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Added descriptions of Jeavons Syndrome and Epilepsy with Myoclonic Absences from open and reliable sources and cite them in syndromes section of the article
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== Cause==
== Cause==
An absence seizure is specifically caused by [[multifactorial inheritance]]. The [[Voltage-gated calcium channel|voltage-gated]] T-type [[T-type calcium channel|calcium channel]] is regulated by [[Gamma-aminobutyric acid receptor subunit gamma-2]] (GABRG2), [[GABRG3]], and [[CACNA1A2]] genes. Inheritance of these genes is involved in the [[etiology]] (cause) of absence seizure.<ref name="Albuja 2021"/> The commonly held belief is that the genetic factor is the primary cause of childhood absence epilepsy. Seizures might be triggered by excessive breathing in sensitive kids. Some specific anticonvulsant drugs such as phenytoin, carbamazepine, and vigabatrin have been identified to raise the chances of experiencing absence seizures.<ref>Posner E. (2013). Absence seizures in children. ''BMJ clinical evidence'', ''2013'', 0317.</ref><!-- Following sentence deleted, not in source cited but may be ref'd elsewhere: "The factors that trigger an absence seizure are lack of sleep and compliance, drinking alcohol, benzodiazepine withdrawal, and medications that reduce the seizure threshold, such as [[isoniazid]] or some [[Antipsychotic|antipsychotics]]." -->
An absence seizure is specifically caused by [[multifactorial inheritance]]. The [[Voltage-gated calcium channel|voltage-gated]] T-type [[T-type calcium channel|calcium channel]] is regulated by [[Gamma-aminobutyric acid receptor subunit gamma-2]] (GABRG2), [[GABRG3]], and [[CACNA1A2]] genes. Inheritance of these genes is involved in the [[etiology]] (cause) of absence seizure.<ref name="Albuja 2021"/> The commonly held belief is that the genetic factor is the primary cause of childhood absence epilepsy. Almost %25 of children suffering from absence seizure has a relative that suffers from seizures.<ref name=":0" />Seizures might be triggered by excessive breathing in sensitive kids. Some specific anticonvulsant drugs such as phenytoin, carbamazepine, and vigabatrin have been identified to raise the chances of experiencing absence seizures.<ref>Posner E. (2013). Absence seizures in children. ''BMJ clinical evidence'', ''2013'', 0317.</ref><!-- Following sentence deleted, not in source cited but may be ref'd elsewhere: "The factors that trigger an absence seizure are lack of sleep and compliance, drinking alcohol, benzodiazepine withdrawal, and medications that reduce the seizure threshold, such as [[isoniazid]] or some [[Antipsychotic|antipsychotics]]." -->


==Signs and symptoms==
==Signs and symptoms==
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==Diagnosis==
==Diagnosis==
The primary diagnostic test for absence seizures is [[electroencephalography]] (EEG).<ref name=medscape>[http://emedicine.medscape.com/article/1183858-overview#aw2aab6b9 Medscape > Absence Seizures] by Scott Segan. Updated: Apr 27, 2011</ref> However, [[brain scan]]s such as by an [[MRI]] can help rule out other diseases, such as a [[stroke]] or a [[brain tumor]].<ref>[http://www.mayoclinic.com/health/petit-mal-seizure/DS00216/DSECTION=tests-and-diagnosis Mayo Clinic > Absence seizure (petit mal seizure)] June 23, 2011</ref>
The primary diagnostic test for absence seizures is [[electroencephalography]] (EEG).<ref name=medscape>[http://emedicine.medscape.com/article/1183858-overview#aw2aab6b9 Medscape > Absence Seizures] by Scott Segan. Updated: Apr 27, 2011</ref> However, [[brain scan]]s such as by an [[MRI]] can help rule out other diseases, such as a [[stroke]] or a [[brain tumor]].<ref name=":0">[http://www.mayoclinic.com/health/petit-mal-seizure/DS00216/DSECTION=tests-and-diagnosis Mayo Clinic > Absence seizure (petit mal seizure)] June 23, 2011</ref>


During EEG, hyperventilation can be used to provoke these seizures.<ref name=medscape/> Ambulatory EEG monitoring over 24 hours can quantify the number of seizures per day and their most likely times of occurrence.<ref name=medscape/>
During EEG, hyperventilation can be used to provoke these seizures.<ref name=medscape/> Ambulatory EEG monitoring over 24 hours can quantify the number of seizures per day and their most likely times of occurrence.<ref name=medscape/>

