cerebral palsy

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 (walking, grasping, chewing, etc.) is primarily accomplished using muscles that are attached to bones, known as the skeletal muscles. 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. In truth, however, 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—a description of a broad but defined group of neurological and physical problems.

The symptoms of CP and their severity are quite variable. Those with CP may have only minor difficulty with fine motor skills, such as grasping and manipulating items with their hands. A severe form of CP could involve significant muscle problems in all four limbs, mental retardation, seizures, and difficulties with vision, speech, and hearing.

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). There can also be a lack of balance and coordination with unsteady movements (ataxia). A combination of any of these problems may also occur. 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 as well.

CP can be caused by a number of different mechanisms at various times—from several weeks after conception, through birth, to early childhood. For many years, it was accepted that most cases of CP were due to brain injuries received during a traumatic birth, known as birth asphyxia. However, extensive research in the 1980s showed that only 5–10% of CP can be attributed to birth trauma. Other possible causes include abnormal development of the brain, prenatal factors that directly or indirectly damage neurons in the developing brain, premature birth, and brain injuries that occur in the first few years of life.

Advances in the medical care of premature infants in the last 20 years 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. About 50% of all cases of CP now being diagnosed are in children who were born prematurely.

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 almost certainly plays a role in some cases of CP. The tendency toward premature delivery runs in families, but the genetic mechanisms are far from clear.

An increase in multiple pregnancies in recent years, especially in the United States, is blamed on 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. Children from twin pregnancies 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 a child of triplets is up to 18 times greater. Furthermore, recent evidence suggests that a baby from a pregnancy in which its twin died before birth is at increased risk for CP.

Approximately 500,000 children and adults in the United States have CP, and it is newly diagnosed in about 6,000 infants and young children each year. The incidence of CP has not changed much in the last 20–30 years. Ironically, advances in medicine have decreased the incidence from some causes, Rh disease for example, but increased it from others, notably, prematurity and multiple pregnancies. No particular ethnic groups seem to be at higher risk for CP. However, people of disadvantaged background are at higher risk due to poorer access to proper prenatal care and advanced medical services.

— Scott J. Polzin, MS

For more information on cerebral palsy, visit Britannica.com.

Definition

Cerebral palsy is a term used to describe a group of chronic conditions affecting body movements and muscle coordination. It is caused by damage to one or more specific areas of the brain, usually occurring during fetal development or during infancy.

Description

Cerebral palsy (CP) is an umbrella-like term used to describe a group of chronic disorders impairing movement control that appear in the first few years of life and generally do not worsen over time. The disorders are caused by faulty development or damage to motor areas in the brain that disrupt the brain's ability to control movement and posture. The causes of such cerebral insults include vascular, metabolic, infectious, toxic, traumatic, hypoxic (lack of oxygen) and genetic causes. The mechanism that originates cerebral palsy involves multi-factorial causes, but much is still unknown.

Cerebral palsy distorts messages from the brain to cause either increased muscle tension (hypertonus) or reduced muscle tension (hypotonus). Sometimes this tension will fluctuate, becoming more or less obvious.

Symptoms of CP include difficulty with fine motor tasks (such as writing or using scissors) and difficulty maintaining balance or walking. Symptoms differ from person to person and may change over time. Some people with CP are also affected by other medical disorders, including seizures or mental impairment. Early signs of CP usually appear before three years of age. Infants with this disease are frequently slow to reach developmental milestones such as learning to roll over, sit, crawl, smile, or walk.

Causes of CP may be congenital (present at birth) or acquired after birth. Several of the causes that have been identified through research are preventable or treatable: head injury, jaundice, Rh incompatibility, and rubella (German measles). Cerebral palsy is diagnosed by testing motor skills and reflexes, examining the medical history, and employing a variety of specialized tests. Although its symptoms may change over time, this disorder by definition is not progressive. If a patient shows increased impairment, the physician considers an alternative diagnosis.

Demographics

Cerebral palsy is one of the most common causes of chronic childhood disability. About 3,000 babies are born with the disorder each year in the United States, and about 1,500 preschoolers are diagnosed with cerebral palsy during the first three years of life. In almost 70% of cases, CP is found with some other disorder, the most common being

mental retardation. In all, around 500,000–700,000 Americans have some degree of cerebral palsy.

The prevalence of CP has remained very stable for many years. The incidence increases with premature or very low-weight babies regardless of the quality of care. Twins are also four times more likely to develop CP than single births.

Despite medical advances, in some cases the incidence of CP has actually increased over time. This may be attributed to medical advances in areas related to premature babies or the increased usage of artificial fertilization techniques.

Causes and symptoms

CP is caused by damage to an infant's brain before, during or shortly after delivery. The part of the brain that is damaged determines what parts of the body are affected.

There are a number of factors which appear to predispose a child to CP including:

• Exposure of the expectant mother to certain infections like rubella, toxoplasmosis and cytomegalovirus,
• Exposure of the expectant mother to certain chemicals like alcohol, cigarettes, cocaine and teratogenic (capable of causing birth defects) agents,
• Severe physical trauma to the mother during pregnancy, multiple births or maternal illness,
• Children who are born prematurely (less than 32 weeks) or who are very low birth weight (less than 1,500 grams or about 3⅓ pounds),
• Failure of the brain to develop properly or neurological damage to the infant's developing brain, including hypoxia (lack of oxygen) during birth,
• Bacterial meningitis and other infections, bleeding in the brain, lack of oxygen, severe jaundice, and head injury during the first few years of a child's life.

Cerebral palsy is categorized into four different groups that are characterized by different symptoms. Generally, babies that are severely affected may have obvious signs immediately following birth. Many infants do not display immediate CP symptoms. Parents are usually able to notice developmental delays, especially if they have another unaffected child. At the age of about three months, parents may notice a lack of facial expressions or that their baby does not respond to some sounds, or does not follow movement with their eyes. Certain other indicative symptoms may appear at around six months of age, including inability to lift the head or roll over and difficulty feeding. An affected child may be unable to crawl, sit, or stand without support and drooling is a common problem because of poor facial and throat muscle control. CP symptoms depend on the individual and the type of CP and, in particular, whether or not there is a mixed form of the condition.

The four main categories of cerebral palsy are:

• Spastic CP: Children with spastic CP have increased muscle tone. Their muscles are stiff and their movements can be awkward. Seventy to eighty percent of people with this disease have spasticity. Spastic CP is usually described further by what parts of the body are affected. In spastic diplegia, the main effect is found in both legs. In spastic hemiplegia, one side of the person's body is affected. Spastic quadriplegia affects a person's whole body (face, trunk, legs, and arms).
• Athetoid or dyskinetic CP: Children with athetoid CP have slow, writhing movements that they cannot control. The movements usually affect a person's hands, arms, feet, and legs. Sometimes the face and tongue are affected and the person has a hard time talking. Muscle tone can change from day to day and can vary even during a single day. Ten to twenty percent of people with CP have the athetoid form of the condition.
• Ataxic CP: Children with ataxic CP have problems with balance and depth perception. They might be unsteady when they walk. They might have a hard time with quick movements or movements that need a lot of control, like writing. Controlling their hands or arms when they reach for something is often difficult. People with ataxic CP can have increased or decreased muscle tone.
• Mixed CP: Some people have more than one type of CP, but this is most often a mixture of spasticity and athetoid movements, with tight muscle tone and involuntary reflexes.

Diagnosis

Diagnosing CP in an infant is often a difficult and slow process that takes time to establish with certainty, as there other health problems that can mimic the condition. The physician may suspect that the infant has CP because of a history of difficulties at birth, seizures, feeding problems or low muscle tone. Detailed medical and developmental history, including the history of the pregnancy and delivery, medications taken by the mother during fetal development, infections and fetal movement are all considered. A detailed family history, including the mother's history of miscarriage, relatives with similar conditions, ethnic background, and consanguinity (marriage between close blood relatives) can also prove helpful. The child's physician will perform a thorough physical examination and may order vision and hearing testing.

Infants suffering from brain injury are often slow to reach developmental milestones including rolling over, sitting up, crawling, walking and talking. Healthcare professionals are often hesitant to reach an early diagnosis because the child may recover and they may use other, less emotive terms in labeling the condition such as: neuromotor dys-function, developmental delay, motor disability, static encephalopathy and central nervous system dysfunction.

Physicians must test the child's motor skills, using many of the techniques outlined above and looking for evidence of slow development, abnormal muscle tone, and unusual posture. Healthcare professionals will move slowly and carefully towards a positive diagnosis only after eliminating all other possible causes of the child's condition.

Neuroimaging studies can help to evaluate brain damage and to determine those at risk of developing CP. No study exists to support definitive diagnosis of CP. Computed tomography (CT) scans provide information to help diagnose congenital malformations and intracranial hemorrhages in the infant. Magnetic resonance imaging (MRI) is most useful after two to three weeks of life, and is also used to detect brain disease in an older child.

Ultrasound in the neonate (newborn) provides information about the structures of the brain as well as diagnostic information on possible hemorrhage or hypoxicischemic (lack of oxygen) injury.

Evoked potentials are used to evaluate the anatomic pathways of the nerves responsible for hearing and vision. Electroencephalogram (EEG) is useful in evaluating severe hypoxic-ischemic injury.

Treatment team

A neurologist may help to differentiate cerebral palsy from other neurological disorders. Consultation with a neurologist also may be helpful in treatment of patients with seizures. Pulmonologists (lung specialists) may help treat the patient with bronchopulmonary dysplasia or frequent aspiration pneumonia. Orthopedic surgery consultation may be needed to help correct any structural deformities. An ophthalmologist may be indicated to follow up with any patient experiencing visual deficits. Audiologists help screen for hearing deficits. A gastroenterologist (specialist on digestive disorders) may help with reflux and constipation and may be helpful in coordinating feedings to regulate weight gain or weight loss if needed. A periodic nutrition consultation is important to make sure the child does not suffer from growth failure or nutritional deficiencies.

Treatment

Drug therapy is used for those who have seizures associated with CP. Anticonvulsant medications are usually very effective in preventing seizures associated with CP. Drugs are also used to control spasticity in some cases. Medications used most often are diazepam, a general relaxant of the brain and body, baclofen, which blocks signals sent from the spinal cord to contract the muscles, and datrolene, which interferes with the process of muscle contraction. These drugs are used for short periods, but long-term control of spasticity is more difficult to achieve.

Persons with athetoid CP are sometimes given drugs to help reduce abnormal movements, usually anticholinergics. Anticholinergics reduce the activity of acetylcholine, a chemical messenger that helps some brain cells communicate and trigger muscle contraction. Physicians may inject drugs directly into a muscle to reduce spasticity for a short period.

Surgery is used when muscle contractures are severe enough to create problems in movement. The surgeons lengthen the muscle that is too short. Lengthening a muscle usually makes it weaker, so surgery for contractures is usually followed by an extended recovery and therapy period. To reduce spasticity in the legs, surgery called selective dorsal root rhizotomy sometimes proves effective. It reduces the amount of stimulation that reaches leg muscles by the nerves.

Recovery and rehabilitation

Cerebral palsy cannot be cured. Treatment can, however, help a person take part in family, school, and work activities as much as possible. There are many treatments, including physical therapy, occupational therapy, medicine, operations, and orthotic devices that help maintain the highest possible state of wellness and activity.

