Cerebral Palsy
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Cerebral palsy
The most common cause of crippling in children, cerebral palsy (CP) is a group of neuromuscular disorders caused by prenatal, perinatal, or postnatal damage to the upper motor neurons. Although nonprogressive, these disorders may become more obvious as an affected infant grows. The three major types of cerebral palsy — spastic, athetoid, and ataxic — may occur alone or in combination. Motor impairment may be minimal (sometimes apparent only during physical activities such as running) or severely disabling. Common associated defects are seizures, speech disorders, and mental retardation. Cerebral palsy occurs in an estimated 1.5 to 5 per 1,000 live births per year. Incidence is highest in premature infants (anoxia plays the greatest role in contributing to cerebral palsy) and in those who are small for gestational age. Almost half of the children with CP are mentally retarded, approximately one-fourth have seizure disorders, and more than threefourths have impaired speech. Additionally, children with CP often have dental abnormalities, vision and hearing defects, and reading disabilities. Cerebral palsy is slightly more common in males than in females and is more common in whites than in other ethnic groups. The prognosis varies. Treatment may make a near-normal life possible for children with mild impairment. Those with severe impairment require special services and schooling. Causes The exact of CP is unknown; however, conditions resulting in cerebral anoxia, hemorrhage, or other CNS damage are probably responsible. Potential causes vary with time of damage. Prenatal causes include: maternal infection (especially rubella) exposure to radiation anoxia toxemia maternal diabetes abnormal placental attachment malnutrition isoimmunization. Perinatal and birth factors may include: forceps delivery breech presentation placenta previa abruptio placentae depressed maternal vital signs from general or spinal anesthesia prolapsed cord with delay in blood delivery to the head premature birth prolonged or unusually rapid labor multiple births (especially infants born last) infection or trauma during infancy. Postnatal causes include: kernicterus resulting from erythroblastosis fetalis brain infection or tumor head trauma prolonged anoxia cerebral circulatory anomalies causing blood vessel rupture systemic disease resulting in cerebral thrombosis or embolus. Pathophysiology In the early stages of brain development, a lesion or abnormality causes structural and functional defects that in turn cause impaired motor function or cognition. Even though the defects are present at birth, problems may not be apparent until months later, when the axons have become myelinated and the basal ganglia are mature. Signs and symptoms Shortly after birth, the infant with CP may exhibit some typical signs and symptoms, including: excessive lethargy or irritability high-pitched cry poor head control weak sucking reflex. Additional physical findings that may suggest CP include: delayed motor development (inability to meet major developmental milestones) abnormal head circumference, typically smaller than normal for age (because the head grows as the brain grows) abnormal postures, such as straightening legs when on back, toes down; holding head higher than normal when prone due to arching of back abnormal reflexes (neonatal reflexes lasting longer than expected, extreme reflexes, or clonus) abnormal muscle tone and performance (scooting on back to crawl, toe-first walking).
