cerebral palsy(redirected from Cerebral paresis)
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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.
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 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, while advances in medicine have decreased the incidence from some causes—Rh disease for example—they have 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 back-ground are at higher risk due to poorer access to proper prenatal care and advanced medical services.
Causes and symptoms
As noted, CP has many causes, making a discussion of the genetics of CP complicated. A number of hereditary/genetic syndromes have signs and symptoms similar to CP, but usually also have problems not typical of CP. Put another way, some hereditary conditions "mimic" CP. Isolated CP, meaning CP that is not a part of some other syndrome or disorder, is usually not inherited.
It might be possible to group the causes of CP into those that are genetic and those that are non-genetic, but most would fall somewhere in between. Grouping causes into those that occur during pregnancy (prenatal), those that happen around the time of birth (perinatal), and those that occur after birth (postnatal), is preferable. CP related to premature birth and multiple pregnancies (twins, triplets, etc., not "many pregnancies") is somewhat different and considered separately.
Although much has been learned about human embryology in the last few decades, a great deal remains unknown. Studying prenatal human development is difficult because the embryo and fetus develop in a closed environment—the mother's womb. However, the relatively recent development of a number of prenatal tests has opened a window on the process. Add to that more accurate and complete evaluations of newborns, especially those with problems, and a clearer picture of what can go wrong before birth is possible.
The complicated process of brain development before birth is susceptible to many chance errors that can result in abnormalities of varying degrees. Some of these errors will result in structural anomalies of the brain, while others may cause undetectable, but significant, abnormalities in how the cerebral cortex is "wired." An abnormality in structure or wiring is sometimes hereditary, but is most often due to chance, or a cause unknown at this time. Whether and how much genetics played a role in a particular brain abnormality depends to some degree on the type of anomaly and the form of CP it causes.
Several maternal-fetal infections are known to increase the risk for CP, including rubella (German measles, now rare in the United States), cytomegalovirus (CMV), and toxoplasmosis. Each of these infections is considered a risk to the fetus only if the mother contracts it for the first time during that pregnancy. Even in those cases, though, most babies will be born normal. Most women are immune to all three infections by the time they reach childbearing age, but a woman's immune status can be determined using the so-called TORCH (for Toxoplasmosis, Rubella, Cytomegalovirus, and Herpes) test before or during pregnancy.
Reserchers continue to study the role of perinatal infection in development of cerebral palsy. New evidence in 2004 linked inflammatory cytokines to possible cerebral injury that could lead to CP. Scientists suggested new research with intravenous immunoglobulin to limit inflammatory damage.
Just as a stroke can cause neurologic damage in an adult, so too can this type of event occur in the fetus. A burst blood vessel in the brain followed by uncontrolled bleeding (coagulopathy), known as intracerebral hemorrhage, could cause a fetal stroke, or a cerebral blood vessel could be obstructed by a clot (embolism). Infants who later develop CP, along with their mothers, are more likely than other mother-infant pairs to test positive for factors that put them at increased risk for bleeding episodes or blood clots. Some coagulation disorders are strictly hereditary, but most have a more complicated basis.
A teratogen is any substance to which a woman is exposed that has the potential to harm the embryo or fetus. Links between a drug or other chemical exposure during pregnancy and a risk for CP are difficult to prove. However, any substance that might affect fetal brain development, directly or indirectly, could increase the risk for CP. Furthermore, any substance that increases the risk for premature delivery and low birth weight, such as alcohol, tobacco, or cocaine, among others, might indirectly increase the risk for CP.
The fetus receives all nutrients and oxygen from blood that circulates through the placenta. Therefore, anything that interferes with normal placental function might adversely affect development of the fetus, including the brain, or might increase the risk for premature delivery. Structural abnormalities of the placenta, premature detachment of the placenta from the uterine wall (abruption), and placental infections (chorioamnionitis) are thought to pose some risk for CP.
