Educational draft · awaiting clinical reviewThe full textbook explains uncertainty but does not replace live national or local guidance, specialist advice, or current prescribing information.
Epilepsy syndromes and antiseizure-medicine principles
Paediatrics and child health · UK scope · Sources checked 27 Aug 2026 · Clinical review pending
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Seizure emergency within chronic epilepsy
A convulsion lasting five minutes, seizure cluster without recovery, new focal deficit, injury, pregnancy exposure concern or rapidly increasing frequency requires urgent assessment rather than routine medicine adjustment.
Action: Follow the child's emergency plan and paediatric status pathway, verify rescue doses and usual medicines, correct acute precipitants and involve paediatric neurology promptly for a new seizure type or loss of control.
Overview
Classify childhood epilepsy by seizure type, age, development and EEG pattern, then choose syndrome-appropriate treatment while managing cognitive, behavioural, reproductive and medicine-specific safety risks.
Epilepsy is an enduring predisposition to unprovoked seizures, not a single test result. Describe the seizure semiology before applying a syndrome name. Focal sensory, motor, autonomic or experiential symptoms indicate a local network; generalised absence, myoclonic or tonic-clonic events engage bilateral networks early. Unknown onset is preferable to forced classification when witness evidence is limited.
Age and development are powerful discriminators. Infantile spasms cluster in the first year and may accompany developmental slowing. Childhood absence usually begins in early school years with many brief lapses. Juvenile myoclonic epilepsy emerges around adolescence with morning jerks. Self-limited centrotemporal epilepsy features nocturnal mouth, face and speech symptoms. Atypical age or regression broadens genetic, structural and metabolic assessment.
EEG supports the hypothesis and should use activation, sleep or prolonged recording when needed. Syndrome-specific patterns guide medicine selection, but false negatives and incidental discharges occur. MRI with an epilepsy protocol identifies structural causes in most diagnosed epilepsy except selected clearly defined generalised or self-limited syndromes where imaging may not be routinely needed under NICE.
Practice
Two practice questions
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Question 1 of 2
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Paediatrics and child healthOriginal SBA
Pure absence treatment
An eight-year-old has frequent typical absence seizures and no myoclonic or tonic-clonic seizures. EEG supports childhood absence epilepsy. Which monotherapy is offered first-line by NICE?
Sources and review status4 sources · checked 27 Aug 2026 · clinical review pending+
Sources
Sources and review status
National guidance is shown before implementation-dependent detail. Typical adult dose examples remain subject to patient factors, contraindications and the live BNF or specialist protocol. Source check completed 27 Aug 2026; clinical approval remains outstanding.
Treatment balances seizure freedom against adverse effects. Match medicine spectrum to seizure type and syndrome, use shared decision-making and explain titration. If the first medicine fails because of inefficacy, introduce the next and only then withdraw the first safely. Abrupt withdrawal can precipitate status. Review formulation, swallowing, school doses, renal or hepatic function and interactions.
Valproate is highly effective for several generalised epilepsies but carries major fetal and possible paternal reproductive risks. Current MHRA measures restrict initiation in people younger than 55 unless two specialists independently document that no effective or tolerated alternative exists, or compelling reasons show reproductive risks do not apply. Girls able to become pregnant require the pregnancy prevention programme unless exempt through the formal route.
After failure of two suitable regimens, do not simply cycle medicines indefinitely. Confirm diagnosis and adherence, obtain tertiary paediatric epilepsy review and assess resective surgery, ketogenic diet, vagus-nerve stimulation or syndrome-specific genetic therapy. Mental health, cognition, education and family sleep are clinical outcomes, not optional extras.
Key points
Classify the event first as focal, generalised, unknown or unclassified, then integrate age at onset, development, examination, EEG and imaging into an epilepsy syndrome where possible.
Typical absence causes frequent abrupt seconds-long lapses with immediate recovery and generalised spike-wave; ethosuximide is first-line when absence is the only seizure type.
Juvenile myoclonic epilepsy causes morning myoclonus with or without absence and tonic-clonic seizures; sleep loss is a common trigger and some focal sodium-channel drugs worsen myoclonus.
Self-limited epilepsy with centrotemporal spikes produces brief nocturnal facial or oropharyngeal focal seizures in otherwise typical school-aged children, but language and learning still deserve assessment.
