eMedicine Specialties > Neurology > Pediatric Neurology

Benign Neonatal Convulsions: Follow-up

Author: Nancy Theresa Rodgers-Neame, MD, Assistant Professor, Department of Molecular Pharmacology and Physiology, University of South Florida; Director, Florida Comprehensive Epilepsy and Seizure Disorders Program
Contributor Information and Disclosures

Updated: Apr 8, 2009

Follow-up

Further Inpatient Care

  • Patients should be observed in the inpatient unit until the physician is satisfied that the patient's condition is stabilized and that the infant is feeding well and is free of seizures that compromise feeding or sleeping. In some situations, patients may be seizure free at discharge, but this is not a requirement. Exclude reasonable alternative diagnoses prior to discharge.
  • The choice to continue or discontinue any medications started can be tailored to each patient. Consider each of the following:
    • Have the seizures abated to the point that they are no longer interfering with function?
    • What is the family's level of comfort? Fully inform the patient's family of the situation and address their questions and concerns prior to discharge.
    • Is the EEG improved? A normal EEG is not required, but improvement in the EEG indicates that the diagnosis is more likely to be benign and that the prognosis is good for continued improvement at home. Likewise, the typical pattern (ie, theta pointu altérnant) indicates a benign course. Conversely, deterioration of the EEG background or development of a less benign pattern may indicate a less benign prognosis.

Further Outpatient Care

  • Follow-up care should consist of one visit soon after discharge to confirm that the patient is physically and neurologically healthy. Perform a repeat EEG at that time.
  • Provide later follow-up care spaced at intervals consistent with the physician's and parents' level of comfort. In general, at least 2 serial assessments spaced several months apart should demonstrate a normal EEG, normal developmental milestones, and normal findings on neurologic examination.

Inpatient & Outpatient Medications

  • No known antiepileptic medications alter the behavior of the potassium channel. Other drugs known to have an effect on potassium transporters are currently being considered for investigation. No studies have revealed any medications that have any advantage over other medications. Select medications on the basis of the following two factors:
    • Appropriateness of the drug in neonates
    • Lack of significant serious adverse effects
  • Currently, the most appropriate medication for neonates that can be given in both IV and PO formulation after discharge remains phenobarbital. In the future, other medications may prove more appropriate.
  • Specifically, valproate and phenytoin are less appropriate.
    • Generally, valproate in very young patients is reserved for serious conditions that do not respond to therapy with other medications, because the high risk of hepatic complications must be outweighed by the risk of the seizures themselves, a situation that normally is not under consideration in a benign condition.
    • Phenytoin is less appropriate because of unpredictable decreased absorption in the neonate when administered orally.
  • The most important consideration in choosing an antiepileptic medication in these patients is to remember that the syndrome is benign. Therefore, any medication chosen should have no risk of serious adverse effects.

Complications

Patients with benign familial neonatal convulsions have an increased risk of developing seizures in later life. Depending on the study, 11-20% of patients develop epilepsy in later life. Some families examined also have demonstrated an increased risk of epilepsy in apparently unaffected siblings.

Prognosis

Overall, as the name implies, benign neonatal convulsions have an excellent prognosis and resolve without neurological sequelae.

Patient Education

  • Inform families with the syndrome of the risk of affected siblings, but reassure them as to the benign nature of the syndrome.
  • Also alert them to the possible development of epilepsy in later life in affected as well as apparently unaffected children.
  • Furthermore, inform them that the incidence of minor neurological problems is the same as expected in the general population.
  • For excellent patient education resources, visit eMedicine's Brain and Nervous System Center. Also, see eMedicine's patient education article Seizures in Children.

Miscellaneous

Medicolegal Pitfalls

  • Careful attention to the differential diagnosis of neonatal seizures and appropriate workup avoids most medicolegal problems. However, benign neonatal convulsions are a retrospective diagnosis and frequently present a difficult diagnostic and treatment dilemma even to the most experienced clinicians.
  • Keep the family appropriately informed at all stages of the workup, diagnosis, and treatment.

Special Concerns

Other seizure types often are intermixed in families with inherited seizure disorders. This also is observed in families with benign neonatal convulsions. Children (and apparently unaffected siblings) who have benign neonatal convulsions are at an increased risk of seizures in later life.

 


More on Benign Neonatal Convulsions

Overview: Benign Neonatal Convulsions
Differential Diagnoses & Workup: Benign Neonatal Convulsions
Treatment & Medication: Benign Neonatal Convulsions
Follow-up: Benign Neonatal Convulsions
References
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References

  1. Quattlebaum TG. Benign familial convulsions in the neonatal period and early infancy. J Pediatr. Aug 1979;95(2):257-9. [Medline].

  2. Mizrahi EM. Seizure disorders in children. Curr Opin Pediatr. Dec 1994;6(6):642-6. [Medline].

  3. Plouin P. Benign idiopathic neonatal convulsions (familial and non-familial): open questions about these syndromes. Epileptic Seizures and Syndromes. 1994;193-201.