Certain conditions in the mother during pregnancy might pose a risk to fetal development leading to CP. Women with autoimmune anti-thyroid or anti-phospholipid (APA) antibodies are at slightly increased risk for CP in their children. A potentially important clue uncovered recently points toward high levels of cytokines in the maternal and fetal circulation as a possible risk for CP. Cytokines are proteins associated with inflammation, such as from infection or autoimmune disorders, and they may be toxic to neurons in the fetal brain. More research is needed to determine the exact relationship, if any, between high levels of cytokines in pregnancy and CP. A woman has some risk of developing the same complications in more than one pregnancy, slightly increasing the risk for more than one child with CP.
Serious physical trauma to the mother during pregnancy could result in direct trauma to the fetus as well, or injuries to the mother could compromise the availability of nutrients and oxygen to the developing fetal brain.
Birth asphyxia significant enough to result in CP is now uncommon in developed countries. Tight nuchal cord (umbilical cord around the baby's neck) and prolapsed cord (cord delivered before the baby) 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 that results in serious illness in the newborn has the potential to produce some neurological damage.
The remaining 15% of CP is 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 now rare in developed countries due to routine screening of maternal blood type and treatment of pregnancies at risk. The routine, effective treatment of jaundice due to other causes has also made it an infrequent cause of CP in developed countries. Rh blood type poses a risk for recurrence of Rh disease if treatment is not provided.
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 infants born healthy 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, poisons, or certain chemicals could cause neurological damage. Accidental overdose of certain medications might also cause similar damage to the central nervous system.
By definition, the defect in cerebral function causing CP is nonprogressive. However, the symptoms of CP often change over time. Most of the symptoms of CP relate in some way to the abnormal control of muscles. To review, CP is categorized first by the type of movement/postural disturbance(s) present, then by a description of which limbs are affected, and finally by the severity of motor impairment. For example, spastic diplegia 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 three-part descriptions are helpful in providing a general picture, but cannot give a complete description of any one person with CP. In addition, the various "forms" of CP do not occur with equal frequency—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 very subjective terms with no firm boundaries between them.
A muscle that is tensed and contracted is hypertonic, while excessively loose muscles are hypotonic. Spastic, hypertonic muscles can cause serious orthopedic problems, including scoliosis (spine curvature), 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, or "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 a "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.
Mechanisms that can cause CP are not always restricted to motor-control areas of the brain. Other neurologically based symptoms may include:
- 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.
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.
Selected developmental milestones, and the ages for normally acquiring them, are given below. If a child does not acquire the skill by the age shown in parentheses, there is some cause for concern.
- sits well unsupported—6 months (8-10 months)
- babbles—six months (eight months)
- crawls—nine months (12 months)
- finger feeds, holds bottle—nine 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 12-18 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 asymmetric crawling or, later on, favoring one leg while climbing stairs.
It must be remembered that children normally progress at somewhat different rates, and slow beginning accomplishment is often followed by normal development. Other causes for developmental delay—some benign, some serious—should be excluded before considering CP as the answer. CP is nonprogressive, so continued loss of previously acquired milestones indicates that CP is not the cause of the problem.
No one test is diagnostic for CP, but certain factors increase suspicion. The Apgar score measures a baby's condition immediately after birth. Babies that 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), periventricular leukomalacia (an abnormality of the area surrounding the ventricles), 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.
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.
Spasticity, muscle weakness, coordination, ataxia, and scoliosis are all significant impairments that affect the posture and mobility of a person with CP. Physical and occupational therapists work with the patient, and the family, to maximize the ability to move affected limbs, develop normal motor patterns, and maintain posture. "Assistive technology," things such as 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. A new experimental physical therapy treatment was tested on children in 2004 that often is used on adults who have had strokes. Called constraint-induced movement therapy, it consists of placing the child's stronger arm in a case for three weeks and giving him or her 21 straight days to retrain the weaker arm.
