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


Status Epilepticus Treatment & Management

  • Author: Julie L Roth, MD; Chief Editor: Stephen A Berman, MD, PhD, MBA  more...
Updated: Feb 19, 2016

Approach Considerations

Both generalized tonic-clonic status epilepticus (SE) and subtle SE must be treated aggressively. Maintenance of vital signs, including respiratory function, is of major importance. Any indication of respiratory insufficiency should be addressed by intubation.

Early treatment measures are performed in concert with diagnostic studies. The treating physician should not wait for a blood level to return from a laboratory test before giving the patient a loading dose of phenytoin. The same protocol should be followed regardless of whether the patient is already taking phenytoin. Assume that the patient is noncompliant because this is the most common cause of SE in patients with known epilepsy.

Even if the patient has been compliant and even if phenytoin levels were already in the therapeutic range (10-20 µg/mL), data suggest that 20-30 µg/mL is more effective than 10-20 µg/mL in stopping seizures.

High doses can cause ataxia and sedation. Because the patient is likely to be hospitalized after the SE is controlled, these adverse effects are less important than they would be in a patient being treated on an outpatient basis. SE is a life-threatening situation, and the patient will be admitted to the hospital after treatment. Therefore, if treatment errs, it should err on the side of excessive medication. Temporary adverse effects are preferred to irreversible brain damage or death.

Finally, systemic acidosis is not a major concern because it is usually transient, and medical treatment to normalize acidosis can lead to a rebound metabolic alkalosis when the SE stops. In addition, evidence suggests that acidosis has antiseizure effects.

The approach to treatment of motor focal SE—specifically, epilepsy partialis continua—is similar to that with generalized convulsive SE. However, the urgency of treatment and the extremes to which a physician may elect to go to terminate the seizure are tempered.

The basic principles of emergency care (ie, attention to airway, breathing, and circulation [ABCs] apply to focal as well as to generalized SE. Although generalized convulsive SE frequently jeopardizes the ABCs, epilepsy partialis continua only infrequently does so.

See the image below for management algorithms for convulsive status epilepticus.

Treatment algorithms for convulsive status epilept Treatment algorithms for convulsive status epilepticus.

Treatment Guidelines

In 2016, the American Epilepsy Society (AES) issued new guidelines for the treatment of SE. The guidelines provide a time-dependent treatment algorithm that includes four phases.[57]

In the stabilization phase, standard first-aid for seizures should be initiated.

In the initial therapy phase, a benzodiazepine (specifically IM midazolam, IV lorazepam, or IV diazepam) is recommended as initial therapy.

In the second phase, options include IV fosphenytoin, valproic acid, or levetiracetam. If none of these is available, IV phenobarbital is a reasonable alternative.

In the third phase, if a patient experiences 40+ minutes of seizure activity, treatment considerations should include repeating second-line therapy or anesthetic doses of thiopental, midazolam, pentobarbital, or propofol.



Prehospital Care

Supportive care, including ABCs, must be addressed in the prehospital setting. If the seizure fails to stop within 4-5 minutes or if the patient is continuing to seize at the time of emergency medical system (EMS) personnel arrival, prompt administration of anticonvulsants may be necessary.

Because of the refrigeration requirements and the infrequent use of most anticonvulsants, diazepam (Valium) is often the only anticonvulsant available in the prehospital setting. Diazepam may be administered intravenously (IV) or per rectum. Midazolam (Versed) is available in some EMS systems and is currently the subject of study because of the option for intramuscular and intranasal administration.

If persons who know the patient, or who witnessed the onset of the seizures, are present at the scene, EMS providers may be able to collect information that offers clues to the cause of the SE.


Emergency Department Care

Regardless of the clinical manifestations of generalized SE, aggressive supportive care and prompt termination of electrical seizure activity are the goals. Care is individualized to the patient.

Establish intravenous access, ideally in a large vein. Intravenous administration is the preferred route for anticonvulsant administration because it allows therapeutic levels to be attained more rapidly. Begin cardiac and other hemodynamic monitoring.