Specialized Therapies

Physical therapy improves infant-caregiver interaction, gives family support, and supplies resources for parental education, as well as promoting motor and developmental skills. Physical therapists teach the parent or caregiver exercises or activities necessary to help the child reach his or her full potential.

Daily range of motion (ROM) exercises are important to prevent or delay contractures (fixed, rigid muscles) secondary to spasticity, and to maintain mobility of joints and soft tissues. Stretching exercises are performed to increase motion. Progressive resistance exercises also increase strength. Age-appropriate play and adaptive toys and games using the desired exercises are important to elicit the child's full cooperation. Strengthening knee extensor muscles helps to improve crouching and stride length. Postural and motor control training is important following the normal developmental sequence of children (i.e., achieve head and neck control if possible before advancing to trunk control).

Occupational therapists keep the child's developmental age in mind and use adaptive equipment as needed to help attain these milestones. For example, if a child is developmentally ready to stand and explore the environment, but is limited by lack of motor control, a stander or modified walker is used. Performance based upon previous success is encouraged to maintain the child's interest and cooperation. Assistive devices and durable medical equipment help attain function that may not be possible otherwise. Orthotic devives frequently are required to maintain functional joint position especially in persons who are non-ambulatory. Frequent reevaluation of orthotic devices is important as children quickly outgrow them and can develop skin irritation from improper use of orthotic devices.

Recreational therapy, especially hippotherapy (horse-back riding therapy) is frequently a well-liked activity of parents and patients alike to help with muscle tone, range of motion, strength, coordination, and balance. Hippotherapy also offers many potential cognitive, physical, and emotional benefits. Incorporation of play into all of a child's therapies is important. The child should view physical and occupational therapy as fun, not work. Caregivers should seek fun and creative ways to stimulate children, especially those who have decreased ability to explore their own environments.

Many children with dyskinetic CP have involvement of the face and oropharynx causing difficulty swallowing properly, drooling, and speech difficulties. Speech therapy can be implemented to help improve swallowing and communication. Those patients with athetoid CP may benefit the most from speech therapy, as most have normal intelligence and communication is an obstacle secondary to abnormal muscle movements that affect their speech. Adequate communication is probably the most important goal for enhancing function in the athetoid CP patient.

Clinical trials

As of mid-2004, there were numerous open clinical trials for the study and treatment of cerebral palsy, including:

• "Botulinum Toxin (BOTOX) for CP," "Relaxation Training to Decrease Pain and Improve Function in Adolescents with CP," and "Constraint-based Therapy to Improve Motor Function in Children with CP," sponsored by the National Institute of Child Health and Human Development (NICHD),
• "Classification of CP Subtypes," "Eye-Hand Coordination in Children with Spastic Diplegia," "Beneficial Effects of Antenatal Magnesium Sulfate (BEAM Trial)," and "Brain Control of Movements in CP," sponsored by National Institute of Neurological Disorders and Stroke (NINDS),
• Study of Tongue Pressures, sponsored by Warren G. Magnuson Clinical Center.

Updated information about these clinical trials can be found at the National Institutes of Health website for clinical trials at www.clinicaltrials.gov.

Prognosis

The prognosis of persons with CP varies according to the severity of the disorder. Some children have only mild problems in muscle tone and no problems with daily activities, while others are unable to purposefully move any part of the body. Regression, or worsening of long-term symptoms, is not characteristic of CP. If regression occurs, it is necessary to look for a different cause of the child's problems. In order for a child to be able to walk, a major cascade of events in motor control have to occur. A child must be able to hold up his head before he can sit up on his own, and he must be able to sit independently before he can walk on his own. It is generally assumed that if a child is not sitting up by himself by age four or walking by age eight, he will never be an independent walker. But a child who starts to walk at age three will certainly continue to walk unless he has a disorder other than CP.

In people with severe CP, motor problems often lead to medical complications, including more frequent and serious infections, severe breathing problems, feeding intolerance, and skin breakdown. These medical complications can lead to frequent hospitalizations and a shortened life expectancy.

Epilepsy also occurs in about a third of children with CP and is more frequent in patients with spastic quadriplegia or mental retardation. Cognitive impairment occurs more frequently in CP than in the general population, and mental delays or some form of learning disability has been estimated to occur in over two thirds of CP cases.

Resources

BOOKS

Anderson, Mery Elizabeth, Dineen Tom. Taking Cerebral Palsy to School. St. Louis: Jayjo Books, 2000.

Mechan, Merlin L. Cerebral Palsy. Austin, TX: Pro-Ed Publishers, 2002.

Pincus, Dion. Everything You Need to Know About Cerebral Palsy (Need to Know Library). New York: Rosen Publishing Group, 1999.

PERIODICALS

Darrah, J., et al. "Conductive education intervention for children with cerebral palsy: an AACPDM evidence report." Dev Med Child Neurol 46 (March 2004): 187–203.

OTHER

"Cerebral Palsy—Facts & Figures." United Cerebral Palsy. (May 1, 2004). http://www.ucp.org/ucp_generaldoc.cfm/1/9/37/37-37/447.

"NINDS Cerebral Palsy Information Page." National Institute of Neurological Disorders and Stroke. (May 1, 2004). http://www.ninds.nih.gov/health_and_medical/disorders/cerebral_palsy.htm.

ORGANIZATIONS

March of Dimes Birth Defects Foundation. 1275 Mamaroneck Avenue, White Plains, NY 10605. (914) 428-7100 or (888) 663-4637; Fax: (914) 428-8203. askus@ marchofdimes.com. http://www.marchofdimes.com.

United Cerebral Palsy (UCP). 1600 L Street, NW, Suite 700, Washington, DC 20036. (202) 776-0406 or (800) USA-5UCP (872-5827); Fax: (202) 776-0414. national@ucp.org. http://www.ucp.org.

Francisco de Paula Careta

Iuri Drumond Louro

A collection of syndromes (not a disease) of nonprogressive motor dysfunction arising from abnormal development of or damage to the brain, either prenatally, at birth, or postnatally. Most cases of cerebral palsy develop in utero. Premature birth is associated with an increased risk of cerebral palsy, with the lowest birth weights carrying the highest risk. A maximum of 15% of cases are related to birth injury or perinatal oxygen deprivation. See also Pregnancy disorders.

Although the brain damage in cerebral palsy is nonprogressive and thus deterioration does not occur, the neurological manifestations of cerebral palsy may change with neurological maturation. The precise form of cerebral palsy rarely can be characterized prior to 6 months of age; often it cannot be characterized until the individual is 2 years old. Cerebral palsy is only rarely familial. Its incidence is stable at 0.1–0.3% of live births.

Cerebral palsy is classified by the form and distribution of the motor handicap. Spasticity, seen in 75% of cases, presents a clinical picture of muscle stiffness, weakness, and imbalance of muscle tone. Common findings are contractures of joints, resulting in shortened heel cords and thus toe walking. Tightness of the adductor muscles in the thigh may result in a scissors gait. Painful dislocation of the hip is a common problem associated with severe spasticity. Dyskinetic syndromes, occuring in 20% of cases, are characterized by a severe lack of voluntary muscle control. Unclear speech (dysarthria) can be quite severe. Ataxic syndromes, characterized by impaired coordination without altered motor tone, are uncommon. A fourth syndrome, characterized by severely decreased motor tone (hypotonia), is called atonic cerebral palsy. Distribution of the altered motor tone (that is, what parts of the body are involved) is of great importance in predicting the degree of handicap, especially in the spastic forms.

Treatment of cerebral palsy is aimed at maximizing lifetime independence within the limitations of the individual's handicap. Common treatment modalities include physical and occupational therapy to prevent contractures and facilitate optimal motor control. Speech therapy is used to improve feeding technique and communication skills. Surgical procedures to correct contractures and improve muscle balance are valuable in the spastic syndromes. Surgical and pharmacological approaches to reducing spasticity and dyskinesia remain largely experimental.

(1) (Central Processor) See processor and CPU.

(2) See control program, control panel and copy protection.

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Cerebral palsy denotes ‘a disorder of movement and posture resulting from a permanent, non-progressive defect or lesion of the immature brain’. There are a number of causative factors, most of which act before birth, but some can act up until the age of 2 years, to cause a non-progressive disorder of the still-developing brain. The overall incidence of cerebral palsy is about 5 per 2000 infants, although there are quite large variations between countries.

In some cases there are prenatal influences which cause failure of brain development: either definite genetic factors, inadequate supply of oxygenated blood to the fetal brain, rubella in the first trimester of pregnancy, toxoplasmosis transmitted across the placenta, or irradiation.

In about half of all instances cerebral palsy is associated with pre-term delivery and low birthweight. Compared to those at full term and of normal weight, such infants are particularly at risk of developing cerebral palsy if they suffer hypoxia or inadequate blood flow to the brain around the time of birth, or if they suffer brain infection (encephalitis, meningitis) or head injury during early life.

There are many variations in the types of cerebral palsy, and often there is a mixture of neurological abnormalities. The children may have increased muscle tone (spasticity), which most commonly affects all four limbs — the condition of spastic tetraplegia; or there may be spastic paraplegia, when the arms are apparently unaffected; or the so-called cerebral diplegia, often associated with premature birth, when the arms are less affected than the legs. There can also be hemiplegia, affecting one half of the body, or monoplegia, affecting one limb.

There may also be involuntary movements, such as the writhing (athetoid) type and various disturbances of co-ordination, depending on the parts of the brain affected. Less commonly, cerebral palsy takes the form of a hypotonic tetraplegia, with no spasticity, when the child has a mobility problem but with floppy muscles.

Children with cerebral palsy frequently have other severe handicaps. About half of them have an IQ less than 70, whilst 25% have an IQ above 90, compared with 3% below 70 and 75% above 90 in the general population. Epileptic seizures are more common than in the population overall. Retarded speech development may parallel the degree of learning disorder, but it is frequently also complicated by the problems of defective muscle control. Different forms of speech defect (dysarthria) accompany the different types of movement disorder.

Although the brain abnormality underlying the cerebral palsy is permanent and cannot be corrected, much help can be given to affected children and their families by way of physiotherapy, play and occupational therapy, speech therapy, orthopaedic surgery, and a variety of nutritional, mobility, and educational aids.

— Forrester Cockburn

See also muscle tone; paralysis.

1. collective term for neurologic defects with associated disturbances of motor function. The disturbances vary in cause and anatomic type (e.g., acquired, hereditary, natal, postnatal, congenital palsy). n 2. nonspecific term representing a group of pathologic conditions having the following common, related characteristics: agenesis, or a lesion of nervous tissue within the cranium; interference with voluntary muscular movements; disabling disorders of a chronic nature, neither acute nor progressive; and occurrence of the original lesion at the date of birth of the patient or before the development of learned human muscular function. 3. a condition caused by damage to the motor centers of the brain, resulting in varying disturbances of motor function and often accompanied by mental subnormality.

Definition

Cerebral palsy (CP), or static encephalopathy, is the name for a collection of movement disorders caused by brain damage that occurs before, during, or shortly after birth. A person with CP is often also affected by other conditions caused by brain damage.