Before fixed contractures develop, muscle-relaxant drugs such as diazepam (Valium), dantrolene (Dantrium), and baclofen (Lioresal) may be prescribed. Botulinum toxin (Botox), a newer and 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).
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.
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. Although knowledgeable and caring medical professionals are indispensable for developing a care plan, a potentially more important source of information and advice is 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.
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 experiences and education consistent with their abilities. The advice and intervention of various professionals remains 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 lifespans, but the lifespan of those with more severe forms may be shortened. However, more than 90% of infants with CP survive into adulthood.
The cause of most cases of CP remains unknown, but it has become clear in recent years that birth difficulties are not to blame in most cases. Rather, developmental problems before birth, usually unknown and generally undiagnosable, are responsible for most cases. The rate of survival for preterm infants has leveled off in recent years, and methods to improve the long-term health of these at-risk babies are now being sought. Current research is also focusing on the possible benefits of recognizing and treating coagulopathies and inflammatory disorders in the prenatal and perinatal periods. 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.
Asphyxia — Lack of oxygen. In the case of cerebral palsy, lack of oxygen to the brain.
Ataxia — A deficiency of muscular coordination, especially when voluntary movements are attempted, such as grasping or walking.
Athetosis — A condition marked by slow, writhing, involuntary muscle movements.
Coagulopathy — A disorder in which blood is either too slow or too quick to coagulate (clot).
Contracture — A tightening of muscles that prevents normal movement of the associated limb or other body part.
Cytokine — A protein associated with inflammation that, at high levels, may be toxic to nerve cells in the developing brain.
Diplegia — Paralysis affecting like parts on both sides the body, such as both arms or both legs.
Dorsal rhizotomy — A surgical procedure that cuts nerve roots to reduce spasticity in affected muscles.
Dyskinesia — Impaired ability to make voluntary movements.
Hemiplegia — Paralysis of one side of the body.
Hypotonia — Reduced or diminished muscle tone.
Quadriplegia — Paralysis of all four limbs.
Serial casting — A series of casts designed to gradually move a limb into a more functional position.
Spastic — A condition in which the muscles are rigid, posture may be abnormal, and fine motor control is impaired.
Spasticity — Increased mucle tone, or stiffness, which leads to uncontrolled, awkward movements.
Static encephalopathy — A disease of the brain that does not get better or worse.
Tenotomy — A surgical procedure that cuts the tendon of a contracted muscle to allow lengthening.
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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.
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"Experimental Treatment Yields New Hope for Children Battling Cerebral Palsy." Drug Week February 27, 2004: 82.
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Epilepsy Foundation of America. 4351 Garden City Dr., Suite 406, Landover, MD 20785-2267. (301) 459-3700 or (800) 332-1000. http://www.epilepsyfoundation.org.
March of Dimes Birth Defects Foundation. 1275 Mamaroneck Ave., White Plains, NY 10605. (888) 663-4637. email@example.com. http://www.modimes.org.
National Easter Seal Society. 230 W. Monroe St., Suite 1800, Chicago, IL 60606-4802. (312) 726-6200 or (800) 221-6827. http://www.easter-seals.org.
National Institute of Neurological Disorders and Stroke. 31 Center Drive, MSC 2540, Bldg. 31, Room 8806, Bethesda, MD 20814. (301) 496-5751 or (800) 352-9424. http://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〉.
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pertaining to the cerebrum.
cerebral palsy a diagnostic term used to describe a type of nonprogressive neuromotor dysfunction; it is a disorder of movement and posture resulting from an insult to the immature brain. Cerebral dysfunction can occur because the central nervous system has not developed properly from the start (a developmental anomaly); or it can be the consequence of an injury to a previously normally developing nervous system. The insult of cerebral palsy is always static and nonprogressive; the lesion itself will not get worse. What often do change over time are the manifestations of the motor disorder and the emergence or recognition of associated deficits as the child grows and the nervous system matures. There is no universally accepted age-of-onset criterion for making the diagnosis. The upper age limit is often set at seven or eight years old for an acquired insult to be classified as cerebral palsy; this is the age when motor areas in the nervous system have largely reached maturation and therefore the potential for motor plasticity significantly diminishes. Prior to this age, function lost by damage to one area of the brain may be partially taken over by another area. However, there is not universal agreement on this age criterion.
