Cerebral palsy: Evaluation and diagnosis

INTRODUCTION — Cerebral palsy (CP) refers to a heterogeneous group of conditions involving permanent motor dysfunction that affects muscle tone, posture, and/or movement. These conditions are due to abnormalities of the developing fetal or infant brain resulting from a variety of nonprogressive causes. Although the disorder itself is not neurodegenerative, the clinical expression may change over time as the central nervous system matures. The motor impairment results in limitations in functional abilities and activity, which can vary in severity. Multiple additional symptoms often accompany the primary motor abnormalities, including altered sensation or perception, intellectual disability, communication and behavioral difficulties, seizures, and musculoskeletal complications [1].

The evaluation and diagnosis of CP are discussed here. The epidemiology, etiologies, classification, clinical features, management, and prevention of CP are discussed separately:

●(See "Cerebral palsy: Epidemiology, etiology, and prevention".)

●(See "Cerebral palsy: Classification and clinical features".)

●(See "Cerebral palsy: Overview of management and prognosis".)

●(See "Cerebral palsy: Treatment of spasticity, dystonia, and associated orthopedic issues".)

DIAGNOSIS — The diagnosis of CP is made clinically in children with permanent, nonprogressive motor dysfunction due to abnormalities in the developing brain. A diagnostic assessment of CP incorporates pre- and postnatal history, physical examination (muscle tone, posture, coordination, upper motor neuron signs), and ancillary testing (imaging, laboratory studies). There is no single test that confirms or excludes CP.

A definitive diagnosis of CP generally requires serial examinations. Key features in the diagnosis of CP include the following [1]:

●Abnormal motor development and posture

●Brain injury is permanent and nonprogressive

●Motor impairment is attributed to an insult that occurred in the developing fetal or infant brain

●Motor impairment results in limitations in functional abilities and activity

●Motor impairment is often accompanied by secondary musculoskeletal problems, epilepsy, and/or disturbances of sensation, perception, cognition, communication, and behavior

The diagnosis should not be based upon an isolated abnormality. Infants with mild hypertonia or hyperreflexia who otherwise have normal functional development should be observed. If the abnormality remains isolated, it will resolve in most cases after the child reaches nine months of age.

OUR APPROACH — For infants and children with risk factors for CP and/or evidence on examination of impairment in motor functioning, we perform a comprehensive clinical and diagnostic evaluation. Serial examinations are used to confirm initial findings and identify any new features. Diagnostic testing is performed to identify the underlying cause and to exclude alternative etiologies (algorithm 1).

Early screening — We suggest screening for CP as soon as risk factors or clinical findings are identified, in agreement with international consensus statements [2]. Clues to an early diagnosis include abnormal behavior (eg, excessive docility or irritability), abnormal tone, abnormal posture, persistence of primitive reflexes, and failure to achieve motor milestones (table 1A). Early signs of CP differ somewhat based upon the CP subtype (table 2). In many cases, spasticity may not be identified until six months of age. Dyskinetic patterns are often not apparent until approximately 18 months. Ataxia may not become obvious until even later. (See "Cerebral palsy: Classification and clinical features", section on 'Early signs of cerebral palsy'.)

Although historical precedent has been to make a CP diagnosis between 12 and 24 months, the diagnosis can be made at even <6 months of age in children with neonatal risk factors, suggestive brain imaging, and suggestive features on a standardized neurologic examination [3]. Early diagnosis is often critical for establishing access to targeted therapy services, which are often most effective when instituted early [4]. The provision of an early diagnosis can be a disease-modifying intervention for some children and their families. Families often suspect a CP diagnosis long before it is given, and some studies report they wish that a CP diagnosis was provided sooner [5,6].

It is important to reconfirm the CP diagnosis as the child ages, particularly with early CP diagnosis. There are certain motor phenotypic, imaging, and history features that make it more likely for a child to have a progressive or neurodegenerative CP "mimic" as opposed to a true CP diagnosis, even if the child meets criteria for a CP diagnosis early in life [7-9]. (See 'Findings suggesting an alternative diagnosis' below.)

The specific CP subtypes are best recognized after five years of age (table 2). The clinical features of these syndromes are discussed in more detail separately. (See "Cerebral palsy: Classification and clinical features".)