Administer a 50-mL bolus of 50% dextrose IV and 100 mg of thiamine. If seizure activity does not terminate within 4-5 minutes, start anticonvulsant medication. If EMS history has already defined SE, treatment should begin immediately. In some settings where drug intoxication might be likely, consider also adding naloxone at 0.4-2.0 mg IV to the dextrose bag.

Administer diazepam (0.15 mg/kg) or lorazepam (0.1 mg/kg) IV over 5 minutes, followed by fosphenytoin or phenytoin. Fosphenytoin is preferable, as it provides the advantage of a potentially rapid rate of administration with less risk of venous irritation (eg, to avoid the risk of purple-glove syndrome with phenytoin).

Fosphenytoin is given in a dose of 15-20 mg phenytoin equivalents [PE]/kg, at a rate not to exceed 150 mg PE/min). The dose of phenytoin is 18-20 mg/kg, at a rate not to exceed 50 mg/min). Never mix phenytoin with a 5% dextrose solution; put it in a normal saline solution to minimize the risk of crystal precipitation.

Ensure airway control. Nasopharyngeal airway placement is sufficient for some patients, particularly if the seizures are stopped and the patient is awakening. For other patients, endotracheal intubation is necessary. In neuromuscular paralysis, rapid sequence induction is necessary at times. Use short-acting paralytics to ensure that ongoing seizure activity is not masked. Use EEG monitoring if long-acting paralytics are used and if a question exists about seizure cessation.

Correct any metabolic imbalances. Control hyperthermia.

If seizures continue after 20 minutes, give additional fosphenytoin (10 mg PE/kg IV) or phenytoin (10 mg/kg IV). Aim for a total serum phenytoin level of about 22-25 µg/mL.

In patients with epilepsy partialis continua who had been receiving AED treatment, knowledge of the patient's usual regimen and current levels may be pivotal. As an alternative to fosphenytoin or phenytoin, supplementation of their routine medication (guided by stat AED levels) may help suppress their seizures.

Failure to respond to optimal benzodiazepine and phenytoin loading operationally defines refractory status epilepticus. If seizures continue after 20 minutes, give phenobarbital (15 mg/kg IV). Use caution when adding barbiturates to benzodiazepines because their coadministration may potentiate ventilatory failure. This may be especially true for patients (eg, elderly patients) with impaired drug clearance.

For this reason, especially in the setting of partially treated epilepsy partialis continua or simple partial SE, in which the morbidity of the underlying illness is less than in generalized convulsive SE, a tempered approach may be preferred. Incremental doses of phenobarbital may offer satisfactory efficacy in these uncommon settings and may be safer than full intravenous loading doses, which increase the risk of respiratory suppression.

Alternatives to phenobarbital that are shorter acting and allow for periodic neurologic assessments include the following[58, 59] :

  • Valproate
  • Levetiracetam
  • Propofol [60, 61]
  • Midazolam
  • Pentobarbital
  • Ketamine [62] }

If seizures continue, consider administering general anesthesia with medications such as propofol, midazolam, or pentobarbital. Ketamine infusion can alternatively (or additionally) be used in the treatment of refractory status epilepticus, with some evidence of safety and efficacy. These agents are given by IV drip and titrated to a burst-suppression pattern in the EEG trace. In a patient with epilepsy partialis continua or simple partial SE, one might even consider rapid oral loading of one of the newer AEDs (eg, topiramate[63] ), depending on the ongoing clinical urgency. Lacosamide is a novel antiepileptic drug available in IV form; though anecdotally it appears safe, its effectiveness in treatment of refractory SE is unknown.

If the patient promptly becomes alert after receiving a benzodiazepine or other AED, that tends to corroborate the diagnosis of SE. Nevertheless, the failure to become alert by no means excludes the diagnosis of SE. Most patients remain sleepy or stuporous after the resolution of a prolonged episode of SE, whether focal or generalized.

For this reason, bedside EEG assessment can be invaluable in guiding treatment decisions. This is true not only early in the treatment paradigm but also late to help gauge the patient's recovery and to ensure that he or she is not having repeated subclinical seizures. Portable computer-aided EEG monitoring (LTM system) can be particularly helpful in this task.