The child with cerebral palsy is at high risk for having associated deficits in neurological, cognitive, and perceptual abilities. Motor deficits are generally identified before delays in language or perceptual abilities are evident.
The child with cerebral palsy is at high risk for having associated deficits in neurological, cognitive, and perceptual abilities. Motor deficits are generally identified before delays in language or perceptual abilities are evident.
Etiology. Cerebral palsy is relatively common, affecting 1 in 200 children. This number takes into account the full spectrum of the disorder, including milder cases, a broad definition of age of insult, and more complete case ascertainment. The exact cause cannot always be determined, but it usually develops before the age of three. The percentage due to prenatal anomalies and insults is usually considered to be 40 to 60 per cent. Damage to the fetal brain can occur as a result of maternal infections, drug or alcohol abuse, other teratogenic exposures, and genetic syndromes. Cerebral palsy is associated with preterm birth between 30 and 50 per cent of the time, but it is not clear whether or not this association is causal in nature. Thirty years ago, the belief was that most cerebral palsy was a consequence of birth-related injury to the brain, and obstetricians often took blame for “causing” the condition. More recently, there has been a shift in emphasis to unknown prenatal events as the causative factors, such as preterm birth, difficult deliveries, and prenatal or perinatal brain injuries. Any situation that interferes with the fetal oxygen supply can produce brain damage and cerebral palsy. These include premature separation of the placenta, prolapsed cord, and chronic placental insufficiency. Other potential causes during the perinatal and early postnatal period include hypoglycemia, which can lead to cell death; hypernatremia, which results in cellular hyperosmolality, vascular lesions, and intracranial hemorrhage; and hyperbilirubinemia. Postnatally acquired cerebral palsy is usually considered to be around 10 per cent of cases. Damage to the brain in childhood can result from infections of the meninges or brain cells; near-drowning or similar anoxic insults; cancers that although successfully treated leave permanent brain damage; head injury; or any of various stroke syndromes.
Classification. The most common classification for cerebral palsy, based on the predominant clinical manifestations, distinguishes three major types: (1) spastic, in which there are exaggerated stretch reflexes, muscle spasticity, and a strong tendency to develop contractures; (2) athetoid, with purposeless, uncontrollable movements and muscle tension; and (3) atactic, in which the child has poor balance, poor coordination, and a staggering gait.
Treatment. This varies according to the nature and extent of brain damage. Muscle relaxants and other medications may help reduce spasms. Orthopedic surgery, casts, braces, and traction can be used to correct or prevent associated deformities. Early muscle training and special exercises may also promote function, prevent deformity, and help the child lead a useful, productive life. If muscle training is not begun early, extensive rehabilitation may be necessary to correct faulty habits and poor muscle patterns the child has established. However, it is never too late for a complete evaluation of the condition of a patient with cerebral palsy. A rehabilitation program can produce good results later in life, not only in childhood. Anticonvulsant drugs are necessary when seizures are among the associated symptoms. Special education is important for children with cognitive impairments, as is attention to the other associated problems.
Bell's palsy see bell's palsy.
birth palsy birth paralysis.
cerebral palsy see cerebral palsy.
crossed leg palsy palsy of the fibular nerve, caused by sitting with one leg crossed over the other.
Erb's palsy (Erb-Duchenne palsy) Erb-Duchenne paralysis.
facial palsy Bell's palsy.
shaking palsy Parkinson's disease.
ce·re·bral pal·sy (CP),
a generic term for various types of nonprogressive motor dysfunction present at birth or beginning in early childhood. Causes are both hereditary and acquired; depending on cause, classified as intrauterine, natal, and early postnatal; motor disturbances include diplegia, hemiplegia, quadriplegia, choreoathetosis, and ataxia.
