Close
New

Medscape is available in 5 Language Editions – Choose your Edition here.

 

Juvenile Myoclonic Epilepsy Treatment & Management

  • Author: James Selph, MD; Chief Editor: Selim R Benbadis, MD  more...
 
Updated: Jun 24, 2016
 

Approach Considerations

Medical therapy with anticonvulsants typically is needed (see Medication). Avoidance of precipitating events such as alcohol use and sleep deprivation may be useful but is not by itself sufficient to control the seizures of juvenile myoclonic epilepsy (JME).

Go to Antiepileptic Drugs and Epilepsy and Seizures for complete information on these topics.

Next

Anticonvulsant Therapy

The selection of antiepileptic drugs for the treatment of JME depends on several factors, including the patient’s comorbidities, preferences, previous history of adverse events, and gender. The US Food and Drug Administration (FDA) has not approved any anticonvulsant solely for the treatment of JME. In 2006, the FDA approved the adjunctive use of levetiracetam for the treatment of JME. Divalproex sodium has been approved as adjunctive therapy for patients with multiple seizure types that include primary generalized epilepsies.

In most patients with JME, seizures are well controlled with monotherapy. Valproic acid has been considered the treatment of choice for JME for many years due to high response rates, but epileptologists are increasingly using other choices as first-line therapies. Approximately 80% of patients with JME become seizure free with valproate monotherapy. Several studies using lamotrigine, topiramate, levetiracetam, and zonisamide have shown similar efficacy to that achieved with divalproex sodium, and in some cases better tolerability.[45]

Levetiracetam is useful for the treatment of myoclonic seizures.[46, 47] Noachtar et al demonstrated in a randomized, double-blinded, placebo-controlled trial that levetiracetam adjunctive therapy reduced all seizure types and myoclonic seizures in patients with JME.[48] Meta-analysis of 2 randomized controlled trials affirm that JME is highly responsive to treatment with levetiracetam.[49] Small, uncontrolled studies of levetiracetam monotherapy in JME suggest efficacy and tolerability.[50, 51]

Lamotrigine may also be a consideration in the treatment of JME. This agent is ideal for patients who cannot tolerate the adverse effects of valproate (eg, weight gain, tremor, stomach upset, and hair loss) or leviteracetam. In some patients, lamotrigine monotherapy controls seizures completely. However, lamotrigine can exacerbate myoclonic jerks. Data from an open-label study suggested that lamotrigine was better tolerated than valproate, with similar efficacy.[52] A European expert opinion study showed that lamotrigine was first-line choice for JME in adolescent females, whereas valproate was the first-line choice in adolescent males.[53]

Topiramate is useful in the treatment of primary generalized seizures; it may effectively prevent the seizures of JME.[54]  Findings from an open-label study also suggested that zonisamide might be effective and well tolerated in patients with JME.[55]

In general, low doses of appropriate anticonvulsants are needed to successfully treat JME. Although treatment with phenytoin, carbamazepine, or phenobarbital may control some seizure components of JME (albeit at high doses), these drugs may increase seizure frequency and occasionally precipitate new seizure types, such as absence seizures. Rarely, they may be considered in combination if the patient’s condition does not respond effectively to other first line drugs.[56]  Other antiepileptic medications noted to exacerbate JME include gabapentin, pregabalin, vigabatrin, oxcarbazepine, and tiagibine. Innapproriate antiepileptic medication selection in JME has been reported to potentiate status epilepticus.

Clonazepam is often used during seizure exacerbations in patients with JME; however, it is inadequate and undesirable as long-term treatment.

A patient’s medication should rarely be changed when he or she is not having seizures and there are no medication side effects or signs of toxicity. In medical school, physicians are taught to treat patients and not proposed serum target concentrations.  The routine checking of levels in a patient without side effects whose seizures are controlled is of little benefit to the patient, and sometimes detremental if it leads to an unnecessary dosing adjustment.  An effective low-dose regimen is not unusual; in fact, many patients with JME need relatively low levels of anticonvulsants to achieve adequate seizure control (as long as it is an appropriate medication for the syndrome).