Clinical assessment — Early diagnosis of CP begins with a detailed medical history and physical examination and involves standardized assessments of neurologic and motor development [3]. The initial assessment may lead to further diagnostic evaluation, which typically includes neuroimaging and laboratory testing.

The goals of the history and physical examination are to:

●Identify the clinical features and suspected classification of the type of CP (table 2), which may provide clues as to the underlying etiology and have implications regarding the likelihood of associated conditions.

●Rule out clinical suspicion of a progressive or neurodegenerative condition. (See 'Findings suggesting an alternative diagnosis' below.)

●Establish treatment goals and priorities. (See "Cerebral palsy: Overview of management and prognosis", section on 'Treatment goals'.)

Birth and family history — The evaluation of children with suspected CP begins with a detailed history, which should include assessment of the following elements:

●Prenatal and birth history, which can identify risk factors for CP (table 3) (see "Cerebral palsy: Epidemiology, etiology, and prevention", section on 'Specific causes and risk factors')

●Newborn screening results, including newborn hearing test results and ophthalmologic evaluation if the child was in the neonatal intensive care unit (NICU) (see "Overview of newborn screening")

●Family history – Relatives with any of the following should raise suspicion for a genetic cause of CP [10]:

•Intellectual disability/developmental disabilities

•Seizures

•CP

•Neuromotor/movement disorders

•Neurobehavioral disorders

•Joint contractures/stiffness

•Thromboses/vascular accidents

•Congenital anomalies

•Infertility

•Recurrent miscarriages

•Stillbirths

•Adult-onset neurodegenerative conditions

Examination and developmental assessment — Standardized assessments of neurologic and motor development are key to early recognition and accurate diagnosis of CP. A comprehensive general physical and neurologic examination should include the following elements:

●Assessment of growth (see "Normal growth patterns in infants and prepubertal children")

●Evaluation of motor tone, posture, and coordination (see "Cerebral palsy: Classification and clinical features", section on 'Motor tone and posture abnormalities')

●Assessment of motor development (table 1A-B) [11] (see "Cerebral palsy: Classification and clinical features", section on 'Developmental reflex changes' and "Cerebral palsy: Classification and clinical features", section on 'Motor milestone delays')

●Screening for attention, behavioral, communication, and/or cognitive concerns (see "Cerebral palsy: Classification and clinical features", section on 'Associated conditions')

●Evaluation of overall functional status and any limitations in functional abilities using a standard measurement such as the Gross Motor Functional Classification System (see "Cerebral palsy: Classification and clinical features", section on 'Functional classification systems')

Assessment begins with routine developmental screening performed by the primary care clinician. Infants and children with risk factors for CP and/or abnormal findings on surveillance screening should subsequently be referred to a specialist such as a child neurologist or developmental-behavioral pediatrician for more detailed evaluation. Standardized assessments such as Hammersmith infant neurological examination (HINE), Prechtl general movements assessment (GMA), and the developmental assessment of young children (DAYC) tools assess the quality of spontaneous movements in early infancy [12,13]. These tests perform well in predicting the risk of CP in young infants, with >85 to 90 percent sensitivity in most reports [3,12-14]. The GMA has a high sensitivity even when performed before the age of five months [14]. The sensitivity of these instruments is increased by using multiple assessment tools in combination with neuroimaging. (See 'Neuroimaging' below.)

Findings suggesting an alternative diagnosis — Some conditions, especially those that are slowly progressive, may be misdiagnosed as CP [15]. It is important to differentiate these progressive conditions which may appear like CP in early life (so-called CP mimics) from genetic contributors to true CP, which may be present in up to 30 percent of individuals with CP [16,17]. (See 'Differential diagnosis' below.)