Antiepileptic Drug Selection

Benzodiazepines are the preferred first-line agents. According to 2016 guidelines from the American Epilepsy Society (AES), any of three benzodiazepines — intramuscular (IM) midazolam, intravenous (IV) lorazepam, or IV diazepam — should be given if first-aid stabilization measures don't stop the seizure within 5 minutes.[57] Although diazepam is familiar to paramedics and emergency physicians, a consensus has evolved among neurologists and epileptologists that lorazepam may be preferred in this setting because of its long distribution half-life. 

A comparison of initial IV treatment for overt generalized convulsive SE by Treiman et al found that lorazepam was more effective than phenytoin alone.[38] Lorazepam was not more effective than phenobarbital or diazepam plus phenytoin, but it was easier to use. Not studied was fosphenytoin, which is theoretically a significant improvement over phenytoin.

A 2014 Cochrane Database review found intravenous lorazepam is better than intravenous diazepam or intravenous phenytoin alone for cessation of seizures.[64]

Intravenous valproic acid has been shown in a pilot study to be equal to or better than phenytoin in aborting generalized SE, and it has been used in some cases of focal status epilepticus.[65, 66]

The use of levetiracetam (Keppra) in treatment of refractory SE has been examined, in part due to its availability in intravenous form, although its use in treating focal SE remains investigational.[67, 68, 69] Anecdotal reports describe the beneficial use of topiramate in some cases of focal SE.

There are several intravenous formulations of antiepileptic drugs (AEDs) at different stages of development.[70] Some of these might be able to help refractory cases with SE as adjunctive therapy.

No data clearly support a best third-line drug. Controlled trials are lacking, and recommendations vary greatly. While phenobarbital has historically been among the most widely used, the list of third-line drugs also includes intravenous agents such as midazolam, propofol, pentobarbital, valproate, levetiracetam, lidocaine,[71] , ketamine[62] } and others. Lacosamide, a novel antiepileptic drug available for intravenous injection, may be used safely as adjunctive therapy for SE, but little data exist on its efficacy.[72]

A clinical practice trend seems to be for use of propofol as a third-line agent, often initiated during induction for endotracheal intubation. However, propofol infusion syndrome and increased mortality is reported when used at high doses and for prolonged periods.[61]

Absence status epilepticus

Benzodiazepines and valproate are the treatments of choice for absence SE. Valproic acid is available in intravenous (IV) form. The theoretical advantage is that it can be continued long term after the acute episode. Valproate is loaded at a dose of 25 mg/kg IV in a 50-mL solution and infused over 10 minutes. The next dose is given 3 hours later, after which every-6-hour dosing can be started. The drug should never be given intramuscularly. Ethosuximide also can be useful, but is not available in parenteral form.

Contributor Information and Disclosures

Julie L Roth, MD Neurologist, Epilepsy and General Neurology, Comprehensive Epilepsy Program, Rhode Island Hospital; Assistant Professor, Department of Neurology, The Warren Alpert Medical School of Brown University

Julie L Roth, MD is a member of the following medical societies: American Academy of Neurology, American Epilepsy Society

Disclosure: Nothing to disclose.


Andrew S Blum, MD, PhD Director, Adult Epilepsy and EEG Laboratory, Comprehensive Epilepsy Program, Rhode Island Hospital; Associate Professor of Neurology, The Warren Alpert Medical School of Brown University

Andrew S Blum, MD, PhD is a member of the following medical societies: American Academy of Neurology, American Epilepsy Society, Massachusetts Medical Society

Disclosure: Received royalty from Springer Publishing for editor of text, the clinical neurophysiology primer.

Chief Editor

Stephen A Berman, MD, PhD, MBA Professor of Neurology, University of Central Florida College of Medicine

Stephen A Berman, MD, PhD, MBA is a member of the following medical societies: Alpha Omega Alpha, American Academy of Neurology, Phi Beta Kappa

Disclosure: Nothing to disclose.


