Idiopathic Generalized Epilepsies
Idiopathic Generalized Epilepsies
What Do You Need to Know?
- Four IGE syndromes (ILAE 2022): CAE, JAE, JME, GTCA — all share generalized spike-wave (2.5–5.5 Hz), normal exam, normal MRI, presumed genetic etiology
- Only CAE is self-limited (65–80% remission); JAE, JME, and GTCA all require lifelong ASM therapy
- JME is the most common IGE: classic triad of morning myoclonus (100%), GTC (80–95%), and absences (15–40%); relapse >80–90% on ASM withdrawal
- AVOID Na channel blockers (CBZ, OXC, PHT) in ALL IGEs — they worsen absence, myoclonic, and atonic seizures
- VPA is the most effective ASM across all IGEs but is teratogenic; LEV is first-line in women of childbearing potential
- Jeavons syndrome: eyelid myoclonia on eye closure, nearly 100% photosensitive, drug-resistant in 40–50%
- Absence status epilepticus: prolonged confusion in IGE patients; treat with IV benzodiazepines; triggered by ASM noncompliance or inappropriate ASM changes
🚩 Don’t Miss — Test-Day Priorities
- CAE = ethosuximide first-line: Glauser NEJM 2010 (CAE trial) showed ETX = VPA > LTG for freedom from treatment failure, and ETX has the best attentional profile — pick ETX for pure absence with no GTC
- Ethosuximide does NOT cover GTC: never use ETX monotherapy in JAE or JME (GTC in ~80–95%) — pick VPA, LEV, or LTG instead
- VPA is teratogenic — pick LEV first-line in women of childbearing potential (SANAD II); VPA stays the most effective ASM in IGE for men
- AVOID Na-channel blockers in IGE: CBZ, OXC, PHT, GBP, PGB, TGB, VGB worsen absence and myoclonic seizures — the most common cause of "drug-resistant" JME is misdiagnosis as focal epilepsy → CBZ/OXC prescribed → worse seizures
- AVOID LTG in prominent myoclonus: lamotrigine may paradoxically worsen myoclonic jerks in JME and eyelid myoclonia in Jeavons — broad-spectrum does NOT mean myoclonus-safe
- Morning myoclonic jerks + GTC in a teenager = JME: ask about "dropping cereal/toothbrush in the morning"; sleep deprivation and alcohol are the dominant triggers; lifelong therapy (>80–90% relapse off ASM)
- Eye-closure–induced eyelid jerking + near-100% photosensitivity in a young girl = Jeavons syndrome; self-induced seizures are epileptic, not behavioral — AVOID LTG, use VPA/LEV/clonazepam
- Only CAE is self-limited (65–80% remit by adolescence); JAE, JME, and GTCA all require lifelong ASM — do not attempt withdrawal in JME
- Consider GLUT1 deficiency (SLC2A1) in atypical/early-onset absence (<4 yrs), microcephaly, paroxysmal exertional dyskinesia, or movement disorder — check CSF:serum glucose ratio <0.45 and start ketogenic diet (disease-modifying)
- Prolonged confusion in an IGE patient after ASM noncompliance or a switch to a Na-channel blocker = absence status epilepticus — emergent EEG and IV benzodiazepines are both diagnostic and therapeutic
🔍 Buzzwords & Pathognomonic FindingsEEG · Clinical · Treatment / pharmacology
EEG signs
- Regular 3-Hz generalized spike-and-wave activated by hyperventilation → CAE
- Generalized 3.5–4.5 Hz spike-and-wave (faster than CAE) → JAE
- Irregular 3.5–6 Hz polyspike-and-wave, often on awakening → JME
- Photoparoxysmal response on intermittent photic stimulation → JME or Jeavons
- Generalized polyspike-wave within 0.5–2 sec of eye closure → Jeavons syndrome
- Focal/frontal-appearing discharges in a teen with morning jerks → JME (NOT focal epilepsy — do not give CBZ)
- Slow (<2.5 Hz) spike-and-wave on an abnormal background → Lennox-Gastaut (atypical absence), NOT IGE
Clinical signs
- School-age child with multiple daily brief blank stares + eyelid flutter or oral automatisms → CAE
- Teen presenting with first GTC + prior history of "spaced-out spells" → JAE
- Morning myoclonic jerks ("dropping the toothbrush / spilling cereal") + GTC after sleep deprivation → JME
- GTC on awakening triggered by sleep deprivation or alcohol, no myoclonus/absences → GTCA
- Eyelid jerks with upward eye deviation triggered by eye closure in a young girl + photosensitivity → Jeavons syndrome
- Seizures triggered by TV / video games / patterned stimuli ("Pokémon stroboscope") → photosensitive IGE (JME, Jeavons)
- Normal neuro exam + normal MRI + family history of epilepsy → IGE hallmark
