Journal of Pediatric Epilepsy 2015; 04(03): 130-136
DOI: 10.1055/s-0035-1558833
Review Article
Georg Thieme Verlag KG Stuttgart · New York

Epilepsy in Adolescents: Rational Treatment and Considerations

Gregory B. Sharp
1   Departments of Pediatrics and Neurology, University of Arkansas for Medical Sciences, Little Rock, Arkansas, United States
› Author Affiliations
Further Information

Publication History

19 January 2015

20 January 2015

Publication Date:
17 August 2015 (online)

Abstract

Human brain development is a dynamic process that proceeds from childhood through the adolescent period into adulthood both anatomically and functionally. Likewise, epilepsy follows a course of change. Childhood seizure disorders may change or remit, and other epilepsies may begin during adolescence. Care of the epilepsy patient should include new or further diagnostic testing that is appropriate for the individual patient, differentiation from other paroxysmal disorders, attention to psychosocial and behavioral concerns, and selection and management of appropriate antiepileptic drug therapy. Attention should also be placed on potential adverse effects that appropriate antiepileptic drugs may impart. Special consideration should be given to adolescent girls who should be considered of childbearing age during adolescence. When epilepsy is refractory to medical therapy, alternative therapies should be considered that include epilepsy surgery, vagus nerve stimulation, and specific diets such as ketogenic diet and modified Atkins diet that can be used to successfully treat epilepsy.

