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Clinical features of cerebral palsy Author Geoffrey Miller, MD Disclosures All topics are updated as new evidence becomes available and our peer review process is complete. Literature review current through: Sep 2013. | This topic last updated: feb 13, 2013. INTRODUCTION Cerebral palsy (CP) consists of a heterogeneous group of nonprogressive clinical syndromes that are characterized by motor and postural dysfunction. These conditions, which range in severity, are due to abnormalities of the developing brain resulting from a variety of causes. Although the disorder itself is not progressive, the appearance of neuropathologic lesions and their clinical expression may change over time as the brain matures. The clinical manifestations of CP are reviewed here. The epidemiology, etiology, diagnosis, and management are discussed separately. (See "Epidemiology and etiology of cerebral palsy" and "Diagnosis and classification of cerebral palsy" and "Management and prognosis of cerebral palsy".) CLINICAL FEATURES The cerebral palsy (CP) syndromes are characterized by abnormalities of motor activity and posture. In affected patients, a voluntary movement that should be complex, coordinated, and varied is instead uncoordinated, stereotypic, and limited. Simple actions that are performed unconsciously by unaffected individuals require marked effort and concentration and often fail in patients with CP. In severely affected individuals, an attempted voluntary movement may evoke a primitive reflex, co-contraction of agonist and antagonist muscles, and mass movements [1]. For example, attempts at flexion may involve all segments of a limb, and extension of all the fingers may accompany extension of the wrist. Discrete movements, such as that of an individual finger, may be impossible. Classification of CP syndromes is based upon the type and distribution of motor abnormalities (table 1). However, there may be substantial overlap among the clinical features. For example, patients with spastic syndromes may have involuntary abnormal movements, and those with dyskinetic and ataxic syndromes may have pyramidal signs. Spastic syndromes The spastic syndromes have variable expression. They may be symmetric or asymmetric, and may involve one or more extremities. These variations are important in identifying etiology, associated findings, and prognosis [2]. Patients with spastic CP have features of an upper motor neuron syndrome, which include positive and negative signs [3,4]. A positive sign is an abnormality that leads to involuntarily increased muscle activity or movement patterns. A negative sign reflects insufficient muscle activity or insufficient control of muscle activity that interferes with function. These differ from signs of upper motor neuron syndrome with adult onset because the developing nervous system may respond differently to insults [5]. Positive signs of spastic CP include: Spastic hypertonia Hyperreflexia caused by hyperexcitability of the stretch reflex Extensor plantar responses Section Editors Marc C Patterson, MD, FRACP Carolyn Bridgemohan, MD Deputy Editor Alison G Hoppin, MD