Treatment / pharmacology pearls
- Ethosuximide → first-line for pure absence (CAE) per Glauser NEJM 2010 — absence only, no GTC coverage
- Valproate → most effective ASM across all IGEs (SANAD II) but teratogenic — avoid in women of childbearing potential
- Levetiracetam → first-line in women of childbearing potential with JME/JAE/GTCA
- Lamotrigine → may worsen myoclonus — use cautiously in JME and Jeavons
- Carbamazepine / oxcarbazepine / phenytoin → worsen absence and myoclonus — AVOID in all IGEs
- Vigabatrin, gabapentin, pregabalin, tiagabine → worsen absence/myoclonus — AVOID in IGE
- Sleep deprivation + alcohol → classic JME triggers; lifestyle counseling is core therapy
- Lifelong therapy with >80–90% relapse on withdrawal → JME
- IV benzodiazepines → absence status epilepticus (rapid resolution, diagnostic + therapeutic)
Terminology: IGE vs GGE (ILAE 2022)
Per ILAE 2022 (Hirsch et al.), IGE = the four electroclinical syndromes (CAE, JAE, JME, GTCA); GGE is the broader category that also includes generalized epilepsies of presumed genetic etiology not meeting any specific IGE syndrome. All IGEs are GGEs, but not all GGEs are IGEs.
Childhood Absence Epilepsy (CAE)
Clinical Features
- Onset: 4–10 years; peak 5–7 years; slight female predominance
- Seizure semiology: Multiple daily absences (10–100+/day); brief (<10 seconds); abrupt onset and offset; no postictal phase
- Behavioral arrest with staring; may have subtle automatisms (lip smacking, fumbling) or mild eyelid flutter
- Often discovered when teachers report "daydreaming" or "inattention" in a school-age child
- GTC seizures rare (<10%) — if present, consider reclassification (JAE or JME)
- Normal neurological examination and (usually) normal baseline cognition
EEG
- Regular 3 Hz generalized spike-and-wave on a normal background (classically 3.5 Hz at onset slowing to 2.5 Hz at offset)
- Hyperventilation provokes absences in >80–90% — the key diagnostic provocation; failure of HV to provoke a typical absence in an untreated patient should prompt reconsideration of the diagnosis
- PPR uncommon (5–15%)
- Ictal pattern is identical to interictal pattern, just sustained
Differential / Mimics
- Consider GLUT1 deficiency (SLC2A1) in atypical/early-onset/microcephalic cases — especially if absences begin before age 4, are paroxysmal-exertional, or are accompanied by movement disorder/microcephaly; check low CSF glucose (CSF:serum ratio <0.45); ketogenic diet is responsive and disease-modifying
- Atypical absences (slower <2.5 Hz spike-wave, abnormal background) suggest a developmental and epileptic encephalopathy (e.g., Lennox-Gastaut), not CAE
Treatment
- First-line: Ethosuximide (ETX) or valproate (VPA)
- Glauser NEJM 2010 (childhood absence epilepsy trial): ETX = VPA > LTG for freedom from treatment failure in CAE without GTC; ETX preferred over VPA due to a better attentional/cognitive profile
- LTG is a reasonable alternative but less efficacious in this trial
- AVOID CBZ, OXC, PHT, VGB, GBP, TGB — all worsen absences
Prognosis
- Self-limited — remission in 65–80% by adolescence
- A minority evolve into JME (myoclonic jerks emerge in adolescence) or JAE (sporadic absences plus GTC)
- Subtle attention/executive deficits may persist even after seizure remission
Juvenile Absence Epilepsy (JAE)
Clinical Features
- Onset: 9–13 years (later than CAE, earlier than JME)
- Absences: Sporadic — often less than daily; less frequent and typically longer than in CAE; consciousness more variably impaired
- GTC seizures in ~80% — frequently the presenting event (a teen presenting with first GTC + history of prior "spaced-out spells" should raise suspicion for JAE)
- Myoclonic jerks rare (~15–20%); if prominent, reclassify as JME
- Normal exam, normal MRI, normal cognition
EEG
- Generalized spike-wave at ~3.5–4 Hz (slightly faster than CAE) on a normal background
- PPR in 15–25%
- Hyperventilation may provoke but is less reliably activating than in CAE
Treatment
- First-line: VPA, LTG, LEV
- In women of childbearing potential, prefer LEV over VPA (see SANAD II); LTG is also a reasonable choice but watch for myoclonic worsening if JAE/JME overlap is suspected
