Origins and Causes of Cerebral Palsy: Symptoms and Diagnosis

By Myers, Scott M.; Shapiro, Bruce K. | The Exceptional Parent, April 1999 | Go to article overview

Origins and Causes of Cerebral Palsy: Symptoms and Diagnosis


Myers, Scott M., Shapiro, Bruce K., The Exceptional Parent


Cerebral palsy is a generic name for a difficulty in coordinating muscle movement or maintaining a normal posture that is caused by a brain dysfunction. This excludes movement problems due to abnormalities of muscles, peripheral nerves, or the spinal cord. The brain abnormality that causes cerebral palsy is static in nature--that is, it will not continue to get worse. For example, if a child has a brain tumor that causes a motor disability of his or her left arm and leg, the youngster is not considered to have cerebral palsy because the tumor, as it grows, can cause further motor problems. If the tumor is successfully removed, but a residual muscle coordination difficulty persists, the child can then be diagnosed as having cerebral palsy.

The "insult" to the brain that causes cerebral palsy occurs in early childhood. The time of onset of that damage can be assigned to one of three periods: prenatal (before labor), perinatal (from the onset of labor through the first few weeks after birth), or postnatal (after the perinatal period). The cause of most cerebral palsy can be identified as prenatal events such as genetic disorders; intrauterine infections (e.g. German measles); exposure to toxins; malformations of the brain structure; complications of multiple births; and abnormalities of blood flow to the brain. Perinatal events--such as asphyxia (lack of oxygen), brain hemorrhage, or very high levels of bilirubin that cause jaundice--account for less than 10 percent of all cases of cerebral palsy. Postnatal events such as traumatic brain injury, brain infection (e.g. encephalitis or meningitis), and cardiac arrest are also uncommon, accounting for less than 10 percent of all cases.

When does it happen?

The modern practice of obstetrics and the technology available to pediatricians working in a neonatal intensive care unit have had mixed results in preventing cerebral palsy. Mortality has decreased as techniques have developed to save babies as small as one pound at birth. While many of these premies grow up normally; a small percentage of them develop cerebral palsy. These babies would not have survived 20-plus years ago.

In the case of full-term newborns who show distress soon after birth and later develop cerebral palsy, blame cannot conclusively be put on adverse perinatal events. We are learning that, occasionally, adverse events have occurrred while the baby is in utero that affected brain development, making the baby more susceptible to complications occuring perinatally. Infections in the uterus that show no symptoms would be an example.

A child's type of cerebral palsy often relates to the time when the brain injury occurred. The developing brain is not equally susceptible to injury at all times during its development. Recent research has resulted in several possible explanations for this selective vulnerability. For example, before 32 to 34 weeks in the womb, the developing brain is most susceptible to injury to "white matter" (long nerve fibers), especially around the cavities of the brain. Immaturity of the blood circulation to the brain and of the cells that produce myelin--the insulating substance that surrounds mature nerve fibers--is a key factor in this time-dependent vulnerability. It also contributes to other forms of early brain damage, such as an intraventricular hemorrhage (IVH: bleeding in the brain's cavities).

In contrast, in the near-term fetus and newborn, the white matter is less vulnerable. The gray matter (or nerve cells) that control voluntary motor movement is more likely to be injured by low oxygen, infections, and inflammation. Most infants who are carried to term are able to withstand even severe levels of low oxygen (hypoxia) without significant damage. However, when a certain threshold of low oxygen and decreased blood flow to the brain is reached, a series of events occur at biochemical and cellular levels that result in "death of neurons" (nerve cells). …

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