Clonus Spastic hypertonia is the velocity-dependent increased resistance that occurs in response to passive muscle stretch. In the classic form, described as clasp-knife, the maximum resistance occurs after a few degrees of passive movement of a joint, which then relaxes after continued effort by the examiner. More rapid movement of the joint increases the degree of resistance, and decreases its time of onset. Spastic hypertonia is increased by stress and during voluntary movement when co-contraction of agonist and antagonist muscles may occur. In the most severe form, the affected part is rigid in flexion or extension. It tends to decrease during sleep. Negative signs of spastic CP include: Slow effortful voluntary movements Impaired fine-motor function Difficulty in isolating individual movements Fatigability Classification of the spastic CP syndromes depends upon the distribution of abnormal upper motor neuron signs. Spastic diplegia occurs when the lower limbs are more affected than the upper limbs. In quadriplegia, all limbs are affected; upper limbs may be equally or more involved than lower limbs. Involvement of one side of the body is termed hemiplegia. The suffix -paresis denotes weakness and -plegia means paralysis. However, these terms often are used interchangeably and do not necessarily imply a difference in severity. Mild dyskinetic signs (eg, involuntary movements) may occur in all the spastic syndromes. Spastic diplegia Spastic diplegia affects both term and preterm infants. Spastic diplegia in preterm infants often is associated with periventricular leukomalacia (PVL), and the risk is greater with increasing prematurity. (See "Periventricular leukomalacia".) The lower limbs are affected predominantly. Patients with mild PVL may have relatively good hand function and fewer associated disabilities. In more severely affected patients, upper limb function also may be compromised, depending upon the degree of spasticity, presence of contractures, sensory loss, associated involuntary movements, and intelligence. Affected patients have variable degrees of flexion at the elbows and knees; and flexion, adduction, and internal rotation of the hips. They may have an equinovalgus or calcaneovarus deformity of the foot. Extension of the fingers, abduction of the thumb, extension of the wrist, and supination of the forearm may be limited. These features may be associated with poor grasp release and involuntary or associated movements. Atrophy below the waist occurs in many patients. Sensory disturbances of central nervous system origin, such as poor two-point discrimination and astereognosis, are common in all the spastic syndromes [6]. Vasomotor abnormalities also occur. More severe associated disabilities usually occur in asymmetric than in symmetric spastic diplegia. Some cases may be caused by PVL and associated unilateral hemorrhagic infarction. Spastic hemiplegia Spastic hemiplegia typically affects term infants of normal birth weight. Most cases in term infants result from maldevelopment, prenatal circulatory disturbances, or neonatal stroke [7-10]. (See "Stroke in the newborn".) Prenatal causes include hypercoagulable states, vasculopathies, abnormal development of blood vessels, and emboli secondary to disorders affecting the placenta or fetus [11]. Causes of strokes that occur during early infancy include sepsis, disseminated intravascular coagulation, venous sinus thrombosis, emboli, and congenital heart disease [12,13]. Some cases are caused by periventricular atrophy or cerebral dysgenesis. Affected patients with nondiagnostic neuroimaging may have maldevelopment at a microscopic level [8,14]. The presentation of congenital spastic hemiplegia is variable. It is usually caused by a cortical lesion. Thus, the arm typically is more affected than the leg. The condition may be missed during the newborn period and become evident during a later examination. It may be detected when an infant's caregiver notices hand dominance, reduced movement, or abnormal posturing on one side. The disorder sometimes is detected after a seizure occurs.