Infantile spasms are a developmental emergency: arrange urgent sleep EEG and a specialist pathway; NICE recommends vigabatrin with high-dose oral prednisolone for most, and vigabatrin alone first-line with tuberous sclerosis.
For focal seizures NICE generally offers lamotrigine or levetiracetam first-line monotherapy, with selection based on age, comorbidity, reproductive safety, interactions and family preference.
Aetiology
01
Genetic generalised epilepsy
Inherited network excitability produces age-linked absence, myoclonic and generalised tonic-clonic seizures without a focal structural lesion.
02
Self-limited focal epilepsy
Developmentally regulated cortical excitability causes childhood focal syndromes that often remit, although learning and sleep effects still require review.
03
Structural focal epilepsy
Malformation, tumour, vascular lesion, perinatal injury or hippocampal damage can generate recurrent seizures from a persistent focal network.
04
Developmental epileptic encephalopathy
Genetic or structural disease causes both seizures and abnormal brain development, while frequent epileptic activity can further disrupt cognitive acquisition.
Pathophysiology
1
Excitation inhibition imbalance
Altered ion channels, neurotransmitters or synaptic organisation lower the threshold for hypersynchronous cortical discharge and recurrent unprovoked seizures.
2
Syndrome-specific networks
Thalamocortical oscillation generates typical absence discharges, while focal cortical networks create local symptoms that may spread bilaterally.
3
Sleep activation
Sleep changes neuronal synchrony and can expose centrotemporal spikes, electrical status or seizures that are sparse during wakefulness.
4
Medicine mechanism matching
Broad-spectrum medicines cover several generalised and focal seizure types, whereas narrow sodium-channel agents may worsen absence or myoclonic activity.
Clinical features and red flags
Typical absence
Abrupt brief staring with impaired response, eyelid flutter and immediate recovery occurs many times daily and can be provoked by hyperventilation.
Juvenile myoclonic pattern
Shock-like bilateral arm jerks after waking, often dropping objects, accompany later tonic-clonic seizures and sensitivity to sleep deprivation.
Centrotemporal focal pattern
Nocturnal unilateral facial twitching, drooling, throat sensation and speech arrest with preserved awareness typifies a self-limited childhood focal syndrome.
Infantile spasms
Repeated brief flexor or extensor movements in clusters, especially after waking, with developmental slowing require same-day specialist assessment.
Focal impaired awareness
Behavioural arrest, automatisms, experiential symptoms or unilateral motor activity followed by confusion indicates focal onset rather than typical absence.
Medicine aggravation
Emergence of myoclonus or more absences after a narrow-spectrum sodium-channel medicine suggests seizure-type mismatch.
Red flags requiring action
Developmental plateau or regression, new movement abnormality or loss of previously acquired language suggests an epileptic encephalopathy or progressive neurological disorder.
Infantile spasms present as brief flexor or extensor clusters, often after waking, and require urgent EEG and specialist treatment to protect development.
Investigations
01Expert seizure and developmental historyFirst step
Why
Define seizure types, triggers, developmental trajectory and syndrome before treatment selection.
Interpretation and limitations
A coherent age-linked phenotype guides targeted EEG and genetics more reliably than an isolated symptom label.
02Syndrome-directed EEG
Why
Identify focal or generalised epileptiform activity and activation by sleep, photic stimulation or hyperventilation.
Interpretation and limitations
Integrate discharges with actual events; a normal interictal recording does not exclude epilepsy.
03Epilepsy-protocol MRI
Why
Identify a surgically remediable or prognostically important structural cause of focal or atypical epilepsy.
Interpretation and limitations
Specialist review of dedicated sequences is preferable to relying on a prior routine scan reported as normal.
04Genetic and metabolic testing
Why
Diagnose developmental epileptic encephalopathy, channelopathy or treatable metabolic disease when phenotype supports it.
Interpretation and limitations
Testing is specialist-directed and results need counselling because uncertain variants do not automatically explain seizures.
05
Differential diagnosis
01
Non-epileptic paroxysms
Syncope, tics, stereotypies, parasomnias, migraine and functional events require positive clinical differentiation before escalating antiseizure treatment.
02
Acute symptomatic seizures
Glucose, electrolyte, infection, toxin or trauma-related seizures do not necessarily establish an enduring childhood epilepsy syndrome.
03
Daydreaming or inattention
Ordinary inattention is interruptible and context-dependent, unlike stereotyped brief absence episodes with abrupt onset and immediate recovery.
