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Pediatric Status Epilepticus Workup

  • Author: Rajesh Ramachandrannair, MBBS, MD, FRCPC; Chief Editor: Timothy E Corden, MD  more...
Updated: Oct 06, 2014

Approach Considerations

Every patient who presents with SE requires electroencephalography (EEG); however, treatment should not be delayed to wait for EEG results. When a seizure persists longer than 30-60 minutes, making immediate arrangements for an EEG is advisable.

Likewise, laboratory testing should proceed concurrently with stabilization. Although routine laboratory studies are not always useful in assessing patients with brief seizures who present to the emergency department (ED), children with generalized tonic-clonic status epilepticus (GTCSE) require a more aggressive workup. Lumbar puncture with opening pressure measurement is performed for prolonged SE of unknown etiology. It is also indicated in immunocompromised patients.

Stabilize all children before CT scanning or other imaging studies are performed. Obtain imaging studies based on likely etiologies


Lab Studies

The choice of laboratory studies is based on age and likely etiologies. They may include the following:

  • Blood glucose level
  • Complete blood count (CBC)
  • Electrolyte levels
  • Calcium and magnesium levels, particularly in neonates
  • Arterial blood gases
  • Toxicology screen
  • Anticonvulsant levels (if indicated by history of ingestion or known therapy [14] )

Stabilization phase studies

While attending to the patient’s airway, breathing, and circulation (ABCs) and inserting an intravenous (IV) line, obtain a CBC and tests for levels of anticonvulsant medication, electrolytes, blood urea nitrogen (BUN) and creatinine, calcium, and magnesium.

Serum glucose measurement is particularly important if the child or another household member uses insulin or other hypoglycemic agents; hypoglycemia may be a contributing factor or cause of seizures. Glucose measurement should be performed with a fast bedside assay (eg, Dextrostix).

The CBC may show elevation of the white blood cell (WBC) count in patients with infection. However, an elevated WBC count may be due to demargination, returning to reference ranges over 12-24 hours.

Calcium and magnesium measurement may be important, especially for infants fed with cows' milk. It is also valuable in older patients with disorders that may produce imbalances in these elements (eg, renal failure, hypoparathyroidism).

Other necessary tests may include urine/serum toxicology, especially in teenagers with unexplained seizures. If school-aged children who have cats (particularly kittens) at home present with unexplained mental status changes and prolonged seizures, evaluate for catscratch fever by measuring indirect fluorescent antibody titers to Bartonella henselae. A lumbar puncture is commonly indicated in children with GTCSE, especially those with unexplained fever or mental status changes preceding or following the seizure episode.

Continued evaluation

Continue evaluation after seizures are controlled. Basic tests recommended by the Epilepsy Foundation Working Group on Status Epilepticus include liver function tests (LFTs), toxicology screen, and brain imaging.[15]

After an SE episode, perform a lumbar puncture for individuals with fever or other evidence of CNS infection. Remember that febrile convulsive status may be associated with CNS infection without typical meningeal signs. Brain imaging should be part of the workup for status epilepticus prior to lumbar puncture for patients with acute neurologic changes suggesting increased intracranial pressure.

A treatment algorithm is shown in the image below.

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

Imaging Studies

Imaging studies are indicated in patients with GTCSE once they are stabilized. A head CT scan is the best diagnostic imaging study, particularly if intracranial hemorrhage, midline shift, or mass lesion is suspected.

In many centers, head CT scanning is available on an emergency basis. If CT scanning is unavailable and the patient is stable and has no signs of increased intracranial pressure, CT scanning can be temporarily deferred.

Perform an imaging study for all patients who have histories of neurologic (including mental status) changes and for patients who have actual deficits on the neurologic examination that persist after cessation of seizures.

Brain imaging should be part of the workup for SE prior to lumbar puncture for patients with acute neurologic changes suggesting increased intracranial pressure.

Children with complex partial seizures preceding or leading to the episode of GTCSE should undergo brain MRI. In many centers, CT scanning is performed in the ED because MRI services are often unavailable after hours. If not immediately available, MRI should be performed in the following days.