Norberto Alvarez, MD Assistant Professor, Department of Neurology, Harvard Medical School; Consulting Staff, Department of Neurology, Boston Children's Hospital; Medical Director, Wrentham Developmental Center

Norberto Alvarez, MD is a member of the following medical societies: American Academy of Neurology, American Epilepsy Society, and Child Neurology Society

Disclosure: Nothing to disclose.

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

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 Medscape Reference articles that I wrote or edited.

Daniel J Dire, MD, FACEP, FAAP, FAAEM Clinical Professor, Department of Emergency Medicine, University of Texas Medical School at Houston; Clinical Professor, Department of Pediatrics, University of Texas Health Sciences Center San Antonio

Daniel J Dire, MD, FACEP, FAAP, FAAEM is a member of the following medical societies: American Academy of Clinical Toxicology, American Academy of Emergency Medicine, American Academy of Pediatrics, American College of Emergency Physicians, and Association of Military Surgeons of the US

Disclosure: Nothing to disclose.

Rick Kulkarni, MD Attending Physician, Department of Emergency Medicine, Cambridge Health Alliance, Division of Emergency Medicine, Harvard Medical School

Rick Kulkarni, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine

Disclosure: WebMD Salary Employment

Edward H Maa, MD Chief of Comprehensive Epilepsy Program, Department of Neurology, Denver Health and Hospitals; Assistant Professor, Department of Neurology, University of Colorado School of Medicine and Veterans Affairs Medical Center

Edward H Maa, MD is a member of the following medical societies: American Academy of Neurology and American Epilepsy Society

Disclosure: UCB Pharma Honoraria Speaking and teaching

Erasmo A Passaro, MD, FAAN Director, Comprehensive Epilepsy Program/Clinical Neurophysiology Lab, Bayfront Medical Center, Florida Center for Neurology

Erasmo A Passaro, MD, FAAN is a member of the following medical societies: American Academy of Neurology, American Academy of Sleep Medicine, American Clinical Neurophysiology Society, American Epilepsy Society, American Medical Association, and American Society of Neuroimaging

Disclosure: Glaxo Smith Kline Honoraria Speaking and teaching; UCB Honoraria Speaking and teaching; Pfizer Honoraria Speaking and teaching; Forest Honoraria Speaking and teaching

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

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

  1. Lüders HO, Rona S, Rosenow F, et al. A semiological classification of status epilepticus. Epileptic Disord. 2005 Jun. 7(2):149-50. [Medline].

  2. Brenner RP. EEG in convulsive and nonconvulsive status epilepticus. J Clin Neurophysiol. 2004 Sep-Oct. 21(5):319-31. [Medline].

  3. Kaplan PW. The EEG of status epilepticus. J Clin Neurophysiol. 2006 Jun. 23(3):221-9. [Medline].

  4. D'Giano CH, Del C Garcia M, Pomata H, Rabinowicz AL. Treatment of refractory partial status epilepticus with multiple subpial transection: case report. Seizure. 2001 Jul. 10(5):382-5. [Medline].

  5. Ma X, Liporace J, O'Connor MJ, Sperling MR. Neurosurgical treatment of medically intractable status epilepticus. Epilepsy Res. 2001 Jul. 46(1):33-8. [Medline].

  6. Duane DC, Ng YT, Rekate HL, et al. Treatment of refractory status epilepticus with hemispherectomy. Epilepsia. 2004 Aug. 45(8):1001-4. [Medline].

  7. Winston KR, Levisohn P, Miller BR, Freeman J. Vagal nerve stimulation for status epilepticus. Pediatr Neurosurg. 2001 Apr. 34(4):190-2. [Medline].

  8. Proceedings and abstracts of the First London Colloquium on Status Epilepticus, University College London, April 12-15, 2007. Epilepsia. 2007. 48 Suppl 8:1-109. [Medline].

  9. Shorvon SD, Trinka E, Walker MC. The proceedings of the First London Colloquium on Status Epilepticus--University College London, April 12-15, 2007. Introduction. Epilepsia. 2007. 48 Suppl 8:1-3. [Medline].

