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Yang, C. Benign Familial Neonatal Seizures. Encyclopedia. Available online: https://encyclopedia.pub/entry/4947 (accessed on 28 September 2026).
Yang C. Benign Familial Neonatal Seizures. Encyclopedia. Available at: https://encyclopedia.pub/entry/4947. Accessed September 28, 2026.
Yang, Catherine. "Benign Familial Neonatal Seizures" Encyclopedia, https://encyclopedia.pub/entry/4947 (accessed September 28, 2026).
Yang, C. (2020, December 24). Benign Familial Neonatal Seizures. In Encyclopedia. https://encyclopedia.pub/entry/4947
Yang, Catherine. "Benign Familial Neonatal Seizures." Encyclopedia. Web. 24 December, 2020.
Benign Familial Neonatal Seizures
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This entry is adapted from the peer-reviewed paper https://medlineplus.gov/genetics/condition/benign-familial-neonatal-seizures

Benign familial neonatal seizures (BFNS) is a condition characterized by recurrent seizures in newborn babies. The seizures begin around day 3 of life and usually go away within 1 to 4 months. The seizures can involve only one side of the brain (focal seizures) or both sides (generalized seizures). Many infants with this condition have generalized tonic-clonic seizures (also known as grand mal seizures). This type of seizure involves both sides of the brain and affects the entire body, causing muscle rigidity, convulsions, and loss of consciousness.

genetic conditions

References

  1. Biervert C, Schroeder BC, Kubisch C, Berkovic SF, Propping P, Jentsch TJ,Steinlein OK. A potassium channel mutation in neonatal human epilepsy. Science.1998 Jan 16;279(5349):403-6.
  2. Castaldo P, del Giudice EM, Coppola G, Pascotto A, Annunziato L, Taglialatela M. Benign familial neonatal convulsions caused by altered gating of KCNQ2/KCNQ3potassium channels. J Neurosci. 2002 Jan 15;22(2):RC199.
  3. Chung HJ, Jan YN, Jan LY. Polarized axonal surface expression of neuronal KCNQchannels is mediated by multiple signals in the KCNQ2 and KCNQ3 C-terminaldomains. Proc Natl Acad Sci U S A. 2006 Jun 6;103(23):8870-5.
  4. Lerche H, Biervert C, Alekov AK, Schleithoff L, Lindner M, Klinger W,Bretschneider F, Mitrovic N, Jurkat-Rott K, Bode H, Lehmann-Horn F, Steinlein OK.A reduced K+ current due to a novel mutation in KCNQ2 causes neonatalconvulsions. Ann Neurol. 1999 Sep;46(3):305-12.
  5. Miceli F, Soldovieri MV, Joshi N, Weckhuysen S, Cooper E, Taglialatela M.KCNQ2-Related Disorders. 2010 Apr 27 [updated 2018 Sep 27]. In: Adam MP, ArdingerHH, Pagon RA, Wallace SE, Bean LJH, Stephens K, Amemiya A, editors. GeneReviews® [Internet]. Seattle (WA): University of Washington, Seattle; 1993-2020. Availablefrom http://www.ncbi.nlm.nih.gov/books/NBK32534/
  6. Rogawski MA. KCNQ2/KCNQ3 K+ channels and the molecular pathogenesis ofepilepsy: implications for therapy. Trends Neurosci. 2000 Sep;23(9):393-8.Review.
  7. Schroeder BC, Kubisch C, Stein V, Jentsch TJ. Moderate loss of function ofcyclic-AMP-modulated KCNQ2/KCNQ3 K+ channels causes epilepsy. Nature. 1998 Dec17;396(6712):687-90.
  8. Singh NA, Westenskow P, Charlier C, Pappas C, Leslie J, Dillon J, Anderson VE,Sanguinetti MC, Leppert MF; BFNC Physician Consortium. KCNQ2 and KCNQ3 potassium channel genes in benign familial neonatal convulsions: expansion of thefunctional and mutation spectrum. Brain. 2003 Dec;126(Pt 12):2726-37.
  9. Soldovieri MV, Miceli F, Bellini G, Coppola G, Pascotto A, Taglialatela M.Correlating the clinical and genetic features of benign familial neonatalseizures (BFNS) with the functional consequences of underlying mutations.Channels (Austin). 2007 Jul-Aug;1(4):228-33.
  10. Volkers L, Rook MB, Das JH, Verbeek NE, Groenewegen WA, van Kempen MJ,Lindhout D, Koeleman BP. Functional analysis of novel KCNQ2 mutations found inpatients with Benign Familial Neonatal Convulsions. Neurosci Lett. 2009 Oct2;462(1):24-9. doi: 10.1016/j.neulet.2009.06.064.
  11. Wang HS, Pan Z, Shi W, Brown BS, Wymore RS, Cohen IS, Dixon JE, McKinnon D.KCNQ2 and KCNQ3 potassium channel subunits: molecular correlates of theM-channel. Science. 1998 Dec 4;282(5395):1890-3.
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Subjects: Genetics & Heredity
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Update Date: 24 Dec 2020
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