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Select item 44036681.

StatPearls [Internet].

Treasure Island (FL): StatPearls Publishing; 2025 Jan-.

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Select item 23871562.

Jasper's Basic Mechanisms of the Epilepsies [Internet]. 4th edition.

Noebels JL, Avoli M, Rogawski MA, et al., editors.

Bethesda (MD): National Center for Biotechnology Information (US); 2012.

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Select item 48538163.

LiverTox: Clinical and Research Information on Drug-Induced Liver Injury [Internet].

Bethesda (MD): National Institute of Diabetes and Digestive and Kidney Diseases; 2012-.

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Select item 14051744.

The Epilepsies: Seizures, Syndromes and Management.

Panayiotopoulos CP.

Oxfordshire (UK): Bladon Medical Publishing; 2005.

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Select item 50644125.

Interventions for adults with a history of complex traumatic events: the INCiTE mixed-methods systematic review.

Melton H, Meader N, Dale H, et al.

Southampton (UK): NIHR Journals Library; 2020 Sep. (Health Technology Assessment, No. 24.43.)

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Select item 28056146.

Effectiveness and Safety of Antiepileptic Medications in Patients With Epilepsy [Internet].

Talati R, Scholle JM, Phung OJ, et al.

Rockville (MD): Agency for Healthcare Research and Quality (US); 2011 Dec. (Comparative Effectiveness Reviews, No. 40.)

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Select item 57048767.

Jasper's Basic Mechanisms of the Epilepsies. 5th edition.

Noebels JL, Avoli M, Rogawski MA, et al., editors.

New York: Oxford University Press; 2024.

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Select item 14134408.

An Introduction to Epilepsy [Internet].

Bromfield EB, Cavazos JE, Sirven JI, editors.

West Hartford (CT): American Epilepsy Society; 2006.

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Select item 55642269.

Cenobamate (Xcopri): CADTH Reimbursement Review: Therapeutic area: Epilepsy, partial onset seizures [Internet].

Ottawa (ON): Canadian Agency for Drugs and Technologies in Health; 2023 Nov.

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Select item 456572810.

Drugs and Lactation Database (LactMed®) [Internet].

Bethesda (MD): National Institute of Child Health and Human Development; 2006-.

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Select item 533756811.

Effectiveness of antiseizure therapies in the treatment of absence seizures: Epilepsies in children, young people and adults: Evidence review G.

National Guideline Alliance (UK).

London: National Institute for Health and Care Excellence (NICE); 2022 Apr. (NICE Guideline, No. 217.)

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Select item 533858612.

Effectiveness of antiseizure therapies in the treatment of idiopathic generalised epilepsies, including juvenile myoclonic epilepsy: Epilepsies in children, young people and adults: Evidence review J.

National Guideline Alliance (UK).

London: National Institute for Health and Care Excellence (NICE); 2022 Apr. (NICE Guideline, No. 217.)

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Select item 533803613.

Add-on therapy for generalised tonic-clonic and focal onset seizures: Epilepsies in children, young people and adults: Evidence review F.

National Guideline Alliance (UK).

London: National Institute for Health and Care Excellence (NICE); 2022 Apr. (NICE Guideline, No. 217.)

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Select item 533799814.

Epilepsies in children, young people and adults.

London: National Institute for Health and Care Excellence (NICE); 2025 Jan 30. (NICE Clinical Guidelines, No. 217.)

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Select item 539225215.

Management of Infantile Epilepsies [Internet].

Treadwell JR, Wu M, Tsou AY.

Rockville (MD): Agency for Healthcare Research and Quality (US); 2022 Oct. (Comparative Effectiveness Review, No. 252.)

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Select item 145898416.

GeneReviews® [Internet].

Adam MP, Bick S, Mirzaa GM, et al., editors.

Seattle (WA): University of Washington, Seattle; 1993-2026.

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Select item 519298017.