 
  • References

  • 1 Craiu D. What is special about the adolescent (JME) brain?. Epilepsy Behav 2013; 28 (Suppl. 01) S45-S51
  • 2 Gogtay N, Giedd JN, Lusk L , et al. Dynamic mapping of human cortical development during childhood through early adulthood. Proc Natl Acad Sci U S A 2004; 101 (21) 8174-8179
  • 3 Sowell ER, Trauner DA, Gamst A, Jernigan TL. Development of cortical and subcortical brain structures in childhood and adolescence: a structural MRI study. Dev Med Child Neurol 2002; 44 (1) 4-16
  • 4 Tau GZ, Peterson BS. Normal development of brain circuits. Neuropsychopharmacology 2010; 35 (1) 147-168
  • 5 Sowell ER, Delis D, Stiles J, Jernigan TL. Improved memory functioning and frontal lobe maturation between childhood and adolescence: a structural MRI study. J Int Neuropsychol Soc 2001; 7 (3) 312-322
  • 6 Sowell ER, Peterson BS, Thompson PM, Welcome SE, Henkenius AL, Toga AW. Mapping cortical change across the human life span. Nat Neurosci 2003; 6 (3) 309-315
  • 7 Sowell ER, Thompson PM, Holmes CJ, Jernigan TL, Toga AW. In vivo evidence for post-adolescent brain maturation in frontal and striatal regions. Nat Neurosci 1999; 2 (10) 859-861
  • 8 Bava S, Thayer R, Jacobus J, Ward M, Jernigan TL, Tapert SF. Longitudinal characterization of white matter maturation during adolescence. Brain Res 2010; 1327: 38-46
  • 9 Barnea-Goraly N, Menon V, Eckert M , et al. White matter development during childhood and adolescence: a cross-sectional diffusion tensor imaging study. Cereb Cortex 2005; 15 (12) 1848-1854
  • 10 Giorgio A, Watkins KE, Douaud G , et al. Changes in white matter microstructure during adolescence. Neuroimage 2008; 39 (1) 52-61
  • 11 Giorgio A, Watkins KE, Chadwick M , et al. Longitudinal changes in grey and white matter during adolescence. Neuroimage 2010; 49 (1) 94-103
  • 12 Schmithorst VJ, Wilke M, Dardzinski BJ, Holland SK. Correlation of white matter diffusivity and anisotropy with age during childhood and adolescence: a cross-sectional diffusion-tensor MR imaging study. Radiology 2002; 222 (1) 212-218
  • 13 Kretschmann HJ. Localisation of the corticospinal fibres in the internal capsule in man. J Anat 1988; 160: 219-225
  • 14 Wierenga L, Langen M, Ambrosino S , et al. Typical development of basal ganglia, hippocampus, amygdala and cerebellum from age 7 to 24. Neuroimage 2014; 96: 67-72
  • 15 Gauthier CT, Duyme M, Zanca M, Capron C. Sex and performance level effects on brain activation during a verbal fluency task: a functional magnetic resonance imaging study. Cortex 2009; 45 (2) 164-176
  • 16 Hamilton LS, Levitt JG, O'Neill J , et al. Reduced white matter integrity in attention-deficit hyperactivity disorder. Neuroreport 2008; 19 (17) 1705-1708
  • 17 Jansen LA, Peugh LD, Roden WH, Ojemann JG. Impaired maturation of cortical GABA(A) receptor expression in pediatric epilepsy. Epilepsia 2010; 51 (8) 1456-1467
  • 18 Escayg A, MacDonald BT, Meisler MH , et al. Mutations of SCN1A, encoding a neuronal sodium channel, in two families with GEFS+2. Nat Genet 2000; 24 (4) 343-345
  • 19 Claes L, Del-Favero J, Ceulemans B, Lagae L, Van Broeckhoven C, De Jonghe P. De novo mutations in the sodium-channel gene SCN1A cause severe myoclonic epilepsy of infancy. Am J Hum Genet 2001; 68 (6) 1327-1332
  • 20 Harkin LA, McMahon JM, Iona X , et al; Infantile Epileptic Encephalopathy Referral Consortium. The spectrum of SCN1A-related infantile epileptic encephalopathies. Brain 2007; 130 (Pt 3) 843-852
  • 21 Zuberi SM, Brunklaus A, Birch R, Reavey E, Duncan J, Forbes GH. Genotype-phenotype associations in SCN1A-related epilepsies. Neurology 2011; 76 (7) 594-600
  • 22 De Vivo DC, Trifiletti RR, Jacobson RI, Ronen GM, Behmand RA, Harik SI. Defective glucose transport across the blood-brain barrier as a cause of persistent hypoglycorrhachia, seizures, and developmental delay. N Engl J Med 1991; 325 (10) 703-709
  • 23 Leen WG, Wevers RA, Kamsteeg EJ, Scheffer H, Verbeek MM, Willemsen MA. Cerebrospinal fluid analysis in the workup of GLUT1 deficiency syndrome: a systematic review. JAMA Neurol 2013; 70 (11) 1440-1444
  • 24 Pong AW, Geary BR, Engelstad KM, Natarajan A, Yang H, De Vivo DC. Glucose transporter type I deficiency syndrome: epilepsy phenotypes and outcomes. Epilepsia 2012; 53 (9) 1503-1510
  • 25 Suls A, Dedeken P, Goffin K , et al. Paroxysmal exercise-induced dyskinesia and epilepsy is due to mutations in SLC2A1, encoding the glucose transporter GLUT1. Brain 2008; 131 (Pt 7) 1831-1844