The following features raise the possibility of a diagnosis other than CP, such as a neurodegenerative disease, genetic disorder, or metabolic condition [7,15,17-19]:

●Loss of previously acquired developmental milestones or skills

●Progressive symptoms

●Muscle atrophy or sensory loss

●Dysmorphic clinical features

●Early-life (eg, during infancy) presence of extrapyramidal symptoms including ataxia, choreoathetosis, or dystonia

●Marked worsening during periods of catabolism (fasting or illness)

●History of term birth

●Family history of childhood neurologic disorder or of consanguinity

●Normal brain magnetic resonance imaging (MRI) (see 'Neuroimaging' below)

Of note, the extrapyramidal symptoms of less common forms of CP such as ataxic or dyskinetic subtypes may become apparent as the child grows and development progresses. Hypotonia and other motor symptoms may be identified during infancy. (See "Cerebral palsy: Classification and clinical features", section on 'Patterns of motor impairment'.)

Diagnostic testing — While the diagnosis of CP is made clinically and no specific test confirms or excludes the diagnosis of CP, a diagnostic evaluation should be performed in all children with CP to identify the underlying cause of CP when possible and to exclude other conditions. We obtain neuroimaging for all patients and perform laboratory testing based on clinical and historic features (algorithm 1).

Neuroimaging — We suggest neuroimaging for all patients with suspected CP to help identify underlying etiology and exclude alternative conditions. Repeat imaging may be warranted for infants and children when neuroimaging performed in the neonatal period did not establish an etiology. MRI without contrast is preferred over computed tomography (CT) because it generally has a higher diagnostic yield in determining the etiology and does not expose the patient to radiation.

●MRI findings – Brain MRI is abnormal in 85 to 90 percent of children with CP [20,21]. The diagnostic yield depends upon the CP phenotype (mixed > quadriplegic > hemiplegic > diplegic > ataxic > dyskinetic) and the timing of birth (preterm > term infants). MRI may also help identify the timing of a causal brain injury if performed during the acute setting. For some patients, this can help determine whether the injury was prenatal, perinatal, or postnatal in onset.

Several MRI abnormalities may be found in patients with CP. These include:

•Periventricular leukomalacia from hypoxic ischemic injury (see "Clinical features, diagnosis, and treatment of neonatal encephalopathy", section on 'Neuroimaging')

•Cortical malformations (eg, lissencephaly, schizencephaly, or pachygyria) (see "Overview of neonatal brain malformations of the cortex")

•Ischemic or hemorrhagic stroke (see "Stroke in the newborn: Classification, manifestations, and diagnosis", section on 'Evaluation and diagnosis')

•Lesions of the basal ganglia (eg, T2 hyperintensities associated with chronic bilirubin encephalopathy)

In a systematic review of six studies including a total of 388 children with spastic or dyskinetic CP, 86 percent had abnormal MRI findings [20]. Periventricular white matter lesions were the most common findings (56 percent) and were seen predominantly in preterm children. Other abnormalities included cortical and deep grey matter lesions (18 percent) and brain malformations or maldevelopments (10 percent), which occurred more often in term children. In a study of 174 infants born at term who had brain MRI for neonatal encephalopathy, the risk of moderate to severe CP was 67 percent (95% CI 36-98) for children with a brain injury pattern on imaging that involved the basal ganglia and thalamus [22]. In another study of 85 infants with neonatal arterial stroke, gray and white matter regions involved in the primary motor pathways were associated with the subsequent diagnosis of CP at a median 2.1 years of age [23].

●Timing of imaging – Early imaging at the time of initial assessment is warranted in severely affected children (eg, considerable motor asymmetry) and those with progressive symptoms or signs.

For children with milder clinical findings, we typically delay imaging until approximately two years of age to increase diagnostic yield for subtle findings that may be missed on imaging performed before completion of cerebral myelination.

MRI should be repeated if there is a significant change or deviation from the expected clinical course or if there are red flags for a progressive neurologic disorder, such as loss of a previously acquired developmental milestone [18].

●Other imaging modalities

•Head CT may be performed as a less sensitive alternative to MRI. CT-based imaging may be more readily available and quicker to perform than MRI in some facilities but involves radiation exposure. Head CT is typically reserved for patients with acute symptoms requiring urgent imaging, such as those with intracranial hemorrhage.

•Cranial ultrasound is a neuroimaging modality that is typically performed in neonates and young infants who have an open anterior fontanel. Some patients presenting for evaluation of suspected CP may be beyond the age where this study can be performed. However, review of prior cranial ultrasounds performed in early infancy (eg, during a NICU stay) can provide helpful information. Ultrasonography can identify hemorrhage, periventricular leukomalacia, and hydrocephalus, but it is not sensitive for white matter injury. For most children with suspected CP, abnormal findings on a cranial ultrasound should generally be followed up with brain MRI for better characterization.