 

Special considerations in pregnant women

All women of childbearing age who are taking anticonvulsants should also take folic acid 1 mg/d. It is also beneficial to provide counsel regarding pregancy planning so that adjustments to an antiepileptic drug regimen can occur in anticipation of a potential pregnancy. As a general consideration, monotherapy is preferred to polytherapy, as is the minimal dose required to control the patient's seizures.

In general, most epileptologists believe that the anticonvulsants that help that patient the most should be continued during pregnancy. Frequent monitoring of drug levels is recommended, as pregnancy induces clinically significant changes in drug metabolism, clearance, and volume of distribution. Women with JME are no different from other women who need to take anticonvulsants.

A great majority of children born to women taking anticonvulsant monotherapy are healthy. Valproic acid and divalproex sodium, however, clearly pose a recognized risk of birth defects (category D) that is higher than the risk associated with other anticonvulsants. Exposure in utero probably contributes to neural tube defects (at a rate of 10-20 times the general population) and facial clefts, possibly contributes to hypospadias, and potentially impacts cognition. Multiple studies have shown valproic acid inferiority in comparison to other AEDs. 

With regards to topiramate, data from the North American AED pregnancy registry reported a prevalence of MCM of 3.8% in 289 women exposed to TPM in the first trimester of pregnancy, versus 1.3% in the unexposed reference group.[57] As of March, 2011, the FDA considers topiramate to be a Category D drug.

Experience is limited with levetiracetam (category C), with one larger prospective database following 197 patients finding no detectable increased fetal risk. Greater data is available with lamotrigine. The North American AED Pregnancy registry prospectively found no increased risk of major congenital malformations; a 10.1 fold risk of cleft palate was noted, however it should be noted that the study included montherapy and polytherapy.[57]  This has failed to be replicated in larger prospective monotherapy reports. The United Kingdom pregnancy registry, a prospective database of 1151 patients on lamotrigine monotherapy, found no significantly increased risk of major congenital malformations or cleft palate.[58]

Previous
Next

Surgical Care

Surgical treatment is not indicated, because JME is a primary generalized epilepsy. Some uncontrolled studies have suggested that vagal nerve stimulation might be helpful for patients with intractable seizures of primary generalized onset, such as JME.

Previous
Next

Modification of Activity

Seizure precautions include warnings about unpredictable lapses of consciousness due to seizures during a variety of activities, including the following:

  • Driving vehicles or flying aircraft
  • Immersing oneself in water (eg, for baths, swimming, and other purposes)
  • Being at heights (eg, on roofs, scaffolds, and ladders)
  • Using fire (eg, on stoves, in ovens, in open fires)
  • Using power tools (eg, drills and saws)

Such precautions, including restrictions on driving, must be observed until seizures that impair consciousness are controlled (ie, the patient is seizure free) for the recommended period—typically 3-12 months, though the length varies from state to state in the United States. Patients with seizures cannot have a commercial driving license until they complete a seizure-free period of 5 years. In addition, patients with seizures are not permitted to fly aircraft.

Studies have shown that patients with JME experience decreases in quality of life similar to those experienced by patients with other epileptic syndromes.[59]

Patients with suspected seizures manifesting as lapses of consciousness during wakefulness should be educated and warned about seizure precautions. Documenting on the patient’s chart that driving and occupational hazards for people with seizures were discussed is helpful. Physicians should be aware of state regulations regarding driving, which vary considerably among states and nations.

Warnings should be tailored to each specific patient, and they should include factors such as seizure control, time of the occurrence of seizures, medication compliance, and the patient’s occupation, among other concerns.

Previous
Next

Consultations

JME is rarely diagnosed in the primary care setting. Most often, an epileptologist diagnoses and manages the condition, sometimes unfortunately after several years of inadequate treatment with medications such as carbamazepine or phenytoin.

