestations: The clinical symptoms of cerebral cysticercus are complex and varied due to the different sites and numbers of cysticercus parasites and the differences in individual reactions of patients. In the acute stage, there may be fever, generalized pain, weakness, loss of appetite and other systemic symptoms. According to the site of lesion and the manifestation of neurological damage, it can be roughly divided into the following types: 1) parenchymal type; 2) ventricular type; 3) meningeal type; 4) spinal type. All types can be combined. Headache is the most common symptom, especially in patients with meningeal type of cysticercosis, which is more severe, and may show increased intracranial pressure such as nausea, vomiting, optic papilledema, and positive signs of meningeal irritation. Paraplegia and urinary and fecal disorders may occur when cysticerci invade the spinal cord. The routine blood picture is normal, with a few mildly increased eosinophil ratios, and eggs can be detected in the stool routine (suggesting intestinal tapeworm disease). Spinal fluid examination pressure can be increased, cerebrospinal fluid leukocytes are mildly to moderately increased, usually 10-100×106/L, sugar is normal or decreased, and protein is mildly increased. Cerebrospinal fluid cytology is generally lymphocytic inflammation, with a mild-moderate increase in the percentage of eosinophils and also plasma cells, etc. The massive death of cysticercus during anthelmintic treatment can aggravate the cerebrospinal fluid response and cause a significant increase in cerebrospinal fluid eosinophils. Immunological methods to detect anti-cysticercosis antibodies or cysticercosis antigen in blood and cerebrospinal fluid can help in the diagnosis and treatment detection of this disease. CT examination of the head has an important role in detecting lesions, location, size and number, and cysticerci are located in the junctional area of white and gray matter of the brain. In the calcification stage, there is no enhancement. MRI of the head can well show the cysticercus in the brain parenchyma, subarachnoid space and ventricles. Diagnosis: The diagnosis of this disease is based on clinical manifestations, epidemiological data, neuroimaging, cerebrospinal fluid examination and immunological tests. Treatment: Pharmacological treatment: commonly used drugs are praziquantel and abendazol. The total adult dose of praziquantel is 200mg/Kg, and the total adult dose of abendazol is 200-300mg/Kg, both of which are recommended to be increased gradually from the dose. Generally 2-4 courses of treatment are required. In the drug worm-killing treatment, the dead cysts may cause severe inflammation and edema, and the intracranial pressure may be significantly increased, which needs to be observed clinically, and glucocorticoids and dehydrating agents may be given. Ophthalmology consultation should also be requested to exclude ocular cysticerci before pharmacological treatment. Surgical treatment: intracerebroventricular cysts can be surgically removed.