As the clinical features evolve, movement and tone on the affected side typically decrease before tone and tendon reflexes abnormally increase. The typical posture appears when the child is approximately two years of age [1]. The arm is adducted at the shoulder and flexed at the elbow, the forearm is pronated, and the wrist and fingers are flexed with the hand closed. The hip is partially flexed and adducted, and the knee and ankle are flexed because of increased tone in the hamstring and plantar flexor muscles. The foot may remain in the equinovarus or calcaneovalgus position. In mildly affected patients, the postural abnormalities are more apparent during walking or running. However, unless severe intellectual disability is present, independent walking usually occurs at the appropriate age or is only slightly delayed. In spastic hemiplegia with a postnatal etiology, motor handicap usually is only mild or moderate. Athetotic posturing sometimes accompanies the spasticity [15,16]. Associated disabilities, such as intellectual impairment, hemianopsia, and seizures, may be worse than in cases with prenatal or perinatal causes. Cognitive deficits tend to be worse in infants with seizures [17]. Insults before the child reaches five years of age are more likely to adversely affect IQ compared to later events [18]. This is because peak synaptic production and elimination occur prior to this period [19,20]. IQ, or the difference between performance and verbal IQ, is not affected by the side of the lesion [17,18]. Verbal-performance discrepancy may be attributable to visuospatial impairment [18,21]. In general, language development is related to cognitive ability. Most children with spastic hemiplegia also have sensory deficits. These are correlated with poor growth of the affected side, although not with the severity of the motor deficit [22]. Spastic quadriplegia Spastic quadriplegia is the most severe form of spastic CP. It usually affects term infants who are small for gestational age, consistent with a prenatal origin, such as cerebral dysgenesis or infection. Other cases result from perinatal or postnatal events or a combination of prenatal and perinatal causes [23]. This disorder also is seen in extremely low birth weight infants [24]. Affected infants typically are severely handicapped. In addition to spasticity, they may have dystonia and feeding and respiratory difficulties because of pseudobulbar palsy. The characteristics of this disorder were investigated in a population-based study of 96 affected children born in Sweden from 1959 to 1978 [23,25]. The etiology was considered prenatal (eg, microcephaly, CNS maldevelopment, intrauterine infection), perinatal (eg, cerebral hemorrhage), or postnatal (eg, CNS infection) in 50 to 55, 30, and 15 to 20 percent, respectively [25]. Among the prenatal and perinatal cases, 21 percent were small for gestational age. All the patients had severe spastic paresis of all limbs, resulting in profound motor disability [23]. All had severe intellectual disability, and none could speak. Seizures occurred in 94 percent. Hip subluxation, contractures, and scoliosis were present in 75, 73, and 72 percent, respectively, and 47 percent had severe visual impairment. Microcephaly was congenital or secondary in 13 and 68 percent, respectively. Dyskinetic syndromes Dyskinetic CP typically affects term infants [26]. In most cases, it results from severe, acute perinatal asphyxia. (See "Etiology and pathogenesis of neonatal encephalopathy".) The disorder is associated with status marmoratus (lesions in the basal ganglia and thalamus with a marbled appearance) that may appear as high-intensity areas on T2-weighted MRI [27,28]. Dyskinetic CP results from selective neuronal necrosis in the hippocampus, thalamus, basal ganglia, reticular formation, and Purkinje cells of the cerebellum [29]. The neonatal presentation includes encephalopathy characterized by lethargy, decreased spontaneous movement, hypotonia, and suppressed primitive reflexes. Multiple organs may be affected. (See "Systemic effects of perinatal asphyxia".) Dyskinetic syndromes are characterized by the involuntary movements of athetosis, chorea, and dystonia. They are divided into two categories, according to the predominant type of abnormal movement [30]. One type is mainly athetoid, in which movements are athetoid, choreiform, or a combination of both. The second type is mainly

dystonic. Athetosis Athetosis consists of slow, smooth, writhing movements that involve distal muscles. There is dyssynergia (antagonistic action) of opposing muscle groups, such as flexion and extension or pronation and supination. Emotion, change in posture, or intended movement may accentuate or induce the abnormal movements. Athetosis is most apparent during reaching, as the fingers extend and abduct. Primitive reflexes often are retained. Oropharyngeal difficulties may result from facial grimacing. Chorea Chorea consists of rapid, irregular, unpredictable contractions of individual muscles or small muscle groups that involve the face, bulbar muscles, proximal extremities, and fingers and toes. Stress, excitement, or fever may exacerbate the chorea. In some cases, fever may result in ballismus, a form of severe, coarse chorea [31]. Dystonia The second category of dyskinetic CP is characterized by dystonia, although tension and persistent neonatal reflex patterns often occur. Dystonia consists of repetitive, patterned, twisting, and sustained movements of the trunk and limbs that may be either slow or rapid. Affected patients usually are severely disabled in all four limbs, the trunk, and pharyngeal muscles. The presentation of dyskinetic CP is variable. The muscle tone typically is normal or hypotonic, especially in early childhood. Infants tend to have retention of primitive reflexes, involuntary grimacing, a tendency to drool, and delayed psychomotor development. The involuntary movements evolve with time and may not be apparent until the child is two to three years of age. Unlike spastic CP, contractures usually do not develop, unless they are positional. If hypertonus develops, it is the "tension" type. Tension is a sudden involuntary increase in tone that affects both flexor and extensor muscles. The limbs become stiff during attempted movement or with emotion. Tendon reflexes are normal or may be difficult to elicit. Clonus and extensor plantar responses are absent, although athetoid movements of the toes may be confusing. Tension may be reduced with relaxation or a change in posture. Patients often have more than one form of involuntary movement, and the types may overlap in some cases. The extent of dysarthria and motor and intellectual disability are variable. However, patients with the dystonic type tend to be more severely affected than those with the other dyskinetic syndromes, and also may have pyramidal signs and anarthria. Ataxic syndromes Although ataxia indicates an incoordination of cerebellar or sensory origin, ataxic CP represents a widespread disorder of motor function. Affected patients usually are born at term. The etiology of ataxic CP is heterogeneous. Most cases are caused by early prenatal events. Some cases have genetic causes. Autosomal recessive conditions include cerebellar hypoplasia, granule cell deficiency [32], and Joubert syndrome [33]. An autosomal dominant form of nonprogressive ataxia has been described [34]. Congenital hypoplasia of the cerebellum and pure ataxia occur rarely [1]. The clinical presentation of ataxic CP is variable [35]. Most patients have congenital hypotonia. Motor milestones and language skills typically are delayed. Ataxia usually improves with time. In general, associated disabilities are worse with increasing severity of motor impairment. Speech, which is related to intellectual ability, typically is slow, jerky, and explosive. The diagnosis of ataxic CP is made by exclusion, as all patients with CP have incoordination and disturbed posture. Other causes of weakness, spasticity, dystonia, or choreoathetosis should be ruled out. Ataxic CP also should be distinguished from progressive neurodegenerative disorders, which may present with some of the same features. Atonic syndromes Atonic syndromes comprise another form of CP. Although first described in 1910, atonic CP often is absent from contemporary classifications [36,37]. Affected infants usually are born at term with severe hypotonia. Many have cerebral dysgenesis, microcephaly, and