- ETX is NOT first-line because it does not cover GTC seizures, which occur in ~80%
- AVOID Na channel blockers (CBZ, OXC, PHT), VGB, GBP, PGB, TGB
Prognosis
- NOT self-limited — typically requires lifelong treatment
- High relapse rate (>70–80%) on ASM withdrawal
- Good seizure control with appropriate ASMs in most patients
Juvenile Myoclonic Epilepsy (JME)
Overview
- Most common IGE syndrome (~27% of all IGE; 5–10% of all epilepsies)
- Peak onset 12–18 years (range 10–24); slight female predominance
- Complex polygenic inheritance; family history of epilepsy in 30–50%
- Susceptibility genes: EFHC1, GABRA1, GABRD, CLCN2, BRD2 — genetic testing is NOT required for diagnosis
- ~70% concordance in monozygotic twins; diagnosis is clinical and electroclinical, not genetic
- Up to 30% misdiagnosed as focal epilepsy → placed on Na channel blockers → seizures worsen
Classic Triad
| Seizure Type | Frequency | Key Features |
|---|---|---|
| Myoclonic jerks | 100% | Morning (within 30–60 min of awakening); bilateral, asymmetric, upper-limb predominant; consciousness preserved; "dropping things in the morning" |
| GTC | 80–95% | Often preceded by myoclonic cluster (myoclonic-tonic-clonic sequence); main reason for presentation; morning predominance |
| Typical absence | 15–40% | Briefer and less frequent than in CAE; may precede myoclonus onset by months to years |
Triggers
- Sleep deprivation — single most potent trigger; nearly universal
- Alcohol — intoxication + associated sleep disruption
- Photic stimulation — PPR ~30–40% on routine IPS; higher with provocative protocols; TV, video games, flickering lights
- Stress and fatigue — examination periods, emotional stress
- Praxis-induced seizures — triggered by complex cognitive tasks (calculation, writing, decision-making) in up to 40% of JME patients
- Menstruation — catamenial worsening of myoclonus and GTC
- ASM noncompliance — common trigger in the adolescent population
EEG Findings
- Interictal: Irregular generalized 3.5–6 Hz polyspike-and-wave discharges; normal background
- Photoparoxysmal response (PPR): ~30–40% on routine IPS; higher with provocative protocols
- Focal-appearing features in 30–40% (often frontal) — do NOT indicate focal epilepsy; do not prescribe Na channel blockers
- Single routine EEG may be normal in 30–50% — sleep-deprived EEG increases yield
- Ictal myoclonic: Generalized polyspike-wave burst time-locked to myoclonic jerk
Frontal Lobe Hypothesis
- VBM shows gray matter volume reductions in frontal lobes and thalamus
- DTI reveals reduced fractional anisotropy in frontal white matter tracts and frontal-thalamic connections
- fMRI shows enhanced motor cortex-thalamus connectivity; disrupted default mode network
- Subtle executive dysfunction: impaired prospective memory, planning, mental flexibility
- Supports cortico-thalamic network model of generalized epilepsy
Treatment
| Medication | Efficacy | Notes |
|---|---|---|
| Valproate (VPA) | 70–85% seizure freedom | Most effective; controls all 3 seizure types; MAJOR teratogen — avoid in women of childbearing age unless no alternative |
| Levetiracetam (LEV) | 60–70% | First-line in women of childbearing potential; less effective for absence; irritability in 10–20% |
| Lamotrigine (LTG) | Good for GTC/absence | May worsen myoclonus in some patients; slow titration (SJS risk); useful in women |
| Topiramate / Zonisamide | Broad-spectrum | TPM: cognitive effects, teratogenic (cleft palate); ZNS: less cognitive impairment |
| Perampanel | Add-on for refractory GTC/myoclonus | AMPA antagonist; aggression at higher doses; FDA-approved as adjunctive therapy for primary GTC seizures (age ≥12) |
Medications That WORSEN JME
- Carbamazepine / Oxcarbazepine — most common cause of treatment failure due to misdiagnosis as focal epilepsy
- Phenytoin — worsens myoclonus; ineffective for generalized seizures
- Vigabatrin — consistently worsens myoclonus and absence
- Gabapentin / Pregabalin — may exacerbate myoclonic and absence seizures
- Lamotrigine — can paradoxically worsen myoclonus in a subset of patients
Prognosis
- NOT self-limited — ILAE classifies JME as "not self-limited"
- Relapse rate >80–90% with ASM withdrawal, even after years of seizure freedom