  • 26 Klepper J. Glucose transporter deficiency syndrome (GLUT1DS) and the ketogenic diet. Epilepsia 2008; 49 (Suppl. 08) 46-49
  • 27 Sulc V, Stykel S, Hanson DP , et al. Statistical SPECT processing in MRI-negative epilepsy surgery. Neurology 2014; 82 (11) 932-939
  • 28 Bouma PA, Bovenkerk AC, Westendorp RG, Brouwer OF. The course of benign partial epilepsy of childhood with centrotemporal spikes: a meta-analysis. Neurology 1997; 48 (2) 430-437
  • 29 Camfield CS, Berg A, Stephani U, Wirrell EC. Transition issues for benign epilepsy with centrotemporal spikes, nonlesional focal epilepsy in otherwise normal children, childhood absence epilepsy, and juvenile myoclonic epilepsy. Epilepsia 2014; 55 (Suppl. 03) 16-20
  • 30 Wirrell EC, Camfield CS, Camfield PR, Gordon KE, Dooley JM. Long-term prognosis of typical childhood absence epilepsy: remission or progression to juvenile myoclonic epilepsy. Neurology 1996; 47 (4) 912-918
  • 31 Trinka E, Baumgartner S, Unterberger I , et al. Long-term prognosis for childhood and juvenile absence epilepsy. J Neurol 2004; 251 (10) 1235-1241
  • 32 Wirrell EC, Grossardt BR, So EL, Nickels KC. A population-based study of long-term outcomes of cryptogenic focal epilepsy in childhood: cryptogenic epilepsy is probably not symptomatic epilepsy. Epilepsia 2011; 52 (4) 738-745
  • 33 Berg AT, Testa FM, Levy SR. Complete remission in nonsyndromic childhood-onset epilepsy. Ann Neurol 2011; 70 (4) 566-573
  • 34 Schmidt D. AED discontinuation may be dangerous for seizure-free patients. J Neural Transm 2011; 118 (2) 183-186
  • 35 French JA, Gazzola DM. Antiepileptic drug treatment: new drugs and new strategies. Continuum (Minneap Minn) 2013; 19 (3 Epilepsy): 643-655
  • 36 Harden CL, Meador KJ, Pennell PB , et al; American Academy of Neurology; American Epilepsy Society. Management issues for women with epilepsy-Focus on pregnancy (an evidence-based review): II. Teratogenesis and perinatal outcomes: Report of the Quality Standards Subcommittee and Therapeutics and Technology Subcommittee of the American Academy of Neurology and the American Epilepsy Society. Epilepsia 2009; 50 (5) 1237-1246
  • 37 Holmes LB, Baldwin EJ, Smith CR , et al. Increased frequency of isolated cleft palate in infants exposed to lamotrigine during pregnancy. Neurology 2008; 70 (22) 2152-2158
  • 38 Foldvary-Schaefer N, Harden C, Herzog A, Falcone T. Hormones and seizures. Cleve Clin J Med 2004; 71 (Suppl. 02) S11-S18
  • 39 Kwan P, Arzimanoglou A, Berg AT , et al. Definition of drug resistant epilepsy: consensus proposal by the ad hoc Task Force of the ILAE Commission on Therapeutic Strategies. Epilepsia 2010; 51 (6) 1069-1077
  • 40 Henry TR. Therapeutic mechanisms of vagus nerve stimulation. Neurology 2002; 59 (6) (Suppl. 04) S3-S14
  • 41 Morris III GL, Gloss D, Buchhalter J, Mack KJ, Nickels K, Harden C. Evidence-based guideline update: vagus nerve stimulation for the treatment of epilepsy: report of the guideline development subcommittee of the American Academy of Neurology. Epilepsy Curr 2013; 13 (6) 297-303
  • 42 Sun FT, Morrell MJ. The RNS System: responsive cortical stimulation for the treatment of refractory partial epilepsy. Expert Rev Med Devices 2014; 11 (6) 563-572
  • 43 Wilder RM. The effects of ketonemia on course of epilepsy. Mayo Clin Proc 1921; 2: 307-308
  • 44 Lutas A, Yellen G. The ketogenic diet: metabolic influences on brain excitability and epilepsy. Trends Neurosci 2013; 36 (1) 32-40
  • 45 Lefevre F, Aronson N. Ketogenic diet for the treatment of refractory epilepsy in children: A systematic review of efficacy. Pediatrics 2000; 105 (4) E46
  • 46 Kossoff EH, Cervenka MC, Henry BJ, Haney CA, Turner Z. A decade of the modified Atkins diet (2003–2013): Results, insights, and future directions. Epilepsy Behav 2013; 29 (3) 437-442
  • 47 Groesbeck DK, Bluml RM, Kossoff EH. Long-term use of the ketogenic diet in the treatment of epilepsy. Dev Med Child Neurol 2006; 48 (12) 978-981
  • 48 Kossoff EH, Zupec-Kania BA, Amark PE , et al; Charlie Foundation, Practice Committee of the Child Neurology Society; Practice Committee of the Child Neurology Society; International Ketogenic Diet Study Group. Optimal clinical management of children receiving the ketogenic diet: recommendations of the International Ketogenic Diet Study Group. Epilepsia 2009; 50 (2) 304-317
  • 49 Martinez CC, Pyzik PL, Kossoff EH. Discontinuing the ketogenic diet in seizure-free children: recurrence and risk factors. Epilepsia 2007; 48 (1) 187-190