Revision as of 11:51, 29 August 2023

Absence seizure
Other namesPetit mal seizures
Pronunciation
SpecialtyNeurology

Absence seizures are one of several kinds of generalized seizures. These seizures are sometimes referred to as petit mal seizures (from the French for "little illness", a term dated in the late 18th century).[1] Absence seizures are characterized by a brief loss and return of consciousness, generally not followed by a period of lethargy (i.e. without a notable postictal state). Absence seizures are most common in children. They affect both sides of the brain.[2][3]

Epidemiology

Absence seizures affect between 0.7 and 4.6 per 100,000 in the general population and 6 to 8 per 100,000 in children younger than 15 years. Childhood absence seizures account for 10% to 17% of all absence seizures. Onset is between 4 and 10 years and peaks at 5 to 7 years. It is more common in girls than in boys.[4]

Cause

An absence seizure is specifically caused by multifactorial inheritance. The voltage-gated T-type calcium channel is regulated by Gamma-aminobutyric acid receptor subunit gamma-2 (GABRG2), GABRG3, and CACNA1A2 genes. Inheritance of these genes is involved in the etiology (cause) of absence seizure.[4] The commonly held belief is that the genetic factor is the primary cause of childhood absence epilepsy. Almost %25 of children suffering from absence seizure has a relative that suffers from seizures.[5]Seizures might be triggered by excessive breathing in sensitive kids. Some specific anticonvulsant drugs such as phenytoin, carbamazepine, and vigabatrin have been identified to raise the chances of experiencing absence seizures.[6]

Signs and symptoms

The clinical manifestations of absence seizures vary significantly among patients.[7][8][9] Impairment of consciousness is the essential symptom, and may be the only clinical symptom, but this can be combined with other manifestations. The hallmark of the absence seizures is abrupt and sudden-onset impairment of consciousness, interruption of ongoing activities, a blank stare, possibly a brief upward rotation of the eyes. If the patient is speaking, speech is slowed or interrupted; if walking, they stand transfixed; if eating, the food will stop on its way to the mouth. Usually, the patient will be unresponsive when addressed. In some cases, attacks are aborted when the patient is called. The attack lasts from a few seconds to half a minute and evaporates as rapidly as it commenced. Absence seizures generally are not followed by a period of disorientation or lethargy (postictal state), in contrast to the majority of seizure disorders.[2] If the patient has jerking gestures during the seizure this might be the indication of another type of seizure occurring onward with the absence seizure.[10]

  1. Absence with impairment of consciousness only as per the above description.[2]
  2. Absence with mild clonic components. Here the onset of the attack is indistinguishable from the above, but clonic components may occur in the eyelids, at the corner of the mouth, or in other muscle groups which may vary in severity from almost imperceptible movements to generalised myoclonic jerks. Objects held in the hand may be dropped.[citation needed]
  3. Absence with atonic components. Here there may be a diminution in tone of muscles subserving posture as well as in the limbs leading to dropping of the head, occasionally slumping of the trunk, dropping of the arms, and relaxation of the grip. Rarely tone is sufficiently diminished to cause this person to fall.[citation needed]
  4. Absence with tonic components. Here during the attack tonic muscular contraction may occur, leading to increase in muscle tone which may affect the extensor muscles or the flexor muscles symmetrically or asymmetrically. If the patient is standing, the head may be drawn backward and the trunk may arch. This may lead to retropulsion, which may cause eyelids to twitch rapidly; eyes may jerk upwards or the patients head may rock back and forth slowly, as if nodding.[11][12][13] The head may tonically draw to one or another side.[citation needed]
  5. Absence with automatisms. Purposeful or quasi-purposeful movements occurring in the absence of awareness during an absence attack are frequent and may range from lip licking and swallowing to clothes fumbling or aimless walking. If spoken to, the patient may grunt, and when touched or tickled may rub the site. Automatisms are quite elaborate and may consist of combinations of the above described movements or may be so simple as to be missed by casual observation.[14]
  6. Absence with autonomic components. These may be pallor, and less frequently flushing, sweating, dilatation of pupils and incontinence of urine.[citation needed]

Mixed forms of absence frequently occur. These seizures can happen a few times a day or in some cases, hundreds of times a day, to the point that the person cannot concentrate in school or in other situations requiring sustained, concentrated attention.[2]