Metabolic and genetic testing — We suggest laboratory testing for infants and children with suspected CP when clinical assessment is suggestive of an underlying infectious, metabolic, or genetic etiology. As an example, children born to mothers who had a varicella infection during gestation warrant evaluation for varicella-zoster virus.

In addition, laboratory testing is warranted when neuroimaging evaluation is suggestive of a specific underlying condition (eg, genetic testing for microdeletion syndromes may be warranted when brain MRI shows lissencephaly) or is nondiagnostic.

●Testing for prenatal or perinatal infections – Several infections that may be acquired in utero or during the birth process can cause morbidity, including developmental anomalies. They may be called TORCH (toxoplasmosis, others [syphilis, Zika virus, varicella-zoster virus], rubella, cytomegalovirus [CMV], and herpes simplex virus) infections, an acronym specifying several such conditions (table 4). Laboratory evaluation is required for infants and children with suspected congenital or perinatal infection based on birth history, examination, or imaging.

TORCH infections are discussed in detail separately. (See "Overview of TORCH infections".)

●Genetic and metabolic testing – Several metabolic or genetic disorders may present with symptoms resembling CP (table 5). Identification of an underlying metabolic disorder is imperative as treatment and interventions often differ from typical management strategies for CP. Identification of a genetic etiology may have implications for family planning both for the patient and for close relatives [24-26].

Metabolic and genetic testing is warranted when:

•Symptoms are atypical for CP or otherwise suggestive of a genetic or metabolic condition (see 'Findings suggesting an alternative diagnosis' above)

•Perinatal history and clinical examination do not identify an etiology

•Abnormal neuroimaging is of uncertain etiology (eg, a brain malformation or injury)

Initial laboratory testing for metabolic diseases includes glucose, creatine kinase, ammonia, lactate, and pyruvate; plasma amino acid analysis; urine organic acid analysis; and measurement of acid-base status (with blood gas or serum bicarbonate level) (table 6). Additional testing for specific disorders is discussed separately. (See "Inborn errors of metabolism: Identifying the specific disorder".)

Genetic testing may involve analysis of targeted gene panels, exome sequencing, or whole-genome sequencing. Genetic disorders were historically thought to be uncommon causes of CP, but studies using next-generation sequencing techniques have detected potentially disease-causing genetic variants in as many as one-third of CP patients who lack an otherwise identified etiology [10,19,24,27,28]. (See "Cerebral palsy: Epidemiology, etiology, and prevention", section on 'Genetic susceptibility'.)

The approach to genetic testing is based on the individual's presentation, clinical findings, and family history. When genetic testing is warranted, it is valuable to undertake it with a clinician with genetics expertise and a genetics counselor. (See "Genetic testing".)

●Other laboratory testing – Thrombophilia testing (table 7) may be appropriate for select children with hemiplegic CP or MRI evidence of cerebral infarction. Perinatal stroke (either known or presumed) is the most common cause of hemiplegic CP, and thrombophilia testing is generally not necessary for most affected patients since it provides little added prognostic or therapeutic value in this setting. However, testing may be reasonable if there is a strong family history of thrombotic disease. Thrombophilia testing in the setting of perinatal stroke is discussed in greater detail separately. (See "Stroke in the newborn: Classification, manifestations, and diagnosis", section on 'Coagulation testing'.)

By contrast, thrombophilia testing is generally warranted for evaluation of ischemic stroke occurring outside of the perinatal period. This accounts for a small minority of patients with hemiplegic CP. Evaluation of ischemic stroke in children is discussed separately. (See "Ischemic stroke in children: Clinical presentation, evaluation, and diagnosis", section on 'Hypercoagulable evaluation'.)

The general approach to thrombophilia testing in children is discussed in greater detail separately. (See "Thrombophilia testing in children and adolescents".)

