Neonatal jaundice, a common phenomenon in neonatal period, is physiologic in most cases. Pathological jaundice, deep in colour, occurs within 24 hours after birth, progresses rapidly, does not resolve for a long time or reappears after a little resolution, and in some affected new-borns it may last for 2-3 months and is accompanied by other symptoms, this being the nuclear jaundice. Nuclear jaundice occurs when excess indirect bilirubin in the blood enters into the brain and produces an irreversible injury to the nerve cells of the brain, so it is also known as bilirubin encephalopathy. In early stage of the disease, the affected new-born displays somnolence, sucking no breast, screaming, restlessness or even convulsion, and in severe cases death may occur. Survivors often have sequelae of nervous system in varying degrees, manifested as feeblemindedness, aphasis, unclear enunciation, torsion dystonia, athetosis, maldevelopment of teeth, strabismus, dysacusis, and salivation, and in severe cases rigidity of extremities, muscular atrophy and convulsion may occur.
There are many complex etiological factors causing hyperbilirubinemia: (1) hereditary RBC glucose-6-phosphate dehydrogenase (G-G6-PD) deficiency, which is more frequently encountered in southern provinces of China; (2) hemolytic nuclear jaundice due to maternal-fetal blood group incompatibility, the most common being ABO blood group incompatibility; (3) infection,
such as neonatal pneumonia, omphalitis,

Author's unit: Guangdong Gaoming Medical and Medicinal Institute of Encephalopathy, Gaoming, Guangdong 528500
septicemia, etc.; (4) premature delivery, such as low birth weight newborn or immature infant; (5) abnormal delivery, such as embryulcia, cesarean birth, premature rupture of fetal membranes, postmature delivery, etc.; (6) birth trauma, such as cephalohematoma in newborn, intracranial hemorrhage in newborn, anoxia, asphyxia, etc.; and (7) abnormal hemoglobinemia, such asα-Mediterranean anemia.
The main hazard of hyperbilirubinemia is the development of bilirubin cerebrosis, anatomicopathological examination reveals basal ganglionic lesion with simultaneous involvement of cerebellar dentate nucleus and posterior commissural nucleus, mesencephalic red nucleus and black substance and reticular structure of brain stem. It severely affects the patient's life quality and is difficult to cure.
Once a newborn is found to have pathological jaundice, early treatment is indicated. At present, the most effective method is phototherapy to change the structure and property of bilirubin in the blood to make it harmless to nervous tissue and excreted outside the body (generally red or blue light is used, sometimes green or white light is used). Pharmacotherapy includes intravenous drip of glucose, adrenocortical hormone and albumin and oral or muscular administration of phenobarbital. The purpose of pharmacotherapy is to accelerate the metabolism and excretion of bilirubin. Exchange transfusion is indicated for those who are extremely affected and do not respond to the treatment mentioned above. For those with G-6-PD deficiency, it is advocated that from the 28th-30th week of gestational period on the pregnant women are given oral administration of phenobarbital every evening till delivery to avoid as far as possible the development of bilirubinemia. Those with sequela of nuclear jaundice may be given neurotrophic agent in combination with rehabilitation. For rehabilitation, the physiocracy of traditional Chinese medicine is preferable, and for neurotrophic agent, cytidine diphosphate choline may be tried out or the brain health nutriment "Naolizhibao" may be used. Tiapride in combination with anticholinergic may be used for treatment.