Risk factors

Typical absences are easily induced by hyperventilation in more than 90% of people with typical absences. This is a reliable test for the diagnosis of absence seizures: a patient suspected of typical absences should be asked to hyperventilate for three minutes, counting breaths. During hyperventilation, the oxygen and carbon dioxide level will become abnormal. This results in weakening of electrical signal which leads to a reduction in the seizure threshold.[15] Intermittent photic stimulation may precipitate or facilitate absence seizures; eyelid myoclonia is a common clinical feature. [citation needed]

A specific mechanism difference exists in absence seizures in that T-type Ca++ channels are believed to be involved. Ethosuximide is specific for these channels and thus it is not effective for treating other types of seizures. Valproate and gabapentin (among others) have multiple mechanisms of action including blockade of T-type Ca++ channels, and are useful in treating multiple seizure types.[citation needed] Gabapentin can aggravate absence seizures.[16]

Pathophysiology

The corticothalamic cortical circuit plays an important role in the pathophysiology of absence seizure. Some of the neurons are important in their occurrence. They are

  • Cortical glutamatergic neurons
  • Thalamic relay neurons
  • Neurons of thalamic nucleus reticularis

Abnormal oscillatory rhythms develop in the thalamic nucleus reticularis. This causes inhibition of GABAergic neurotransmission and excitation of glutamate neurotransmission. Abnormal oscillatory spikes are produced by the low threshold T-type calcium channel. This explains how inheritance of gene code for T-type calcium channel leads to an absence seizure. Antiepileptic drugs such as Gabapentin, Tiagabine and Vigabatrin cause inhibition of GABA resulting in exacerbation of absence seizures.[17][18]

Diagnosis

The primary diagnostic test for absence seizures is electroencephalography (EEG).[19] However, brain scans such as by an MRI can help rule out other diseases, such as a stroke or a brain tumor.[5]

During EEG, hyperventilation can be used to provoke these seizures.[19] Ambulatory EEG monitoring over 24 hours can quantify the number of seizures per day and their most likely times of occurrence.[19]

Absence seizures are brief (usually less than 20 seconds) generalized epileptic seizures of sudden onset and termination. When someone experiences an absence seizure they are often unaware of their episode.[20] Those most susceptible to this are children, and the first episode usually occurs between 4–14 years old. It is very rare that someone older will experience their first absence seizure.[21] Episodes of absence seizures can often be mistaken for inattentiveness when misdiagnosed, and can occur 50–100 times a day. They can be so difficult to detect that some people may go months or years before being given a proper diagnosis. The majority of children experiencing typical absence seizures have an overall normal health condition. However, these absence seizures can disrupt the learning process and hinder concentration in a school environment. This underscores the crucial significance of treatment[22] There are no known before or after effects of absence seizures.[23]

Absence seizures have two essential components:[7][8][9]

  • Clinical - the impairment of consciousness (absence)
  • EEG - the EEG shows generalized spike-and-slow wave discharges

Absence seizures are broadly divided into typical and atypical types:

  • Typical absence seizures usually occur in the context of idiopathic generalised epilepsies and an EEG shows fast >2.5 Hz generalised spike-wave discharges. The prefix "typical" is to differentiate them from atypical absences rather than to characterise them as "classical" or characteristic of any particular syndrome.
  • Atypical absence seizures:
    • Occur only in the context of mainly severe symptomatic or cryptogenic epilepsies of children with learning difficulties who also have frequent seizures of other types, such as atonic, tonic and myoclonic.
    • Have slower onset and termination and changes in tone are more pronounced.
    • Have particular ictal characteristics: EEG is of slow (less than 2.5 Hz) spike and slow wave. The discharge is heterogeneous, often asymmetrical and may include irregular spike and slow wave complexes, fast and other paroxysmal activity. Background interictal EEG is usually abnormal.

Syndromes

Absence seizure syndromes are childhood absence epilepsy, epilepsy with myoclonic absences, juvenile absence epilepsy and juvenile myoclonic epilepsy. Other proposed syndromes are Jeavons syndrome (eyelid myoclonia with absences), and genetic generalised epilepsy with phantom absences.

Absence seizures are also known to occur to patients with porphyria and can be triggered by stress or other porphyrin-inducing factors.

