Neonatal cerebral infarction is a cerebrovascular event that occurs between 28 weeks of gestational age and 28 days after birth. With an incidence of 1/4000-1/1578, it is the second most common cause of neonatal convulsions. The arteries of the brain are derived from the internal carotid artery, which supplies the anterior 2/3 of the cerebral hemisphere and part of the mesencephalon, and the vertebral artery, which is bounded by the parieto-occipital sulcus, which supplies the posterior 1/3 of the cerebral hemisphere and part of the mesencephalon, brainstem and cerebellum. The branches of the two arteries in the brain can be divided into cortical and central branches, with the former nourishing the cerebral cortex and deep medulla, and the latter supplying the basal nucleus, internal capsule and mesencephalon. Cerebral infarction in neonates most often occurs in the middle cerebral artery region and is mostly unilateral, with left-sided involvement being more common than right-sided involvement. Infarcts in the middle cerebral artery are divided into trunk infarcts, cortical branch infarcts (watershed infarcts), and central branch infarcts (doublestem artery infarcts). Preterm infants born at 28-32 weeks of gestational age are commonly affected by one or more bean and striatal branches, and preterm and term infants born at >32 weeks of gestational age are prone to trunk branch infarcts. Etiology and risk factors The etiology of neonatal cerebral infarction is usually considered to be related to thromboembolism of intracranial or extracranial vascular, cardiac or placental origin. The antenatal and postnatal days are a special period of risk for cerebral infarction for both the mother and the baby, which may be related to the activation of coagulation mechanisms during this period. Prenatal high-risk factors: pre-eclampsia, first birth, infertility, reduced amniotic fluid, chorioamnionitis, delayed rupture of membranes, decreased fetal movement, prolonged second stage of labor, abnormal fetal heartbeat, intrauterine growth restriction. Intrapartum high-risk factors: emergency cesarean section, fetal head extraction, 5-minute Arrhenius score of 7, experiencing birth resuscitation, etc. Postnatal high-risk factors: congenital heart disease, infection, dehydration, erythrocytosis, homocysteinemia, etc. Other high-risk factors: maternal smoking, substance use, social status and economic conditions, etc. Recent studies have shown that birth asphyxia is not significantly associated with neonatal cerebral infarction. Clinical manifestations: lack of specific manifestations, which may be convulsive seizures, apnea, lethargy, reduced muscle tone, feeding abnormalities or no manifestations. The lack of specific manifestations has been suggested to be explained by the lack of specialized neurological functions in the mature brain at the end of the neonatal period. Imaging manifestations Ultrasound is preferred, with strong echogenic reflexes at the infarct site and hypoechoic or no echogenicity in late stages. CT: decreased tissue density in the infarcted area. MRI: T2 sites show significant high signal, T1-weighted shows low signal or is not significant. Diffusion-weighted imaging: its advantage is that it can indeed detect intracellular edema, the hallmark of localized ischemic seizure injury in the brain. The lesion area shows a high bright white high signal. Treatment: The most common symptom is convulsions, and the treatment taken is basically anticonvulsant therapy. Prognosis: The outcome is death, mild hemiparesis, epilepsy and normal neurological performance. The long-term prognosis is more optimistic than in adults and older children.