Previous
 
 
Contributor Information and Disclosures
Author

James Selph, MD Assistant Professor of Neurology, University of South Carolina School of Medicine; Director of Neurophysiology Lab and Services, Palmetto Richland Hospital

James Selph, MD is a member of the following medical societies: American Association of Neuromuscular and Electrodiagnostic Medicine, American Epilepsy Society

Disclosure: Nothing to disclose.

Coauthor(s)

Souvik Sen, MD, MPH, MS, FAHA Professor and Chair, Department of Neurology, University of South Carolina School of Medicine

Souvik Sen, MD, MPH, MS, FAHA is a member of the following medical societies: American Academy of Neurology, Association for Patient-Oriented Research, American Heart Association

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Chief Editor

Selim R Benbadis, MD Professor, Director of Comprehensive Epilepsy Program, Departments of Neurology and Neurosurgery, Tampa General Hospital, University of South Florida College of Medicine

Selim R Benbadis, MD is a member of the following medical societies: American Academy of Neurology, American Medical Association, American Academy of Sleep Medicine, American Clinical Neurophysiology Society, American Epilepsy Society

Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: Cyberonics; Eisai; Lundbeck; Sunovion; UCB; Upsher-Smith<br/>Serve(d) as a speaker or a member of a speakers bureau for: Cyberonics; Eisai; Glaxo Smith Kline; Lundbeck; Sunovion; UCB<br/>Received research grant from: Cyberonics; Lundbeck; Sepracor; Sunovion; UCB; Upsher-Smith.

Additional Contributors

Jose E Cavazos, MD, PhD, FAAN, FANA, FACNS Professor with Tenure, Departments of Neurology, Pharmacology, and Physiology, Assistant Dean for the MD/PhD Program, Program Director of the Clinical Neurophysiology Fellowship, University of Texas School of Medicine at San Antonio; Co-Director, South Texas Comprehensive Epilepsy Center, University Hospital System; Director, San Antonio Veterans Affairs Epilepsy Center of Excellence and Neurodiagnostic Centers, Audie L Murphy Veterans Affairs Medical Center

Jose E Cavazos, MD, PhD, FAAN, FANA, FACNS is a member of the following medical societies: American Academy of Neurology, American Clinical Neurophysiology Society, American Neurological Association, Society for Neuroscience, American Epilepsy Society

Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: Brain Sentinel, consultant.<br/>Stakeholder (<5%), Co-founder for: Brain Sentinel.

Ramon Diaz-Arrastia, MD, PhD Professor, Department of Neurology, University of Texas Southwestern Medical Center at Dallas, Southwestern Medical School; Director, North Texas TBI Research Center, Comprehensive Epilepsy Center, Parkland Memorial Hospital

Ramon Diaz-Arrastia, MD, PhD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Neurology, New York Academy of Sciences, Phi Beta Kappa

Disclosure: Nothing to disclose.

Elizabeth Carroll, DO Resident Physician, Department of Neurology, University of South Florida College of Medicine

Elizabeth Carroll, DO is a member of the following medical societies: American Academy of Neurology, American Osteopathic Association, Florida Osteopathic Medical Association

Disclosure: Nothing to disclose.

Acknowledgements

Mark Spitz, MD Professor, Department of Neurology, University of Colorado Health Sciences Center

Mark Spitz, MD is a member of the following medical societies: American Academy of Neurology, American Clinical Neurophysiology Society, and American Epilepsy Society

Disclosure: pfizer Honoraria Speaking and teaching; ucb Honoraria Speaking and teaching; lumdbeck Honoraria Consulting

References
  1. Herpin TH. Des asces incomplets de l'epilepsie. J Balliere et Fils. 1867.