Childhood Absence Epilepsy

Childhood absence epilepsy (CAE) is a type of idiopathic epilepsy characterized by its non-convulsive, generalized nature and a genetic origin influenced by multiple factors[24]

Epilepsy with Myoclonic Absences

Myoclonic Absence Epilepsy is an infrequent type of childhood epilepsy characterized by a high occurrence of intellectual impairments and resistance to treatment.[25]

Juvenile Absence Epilepsy

Juvenile Absence Epilepsy is considered an Idiopathic GED (Idiopathic Major Epilepsy) Syndrome and is officially categorized as Idiopathic Generalized Epilepsy by the ILAE. This condition typically begins in adolescents during the puberty stage and is distinguished by the occurrence of absence seizures and Generalized Tonic-Clonic Seizures.[26]

Juvenile Myoclonic Epilepsy

Juvenile Myoclonic Epilepsy (JME), also referred to as Janz Syndrome and Impulsive Petit Mal, is a form of epilepsy that is characterized by absence, Myoclonic, and Generalized Tonic-Clonic Seizures. This epilepsy variant is marked by its idiopathic and hereditary characteristics, as well as its generalization across seizures. The initial documentation of JME dates back to 1867 by Herpin, followed by Janz and Christian labeling it as 'Impulsive Petit Mal' in 1957, and Lund's 1975 designation of 'JME'.[27]

Jeavons Syndrome

Reflex Epilepsy (JS) is a form of epilepsy usually categorized within the spectrum of genetically-linked Generalized Epilepsy (GGE). While EM (Epileptic Myoclonus) is commonly acknowledged as a type of seizure, the formal recognition of JS as a separate medical entity by the International League Against Epilepsy (ILAE) has not yet occurred.[28]

Treatment

Treatment of patients with absence seizures only is mainly with ethosuximide or valproic acid, which are of equal efficacy controlling absences in around 75% of patients. Lamotrigine monotherapy is less effective, controlling absences in around 50% of patients. This summary has been recently confirmed by Glauser et al. (2010),[29] who studied the effects of ethosuximide, valproic acid, and lamotrigine in children with newly diagnosed childhood absence epilepsy. Drug dosages were incrementally increased until the child was free of seizures, the maximal allowable dose was reached, or a criterion indicating treatment failure was met. The primary outcome was freedom from treatment failure after 16 weeks of therapy; the secondary outcome was attentional dysfunction. After 16 weeks of therapy, the freedom-from-failure rates for ethosuximide and valproic acid were similar and were higher than the rate for lamotrigine. There were no significant differences between the three drugs with regard to discontinuation because of adverse events. Attentional dysfunction was more common with valproic acid than with ethosuximide. If monotherapy fails or unacceptable adverse reactions appear, replacement of one by another of the three antiepileptic drugs is the alternative. Adding small doses of lamotrigine to sodium valproate may be the best combination in resistant cases.

Although ethosuximide is effective in treating only absence seizures, valproic acid is effective in treating multiple seizure types including tonic-clonic seizure and partial seizure, suggesting it is a better choice if a patient is exhibiting multiple types of seizures.[30] Similarly, lamotrigine treats multiple seizure types including partial seizures and generalized seizures, therefore it is also an option for patients with multiple seizure types.[31] Clonazepam (Klonopin, Rivotril) is effective in the short term but is not generally recommended for treatment of absence seizure because of the rapid development of tolerance and high frequency of side effects.[32] If medication is not effective in treating absence seizures, surgical treatment such as deep brain stimulation can reduce seizure episodes.[33]

Roughly 70% of children experiencing absence seizures will see these seizures naturally cease before they reach the age of 18. In such instances, the need for medications might no longer be relevant in adulthood. It's worth noting that children who develop absence seizures prior to turning 9 are more inclined to outgrow them compared to those whose absence seizures commence after the age of 10.[34]

Prevention

Appropriate medication is the best way to manage absence seizures, but prevention can be considerably enhanced by life-style changes such as exercise, stress reduction, good sleep hygiene, and healthy diet.[35] In particular, a therapeutic ketogenic diet can be very beneficial. In a review of studies of childhood and juvenile patients, this diet reduced seizure episodes in most patients by more than half; of those with clear outcomes, a quarter to a third became seizure free.[36]

Medications that should not be used

Carbamazepine, vigabatrin, and tiagabine are contraindicated in the treatment of absence seizures, irrespective of cause and severity. This is based on clinical and experimental evidence.[9] In particular, the GABA agonists vigabatrin and tiagabine are used to induce, not to treat, absence seizures and absence status epilepticus.[37] Similarly, oxcarbazepine, phenytoin, phenobarbital, gabapentin, and pregabalin should not be used in the treatment of absence seizures because these medications may worsen absence seizures.[31]