Description

The affected muscles of a person with CP may become rigid or excessively loose. The person may lose control of muscles, or have problems with balance and coordination. A combination of these is also possible. Those with CP may be primarily affected in the legs (paraplegia or diplegia), or in the arm and leg of one side of the body (hemiplegia), or all four limbs may be involved (quadriplegia).

A person with CP may also be affected by a number of other problems, including a seizure disorder, visual deficits, hearing problems, mental retardation, learning disabilities, and attention-deficit hyperactivity disorder. None of these is necessarily part of CP, however, they may accompany the disorder.

CP affects approximately 500,000 children and adults in the United States, and is diagnosed in more than 6,000 newborns and young children each year. It is not an inherited disorder, and as of yet there is no way to predict with certainty which children will develop CP. It is not a disease, and is not communicable. CP is a nonprogressive disorder, which means that symptoms neither worsen nor improve over time. However manifestation of the symptoms may become more severe over time. For example, rigidity of muscles can lead to contractures and deformities that require a variety of interventions.

Causes & Symptoms

Causes

Cerebral palsy is caused by damage to the motor control centers of the brain. When the nerve cells (neurons) in these regions die, the appropriate signals can no longer be sent to the muscles under their control. The resulting poor control of these muscles causes the symptoms of CP.

The brain damage leading to CP may be caused by lack of oxygen (asphyxia), infection, trauma, malnutrition, drugs or other chemicals, or hemorrhage. In most cases it is impossible to determine the actual cause, although premature birth is recognized as a significant risk factor. It was once thought that difficult or prolonged delivery was responsible for many cases of CP, but most researchers now believe that the great majority of cases result from brain damage occurring before birth. The same injury that damages the motor areas can harm other areas as well, leading to problems commonly associated with CP.

If brain cells do not get enough oxygen because of poor circulation, they may die. Defects in circulation in the developing brain may cause CP in some cases. Asphyxia during birth is also possible, and about half of newborns known to have suffered asphyxia during birth (perinatal asphyxia) develop CP. However, asphyxia during birth is usually considered a symptom of an underlying neurological problem in a newborn, rather than its cause, and the resulting CP may be another sign of that problem. Asphyxia after birth can be caused by choking, poisoning (such as from carbon monoxide or barbiturates), or near-drowning.

The fetal brain may be damaged by an infection contracted by the mother. Infections correlated with CP include rubella (German measles), toxoplasmosis (often contracted from cat feces), cytomegalovirus (a herpes virus), and HIV (the virus that causes AIDS). Encephalitis and meningitis, infections of the brain and its coverings, can also cause CP when contracted by infants.

Physical trauma to the pregnant mother or infant may cause brain damage. Blows to the infant's head, as from a motor vehicle accident, violent shaking, or other physical abuse can damage the infant's brain. Maternal malnutrition may cause brain damage, as can the use of drugs, including cocaine or alcohol. Although these factors may cause CP, they may be more likely to cause mental retardation or other impairments.

Incompatibility between the Rh blood types of mother and child was once a major cause of athetoid CP, one type of movement impairment seen in cerebral palsy. In some cases, this incompatibility can cause the mother's defense (immune) system to attack and destroy the child's blood cells during pregnancy, a condition called erythroblastosis fetalis. High levels of a blood cell breakdown product called bilirubin in a child's circulation, leading to yellowish pigmentation of the skin caused by bile (jaundice) can result in brain damage. This condition is now rare because of testing procedures that identify potential Rh incompatibility, and treatment that prevents the mother's immune system from attacking the child's blood cells. Jaundice that does occur can be treated with special lights that help the breakdown of bilirubin. Blood transfusions for the child are also possible in extreme cases. Despite the virtual elimination of this cause of CP in the last few decades, CP rates have not declined, largely because of the increase of survival of premature babies.

Prematurity is one of the most significant risk factors for CP. About 7% of babies weighing less than three pounds at birth develop CP, and the risk increases dramatically as weight falls. Prematurity may increase the risk of CP because of the increased likelihood of hemorrhaging in the brain associated with low birth weight. Brain hemorrhage is most common in babies weighing less than four pounds at birth, and the risk increases as weight decreases. The hemorrhage may destroy brain tissue, either through asphyxia or release of toxic breakdown products.

Researchers in Sweden reported in 2002 that babies conceived through in vitro fertilization (IVF) were 3.7 times more likely to have CP than babies conceived naturally. Some of the reason can be attributed to a higher rate of twins, low birthweight, and premature births associated with IVF babies, but some single births also have higher rates of CP.

Symptoms

The symptoms of CP are usually not noticeable at birth. As children develop in the first 18 months of life, however, they progress through a predictable set of developmental milestones. Children with CP will develop these skills more slowly because of their motor impairments, and delay in reaching milestones is usually the first symptom of CP. The more severe the CP, the earlier the diagnosis is usually made.

Selected developmental milestones, and the ages at which a child will normally acquire them, are given below. There is some cause for concern if the child does not acquire the skill by the age shown in parentheses:

• sits well unsupported, 6 months (8-10 months)
• babbles, 6 months (8 months)
• crawls, 9 months (12 months)
• finger feeds, holds bottle, 9 months (12 months)
• walks alone, 12 months (15-18 months)
• uses one or two words other than dada/mama, 12 months (15 months)
• walks up and down steps, 24 months (24-36 months)
• turns pages in books, removes shoes and socks, 24 months (30 months)

Children do not consistently favor one hand over the other before 18 months, and doing so may be a sign that the child has difficulty using the other hand. This same preference for one side of the body may show up as an asymmetric crawling effort, or continuing to use only one leg for the work of stair climbing after age three.

It must be remembered that children normally progress at somewhat different rates, and slow initial accomplishment is often followed by normal development. There are also other causes for delay in reaching some milestones, including problems with vision or hearing. Because CP is a non-progressive disease, loss of previously acquired milestones indicates that CP is not the cause of the problem.

The impairments of CP become recognizable in early childhood. The type of motor impairment and its location are used as the basis for classification. There are five generally recognized types of impairment:

• Spastic. Muscles are rigid, posture may be abnormal, and fine motor control is impaired.
• Athetoid. It is marked by slow, writhing, involuntary movements.
• Hypotonic. Muscles are floppy, without tone.
• Ataxic. Balance and coordination are impaired.
• Dystonic. Impairment is mixed.

The location of the impairment usually falls into one of three broad categories:

• Hemiplegia. One arm and one leg on the same side of the body are involved
• Diplegia. Both legs; arms may be partially involved.
• Quadriplegia. All four extremities are involved.

A person with CP may be said to have spastic diplegia, or ataxic hemiplegia, for instance. CP is also termed mild, moderate, or severe, although these are subjective categories with no firm boundaries.

Loss of muscle control, especially of the spastic type, can cause serious orthopedic problems, including scoliosis (spine curvature), hip dislocation, or contractures. Contracture is shortening of a muscle, caused by an imbalance of opposing force from a neighboring muscle. Contractures begin as prolonged contractions, but can become fixed or irreversible without regular range of motion exercises. A fixed contracture occurs when the contracted muscle adapts by reducing its overall length. Fixed contractures may cause postural abnormalities in the affected limbs, including clenched fists, tightly pressed or crossed thighs, or equinus. In equinus, the most common postural deformity, the foot is extended by the strong pull of the rear calf muscles, causing the toes to point. The foot is commonly pulled inward as well, a condition called equinovarus. Contractures of all kinds may be painful, and may interfere with normal activities of daily living, including hygiene and mobility.

As noted, the brain damage that causes CP may also cause a large number of other disorders. These may include:

• mental retardation
• learning disabilities
• attention-deficit hyperactivity disorder
• seizure disorder
• visual impairment, especially strabismus ("cross-eye")
• hearing loss
• speech impairment

These problems may have an even greater impact on the child's life than the physical impairment of CP, although not all children with CP are affected by other problems. About one-third of children with CP have moderate to severe mental retardation, one-third have mild mental retardation, and one-third have normal to above average intelligence.

Diagnosis

The tracking of developmental progress is the most important test the physician has in determining whether a child has cerebral palsy. Most children with CP can be confidently diagnosed by 18 months. However, diagnosing CP is not always easy, since variations in child development may account for delays in achieving milestones, and since even children who are obviously delayed may continue to progress through the various developmental stages, attaining a normal range of skills later on. Serious or prolonged childhood illness may cause delays that are eventually caught up.

Evidence of other risk factors may aid the diagnosis. The Apgar score, evaluated immediately after birth, measures a newborn's heart rate, cry, color, muscle tone, and motor reactions. Apgar scores of less than three out of a possible 10 are associated with a highly increased indication of CP. Presence of abnormal muscle tone or movements may signal CP, as may the persistence of infantile reflexes. A child with seizures or congenital organ malformation has an increased likelihood of CP. Ultra-sound examination, a diagnostic technique that creates a two-dimensional image of internal body structures, may help to identify brain abnormalities, such as enlarged ventricles (chambers containing fluid) or periventricular leukomalacia (an abnormality of the area surrounding the ventricles), which may be associated with CP.

X rays, magnetic resonance imaging (MRI) studies, and computed tomography (CT) scans are often used to look for scarring, cysts, expansion of the cerebral ventricles (hydrocephalus), or other brain abnormalities that may indicate the cause of symptoms. Blood tests and genetic tests may be used to rule out other possible causes, including muscular dystrophy (a disease characterized by the progressive wasting of muscles), mitochondrial (cellular) disease, and other inherited disorders or infections.

Treatment

A number of people with cerebral palsy, both children and adults, have found systematic relief and enhanced quality of life from a combination of alternative and complementary treatments, including nutritional therapy, craniosacral therapy, bodywork, herbal therapy, homeopathy, and acupuncture.

General Recommendations

Pregnant women should avoid cleaning cat litter, which may contain toxoplasma parasite. This organism causes severe brain damage or death in the unborn fetus. Unprotected sex increases risk of contracting sexually transmitted diseases such as genital herpes, which can infect the unborn child. Women should also vaccinate before getting pregnant to prevent measles and rubella, which can cause severe brain damage to the fetus. They should avoid taking certain drugs, smoking, or drinking alcohol. Cocaine, heroine, nicotine and alcohol are toxic to the developing brain of the fetus.

Nutritional Therapy

The following dietary adjustments have been recommended to alleviate some symptoms in patients with cerebral palsy:

• Those with CP should avoid potential allergenic foods. Allergic foods are believed to worsen symptoms in many CP patients.
• CP patients should also avoid preservatives and food additives such as MSG (which are potentially toxic to the brain) by eating fresh and unprocessed foods such as whole grains, vegetables, beans, fruits, nuts, and seeds.
• To improve muscle tone, CP patients should supplement their diets with magnesium, thiamine, pyridoxine, vitamin C, and bioflavonoids. Alternatively, they can take daily multivitamin/mineral supplements that can provide all these helpful nutrients and make sure they are getting adequate protein in diet or supplements.

Osteopathy

Craniosacral therapy, a special form of osteopathic treatment, may be successful in preventing cerebral palsy if performed right after a difficult labor or delivery by forceps. This manipulation of bones of the newborn's skull may prevent stress and distortion of the child's head occurring during traumatic delivery. Craniosacral therapy is less successful, however, in established cerebral palsy in an older child.