Brain imaging may be unnecessary for patients who have already had MRI performed as part of a workup for epilepsy or when the cause or precipitant for their episode of SE is obvious (eg, low anticonvulsant levels, acute infection).

On follow-up, many patients with documented a priori normal MRI findings may develop an increased T2, diffusion and fluid attenuated inverted recovery (FLAIR) signal. This is especially true in cases of prolonged partial seizures leading to secondary GTCSE. Most of these changes are due to transient vasogenic or cytotoxic edema.



The EEG helps in differentiating convulsive SE from pseudoseizure (nonepileptic or psychogenic seizure). Nonconvulsive status epilepticus (NCSE) may need to be differentiated from postictal state–related depression and unresponsiveness from metabolic encephalopathies (renal and hepatic) as well as anoxic encephalopathies. This is especially the case when treatment with anticonvulsant medication does not improve the patient’s alertness.

Patients who ultimately require continuous infusion with a barbiturate or benzodiazepine should undergo continuous EEG monitoring.

During a prolonged seizure, EEG manifestations follow a sequence of partial (focal) EEG seizures, leading to discrete generalized tonic-clonic seizures that eventually become fused (ie, continuous EEG seizure). Rhythmic lateralized or generalized discharges later appear to slow in frequency and may appear similar to periodic lateralizing epileptiform discharges (PLEDs).

A patient who arrives at the ED may be at any of these EEG stages; historical information concerning seizure progression usually correlates somewhat with stage. Patients at the later stages of EEG with GTCSE may be more difficult to treat.

Patients who cannot be aroused following a seizure should have an EEG performed to rule out subclinical SE. An EEG can confirm the seizure pattern and help indicate the most appropriate long-term treatment, if necessary.


Workup for Prolonged Refractory Status Epilepticus

Seizures not responding to appropriate therapy in 60 minutes or to the first- and second-lines drugs (initial doses of benzodiazepines, IV phenytoin/fosphenytoin, and phenobarbital) should be considered refractory status epilepticus. Prolonged refractory status epilepticus (seizures persisting beyond 24 h) needs further workup if routine blood work, MRI of the brain, and microbiological studies in serum and cerebrospinal fluid (CSF) do not provide clues to the etiology of the seizures. The following investigations are considered:

  • Urine organic acids, porphyrins (porphyria), and sulfites (sulfite oxidase deficiency and molybdenum co-factor deficiency)
  • Serum T4, T3, thyrotropin, and antiperoxidase antibody (autoimmune epilepsy)
  • Serological markers for collagen-vascular disorders
  • Serum and CSF NMDA-R antibody, ultrasound/CT/MRI of testes and abdomen to look for solid tumors (anti NMDA-R antibody encephalitis)
  • Other paraneoplastic antibodies (anti Hu, Yo, Ri)

If the patient continues to be in refractory status epilepticus beyond 72 hours, additional investigations are suggested, as follows:

  • Repeat MRI brain with gadolinium
  • Cerebral angiography (CT angiography or conventional 4-vessel angiography) to look for evidence of vasculitis
  • CSF neurotransmitters

If the above-mentioned investigations do not identify the etiology of seizures within a week, brain biopsy may be considered.

Contributor Information and Disclosures

Rajesh Ramachandrannair, MBBS, MD, FRCPC Associate Professor, McMaster University School of Medicine; Staff Neurologist, McMaster Children's Hospital, Canada

Disclosure: Nothing to disclose.


Marcio Sotero de Menezes, MD Clinical Associate Professor, Department of Neurology, Division of Pediatric Neurology, Seattle Children's Hospital, University of Washington School of Medicine; Director, Pediatric Neuroscience Center and Genetic Epilepsy Clinic, Swedish Neuroscience Institute

Marcio Sotero de Menezes, MD is a member of the following medical societies: American Academy of Neurology, American Epilepsy Society

Disclosure: Received salary from Novartis for speaking and teaching; Received salary from Cyberonics for speaking and teaching; Received salary from Athena diagnostics for speaking and teaching.

Ednea Simon, MD Consulting Staff, Swedish Pediatric Neuroscience Center

Ednea Simon, MD is a member of the following medical societies: American Academy of Neurology, American Epilepsy Society, Child Neurology Society

Disclosure: Nothing to disclose.

