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 non-progressive 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, etiology, 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".)
EVALUATION — Early diagnosis of CP begins with a detailed medical history and physical examination and involves standardized assessments of neurologic and motor development [2].The initial assessment may lead to further diagnostic evaluation, which typically includes neuroimaging.
History and physical examination — The evaluation of children with suspected CP begins with a detailed history and physical examination, which should include the following elements:
●Review of prenatal and birth history, which can identify risk factors for CP (table 1) (see "Cerebral palsy: Epidemiology, etiology, and prevention", section on 'Risk factors')
●Review of the newborn screening results, including newborn hearing test results and ophthalmologic evaluation if the child was in the NICU (see "Newborn screening")
●Review of the family history – Relatives with any of the following should raise suspicion for a genetic cause of CP [3]:
•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
●Assessment of motor development (table 2A-B) [4] (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
●Evaluation of any limitations in functional abilities (see "Cerebral palsy: Overview of management and prognosis", section on 'Functional evaluation')
●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')
The goals of the history and physical examination are to:
●Identify the clinical features and suspected classification of the type of CP (table 3), 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'.)
The evaluation of a child with CP often requires serial examinations. Although CP is nonprogressive, clinical signs evolve as the nervous system matures. The diagnosis is typically made between the age of 12 to 24 months, though earlier diagnosis is becoming increasingly common [2].
Standardized developmental assessment — Standardized assessments of neurologic and motor development are key to early recognition and accurate diagnosis of CP. Assessment begins with routine developmental screening performed by the primary care provider, with subsequent referral to a specialist such as a pediatric neurologist or developmental-behavioral pediatrician for more detailed evaluation. Details of developmental screening in the primary care setting are provided separately. (See "Developmental-behavioral surveillance and screening in primary care".)
Standardized assessments such as Prechtl’s general movements assessment (GMA), Hammersmith infant neurological examination (HINE), and the developmental assessment of young children (DAYC) tools assess the quality of spontaneous movements in early infancy [5,6]. These tests perform well in predicting risk of CP in young infants, with >85 to 90 percent sensitivity in most reports [2,5-7]. The GMA has a high sensitivity even when performed before the age of five months [7]. 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 [8]. (See 'Differential diagnosis' below.)
The following features raise the possibility of a diagnosis other than CP, such as a neurodegenerative disease or metabolic disorder [8,9]:
●Absence of a known risk factor for CP (table 1) (see "Cerebral palsy: Epidemiology, etiology, and prevention", section on 'Risk factors')
●Family history of a similar neurologic condition
●Loss of previously acquired developmental milestones
●Extrapyramidal symptoms including ataxia, choreoathetosis, or dystonia (though they can also be features of dyskinetic CP)
●Muscle atrophy or sensory loss
●Weakness that is equal to or greater than the degree of hypotonia (see "Approach to the infant with hypotonia and weakness")
●Rapid deterioration of neurologic signs
●Marked worsening during periods of catabolism (fasting or illness)
Diagnostic evaluation — The diagnosis of CP is made clinically. No specific test confirms or excludes the diagnosis of CP. However, 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 (algorithm 1).
We obtain neuroimaging, typically with magnetic resonance imaging (MRI) of the brain for all children with suspected CP. (See 'Neuroimaging' below.)
Other testing is dependent on clinical and historic concerns and may include:
●Metabolic and genetic testing if there are atypical symptoms, atypical MRI findings (eg, a brain malformation or injury), or if no etiology is identified by clinical history and neuroimaging. (See 'Metabolic and genetic testing' below.)
●Electroencephalogram (EEG) if seizure activity is suspected. (See 'Seizures' below.)
●Infectious work-up (TORCH titers) if pre- or perinatal history is suggestive (table 4). (See "Overview of TORCH infections".)
●Thrombophilia testing is not necessary for most patients with known or presumed perinatal stroke; however, testing may be warranted if there is a strong family history of thrombosis or if the stroke occurred outside of the perinatal period. (See 'Other tests' below.)
These tests are described in detail below. Our recommendations are consistent with the practice parameter from the American Academy of Neurology (AAN) and the Child Neurology Society (CNS) [10].
Neuroimaging — MRI of the brain should be performed if the etiology has not yet been established (eg, by neuroimaging in the neonatal period) (algorithm 1) [10]. The timing of when to perform the MRI depends on the clinical circumstances. Early imaging is warranted in severely affected children and those with concerning findings (eg, considerable motor asymmetry). For children with subtle clinical findings, waiting until approximately two years of age to account for myelination may be a better option since subtle findings may be missed on earlier imaging. MRI should be repeated if there is a notable change or deviation from the expected clinical course or if there are red flags for a progressive neurologic disorder [9]. (See 'Findings suggesting an alternative diagnosis' above.)