Evidence review for pharmacological management for chronic primary pain: Chronic pain (primary and secondary) in over 16s: assessment of all chronic pain and management of chronic primary pain: Evidence review J.

National Guideline Centre (UK).

London: National Institute for Health and Care Excellence (NICE); 2021 Apr. (NICE Guideline, No. 193.)

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Select item 265918218.

Database of Abstracts of Reviews of Effects (DARE): Quality-assessed Reviews [Internet].

York (UK): Centre for Reviews and Dissemination (UK); 1995-.

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Select item 470897219.

Pharmacotherapy for Stimulant Use Disorders: A Systematic Review [Internet].

Chan B, Kondo K, Ayers C, et al.

Washington (DC): Department of Veterans Affairs (US); 2018 Aug.

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Select item 533761620.

Effectiveness of antiseizure therapies in the treatment of tonic or atonic seizures/drop attacks: Epilepsies in children, young people and adults: Evidence review I.

National Guideline Alliance (UK).

London: National Institute for Health and Care Excellence (NICE); 2022 Apr. (NICE Guideline, No. 217.)

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Figure 10.4Samples from a video EEG showing idiopathic and symptomatic myoclonic absence seizures. The EEG GSWD are similar with no apparent differentiating features or asymmetry in the symptomatic patient.

Top: Video EEG of a boy aged 8 years with myoclonic absences from the age of 6 years. These were frequent, hundreds per day, and manifested with rhythmic myoclonic jerks and unresponsiveness. Valproate failed to achieve control, but absences ceased completely when ethosuximide was added at the age of 8 years. Medication was withdrawn at 11 years of age. No further seizures occurred in the next 8 years of follow-up and he is academically successful.
The absence is terminated by somatosensory stimulation (tapping his shoulder).
Bottom: Video EEG of a girl aged 15 months with myoclonic absences due to birth anoxia. Myoclonic absences started at 15 months of age, occurred many times a day, lasted for 8–10 s and were characterised by synchronous and bilateral myoclonic jerks of the limbs and head with apparent loss of consciousness. Subsequently, she developed frequent, mainly nocturnal GTCS while myoclonic absences continued. These were intractable to any appropriate medication. At 8 years of age, she had severe learning difficulties and spastic quadraparesis.

Idiopathic Generalised Epilepsies.

Panayiotopoulos CP. The Epilepsies: Seizures, Syndromes and Management. Oxfordshire (UK): Bladon Medical Publishing; 2005.
Figure 10.16Diagnostic Errors in PMA

Top: Video EEG recording of an 18-year-old woman with perioral myoclonia with absences (case 6 in ref 328). She was referred because of ‘focal motor seizures and secondarily GTCS’. She had onset of GTCS and absences at 11 years of age, which continued despite treatment with various combinations of valproate, ethosuximide, clonazepam, lamotrigine and acetazolamide. Absences were frequent, often in daily clusters and consisted of brief (about 5 s) moderate impairment of consciousness with violent rhythmic jerking of the jaw. GTCS occurred 1–10 times a year, usually after awakening, preceded by clusters of absences with the jaw myoclonus spreading to limb jerks prior to generalised convulsions. She was more concerned about the absences because they interfered with her daily life “everyone notices the jerks of my jaw” and less about the GTCS, which usually occurred at home. The initial misdiagnosis of ‘focal motor seizures’ was because the jaw jerking was perceived and described by her mother as unilateral.
Bottom: EEG of 23-year-old woman while in perioral status epilepticus (case 2 in ref 328). She was mildly confused with continuous perioral twitching. This ended with a GTCS. Initial presentation at 11 years of age was with GTCS. PMA was noted at the same time and was diagnosed as focal motor seizures. Despite medication with valproate, she continues having infrequent episodes of ASE terminated with self-administered benzodiazepines.

Idiopathic Generalised Epilepsies.

