The direct cause of cerebral palsy is a syndrome in which brain injury and/or developmental defects lead to movement disorders and postural abnormalities before the brain matures. There are numerous causes of brain injury, and although understanding the exact cause is of little significance for the treatment of cerebral palsy movement disorders, it is important for determining prognosis and promoting growth and development, and for an in-depth discussion of pathogenesis and prevention measures, and it is also helpful for parents of affected children to understand why their children have cerebral palsy. The timing of brain injury and brain developmental defects can be divided into three stages, namely prenatal, perinatal and postnatal. Some people have analyzed this using both congenital and acquired factors. The traditional view is that perinatal causes are the main cause of cerebral palsy, and recently it is believed that 70% to 80% of cerebral palsy occurs before birth, with some of the causes unknown. Therefore, in recent years, it is believed that the research on the etiology of cerebral palsy should be transferred to the field of embryonic developmental biology. The prenatal factors include maternal factors and genetic factors. Maternal factors: maternal smoking, alcoholism, physical and chemical factors, infection during pregnancy, pre-eclampsia, medication, gestational toxicity, trauma, rheumatism, diabetes, toxoplasmosis, circulatory disorders during fetal life, maternal mental retardation, maternal nutritional disorders, severe anemia, etc. Recent studies have found that intraventricular hemorrhage and periventricular lucency (PVL) are an important risk factor for cerebral palsy in preterm infants, and infection is one of the causes of PVL. Genetic factors: Recent studies have suggested that genetic factors are important in the development of cerebral palsy, and that twins with cerebral palsy at the same time and children with cerebral palsy in the family are more likely to have cerebral palsy. It has been reported that simple ataxic cerebral palsy is associated with autosomal recessive inheritance, and some children with spastic diplegia and hemiplegia have a genetic predisposition. 2. Perinatal factors are mainly associated with prematurity and intrapartum factors, which can lead to different types of brain damage. However, the immature brain has strong potential and plasticity, which mainly shows that the uninjured parts have strong functional reorganization ability to cope with brain injury, so immature brain injury has obvious differences from mature brain injury. (1) The risk of developing cerebral palsy increases with the degree to which birth weight deviates from the standard weight for the same gestational age, and low birth weight or large infants are tens of times more likely to develop cerebral palsy than normal weight. (2) Prematurity is by far one of the most important factors in the detection of cerebral palsy. (3) Placental insufficiency, hypoxia-ischemia, meconium aspiration, Rh or ABO blood group incompatibility, glucose-6-phosphate dehydrogenase deficiency, and hyperbilirubinemia are also thought to be associated with cerebral palsy. Placental abruption, placenta praevia, cord winding, or meconium aspiration in full-term pregnancies may cause neonatal asphyxia, leading to the development of cerebral palsy from hypoxic-ischemic encephalopathy (HIE). Severe hypoxic-ischemic encephalopathy can lead to subcortical polycystic cerebral softening, and when this occurs, it mostly causes severe tetraplegia with severe mental retardation. Polycystic cerebral softening involving the thalamus or basal ganglia can lead to dystonia. (4) Neonatal stroke can occur in preterm or term infants and usually involves the middle cerebral artery. Wedge-shaped defects and cysts in one cerebral hemisphere can occur, often leading to hemiparesis. Therefore, even if the defect or cyst is large, the child’s function is not greatly affected, and cognitive function in particular is generally good. (5) Certain intrauterine viral infections can lead to the development of cerebral palsy, such as the rodent-transmitted sarcoid virus that can cause lymphatic choroid plexus meningitis with non-progressive lesions that can lead to cerebral palsy. Immunodeficiency virus (HIV) infection can also lead to neurological sequelae, but is progressive and the affected child has a short life span. Most commonly, Toxoplasma gondii infection with cats as the host leads to cerebral palsy and mental retardation with a chance of about 30%. 3. Postnatal factors Postnatal factors can overlap with prenatal and natal factors, but trauma, infection, convulsions, hypoxic-ischemic encephalopathy, intracranial hemorrhage, hydrocephalus, bilirubin encephalopathy, and poisoning are considered to be the main factors. Cerebral palsy due to postnatal factors accounts for 10% to 15%. Neonatal convulsions, respiratory distress syndrome, aspiration pneumonia, sepsis, hypoxic-ischemic encephalopathy, intracranial hemorrhage, hydrocephalus, bilirubin encephalopathy, and brain infections, hypoglycemia, and traumatic brain injury are considered to be risk factors for cerebral palsy. Child abuse or accidental trauma can result in blunt trauma with skull fracture. Falls or violent shaking to quiet the infant can lead to the development of shaken baby syndrome, often before the age of 1 year, which mostly results in severe spastic quadriplegia with a poor prognosis due to pulling, shearing and tearing of the long axons of the cortical capillaries and neuronal axons. Direct injury to the brain or secondary brain swelling due to traffic accidents often leads to hemiparesis if the injury site is on one side. If the injury occurs on the left side, it can lead to speech impairment in addition to motor impairment. In addition, many children with closed craniosynostosis have ataxia as their primary functional impairment. Most children with closed craniocerebral injury will make substantial progress within 1 year; very few will require surgical correction of secondary injuries such as contractures at a later stage, and most will have sustained improvement within 3 years of injury, although early tetanic spasticity may also turn into later dystonia. Permanent, nonprogressive central nervous system injury due to various infections should be diagnosed as cerebral palsy, with prenatal and neonatal infections being the most common. 90% of children with cytomegalovirus (CMV) infection result in mental retardation and deafness, and 50% develop cerebral palsy and motor deficits. Congenital rubella virus infection causing mental retardation is very common and 15% can develop cerebral palsy. Neonatal herpes simplex virus infection has a high mortality rate, with 30% to 60% of survivors left with neurological sequelae including cerebral palsy. 30% to 50% of newborns with bacterial meningitis will eventually develop cerebral palsy. In addition, heavy metal and organophosphorus pesticide poisoning, streptocytic anemia, and severe precocious heart disease are also associated with the occurrence of cerebral palsy.