Bodywork

Bodywork such as massage, reflexology, Feldenkrais, or rolfing can help improve blood circulation and muscle tone and reduce muscle spasms in patients with cerebral palsy.

Other Therapies

Other potentially helpful treatments include acupuncture, homeopathy and herbal therapy, and dance and music therapy. Although still not proven in clinical trials, hyperbaric oxygen therapy (HBOT) has been used to alleviate many symptoms of CP. It provides pure oxygen at higher-tha-normal pressure in an enclosed chamber and is more commonly known for treating divers with compression sickness. A Cornell University study in 1999–2000 studied the effects of 40 one-hour sessions on 23 children with moderate to severe CP. They noted improvements in motor skills, attention, language, and play.

Allopathic Treatment

Cerebral palsy cannot be cured, but many of the disabilities it causes can be managed through planning and timely care. Treatment for a child with CP depends on the severity, nature, and location of the impairment, as well a child's associated problems. Optimal care of a child with mild CP may involve regular interaction with only physical and occupational therapists, whereas care for a more severely affected child may include a speech-language therapist, special education teacher, adaptive sports therapist, nutritionist, orthopedic surgeon, and neurosurgeon.

Parents of a child newly diagnosed with CP are not likely to have the necessary expertise to coordinate the full range of care their child will need. Support groups for parents of physically or mentally impaired children can be significant sources of both practical advice and emotional support. Many cities have support groups that can be located through the United Cerebral Palsy Association or a local hospital or social service agency. Children with CP are also eligible for special education services. The diagnosing doctor should refer parents to the local school district for these services. Even children aged birth to three years are eligible through early intervention programs.

Influence of Cp on Development

Cerebral palsy may restrict a child's ability to reach for and grasp objects, to move about, to explore the properties of toys, and to communicate with others, which are all central activities in the child's growth and development. Therefore, the disease inhibits acquisition of motor skills, knowledge of the world, and social competence. The family can do much to overcome these restrictions by adapting the child's environment to meet his or her needs and providing challenges within the child's abilities to accomplish. The advice and direction of an occupational therapist can be critical to promoting normal development of the child with CP.

Posture and Mobility

Spasticity, muscle coordination, ataxia, and scoliosis are all significant impairments that affect the posture and mobility of a person with cerebral palsy. Physical therapists work with the family to maximize the child's ability to move affected limbs, to develop normal motor patterns, and to maintain posture. Adaptive equipment may be needed, including wheelchairs, walkers, shoe inserts, crutches, or braces. The need for adaptive equipment may change as the person develops, or as new treatments are introduced.

SPASTICITY. Spasticity causes muscles to shorten, joints to tighten, and postures to change. Spasticity can affect the ability to walk, use a wheelchair, and sit unaided; and it can prevent independent feeding, dressing, hygiene, or other activities of daily living. Contracture and dislocations are common consequences of spasticity.

Mild spasticity may be treated by regular stretching of the affected muscles through their full range of motion. This usually is done at least daily. Moderate spasticity may require bracing to keep a limb out of the abnormal position, or serial casting to return it to its normal position. Ankle-foot braces (orthoses) made of lightweight plastic are often used to increase a child's stability and to promote proper joint alignment.

Spasticity may also be treated with muscle relaxing drugs, including diazepam (Valium), dantrolene (Dantrium), and baclofen (Lioresal). A variety of experimental surgeries have been tried for people with cerebral palsy to control spasticity. Most of these have not proven effective.

ATAXIA AND COORDINATION Ataxia, or lack of balance control, is another factor affecting mobility. Physical therapy is an important tool to help the child with CP maximize balance. Coordination can be worsened if one member of a muscle pair is overly strong; bracing or surgical transfer of the muscle to a less over-powering position may help.

SCOLIOSIS. Scoliosis, or spine curvature, can develop when the muscles that hold the spine in place become either weak or spastic. This can cause pain, as well as interfere with normal posture and internal organ function. Scoliosis may be treated with a trunk brace. If this proves unsuccessful, spinal fusion surgery may be needed to join the vertebrae together, which keeps the spine straight.

Seizures

Seizures occur in 30-50% of children with CP. Seizures may be treated with drugs, most commonly carbamazepine (Tegretol) or ethosuximide (Zarontin). A combination of a ketogenic diet and fasting may also be used to control seizures. Although the need for anti-seizure medication is temporary in some children, it may be required throughout life for others.

Strabismus

Strabismus, or squinting and lack of parallelism in the eyes, occurs in nearly half of all people with spastic CP. Strabismus may be treated with patching and corrective lenses. When these do not work, it may be treated with either surgery on the eye muscles causing the problem or by injection of botulinum toxin.

Nutrition

Due to poor muscle coordination, CP children may not take in adequate nutrition for full growth and development, worsening the results of the disorder. Careful attention to nutritional needs and nutritional supplements is required. Poor swallowing coordination may lead to aspiration, or inhaling of food or saliva. A speech-language therapist may be able to teach the person more effective movement patterns to avoid aspiration. In severe cases, a gastrostomy tube may be required to provide adequate nutrition directly into the digestive system while preventing aspiration.

Other Common Medical Problems

Drooling, dental caries (cavities), and gum disease are more common in people with CP than in the general population, partly because of lowered coordination and increased muscle tightness in the mouth and jaw. Each of these can be prevented to some degree, either through behavioral changes alone or in combination with drug therapy. Constipation is more common as well, and may be treated through dietary changes, or with enemas or suppositories when necessary.

Communication

Poor coordination of the tongue and mouth muscles can also affect speech. Children may benefit from picture boards or other communication devices that allow them to point to make their desires known. For school-age children or older persons with CP, there are a large number of augmentative communication devices, including shorthand typing programs and computer-assisted speech devices. A speech-language therapist can offer valuable advice on the types of equipment available.

Education

The best choice of school for the child with CP depends on the presence and degree of mental impairment and physical impairment, as well as the facilities available in the area. "Inclusion," or mainstreaming the child in a regular public school classroom, may work well for the child with mild physical impairment. Separate classrooms or special schools may be needed for more severely involved children. Schooling for disabled students is governed by the Individuals with Disabilities Education Act (IDEA) at the federal level and state special education rules at the local level. An educational specialist within the school system or from a community social services agency may be able to help the family navigate the various bureaucratic pathways that will ensure the best schooling available.

The process of developing an educational plan for a child with CP begins with an assessment of the child's needs. The assessment is carried out under state guidelines by a team of medical professionals. After the assessment, the school district works with the parents and others involved in the child's education and treatment to develop an Individualized Educational Plan (IEP). The IEP states the child's specific needs for special instruction and indicates what services will be provided. The special services may be as simple as allowing extra time to travel between classes or as extensive as individualized instruction, adapted classroom equipment, and special testing procedures. More information about assessments and IEPs is available through the National Information Center for Children and Youth with Disabilities. The United Cerebral Palsy Assocation is another resource for advocacy, information, and legal rights.

Behavioral and Mental Health Services

The child with CP may have behavioral problems or emotional issues that affect psychological development and social interactions. These may require special intervention or treatment, including behavior modification programs or individual and family counseling. Attention-deficit hyperactivity disorder is common in children with CP, and may require behavioral, educational, and medical intervention.

Expected Results

Cerebral palsy can affect every stage of maturation, from childhood through adolescence to adulthood. At each stage, the person with CP and his or her caregivers must strive to achieve and maintain the fullest range of experiences and education consistent with the person's abilities. The advice and intervention of professionals remains crucial for many people with CP.

Although CP is not a terminal disorder, it can affect a person's lifespan by increasing the risk of infection, especially lung infections. Poor nutrition can contribute to the likelihood of infection. People with mild cerebral palsy may have near-normal lifespans. The lifespan of those with more severe forms, especially spastic quadriplegia, is often considerably shortened. However, over 90% of infants with CP survive into adulthood.

In 2002, a radical new method for repairing the damage caused by lack of oxygen at delivery of babies with CP was being funded for study. The possible treatment involved transplanting mature stem cells into babies' circulations, which will then migrate to the site of injury caused by oxygen deprivation, hopefully promoting natural repair of the brain damage. However, this treatment was in very early stages of testing in animals only as of late 2002.

Prevention

The cause of most cases of CP is unknown, but it has become clear in recent years that birth difficulties are not to blame in most cases. Developmental problems before birth, usually unknown and generally undiagnosable, are responsible for most cases. Although the incidence of CP caused by Rh factor incompatibility has declined markedly, the incidence of CP as a consequence of prematurity has increased, because of the increasing success of medical intervention in keeping premature babies alive.

The risk of CP can be decreased through good maternal nutrition, avoidance of drugs or alcohol during pregnancy, and prevention or prompt treatment of infections. Recent preliminary research suggests that magnesium sulfate may reduce the risk of CP in mothers taking it for the medical treatment of preeclampsia and preterm labor

Resources

Books

The Burton Goldberg Group. "Cerebral Palsy." Alternative Medicine: The Definitive Guide. Tiburon, CA: Future Medicine Publishing, Inc., 1999.

"Cerebral Palsy." Reader's Digest Guide to Medical Cures and Treatments. Canada: The Reader's Digest Association, Inc., 1996.

Kramer, Laura. Uncommon Voyage: Parenting a Special Needs Child in the World of Alternative Medicine. Faber & Faber, 1996.

Miller, Freema, and Steven J. Bachrach. Cerebral Palsy: A Complete Guide for Caregiving. Johns Hopkins University Press, 1995.

Vickers, Andrew. Health Options: Complementary Therapies for Cerebral Palsy and Related Conditions. Element Publications, 1994.

Periodicals

Exceptional Parent Magazine. 555 Kinderkamack Road, Oradell, NJ 07649-1517; 800-EPARENT, or 201-634-6550.

"Hyperbaric Oxygen Therapy." The Exceptional Parent (July 2002): 52.

"IVF Babies at Increased Risk of Cerebral Palsy." Contemporary OB/GYN (July 2002): 41.

Kuban, KCK, and A. Leviton. "Cerebral Palsy." New England Journal of Medicine (1994): 188-95.

"Mature Stem Cell Transplants Linked to Treatment." Pain & Central Nervous System Week (July 22, 2002): 11.

Organization

Cranial Academy. 3500 Depaw Boulevard. Indianapolis, IN 46268. (317) 879-0713.

National Information Center for Children and Youth with Disabilities. PO Box 1492, Washington DC 20013-1492. (800) 695-0285.

United Cerebral Palsy Association. 1660 L Street, NW Washington, DC 20036-5602. (800) USA-5-UCP,(202) 776-0406, (202) 973-7197 (TTY). Fax: (202) 776-0414. ucpnatl@ucpa.org. http://www.ucpa.org.

Other

Electronic forum for cerebral palsy. http://neuro-www.mgh.harvard.edu/forum/CerebralPalsyMenu.html.

[Article by: Mai Tran; Teresa G. Odle]

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.

Demographics

Approximately 500,000 children and adults in the United States have CP, and it is newly diagnosed in about 6,000 infants and young children each year, representing about two to three children in 1,000 live births. No particular ethnic group seems to be at higher risk for CP. However, some low income families may be at higher risk due to poorer access to proper prenatal care and advanced medical services.