Chief Editor

Timothy E Corden, MD Associate Professor of Pediatrics, Co-Director, Policy Core, Injury Research Center, Medical College of Wisconsin; Associate Director, PICU, Children's Hospital of Wisconsin

Timothy E Corden, MD is a member of the following medical societies: American Academy of Pediatrics, Phi Beta Kappa, Society of Critical Care Medicine, Wisconsin Medical Society

Disclosure: Nothing to disclose.


G Patricia Cantwell, MD, FCCM Professor of Clinical Pediatrics, Chief, Division of Pediatric Critical Care Medicine, University of Miami, Leonard M Miller School of Medicine; Medical Director, Palliative Care Team, Director, Pediatric Critical Care Transport, Holtz Children's Hospital, Jackson Memorial Medical Center; Medical Manager, FEMA, Urban Search and Rescue, South Florida, Task Force 2; Pediatric Medical Director, Tilli Kids – Pediatric Initiative, Division of Hospice Care Southeast Florida, Inc

G Patricia Cantwell, MD, FCCM is a member of the following medical societies: American Academy of Hospice and Palliative Medicine, American Academy of Pediatrics, American Heart Association, American Trauma Society, National Association of EMS Physicians, Society of Critical Care Medicine, and Wilderness Medical Society

Disclosure: Nothing to disclose.

Barry J Evans, MD Assistant Professor of Pediatrics, Temple University Medical School; Director of Pediatric Critical Care and Pulmonology, Associate Chair for Pediatric Education, Temple University Children's Medical Center

Barry J Evans, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Chest Physicians, American Thoracic Society, and Society of Critical Care Medicine

Disclosure: Nothing to disclose.

Garry Wilkes MBBS, FACEM, Director of Emergency Medicine, Calvary Hospital, Canberra, ACT; Adjunct Associate Professor, Edith Cowan University; Clinical Associate Professor, Rural Clinical School, University of Western Australia

Disclosure: Nothing to disclose.

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Wayne Wolfram, MD, MPH Associate Professor, Department of Emergency Medicine, Mercy St Vincent Medical Center

Wayne Wolfram, MD, MPH is a member of the following medical societies: American Academy of Emergency Medicine, American Academy of Pediatrics, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Grace M Young, MD Associate Professor, Department of Pediatrics, University of Maryland Medical Center

Grace M Young, MD is a member of the following medical societies: American Academy of Pediatrics and American College of Emergency Physicians

Disclosure: Nothing to disclose.

  1. De Novo Mutations in Synaptic Transmission Genes Including DNM1 Cause Epileptic Encephalopathies. Am J Hum Genet. 2014 Sep 24. [Medline].

  2. Mitchell WG. Status epilepticus and acute serial seizures in children. J Child Neurol. 2002 Jan. 17 Suppl 1:S36-43. [Medline].

  3. Tassinari CA, Daniele O, Michelucci R, Bureau M, Dravet C, Roger J. Benzodiazepines: efficacy in status epilepticus. Adv Neurol. 1983. 34:465-75. [Medline].

  4. Meldrum BS, Horton RW, Brierley JB. Epileptic brain damage in adolescent baboons following seizures induced by allylgycine. Brain. 1974 Jun. 97(2):407-18. [Medline].

  5. Meldrum BS, Vigouroux RA, Brierley JB. Systemic factors and epileptic brain damage. Prolonged seizures in paralyzed, artificially ventilated baboons. Arch Neurol. 1973 Aug. 29(2):82-7. [Medline].

  6. Chin RF, Neville BG, Scott RC. Meningitis is a common cause of convulsive status epilepticus with fever. Arch Dis Child. 2005 Jan. 90(1):66-9. [Medline]. [Full Text].

  7. Raspall-Chaure M, Chin RF, Neville BG, Bedford H, Scott RC. The epidemiology of convulsive status epilepticus in children: a critical review. Epilepsia. 2007 Sep. 48(9):1652-63. [Medline].

  8. Maytal J, Shinnar S, Moshé SL, Alvarez LA. Low morbidity and mortality of status epilepticus in children. Pediatrics. 1989 Mar. 83(3):323-31. [Medline].