  2. Rabot T. De la myoclonia epileptique. Paris, France: Medical thesis; 1899.

  3. Lundborg H. Die Progresive Myoklonusepilepsie (Unverricht's Myoklonie). Stockholm, Sweden: Almqvist & Wiksell; 1903.

  4. Janz D, Mathes A. Die Propulsiv Petit Mal Epilepsie. New York, NY: Garger; 1955.

  5. Janz D, Christian W. Impulsive petit mal. Deutsche Leitschrift f Nervenheilkunde. 1957. 176:346-386.

  6. Lund M, Reintoft H, Simonsen N. Ein kontrolleret social og psychologisk Undersgelse af Patienter med Juvenil Myoklon Epilepsi. Ugeskr Laeg. 1975. 137:2415-18.

  7. Proposal for revised classification of epilepsies and epileptic syndromes. Commission on Classification and Terminology of the International League Against Epilepsy. Epilepsia. 1989 Jul-Aug. 30(4):389-99. [Medline].

  8. Bradley CA, Taghibiglou C, Collingridge GL, Wang YT. Mechanisms involved in the reduction of GABAA receptor alpha1-subunit expression caused by the epilepsy mutation A322D in the trafficking-competent receptor. J Biol Chem. 2008 Aug 8. 283(32):22043-50. [Medline].

  9. Macdonald RL, Kang JQ. Molecular Pathology of Genetic Epilepsies Associated with GABA(A) Receptor Subunit Mutations. Epilepsy Curr. 2009 Jan-Feb. 9(1):18-23. [Medline]. [Full Text].

  10. Ciumas C, Wahlin TB, Jucaite A, Lindstrom P, Halldin C, Savic I. Reduced dopamine transporter binding in patients with juvenile myoclonic epilepsy. Neurology. 2008 Sep 9. 71(11):788-94. [Medline].

  11. Delgado-Escueta AV. Advances in genetics of juvenile myoclonic epilepsies. Epilepsy Curr. 2007 May-Jun. 7(3):61-7. [Medline].

  12. Wallace R. Identification of a new JME gene implicates reduced apoptotic neuronal death as a mechanism of epileptogenesis. Epilepsy Curr. 2005 Jan-Feb. 5(1):11-3. [Medline].

  13. Suzuki T, Delgado-Escueta AV, Aguan K, et al. Mutations in EFHC1 cause juvenile myoclonic epilepsy. Nat Genet. 2004 Aug. 36(8):842-9. [Medline].

  14. Medina MT, Suzuki T, Alonso ME, Durón RM, Martínez-Juárez IE, Bailey JN, et al. Novel mutations in Myoclonin1/EFHC1 in sporadic and familial juvenile myoclonic epilepsy. Neurology. 2008 May 27. 70(22 Pt 2):2137-44. [Medline].

  15. Kinirons P, Rabinowitz D, Gravel M, Long J, Winawer M, Sénéchal G, et al. Phenotypic concordance in 70 families with IGE-implications for genetic studies of epilepsy. Epilepsy Res. 2008 Nov. 82(1):21-28. [Medline]. [Full Text].

  16. Tóth V, Rásonyi G, Fogarasi A, Kovács N, Auer T, Janszky J. Juvenile myoclonic epilepsy starting in the eighth decade. Epileptic Disord. 2007 Sep. 9(3):341-5. [Medline].

  17. Camfield CS, Camfield PR. Juvenile myoclonic epilepsy 25 years after seizure onset: a population-based study. Neurology. 2009 Sep 29. 73(13):1041-5. [Medline].

  18. Hirano Y, Oguni H, Funatsuka M, Imai K, Osawa M. Differentiation of myoclonic seizures in epileptic syndromes: a video-polygraphic study of 26 patients. Epilepsia. 2009 Jun. 50(6):1525-35. [Medline].

  19. Baykan B, Altindag EA, Bebek N, Ozturk AY, Aslantas B, Gurses C, et al. Myoclonic seizures subside in the fourth decade in juvenile myoclonic epilepsy. Neurology. 2008 May 27. 70(22 Pt 2):2123-9. [Medline].