Panayiotopoulos CP. The Epilepsies: Seizures, Syndromes and Management. Oxfordshire (UK): Bladon Medical Publishing; 2005.
Figure 3The tonic GABAA inhibition in TC neurons is both necessary and sufficient for typical absence seizure generation

A. Bilateral (L = left, R = right hemispheres) EEG traces from a freely moving GAT-1 knockout (KO) mouse showing spontaneous SWDs (spectrogram of the R trace is illustrated below). B. Bilateral EEG traces from a normal Wistar rat following intra-thalamic administration by reverse microdialysis of 200μM of the selective GAT-1 blocker NO711 (spectrogram of the L trace is illustrated below). C. Bilateral EEG traces from a normal Wistar rat following intra-thalamic administration by reverse microdialysis of 100μM THIP (spectrogram of the R trace is illustrated below). D. Time-course of the induction of SWDs by intra-thalamic administration of NO711. E. SWDs are substantially reduced in GAERS 1 and 2 days following a single intrathalamic injection of a small and large dose of a δ-subunit antisense oligodeoxynucleotide (Anti-1 and Anti-2, respectively), but not of a missense oligo (Mis). F. Summary histograms showing the cumulative (over 1–2 hours) time spent in seizures for different transgenic and pharmacological mice and rat models, and the abolition of their SWDs by systemic administration of ethosuximide (100 or 200 mg/kg/ip). * p<0.05, ** p<0.01 and ***p<0.001. (A-F: reproduced with permission from Cope et al., 2009, © Nature Publishing Group).

GABA-A Receptor Function in Typical Absence Seizures.

Noebels JL, Avoli M, Rogawski MA, et al., editors. Jasper's Basic Mechanisms of the Epilepsies [Internet]. 4th edition. Bethesda (MD): National Center for Biotechnology Information (US); 2012.
Figure 4Baseline ECoG recording from the electrodes placed in cerebral cortex of a wild-type mouse and from the cortex of LN3-1, LN2-4, and LN3-5 transgenic mice

The traces denote differential signal between either the left frontal parietal electrodes (LF-P) or the right frontal parietal electrodes (RF-P). Note that the frequency of the seizure is 3–6 Hz. All subjects were 2 months of age or older at the time of the recordings. (B) Higher resolution tracing illustrating the spike and wave components of the ictal event from the cortex of an LN3-1 transgenic mouse. (C) Comparison of the spontaneous SWD activity between the different transgenic mouse lines. Although the frequency of the seizure was consistent between the different lines, the amount of seizure activity per hour differed significantly between the different lines. Note that the amount of seizure activity present in each line correlates with the amount of immunoreactive transgene expressed within each line (see Figure 1). Data are presented as the mean and standard error of the seizure duration per hour of recording from n=10 (LN2-4); n=11 (LN3-5); n=10 (LN2-3); and n=12 (LN3-1) transgenic mice. (D) The pharmacological responsiveness of the spontaneous SWD in the GABABR1a transgenic mice is consistent with absence epilepsy. The cumulative SWD duration in transgenic line LN3-1 was measured for 1 h either following saline injection or following the administration of the proabsence drug γ-butyrolactone (GBL), the GABABR agonist (−)baclofen (BAC), the GABABR antagonist, CGP 35348 (CGP), or the anti-absence drug ethosuximide (ETO). As shown in the figure, the duration of the SWD was significantly (p<0.01, n=8–10) reduced by pretreatment with either ETO or CGP and exacerbated by GBL or BAC. Note that the injection of the control saline was sufficient to reduce SWDduration (compare panels C and D). Asterisks denote significant differences from their littermate wild type (p<0.05 student’s unpaired t-test). (With Permission from Wu et al. Neurobiology of Disease 26 (2007) 439–451)

GABAB Receptor and Absence Epilepsy.

Noebels JL, Avoli M, Rogawski MA, et al., editors. Jasper's Basic Mechanisms of the Epilepsies [Internet]. 4th edition. Bethesda (MD): National Center for Biotechnology Information (US); 2012.