Other tests — Additional testing that may be useful in select circumstances includes:

●Lumbar puncture – Lumbar puncture is not routinely performed for the evaluation of most children with CP. Increased availability of genetic testing has greatly reduced the need for cerebrospinal fluid studies. Lumbar puncture may occasionally be warranted to evaluate for rare causes of seizure disorders (eg, glucose transporter [GLUT1] deficiency) or movement disorders (eg, dopa-responsive dystonia) based upon the clinical findings. These issues are discussed separately. (See "Seizures and epilepsy in children: Clinical and laboratory diagnosis", section on 'Laboratory and genetic testing in undiagnosed epilepsy' and "Etiology, clinical features, and diagnostic evaluation of dystonia", section on 'Dopa-responsive dystonia'.)

●Examination of the placenta – Clinical and pathologic examination of the placenta, if performed at birth, can provide clues to the etiology of CP. It may indicate infection or chronic pathologic changes due to ischemia [29]. Pathologic findings associated with asphyxia include chronic ischemic change, meconium staining, nucleated red blood cells, intravillous hemorrhages, and chronic ischemic changes [30].

●Electroencephalogram – Electroencephalogram (EEG) is performed if seizure activity is suspected. Seizures may occur as a CP mimic, as in some neurodegenerative conditions, or as an associated condition in some children with CP. (See "Overview of infantile epilepsy syndromes" and 'Epilepsy' below.)

DIFFERENTIAL DIAGNOSIS — Typical symptoms and signs of CP may be present in many other conditions (eg, early hypotonia, spasticity, and dystonia and/or choreoathetosis). These include neurodegenerative diseases, conditions associated with inborn errors of metabolism (table 5), developmental or traumatic lesions of the brain or spinal cord, neuromuscular or movement disorders, and neoplasm [15]. Neuroimaging, laboratory studies, and the clinical course distinguish these conditions from CP. They may be categorized by the predominating clinical feature:

●Muscle weakness – Hypotonia and muscle weakness may be present in many conditions. In infants with muscular dystrophy or myopathy, muscle weakness may be mistaken for hypotonia, which often occurs in infants with CP. In most cases of CP, the degree of hypotonia exceeds or is equivalent to the degree of muscle weakness, whereas muscle weakness is more prominent in children with myopathies. The diagnostic approach to infants with hypotonia and weakness is discussed separately. (See "Approach to the infant with hypotonia and weakness".)

●Spastic diplegia or quadriplegia – Spasticity common among individuals with CP may also occur in urea cycle disorders, leukodystrophies, and other neurodegenerative disorders. These disorders may be distinguished from CP based upon their progressive clinical course, through metabolic and genetic testing, or imaging features on MRI of the brain. (See "Urea cycle disorders: Clinical features and diagnosis" and "Clinical features, evaluation, and diagnosis of X-linked adrenoleukodystrophy" and "Hereditary spastic paraplegia".)

●Dystonia and choreoathetosis – Dystonia and choreoathetosis are prominent features in a number of genetic and metabolic syndromes but can also been seen in patients with CP if there is injury to the basal ganglia or cerebellum. Acquired causes resulting in CP include acute rheumatic fever, cardiac bypass, and kernicterus. The diagnostic approach to hyperkinetic movement disorders is discussed separately. (See "Hyperkinetic movement disorders in children".)

●Ataxia – Ataxic CP is rare and should be distinguished from progressive neurodegenerative disorders. Hereditary causes of ataxia are discussed separately. (See "Overview of the hereditary ataxias".)

ASSESSING FOR ASSOCIATED CONDITIONS — Children with CP may have motor and nonmotor dysfunction depending on underlying causes. All children with CP should be evaluated for other conditions associated with CP [31] (see "Cerebral palsy: Classification and clinical features", section on 'Associated conditions'):

Learning disorders and intellectual disability — Intellectual disability occurs in approximately 50 percent of patients with CP. Infants and children with CP should undergo developmental surveillance at every well-child visit using standardized screening tools. If cognitive and/or adaptive delays are identified, further developmental testing may be indicated. (See "Intellectual disability (ID) in children: Clinical features, evaluation, and diagnosis" and "Developmental-behavioral surveillance and screening in primary care", section on 'Approach to surveillance'.)