  4. Pettit RE, Fenichel GM. Benign familial neonatal seizures. Arch Neurol. Jan 1980;37(1):47-8. [Medline].

  5. Singh NA, Westenskow P, Charlier C, et al. KCNQ2 and KCNQ3 potassium channel genes in benign familial neonatal convulsions: expansion of the functional and mutation spectrum. Brain. Dec 2003;126:2726-37. [Medline].

  6. Singh NA, Charlier C, Stauffer D, et al. A novel potassium channel gene, KCNQ2, is mutated in an inherited epilepsy of newborns. Nat Genet. Jan 1998;18(1):25-9. [Medline].

  7. Plouin P. [Value of video electroencephalography in neonatology]. Arch Pediatr. May 2000;7 Suppl 2:332s-333s. [Medline].

  8. Biervert C, Schroeder BC, Kubisch C, et al. A potassium channel mutation in neonatal human epilepsy. Science. Jan 16 1998;279(5349):403-6. [Medline].

  9. Hirose S, Zenri F, Akiyoshi H, et al. A novel mutation of KCNQ3 (c.925T-->C) in a Japanese family with benign familial neonatal convulsions. Ann Neurol. Jun 2000;47(6):822-6. [Medline].

  10. Schroeder BC, Kubisch C, Stein V, et al. Moderate loss of function of cyclic-AMP-modulated KCNQ2/KCNQ3 K+ channels causes epilepsy. Nature. Dec 17 1998;396(6712):687-90. [Medline].

  11. Schwake M, Pusch M, Kharkovets T, et al. Surface expression and single channel properties of KCNQ2/KCNQ3, M-type K+ channels involved in epilepsy. J Biol Chem. May 5 2000;275(18):13343-8. [Medline].

  12. Singh NA, Charlier C, Stauffer D, et al. A novel potassium channel gene, KCNQ2, is mutated in an inherited epilepsy of newborns. Nat Genet. Jan 1998;18(1):25-9. [Medline].

  13. Kananura C, Biervert C, Hechenberger M, et al. The new voltage gated potassium channel KCNQ5 and neonatal convulsions. Neuroreport. Jun 26 2000;11(9):2063-7. [Medline].

  14. Beck C, Moulard B, Steinlein O, et al. A nonsense mutation in the alpha4 subunit of the nicotinic acetylcholine receptor (CHRNA4) cosegregates with 20q-linked benign neonatal familial convulsions (EBNI). Neurobiol Dis. Nov 1994;1(1-2):95-9. [Medline].

  15. Steinlein O, Sander T, Stoodt J, et al. Possible association of a silent polymorphism in the neuronal nicotinic acetylcholine receptor subunit alpha4 with common idiopathic generalized epilepsies. Am J Med Genet. Jul 25 1997;74(4):445-9. [Medline].

  16. Lerche H, Biervert C, Alekov AK, et al. A reduced K+ current due to a novel mutation in KCNQ2 causes neonatal convulsions. Ann Neurol. Sep 1999;46(3):305-12. [Medline].

  17. Zhu G, Okada M, Murakami T, et al. Dysfunction of M-channel enhances propagation of neuronal excitability in rat hippocampus monitored by multielectrode dish and microdialysis systems. Neurosci Lett. Nov 10 2000;294(1):53-7. [Medline].

  18. Burgess DL. Neonatal epilepsy syndromes and GEFS+: mechanistic considerations. Epilepsia. 2005;46 Suppl 10:51-8. [Medline].

  19. Lehmann-Horn F, Jurkat-Rott K. Voltage-gated ion channels and hereditary disease. Physiol Rev. Oct 1999;79(4):1317-72.

  20. Mulley JC, Scheffer IE, Petrou S, et al. Channelopathies as a genetic cause of epilepsy. Curr Opin Neurol. Apr 2003;16(2):171-6. [Medline].

  21. Webb R, Bobele G. 'Benign' familial neonatal convulsions. J Child Neurol. Oct 1990;5(4):295-8. [Medline].

  22. Tharp BR. Neonatal seizures and syndromes. Epilepsia. 2002;43 Suppl 3:2-10. [Medline].

  23. DeLorenzo RJ. The challenging genetics of epilepsy. Epilepsy Res Suppl. 1991;4:3-17. [Medline].

  24. Hirose S, Mitsudome A, Okada M, et al. Genetics of idiopathic epilepsies. Epilepsia. 2005;46 Suppl 1:38-43. [Medline].

  25. Ben-Ari Y, Khazipov R, Leinekugel X, et al. GABAA, NMDA and AMPA receptors: a developmentally regulated 'ménage à trois'. Trends Neurosci. Nov 1997;20(11):523-9. [Medline].

  26. Dzhala VI, Talos DM, Sdrulla DA, et al. NKCC1 transporter facilitates seizures in the developing brain. Nat Med. Nov 2005;11(11):1205-13. [Medline].

  27. Leinekugel X, Medina I, Khalilov I, et al. Ca2+ oscillations mediated by the synergistic excitatory actions of GABA(A) and NMDA receptors in the neonatal hippocampus. Neuron. Feb 1997;18(2):243-55. [Medline].