  20. Sadleir LG, Scheffer IE, Smith S, Carstensen B, Carlin J, Connolly MB, et al. Factors influencing clinical features of absence seizures. Epilepsia. 2008 Dec. 49(12):2100-7. [Medline].

  21. Badawy RA, Macdonell RA, Jackson GD, Berkovic SF. Why do seizures in generalized epilepsy often occur in the morning?. Neurology. 2009 Jul 21. 73(3):218-22. [Medline].

  22. Filho GM, Rosa VP, Lin K, Caboclo LO, Sakamoto AC, Yacubian EM. Psychiatric comorbidity in epilepsy: a study comparing patients with mesial temporal sclerosis and juvenile myoclonic epilepsy. Epilepsy Behav. 2008 Jul. 13(1):196-201. [Medline].

  23. Piazzini A, Turner K, Vignoli A, Canger R, Canevini MP. Frontal cognitive dysfunction in juvenile myoclonic epilepsy. Epilepsia. 2008 Apr. 49(4):657-62. [Medline].

  24. Iqbal N, Caswell HL, Hare DJ, Pilkington O, Mercer S, Duncan S. Neuropsychological profiles of patients with juvenile myoclonic epilepsy and their siblings: a preliminary controlled experimental video-EEG case series. Epilepsy Behav. 2009 Mar. 14(3):516-21. [Medline].

  25. Specchio N, Boero G, Michelucci R, Gambardella A, Giallonardo AT, Fattouch J, et al. Effects of levetiracetam on EEG abnormalities in juvenile myoclonic epilepsy. Epilepsia. 2008 Apr. 49(4):663-9. [Medline].

  26. Sadleir LG, Scheffer IE, Smith S, Carstensen B, Farrell K, Connolly MB. EEG features of absence seizures in idiopathic generalized epilepsy: impact of syndrome, age, and state. Epilepsia. 2009 Jun. 50(6):1572-8. [Medline].

  27. Lu Y, Waltz S, Stenzel K, Muhle H, Stephani U. Photosensitivity in epileptic syndromes of childhood and adolescence. Epileptic Disord. 2008 Jun. 10(2):136-43. [Medline].

  28. Leutmezer F, Lurger S, Baumgartner C. Focal features in patients with idiopathic generalized epilepsy. Epilepsy Res. 2002 Aug. 50 (3):293-300. [Medline].

  29. Labate A, Ambrosio R, Gambardella A, Sturniolo M, Pucci F, Quattrone A. Usefulness of a morning routine EEG recording in patients with juvenile myoclonic epilepsy. Epilepsy Res. 2007 Oct. 77(1):17-21. [Medline].

  30. Park KI, Lee SK, Chu K, Lee JJ, Kim DW, Nam H. The value of video-EEG monitoring to diagnose juvenile myoclonic epilepsy. Seizure. 2009 Mar. 18(2):94-9. [Medline].

  31. Stefan H, Paulini-Ruf A, Hopfengärtner R, Rampp S. Network characteristics of idiopathic generalized epilepsies in combined MEG/EEG. Epilepsy Res. 2009 Aug. 85(2-3):187-98. [Medline].

  32. Lin K, Jackowski AP, Carrete H Jr, de Araújo Filho GM, Silva HH, Guaranha MS, et al. Voxel-based morphometry evaluation of patients with photosensitive juvenile myoclonic epilepsy. Epilepsy Res. 2009 Oct. 86(2-3):138-45. [Medline].

  33. Saini J, Sinha S, Bagepally BS, Ramchandraiah CT, Thennarasu K, Prasad C, et al. Subcortical structural abnormalities in juvenile myoclonic epilepsy (JME): MR volumetry and vertex based analysis. Seizure. 2013 Apr. 22(3):230-5. [Medline].