  10. Kälviäinen R. Status epilepticus treatment guidelines. Epilepsia. 2007. 48 Suppl 8:99-102. [Medline].

  11. Wilson JV, Reynolds EH. Texts and documents. Translation and analysis of a cuneiform text forming part of a Babylonian treatise on epilepsy. Med Hist. 1990 Apr. 34(2):185-98. [Medline].

  12. Wolf P, Trinka E, Bauer G. Absence status epilepticus: the first documented case?. Epilepsia. 2007. 48 Suppl 8:4-5. [Medline].

  13. Epilepsy Foundation of America. Treatment of convulsive status epilepticus. Recommendations of the Epilepsy Foundation of America's Working Group on Status Epilepticus. JAMA. 1993 Aug 18. 270(7):854-9. [Medline].

  14. Lowenstein DH, Bleck T, Macdonald RL. It's time to revise the definition of status epilepticus. Epilepsia. 1999 Jan. 40(1):120-2. [Medline].

  15. Lowenstein DH, Cloyd J. Out-of-hospital treatment of status epilepticus and prolonged seizures. Epilepsia. 2007. 48 Suppl 8:96-8. [Medline].

  16. Geier S, Bancaud J, Bonis A, Enjelvin M. [Tele-E.E.G. recordings of three epileptic attacks classified as episodes of PM status (author's transl)]. Rev Electroencephalogr Neurophysiol Clin. 1977 Apr-Jun. 7(2):201-2. [Medline].

  17. Ellis JM, Lee SI. Acute prolonged confusion in later life as an ictal state. Epilepsia. 1978 Apr. 19(2):119-28. [Medline].

  18. Niedermeyer E, Fineyre F, Riley T, Uematsu S. Absence status (petit mal status) with focal characteristics. Arch Neurol. 1979 Jul. 36(7):417-21. [Medline].

  19. Celesia GG. Modern concepts of status epilepticus. JAMA. 1976 Apr 12. 235(15):1571-4. [Medline].

  20. Treiman DM. Generalized convulsive, nonconvulsive, and focal status epilepticus. In: Feldman E, ed. Current Diagnosis in Neurology. St. Louis: Mosby-Year Book. 1994:11-8.

  21. Lennox W, Lennow MA. Epilepsy and Related Disorders. Boston, MA: Little Brown;. 1960.

  22. Cascino GD. Nonconvulsive status epilepticus in adults and children. Epilepsia. 1993. 34 Suppl 1:S21-8. [Medline].

  23. Shorvon S. The outcome of tonic-clonic status epilepticus. Curr Opin Neurol. 1994 Apr. 7(2):93-5. [Medline].

  24. White PT, Grant P, Mosier J, Craig A. Changes in cerebral dynamics associated with seizures. Neurology. 1961 Apr. 11(4)Pt 1:354-61. [Medline].

  25. Aminoff MJ, Simon RP. Status epilepticus. Causes, clinical features and consequences in 98 patients. Am J Med. 1980 Nov. 69(5):657-66. [Medline].

  26. Meldrum BS, Horton RW. Physiology of status epilepticus in primates. Arch Neurol. 1973 Jan. 28(1):1-9. [Medline].

  27. Naylor DE, Liu H, Wasterlain CG. Trafficking of GABA(A) receptors, loss of inhibition, and a mechanism for pharmacoresistance in status epilepticus. J Neurosci. 2005 Aug 24. 25(34):7724-33. [Medline].

  28. Sloviter RS, Zappone CA, Bumanglag AV, Norwood BA, Kudrimoti H. On the relevance of prolonged convulsive status epilepticus in animals to the etiology and neurobiology of human temporal lobe epilepsy. Epilepsia. 2007. 48 Suppl 8:6-10. [Medline].

  29. Goodkin HP, Sun C, Yeh JL, Mangan PS, Kapur J. GABA(A) receptor internalization during seizures. Epilepsia. 2007. 48 Suppl 5:109-13. [Medline].