  28. Rivera C, Voipio J, Payne JA, et al. The K+/Cl- co-transporter KCC2 renders GABA hyperpolarizing during neuronal maturation. Nature. Jan 21 1999;397(6716):251-5. [Medline].

  29. Miles DK, Holmes GL. Benign neonatal seizures. J Clin Neurophysiol. Jul 1990;7(3):369-79. [Medline].

  30. Lewis TB, Leach RJ, Ward K, et al. Genetic heterogeneity in benign familial neonatal convulsions: identification of a new locus on chromosome 8q. Am J Hum Genet. Sep 1993;53(3):670-5. [Medline].

  31. Treiman LJ. Genetics of epilepsy: an overview. Epilepsia. 1993;34 Suppl 3:S1-11. [Medline].

  32. Turnbull J, Lohi H, Kearney JA, et al. Sacred disease secrets revealed: the genetics of human epilepsy. Hum Mol Genet. Sep 1 2005;14(17):2491-500. [Medline].

  33. Jallon P, Latour P. Epidemiology of idiopathic generalized epilepsies. Epilepsia. 2005;46 Suppl 9:10-4. [Medline].

  34. Concordance of clinical forms of epilepsy in families with several affected members. Italian League Against Epilepsy Genetic Collaborative Group. Epilepsia. Sep-Oct 1993;34(5):819-26. [Medline].

  35. North KN, Storey, GNB, Henderson-Smart, D.J. Fifth day fits in the newborn. Journal of Paediatrics and Child Health,. March 2008;25(5):284-287.

  36. Leppert M, Anderson VE, Quattlebaum T, et al. Benign familial neonatal convulsions linked to genetic markers on chromosome 20. Nature. Feb 16 1989;337(6208):647-8. [Medline].

  37. Leppert M. Novel K+ channel genes in benign familial neonatal convulsions. Epilepsia. Aug 2000;41(8):1066-7. [Medline].

  38. Lewis TB, Shevell MI, Andermann E, et al. Evidence of a third locus for benign familial convulsions. J Child Neurol. May 1996;11(3):211-4. [Medline].

  39. Elmslie F, Gardiner M. Genetics of the epilepsies. Curr Opin Neurol. Apr 1995;8(2):126-9. [Medline].

  40. Gardiner M. Genetics of idiopathic generalized epilepsies. Epilepsia. 2005;46 Suppl 9:15-20. [Medline].

  41. Camfield PR, Dooley J, Gordon K, et al. Benign familial neonatal convulsions are epileptic. J Child Neurol. Oct 1991;6(4):340-2. [Medline].

  42. Tibbles JA. Dominant benign neonatal seizures. Dev Med Child Neurol. Oct 1980;22(5):664-7. [Medline].

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

  44. Delgado-Escueta AV, Serratosa JM, Liu A, et al. Progress in mapping human epilepsy genes. Epilepsia. 1994;35 Suppl 1:S29-40. [Medline].

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Further Reading

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Keywords

benign neonatal convulsions, second day seizures, benign neonatal seizures, benign familial neonatal convulsions, benign idiopathic neonatal convulsions, benign familial neonatal seizures, benign idiopathic neonatal seizures, fifth day disease, fifth day fits, seizure epilepsy treatment, symptoms, BFNC, BINC

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Contributor Information and Disclosures

Author

Nancy Theresa Rodgers-Neame, MD, Assistant Professor, Department of Molecular Pharmacology and Physiology, University of South Florida; Director, Florida Comprehensive Epilepsy and Seizure Disorders Program
Nancy Theresa Rodgers-Neame, MD is a member of the following medical societies: American Academy of Neurology, American Epilepsy Society, American Medical Women's Association, Society for Neuroscience, Southern Clinical Neurological Society, and Southern Medical Association
Disclosure: Nothing to disclose.

Medical Editor

Robert Baumann, MD, Program Director, Professor, Departments of Neurology and Pediatrics, University of Kentucky
Robert Baumann, MD is a member of the following medical societies: American Academy of Neurology, American Academy of Pediatrics, American College of Epidemiology, American Epilepsy Society, and Child Neurology Society
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Kenneth J Mack, MD, PhD, Senior Associate Consultant, Department of Child and Adolescent Neurology, Mayo Clinic
Kenneth J Mack, MD, PhD is a member of the following medical societies: American Academy of Neurology, Child Neurology Society, Phi Beta Kappa, and Society for Neuroscience
Disclosure: Nothing to disclose.

CME Editor

Selim R Benbadis, MD, Professor, Director of Comprehensive Epilepsy Program, Departments of Neurology and Neurosurgery, University of South Florida School of Medicine, Tampa General Hospital
Selim R Benbadis, MD is a member of the following medical societies: American Academy of Neurology, American Academy of Sleep Medicine, American Clinical Neurophysiology Society, American Epilepsy Society, and American Medical Association
Disclosure: Nothing to disclose.

Chief Editor

Amy Kao, MD, Assistant Professor, Department of Pediatrics, Division of Pediatric Neurology, Department of Neurology, Oregon Health and Science University; Consulting Staff, Shriners Hospital for Children
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.

 
 
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