Each type of cerebral palsy typically produces a distinctive set of clinical features, although some children display a mixed form of the disease. Complications Complications depend on the type of CP and the severity of the involvement. Possible complications include: contractures skin breakdown and ulcer formation muscle atrophy malnutrition seizure disorders speech, hearing, and vision problems language and perceptual deficits mental retardation dental problems respiratory difficulties, including aspiration from poor gag and swallowing reflexes. Diagnosis No diagnostic tests are specific to CP. However, neurologic screening will exclude other possible conditions, such as infection, spina bifida, or muscular dystrophy. Diagnostic tests that may be performed include: Developmental screening reveals delay in achieving milestones. Vision and hearing screening demonstrates degree of impairment. Electroencephalogram identifies the source of seizure activity. Treatment Cerebral palsy can't be cured, but proper treatment can help affected children reach their full potential within the limits set by this disorder. Such treatment requires a comprehensive and cooperative effort, involving doctors, nurses, teachers, psychologists, the child's family, and occupational, physical, and speech therapists. Home care is often possible. Treatment usually includes: braces, casts, or splints and special appliances, such as adapted eating utensils and a low toilet seat with arms, to help these children perform activities of daily living independently an artificial urinary sphincter for the incontinent child who can use the hand controls range-of-motion exercises to minimize contractures anticonvulsant to control seizures muscle relaxants (sometimes) to reduce spasticity surgery to decrease spasticity or correct contractures muscle transfer or tendon lengthening surgery to improve function of joints rehabilitation including occupational, physical, and speech therapy to maintain or improve functional abilities. ASSESSING SIGNS OF CP Each type of cerebral palsy (CP) is manifested by specific signs. This chart highlights the major signs and symptoms associated with each type of CP. The manifestations reflect impaired upper motor neuron function and disruption of the normal stretch reflex. TYPE OF CP Spastic CP (due to impairment of the pyramidal tract [most common type]) SIGNS AND SYMPTOMS Hyperactive deep tendon reflexes Increased stretch reflexes Rapid alternating muscle contraction and relaxation Muscle weakness Underdevelopment of affected limbs Muscle contraction in response to manipulation Tendency toward contractures Typical walking on toes with a scissors gait, crossing one foot in front of the other Involuntary movements usually affecting arms more severely than legs, including: –grimacing –wormlike writhing –dystonia –sharp jerks Difficulty with speech due to involuntary facial movements Increasing severity of movements during stress; decreased with relaxation and disappearing entirely during sleep
Athetoid CP (due to impairment of the extrapyramidal tract)
Ataxic CP (due to impairment of the extrapyramidal tract)
Mixed CP
Disturbed balance Incoordination (especially of the arms) Hypoactive reflexes Nystagmus Muscle weakness Tremor Lack of leg movement during infancy Wide gait as the child begins to walk Sudden or fine movements impossible (due to ataxia) Spasticity and athetoid movements Ataxic and athetoid movements (resulting in severe impairment)
The most common cause of crippling in children, cerebral palsy (CP) is a group of neuromuscular disorders caused by prenatal, perinatal, or postnatal damage to the upper motor neurons. Although nonprogressive, these disorders may become more obvious as an affected infant grows. The three major types of cerebral palsy — spastic, athetoid, and ataxic — may occur alone or in combination. Motor impairment may be minimal (sometimes apparent only during physical activities such as running) or severely disabling. Common associated defects are seizures, speech disorders, and mental retardation. Cerebral palsy occurs in an estimated 1.5 to 5 per 1,000 live births per year. Incidence is highest in premature infants (anoxia plays the greatest role in contributing to cerebral palsy) and in those who are small for gestational age. Almost half of the children with CP are mentally retarded, approximately one-fourth have seizure disorders, and more than threefourths have impaired speech. Additionally, children with CP often have dental abnormalities, vision and hearing defects, and reading disabilities. Cerebral palsy is slightly more common in males than in females and is more common in whites than in other ethnic groups. The prognosis varies. Treatment may make a near-normal life possible for children with mild impairment. Those with severe impairment require special services and schooling. Causes The exact of CP is unknown; however, conditions resulting in cerebral anoxia, hemorrhage, or other CNS damage are probably responsible. Potential causes vary with time of damage. Prenatal causes include: maternal infection (especially rubella) exposure to radiation anoxia toxemia maternal diabetes abnormal placental attachment malnutrition isoimmunization. Perinatal and birth factors may include: forceps delivery breech presentation placenta previa abruptio placentae depressed maternal vital signs from general or spinal anesthesia prolapsed cord with delay in blood delivery to the head premature birth prolonged or unusually rapid labor multiple births (especially infants born last) infection or trauma during infancy. Postnatal causes include: kernicterus resulting from erythroblastosis fetalis brain infection or tumor head trauma prolonged anoxia cerebral circulatory anomalies causing blood vessel rupture systemic disease resulting in cerebral thrombosis or embolus. Pathophysiology In the early stages of brain development, a lesion or abnormality causes structural and functional defects that in turn cause impaired motor function or cognition. Even though the defects are present at birth, problems may not be apparent until months later, when the axons have become myelinated and the basal ganglia are mature. Signs and symptoms Shortly after birth, the infant with CP may exhibit some typical signs and symptoms, including: excessive lethargy or irritability high-pitched cry poor head control weak sucking reflex. Additional physical findings that may suggest CP include: delayed motor development (inability to meet major developmental milestones) abnormal head circumference, typically smaller than normal for age (because the head grows as the brain grows) abnormal postures, such as straightening legs when on back, toes down; holding head higher than normal when prone due to arching of back abnormal reflexes (neonatal reflexes lasting longer than expected, extreme reflexes, or clonus) abnormal muscle tone and performance (scooting on back to crawl, toe-first walking).