  9. zz. zz.

  10. Sahin M, Menache CC, Holmes GL, Riviello JJ Jr. Prolonged treatment for acute symptomatic refractory status epilepticus: outcome in children. Neurology. 2003 Aug 12. 61(3):398-401. [Medline].

  11. Pohlmann-Eden B, Gass A, Peters CN, Wennberg R, Blumcke I. Evolution of MRI changes and development of bilateral hippocampal sclerosis during long lasting generalised status epilepticus. J Neurol Neurosurg Psychiatry. 2004 Jun. 75(6):898-900. [Medline]. [Full Text].

  12. Pujar SS, Neville BG, Scott RC, Chin RF. Death within 8 years after childhood convulsive status epilepticus: a population-based study. Brain. 2011 Oct. 134:2819-27. [Medline]. [Full Text].

  13. Haffey S, McKernan A, Pang K. Non-convulsive status epilepticus: a profile of patients diagnosed within a tertiary referral centre. J Neurol Neurosurg Psychiatry. 2004 Jul. 75(7):1043-4. [Medline]. [Full Text].

  14. Riviello JJ Jr, Ashwal S, Hirtz D, Glauser T, Ballaban-Gil K, Kelley K, et al. Practice parameter: diagnostic assessment of the child with status epilepticus (an evidence-based review): report of the Quality Standards Subcommittee of the American Academy of Neurology and the Practice Committee of the Child Neurology Society. Neurology. 2006 Nov 14. 67(9):1542-50. [Medline].

  15. Epilepsy Foundation of America's Working Group on Status Epilepticus. 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].

  16. Chin RF, Verhulst L, Neville BG, Peters MJ, Scott RC. Inappropriate emergency management of status epilepticus in children contributes to need for intensive care. J Neurol Neurosurg Psychiatry. 2004 Nov. 75(11):1584-8. [Medline]. [Full Text].

  17. Brevoord JC, Joosten KF, Arts WF, van Rooij RW, de Hoog M. Status epilepticus: clinical analysis of a treatment protocol based on midazolam and phenytoin. J Child Neurol. 2005 Jun. 20(6):476-81. [Medline].

  18. [Guideline] Meierkord H, Boon P, Engelsen B, Göcke K, Shorvon S, Tinuper P, et al. EFNS guideline on the management of status epilepticus. Eur J Neurol. 2006 May. 13(5):445-50. [Medline].

  19. Lang ES, Andruchow JE. Evidence-based emergency medicine. What is the preferred first-line therapy for status epilepticus?. Ann Emerg Med. 2006 Jul. 48(1):98-100. [Medline].

  20. Prasad K, Al-Roomi K, Krishnan PR, Sequeira R. Anticonvulsant therapy for status epilepticus. Cochrane Database Syst Rev. 2005 Oct 19. CD003723. [Medline].

  21. Choudhery V, Townend W. Best evidence topic reports. Lorazepam or diazepam in paediatric status epilepticus. Emerg Med J. 2006 Jun. 23(6):472-3. [Medline]. [Full Text].

  22. Chamberlain JM, Capparelli EV, Brown KM, Vance CW, Lillis K, Mahajan P, et al. Pharmacokinetics of Intravenous Lorazepam in Pediatric Patients with and without Status Epilepticus. J Pediatr. 2011 Nov 1. [Medline].

  23. Holsti M, Dudley N, Schunk J, Adelgais K, Greenberg R, Olsen C, et al. Intranasal midazolam vs rectal diazepam for the home treatment of acute seizures in pediatric patients with epilepsy. Arch Pediatr Adolesc Med. 2010 Aug. 164(8):747-53. [Medline].

  24. Morrison G, Gibbons E, Whitehouse WP. High-dose midazolam therapy for refractory status epilepticus in children. Intensive Care Med. 2006 Dec. 32(12):2070-6. [Medline].

  25. Tasker RC. Midazolam for refractory status epilepticus in children: higher dosing and more rapid and effective control. Intensive Care Med. 2006 Dec. 32(12):1935-6. [Medline].

