Neonatal Seizures Treatment & Management

  • Author: Raj D Sheth, MD; Chief Editor: Amy Kao, MD   more...
 
Updated: Oct 31, 2011
 

Medical Care

Acute neonatal seizures should be treated aggressively, although controversy exists as to the optimal treatment for them.[10, 14]

When clinical seizures are present, a rigorous workup to determine an underlying etiologic cause should be initiated quickly. Electrolyte imbalances should be corrected through a central venous site. Hypocalcemia should be treated cautiously with calcium, since leakage of calcium into subcutaneous tissue can cause scarring.

When an inborn error of metabolism is suspected, discontinue feeding, since feeding may exacerbate the seizures and encephalopathy. Institute intravenous solutions.

Once these issues have been addressed, antiepileptic drug (AED) therapy should be considered. Phenobarbital is the initial drug of choice. If seizures persist, the use of phenytoin should be considered.

Patients with seizures resulting from intracranial hemorrhage should have head circumference measurements performed daily. A rapid increase in head circumference may indicate hydrocephalus.

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Seizure Medications

Seizure medication concentrations should be monitored during the acute period. These drugs often are discontinued between ages 3 and 6 months if further seizures have not occurred. A trend toward earlier discontinuation has met with good results.

A general recommendation is to use AEDs for 3 months, but electroencephalography may be helpful in deciding when to stop AEDs.

If the patient remains seizure free, then medications may be tapered gradually. If the patient is on 2 AEDs, then one should be tapered first before considering withdrawal of the other.

If seizures recur, then the patient should be placed back on AEDs. The patient may be placed on the original AED, or carbamazepine may be considered.

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Contributor Information and Disclosures
Author

Raj D Sheth, MD  Professor, Mayo College of Medicine; Chief, Division of Pediatric Neurology, Nemours Children's Clinic

Raj D Sheth, MD is a member of the following medical societies: American Academy of Neurology, American Academy of Pediatrics, American Epilepsy Society, American Neurological Association, and Child Neurology Society

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

Robert Stanley Rust Jr, MD, MA Thomas E Worrell Jr Professor of Epileptology and Neurology, Co-Director of FE Dreifuss Child Neurology and Epilepsy Clinics, Director, Child Neurology, University of Virginia; Chair-Elect, Child Neurology Section, American Academy of Neurology

Robert Stanley Rust Jr, MD, MA is a member of the following medical societies: American Academy of Neurology, American Epilepsy Society, American Headache Society, American Neurological Association, Child Neurology Society, International Child Neurology Association, and Society for Pediatric Research

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Senior Pharmacy Editor, eMedicine

Disclosure: eMedicine Salary Employment

References

  1. Volpe JJ. Hypoxic-Ischemic Encephalopathy: Biochemical and Physiological Aspects. In: Neurology of the Newborn. 4th ed. Philadelphia: WB Saunders; 2000:217-276.

  2. Lombroso CT. Neonatal seizures: gaps between the laboratory and the clinic. Epilepsia. 2007;48 Suppl 2:83-106. [Medline].

  3. Sheth RD. Electroencephalogram confirmatory rate in neonatal seizures. Pediatr Neurol. Jan 1999;20(1):27-30. [Medline].

  4. Silverstein FS, Jensen FE. Neonatal seizures. Ann Neurol. Aug 2007;62(2):112-20. [Medline].

  5. Sheth RD, Hobbs GR, Mullett M. Neonatal seizures: incidence, onset, and etiology by gestational age. J Perinatol. Jan 1999;19(1):40-3. [Medline].

  6. Sheth RD. Frequency of neurologic disorders in the neonatal intensive care unit. J Child Neurol. Sep 1998;13(9):424-8. [Medline].

  7. Sheth RD, Bodensteiner JB. Delayed postanoxic encephalopathy: possible role for apoptosis. J Child Neurol. Jul 1998;13(7):347-8. [Medline].

  8. [Best Evidence] Pisani F, Sisti L, Seri S. A scoring system for early prognostic assessment after neonatal seizures. Pediatrics. Oct 2009;124(4):e580-7. [Medline].

  9. Vigevano F. Benign familial infantile seizures. Brain Dev. Apr 2005;27(3):172-7. [Medline].

  10. Sheth RD, Buckley DJ, Gutierrez AR, et al. Midazolam in the treatment of refractory neonatal seizures. Clin Neuropharmacol. Apr 1996;19(2):165-70. [Medline].

  11. Cherian PJ, Deburchgraeve W, Swarte RM, De Vos M, Govaert P, Van Huffel S, et al. Validation of a new automated neonatal seizure detection system: a clinician's perspective. Clin Neurophysiol. Aug 2011;122(8):1490-9. [Medline].

  12. Sheth RD. Electroencephalogram in developmental delay: specific electroclinical syndromes. Semin Pediatr Neurol. Mar 1998;5(1):45-51. [Medline].

  13. Scher MS, Trucco GS, Beggarly ME, et al. Neonates with electrically confirmed seizures and possible placental associations. Pediatr Neurol. Jul 1998;19(1):37-41. [Medline].

  14. Sankar R, Painter MJ. Neonatal seizures: after all these years we still love what doesn't work. Neurology. Mar 8 2005;64(5):776-7. [Medline].

  15. Painter MJ, Scher MS, Stein AD, et al. Phenobarbital compared with phenytoin for the treatment of neonatal seizures. N Engl J Med. Aug 12 1999;341(7):485-9. [Medline].

  16. Sheth RD. Frequency of neurologic disorders in the neonatal intensive care unit. J Child Neurol. Sep 1998;13(9):424-8. [Medline].

 
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Onset of neonatal seizure demonstrating a focal onset in the right frontal (FP4) region. At this point, the child had head and eye deviation to the left.
Twenty seconds into a seizure that had focal onset in the right frontal (FP4) region, the seizure shows a rhythmic buildup of activity in the right frontocentral region.
This seizure had focal onset in the right frontal (FP4) region and subsequent buildup of activity in the right frontocentral region. As the seizure evolves, the electroencephalogram shows diffuse involvement of both cerebral hemispheres.
 
 
 
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