Cerebral Palsy Health Article

Definition

Cerebral palsy (CP) is the term used for a group of nonprogressive disorders of movement and posture caused by abnormal development of, or damage to, motor control centers of the brain. CP is caused by events before, during, or after birth. The abnormalities of muscle control that define CP are often accompanied by other neurological and physical abnormalities.

Description

Voluntary movement (for example, walking, grasping, chewing) is primarily accomplished using skeletal muscles (muscles attached to bones). Control of the skeletal muscles originates in the cerebral cortex, the largest portion of the brain. Palsy means paralysis but may also be used to describe uncontrolled muscle movement. Therefore, cerebral palsy encompasses any disorder of abnormal movement and paralysis caused by abnormal function of the cerebral cortex. CP does not include conditions due to progressive disease or degeneration of the brain. For this reason, CP is also referred to as static (nonprogressive) encephalopathy (disease of the brain). Also excluded from CP are any disorders of muscle control that arise in the muscles themselves and/or in the peripheral nervous system (nerves outside the brain and spinal cord). CP is not a specific diagnosis but is more accurately considered a description of a broad but defined group of neurological and physical problems.v

Because CP is not one disorder, it is difficult to classify. It has been divided into four general types: spastic, athetoid, ataxic, and mixed. Another general categorization describes spastic, dyskinetic, and ataxic CP as follows:

• Spastic refers to diplegic impairment of either legs or arms, quadriplegic involving all four extremities, hemiplegic or one-sided involvement of arms and legs, or double hemiplegic impairment of both sides, arms and legs. Spasticity means having an increased stretch reflex.
• Dyskinetic refers to abnormal movements caused by inadequate regulation of muscle tone and coordination. The category includes athetoid or choreoathetoid CP; both are hyperkinetic forms of the disease.
• Ataxic refers to disturbances in coordination of voluntary movements; it includes mixed forms of CP, with mixed characteristics and symptoms.

Muscles that receive defective messages from the brain may be constantly contracted and tight (spastic), exhibit involuntary writhing movements (athetosis), or have difficulty with voluntary movement (dyskinesia). A lack of balance and coordination with unsteady movements (ataxia) may also be present. Spastic CP and mixed CP constitute the majority of cases. Effects on the muscles can range from mild weakness or partial paralysis (paresis) to complete loss of voluntary control of a muscle or group of muscles (plegia). CP is also designated by the number of limbs affected. For instance, affected muscles in one limb is monoplegia, both arms or both legs is diplegia, both limbs on one side of the body is hemiplegia, and in all four limbs is quadriplegia. Muscles of the trunk, neck, and head may be affected.

About 50 percent of all cases of CP diagnosed are in children who are born prematurely. Advances in the medical care of premature infants since the 1980s have dramatically increased the rate of survival of these fragile newborns. However, as gestational age at delivery and birth weight of a baby decrease, the risk for CP dramatically increases. A term pregnancy is delivered at 37–41 weeks gestation. The risk for CP in a preterm infant (32–37 weeks) is increased about five-fold over the risk for an infant born at term. Survivors of extremely preterm births (less than 28 weeks) face as much as a 50-fold increase in risk.

Two factors are involved in the risk for CP associated with prematurity. First, premature babies are at higher risk for various CP-associated medical complications, such as intracerebral hemorrhage, infection, and difficulty in breathing, to name a few. Second, the onset of premature labor may be induced, in part, by complications that have already caused neurologic damage in the fetus. A combination of both factors may play a role in some cases of CP. The tendency toward premature delivery runs in families, but genetic mechanisms are not fully clear.

An increase in multiple births in the early 2000s, especially in the United States, is associated with the increased use of fertility drugs. As the number of fetuses in a pregnancy increases, the risks for abnormal development and premature delivery also increase. Twins, for example, have four times the risk of developing CP as children from singleton pregnancies, owing to the fact that more twin pregnancies are delivered prematurely. The risk for CP in one of triplets is up to 18 times greater. Furthermore, evidence suggests that a baby from a pregnancy in which its twin died before birth is at increased risk for CP.

Although CP is the leading cause of disability in children, its incidence in the United States did not changed much between the 1980s and the early 2000s. Advances in medicine have decreased the incidence from some causes. Rh disease, for example, has been controlled by the advent of anti-Rh globulin; its administration to Rh-negative mothers has reduced one risk factor for CP. The risk has still increased from other causes, however, notably prematurity and multiple-birth pregnancies. The cause of most cases of CP remains unknown, but it has become clear in the early 2000s that birth difficulties are not to blame in most cases. Rather, developmental problems before birth, usually unknown and generally undiagnosable, are largely responsible. The rate of survival for preterm infants has leveled off in the early 2000s, and methods to improve the long-term health of these at-risk babies are being sought.