  34. Tae WS, Kim SH, Joo EY, Han SJ, Kim IY, Kim SI, et al. Cortical thickness abnormality in juvenile myoclonic epilepsy. J Neurol. 2008 Apr. 255(4):561-6. [Medline].

  35. Roebling R, Scheerer N, Uttner I, Gruber O, Kraft E, Lerche H. Evaluation of cognition, structural, and functional MRI in juvenile myoclonic epilepsy. Epilepsia. 2009 Jun 1. [Medline].

  36. Kim JH, Lee JK, Koh SB, Lee SA, Lee JM, Kim SI, et al. Regional grey matter abnormalities in juvenile myoclonic epilepsy: a voxel-based morphometry study. Neuroimage. 2007 Oct 1. 37(4):1132-7. [Medline].

  37. Pulsipher DT, Seidenberg M, Guidotti L, Tuchscherer VN, Morton J, Sheth RD, et al. Thalamofrontal circuitry and executive dysfunction in recent-onset juvenile myoclonic epilepsy. Epilepsia. 2009 May. 50(5):1210-9. [Medline].

  38. de Araújo Filho GM, Lin K, Lin J, Peruchi MM, Caboclo LO, Guaranha MS, et al. Are personality traits of juvenile myoclonic epilepsy related to frontal lobe dysfunctions? A proton MRS study. Epilepsia. 2009 May. 50(5):1201-9. [Medline].

  39. de Araujo Filho GM, de Araujo TB, Sato JR, Silva Id, Lin K, Júnior HC, et al. Personality traits in juvenile myoclonic epilepsy: evidence of cortical abnormalities from a surface morphometry study. Epilepsy Behav. 2013 May. 27(2):385-92. [Medline].

  40. Deppe M, Kellinghaus C, Duning T, Möddel G, Mohammadi S, Deppe K, et al. Nerve fiber impairment of anterior thalamocortical circuitry in juvenile myoclonic epilepsy. Neurology. 2008 Dec 9. 71(24):1981-5. [Medline].

  41. Lin K, Carrete H Jr, Lin J, Peruchi MM, de Araújo Filho GM, Guaranha MS, et al. Magnetic resonance spectroscopy reveals an epileptic network in juvenile myoclonic epilepsy. Epilepsia. 2009 May. 50(5):1191-200. [Medline].

  42. de Araújo Filho GM, Jackowski AP, Lin K, Guaranha MS, Guilhoto LM, da Silva HH, et al. Personality traits related to juvenile myoclonic epilepsy: MRI reveals prefrontal abnormalities through a voxel-based morphometry study. Epilepsy Behav. 2009 Jun. 15(2):202-7. [Medline].

  43. [Guideline] Gaillard WD, Chiron C, Cross JH, Harvey AS, Kuzniecky R, Hertz-Pannier L, et al. Guidelines for imaging infants and children with recent-onset epilepsy. Epilepsia. 2009 Sep. 50(9):2147-53. [Medline].

  44. Akgun Y, Soysal A, Atakli D, Yuksel B, Dayan C, Arpaci B. Cortical excitability in juvenile myoclonic epileptic patients and their asymptomatic siblings: a transcranial magnetic stimulation study. Seizure. 2009 Jul. 18(6):387-91. [Medline].

  45. Park KM, Kim SH, Nho SK, Shin KJ, Park J, Ha SY, et al. A randomized open-label observational study to compare the efficacy and tolerability between topiramate and valproate in juvenile myoclonic epilepsy. J Clin Neurosci. 2013 May 11. [Medline].

  46. Sullivan JE, Dlugos DJ. Idiopathic Generalized Epilepsy. Curr Treat Options Neurol. 2004 May. 6(3):231-242. [Medline].

  47. Specchio LM, Gambardella A, Giallonardo AT, Michelucci R, Specchio N, Boero G, et al. Open label, long-term, pragmatic study on levetiracetam in the treatment of juvenile myoclonic epilepsy. Epilepsy Res. 2006. 71(1):32-39. [Medline].