  26. Tarulli A, Drislane FW. The use of topiramate in refractory status epilepticus. Neurology. 2004 Mar 9. 62(5):837. [Medline].

  27. Kahriman M, Minecan D, Kutluay E, Selwa L, Beydoun A. Efficacy of topiramate in children with refractory status epilepticus. Epilepsia. 2003 Oct. 44(10):1353-6. [Medline].

  28. Perry MS, Holt PJ, Sladky JT. Topiramate loading for refractory status epilepticus in children. Epilepsia. 2006 Jun. 47(6):1070-1. [Medline].

  29. Chez MG, Hammer MS, Loeffel M, Nowinski C, Bagan BT. Clinical experience of three pediatric and one adult case of spike-and-wave status epilepticus treated with injectable valproic acid. J Child Neurol. 1999 Apr. 14(4):239-42. [Medline].

  30. Sheth RD, Gidal BE. Intravenous valproic acid for myoclonic status epilepticus. Neurology. 2000 Mar 14. 54(5):1201. [Medline].

  31. Uberall MA, Trollmann R, Wunsiedler U, Wenzel D. Intravenous valproate in pediatric epilepsy patients with refractory status epilepticus. Neurology. 2000 Jun 13. 54(11):2188-9. [Medline].

  32. Abend NS, Dlugos DJ. Treatment of refractory status epilepticus: literature review and a proposed protocol. Pediatr Neurol. 2008 Jun. 38(6):377-90. [Medline].

  33. 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].

  34. Gallentine WB, Hunnicutt AS, Husain AM. Levetiracetam in children with refractory status epilepticus. Epilepsy Behav. 2009 Jan. 14(1):215-8. [Medline].

  35. Shorvon S. Emergency treatment of epilepsy. Handbook of Epilepsy Treatment. Oxford, UK: Blackwell Science; 2000. 173-93.

  36. Parke TJ, Stevens JE, Rice AS, Greenaway CL, Bray RJ, Smith PJ, et al. Metabolic acidosis and fatal myocardial failure after propofol infusion in children: five case reports. BMJ. 1992 Sep 12. 305(6854):613-6. [Medline]. [Full Text].

  37. Bray RJ. Propofol infusion syndrome in children. Paediatr Anaesth. 1998. 8(6):491-9. [Medline].

  38. Coetzee JF, Coetzer M. Propofol in paediatric anaesthesia. Curr Opin Anaesthesiol. 2003 Jun. 16(3):285-90. [Medline].

  39. Corbett SM, Montoya ID, Moore FA. Propofol-related infusion syndrome in intensive care patients. Pharmacotherapy. 2008 Feb. 28(2):250-8. [Medline].

  40. Hill M, Peat W, Courtman S. A national survey of propofol infusion use by paediatric anaesthetists in Great Britain and Ireland. Paediatr Anaesth. 2008 Jun. 18(6):488-93. [Medline].

  41. Fodale V, La Monaca E. Propofol infusion syndrome: an overview of a perplexing disease. Drug Saf. 2008. 31(4):293-303. [Medline].

  42. Anderson P. Convulsive Status Epilepticus Has Prolonged Cognitive Effect. Medscape Medical News. April 10, 2013. Available at Accessed: April 22, 2013.

  43. Baumeister FA, Oberhoffer R, Liebhaber GM, Kunkel J, Eberhardt J, Holthausen H, et al. Fatal propofol infusion syndrome in association with ketogenic diet. Neuropediatrics. 2004 Aug. 35(4):250-2. [Medline].

  44. Brooks M. Lorazepam, diazepam similar in pediatric status epilepticus. Medscape Medical News. April 30, 2014. [Full Text].

  45. Chamberlain JM, Capparelli EV, Brown KM, Vance CW, Lillis K, Mahajan P, et al. Pharmacokinetics of Intravenous Lorazepam in Pediatric Patients with and without Status Epilepticus. J Pediatr. 2011 Nov 1. [Medline].

  46. Chamberlain JM, Okada P, Holsti M, et al. Lorazepam vs diazepam for pediatric status epilepticus: a randomized clinical trial. JAMA. 2014 Apr 23-30. 311(16):1652-60. [Medline].