profound intellectual disability. Development is extremely delayed, and affected children never stand or walk. Typical findings that characterize other CP syndromes are absent in this disorder. Tone often remains decreased for approximately 12 to 18 months and then becomes variable and paratonic (ie, with passive movement of a joint, resistance increases proportionally to the amount of pressure applied). ASSOCIATED DISORDERS Cerebral palsy (CP) often is accompanied by other disorders of cerebral function. Associated abnormalities may affect cognition, vision, hearing, language, cortical sensation, attention, vigilance, and behavior. Some children have epilepsy, and many have disturbed gastrointestinal function and growth. Dyspraxias and agnosias may interfere with skilled tasks, regardless of the severity of motor deficit. In a child with relatively mild CP, for example, disorders of higher cortical function may interfere with activities of daily living, such as dressing or managing buttons. A systematic review of published literature estimated the following frequencies of impairment [38]: Developmental: Intellectual disability (50 percent); epilepsy (25 percent); behavior disorder (25 percent); sleep disorder (20 percent) Functional: Unable to walk (30 percent); unable to talk (25 percent); blind (10 percent); deaf (4 percent) Physical: Pain (75 percent); hip displacement (30 percent); bladder control problems (25 percent); drooling (20 percent); requiring tube feedings (7 percent) In general, children with more severe disabilities in one area also are more likely to have disabilities in other areas. Because of these risks, children with CP should undergo routine screening for intellectual, visual, auditory and speech impairment [39]. Abnormal screening results call for more detailed evaluation. Intellectual disability Intellectual disability (mental retardation) occurs in approximately 50 percent of patients with CP [38,39]. The severity of intellectual disability often correlates with the extent of motor handicap, particularly in children with spastic CP. However, there is substantial variability in cognitive ability among affected individuals. Children with spastic quadriplegia are typically the most severely affected, while cognitive function usually is better with dyskinetic CP that is mainly athetoid. (See "Intellectual disability (mental retardation) in children: Definition; causes; and diagnosis".) Language development in hemiplegia is related to cognitive ability rather than to the side of the lesion. As a group, children born at term do better with congenital than postnatally acquired hemiplegia [1]. Patients without frank intellectual disability may still have learning disabilities that can affect educational potential [40]. (See "Specific learning disabilities in children: Clinical features", section on 'Risk factors'.) Strategies for devising communication techniques, activities of daily living, and education are based on what a disabled child will understand. Psychometric assessments require time, repetition, and experience, as well as the use of a multidimensional approach that combines results from norm-, criterion-, and observation-referenced tests [41]. Psychiatric disorders Patients with CP commonly have behavioral, emotional, and/or psychiatric disorders. These may be related to the primary neurologic manifestations, including emotional lability, poor attention and vigilance, and obsessive-compulsive traits [42]. The secondary effects of dependency, frustration, and low selfesteem also may play a role. Epilepsy Epilepsy occurs in 25 to 45 percent of patients with CP [38,39]. Seizures are most common in patients with spastic quadriplegia and acquired hemiplegia, and less common in mild symmetric spastic diplegia and CP that is mainly athetoid. The onset of seizures is typically during the first two years of life. Partial seizures with secondary generalization are the most common type. Infantile spasms occur in some infants, particularly those with microcephaly and spastic

