Neonatal jaundice is a common disease in the neonatal period, especially in premature infants. It refers to the clinical symptoms of mucous membrane, sclera, and skin yellowing in newborns, and jaundice can affect the level of their intellectual development in severely jaundiced children. Jaundice, which often occurs in newborns, can be divided into two categories: physiological jaundice and pathological jaundice. For physiological jaundice usually does not require special treatment and clinical observation is all that is needed. A significant proportion of jaundice is characterized by long duration and high serum bilirubin levels, which are pathological jaundice. Pathological jaundice is mostly characterized by elevated indirect bilirubin, which can be deposited in the brain to cause bilirubin encephalopathy if not treated in a timely manner, and may also affect the liver function of the newborn, seriously threatening the health of the newborn, and may even lead to neonatal death, with a mortality rate of 50% to 70% in the acute phase; and about 80% of surviving patients will have more serious neurological sequelae, so how to promptly Therefore, it is very important to diagnose and treat pathological jaundice in newborns to prevent bilirubin encephalopathy. Blue light therapy (light irradiation with a wavelength of 420-470 nm) is the primary clinical treatment for neonatal jaundice and can transform indirect bilirubin in the child’s body into a nontoxic water-soluble derivative, thereby reducing the serum bilirubin level in the child and preventing the occurrence of bilirubin encephalopathy. Currently, two types of blue light irradiation treatment are often used clinically: intermittent blue light irradiation and continuous blue light irradiation. If the jaundice index is too high and the treatment is not timely, it will have a great impact on the neonate’s intellectual development and can lead to bilirubin encephalopathy in severe cases, which can cause irreversible damage to the child’s brain with serious consequences. Therefore, the prevention and treatment of neonatal jaundice should be given sufficient attention. Blue light irradiation therapy has been clinically recognized as one of the most effective cures for jaundice in preterm infants. Foreign studies have concluded that the toxic effects of nuclear jaundice on the nervous system can lead to severe clinical manifestations, and it is also believed that safer serum bilirubin levels often cause intellectual, hearing, and neurological abnormalities. The main etiology of involuntary motor cerebral palsy is due to hypoxic-ischemic brain injury and bilirubin encephalopathy, and different parts of the basal nucleus region in infants and children are selective for damage. Bilirubin mainly damages the pallidum, whereas hypoxia-ischemia mainly damages the nucleus accumbens and thalamus. The main target cells of bilirubin neurotoxicity are neurons and astrocytes. Under the effect of the same dose of bilirubin, neurons mainly show apoptosis while astrocytes show altered mitochondrial function excitatory amino acids are involved in the apoptotic process, and only under the effect of high dose of bilirubin do neurons mainly show necrosis. Bilirubin in neonates with impaired blood-brain barrier is prone to aggregation, binding and deposition at the cell membrane through this barrier, causing neuronal damage, blocking cell membrane potential conduction and affecting the functional state of brain cells reducing brain cell energy metabolism. Bilirubin is deposited differently in different parts of the brain, with the brainstem being the earliest and highest. Brainstem auditory channels are particularly sensitive to the toxic effects of bilirubin. Unconjugated bilirubin can not only be deposited in the cochlear nucleus of inner ear hair cells, but also damage the entire brainstem tissue, causing abnormalities in the central auditory conduction pathway. The negative performance of CT may be due to: (1) mild damage; (2) hidden sites of damage, such as the midbrain and cerebral bridge. Therefore, the rate of abnormalities in children with cerebral palsy caused by neonatal hyperbilirubinemic encephalopathy is higher than their imaging when BAEP is applied.