MRI is preferred over computed tomography (CT) because it generally has a higher diagnostic yield and can be helpful in determining both the etiology and the timing of insult [10]. Additionally, CT exposes the developing brain to a large dose of radiation. CT can be helpful in urgent settings such as intracranial hemorrhage.
Cranial ultrasound is a neuroimaging modality that can be used 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 neonatal intensive care unit stay) can provide helpful information. Ultrasonography can identify hemorrhage, periventricular leukomalacia, and hydrocephalus, but it is not sensitive for white matter injury. In the context of evaluating a child for CP, abnormal findings on cranial ultrasound should generally be followed up with MRI.
The MRI is abnormal in 85 to 90 percent of children with CP [10,11]. The diagnostic yield depends upon the CP type and pattern (mixed > quadriplegic > hemiplegic > diplegic > ataxic > dyskinetic) and the timing of birth (scans are more often abnormal in preterm compared with term infants). MRI, in combination with the clinical history, can help determine whether the injury was prenatal, perinatal, or postnatal in onset. Timing of an injury cannot be determined by MRI alone unless obtained in the acute setting.
MRI abnormalities in patients with CP include evidence of hypoxic ischemia (eg, periventricular leukomalacia), cortical malformations, and lesions of the basal ganglia. In a systematic review of six studies including a total of 388 children with spastic or dyskinetic CP, 86 percent had abnormal MRI findings [11]. 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.
Metabolic and genetic testing — A number of metabolic disorders may present with symptoms resembling CP (table 5). Additionally, there is a growing appreciation for genetic causes of CP. 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 for the patient and close relatives [12].
Metabolic and genetic testing is appropriate in the following circumstances (algorithm 1) [10]:
●If there are features in the history or clinical examination that are atypical for CP, or otherwise suggestive of a genetic or metabolic abnormality (eg, history of progressive rather than static encephalopathy, episodes of metabolic decompensation, family history of childhood neurologic disorder associated with CP, history of consanguinity).
●If brain imaging reveals a developmental brain malformation (eg, lissencephaly, schizencephaly, or pachygyria) or frontal/temporal atrophy
●If dysmorphic features are present
●If no etiology is identified by history, physical examination, and neuroimaging
Initial laboratory testing for metabolic diseases includes serum concentrations of 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). Additional testing for specific disorders is discussed separately. (See "Inborn errors of metabolism: Identifying the specific disorder".)
The genetic evaluation in children with CP begins with a detailed family history. The approach to genetic testing is based on the individual's presentation, clinical findings, and family history. When genetic testing is warranted, it should be undertaken in consultation with a clinical geneticist. Numerous genetic disorders can present with findings of CP (table 5). 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 [3,12]. (See "Next-generation DNA sequencing (NGS): Principles and clinical applications".)
Genetic evaluation for hereditary spastic paraplegia, which is a diverse group of neurologic disorders characterized by progressive lower extremity spasticity, may also be considered. (See "Hereditary spastic paraplegia".)
Genetic susceptibility as an etiology of CP is discussed in greater detail separately. (See "Cerebral palsy: Epidemiology, etiology, and prevention", section on 'Genetic susceptibility'.)
Other tests — Additional testing that may be useful in select circumstances includes:
●Thrombophilia testing – Thrombophilia testing (table 6) 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".)
●Lumbar puncture – Lumbar puncture is not routinely necessary in 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 – In children diagnosed with CP, it can be helpful to obtain records from the birth hospitalization to determine whether the placenta underwent pathologic examination. Examination of the placenta, if performed, can provide clues to the etiology of CP. It may indicate infection or chronic pathologic changes due to ischemia. Pathologic findings associated with asphyxia include chronic ischemic change, meconium staining, nucleated red blood cells, intravillous hemorrhages, and chronic ischemic changes [13].
Screening for associated conditions — Children with CP should be evaluated for other conditions that are commonly associated with CP [14] (see "Cerebral palsy: Classification and clinical features", section on 'Associated conditions'):
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'.)
Seizures — Seizures occur in approximately 45 percent of children with CP. Children with CP and suspected seizure activity should undergo 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. Screening for vision problems in children with CP should begin in infancy (table 7). (See "Vision screening and assessment in infants and children", section on 'Vision assessment in children with special needs'.)
Hearing impairment — Hearing impairment occurs in 10 to 20 percent of children with CP, and approximately 5 percent are deaf. All infants should be screened 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".)
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. Screening 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 8), 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".)
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 [15]. 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 [16].
Growth charts specific to CP have been developed that use weight-for-age (not weight-for-height) to measure nutritional status [17]. 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'.)
DIAGNOSIS — The diagnosis of CP is made clinically, taking into account the 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. In severe cases, the diagnosis can be made soon after birth, but, for the majority, the diagnosis is established within the first two years of life [18].
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, in most cases, it will resolve progressively after the child reaches nine months of age.
A definitive diagnosis of CP generally requires serial examinations. In a study of infants at high risk for CP who had serial examinations for two years, the presence of three or more abnormal signs at eight months of age was highly predictive of CP [19]. However, CP often was missed at one month and sometimes over-diagnosed at four months.