Causes and Symptoms

CP can be caused by a number of different mechanisms at various times of life, ranging from several weeks after conception, through birth, to early childhood. In the twentieth century, it was accepted that most cases of CP were due to brain injuries received during a traumatic birth, a condition known as birth asphyxia. However, extensive research in the 1980s showed that only 5 to 10 percent of CP can be attributed to birth trauma. Other possible causes include abnormal development of the brain, prenatal factors that directly or indirectly damage neurons in the developing brain, premature birth, and brain injuries that occur in the first few years of life.

The causes of CP could be grouped into those that are genetic and those that are non-genetic, although 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 births is somewhat different and considered separately.

Prenatal Causes

Although much was learned about human embryology in the last couple of decades of the twentieth century, a great deal remains unknown in the early 2000s. Studying prenatal human development is difficult because the embryo and fetus develop in a closed environment—the mother's womb. However, the 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 some unknown cause. The possible role genetics plays 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, most babies are 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 occur in an adult and 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 (intracerebral hemorrhage) can cause a fetal stroke, or a clot (embolism) can obstruct a cerebral blood vessel. Infants who later develop CP, along with their mothers, are more likely than other mother-infant pairs to have coagulation disorders (coagulopathies) that put them at increased risk for bleeding episodes or blood clots. Certain coagulation disorders are inherited while others may be deficiencies in essential clotting factors or defects in the coagulation process.

Any substance that might affect fetal brain development, directly or indirectly, can increase the risk for CP. Likewise, 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. Links between a drug or other chemical exposure during pregnancy and a risk for CP are difficult to prove.

Because the fetus receives all nutrients and oxygen from blood that circulates through the placenta, 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 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.

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.

Perinatal Causes

Birth asphyxia that is significant enough to result in CP is uncommon in developed countries. An umbilical cord around the baby's neck (tight nuchal cord) and the cord delivered before the baby (prolapsed cord) are possible causes of birth asphyxia, as are bleeding and other complications associated with placental abruption and placenta previa (placenta lying over the cervix).

Infection in the mother is sometimes not passed to the fetus through the placenta but is transmitted to the baby during delivery. Any such infection, such as herpes, that results in serious illness in the newborn has the potential to produce some neurological damage.

Postnatal Causes

The remaining 15 percent of CP cases are due to neurologic injury sustained after birth. CP that has a postnatal cause is sometimes referred to as acquired CP, but this is only accurate for those cases caused by infection or trauma.

Incompatibility between the Rh blood types of mother and child (mother Rh negative, baby Rh positive) can result in severe anemia in the baby (erythroblastosis fetalis). This may lead to other complications, including severe jaundice, which can cause CP. Rh disease in the newborn is rare in developed countries due to routine screening of maternal blood type and routine prevention of anti-Rh antibodies in Rh negative women after each birth of an Rh positive infant. The routine, effective treatment of jaundice due to other causes has also made it an infrequent cause of CP in developed countries.

Serious infections that affect the brain directly, such as meningitis and encephalitis, may cause irreversible damage to the brain, leading to CP. A seizure disorder early in life may cause CP or may be the product of a hidden problem that causes CP in addition to seizures. Unexplained (idiopathic) seizures are hereditary in only a small percentage of cases. Although rare in healthy infants born at or near term, intracerebral hemorrhage and brain embolism, like fetal stroke, are sometimes genetic.

Physical trauma to an infant or child resulting in brain injury, such as from abuse, accidents, or near drowning/suffocation, might cause CP. Likewise, ingestion of a toxic substance such as lead, mercury, other poisons, or certain chemicals could cause neurological damage. Accidental overdose of certain medications might also cause similar damage to the central nervous system.

Symptoms

The symptoms of CP and their severity are variable. Those who have CP may have only minor difficulty with fine motor skills, such as grasping and manipulating items with their hands. A severe form of CP could involve significant muscle problems in all four limbs, mental retardation, seizures, and difficulties with vision, speech, and hearing.

Although the defect in cerebral function that causes CP is not progressive, the symptoms of CP often change over time. Most of the symptoms relate in some way to the aberrant control of muscles. CP is categorized first by the type of movement/postural disturbance(s) present, rather than by a description of which limbs are affected. The severity of motor impairment is also a factor. Spastic diplegia, for example, refers to continuously tight muscles that have no voluntary control in both legs, while athetoid quadraparesis describes uncontrolled writhing movements and muscle weakness in all four limbs. These may describe CP symptoms generally but do not describe all people with CP. Spastic diplegia is seen in more individuals than is athetoid quadraparesis. CP can also be loosely categorized as mild, moderate, or severe, but these are subjective terms.

A muscle that is tensed and contracted is hypertonic, while excessively loose muscles are hypotonic. Spastic, hypertonic muscles can cause serious orthopedic problems, including curvature of the spine (scoliosis), hip dislocation, or contractures. A contracture is shortening of a muscle, aided sometimes by a weak-opposing force from a neighboring muscle. Contractures may become permanent, i.e., fixed, without some sort of intervention. Fixed contractures may cause postural abnormalities in the affected limbs. Clenched fists and contracted feet (equinus or equinovarus) are common in people with CP. Spasticity in the thighs causes them to turn in and cross at the knees, resulting in an unusual method of walking known as scissors gait. Any of the joints in the limbs may be stiff (immobilized) due to spasticity of the attached muscles.

Athetosis and dyskinesia often occur with spasticity but do not often occur alone. The same is true of ataxia. It is important to remember that mild CP or severe CP refers not only to the number of symptoms present but also to the level of involvement of any particular class of symptoms.

Other neurologically based symptoms may include the following:

• mental retardation/learning disabilities
• behavioral disorders
• seizure disorders
• visual impairment
• hearing loss
• speech impairment (dysarthria)
• abnormal sensation and perception

These problems may have a greater impact on a child's life than the physical impairments of CP, although not all children with CP are affected by other problems. Many infants and children with CP have growth impairment. About one third of individuals with CP have moderate-to-severe mental retardation, one third have mild mental retardation, and one third have normal intelligence.

When to Call the Doctor

Parents should seek medical advice when they notice what seems to be slow development in movement, speech, or cognitive ability in their young child. If a child does not acquire certain skills within a normal time frame, there may be some cause for concern. However, it is known that children progress at somewhat different rates, and a slow beginning is often followed by normal development.

Normal developmental milestones with typical ages for acquiring them, include the following:

• sits well unsupported at about six months (eight to ten months)
• babbles at about six months (up to eight months)
• crawls at about nine months (up to 12 months)
• finger feeds, holds bottle at about nine months (up to 12 months)
• walks alone at about 12 months (up to 15–18 months)
• uses one or two words other than dada/mama at about 12 months (up to 15 months)
• walks up and down steps at about 24 months (24 to 36 months)
• turns pages in books and removes shoes and socks at about 24 months (to 30 months)

Children do not consistently favor one hand over the other before 12 to 18 months of age, and doing so may be a sign that the child has difficulty using the other hand. This same preference for one side of the body may show up as asymmetric crawling or, later on, favoring one leg while climbing stairs. Because CP is nonprogressive, continued loss of previously acquired milestones may indicate that CP is not the cause of the problem; medical evaluation is needed to determine the cause.

Diagnosis

The signs of CP are not usually noticeable at birth. Children normally progress through a predictable set of developmental milestones through the first 18 months of life. Children with CP, however, tend to develop these skills more slowly because of their motor impairments, and delays in reaching milestones are usually the first symptoms of CP. Babies with more severe cases of CP are usually diagnosed earlier than others.

No one test is diagnostic for CP, but certain factors increase suspicion. The Apgar score measures a baby's condition immediately after birth. Babies who have low Apgar scores are at increased risk for CP. Presence of abnormal muscle tone or movements may indicate CP, as may the persistence of infantile reflexes. Imaging of the brain using ultrasound, x rays, MRI, and/or CT scans may reveal a structural anomaly. Some brain lesions associated with CP include scarring, cysts, expansion of the cerebral ventricles (hydrocephalus), abnormality of the area surrounding the ventricles (periventricular leukomalacia), areas of dead tissue (necrosis), and evidence of an intracerebral hemorrhage or blood clot. Blood and urine biochemical tests, as well as genetic tests, may be used to rule out other possible causes, including muscle and peripheral nerve diseases, mitochondrial and metabolic diseases, and other inherited disorders. Evaluations by a pediatric developmental specialist and a geneticist may be of benefit.

Treatment

Cerebral palsy cannot be cured, but many of the disabilities it causes can be managed through planning and timely care. Treatment for a child with CP depends on the severity, nature, and location of the primary muscular symptoms, as well as any associated problems that might be present. Optimal care of a child with mild CP may involve regular interaction with only a physical therapist and occupational therapist, whereas care for a more severely affected child may include visits to multiple medical specialists throughout life. With proper treatment and an effective plan, most people with CP can lead productive, happy lives.

Physical, Occupational, and Speech Therapy

Spasticity, muscle weakness, coordination, ataxia, and scoliosis are all significant impairments that affect the posture and mobility of children and adults with CP. Physical and occupational therapists work with the patient and the family to maximize the patient's ability to move affected limbs, develop normal motor patterns, and maintain posture. Assistive technology, including wheelchairs, walkers, shoe inserts, crutches, and braces, are often required. A speech therapist and high-tech aids such as computer-controlled communication devices can make a tremendous difference in the life of those who have speech impairments.

Drug Therapy

Before fixed contractures develop, muscle-relaxant drugs such as diazepam (Valium), dantrolene (Dantrium), and baclofen (Lioresal) may be prescribed. Botulinum toxin (Botox), a highly effective treatment, is injected directly into the affected muscles. Alcohol or phenol injections into the nerve controlling the muscle are another option. Multiple medications are available to control seizures, and athetosis can be treated using medications such as trihexyphenidyl HCl (Artane) and benztropine (Cogentin).

Surgery

Fixed contractures are usually treated with either serial casting or surgery. The most commonly used surgical procedures are tenotomy, tendon transfer, and dorsal rhizotomy. In tenotomy, tendons of the affected muscle are cut, and the limb is cast in a more normal position while the tendon regrows. Alternatively, tendon transfer involves cutting and reattaching a tendon at a different point on the bone to enhance the length and function of the muscle. A neurosurgeon performing dorsal rhizotomy carefully cuts selected nerve roots in the spinal cord to prevent them from stimulating the spastic muscles. Neurosurgical techniques in the brain such as implanting tiny electrodes directly into the cerebellum or cutting a portion of the hypothalamus have very specific uses and have had mixed results.

Prognosis

Cerebral palsy can affect every stage of maturation, from childhood through adolescence to adulthood. At each stage, those with CP, along with their caregivers, must strive to achieve and maintain the fullest range of experience and education consistent with their abilities. The advice and intervention of various professionals are crucial for many people with CP. Although CP itself is not considered a terminal disorder, it can affect a person's lifespan by increasing the risk for certain medical problems. People with mild cerebral palsy may have near-normal lifespan, but the lifespan of those with more severe forms may be shortened. However, over 90 percent of infants with CP survive into adulthood.

