Generalized Tonic-Clonic Seizures Clinical Presentation

  • Author: David Y Ko, MD; Chief Editor: Selim R Benbadis, MD   more...
 
Updated: Jun 8, 2011
 

History

Patients with generalized tonic-clonic seizures may report having a prodrome, which comprises premonitory symptoms occurring hours or days before a seizure. Common prodromes include mood changes, sleep disturbances, lightheadedness, anxiety, irritability, difficulty concentrating and, rarely, an ecstatic feeling.

Patients with generalized tonic-clonic seizures do not have auras. An aura represents a simple partial seizure, and a reliable history of aura identifies the seizure as partial and not generalized.

Other symptoms that have been described less consistently are abdominal pain, facial pallor, or headache. Witnesses of a patient's seizure should be asked about the stereotypical ictal cry, which is strongly associated with generalized tonic-clonic seizures.[2]

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Physical Examination

The patient may have completely nonfocal findings on neurologic examination when not having seizures. Seizures typically are divided into tonic, clonic, and postictal phases, which are described in detail in this section.

Tonic phase

This stage lasts for 10-20 seconds. Generalized convulsive seizures may begin with myoclonic jerks or, rarely, with absences. The tonic phase begins with flexion of the trunk and elevation and abduction of the elbows. Subsequent extension of the back and neck is followed by extension of arms and legs. This can be accompanied by apnea, which is secondary to laryngeal spasm.

Autonomic signs are common during this phase and include increase in pulse rate and blood pressure, profuse sweating, and tracheobronchial hypersecretion. Although urinary bladder pressure rises, voiding does not occur because of sphincter muscle contraction.

Clonic phase

The tonic stage gives way to clonic convulsive movements, in which the tonic muscles relax intermittently for a variable period of time.

During the clonic stage, a generalized movement occurs at a rate of about 4-8 Hz. This is because phases of atonia alternate with repeated violent flexor spasms. Each spasm is accompanied by pupillary contraction and dilation. Some patients may bite their tongue or cheek.

The atonic periods gradually become longer until the last spasm. Voiding may occur at the end of the clonic phase as sphincter muscles relax. The atonic period lasts about 30 seconds. The patient continues to be apneic during this phase.

The convulsion, including tonic and clonic phases, lasts around 1-2 minutes.

Postictal state

The postictal state includes a variable period of unconsciousness during which the patient becomes quiet and breathing resumes. The patient gradually awakens, often after a period of stupor or sleep, and often is confused, with some automatic behavior. Headache and muscular pain are common. The patient does not recall the seizure itself.

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Contributor Information and Disclosures
Author

David Y Ko, MD  Associate Professor of Clinical Neurology, Associate Director, USC Adult Epilepsy Program, Keck School of Medicine of the University of Southern California

David Y Ko, MD is a member of the following medical societies: American Academy of Neurology, American Clinical Neurophysiology Society, American Epilepsy Society, and American Headache Society

Disclosure: GSK Honoraria Speaking and teaching; UCB Honoraria Speaking and teaching; Lundbeck Consulting fee Consulting; Westward Consulting fee Consulting

Coauthor(s)

Soma Sahai-Srivastava, MD  Director of Neurology Ambulatory Care Services, LAC and USC Medical Center; Assistant Professor, Department of Neurology, Keck School of Medicine of the University of Southern California

Soma Sahai-Srivastava, MD is a member of the following medical societies: American Academy of Neurology, American Headache Society, and American Medical Association

Disclosure: Nothing to disclose.

Specialty Editor Board

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, and Phi Beta Kappa

Disclosure: Nothing to disclose.

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

Disclosure: Medscape Salary Employment

Jose E Cavazos, MD, PhD, FAAN  Associate Professor with Tenure, Departments of Neurology, Pharmacology, and Physiology, 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 of the San Antonio Veterans Affairs Epilepsy Center of Excellence and Neurodiagnostic Centers, Audie L Murphy Veterans Affairs Medical Center

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

Disclosure: GXC Global, Inc. Intellectual property rights Medical Director - company is to develop a seizure detecting device. No conflict with any of the eMedicine articles that I wrote or edited.

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 Academy of Sleep Medicine, American Clinical Neurophysiology Society, American Epilepsy Society, and American Medical Association

Disclosure: UCB Pharma Honoraria Speaking, consulting; Lundbeck Honoraria Speaking, consulting; Cyberonics Honoraria Speaking, consulting; Glaxo Smith Kline Honoraria Speaking, consulting; Pfizer Honoraria Speaking, consulting; Sleepmed/DigiTrace Honoraria Speaking, consulting

References
  1. Walczak TS, Leppik IE, D'Amelio M, Rarick J, So E, Ahman P, et al. Incidence and risk factors in sudden unexpected death in epilepsy: a prospective cohort study. Neurology. Feb 27 2001;56(4):519-25. [Medline].

  2. Elzawahry H, Do CS, Lin K, Benbadis SR. The diagnostic utility of the ictal cry. Epilepsy Behav. Jul 2010;18(3):306-7. [Medline].

  3. Morrell MJ. Differential diagnosis of seizures. Neurol Clin. Nov 1993;11(4):737-54. [Medline].

  4. [Best Evidence] Marson AG, Al-Kharusi AM, Alwaidh M, Appleton R, Baker GA, Chadwick DW, et al. The SANAD study of effectiveness of valproate, lamotrigine, or topiramate for generalised and unclassifiable epilepsy: an unblinded randomised controlled trial. Lancet. Mar 24 2007;369(9566):1016-26. [Medline]. [Full Text].

  5. Peters DH, Sorkin EM. Zonisamide. A review of its pharmacodynamic and pharmacokinetic properties, and therapeutic potential in epilepsy. Drugs. May 1993;45(5):760-87. [Medline].

  6. Kluger G, Bauer B. Role of rufinamide in the management of Lennox-Gastaut syndrome (childhood epileptic encephalopathy). Neuropsychiatr Dis Treat. Feb 2007;3(1):3-11. [Medline]. [Full Text].

  7. [Best Evidence] Glauser T, Kluger G, Sachdeo R, Krauss G, Perdomo C, Arroyo S. Rufinamide for generalized seizures associated with Lennox-Gastaut syndrome. Neurology. May 20 2008;70(21):1950-8. [Medline].

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