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Cerebral Palsy Workup

  • Author: Hoda Z Abdel-Hamid, MD; Chief Editor: Amy Kao, MD  more...
 
Updated: Dec 23, 2015
 

Approach Considerations

The 2003 American Academy of Neurology (AAN) practice parameter on cerebral palsy suggests laboratory studies if[24] : (1) the clinical history or findings from neuroimaging do not indicate a specific structural abnormality, (2) additional and atypical features are present in the history or clinical examination, or (3) a brain malformation is detected in a child with cerebral palsy. In addition, diagnostic testing for coagulation disorders is recommended if a cerebral infarction is seen; however, available data were insufficient for guiding what precise studies should be ordered.

If a diagnosis of a hereditary or neurodegenerative disorder is suspected, screening for an underlying metabolic or genetic disorder should be performed. However, specific studies were not recommended by the AAN practice parameters, as such studies should be guided by the clinical picture.[24]

The AAN practice parameter did not recommend an electroencephalogram (EEG) unless suspicion for epilepsy or an epileptic syndrome is present, but it did recommend neuroimaging "to establish that a brain abnormality exists in children with cerebral palsy, that may, in turn, suggest an etiology and prognosis."[24] Note that a normal brain imaging study does not mean that the child does not have cerebral palsy, because the diagnosis is always based only on physical examination findings.

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Potentially Helpful Laboratory Tests

There are no definitive laboratory studies for diagnosing cerebral palsy, only studies to rule out other symptom causes, such as metabolic or genetic abnormalities, as deemed necessary based on clinical examination. Such studies may include the following:

  • Thyroid function studies - Abnormal thyroid function may be related to abnormalities in muscle tone or deep tendon reflexes or to movement disorders.
  • Lactate and pyruvate levels - Abnormalities may indicate an abnormality of energy metabolism (ie, mitochondrial cytopathy).
  • Ammonia levels - Elevated ammonia levels may indicate liver dysfunction or urea cycle defect.
  • Organic and amino acids - Serum quantitative amino acid and urine quantitative organic acid values may reveal inherited metabolic disorders.
  • Chromosomal analysis - Chromosomal analysis, including karyotype analysis and specific DNA testing may be indicated to rule out a genetic syndrome, if dysmorphic features or abnormalities of various organ systems are present.
  • Cerebrospinal protein - levels may assist in determining asphyxia in the neonatal period. Protein levels can be elevated, as can the lactate-to-pyruvate ratio.
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Cranial Imaging Studies

Neuroimaging studies can help to evaluate brain damage and to identify persons who are at risk for cerebral palsy. Data to support a definitive diagnosis of cerebral palsy are lacking.

Cranial ultrasonography performed in the early neonatal period can be helpful in medically unstable infants until they are able to tolerate transport for more detailed neuroimaging. Ultrasonography can delineate clear-cut structural abnormalities and show evidence of hemorrhage or hypoxic-ischemic injury. For example, neonatal cranial ultrasonography provides information about the ventricular system, basal ganglia, and corpus callosum, as well as diagnostic information on intraventricular hemorrhage and hypoxic-ischemic injury to the periventricular white matter. Periventricular leukomalacia initially appears as an echodense area that converts to an echolucent area when the patient is approximately age 2 weeks. Periventricular leukomalacia is strongly associated with cerebral palsy.

In infants, computed tomography (CT) scanning of the brain helps to identify congenital malformations, intracranial hemorrhage, and periventricular leukomalacia more clearly than ultrasonography.

Magnetic resonance imaging (MRI) of the brain is most useful after 2-3 weeks of life and is the diagnostic neuroimaging study of choice for older children, because this modality defines cortical and white matter structures and abnormalities more clearly than any other method. MRI also allows for the determination of appropriate myelination for a given age. In children with spasticity of the legs and worsening of bowel and bladder function, a spine MRI may help identify a tethered spinal cord.

Although the precise role for MRI in the diagnosis and workup of children with cerebral palsy or suspected cerebral palsy has not been fully elucidated, the literature suggests that MRI should be strongly considered in all cases; in one study, 89% children with cerebral palsy were found to have abnormal MRIs.[35] Additionally, MRI may have a role in predicting neurodevelopmental outcomes in preterm infants.[36] See the following images.

Magnetic resonance image (MRI) of a 1-year-old boy Magnetic resonance image (MRI) of a 1-year-old boy who was born at gestational week 27. The clinical examination was consistent with spastic diplegic cerebral palsy. Pseudocolpocephaly and decreased volume of the white matter posteriorly were consistent with periventricular leukomalacia. Evidence of diffuse polymicrogyria and thinning of the corpus callosum is noted in this image.
Magnetic resonance image (MRI) of a 16-month-old b Magnetic resonance image (MRI) of a 16-month-old boy who was born at term but had an anoxic event at delivery. Examination findings were consistent with a spastic quadriplegic cerebral palsy with asymmetry (more prominent right-sided deficits). Cystic encephalomalacia in the left temporal and parietal regions, delayed myelination, decreased white matter volume, and enlarged ventricles can be seen in this image. These findings are most likely the sequelae of a neonatal insult (eg, periventricular leukomalacia with a superimposed left-sided cerebral infarct).
Magnetic resonance image (MRI) of a 9-day-old girl Magnetic resonance image (MRI) of a 9-day-old girl who was born at full term and had a perinatal hypoxic-ischemic event. Examination of the patient at 1 year revealed findings consistent with a mixed quadriparetic cerebral palsy notable for dystonia and spasticity. Severe hypoxic-ischemic injury to the medial aspect of the cerebellar hemispheres, medial temporal lobes, bilateral thalami, and bilateral corona radiata is observed in this image.