Behavioral and psychiatric conditions — Children with CP may have behavioral dysfunction and/or psychiatric conditions such as anxiety, depression, and obsessive-compulsive traits. Attention-deficit hyperactivity disorder may be identified in school-aged children with CP. (See "Anxiety disorders in children and adolescents: Epidemiology, pathogenesis, clinical manifestations, and course" and "Pediatric unipolar depression: Epidemiology, clinical features, assessment, and diagnosis" and "Attention deficit hyperactivity disorder in adults: Epidemiology, clinical features, assessment, and diagnosis".)

Epilepsy — Seizures occur in approximately 45 percent of children with CP. Children with CP and suspected seizure activity should undergo electroencephalogram (EEG) to diagnose and manage the epilepsy. However, there is no clinical value of performing EEG testing in children with no evidence of seizure activity, and EEG testing is not useful in establishing the cause of CP. (See "Seizures and epilepsy in children: Clinical and laboratory diagnosis" and "Cerebral palsy: Classification and clinical features", section on 'Epilepsy'.)

Vision impairment — Strabismus, refractory errors, and other vision disorders are common in children with CP, occurring in 30 to 50 percent. The risk is greater in preterm infants. Assessing for vision problems in children with CP should begin in infancy (table 8). (See "Vision screening and assessment in infants and children", section on 'Vision assessment in children with special health care needs'.)

Speech and language impairment — Disorders of speech and language, including aphasia and dysarthria, occur in approximately 40 to 50 percent of children with CP, and approximately 25 percent are nonverbal. Assessing for speech and language problems involves obtaining a history of speech development from the parent or caregiver and directly observing the child to assess the precursors of speech and language development (table 9), adequacy of speech and language, nonverbal cognition, and social interaction. If concerns are raised through this assessment, the child should be referred for formal speech and language evaluation. (See "Evaluation and treatment of speech and language disorders in children".)

Hearing impairment — Hearing impairment occurs in 10 to 20 percent of children with CP, and approximately 5 percent are deaf. All infants should be assessed for hearing loss in the newborn period. In addition to newborn screening, children with CP should have at least one formal audiologic assessment by 24 to 30 months of age or sooner if concerns are raised in the history and clinical assessment. (See "Screening the newborn for hearing loss" and "Hearing loss in children: Screening and evaluation".)

Nutrition and growth — Patients with CP often have growth failure, which is primarily due to poor nutrition. Growth should be monitored closely in children with CP. Those with milder CP may have normal growth, while those with more severe motor impairment often have growth failure [32]. Frequently, this correlates with inadequate nutritional intake, which can be multifactorial in etiology. Children with quadriplegic CP are at increased risk for poor growth compared with those with diplegic or hemiplegic CP [33].

Growth charts specific to CP have been developed that use weight-for-age (not weight-for-height) to measure nutritional status [34]. Separate growth charts are used in each of five levels of CP severity (as defined by the Gross Motor Function Classification System [GMFCS]) to define a weight threshold below which the child has an increased risk of morbidity and mortality. Patients who fail to maintain weight-for-age growth trajectories and those with weights below the threshold for their GMFCS should undergo a nutritional evaluation, including assessment of caloric intake and exploration of alternative explanations for low body weight, such as growth hormone deficiency or familial short stature. If undernutrition is confirmed, concerted efforts should be made to boost nutrition through oral supplements or enteral feeds with the guidance of a dietician who has expertise in children with CP. (See "Cerebral palsy: Overview of management and prognosis", section on 'Growth and nutrition'.)

Gastrointestinal disorders — Growth failure in children with CP may be due to other gastrointestinal disorders common among children with CP. These include chronic constipation, gastroesophageal reflux, or chronic abdominal pain. Diagnostic testing may be guided by specific gastrointestinal symptoms. (See "Constipation in infants and children: Evaluation" and "Gastroesophageal reflux in infants" and "Clinical manifestations and diagnosis of gastroesophageal reflux disease in children and adolescents" and "Chronic abdominal pain in children and adolescents: Approach to the evaluation".)

Pulmonary disease — Chronic aspiration is common in many children with CP. Symptoms may be due to oropharyngeal dysphagia, sialorrhea, or gastroesophageal reflux. (See "Aspiration due to swallowing dysfunction in children" and "Cerebral palsy: Overview of management and prognosis", section on 'Sialorrhea' and "Gastroesophageal reflux in infants" and "Clinical manifestations and diagnosis of gastroesophageal reflux disease in children and adolescents".)