  48. Noachtar S, Andermann E, Meyvisch P, Andermann F, Gough WB, Schiemann-Delgado J. Levetiracetam for the treatment of idiopathic generalized epilepsy with myoclonic seizures. Neurology. 2008 Feb 19. 70(8):607-16. [Medline].

  49. Rosenfeld WE, Benbadis S, Edrich P, Tassinari CA, Hirsch E. Levetiracetam as add-on therapy for idiopathic generalized epilepsy syndromes with onset during adolescence: analysis of two randomized, double-blind, placebo-controlled studies. Epilepsy Res. 2009 Jul. 85(1):72-80. [Medline].

  50. Sharpe DV, Patel AD, Abou-Khalil B, Fenichel GM. Levetiracetam monotherapy in juvenile myoclonic epilepsy. Seizure. 2008 Jan. 17(1):64-8. [Medline].

  51. Verrotti A, Cerminara C, Coppola G, Franzoni E, Parisi P, Iannetti P, et al. Levetiracetam in juvenile myoclonic epilepsy: long-term efficacy in newly diagnosed adolescents. Dev Med Child Neurol. 2008 Jan. 50(1):29-32. [Medline].

  52. Morris GL, Hammer AE, Kustra RP, Messenheimer JA. Lamotrigine for patients with juvenile myoclonic epilepsy following prior treatment with valproate: results of an open-label study. Epilepsy Behav. 2004 Aug. 5(4):509-12. [Medline].

  53. Wheless JW, Clarke DF, Arzimanoglou A, Carpenter D. Treatment of pediatric epilepsy: European expert opinion, 2007. Epileptic Disord. 2007 Dec. 9(4):353-412. [Medline].

  54. Prasad A, Kuzniecky RI, Knowlton RC, et al. Evolving antiepileptic drug treatment in juvenile myoclonic epilepsy. Arch Neurol. 2003 Aug. 60(8):1100-5. [Medline].

  55. Kothare SV, Valencia I, Khurana DS, et al. Efficacy and tolerability of zonisamide in juvenile myoclonic epilepsy. Epileptic Disord. 2004 Dec. 6(4):267-70. [Medline].

  56. Nicolson A, Appleton RE, Chadwick DW, Smith DF. The relationship between treatment with valproate, lamotrigine, and topiramate and the prognosis of the idiopathic generalised epilepsies. J Neurol Neurosurg Psychiatry. 2004 Jan. 75(1):75-9. [Medline].

  57. The North American Antiepileptic Drug Pregnancy Registry. Available at http://www.aedpregnancyregistry.org/. Accessed: June 24, 2016.

  58. UK Epilepsy and Pregnancy Register. Available at http://www.epilepsyandpregnancy.co.uk/. Accessed: June 24, 2016.

  59. Westphal-Guitti AC, Alonso NB, Migliorini RC, da Silva TI, Azevedo AM, Caboclo LO, et al. Quality of life and burden in caregivers of patients with epilepsy. J Neurosci Nurs. 2007 Dec. 39(6):354-60. [Medline].

  60. Wolf P, Yacubian EM, Avanzini G, Sander T, Schmitz B, Wandschneider B, et al. Juvenile myoclonic epilepsy: A system disorder of the brain. Epilepsy Res. 2015 Aug. 114:2-12. [Medline].

 
Previous
Next
 
Findings in a man with a history of generalized tonic-clonic seizures (mostly nocturnal) and myoclonic jerks (mostly in the morning) since the age of 14 years. Carbamazepine exacerbated his myoclonic seizures. Sleep-deprived EEG was digitally recorded and then plotted by using an analog paper machine. The patient was getting drowsy when this burst of polyspike and slow wave was recorded.
 
 
 
All material on this website is protected by copyright, Copyright © 1994-2016 by WebMD LLC. This website also contains material copyrighted by 3rd parties.