Any of a group of disorders of varying severity caused by brain injury usually at or before birth, resulting in impairment of muscle movement that may include spasticity, involuntary movement, or problems maintaining balance.
cerebral palsy (CP)
Etymology: L, cerebrum + Gk, para, beyond, lysis, loosening
a motor function disorder caused by a permanent, nonprogressive brain defect or lesion present at birth or shortly thereafter. The neurological deficit may result in spastic hemiplegia, monoplegia, diplegia, or tetraplegia; athetosis or ataxia; seizures; paresthesia; varying degrees of mental retardation; and impaired speech, vision, and hearing. The disorder is usually associated with premature or abnormal birth and intrapartum asphyxia, causing damage to the nervous system. Abnormalities in breathing, sucking, swallowing, and responsiveness are usually apparent soon after birth, but the characteristic stiff, awkward movements of the infant's limbs may be overlooked for several months. Walking is usually delayed, and, when it is attempted, the child manifests a typical scissors gait. The arms may be affected only slightly, but the fingers are often spastic. Deep-tendon reflexes are exaggerated, and there may be slurred speech, delay in development of sphincter control, and athetotic movements of the face and hands. Early identification of the disorder facilitates the handling of infants with cerebral palsy and the initiation of an exercise and training program. Treatment is individualized and may include the use of braces, surgical correction of deformities, speech therapy, and various indicated drugs, such as muscle relaxants and anticonvulsants. Also called congenital cerebral diplegia, Little's disease.
cerebral palsyLittle's disease Neurology A persistent, nonprogressive SX complex affecting up to 0.4% of term births, attributed to intrauterine and/or perinatal hypoxia; characterized by defective motor development, with spastic paraplegia, gait defects, incoordination, seizures, ataxia, speech defects, ±mental retardation
ce·re·bral pal·sy(CP) (ser'ĕ-brăl pawl'zē)
A condition that involves the brain and causes motor defects as well as sensory and cognitive problems, symptoms vary with the type of CP.
cerebral palsySee SPASTIC PARALYSIS.
cerebral palsychronic disorder of motor function, with associated impaired mental ability in 60% of cases; becomes evident during second year of life, but present since, or before, birth; associated with birth injury, premature birth or perinatal brain anoxia; presents as upper motor neurone lesion of variable severity (depending on cause) affecting pyramidal tracts and/or extrapyramidal tract function, with loss of motor control and characteristic limb effects (Table 1and Table 2; see mixed cerebral palsy)
|Limb muscle||Tone much reduced; bulk somewhat reduced; thin limbs|
|Limb movement||Asymmetrical movements|
|Normal childhood milestones not met/much delayed|
|Reflexes||Exaggerated (hyperreflexia); clonus; extensor plantar response|
|Hips||Internal rotation due to hip flexor and adductor spasticity|
|Knees||Toe walking due to knee flexor and foot extensor spasticity|
|Type of CP (prevalence)||Site of brain injury||Clinical effect|
|Spastic CP (70%)|
|Spasticity of limb/ipsilateral limbs|
Spasticity of both arms/both legs
|Athetoid CP (10-20%)||Basal ganglia lesion||Uncontrolled/uncoordinated movements|
|Ataxic CP (5-10%)||Cerebellar lesion||Non-coordination of movements/balance|
|Mixed CP (10%)||Combined lesion||Spastic/athetoid effects|
cerebral palsy (serˑ··brl plˑ·zē),
n neuromuscular disorder sometimes caused by brain damage in utero or at birth, characterized by loss of coordination and muscle control.
ce·re·bral pal·sy(ser'ĕ-brăl pawl'zē)
Generic term for nonprogressive motor dysfunction present at birth or beginning in early childhood. Causes are both hereditary and acquired.