Orthopedic disorders — Motor dysfunction in CP can contribute to several orthopedic conditions such as contractures, hip dysplasia, and scoliosis. Orthopedic conditions may also lead to acute and chronic pain. Routine surveillance is warranted for early identification and treatment. (See "Cerebral palsy: Treatment of spasticity, dystonia, and associated orthopedic issues".)

Sleep disorders — Motor dysfunction may lead to sleep disorders in children with CP due to multiple causes including pulmonary disorders, visual impairment, muscle weakness, and behavioral conditions. These issues may be more prominent in children with severe CP. Sleep quality and underlying causes should be assessed during routine clinical evaluations. (See "Assessment of sleep disorders in children".)

Urinary control — More than half of children with CP may have bladder control issues, such as enuresis, frequency, urgency, or stress incontinence. Children with severe CP may have vesicoureteral reflux and recurrent lower urinary infections. Assessing for urinary control issues is warranted during clinical evaluations. (See "Cerebral palsy: Overview of management and prognosis", section on 'Urinary control'.)

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Cerebral palsy".)

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 5^th to 6^th 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 10^th to 12^th 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 education: Cerebral palsy (The Basics)")

SUMMARY AND RECOMMENDATIONS

●Diagnosis – The diagnosis of CP is made clinically in children with permanent, nonprogressive motor dysfunction due to abnormalities in the developing brain. A diagnostic assessment of CP incorporates pre- and postnatal history, physical examination (muscle tone, posture, coordination, upper motor neuron signs), and ancillary testing (imaging, laboratory studies). There is no test that confirms or excludes CP. (See 'Diagnosis' above.)

For infants and children with risk factors for CP and/or evidence on examination of impairment in motor functioning, we perform a comprehensive clinical and diagnostic evaluation. Serial examinations are used to confirm initial findings and identify any new features. Diagnostic testing is performed to identify the underlying cause and to exclude alternative etiologies (algorithm 1). (See 'Our approach' above.)

•Clinical assessment – Early diagnosis of CP begins with a detailed birth and family history to identify risk factors for CP (table 3) and physical examination and involves standardized assessments of neurologic and motor development (table 1A). (See 'Clinical assessment' above.)

•Neuroimaging – We suggest neuroimaging for all patients with suspected CP to help identify underlying etiology and exclude alternative conditions. Repeat imaging may be warranted for infants and children when neuroimaging performed in the neonatal period did not establish an etiology. (See 'Neuroimaging' above.)

•Metabolic and genetic testing – We suggest laboratory testing for infants and children with suspected CP when clinical assessment is suggestive of an underlying infectious, metabolic, or genetic etiology (table 4 and table 5). In addition, laboratory testing is warranted when neuroimaging evaluation is suggestive of a specific underlying condition (eg, genetic testing for microdeletion syndromes may be warranted when brain MRI shows lissencephaly) or is nondiagnostic. (See 'Metabolic and genetic testing' above.)

●Differential diagnosis – Typical symptoms and signs of CP (eg, early hypotonia, spasticity, and dystonia and/or choreoathetosis) may be present in other conditions. These include neurodegenerative diseases, conditions associated with inborn errors of metabolism, developmental or traumatic lesions of the brain or spinal cord, neuromuscular or movement disorders, and neoplasm. Neuroimaging, laboratory studies, and the clinical course distinguish these conditions from CP. (See 'Differential diagnosis' above.)

●Associated conditions – Children with CP should be evaluated for other conditions that may occur with CP. These include learning disorders and intellectual disability, behavioral and psychiatric conditions, epilepsy, visual impairment, speech and/or language impairment, hearing impairment, nutrition and growth issues, gastrointestinal disorders, pulmonary disease, orthopedic disorders, sleep disorders, and urinary control disorders. (See 'Assessing for associated conditions' above.)

ACKNOWLEDGMENTS — The UpToDate editorial staff acknowledges Geoffrey Miller, MD and Laurie Glader, MD, who contributed to earlier versions of this topic review.