Neonatal hypoxic-ischemic encephalopathy is brain damage in the fetus and newborn caused by perinatal neonatal hypoxia and ischemia. It is mainly caused by intrauterine distress and neonatal asphyxia and hypoxia. It is the most common cause of death and disability from perinatal brain injury in full-term infants. Severe encephalopathy can leave sequelae such as epilepsy, mental retardation and cerebral palsy, which bring a great burden to families and society. The diagnosis of neonatal hypoxic-ischemic encephalopathy requires the following conditions: (1) abnormal obstetric history and severe intrauterine distress (fetal heart rate <100 beats/min for more than 5 min; and/or amniotic fluid III contamination), or a history of significant asphyxia during delivery; (2) severe asphyxia, defined as an Apgar score of ≤3 for 1 min that continues to be ≤5 for 5 min (3) neurological symptoms (consciousness, muscle tone, reflexes) soon after birth and lasting for more than 24 h. In severe cases, there may be convulsions, brainstem signs (altered respiratory rhythm, pupillary changes, dull or absent light response) and increased fontanelle tone; (4) exclude electrolyte disorders, intracranial hemorrhage and birth injuries that cause convulsions, as well as intrauterine infections, genetic (4) exclude convulsions caused by electrolyte disorders, intracranial hemorrhage and birth injuries, as well as brain damage caused by intrauterine infection, genetic diseases and other congenital diseases. Ancillary tests include cranial CT, MRI, ultrasound, EEG and other abnormalities. Neonatal hypoxic-ischemic encephalopathy can be classified as mild, moderate, or severe based on medical history, symptoms, signs, and imaging findings. Mild encephalopathy usually returns to normal symptoms and signs within 3 days and leaves no sequelae, while moderate and severe encephalopathy can leave sequelae. It is important that a history of fetal or neonatal hypoxia should be present to diagnose neonatal hypoxic-ischemic encephalopathy. After birth, there should also be neurological abnormalities, such as altered consciousness and muscle tone, which may be manifested by crying, shrill crying, excitement and irritability, little sleep with eyes open, or neurological depression, such as drowsiness, no crying, no response to stimulation, tight and shaky limbs, or floppy limbs. Ancillary tests such as cranial CT with hypointense shadow and cranial ultrasound with cerebral edema can help in the diagnosis. In our clinical work, we often encounter infants diagnosed with hypoxic-ischemic encephalopathy by local doctors, but they are born smoothly with no history of intrauterine or birth asphyxia or hypoxia, and are diagnosed with hypoxic-ischemic encephalopathy just because of the hypodense shadow found on cranial CT, even if the child does not even show neurological abnormalities, so they are given transvenous infusion of nutritional brain cells for several months. This practice is actually very inappropriate. Even if a newborn has the above-mentioned symptoms of brain injury and has abnormal head CT or MRI or ultrasound, it does not necessarily mean that it is hypoxic-ischemic encephalopathy. Because there are many causes of brain injury, including severe jaundice, intracranial hemorrhage, intrauterine viral infections, genetic and metabolic diseases, all of which can have abnormal neurological manifestations, newborns confirmed to have no history of hypoxia should not be casually diagnosed with hypoxic-ischemic encephalopathy. Mild encephalopathy usually does not require treatment because it does not leave sequelae, and the course of treatment for moderate to severe encephalopathy also depends on the effectiveness of treatment and the performance of the child. Several months of continuous intravenous brain cell-nourishing medication is not required for infants without signs and symptoms of neurological abnormalities. For infants with sequelae of brain injury, such as those who exhibit mental retardation and abnormal muscle tone, rehabilitation should also be the main focus of treatment, while the efficacy of brain cell-nourishing drugs cannot be determined, which is also controversial internationally, so the focus of treatment should be on rehabilitation.