- 80–90% achieve excellent control with appropriate ASMs
- 10–20% have drug-resistant seizures (usually persistent myoclonus)
- Some patients (<20%) may achieve seizure freedom off medication after the 4th–5th decade
Epilepsy With GTC Seizures Alone (GTCA)
Clinical Features
- Onset: 10–25 years; may present later than other IGEs
- GTC seizures as the sole seizure type — no clinically apparent myoclonus or absences
- GTC preferentially on awakening or after relaxation; infrequent (yearly or less)
- Triggers: sleep deprivation, alcohol, stress (same as JME)
- Normal neurological examination and cognition
EEG
- Generalized 3–5.5 Hz spike-wave or polyspike-wave discharges
- Interictal EEG normal in up to 50% — a single routine EEG has low sensitivity
- Sleep-deprived EEG or prolonged monitoring increases diagnostic yield
Key Differentiator: GTCA vs. Focal to Bilateral TLC
| Feature | GTCA | Focal to Bilateral TLC |
|---|---|---|
| Age | 10–25 years | Any age |
| Aura / focal onset | Absent | Often present (may be unrecognized) |
| Todd paralysis | Absent | May be present |
| EEG | Generalized spike-wave | Focal epileptiform discharges |
| MRI | Normal | May show structural lesion |
| Family history | IGE/GGE common | Less common |
Treatment & Prognosis
- First-line: VPA, LEV, LTG
- Avoid: CBZ, PHT, VGB, GBP/PGB
- NOT self-limited — lifelong treatment generally required; high relapse with ASM withdrawal
- Diagnostic challenge: Video-EEG monitoring may be needed when interictal EEG is nondiagnostic; misdiagnosis as focal epilepsy leads to inappropriate Na channel blocker selection
- Lifestyle counseling (sleep hygiene, alcohol avoidance) is critical — triggers are identical to JME
Jeavons Syndrome (Eyelid Myoclonia With Absences)
Clinical Features
- Onset: Childhood (typically 2–14 years; peak 6–8 years); persists into adulthood
- Defining feature: Rapid (3–6 Hz) rhythmic eyelid jerking with upward eye deviation, triggered by eye closure
- Photosensitivity: Nearly 100% — PPR on EEG in virtually all patients
- Other seizures: GTC (~50%), myoclonic jerks, typical absences
- Self-induced seizures: Some patients intentionally trigger eyelid myoclonia via eye closure or hand waving near a light source — this is an epileptic phenomenon, not a behavioral disorder
EEG
- Eye closure sensitivity: Generalized polyspike-wave within 0.5–2 seconds of eye closure — the hallmark
- PPR nearly universal on IPS
- Interictal: generalized 3–6 Hz polyspike-wave; brief discharges easily overlooked
Treatment & Prognosis
- Drug-resistant in 40–50% — eyelid myoclonia is the hardest seizure type to control
- ASMs: VPA (most effective), LEV, LTG (caution: may worsen eyelid myoclonia in some), ETX as adjunct for absence component only — does NOT cover eyelid myoclonia or GTC; never use as monotherapy in Jeavons; clobazam as adjunct
- Avoid: CBZ, PHT, VGB, GBP/PGB
- NOT self-limited — eyelid myoclonia and photosensitivity persist lifelong
- Photosensitivity management: Blue-tinted lenses (Z1 lenses); ambient lighting; screen brightness reduction
- Classification note: ILAE 2022 places EEM as a childhood-onset epilepsy that may be associated with epileptic encephalopathy in some patients (when cognitive impairment develops)
4-Syndrome IGE Comparison
| Feature | CAE | JAE | JME | GTCA |
|---|---|---|---|---|
| Onset age | 4–10 y | 9–13 y | 10–24 y | 10–25 y |
| Predominant seizure | Absences (multiple daily) | Absences (less frequent) | Myoclonic jerks (morning) | GTC only |
| GTC seizures | Rare (<10%) | ~80% | 80–95% | 100% |
| Myoclonic jerks | Absent | Rare (~15–20%) | 100% (defining) | Absent |
| EEG pattern | Regular 3 Hz SW | Regular 3–5.5 Hz SW | Irregular 3.5–6 Hz PSW | 3–5.5 Hz SW (often normal) |
| PPR | 5–15% | 15–25% | ~30–40% (routine IPS) | Variable |
| HV provocation | Strong | Moderate | Variable | Variable |
| Self-limited? | Yes (65–80%) | No | No | No |
| Lifelong Rx | Not usually | Yes | Yes | Yes |
Board Pearl
Only CAE is self-limited among the IGEs. JAE, JME, and GTCA all require lifelong ASM therapy with high relapse rates (>60–90%) on withdrawal. CAE may evolve into JME in some patients — reclassify the syndrome if myoclonic jerks emerge in adolescence.