  30. Holmes GL. Influence of brain development on status epilepticus. Epilepsia. 2007. 48 Suppl 8:19-20. [Medline].

  31. DeLorenzo RJ, Pellock JM, Towne AR, Boggs JG. Epidemiology of status epilepticus. J Clin Neurophysiol. 1995 Jul. 12(4):316-25. [Medline].

  32. Shinnar S, Pellock JM, Moshe SL, et al. In whom does status epilepticus occur: age-related differences in children. Epilepsia. 1997 Aug. 38(8):907-14. [Medline].

  33. DeLorenzo RJ, Hauser WA, Towne AR, et al. A prospective, population-based epidemiologic study of status epilepticus in Richmond, Virginia. Neurology. 1996 Apr. 46(4):1029-35. [Medline].

  34. Shorvon S. Definition, classification and frequency of status epilepticus. In: Shorvon S, ed. Epilepticus: Its Clinical Features and Treatment in Children and Adults. Cambridge: Cambridge University Press; 1994. 21-33.

  35. Waterhouse EJ, DeLorenzo RJ. Status epilepticus in older patients: epidemiology and treatment options. Drugs Aging. 2001. 18(2):133-42. [Medline].

  36. Drislane FW, Blum AS, Lopez MR, Gautam S, Schomer DL. Duration of refractory status epilepticus and outcome: Loss of prognostic utility after several hours. Epilepsia. 2009 Jan 19. [Medline].

  37. Rossetti AO, Oddo M, Liaudet L, Kaplan PW. Predictors of awakening from postanoxic status epilepticus after therapeutic hypothermia. Neurology. 2009 Feb 24. 72(8):744-9. [Medline].

  38. Treiman DM, Meyers PD, Walton NY, et al. A comparison of four treatments for generalized convulsive status epilepticus. Veterans Affairs Status Epilepticus Cooperative Study Group. N Engl J Med. 1998 Sep 17. 339(12):792-8. [Medline].

  39. Thomas P. How urgent is the treatment of nonconvulsive status epilepticus?. Epilepsia. 2007. 48 Suppl 8:44-5. [Medline].

  40. Aicardi J, Chevrie JJ. Convulsive status epilepticus in infants and children. A study of 239 cases. Epilepsia. 1970 Jun. 11(2):187-97. [Medline].

  41. Lowenstein DH, Alldredge BK. Status epilepticus. N Engl J Med. 1998 Apr 2. 338(14):970-6. [Medline].

  42. Hauser WA. Status epilepticus: epidemiologic considerations. Neurology. 1990 May. 40(5 Suppl 2):9-13. [Medline].

  43. Boggs JG, Marmarou A, Agnew JP, et al. Hemodynamic monitoring prior to and at the time of death in status epilepticus. Epilepsy Res. 1998 Aug. 31(3):199-209. [Medline].

  44. Krumholz A, Sung GY, Fisher RS, Barry E, Bergey GK, Grattan LM. Complex partial status epilepticus accompanied by serious morbidity and mortality. Neurology. 1995 Aug. 45(8):1499-504. [Medline].

  45. Treiman DM, Walton NY, Kendrick C. A progressive sequence of electroencephalographic changes during generalized convulsive status epilepticus. Epilepsy Res. 1990 Jan-Feb. 5(1):49-60. [Medline].

  46. Treiman DM, Meyers PD, Walton NY. DVA Status Epilepticus Cooperative Study Group. Duration of generalized convulsive status epilepticus: relationship to clinical symptomatology and response to treatment. Epilepsia. 1992. 33(Suppl 3):66.

  47. Treiman DM. Electroclinical features of status epilepticus. J Clin Neurophysiol. 1995 Jul. 12(4):343-62. [Medline].

  48. Bien CG, Elger CE. Epilepsia partialis continua: semiology and differential diagnoses. Epileptic Disord. 2008 Mar. 10(1):3-7. [Medline].

  49. Leis AA, Ross MA, Summers AK. Psychogenic seizures: ictal characteristics and diagnostic pitfalls. Neurology. 1992 Jan. 42(1):95-9. [Medline].