Head ultrasonography, CT scanning, and MRI may be helpful for diagnosing and monitoring findings of hydrocephalus.

Patients who present clinically with cerebral palsy may have normal results from brain imaging studies. Normal results from a neuroimaging studies do not exclude a clinical diagnosis of this disorder. However, in these cases, other underlying metabolic and genetic etiologies should be considered and excluded before diagnosing a child with cerebral palsy.

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Electroencephalography

Electroencephalography (EEG) is useful in evaluating severe hypoxic-ischemic injury. This study is important in the diagnosis of seizure disorders; findings initially show marked suppression of amplitude and slowing, followed by a discontinuous pattern of voltage suppression, with bursts of high-voltage sharp and slow waves at 24-48 hours. However, EEG is not indicated if seizures are not suspected along with cerebral palsy.

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EMG and Nerve Conduction Studies

Electromyography (EMG) and nerve conduction studies are helpful when a muscle or nerve disorder is suspected (eg, a hereditary motor or sensory neuropathy as a basis for equinus foot deformities and toe walking).

Evoked potentials are used to evaluate the anatomic pathways of the auditory and visual systems.

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Contributor Information and Disclosures
Author

Hoda Z Abdel-Hamid, MD Assistant Professor, Department of Pediatrics, University of Pittsburgh School of Medicine; Director of EMG Laboratory and Neuromuscular Program, Director of Pediatric MDA Clinic, Division of Child Neurology, Children’s Hospital of Pittsburgh, University of Pittsburgh Medical Center

Hoda Z Abdel-Hamid, MD is a member of the following medical societies: American Academy of Neurology, American Association of Neuromuscular and Electrodiagnostic Medicine, Child Neurology Society

Disclosure: Nothing to disclose.

Coauthor(s)

Boosara Ratanawongsa, MD Clinical Assistant Professor of Pediatrics, Pennsylvania State University College of Medicine; Pediatric Neurologist, Pediatric Specialists of Lehigh Valley, Lehigh Valley Physician Group

Boosara Ratanawongsa, MD is a member of the following medical societies: American Academy of Neurology, Child Neurology Society

Disclosure: Nothing to disclose.

Ari S Zeldin, MD, FAAP, FAAN Staff Pediatric Neurologist, Naval Medical Center San Diego

Ari S Zeldin, MD, FAAP, FAAN is a member of the following medical societies: American Academy of Neurology, American Academy of Pediatrics, Child Neurology Society

Disclosure: Nothing to disclose.

Alicia T F Bazzano, MD, PhD, MPH Clinical Faculty, Division of Pediatric Emergency Medicine, Harbor/UCLA Medical Center; Chief Physician, Westside Regional Center

Alicia T F Bazzano, MD, PhD, MPH is a member of the following medical societies: Alpha Omega Alpha, American Academy of Pediatrics, American Public Health Association, American Society for Bioethics and Humanities

Disclosure: Nothing to disclose.

Chief Editor

Amy Kao, MD Attending Neurologist, Children's National Medical Center

Amy Kao, MD is a member of the following medical societies: American Academy of Neurology, American Epilepsy Society, Child Neurology Society

Disclosure: Have stock from Cellectar Biosciences; have stock from Varian medical systems; have stock from Express Scripts.

Acknowledgements

Ann M Neumeyer, MD Medical Director, Lurie Family Autism Center/LADDERS; Assistant Professor of Neurology, Harvard Medical School

Ann M Neumeyer, MD is a member of the following medical societies: American Academy of Neurology, Child Neurology Society, and Massachusetts Medical Society

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

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Magnetic resonance image (MRI) of a 1-year-old boy who was born at gestational week 27. The clinical examination was consistent with spastic diplegic cerebral palsy. Pseudocolpocephaly and decreased volume of the white matter posteriorly were consistent with periventricular leukomalacia. Evidence of diffuse polymicrogyria and thinning of the corpus callosum is noted in this image.
Magnetic resonance image (MRI) of a 16-month-old boy who was born at term but had an anoxic event at delivery. Examination findings were consistent with a spastic quadriplegic cerebral palsy with asymmetry (more prominent right-sided deficits). Cystic encephalomalacia in the left temporal and parietal regions, delayed myelination, decreased white matter volume, and enlarged ventricles can be seen in this image. These findings are most likely the sequelae of a neonatal insult (eg, periventricular leukomalacia with a superimposed left-sided cerebral infarct).
Magnetic resonance image (MRI) of a 9-day-old girl who was born at full term and had a perinatal hypoxic-ischemic event. Examination of the patient at 1 year revealed findings consistent with a mixed quadriparetic cerebral palsy notable for dystonia and spasticity. Severe hypoxic-ischemic injury to the medial aspect of the cerebellar hemispheres, medial temporal lobes, bilateral thalami, and bilateral corona radiata is observed in this image.
 
 
 
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