Key Principles Across All IGEs
ASM Selection by Seizure Type in IGE
| Seizure Type | Preferred ASMs | ASMs to AVOID |
|---|---|---|
| Absence | ETX (absence only), VPA, LTG | CBZ, PHT, VGB, GBP, TGB |
| Myoclonic | VPA, LEV, clonazepam, PER | CBZ, PHT, VGB, GBP, sometimes LTG |
| GTC | VPA, LEV, LTG, PER, TPM | VGB; CBZ may not worsen GTC but may provoke absences/myoclonus |
| Multiple types | VPA (broadest); LEV + LTG combo; add PER or CLB if refractory | All Na channel blockers if myoclonic/absence component present |
General ASM Principles
- AVOID Na channel blockers (CBZ, OXC, PHT) in all IGEs — worsen absence, myoclonic, and atonic seizures (a teaching simplification: worsening is most consistent for absence and myoclonic; GTC seizures may not clearly worsen in every patient)
- AVOID vigabatrin, gabapentin, pregabalin, tiagabine — may worsen absence and myoclonic seizures in IGEs (vigabatrin and tiagabine more consistently; gabapentin/pregabalin variable)
- VPA is the broadest-spectrum and most effective ASM but teratogenic — use LEV or LTG first-line in women of childbearing potential
- In refractory IGE, consider combination therapy: VPA + LTG, LEV + VPA, or addition of PER
Evidence: SANAD II (Marson et al., Lancet 2021)
- In generalized or unclassifiable epilepsy, VPA was superior to LEV for 12-month seizure freedom and for time-to-treatment-failure in men
- In women of childbearing potential, LEV was non-inferior and is the practical first-line; VPA is avoided in PWECP if clinically feasible and is not routine first-line in this population
- Established the evidence base for current VPA vs LEV decision-making in IGE/GGE: VPA remains the most effective ASM, but LEV is the appropriate first-line in any patient for whom teratogenicity is a relevant consideration
Overlap Syndromes
- CAE → JME in some patients as myoclonic jerks emerge in adolescence
- JAE/JME overlap: absences + myoclonus; classify based on predominant seizure type
- Phenotypic heterogeneity within families — proband may have JME while sibling has CAE
- IGE vs. GGE: if criteria for any specific IGE syndrome are not met, classify as GGE
Absence Status Epilepticus
- Presentation: Prolonged confusion, psychomotor slowing, or near-stupor in an IGE patient; subtle eyelid fluttering or perioral twitching may be the only motor signs
- Duration: May last hours to days if unrecognized
- EEG: Continuous or near-continuous generalized spike-wave (2.5–4 Hz)
- Common triggers: ASM noncompliance, switching from broad-spectrum to Na channel blocker, sleep deprivation, alcohol
- Treatment: IV benzodiazepines (lorazepam, diazepam) — highly effective with rapid resolution
- Prognosis: Excellent with appropriate treatment; no lasting cognitive sequelae
Board Pearl
Sodium channel blockers worsen IGE. CBZ, OXC, and PHT paradoxically promote thalamocortical oscillations in generalized epilepsies, worsening absence, myoclonic, and GTC seizures. The most common cause of "drug-resistant epilepsy" in JME is misdiagnosis as focal epilepsy followed by inappropriate Na channel blocker prescription.