Prevention

Research in the early 2000s is focused on the possible benefits of recognizing and treating coagulopathies and inflammatory disorders in the prenatal and perinatal periods in order to reduce the incidence of CP and other congenital diseases. The use of magnesium sulfate in pregnant women with preeclampsia or threatened preterm delivery may reduce the risk of CP in very preterm infants. Finally, the risk of CP can be decreased through good maternal nutrition, avoidance of drugs and alcohol during pregnancy, and prevention or prompt treatment of infections.

Parental Concerns

Parents of a child diagnosed with CP may not feel that they have the necessary expertise to coordinate the full range of care their child needs. Although knowledgeable and caring medical professionals are indispensable for developing a care plan, a potentially more important source of information and advice can be gained from other parents who have dealt with the same set of difficulties. Support groups for parents of children with CP can be significant sources of both practical advice and emotional support. Many cities have support groups that can be located through the United Cerebral Palsy Association, and most large medical centers have special multidisciplinary clinics for children with developmental disorders.

See also Febrile seizures; TORCH test; Seizure disorder.

Resources

Books

Peacock, Judith. Cerebral Palsy. Mankato, MN: Capstone Press, 2000.

Pimm, Paul. Living with Cerebral Palsy. Austin, TX: Raintree Steck-Vaughn Publishers, 2000.

Pincus, Dion. Everything You Need to Know about Cerebral Palsy. New York: Rosen Publishing Group Inc., 2000.

Organizations

National Institute of Neurological Disorders and Stroke. 31 Center Drive, MSC 2540, Bldg. 31, Room 8806, Bethesda, MD 20814. Web site: www.ninds.nih.gov.

National Society of Genetic Counselors. 233 Canterbury Dr., Wallingford, PA 19086–6617. (610) 872–1192. http://www.nsgc.org/GeneticCounselingYou.asp.

United Cerebral Palsy Association Inc. (UCP). 1660 L St. NW, Suite 700, Washington, DC 20036–5602. Web site: www.ucpa.org.

Web Sites

"Cerebral Palsy: Hope Through Research." National Institute of Neurological Disorders and Stroke, 2004. Available online at www.ninds.nih.gov/health_and_medical/pubs/cerebral_palsyhtr.htm (accessed November 29, 2004).

"NINDS Cerebral Palsy Information Page." National Institute of Neurological Disorders and Stroke, October 2004. Available online at www.ninds.nih.gov/disorders/cerebral_palsy/cerebral_palsy.htm (accessed November 29, 2004).

[Article by: L. Lee Culvert Scott J. Polzin, MS]

A disorder marked by lack of muscle coordination and sometimes accompanied by speech defects. It is caused by brain damage present at birth or experienced during birth or infancy.

Cerebral palsy
Classification and external resources
The motor tract.
ICD-10	G80.
ICD-9	343
OMIM	603513 605388
DiseasesDB	2232
eMedicine	neuro/533 pmr/24
MeSH	D002547

This article is about cerebral palsy as an overall umbrella term. For the most common type of cerebral palsy worldwide, see the article on spastic diplegia. For specifics on other types of CP, see their corresponding articles.

Cerebral palsy (CP) (also cerebral pares) is an umbrella term encompassing a group of non-progressive,^[1][2] non-contagious motor conditions that cause physical disability in human development.^[3]

Cerebral refers to the cerebrum, which is the affected area of the brain (although the disorder most likely involves connections between the cortex and other parts of the brain such as the cerebellum), and palsy refers to disorder of movement. CP is caused by damage to the motor control centers of the developing brain and can occur during pregnancy (about 75 percent), during childbirth (about 5 percent) or after birth (about 15 percent) up to about age three.^[4][5] Further research is needed on adults with CP as the current literature is highly focused on the pediatric patient.

Cerebral palsy describes a group of permanent disorders of the development of movement and posture, causing activity limitation, that are attributed to nonprogressive disturbances that occurred in the developing fetal or infant brain. The motor disorders of cerebral palsy are often accompanied by disturbances of sensation, perception, cognition, communication, and behaviour, by epilepsy, and by secondary musculoskeletal problems.^[6]

There is no known cure for CP. Medical intervention is limited to the treatment and prevention of complications arising from CP's effects. A 2003 study put the economic cost for CP sufferers in the US at $921,000 per case, including lost income.^[7]

In another study, the incidence in six countries surveyed was 2.12–2.45 per 1,000 live births,^[8] indicating a slight rise in recent years. Improvements in neonatal nursing have helped reduce the number of babies who develop cerebral palsy, but the survival of babies with very low birth weights has increased, and these babies are more likely to have cerebral palsy.^[9][10]

Contents 1 Classification 1.1 Spastic 1.2 Ataxic 1.3 Athetoid/dyskinetic 2 Incidence and prevalence 3 Symptoms 4 History 5 Causes 6 Diagnosis 7 Presentation: bones 8 Prognosis 9 Treatment 10 Cultural aspects 10.1 Economic Impact Of Cerebral Palsy In Australia 10.2 Use of terms when referring to people with CP 10.3 Misconceptions 11 Notable people 12 References 13 External links

Classification

CP is divided into three major classifications to describe different movement impairments. These classifications also reflect the areas of the brain that are damaged. The three major classifications are:

Spastic

For details on the most common form of cerebral palsy, see spastic diplegia.

Spastic cerebral palsy is by far the most common type, occurring in 70% to 80% of all cases. Moreover, spastic CP accompanies one of the other types in 30% of all cases. People with this type are hypertonic and have a neuromuscular condition stemming from damage to the corticospinal tract or the motor cortex that affects the nervous system's ability to receive gamma amino butyric acid in the area(s) affected by the disability. Spastic CP is further classified by topography dependent on the region of the body affected; these include:

• Spastic hemiplegia (one side being affected). Generally, injury to muscle-nerves controlled by the brain's left side will cause a right body deficit, and vice versa. Typically, people that have spastic hemiplegia are the most ambulatory, although they generally have dynamic equinus on the affected side and are primarily prescribed ankle-foot orthoses to prevent said equinus.^[11]
• Spastic diplegia (the lower extremities are affected with little to no upper-body spasticity). The most common form of the spastic forms. Most people with spastic diplegia are fully ambulatory and have a scissors gait. Flexed knees and hips to varying degrees are common. Hip problems, dislocations, and in three-quarters of spastic diplegics, also strabismus (crossed eyes), can be present as well. In addition, these individuals are often nearsighted. The intelligence of a person with spastic diplegia is unaffected by the condition.
• Spastic tetraplegia (all four limbs affected equally). People with spastic quadriplegia are the least likely to be able to walk, or if they can, to want to walk, because their muscles are too tight and it is too much effort to do so. Some children with quadriplegia also have hemiparetic tremors, an uncontrollable shaking that affects the limbs on one side of the body and impairs normal movement.

Occasionally, terms such as monoplegia, paraplegia, triplegia, and pentaplegia may also be used to refer to specific manifestations of the spasticity.

Ataxic

Ataxia (ICD-10 G80.4) type symptoms can be caused by damage to the cerebellum. The forms of ataxia are less common types of cerebral palsy, occurring in at most 10% of all cases. Some of these individuals have hypotonia and tremors. Motor skills such as writing, typing, or using scissors might be affected, as well as balance, especially while walking. It is common for individuals to have difficulty with visual and/or auditory processing.

Athetoid/dyskinetic

Athetoid or dyskinetic is mixed muscle tone — and sometimes hypotonia (Hypotonia will usually occur before 1 year old; the muscle tone will be increased with age and progress to Hypertonia). People with athetoid CP have trouble holding themselves in an upright, steady position for sitting or walking, and often show involuntary motions. For some people with athetoid CP, it takes a lot of work and concentration to get their hand to a certain spot (like scratching their nose or reaching for a cup). Because of their mixed tone and trouble keeping a position, they may not be able to hold onto objects (such as a toothbrush or pencil). About one quarter of all people with CP have athetoid CP. The damage occurs to the extrapyramidal motor system and/or pyramidal tract and to the basal ganglia. It occurs in 10% to 20% percent of all cases.^[12]. In newborn infants, high bilirubin levels in the blood, if left untreated, can lead to brain damage in certain areas (kernicterus). This may also lead to athetoid cerebral palsy.

Incidence and prevalence

In the industrialized world, the incidence of cerebral palsy is about 2 per 1000 live births.^[13] The incidence is higher in males than in females; the Surveillance of Cerebral Palsy in Europe (SCPE) reports a M:F ratio of 1.33:1.^[14] Variances in reported rates of incidence across different geographical areas in industrialised countries are thought to be caused primarily by discrepancies in the criteria used for inclusion and exclusion. When such discrepancies are taken into account in comparing two or more registers of patients with cerebral palsy (for example, the extent to which children with mild cerebral palsy are included), the incidence rates converge toward the average rate of 2:1000.

In the United States, approximately 10,000 infants and babies are diagnosed with CP each year, and 1200–1500 are diagnosed at preschool age.^[15]

Overall, advances in care of pregnant mothers and their babies has not resulted in a noticeable decrease in CP. This is generally attributed to medical advances in areas related to the care of premature babies (which results in a greater survival rate). Only the introduction of quality medical care to locations with less-than-adequate medical care has shown any decreases. The incidence of CP increases with premature or very low-weight babies regardless of the quality of care.^{[citation needed]}

Prevalence of cerebral palsy is best calculated around the school entry age of about six years, the prevalence in the U.S. is estimated to be 2.4 out of 1000 children^[16]

The SCPE reported the following incidence of comorbidities in children with CP (the data are from 1980–1990 and included over 4,500 children over age 4 whose CP was acquired during the prenatal or neonatal period):

• Mental disadvantage (IQ < 50): 31%
• Active seizures: 21%
• Mental disadvantage (IQ < 50) and not walking: 20%
• Blindness: 11%^[14]

The SCPE noted that the incidence of comorbidities is difficult to measure accurately, particularly across centers. For example, the actual rate of mental retardation may be difficult to determine, as the physical and communicational limitations of people with CP would likely lower their scores on an IQ test if they were not given a correctly modified version.

Apgar scores have sometimes been used as one factor to predict whether or not an individual will develop CP.^[17]

Symptoms

All types of CP are characterized by abnormal muscle tone (i.e. slouching over while sitting), reflexes, or motor development and coordination. There can be joint and bone deformities and contractures (permanently fixed, tight muscles and joints). The classical symptoms are spasticities, spasms, other involuntary movements (e.g. facial gestures), unsteady gait, problems with balance, and/or soft tissue findings consisting largely of decreased muscle mass. Scissor walking (where the knees come in and cross) and toe walking (which can contribute to a gait reminiscent of a marionette) are common among people with CP who are able to walk, but taken on the whole, CP symptomatology is very diverse. The effects of cerebral palsy fall on a continuum of motor dysfunction which may range from slight clumsiness at the mild end of the spectrum to impairments so severe that they render coordinated movement virtually impossible at the other end the spectrum.

Babies born with severe CP often have an irregular posture; their bodies may be either very floppy or very stiff. Birth defects, such as spinal curvature, a small jawbone, or a small head sometimes occur along with CP. Symptoms may appear or change as a child gets older. Some babies born with CP do not show obvious signs right away. Classically, CP becomes evident when the baby reaches the developmental stage at 6/12 to 9/12 months and is starting to mobilise, where preferential use of limbs, asymmetry or gross motor developmental delay is seen.

