What are the symptoms of cerebral palsy caused by jaundice?

Newborns often experience jaundice, which is divided into physiological jaundice and pathological jaundice. If the pathological jaundice is severe, it may even cause cerebral palsy in the child. We know that cerebral palsy often leads to more serious sequelae, causing intellectual problems in children, difficulty swallowing, and limb paralysis, which has a huge impact on the child's future.

Symptoms of cerebral palsy

1. Often "sensitive" or excited

However, if the child (especially a low birth weight baby) only shows such symptoms when hungry, it is of little significance.

It is difficult for children to abduct their thighs when they are "sensitive" to noise or changes in body position, and it is difficult to open their fists when taking a bath. Parents often report that "their children do not like taking a bath". When their feet touch the edge of the bathtub, their backs become stiff and arched.

2. Over-irritability

Continuous crying and difficulty falling asleep. About 30% of children with cerebral palsy have symptoms similar to severe "colic" in the first 3 months after birth.

3. Difficulty feeding

Poor coordination in sucking and swallowing, difficulty nursing, frequent spitting up, and persistent failure to gain weight.

4. Muscle tension

It is difficult to abduct the thighs when changing diapers for children, it is difficult to open the fists when washing hands, the child does not like to take a bath, cries during the bath, the muscles of the whole body are tense, and the child stands on tiptoe. There is noticeable muscle tension when the child moves his limbs.

5. Abnormal movement

When other children can sit up, my child can't lift his head or turn over; when other children can walk, my child can't sit up or crawl. His motor function is obviously behind other children, and he has obvious abnormal posture and abnormal movement patterns during activities.

Can neonatal jaundice cause cerebral palsy?

Neonatal unconjugated hyperbilirubinemia is a type of hyperbilirubinemia caused by a variety of pathological reasons and is relatively common in clinical practice. In hyperbilirubinemia, bilirubin passes through the blood-brain barrier and damages certain nerve nuclei of the central nervous system, causing bilirubin encephalopathy and leading to cerebral palsy. It is generally believed that this is caused by free bilirubin passing through the blood-brain barrier.

Because under normal circumstances bilirubin binds to plasma proteins and cannot pass through the blood-brain barrier, if there is excessive bilirubin in the blood, such as in hemolysis or sepsis, a large number of red blood cells are destroyed or the blood albumin is too low, a part of the bilirubin cannot bind to albumin and becomes free. This free bilirubin can easily pass through the blood-brain barrier and deposit on the nerve cell membrane and mitochondrial biological membrane, causing cell degeneration and necrosis.

In some children, the increase of bilirubin in the blood is not obvious due to the reduced blood-brain barrier function. This is more common in premature infants, low-birth-weight infants, and children with respiratory distress syndrome, hypoxia, acidosis and infection. Damage to the cerebral vascular endothelium can also lead to a decrease in the blood-brain barrier function, and bilirubin bound to plasma proteins can also enter the brain tissue.