Cerebral palsy (CP) is a general term used for a group of nonprogressive disorders of movement and posture caused by abnormal development of, or damage to, parts of the brain that control muscle movements.1 The term does not imply severity, cause, treatment, or prognosis. The overall prevalence of the condition ranges from 1.9 to 2.6 of every 1000 live-born children in the Western world.2 The rate of CP is much higher in preterm versus term infants and increases with decreasing birth weight and gestational age. It increases at the extremes of birth weight across gestational ages.3 CP is newly diagnosed in approximately 6000 infants and young children every year in the United States. This overall amount has not changed in the last 20 to 30 years, although recent studies suggest that there may be a decreasing trend.2,4,5

CP is caused by events occurring before, during, or after birth up to age 3 years.6 The etiology is multifactorial. Birth injuries such as hypoxic ischemic encephalopathy, or head injuries after delivery such as those from car accidents, child abuse, falls, or intracranial hemorrhages, can lead to CP. Illnesses such as meningitis in the first few weeks or months of life, or strokes that occur in the newborn period, may result in cerebral palsy. CP is often, but not always, diagnosed in children with congenital cerebral malformations of microcephaly or hydrocephalus. Perinatal asphyxia, intrapartum hypoxia, prematurity, intrauterine growth retardation, intrauterine infection, antepartum hemorrhage, severe placental abnormalities, and multiple pregnancies can all be associated pathologies.7 Unfortunately, the cause is not always clear.8

CP is characterized by abnormalities of movement and posture. Young children are often identified with signs of CP when motor milestones are not met. Children may also have increased (stiffness) and/or decreased tone on the motor exam or asymmetries may be found.

These children may show a lack of muscle coordination when performing voluntary movements. A young child may appear ataxic when ambulating. Spasticity may be noted as the child has stiff or tight muscles in his or her arms and/or legs, exaggerated reflexes, walking with one foot or leg dragging, toe walking, a crouched, or a “scissored” gait, and muscle tone that is either too stiff or too floppy.9 Common terms used to describe the clinical presentation of CP include static encelphalopathy, spasticity, or developmental delay.10

The classification of CP is based on the number of limbs involved and the associated resting tone, or movement abnormalities (Figure 11-1).

Types of Cerebral Palsy

• Spastic CP—Most common type accounting for approximately 80%, is due to pyramidal tract lesions with subsequent rate-dependent increase in tone, hyperreflexia, clonus, and an abnormal Babinski reflex.11 Muscles are stiff, body position may be abnormal, and fine motor control is affected.
  
• Dyskinetic CP (Athetoid CP, dystonic CP, and choreoathetoid CP)—Extrapyramidal signs characterized by involuntary movements such as twisting, jerking, rigid posturing or other movements; increased tone is often present.11
  
• Ataxic CP—Abnormal movements involving tremors, unsteady gain, and loss of coordination.
  
• Mixed CP—May have both hyper and hypotonia and there is often a mixture of spastic and dyskinetic components.6
  
• Hypotonic CP—Hypotonia in both trunk and extremities with increased reflexes and persistent primitive reflexes; occurs infrequently.6

The location usually of impairment falls into one of three broad categories11:

• Hemiplegia—CP predominantly affecting one side of the body, with the arm usually more impaired than the leg.
  
• Diplegia—CP affecting bilateral lower extremities; arms may be partially involved.
  
• Quadriplegia—CP affecting all 4 extremities (full body).

CP may also be termed mild, moderate, or severe, although there are no firm boundaries.

Children with CP usually present with a delay in reaching early developmental milestones. The diagnosis of CP depends upon a combination of findings including motor delay, tone abnormalities, weakness, persistence or asymmetry of primitive reflexes, and abnormal postural reactions. A detailed history and thorough physical and neurological examinations are necessary to rule out other potential causes such as progressive neurodegenerative disorders or other inherited or metabolic diseases. It is important to note that these children are not losing motor skills.

Infants with an abnormal obstetric or perinatal history should be monitored closely as they may be at increased risk to develop CP. Potential findings include abnormal behavior such as excessive passivity or irritability, poor feeding and/or sleeping, and poor visual attention. The baby may be hypotonic or hypertonic, have increased tendon reflexes, and clonus. Primitive reflexes such as fisting may be asymmetric or persistent, and postural reflexes may be exaggerated or their disappearance may be delayed. Oromotor skills may be abnormal with tongue retraction and thrust, tonic bite, oral hypersensitivity, and grimacing. Furthermore, achievement of motor milestones should be evaluated. Serial examination of motor milestones can be an effective screening tool for CP.12,13 It should also be noted that although the damage in CP is nonprogressive, clinical signs develop as the nervous system matures. An absolute diagnosis usually requires repeated examinations and often is not possible until later infancy or early childhood.