Data limitations

In the treatment of absence seizures there is often insufficient evidence for which of the available medications has the best combination of safety and efficacy for a particular patient.[38] Nor is it easily known how long a medication must be continued before an off-medication trial should be conducted to determine whether the patient has outgrown the absence seizures, as is often the case in children. To date there have been no published results of any large, double-blind, placebo-controlled studies comparing the efficacy and safety of these or any other medications for absence seizures.[citation needed] A 2019 Cochrane review found that ethosuximide was the best mono-therapy for children and adolescents but noted that if absence seizures co-exist with tonic-clonic seizures then valproate should be preferred.[39][40]

References

  1. ^ Daly, D. D. (1968). "Reflections on the Concept of Petit Mal". Epilepsia. 9 (3): 175–8. doi:10.1111/j.1528-1157.1968.tb04618.x. PMID 4975023. S2CID 45169328.
  2. ^ a b c d "Absence Seizures". Epilepsy Foundation. Retrieved 2021-12-18.
  3. ^ "Ethosuximide - an overview | ScienceDirect Topics". www.sciencedirect.com. Retrieved 2021-12-18.
  4. ^ a b Albuja, Ana C.; Khan, Gulam Qutubuddin (2021), "Absence Seizure", StatPearls, Treasure Island (FL): StatPearls Publishing, PMID 29763042, retrieved 2021-12-20
  5. ^ a b Mayo Clinic > Absence seizure (petit mal seizure) June 23, 2011
  6. ^ Posner E. (2013). Absence seizures in children. BMJ clinical evidence, 2013, 0317.
  7. ^ a b "Proposal for revised clinical and electroencephalographic classification of epileptic seizures. From the Commission on Classification and Terminology of the International League Against Epilepsy". Epilepsia. 22 (4): 489–501. 1981. doi:10.1111/j.1528-1157.1981.tb06159.x. PMID 6790275. S2CID 22190102.
  8. ^ a b Panayiotopoulos, Chrysostomos P. (2008). "Typical absence seizures and related epileptic syndromes: Assessment of current state and directions for future research". Epilepsia. 49 (12): 2131–9. doi:10.1111/j.1528-1167.2008.01777.x. PMID 19049569. S2CID 36248499.
  9. ^ a b c Panayiotopoulos, C. P. (2010). A clinical guide to epileptic syndromes and their treatment (2nd ed.). London: Springer.[page needed]
  10. ^ "Absence Seizures". www.hopkinsmedicine.org. 22 August 2023. Retrieved 2023-08-22.
  11. ^ Takahashi S, Yamamoto S, Tanaka R, Okayama A, Araki A, Azuma H (2015). "Focal frontal epileptiform discharges in a patient with eyelid myoclonia and absence seizures". Epilepsy Behav Case Rep. 4: 35–7. doi:10.1016/j.ebcr.2015.06.006. PMC 4491640. PMID 26155465.
  12. ^ John S. Duncan (1996). Eyelid Myoclonia with Absences. John Libbey Eurotext. pp. 52–. ISBN 978-0-86196-550-2.
  13. ^ Antonio V. Delgado-Escueta (2005). Myoclonic Epilepsies. Lippincott Williams & Wilkins. pp. 104–. ISBN 978-0-7817-5248-0.
  14. ^ Myers, Kenneth (May 2018). "Myoclonic absence seizures with complex gestural automatisms". European Journal of Paediatric Neurology. 22 (3): 532–535. doi:10.1016/j.ejpn.2017.12.003. ISSN 1090-3798. PMID 29325826. Retrieved 24 February 2019.
  15. ^ "Seizure Threshold Is Controlled by Breathing Pattern and Blood Gases". Epilepsy Foundation. Archived from the original on 2021-12-20. Retrieved 2021-12-20.
  16. ^ Perucca, Gram, Avanzini, and Dulac, 1998, "Antiepileptic drugs as a cause of worsening seizures."
  17. ^ "What is the pathophysiology of absence seizures?". www.medscape.com. Retrieved 2021-12-21.
  18. ^ Albuja, Ana C.; Khan, Gulam Qutubuddin (2021), "Absence Seizure", StatPearls, Treasure Island (FL): StatPearls Publishing, PMID 29763042, retrieved 2021-12-21
