Neonatal nuclear jaundice, also known as bilirubin encephalopathy, refers to neonatal hyperbilirubinemia in which unconjugated bilirubin crosses the blood-brain barrier and damages the central nervous system, causing cerebral palsy as the nucleus basalis, subthalamic nucleus, pallidum and other nuclei of the brain are yellowed. The severity of the symptoms is related to the concentration of serum unconjugated bilirubin and the age of the patient. There are four phases: the warning phase, which is mainly characterized by drowsiness, refusal of breast milk, hypotonia, weakening or disappearance of embrace reflex and other inhibitory symptoms, as well as apnea and bradycardia, and enters the spastic phase after about half a day to one day. The spastic period is characterized by spasms, increased muscle tone, screaming, nystagmus, dyspnea, convulsions or corns and other excitatory symptoms, and spasms and other symptoms in preterm infants may not be obvious. The recovery period starts with gradual recovery of sucking and response, followed by improvement of breathing, relief of convulsions, and reduction and disappearance of spasms, which lasts for about 2 weeks. Sequelae period Usually appear 2 months to 6 months after birth, manifesting as involuntary movement of limbs, head and trunk twisting, difficulty in turning the eyes upward or strabismus, hearing impairment, underdeveloped dental enamel, crying and restlessness, intellectual backwardness, and eventually developing into hand-foot tachyphyseal cerebral palsy. Causes of nuclear jaundice Neonatal jaundice is caused by an increase in the concentration of free bilirubin and conjugated bilirubin in the blood. Free bilirubin (i.e., unconjugated bilirubin in the part of the blood that is not bound to albumin) has a strong lipophilicity and can pass through cell membranes, and when it enters brain tissue, it can produce the toxic effects of bilirubin and cause bilirubin encephalopathy. The neurotoxic effect of bilirubin is to block the mitochondrial oxygen utilization of brain cells, so that the “respiration” and energy production of brain cells are inhibited, thus affecting the normal function of the brain. Therefore, the risk of nuclear jaundice is usually estimated clinically by the serum bilirubin concentration, and it is generally believed that there is a risk of bilirubin encephalopathy when the serum total bilirubin concentration is higher than 342 μmol/L (20 mg/d1), but the increase in free bilirubin is usually the main cause. ”What is the manifestation of cerebral palsy after nuclear jaundice? Most children with nuclear jaundice have tardive dyskinesia. Due to the degeneration and necrosis of nerve cells in the basal nucleus of the brain, the child shows signs and symptoms of extrapyramidal damage, as well as varying degrees of mental retardation, mainly in the form of involuntary, purposeless and uncoordinated movements of the limbs, which are aggravated by stress; facial muscles, articulatory and phonological organs are also involved, showing drooling, difficulty in chewing and speech disorders; hearing disorders, etc.