Board Pearls & Clinical Pearls
Board Pearls
- Morning myoclonus + GTC in a teenager = JME until proven otherwise. Always ask about "dropping things in the morning" or "morning clumsiness" in any young patient presenting with a first GTC seizure
- JME with focal EEG features: Up to 30–40% of JME patients show focal or asymmetric (often frontal) discharges — these do NOT indicate focal epilepsy and must not lead to Na channel blocker prescription
- Praxis-induced seizures: Up to 40% of JME patients have seizures triggered by complex cognitive tasks — board exams, calculations, writing; counsel patients about task breaks during prolonged mental effort
- PPR + GTC + morning jerks in a teenager = virtually diagnostic of JME; no further workup needed if exam and background EEG are normal
- Worsening seizures on CBZ/PHT? Reconsider the diagnosis — misdiagnosed JME is one of the most common causes of pseudoresistance in epilepsy
- Eyelid myoclonia on eye closure + near-universal photosensitivity = Jeavons syndrome. Self-induced seizures in these patients are an epileptic phenomenon requiring treatment adjustment, not a behavioral disorder
Clinical Pearl
Avoid VPA in people with epilepsy of childbearing potential (PWECP) if clinically feasible — not routine first-line (dose-dependent MCM rate ~6–10%, higher at doses >1000 mg/day; reduced IQ by 8–11 points; increased autism risk). LEV is preferred first-line in this population. If VPA is unavoidable, use the lowest effective dose, ensure at least 0.4 mg/day folic acid (higher doses are specialist-guided rather than evidence-proven), and enroll in pregnancy prevention counseling (formal Pregnancy Prevention Programme in EU/UK; REMS-style risk counseling in the US).
Clinical Pearl
An IGE patient with acute-onset unexplained confusion — especially after recent ASM change or noncompliance — should prompt consideration of absence status epilepticus. Emergent EEG or empiric IV benzodiazepine trial is both diagnostic (rapid resolution) and therapeutic. Do not assume psychiatric or metabolic etiology without ruling out nonconvulsive status.
Clinical Pearl
JME is a lifelong condition. Counsel patients that >80–90% relapse on ASM withdrawal. Do not attempt withdrawal unless the patient has been seizure-free for many years AND a recurrence would have minimal functional impact. Most patients require lifelong therapy.
References
- Hirsch E, French J, Scheffer IE, et al. ILAE definition of the idiopathic generalized epilepsy syndromes: position statement by the ILAE Task Force on Nosology and Definitions. Epilepsia 2022;63(6):1475–1499.
- Riney K, Bogacz A, Somerville E, et al. International League Against Epilepsy classification and definition of epilepsy syndromes with onset at a variable age. Epilepsia 2022;63(6):1443–1474.
- Scheffer IE, Berkovic S, Capovilla G, et al. ILAE classification of the epilepsies: position paper of the ILAE Commission for Classification and Terminology. Epilepsia 2017;58(4):512–521.
- Kasteleijn-Nolst Trenité DG, Schmitz B, Janz D, et al. Consensus on diagnosis and management of JME: from founder's observations to current trends. Epilepsy Behav 2013;28(Suppl 1):S87–S90.
- Camfield CS, Camfield PR. Juvenile myoclonic epilepsy 25 years after seizure onset: a population-based study. Neurology 2009;73(13):1041–1045.
- Baykan B, Wolf P. Juvenile myoclonic epilepsy as a spectrum disorder: a focused review. Seizure 2017;49:36–41.
- Genton P, Thomas P, Kasteleijn-Nolst Trenité DG, et al. Clinical aspects of juvenile myoclonic epilepsy. Epilepsy Behav 2013;28(Suppl 1):S8–S14.
- Striano S, Capovilla G, Sofia V, et al. Eyelid myoclonia with absences (Jeavons syndrome): a well-defined idiopathic generalized epilepsy syndrome or a spectrum of photosensitive conditions? Epilepsia 2009;50(Suppl 5):15–19.
- Genton P, Gelisse P, Thomas P, Dravet C. Do carbamazepine and phenytoin aggravate juvenile myoclonic epilepsy? Neurology 2000;55(8):1106–1109.
- Tomson T, Battino D, Perucca E. Teratogenicity of antiepileptic drugs. Curr Opin Neurol 2019;32(2):246–252.
- Mullen SA, Berkovic SF, Lowenstein DH, et al. Genetic generalized epilepsies. Epilepsia 2018;59(6):1148–1153.
- Specchio N, Wirrell EC, Scheffer IE, et al. International League Against Epilepsy classification and definition of epilepsy syndromes with onset in childhood. Epilepsia 2022;63(6):1398–1442.
- Marson A, Burnside G, Appleton R, et al. The SANAD II study of the effectiveness and cost-effectiveness of valproate versus levetiracetam for newly diagnosed generalised and unclassifiable epilepsy: an open-label, non-inferiority, multicentre, phase 4, randomised controlled trial. Lancet 2021;397(10282):1375–1386.
- Glauser TA, Cnaan A, Shinnar S, et al. Ethosuximide, valproic acid, and lamotrigine in childhood absence epilepsy. N Engl J Med 2010;362(9):790–799.
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