Secondary conditions can include seizures, epilepsy, apraxia, dysarthria or other communication disorders, eating problems, sensory impairments, mental retardation, learning disabilities, and/or behavioral disorders.

Speech and language disorders are common in people with Cerebral Palsy. The incidence of dysarthria is estimated to range from 31% to 88%. Speech problems are associated with poor respiratory control, laryngeal and velopharyngeal dysfunction as well as oral articulation disorders that are due to restricted movement in the oral-facial muscles. There are three major types of dysarthria in cerebral palsy: spastic, dyskinetic (athetosis) and ataxic. Speech impairments in spastic dysarthria involves four major abnormalities of voluntary movement: spasticity, weakness, limited range of motion and slowness of movement. Speech mechanism impairment in athetosis involves a disorder in the regulation of breathing patterns, laryngeal dysfunction (monopitch, low, weak and breathy voice quality). It is also associated with articulatory dysfunction (large range of jaw movements), inappropriate positioning of the tongue, instability of velar elevation. Athetoid dysarthria is caused by disruption of the internal sensorimotor feedback system for appropriate motor comands, which leads to the generation of faulty movements that are perceived by others as involuntary. Ataxic dysarthria is uncommon in cerebral palsy. The speech characteristics are: imprecise consonants, irregular articulatory breakdown, distorted vowels, excess and equal stress, prolonged phonemes, slow rate, monopitch, monoloudness and harsh voice.^[18] Overall language delay is associated with problems of mental retardation, hearing impairment and learned helplessness^[3]. Children with cerebral palsy are at risk of learned helplessness and becoming passive communicators, initiating little communication.^[3] Early intervention with this clientele often targets situations in which children communicate with others, so that they learn that they can control people and objects in their environment through this communication, including making choices, decisions and mistakes.^[3]

History

CP, formerly known as "Cerebral Paralysis," was first identified by English surgeon William Little in 1860. Little raised the possibility of asphyxia during birth as a chief cause of the disorder. It was not until 1897 that Sigmund Freud, then a neurologist, suggested that a difficult birth was not the cause but rather only a symptom of other effects on fetal development.^[19] Research conducted during the 1980s by the National Institute of Neurological Disorders and Stroke (NINDS) suggested that only a small number of cases of CP are caused by lack of oxygen during birth.^[20]

Causes

While in certain cases there is no identifiable cause, other etiologies include problems in intrauterine development (e.g. exposure to radiation, infection), asphyxia before birth, hypoxia of the brain, and birth trauma during labor and delivery, and complications in the perinatal period or during childhood.^[3] CP is also more common in multiple births.

Studies at the University of Liverpool have led to the hypothesis that many cases of cerebral palsy, and other conditions that an infant has at birth, are caused by the death in very early pregnancy of an identical twin. This may occur when twins have a joint circulation through sharing the same placenta. Not all identical twins share the same blood supply (monochorionic twins), but if they do, the suggestion is that perturbations in blood flow between them can cause the death of one and damage to the development of the surviving fetus.^[21][22][23] It is common knowledge amongst obstetricians and midwives that a small dead fetus (fetus papyraceus) may sometimes be found attached to a placenta following birth. In the past, this has not been considered important and knowledge of the so called ‘vanishing twin’ has been suppressed to avoid triggering feelings of loss, grief, or guilt in mothers. The pathological consequences depend on the severity and the stage of development of the fetus when the imbalances in blood flow between the fetuses occur. It has been proposed that such pathology could account, not just for cerebral palsy, but for developmental abnormalities of the eye, heart, and gut, and other specific brain abnormalities such as neuronal migration disorders e.g. lissencephaly and holoprosencephaly. Studies at the University of Liverpool have led to the hypothesis that many cases of cerebral palsy, and other conditions that an infant has at birth, are caused by the death in very early pregnancy of an identical twin. This may occur when twins have a joint circulation through sharing the same placenta. Not all identical twins share the same blood supply (monochorionic twins), but if they do, the suggestion is that perturbations in blood flow between them can cause the death of one and damage to the development of the surviving fetus.^[24][25][26]

Between 40% and 50% of all children who develop cerebral palsy were born prematurely. Premature infants are vulnerable, in part because their organs are not fully developed, increasing the risk of hypoxic injury to the brain that may manifest as CP. A problem in interpreting this is the difficulty in differentiating between CP caused by damage to the brain that results from inadequate oxygenation and CP that arises from prenatal brain damage that then precipitates premature delivery.

Recent research has demonstrated that intrapartum asphyxia is not the most important cause, probably accounting for no more than 10 percent of all cases; rather, infections in the mother, even infections that are not easily detected, may triple the risk of the child developing the disorder, mainly as the result of the toxicity to the fetal brain of cytokines that are produced as part of the inflammatory response.^[27] Low birthweight is a risk factor for CP—and premature infants usually have low birth weights, less than 2.0 kg, but full-term infants can also have low birth weights. Multiple-birth infants are also more likely than single-birth infants to be born early or with a low birth weight.

After birth, other causes include toxins, severe jaundice, lead poisoning, physical brain injury, shaken baby syndrome, incidents involving hypoxia to the brain (such as near drowning), and encephalitis or meningitis. The three most common causes of asphyxia in the young child are: choking on foreign objects such as toys and pieces of food, poisoning, and near drowning.

Some structural brain anomalies such as lissencephaly may present with the clinical features of CP, although whether that could be considered CP is a matter of opinion (some people say CP must be due to brain damage, whereas people with these anomalies didn't have a normal brain). Often this goes along with rare chromosome disorders and CP is not genetic or hereditary.

Diagnosis

The diagnosis of cerebral palsy has historically rested on the patient's history and physical examination. Once diagnosed with cerebral palsy, further diagnostic tests are optional. The American Academy of Neurology published an article in 2004 reviewing the literature and evidence available on CT and MRI imaging. They suggested that neuroimaging with CT or MRI is warranted when the etiology of a patient's cerebral palsy has not been established - an MRI is preferred over CT due to diagnostic yield and safety. When abnormal, the neuroimaging study can suggest the timing of the initial damage. The CT or MRI is also capable of revealing treatable conditions, such as hydrocephalus, porencephaly, arteriovenous malformation, subdural hematomas and hygromas, and a vermian tumor^[28] (which a few studies suggest are present 5 to 22%). Furthermore, an abnormal neuroimaging study indicates a high likelihood of associated conditions, such as epilepsy and mental retardation.^[29]

Presentation: bones

In order for bones to attain their normal shape and size, they require the stresses from normal musculature. Osseous findings will therefore mirror the specific muscular deficits in a given person with CP. The shafts of the bones are often thin (gracile). When compared to these thin shafts (diaphyses) the metaphyses often appear quite enlarged (ballooning). With lack of use, articular cartilage may atrophy, leading to narrowed joint spaces. Depending on the degree of spasticity, a person with CP may exhibit a variety of angular joint deformities. Because vertebral bodies need vertical gravitational loading forces to develop properly, spasticity and an abnormal gait can hinder proper and/or full bone and skeletal development. People with CP tend to be shorter in height than the average person because their bones are not allowed to grow to their full potential. Sometimes bones grow to different lengths, so the person may have one leg longer than the other.

Prognosis

CP is not a progressive disorder (meaning the brain damage neither improves nor worsens), but the symptoms can become more severe over time due to subdural damage. A person with the disorder may improve somewhat during childhood if he or she receives extensive care from specialists, but once bones and musculature become more established, orthopedic surgery may be required for fundamental improvement. People who have CP tend to develop arthritis at a younger age than normal because of the pressure placed on joints by excessively toned and stiff muscles.

The full intellectual potential of a child born with CP will often not be known until the child starts school. People with CP are more likely to have some type of learning disability, but this is not related to a person's intellect or IQ level. Intellectual level among people with CP varies from genius to mentally retarded, as it does in the general population, and experts have stated that it is important to not underestimate a person with CP's capabilities and to give them every opportunity to learn.^[30]

The ability to live independently with CP varies widely depending on the severity of each case. Some individuals with CP will require personal assistant services for all activities of daily living. Others can lead semi-independent lives, needing support only for certain activities. Still others can live in complete independence. The need for personal assistance often changes with increasing age and associated functional decline. However, in most cases persons with CP can expect to have a normal life expectancy; survival has been shown to be associated with the ability to ambulate, roll, and self-feed.^[31] As the condition does not directly affect reproductive function, some persons with CP have children and parent successfully.

According to OMIM, only 2% of cases of CP are inherited (with glutamate decarboxylase-1 as one known enzyme involved.)^[32] There is no evidence of an increased chance of a person with CP having a child with CP.

Treatment

There is no cure for CP, but various forms of therapy can help a person with the disorder to function and live more effectively. In general, the earlier treatment begins the better chance children have of overcoming developmental disabilities or learning new ways to accomplish the tasks that challenge them. The earliest proven intervention occurs during the infant's recovery in the neonatal intensive care unit (NICU). Treatment may include one or more of the following: physical therapy; occupational therapy; speech therapy; drugs to control seizures, alleviate pain, or relax muscle spasms (e.g. benzodiazepienes, baclofen and intrathecal phenol/baclofen); hyperbaric oxygen; the use of Botox to relax contracting muscles; surgery to correct anatomical abnormalities or release tight muscles; braces and other orthotic devices; rolling walkers; and communication aids such as computers with attached voice synthesizers. For instance, the use of a standing frame can help reduce spasticity and improve range of motion for people with CP who use wheelchairs. Nevertheless, there is only some benefit from therapy. Treatment is usually symptomatic and focuses on helping the person to develop as many motor skills as possible or to learn how to compensate for the lack of them. Non-speaking people with CP are often successful availing themselves of augmentative and alternative communication systems such as Blissymbols.

Early Nutritional Support In one cohort study of 490 premature infants discharged from the NICU, the rate of growth during hospital stay was related to neurological function at 18 and 22 months of age. The study found a significant decrease in the incidence of cerebral palsy in the group of premature infants with the highest growth velocity. This study suggests that adequate nutrition and growth play a protective role in the development of cerebral palsy.^[33]

Physical therapy (PT) programs are designed to encourage the patient to build a strength base for improved gait and volitional movement, together with stretching programs to limit contractures. Many experts believe that life-long physical therapy is crucial to maintain muscle tone, bone structure, and prevent dislocation of the joints.

Occupational therapy helps adults and children maximise their function, adapt to their limitations and live as independently as possible.^[34][35]

Orthotic devices such as ankle-foot orthoses (AFOs) are often prescribed to minimise gait irregularities. AFOs have been found to improve several measures of ambulation, including reducing energy expenditure^[36] and increasing speed and stride length.^[37]

Speech therapy helps control the muscles of the mouth and jaw, and helps improve communication. Just as CP can affect the way a person moves their arms and legs, it can also affect the way they move their mouth, face and head. This can make it hard for the person to breathe; talk clearly; and bite, chew and swallow food. Speech therapy often starts before a child begins school and continues throughout the school years.^[38]

Hyperbaric oxygen therapy (HBOT), in which pressurized oxygen is inhaled inside a hyperbaric chamber, has been used to treat CP under the theory that improving oxygen availability to damaged brain cells can reactivate some of them to function normally. Its use to treat CP is controversial. A 2007 systematic review concluded that the effect of HBOT on CP is not significantly different from that of pressurized room air, and that some children undergoing HBOT will experience adverse events such as seizures and the need for ear pressure equalization tubes; due to poor quality of data assessment the review also concluded that estimates of the prevalence of adverse events are uncertain.^[39]

Nutritional counseling may help when dietary needs are not met because of problems with eating certain foods.