  47. Krishnamurthy KB, Drislane FW. Depth of EEG suppression and outcome in barbiturate anesthetic treatment for refractory status epilepticus. Epilepsia. 1999 Jun. 40(6):759-62. [Medline].

  48. Martinos MM, Yoong M, Patil S, Chong WK, Mardari R, Chin RF, et al. Early developmental outcomes in children following convulsive status epilepticus: A longitudinal study. Epilepsia. 2013 Apr 8. [Medline].

  49. Mathews HM, Carson IW, Lyons SM, Orr IA, Collier PS, Howard PJ, et al. A pharmacokinetic study of midazolam in paediatric patients undergoing cardiac surgery. Br J Anaesth. 1988 Sep. 61(3):302-7. [Medline].

  50. Neville BG, Chin RF, Scott RC. Childhood convulsive status epilepticus: epidemiology, management and outcome. Acta Neurol Scand Suppl. 2007. 186:21-4. [Medline].

Treatment algorithms for convulsive status epilepticus.
Table 1. Medical Treatment of Seizures and Status Epilepticus Based on Time Elapsed Since Seizure Onset (Steps 2-4)
Step Medication Dose Alternatives
Step 2 (6-15 min) Diazepam (Valium) 5-20 mg IV slowly; not to exceed infusion rate of 2 mg/min; pediatric dose is 0.3 mg/kg If IV line is unavailable, use rectally administered (PR) diazepam at 0.5 mg/kg (not to exceed 10 mg) or midazolam (Versed) at 0.2 mg/kg intramuscularly (IM)*, IV, or intranasally*
Lorazepam* (Ativan) 2-4 mg IV slowly*; not to exceed infusion rate of 2 mg/min or 0.05 mg/kg over 2-5 min; pediatric dose is 0.05-0.1 mg/kg
Step 3 (16-35 min) Phenytoin (Dilantin) or fosphenytoin (Cerebyx)† 20 mg/kg IV over 20 min; not to exceed infusion rate of 1 mg/kg/min; do not dilute in 5% dextrose in water (D5W)

If seizures persist, administer 5 mg/kg for 2 doses (if blood pressure is within the reference range and no history of cardiac disease is present)

If unsuccessful, administer phenobarbital 10-20 mg/kg IV (not to exceed 700 mg IV); increase infusion rate by 100 mg/min; phenobarbital may be used in infants before phenytoin; be prepared to intubate patient; closely monitor hemodynamics and support blood pressure as indicated
Step 4 (45-60 min)‡ Pentobarbital anesthesia (patient already intubated) Loading dose: 5-7 mg/kg IV; may repeat 1-mg/kg to 5-mg/kg boluses until EEG exhibits burst suppression; closely monitor hemodynamics and support blood pressure as indicated

Maintenance dose: 0.5-3 mg/kg/h IV; monitor EEG to keep burst suppression pattern at 2-8 bursts/min

Midazolam* infusion loading dose: 100-300 mcg/kg IV followed by IV infusion of 1-2 mcg/kg/min; increase by 1-2 mcg/kg/min every 15 min if seizures persist (effective range 1-24 mcg/kg/min); closely monitor hemodynamics and support blood pressure as indicated; when seizures stop, continue same dose for 48 h then wean by decrements of 1-2 mcg/kg/min every 15 min

Propofol* initial bolus: 2 mg/kg IV; repeat if seizures continue and follow by IV infusion of 5-10 mg/kg/h, if necessary, guided by EEG monitoring; taper dose 12 h after seizure activity stops; closely monitor hemodynamics and support blood pressure as indicated

With phenobarbital-induced anesthesia, repeated boluses of 10 mg/kg are administered until cessation of ictal activity or appearance of hypotension; closely monitor hemodynamics and support blood pressure as indicated

*Not approved by the FDA for the indicated use.

†Doses for fosphenytoin administered in phenytoin equivalents (PE).

‡An alternative third step preferred by some authors is midazolam

administered by continuous IV infusion with a loading dose 0.1-0.3 mg/kg followed by infusion at a rate of 0.1-0.3 mg/kg/h.

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