Cerebral Palsy Health Article

Causes and symptoms

As noted, CP has many causes, making a discussion of the genetics of CP complicated. A number of hereditary/genetic syndromes have signs and symptoms similar to CP, but usually also have problems not typical of CP. Put another way, some hereditary conditions "mimic" CP. Isolated CP, meaning CP that is not a part of some other syndrome or disorder, is usually not inherited.

It might be possible to group the causes of CP into those that are genetic and those that are non-genetic, but most would fall somewhere in between. Grouping causes into those that occur during pregnancy (prenatal), those that happen around the time of birth (perinatal), and those that occur after birth (postnatal), is preferable. CP related to premature birth and multiple pregnancies (twins, triplets, etc., not "many pregnancies") is somewhat different and considered separately.

Prenatal causes

Although much has been learned about human embryology in the last couple of decades, a great deal remains unknown. Studying prenatal human development is difficult because the embryo and fetus develop in a closed environment—the mother's womb. However, the relatively recent development of a number of prenatal tests has opened a window on the process. Add to that more accurate and complete evaluations of newborns, especially those with problems, and a clearer picture of what can go wrong before birth is possible.

The complicated process of brain development before birth is susceptible to many chance errors that can result in abnormalities of varying degrees. Some of these errors will result in structural anomalies of the brain, while others may cause undetectable, but significant, abnormalities in how the cerebral cortex is "wired." An abnormality in structure or wiring is sometimes hereditary, but is most often due to chance, or a cause unknown at this time. Whether and how much genetics played a role in a particular brain abnormality depends to some degree on the type of anomaly and the form of CP it causes.

Several maternal-fetal infections are known to increase the risk for CP, including rubella (German measles, now rare in the United States), cytomegalovirus (CMV), and toxoplasmosis. Each of these infections is considered a risk to the fetus only if the mother contracts it for the first time during that pregnancy. Even in those cases, though, most babies will be born normal. Most women are immune to all three infections by the time they reach childbearing age, but a woman's immune status can be determined using the so-called TORCH (for Toxoplasmosis, Rubella, Cytomegalovirus, and Herpes) test before or during pregnancy.

Just as a stroke can cause neurologic damage in an adult, so too can this type of event occur in the fetus. A burst blood vessel in the brain followed by uncontrolled bleeding (coagulopathy), known as intracerebral hemorrhage, could cause a fetal stroke, or a cerebral blood vessel could be obstructed by a clot (embolism). Infants who later develop CP, along with their mothers, are more likely than other mother-infant pairs to test positive for factors that put them at increased risk for bleeding episodes or blood clots. Some coagulation disorders are strictly hereditary, but most have a more complicated basis.

A teratogen is any substance to which a woman is exposed that has the potential to harm the embryo or fetus. Links between a drug or other chemical exposure during pregnancy and a risk for CP are difficult to prove. However, any substance that might affect fetal brain development, directly or indirectly, could increase the risk for CP. Furthermore, any substance that increases the risk for premature delivery and low birth weight, such as alcohol, tobacco, or cocaine, among others, might indirectly increase the risk for CP.

The fetus receives all nutrients and oxygen from blood that circulates through the placenta. Therefore, anything that interferes with normal placental function might adversely affect development of the fetus, including the brain, or might increase the risk for premature delivery. Structural abnormalities of the placenta, premature detachment of the placenta from the uterine wall (abruption), and placental infections (chorioamnionitis) are thought to pose some risk for CP.

Certain conditions in the mother during pregnancy might pose a risk to fetal development leading to CP. Women with autoimmune anti-thyroid or anti-phospholipid (APA) antibodies are at slightly increased risk for CP in their children. A potentially important clue uncovered recently points toward high levels of cytokines in the maternal and fetal circulation as a possible risk for CP. Cytokines are proteins associated with inflammation, such as from infection or autoimmune disorders, and they may be toxic to neurons in the fetal brain. More research is needed to determine the exact relationship, if any, between high levels of cytokines in pregnancy and CP. A woman has some risk of developing the same complications in more than one pregnancy, slightly increasing the risk for more than one child with CP.

Serious physical trauma to the mother during pregnancy could result in direct trauma to the fetus as well, or injuries to the mother could compromise the availability of nutrients and oxygen to the developing fetal brain.