  50. Jagoda A, Richey-Klein V, Riggio S. Psychogenic status epilepticus. J Emerg Med. 1995 Jan-Feb. 13(1):31-5. [Medline].

  51. Holtkamp M, Othman J, Buchheim K, Meierkord H. Diagnosis of psychogenic nonepileptic status epilepticus in the emergency setting. Neurology. 2006 Jun 13. 66(11):1727-9. [Medline].

  52. Kutluay E, Beattie J, Passaro EA, Edwards JC, Minecan D, Milling C, et al. Diagnostic and localizing value of ictal SPECT in patients with nonconvulsive status epilepticus. Epilepsy Behav. 2005 Mar. 6(2):212-7. [Medline].

  53. Assal F, Papazyan JP, Slosman DO, Jallon P, Goerres GW. SPECT in periodic lateralized epileptiform discharges (PLEDs): a form of partial status epilepticus?. Seizure. 2001 Jun. 10(4):260-5. [Medline].

  54. Karlov VA. Complex partial status epilepticus. Epilepsia. 2007 Sep. 48(9):1815. [Medline].

  55. DeLorenzo RJ, Waterhouse EJ, Towne AR, et al. Persistent nonconvulsive status epilepticus after the control of convulsive status epilepticus. Epilepsia. 1998 Aug. 39(8):833-40. [Medline].

  56. Szabo K, Poepel A, Pohlmann-Eden B, Hirsch J, Back T, Sedlaczek O, et al. Diffusion-weighted and perfusion MRI demonstrates parenchymal changes in complex partial status epilepticus. Brain. 2005 Jun. 128:1369-76. [Medline].

  57. [Guideline] Glauser, T. et al. Treatment of Convulsive Status Epilepticus in Children and Adults: Report of the Guideline Committee of the American Epilepsy Society. Epilepsy Currents. Jan/Feb 2016. 16(1):48-61. [Full Text].

  58. Rossetti AO. Which anesthetic should be used in the treatment of refractory status epilepticus?. Epilepsia. 2007. 48 Suppl 8:52-5. [Medline].

  59. Arif H, Hirsch LJ. Treatment of status epilepticus. Semin Neurol. 2008 Jul. 28(3):342-54. [Medline].

  60. Parviainen I, Uusaro A, Kalviainen R, et al. Propofol in the treatment of refractory status epilepticus. Intensive Care Med. 2006 Jul. 32(7):1075-9. [Medline].

  61. Iyer VN, Hoel R, Rabinstein AA. Propofol infusion syndrome in patients with refractory status epilepticus: an 11-year clinical experience. Crit Care Med. 2009 Dec. 37(12):3024-30. [Medline].

  62. Synowiec AS, Singh DS, Yenugadhati V, Valeriano JP, Schramke CJ, Kelly KM. Ketamine use in the treatment of refractory status epilepticus. Epilepsy Res. 2013 Jan 28. [Medline].

  63. Blumkin L, Lerman-Sagie T, Houri T, Gilad E, Nissenkorn A, Ginsberg M, et al. Pediatric refractory partial status epilepticus responsive to topiramate. J Child Neurol. 2005 Mar. 20(3):239-41. [Medline].

  64. Prasad M, Krishnan PR, Sequeira R, Al-Roomi K. Anticonvulsant therapy for status epilepticus. Cochrane Database Syst Rev. 2014 Sep 10. 9:CD003723. [Medline].

  65. Misra UK, Kalita J, Patel R. Sodium valproate vs phenytoin in status epilepticus: a pilot study. Neurology. 2006 Jul 25. 67(2):340-2. [Medline].

  66. Limdi NA, Shimpi AV, Faught E, Gomez CR, Burneo JG. Efficacy of rapid IV administration of valproic acid for status epilepticus. Neurology. 2005 Jan 25. 64(2):353-5. [Medline].

  67. Rossetti AO, Bromfield EB. Levetiracetam in the treatment of status epilepticus in adults: a study of 13 episodes. Eur Neurol. 2005. 54(1):34-8. [Medline].