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 2A-B). Early signs of CP differ somewhat based upon the CP subtype (table 3). 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'.)
In most cases, the diagnosis can be established by the age of two years using the above criteria. In a study using data from the Canadian CP registry that included 1683 children with a definitive or probable diagnosis of CP at two years of age, only 48 (2.9 percent) received an alternative diagnosis by age 5 years [20]. In approximately half of these cases, the alternative diagnosis was a specific metabolic or genetic syndrome. Interestingly, in 10 children (0.6 percent of the entire cohort), neuromotor abnormalities improved or resolved by the age of five years, such that they no longer met diagnostic criteria for CP. These children were more likely to be born at term, lack perinatal adversity, and have normal magnetic resonance imaging.
The specific CP subtypes are best recognized after five years of age (table 3). The clinical features of these syndromes are discussed in more detail separately. (See "Cerebral palsy: Classification and clinical features".)
DIFFERENTIAL DIAGNOSIS — CP is a diagnosis of exclusion. 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, inborn errors of metabolism (table 5), developmental or traumatic lesions of the brain or spinal cord, neuromuscular or movement disorders, and neoplasm [8]. Neuroimaging, metabolic studies, and the clinical course distinguish these conditions from CP.
Muscle weakness — In infants with muscular dystrophy or myopathy, muscle weakness may be mistaken for hypotonia, which often occurs in infants with CP. As a general rule, in children with CP, the degree of hypotonia exceeds or is equivalent to the degree of muscle weakness, whereas muscle weakness is more prominent in children with myopathy. 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 may 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 magnetic resonance imaging of the brain. (See "Urea cycle disorders: Clinical features and diagnosis" and "X-linked adrenoleukodystrophy and adrenomyeloneuropathy" 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".)
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 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 education: Cerebral palsy (The Basics)")
SUMMARY AND RECOMMENDATIONS
●Aims of the history and physical examination – A detailed history and physical examination should be performed in all children with suspected cerebral palsy (CP). The goals of the history and physical examination are to:
•Identify the clinical features of CP
•Determine that the child's condition is static rather than progressive or neurodegenerative
•Classify, when possible, the type of CP (table 3), which may provide clues as to the underlying etiology and may have implications regarding the likelihood of associated conditions
•Rule out clinical suspicion of a progressive or neurodegenerative condition
•Establish treatment goals and priorities (see "Cerebral palsy: Overview of management and prognosis", section on 'Treatment goals')
This generally requires repeated examinations over time. (See 'History and physical examination' above.)
●Diagnostic evaluation – Our approach to the evaluation of a child with CP is as follows (algorithm 1):
•Magnetic resonance imaging (MRI) of the brain is performed if the etiology has not yet been established (eg, by neuroimaging in the neonatal period). (See 'Neuroimaging' above.)
•Other testing is dependent on clinical and historic concerns and may include:
-Metabolic and genetic testing are performed if there are atypical symptoms, atypical MRI findings (eg, a brain malformation or injury), dysmorphic features, or if no etiology is identified by clinical history and neuroimaging (table 5). (See 'Metabolic and genetic testing' above.)
-Electroencephalogram (EEG) if seizure activity is suspected. (See 'Seizures' above and "Seizures and epilepsy in children: Clinical and laboratory diagnosis".)
-Infectious work-up (TORCH titers) if pre- or perinatal history is suggestive (table 4). (See "Overview of TORCH infections".)
-Thrombophilia testing (table 6) is not necessary for most patients with known or presumed perinatal stroke; however, testing may be warranted if there is a strong family history of thrombosis or if the stroke occurred outside of the perinatal period. (See "Stroke in the newborn: Classification, manifestations, and diagnosis", section on 'Coagulation testing' and "Ischemic stroke in children: Clinical presentation, evaluation, and diagnosis", section on 'Hypercoagulable evaluation'.)
•All children with CP should be screened for commonly associated conditions, including intellectual disability, ophthalmologic abnormalities, hearing impairment, speech and language disorders, and growth failure. (See "Cerebral palsy: Classification and clinical features", section on 'Associated conditions'.)
●Key diagnostic features – The diagnosis of CP is based upon a combination of clinical findings; a single clinical finding is generally not sufficient to establish the diagnosis. Key features in the diagnosis of CP include the following (see 'Diagnosis' above):
•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
●Differential diagnosis – Typical symptoms and signs of CP may be present in other conditions, including neurodegenerative diseases, inborn errors of metabolism (table 5), developmental or traumatic lesions of the brain or spinal cord, neuromuscular or movement disorders, and neoplasm. (See 'Differential diagnosis' above.)
ACKNOWLEDGMENTS — The UpToDate editorial staff acknowledges Geoffrey Miller, MD and Laurie Glader, MD, who contributed to earlier versions of this topic review.
