Childhood Migraine Variants Workup

  • Author: Wendy G Mitchell, MD; Chief Editor: Amy Kao, MD   more...
 
Updated: Mar 29, 2012
 

Approach Considerations

During the first or worst episode, perform appropriate laboratory and neuroradiologic studies to exclude other causes of the symptoms.[10]

Although alternative causes of symptoms are rare, most patients are not satisfied with a simple explanation, and neuroimaging is often performed to rule out serious alternative pathology (eg, intracranial hemorrhage, tumor, or hydrocephalus). If the physician decides that imaging is not indicated (eg, on the grounds that it has been repeatedly performed for similar attacks), the reasoning should be well documented in the medical record, and a clear explanation should be given to the patient and the family.

For aura without headache, the differential diagnosis often includes simple partial (focal) seizures. Therefore, electroencephalography (EEG) or video EEG may help in the diagnosis. For other migraine variants, EEG generally does not confirm or exclude migraine or other alternatives, since epileptiform EEG changes can be observed in migraineurs.

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Laboratory Studies

Laboratory studies generally are not helpful between episodes when the patient has a history of multiple, recurrent episodes and complete clearing between episodes. Evaluate a child with cyclic vomiting with or without head pain for metabolic disease, particularly mitochondrial cytopathy.

Studies performed during attacks have higher yield than those performed while the child is feeling well. During the attack, perform the following investigations:

  • Serum lactate
  • Serum pyruvate
  • Urine organic acids
  • Serum ammonia

Samples must be collected carefully and handled appropriately by the laboratory. If suspicion of mitochondrial cytopathy is high, blood may be collected at any time to allow examination of the DNA for mitochondrial point mutations and deletions.

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CT, MRI, and SPECT

Neuroimaging with computed tomography (CT) or magnetic resonance imaging (MRI) is indicated during the first or worst attack that presents with simultaneous focal neurologic deficits or altered mental status; it should also be done if any focal findings persist between attacks. Perform these studies to exclude other acute causes of the symptoms.

Neuroimaging is less important if the patient presents during a symptom-free interlude, with a history of multiple attacks followed by complete recovery. In these patients, the clinician can usually rule out acute life-threatening conditions and can more reasonably make a diagnosis of migraine on the basis of the history.

During or immediately after an attack, functional neuroimaging may support the diagnosis, though migraine is most often a clinical diagnosis. Single-photon emission CT (SPECT) may show hypoperfusion during an aura or episode. Functional MRI (fMRI), a research technique, also may demonstrate abnormalities of perfusion. Gadolinium-enhanced MRI may show focal enhancement during or immediately after the attack. This can cause confusion with ischemic stroke, inflammatory conditions, or infection.

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Electroencephalography

EEG may yield abnormal results during or immediately after an episode, showing a slowing in focal or generalized patterns. In general, nonspecific interictal EEG abnormalities, including epileptiform activity, are reported in higher frequencies in migraineurs.

Continuous ambulatory or video EEG may be useful in the rare patient with episodic confusion, hallucinations, or focal neurologic deficits; partial seizures or nonconvulsive status epilepticus are included in the differential diagnosis for the attack.

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Contributor Information and Disclosures
Author

Wendy G Mitchell, MD  Professor of Neurology, Keck School of Medicine of the University of Southern California; Consulting Staff, Division of Child Neurology, Children's Hospital Los Angeles, LAC-USC

Wendy G Mitchell, MD is a member of the following medical societies: American Academy of Neurology, American Academy of Pediatrics, American Epilepsy Society, Child Neurology Society, and International Child Neurology Association

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 Academy of Pediatrics, American Epilepsy Society, and Child Neurology Society

Disclosure: Nothing to disclose.

Additional Contributors

James J Riviello Jr, MD George Peterkin Endowed Chair in Pediatrics, Professor of Pediatrics, Section of Neurology and Developmental Neuroscience, Professor of Neurology, Peter Kellaway Section of Neurophysiology, Baylor College of Medicine; Chief of Neurophysiology, Director of the Epilepsy and Neurophysiology Program, Texas Children's Hospital

James J Riviello Jr, MD is a member of the following medical societies: American Academy of Pediatrics

Disclosure: Up To Date Royalty Section Editor

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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