quadriplegic or atonic CP [43,44]. (See "Clinical features and diagnosis of infantile spasms".) Intellectual disability is more common in CP patients with seizures than in those without seizures, and severe intellectual disability is more likely in those with multiple seizure types. Epilepsy can impose an additional handicap when it is difficult to control, or if anticonvulsant drug doses cause sedation that further impairs learning and socialization. Visual disorders Ocular and visual disorders are common in CP [38,39,45-50]. As an example, in a study of 120 school age children with CP, the eye examination was abnormal in 80 percent, strabismus and clinically significant refractive errors each occurred in 50 percent, and amblyopia and visual field defects each occurred in 10 to 15 percent [45]. Low visual acuity may be due to cortical impairment. This was illustrated by a study of visual acuity in children with CP [48]. In 36 of 43 patients (84 percent) with low visual acuity not explained by ophthalmological examination, cerebral visual disturbance was considered a likely cause. Severe dyskinetic eye movements also can result in slow, variable, and highly inefficient visual function [49,51]. The incidence of ocular abnormalities after preterm birth is greater in children with than without CP. In one report, 558 children born before 32 weeks gestation (54 with CP) were examined at age two years [52]. Children with CP were significantly more likely to have cicatricial retinopathy of prematurity (15 versus 2 percent), cortical visual impairment (11 versus 0.2 percent), and strabismus (52 versus 8 percent). The rate of refractive error without other ocular abnormalities was similar in the two groups. Speech impairment Disorders of speech and language, including aphasia and dysarthria, occur in about 40 to 50 percent of children with CP, and about 25 percent are nonverbal [38,39,53]. Abnormal function of oropharyngeal muscles and lack of coordination of breathing patterns contribute to speech disorders in some patients. Hearing impairment and intellectual disability may also play a role. Hearing impairment Hearing impairment occurs in 10 to 20 percent of children with CP and about 5 percent are deaf [38,39]. It is most common in those with very low birthweight or severe hypoxic-ischemic insults. In a series of 75 children with spastic CP, brainstem auditory evoked potentials were abnormal in 23 percent [54]. Sensorineural hearing loss is also a feature of CP caused by kernicterus, which also includes choreoathetosis. Early diagnosis and treatment of hearing loss in infants at risk may improve learning and language development. (See "Screening the newborn for hearing loss" and "Evaluation of hearing impairment in children" and "Epidemiology and etiology of cerebral palsy", section on 'Kernicterus'.) Growth failure Patients with CP often have growth failure, which is primarily due to poor nutrition. In one report, 23 percent of 154 children ages 2 to 17 years with diplegic or hemiplegic CP had stunted growth [55]. Linear growth was significantly reduced compared to healthy children. Approximately 30 percent of the patients were poorly nourished, as indicated by reduced body weight or diminished triceps skinfold measurement. Findings were similar in children with quadriplegic CP [56]. Poor nutritional status is caused by both inadequate intake and gastrointestinal abnormalities [55-59]. More than 90 percent of patients may have clinically significant gastrointestinal symptoms [59]. These include swallowing disorders, chronic constipation, regurgitation and/or vomiting, chronic aspiration, and abdominal pain which, in one series, occurred in 60, 74, 32, 41, and 32 percent of patients, respectively [59]. Gastroesophageal reflux also contributes to dental abnormalities, such as tooth erosion [60]. Non-nutritional factors also affect growth in CP. In one report, growth was assessed on each side of the body in 20 children with hemiplegic CP who had normal stature and triceps skinfold measurements [61]. Measurements of length, breadth, and circumference were smaller on the affected side. Factors related to this differential growth are poorly understood. Pulmonary disease Chronic pulmonary disease is a leading cause of death among patients with severe CP [62]. In these patients, pulmonary disease typically is caused by recurrent aspiration due to gastroesophageal