Both massage therapy^[40] and hatha yoga^{[citation needed]} are designed to help relax tense muscles, strengthen muscles, and keep joints flexible. Hatha yoga breathing exercises are sometimes used to try to prevent lung infections. More research is needed to determine the health benefits of these therapies for people with CP.

Surgery for people with CP usually involves one or a combination of:

• Loosening tight muscles and releasing fixed joints, most often performed on the hips, knees, hamstrings, and ankles. In rare cases, this surgery may be used for people with stiffness of their elbows, wrists, hands, and fingers.

• The insertion of a Baclofen Pump usually during the stages while a patient is a young adult. This is usually placed in the left abdomen. It is a pump that is connected to the spinal cord, whereby it sends bits of Baclofen alleviating the continuous muscle flexion. Baclofen is a muscle relaxant and is often given PO to patients to help counter the effects of spasticity.

• Straightening abnormal twists of the leg bones, i.e. femur (termed femoral anteversion or antetorsion) and tibia (tibial torsion). This is a secondary complication caused by the spastic muscles generating abnormal forces on the bones, and often results in intoeing (pigeon-toed gait). The surgery is called derotation osteotomy, in which the bone is broken (cut) and then set in the correct alignment.^[41]

• Cutting nerves on the limbs most affected by movements and spasms. This procedure, called a rhizotomy, "rhizo" meaning root and "tomy" meaning "a cutting of" from the Greek suffix 'tomia' reduces spasms and allows more flexibility and control of the affected limbs and joints.^[42]

• Botulinum Toxin A (Botox) injections into muscles that are either spastic or have contractures, the aim being to relieve the disability and pain produced by the inappropriately contracting muscle.^[43]

A new study has found that cooling the bodies and blood of high-risk full-term babies shortly after birth may significantly reduce disability or death.^[44]

Cord Blood Therapy: There are no published randomized controlled trials or meta-analysis of this treatment modality in cerebral palsy. In March 2008 a boy diagnosed with cerebral palsy appeared on the Today Show with his family.^[45] The parents noted that he could not walk on his own and appeared to be "swallowing his tongue" at times. He was eventually diagnosed with cerebral palsy and could only walk with the aid of a walker for a short time. Earlier that year he participated in a clinical trial involving his own cord blood that his parents had saved when he was born. His parents reported that within 5 days after the procedure he was walking on his own and talking, something his mother said he was not capable of on his own and it was doubtful he would ever be able to do on his own. They also reported that the doctors also told them that if his rate of progress continues uninterrupted until he is 7 he will be pronounced cured.

Conductive education (CE) was developed in Hungary from 1945 based on the work of András Pető. It is a unified system of rehabilitation for people with neurological disorders including cerebral palsy, Parkinson's disease and multiple sclerosis, amongst other conditions. It is theorised to improve mobility, self-esteem, stamina and independence as well as daily living skills and social skills. The conductor is the professional who delivers CE in partnership with parents and children. Skills learned during CE should be applied to everyday life and can help to develop age-appropriate cognitive, social and emotional skills. It is available at specialized centers.

Biofeedback is an alternative therapy in which people with CP learn how to control their affected muscles. Some people learn ways to reduce muscle tension with this technique. Biofeedback does not help everyone with CP.

Neuro-cognitive therapy. A new approach to treating cerebral palsy from Snowdrop. It is based upon two proven principles. (1) Neural Plasticity. The brain is capable of altering its own structure and functioning to meet the demands of any particular environment. Consequently if the child is provided with an appropriate neurological environment, he will have the best chance of making progress. (2) Learning can lead to development. As early as the early 1900s, this was being proven by a psychologist named Lev Vygotsky. He proposed that children's learning is a social activity, which is achieved by interaction with more skilled members of society. There are many studies, which provide evidence for this claim. there are however, as yet no controlled studies on neuro-cognitive therapy.

Patterning is a controversial form of alternative therapy for people with CP. The method is promoted by The Institutes for the Achievement of Human Potential (IAHP), a Philadelphia nonprofit, but has been criticized by the American Academy of Pediatrics.^[46] The IAHP's methods have been endorsed by Linus Pauling,^[47] as well as some parents of children treated with their methods.^[48][49][50]

Cultural aspects

Economic Impact Of Cerebral Palsy In Australia

Access Economics has released a report on the economic impact of cerebral palsy in Australia. Launched by the Hon. Bill Shorten, MP, the report found that, in 2007, the financial cost of cerebral palsy (CP) in Australia was $1.47 billion or 0.14% of GDP. When the value of lost well-being (disability and premature death) was added, the cost rose a further $2.4 billion.^[51]

In 2007, the financial cost of CP was $1.47 billion (0.14% of GDP). Of this:

• 1.03 billion (69.9%) was productivity lost due to lower employment, absenteeism and premature death of Australians with CP;

• 141 million (9.6%) was the DWL from transfers including welfare payments and taxation forgone;

• 131 million (9.0%) was other indirect costs such as direct program services, aides and home modifications and the bringing-forward of funeral costs;

• 129 million (8.8%) was the value of the informal care for people with CP; and

• 40 million (2.8%) was direct health system expenditure.

Additionally, the value of the lost well-being (disability and premature death) was a further $2.4 billion.

In per capita terms, this amounts to a financial cost of $43,431 per person with CP per annum. Including the value of lost well-being, the cost is over $115,000 per person per annum.

Individuals with CP bear 37% of the financial costs, and their families and friends bear a further 6%. Federal government bears around one third (33%) of the financial costs (mainly through taxation revenues forgone and welfare payments). State governments bear under 1% of the costs, while employers bear 5% and the rest of society bears the remaining 19%. If the burden of disease (lost well-being) is included, individuals bear 76% of the costs.

Use of terms when referring to people with CP

Many people would rather be referred to as a person with a disability instead of handicapped. "Cerebral Palsy: A Guide for Care" at the University of Delaware offers the following guidelines:^[52]

Impairment is the correct term to use to define a deviation from normal, such as not being able to make a muscle move or not being able to control an unwanted movement. Disability is the term used to define a restriction in the ability to perform a normal activity of daily living which someone of the same age is able to perform. For example, a three year old child who is not able to walk has a disability because a normal three year old can walk independently. Handicap is the term used to describe a child or adult who, because of the disability, is unable to achieve the normal role in society commensurate with his age and socio-cultural milieu. As an example, a sixteen-year-old who is unable to prepare his own meal or care for his own toileting or hygiene needs is handicapped. On the other hand, a sixteen-year-old who can walk only with the assistance of crutches but who attends a regular school and is fully independent in activities of daily living is disabled but not handicapped. All disabled people are impaired, and all handicapped people are disabled, but a person can be impaired and not necessarily be disabled, and a person can be disabled without being handicapped.

The term "spastic" describes the attribute of spasticity in types of spastic CP. In 1952 a UK charity called The Spastics Society was formed.^[53] The term "spastics" was used by the charity as a term for people with CP. The words "spastic" and "spaz" have since been used extensively as a general insult to disabled people, which some see as extremely offensive. They are also frequently used to insult able-bodied people when they seem overly uncoordinated, anxious, or unskilled in sports. The charity changed its name to Scope in 1994.^[53] In the United States the word spaz has the same usage as an insult, but is not generally associated with CP.^[54]

Misconceptions

A common misconception about those born with Cerebral Palsy is that they are less intelligent than those born without it. Cerebral Palsy is defined as damage to the part of the brain that controls movement; areas of the brain that define a person's intelligence are not affected by CP.

Spastic Cerebral Palsy, the most common form of CP, causes the muscles to be tense, rigid and movements are slow and difficult. This can be misinterpreted as cognitive delay due to difficulty of communication. Individuals with cerebral palsy can have learning difficulties, but sometimes it is the sheer magnitude of problems caused by the underlying brain injury that prevents the individual from expressing what cognitive abilities they do possess.^[55]

Notable people

• Christy Brown, Irish writer and painter who wrote My Left Foot, which was later adapted into an Oscar winning movie of the same name starring Daniel Day Lewis
• Eric S. Raymond, an open source computer programmer.
• Christopher Widdows aka Steady Eddy, Australian comedian
• Francesca Martinez, English stand-up comedian.
• Joel Gausten, American journalist, author and musician.
• Josh Blue, comedian and winner of the fourth season of Last Comic Standing, who often jokes about his condition.
• Gianna Jessen, singer-songwriter and pro-life activist, and a abortion survivor.
• Stephen Hopkins, signer of USA Declaration of Independence, reputed to have stated, "My hand trembles, but my heart does not."^[56]
• Bill Porter, a salesman for Watkins Incorporated whose life story was told in the TV movie Door to Door.
• Karen Killilea, the subject of the book Karen (1952) and its sequel, With Love from Karen (1963), by her mother Marie Killilea.^[57]
• RJ Mitte, American actor known for his role in the AMC series Breaking Bad
• Gabriela Brimmer, poet and disability rights activist
• Geri Jewell, actress and comedienne best known for her roles on the TV series The Facts of Life and later Deadwood
• Cara Readle, young actress known for her role as Layla on CBBC's Tracy Beaker
• Paul Henshall, British TV actor
• Ruben Gallego, writer of White on Black: A Boy's Story, a memoir book on his early life in Russian institutes.
• David Ring, American Christian evangelist and motivational speaker
• Emperor Claudius, the Roman Emperor who was also a stutterer and walked with a limp is believed to have had CP.^[58]
• Susie Maroney, world-record holding marathon swimmer.
• Baruch Kimmerling, Israeli sociologist and political dissident
• Greg Walloch, American writer, actor and comedian
• Joey Deacon, British author and television personality
• Eric Gores, American actor who starred in The Kid & I
• Maysoon Zayid, Palestinian-American actor and comedienne.
• Christopher Nolan, Irish poet and author, died on Feb 20, 2009, after choking on food.^[59]

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External links

Look up cerebral palsy in Wiktionary, the free dictionary.

• Cerebral palsy at the Open Directory Project: Includes links to more than a dozen sites with information on CP, as well as support groups and CP organisations.
• A Guide to Cerebral Palsy
• NINDS Cerebral Palsy Information Page
• Cerebral Palsy Guide for Parents

v • d • e Cerebral palsy and other paralytic syndromes (G80-G83, 342-344) Paresis and plegia NOS Paralysis · Quadriplegia · Triplegia · Hemiplegia/Hemiparesis · Paraplegia/Diplegia · Monoplegia Flaccid vs. spastic Upper motor neuron lesion: Spastic diplegia · Spastic paraplegia (Hereditary spastic paraplegia) Lower motor neuron lesion: Flaccid paralysis Specific types Cerebral palsy · Cauda equina syndrome · Locked-in syndrome

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