  68. Patel NC, Landan IR, Levin J, Szaflarski J, Wilner AN. The use of levetiracetam in refractory status epilepticus. Seizure. 2006 Apr. 15(3):137-41. [Medline].

  69. Hirsch LJ. Levitating Levetiracetam''s Status for Status Epilepticus. Epilepsy Curr. 2008 Sep-Oct. 8(5):125-6. [Medline]. [Full Text].

  70. Bialer M. Clinical pharmacology of parenteral use of antiepileptic drugs. Epilepsia. 2007. 48 Suppl 8:46-8. [Medline].

  71. Aggarwal P, Wali JP. Lidocaine in refractory status epilepticus: a forgotten drug in the emergency department. Am J Emerg Med. 1993 May. 11(3):243-4. [Medline].

  72. Koubeissi MZ, Mayor CL, Estephan B, Rashid S, Azar NJ. Efficacy and safety of intravenous lacosamide in refractory nonconvulsive status epilepticus. Acta Neurol Scand. 2011 Feb. 123(2):142-6. [Medline].

  73. Costello DJ, Simon MV, Eskandar EN, Frosch MP, Henninger HL, Chiappa KH, et al. Efficacy of surgical treatment of de novo, adult-onset, cryptogenic, refractory focal status epilepticus. Arch Neurol. 2006 Jun. 63(6):895-901. [Medline].

  74. McIntyre J, Robertson S, Norris E, Appleton R, Whitehouse WP, Phillips B, et al. Safety and efficacy of buccal midazolam versus rectal diazepam for emergency treatment of seizures in children: a randomised controlled trial. Lancet. 2005 Jul 16-22. 366(9481):205-10. [Medline].

  75. de Haan GJ, van der Geest P, Doelman G, Bertram E, Edelbroek P. A comparison of midazolam nasal spray and diazepam rectal solution for the residential treatment of seizure exacerbations. Epilepsia. 2010 Mar. 51(3):478-82. [Medline].

Treatment algorithms for convulsive status epilepticus.
Focal status epilepticus. Electroencephalograph (EEG) in a patient with epilepsia partialis continua caused by Rasmussen encephalitis before hemispherectomy. The patient had long-standing, intractable partial epilepsy since the first decade of life. Seizures included complex partial with occasional secondary generalization and repetitive myoclonus involving the left side of the body. Note the frequent epileptiform discharges at 1-2 Hz involving the right frontocentral channels. These were evident on many of the patient's routine EEGs. Clinical myoclonus is often correlated with high-voltage bursts of such activity.
Focal status epilepticus. Electroencephalograph (EEG) in a 35-year-old patient with a history of intractable partial epilepsy, in complex partial status epilepticus. The patient underwent a rapid antiepileptic drug taper as an inpatient for long-term video/EEG monitoring as a presurgical candidate. On clinical observation, the patient abruptly stopped and stared, exhibiting automatisms. This first of 2 EEG fragments covers approximately 30 seconds and illustrates the start and evolution of a seizure in the right temporal lobe. The onset appears to be at Sp2 and T4. Note the time of the event, 18:35 on May 9.
Focal status epilepticus. This electroencephalographic (EEG) fragment was obtained at approximately 12:39 on May 10, 18 hours after the onset of complex partial status epilepticus originating in the right temporal lobe, in a 35-year-old patient with a history of intractable partial epilepsy. Other EEG acquisitions over the interval were identical. On clinical observation, the patient was lethargic, sluggish, and vague, with variable responsivity to examiners. Note the persistent epileptiform discharges at 1.5-2.5 Hz with phase reversal mainly at Sp2 though infrequently shifting to Sp1 and F7. The bulk of the discharges are maximal at Sp2, reflecting their mesial temporal origin, with rare, subtle, and low-amplitude reflection from lateral neocortical channels (F8). Background activities are slow with admixed beta frequencies. This finding corresponds to complex partial status epilepticus.
All material on this website is protected by copyright, Copyright © 1994-2016 by WebMD LLC. This website also contains material copyrighted by 3rd parties.