Each type of cerebral palsy typically produces a distinctive set of clinical features, although some children display a mixed form of the disease. Complications Complications depend on the type of CP and the severity of the involvement. Possible complications include: contractures skin breakdown and ulcer formation muscle atrophy malnutrition seizure disorders speech, hearing, and vision problems language and perceptual deficits mental retardation dental problems respiratory difficulties, including aspiration from poor gag and swallowing reflexes. Diagnosis No diagnostic tests are specific to CP. However, neurologic screening will exclude other possible conditions, such as infection, spina bifida, or muscular dystrophy. Diagnostic tests that may be performed include: Developmental screening reveals delay in achieving milestones. Vision and hearing screening demonstrates degree of impairment. Electroencephalogram identifies the source of seizure activity. Treatment Cerebral palsy can't be cured, but proper treatment can help affected children reach their full potential within the limits set by this disorder. Such treatment requires a comprehensive and cooperative effort, involving doctors, nurses, teachers, psychologists, the child's family, and occupational, physical, and speech therapists. Home care is often possible. Treatment usually includes: braces, casts, or splints and special appliances, such as adapted eating utensils and a low toilet seat with arms, to help these children perform activities of daily living independently an artificial urinary sphincter for the incontinent child who can use the hand controls range-of-motion exercises to minimize contractures anticonvulsant to control seizures muscle relaxants (sometimes) to reduce spasticity surgery to decrease spasticity or correct contractures muscle transfer or tendon lengthening surgery to improve function of joints rehabilitation including occupational, physical, and speech therapy to maintain or improve functional abilities. ASSESSING SIGNS OF CP Each type of cerebral palsy (CP) is manifested by specific signs. This chart highlights the major signs and symptoms associated with each type of CP. The manifestations reflect impaired upper motor neuron function and disruption of the normal stretch reflex. TYPE OF CP Spastic CP (due to impairment of the pyramidal tract [most common type]) SIGNS AND SYMPTOMS Hyperactive deep tendon reflexes Increased stretch reflexes Rapid alternating muscle contraction and relaxation Muscle weakness Underdevelopment of affected limbs Muscle contraction in response to manipulation Tendency toward contractures Typical walking on toes with a scissors gait, crossing one foot in front of the other Involuntary movements usually affecting arms more severely than legs, including: –grimacing –wormlike writhing –dystonia –sharp jerks Difficulty with speech due to involuntary facial movements Increasing severity of movements during stress; decreased with relaxation and disappearing entirely during sleep
Athetoid CP (due to impairment of the extrapyramidal tract)
Ataxic CP (due to impairment of the extrapyramidal tract)
Mixed CP
Disturbed balance Incoordination (especially of the arms) Hypoactive reflexes Nystagmus Muscle weakness Tremor Lack of leg movement during infancy Wide gait as the child begins to walk Sudden or fine movements impossible (due to ataxia) Spasticity and athetoid movements Ataxic and athetoid movements (resulting in severe impairment)