reflux and palatopharyngeal incoordination, or restrictive disease related to scoliosis. Gastrostomy feeding reduces aspiration during swallowing, but does not address aspiration of oral secretions, and may exacerbate gastroesophageal reflux. (See "Management and prognosis of cerebral palsy", section on 'Survival' and "Management and prognosis of cerebral palsy", section on 'Feeding disorders'.) The respiratory problems may be exacerbated by poor coordination of respiratory muscles and chest deformity. Orthopedic disorders Orthopedic disorders common in children with CP include subluxation, dislocation, and progressive dysplasia of the hip, foot deformities, and scoliosis [63,64]. These may require orthotics, postural management, and/or surgical intervention. Adults with CP frequently report back, neck, and joint pain [65]. (See "Management and prognosis of cerebral palsy", section on 'Orthopedic interventions'.) Osteopenia Multiple factors contribute to the development of osteopenia in patients with CP, including lack of mobility, feeding dysfunction, nutritional deficiency, and antiepileptic drug use, and can result in frequent fractures [66-69]. More than 70 percent of children with moderate to severe CP have reduced bone mineral density in the femur [69]. Osteopenia in children with CP appears to be related to a diminished rate of bone growth rather than bone loss [70]. Treatment with high doses of intravenous pamidronate for 12 months increased bone mineral density in a small randomized trial [71]. Lower doses also appeared to be effective in an open label trial [72]. A systematic review concluded that there is weak evidence that bisphosphonates reduce fracture rates, and there are some concerns that pamidronate and other bisphosphonates may make bones more brittle, and information about long-term risks of these drugs is lacking [73]. Therefore, these drugs are generally reserved for pediatric patients with severe reductions in bone mineral density and pathological extremity fractures or vertebral compression. Weight-bearing regimens and supplementation of calcium and vitamin D have shown some merit, but the evidence is limited [68,7376]. Urinary disorders Thirty to 60 percent of children with CP have dysfunctional voiding symptoms, including enuresis, frequency, urgency, and stress incontinence [77-79]. Symptomatic neurogenic bladder and incontinence is most common in individuals with bilateral CP [79]. Continence often improves with age, but may relapse as the neurogenic bladder dysfunction progresses [78-80]. Children with incontinence have difficulty sensing bladder fullness and tend to have lower bladder capacity [81]. The dysfunction is caused by urodynamic abnormalities, such as bladder hyperreflexia, detrusor sphincter dyssynergia, bladder hypertonia with leakage, and periodic relaxation of the distal sphincter during filling [77]. Other contributing factors can include reduced mobility and communication, poor cognition, low expectations of caregivers, and neurogenic dysfunction [82]. Urinary infection and vesicoureteral reflux are not common in children with CP. Most children have normal storage pressures as measured by urodynamic testing, and the kidneys and bladder wall thickness are usually normal on ultrasonographic imaging [78]. In a series of patients with CP undergoing urodynamic testing, the following disorders were seen [77]: Upper motor neuron lesion, with detrusor overactivity (86 percent) Mixed upper and lower motor neuron lesion (9 percent) Incomplete lower motor neuron lesion (2 percent) No urodynamic lesion (3 percent) Children with milder forms of CP (ie, without significant limb spasticity) are also prone to detrusor overactivity, leading to urgency and/or daytime and nighttime incontinence [83]. The approach to CP patients with urinary incontinence is similar to that of patients without CP. The treatment of choice for detrusor overactivity is anticholinergic medication. However, this must be done judiciously, with careful monitoring of residual urine to prevent the development of retention (see "Management of bladder dysfunction in children", section on 'Anticholinergic agents'). For children with CP who have features of a neurogenic bladder, management depends on whether the bladder is underactive or overactive, and may include anticholinergic