  19. ^ a b c Medscape > Absence Seizures by Scott Segan. Updated: Apr 27, 2011
  20. ^ Carlson, Neil R. (2013). Physiology of Behavior.
  21. ^ "Absence Seizures". www.hopkinsmedicine.org. 22 August 2023. Retrieved 2023-08-16.
  22. ^ "Absence Seizures". www.hopkinsmedicine.org. 22 August 2023. Retrieved 2023-08-22.
  23. ^ Epilepsy Therapy Project. "Absence Seizures". Epilepsy Foundation. Retrieved 8 May 2013.
  24. ^ V. Crunelli, N. Leresche Childhood absence epilepsy: genes, channels, neurons and networks Nat Rev Neurosci, 3 (2002), pp. 371-382
  25. ^ Manonmani V, Wallace SJ. Epilepsy with myoclonic absences. Arch Dise Child 1994; 70: 288–90.
  26. ^ Yadala, S., & Nalleballe, K. (2023). Juvenile Absence Epilepsy. In StatPearls. StatPearls Publishing.
  27. ^ Amrutkar, C., & Riel-Romero, R. M. (2023). Juvenile Myoclonic Epilepsy. In StatPearls. StatPearls Publishing.
  28. ^ Nilo, A., Crespel, A., Genton, P., Macorig, G., Gigli, G. L., & Gelisse, P. (2021). Epilepsy with eyelid myoclonias (Jeavons syndrome): An electro-clinical study of 40 patients from childhood to adulthood. Seizure, 87, 30–38. https://doi.org/10.1016/j.seizure.2021.02.028
  29. ^ Glauser, Tracy A.; Cnaan, Avital; Shinnar, Shlomo; Hirtz, Deborah G.; Dlugos, Dennis; Masur, David; Clark, Peggy O.; Capparelli, Edmund V.; Adamson, Peter C. (2010). "Ethosuximide, Valproic Acid, and Lamotrigine in Childhood Absence Epilepsy". New England Journal of Medicine. 362 (9): 790–9. doi:10.1056/NEJMoa0902014. PMC 2924476. PMID 20200383.
  30. ^ Kahan, Scott; Brillman, Jon (2005). In A Page Neurology. Hagerstwon, MD: Lippincott Williams & Wilkins. p. 47. ISBN 978-1-4051-0432-6.
  31. ^ a b "NICE Guidelines". Retrieved 3 November 2014.
  32. ^ Dreifuss, FE (1983). "Treatment of the nonconvulsive epilepsies". Epilepsia. 24 Suppl 1: S45–54. doi:10.1111/j.1528-1157.1983.tb04642.x. PMID 6413201. S2CID 37633941.
  33. ^ "Absence Epilepsy on The Rise Among Children". Medindia. 2016-11-26. Retrieved 2021-12-18.
  34. ^ "Absence Seizures". Epilepsy Foundation. Retrieved 08-22-2023
  35. ^ "Absence Seizures". www.hopkinsmedicine.org. 19 November 2019. Retrieved 2021-12-19.
  36. ^ Groomes, Laura B.; Pyzik, Paula L.; Turner, Zahava; Dorward, Jennifer L.; Goode, Victoria H.; Kossoff, Eric H. (2011-02-01). "Do Patients With Absence Epilepsy Respond to Ketogenic Diets?". Journal of Child Neurology. 26 (2): 160–165. doi:10.1177/0883073810376443. ISSN 0883-0738. PMID 20647578. S2CID 21958807.
  37. ^ Knake, S; Hamer, HM; Schomburg, U (August 8, 1999). "Tiagabine-induced absence status in idiopathic generalized epilepsy". European Journal of Epilepsy. 8 (5): 314–317. doi:10.1053/seiz.1999.0303. PMID 10486298. Retrieved 3 November 2014.
  38. ^ Posner, Ewa B; Mohamed, Khalid K; Marson, Anthony G (2005). Posner, Ewa B (ed.). "Ethosuximide, sodium valproate or lamotrigine for absence seizures in children and adolescents". Cochrane Database of Systematic Reviews (4): CD003032. doi:10.1002/14651858.CD003032.pub2. PMID 16235312.
  39. ^ Brigo, Francesco; Igwe, Stanley C.; Lattanzi, Simona (8 February 2019). "Ethosuximide, sodium valproate or lamotrigine for absence seizures in children and adolescents". The Cochrane Database of Systematic Reviews. 2 (2): CD003032. doi:10.1002/14651858.CD003032.pub4. ISSN 1469-493X. PMC 6367681. PMID 30734919.
  40. ^ Posner, Ewa B.; Mohamed, Khalid; Marson, Anthony G. (2005). "A systematic review of treatment of typical absence seizures in children and adolescents with ethosuximide, sodium valproate or lamotrigine". Seizure. 14 (2): 117–22. doi:10.1016/j.seizure.2004.12.003. PMID 15694565.
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