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Juvenile Myoclonic Epilepsy Clinical Presentation

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


Juvenile myoclonic epilepsy (JME) is diagnosed on the basis of clinical findings. Video-electroencephalography (EEG) monitoring of typical seizures is the criterion standard, but in the great majority of patients, a working diagnosis of probable JME is made on the basis of the clinical history, often with supportive interictal EEG correlates.

Although observers’ descriptions of seizures are helpful, caution must be used regarding their validity. The most important element in the diagnosis of JME is the patient’s history. Any patient who presents with generalized tonic-clonic seizures (GTCSs) without an aura should be questioned about myoclonic jerks, the time of day when the seizures occurred, and any precipitating factors.

About 17-49% of patients have a family history of epilepsy. Symptoms usually begin in adolescence. The leading symptom is jerky movements that occur in the morning (typically, shortly after awakening) but might occur throughout the day, without loss of consciousness.

Patients may have myoclonic jerks plus other seizure types. In about 60% of patients, JME begins with myoclonic jerks, followed by the onset of relatively uncommon GTCSs a few years later. The finding of myoclonic jerks plus absence seizures and GTCSs is the next most common combination, occurring in approximately 30% of patients with JME. The combination of myoclonic jerks and absence seizures without GTCSs is rare, occurring in only 2% of patients.

Myoclonic jerks or seizures

Myoclonic jerks or seizures without impairment of consciousness are the cardinal symptoms of JME. Although an occasional strong myoclonic jerk may make patients momentarily seem to be “in a fog,” a key feature is that consciousness is preserved during these jerks.

The jerks are usually brief, bilateral, arrhythmic contractions that mainly involve the shoulders and arms. However, some patients report jerking in the lower limbs, trunk, or head. Some jerks occur unilaterally. In a video-EEG study, Hirano et al characterized myoclonic jerks in patients with JME as being more likely to occur in clusters, with distal predominance, and involving extension muscles.[18]

The frequency and intensity of myoclonic jerks may vary. For instance, they may be perceived only internally, as an electric shock–like sensation. If the jerks are violent, patients may throw objects they are holding or even fall to the floor. Myoclonic jerks can occur in rapid succession and even progress to myoclonic status epilepticus. However, more often a rapid succession of myoclonic jerks evolves into a primary GTCS.

Myoclonic jerks occur as the only seizure type in approximately 17% of patients with JME; the remaining patients have a combination of myoclonic jerks, GTCSs, and absence seizures. Myoclonic seizures tend to subside by the fourth decade,[19] but the other seizure types might persist.

Generalized tonic-clonic seizures

GTCSs occur in approximately 80% of patients with JME. The GTCSs seen in JME are typically symmetric, with a prolonged tonic phase that may lead to cyanosis and tongue biting.

GTCSs are sometimes preceded by a series of myoclonic jerks of increasing severity that evolve into an initial clonic phase of a GTCS. The GTCSs often cause a patient with JME to seek medical attention; in this setting, patients should be questioned specifically about myoclonic jerks because most patients do not mention them.

Absence seizures

In JME, absence seizures are somewhat less common than GTCSs. Janz reported that 28% of his patients with JME also had absence seizures.[4, 5] When absence seizures are a feature of JME, they are often the first clinical manifestation of the syndrome, with myoclonic jerks typically following 1-9 years later. A clue to this diagnosis is the development of GTCSs or myoclonic seizures within a couple of years after starting treatment with ethosuximide. Approximately 3-8% of children who present with absence seizures ultimately receive a diagnosis of JME.

In JME, absence seizures are typically short, lasting a few seconds, and usually not accompanied by motor signs.

The severity of absence seizures in JME is somewhat age dependent. When they appear in children younger than 10 years, absence seizures of JME are reported less often than those of childhood absence epilepsy. Some recollection of the ictal events is common, particularly in patients that have persistence of these seizures during adulthood. Automatism is rare.

When absence seizures of JME begin in children aged 10 years or older, they may be even less severe than they otherwise would be, with merely a brief interruption in the patient’s ability to concentrate. In a video-EEG monitoring study of patients with absence seizures, Sadleir et al found that patients with JME tend to have shorter seizures than patients with other epileptic syndromes with absences.[20]

Precipitating factors for seizures

Seizures of JME often are precipitated by (1) lack of sleep, (2) psychological stress, (3) alcohol consumption, and (4) noncompliance with medication regimens. These factors can all be a particular problem in adolescents, particularily after moving out of the parents household or after matriculation into college.

The time of day is also important because JME has a characteristic circadian pattern of activity. Myoclonic jerks, GTCSs, and absence seizures all tend to occur in the early morning after the patient awakens (though they also occur, to a lesser extent, in the evening when the patient is relaxing). When myoclonic jerks occur in the mornings, patients may have difficulty in eating breakfast or brushing their teeth. In some studies, nearly 90% of patients with JME had myoclonic jerks on awakening; the rest had either random jerks throughout the day or jerks at night.

In a study using transcranial magnetic stimulation (TMS) to examine the diurnal variability of cortical excitability, Badawy et al demonstrated that short and long intracortical inhibition was considerably more impaired in the mornings than in the afternoons in patients with JME.[21] This might suggest a biological basis for the clinical observation of increased seizure frequency within the first hour upon awakening in patients with JME.

Precipitating factors can be summarized as follows:

  • Sleep deprivation
  • Psychological stress
  • Alcohol use
  • Noncompliance of medication
  • Menses
  • Time of day - Usually mornings

Physical Examination

Physical examination usually does not identify any abnormalities in patients with JME. Intelligence is normal; this observation is in contrast to findings with diseases such as progressive myoclonic epilepsies, in which progressive mental deterioration is the rule.



Comorbidities associated with JME include psychiatric and neurologic disorders.

Psychiatric comorbidities have been described in patients with JME. In one study, 49% of patients with JME had a psychiatric comorbidity.[22] Anxiety and mood disorders were reported in 23% and 19% of patients with JME, respectively.

Neuropsychological testing of patients with JME has demonstrated selected frontal lobe dysfunction in tests such as the Wisconsin Card Sorting test and the Word Fluency test.[23] This dysfunction occurs despite having normal intelligence quotient (IQ) results obtained testing through conventional Wechsler testing. Impairment in executive function has also been reported.[24]



Both myoclonic status epilepticus and nonconvulsive status epilepticus (NCSE) have been reported in JME. 

The prevalence of NCSE in JME can be estimated at 5.8%, and the incidence at 1.2% per year with a clear preponderance of female gender. 

Absence and myoclonic status epilepticus precipitated by inappropriate antiepileptic drugs can occur in idiopathic generalized epilepsy, including JME.

Contributor Information and Disclosures

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.


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.


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

  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 Accessed: June 24, 2016.

  58. UK Epilepsy and Pregnancy Register. Available at 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].

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.
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