medication, alterations of the toileting schedule or environment, and/or clean intermittent catheterization [79]. The management of these patients is similar to that in patients with myelomeningocele. (See "Urinary tract complications of myelomeningocele (spina bifida)".) NEUROLOGIC DETERIORATION Although the primary lesion in cerebral palsy (CP) is static, neurologic signs may change or worsen with increasing age. In some cases, neurologic deterioration is due to cervical spondylotic myelopathy resulting from exaggerated neck flexion or extension [84,85]. Dystonia and other progressive movement disorders (eg, tremor, parkinsonism, myoclonus, chorea) may develop in patients with CP [86-88]. In one report of patients with static brain injury beginning at birth or during infancy, the onset of movement disorder occurred at an average of 26 years of age [86]. The latency period was shorter in patients who sustained later insults. The mechanism is uncertain, although it may be related to continuing aberrant development of the nervous system [88]. Dystonic reactions also may occur in brain-damaged children following ingestion of carbamazepine or phenytoin [89,90]. INFORMATION FOR PATIENTS UpToDate offers two types of patient education materials, The Basics and Beyond the Basics. The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon. Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on patient info and the keyword(s) of interest.) Basics topics (see "Patient information: Cerebral palsy (The Basics)") SUMMARY The cerebral palsy (CP) syndromes are characterized by abnormalities of motor activity and posture. In affected patients, a voluntary movement that should be complex, coordinated, and varied is instead uncoordinated, stereotypic, and limited. Classification of CP syndromes is based upon the type of motor abnormalities (spastic, dyskinetic, or ataxic) and their distribution (table 1). There may be substantial overlap among the clinical features. Spastic CP is an upper motor neuron syndrome, which includes spastic hypertonia, hyperreflexia, extensor plantar responses, and clonus. Affected patients also have slow effortful voluntary movements, impaired finemotor function, difficulty in isolating individual movements, and fatigability. (See 'Spastic syndromes' above.) Dyskinetic CP typically affects term infants and usually results from severe, acute perinatal asphyxia. The neonatal presentation includes encephalopathy characterized by lethargy, decreased spontaneous movement, hypotonia, and suppressed primitive reflexes. Affected individuals later develop involuntary movements of athetosis, chorea, and dystonia. (See 'Dyskinetic syndromes' above.) Ataxic CP is characterized by ataxic movements and speech, usually associated with widespread disorders of motor function. It has multiple causes, including early prenatal events and genetic defects. The diagnosis of ataxic CP is made by exclusion, and other causes of weakness, spasticity, dystonia, or choreoathetosis should be ruled out, including progressive neurodegenerative disorders. (See 'Ataxic syndromes' above.) CP often is accompanied by other disorders of cerebral function, including intellectual disability or specific learning disabilities, behavioral and emotional disorders, seizures and impaired vision and speech.

Secondary consequences of CP may include poor growth and nutrition, orthopedic problems (eg, joint subluxations and dislocations and hip dysplasia), osteopenia, and urinary disorders. (See 'Associated disorders' above.)

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GRAPHICS
Cerebral palsy syndromes
Spastic
Diplegia
Good hand funtion Poor hand function Asymmetric

Hemiplegia
Arm involved more than leg Leg involved as much as or more than arm

Quadriplegia

Dyskinetic
Mainly dystonic Mainly athetoid

Ataxia
Simple ataxia Ataxic diplegia Reproduced with permission from: Miller G. Cerebral palsies. In: Static Encephalopathies of Infancy and Childhood, Miller G, Ramer JC (Eds), Raven, New York 1992. Copyright 1992 Lippincott Williams & Wilkins.

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