04
Movement disorder
Dystonia, tremor and paroxysmal dyskinesia often preserve awareness and have triggers or durations inconsistent with cortical seizure activity.
05
Sleep disorder
Night terrors, confusional arousals and REM behaviours arise from characteristic sleep stages and may need video EEG when stereotyped or injurious.
Management
01ClassifyDefine seizure and syndromeFirst stepRecurrent unprovoked events or high recurrence risk establishes epilepsy.+
1Describe onset, awareness, motor pattern, duration, recovery, age and developmental context.
2Use EEG, MRI and genetic testing only to answer syndrome-specific questions.
3Record uncertainty explicitly and avoid a medicine likely to worsen plausible seizure types.
02Start treatmentMatch medicine to syndromeSpecialist and family decide seizure-prevention benefit exceeds treatment burden.+
1First lineSelect a NICE-recommended first-line option after interaction, organ and reproductive review.
2Titrate gradually using one formulation and provide a written missed-dose and adverse-effect plan.
3
Complications
01
Status and injury
Breakthrough convulsions can become prolonged and cause aspiration, burns, drowning, trauma or critical illness without a practical rescue plan.
02
Learning and behavioural burden
Underlying brain disorder, sleep disruption, interictal activity and medicine adverse effects can impair attention, mood and school participation.
03
Sudden unexpected death
SUDEP risk rises particularly with uncontrolled generalised tonic-clonic seizures, making adherence, nocturnal discussion and seizure control important.
04
Medicine and reproductive harm
Teratogenicity, endocrine effects, bone health, organ toxicity and interactions require planned surveillance and age-appropriate reproductive counselling.
05
Psychosocial exclusion
Stigma and disproportionate restriction can limit independence, sport, education and employment beyond what individual seizure risk requires.
Monitoring and follow-up
Track each seizure type separately with duration, injury, rescue treatment, sleep and likely trigger.
Review adherence and the actual formulation and dose at every apparent treatment failure.
Monitor growth, school progress, attention, mood, sleep and family wellbeing alongside seizure counts.
Apply medicine-specific blood, renal, liver, dermatological, bone and reproductive surveillance rather than indiscriminate panels.
Revisit valproate safeguards and pregnancy-prevention documentation at every required specialist review.
Assess rescue-plan technique, expiry and availability at home, school and respite settings.
Escalate after two appropriate failures for tertiary surgery, ketogenic-diet or device assessment.
Special situations
Syndrome changes prescribing
The same tonic-clonic appearance can belong to focal or generalised epilepsy and lead to different safest medicine choices.
Morning jerks are clues
Adolescents may describe dropping toothbrushes or breakfast objects rather than volunteering the term myoclonus.
Spasms are easily mislabelled
Brief clustered infant movements can be mistaken for reflux or startle while developmental opportunity is being lost.
Normal concentration is not success
A therapeutic serum range cannot compensate for wrong syndrome, non-adherence or unacceptable cognitive and behavioural effects.
Resistance prompts reconsideration
Two failed appropriate medicines should trigger diagnostic and surgical review rather than endless empiric polypharmacy.
Common pitfalls
01
Calling every staring episode absence epilepsy.
02
Selecting medicine before identifying seizure type.
03
Using carbamazepine for unrecognised myoclonic or absence epilepsy.
04
Increasing doses without checking adherence, sleep and formulation.
05
Missing developmental regression in a child with frequent seizures.
06
Starting valproate outside current MHRA safeguards.
07
Delaying tertiary referral after two appropriate treatment failures.
Do not infer treatment from one EEG label; review actual seizure types, because carbamazepine, oxcarbazepine and phenytoin can aggravate absence or myoclonic seizures.
Start low and titrate, change one drug at a time where safe, check adherence and sleep before declaring resistance, and use a seizure diary with functional outcomes.
Drug-resistant epilepsy means failure of two appropriately chosen, tolerated regimens to achieve sustained seizure freedom and should trigger tertiary review for surgery, diet or device options.
Every review should cover rescue plan, school, swimming and bathing, driving when age-relevant, contraception and pregnancy, bone health, mood, cognition and SUDEP proportionately.
Myoclonic jerks after waking with generalised tonic-clonic seizures suggest juvenile myoclonic epilepsy; sodium-channel medicines can aggravate some generalised seizure types.
New focal seizures, persistent focal deficit, raised intracranial-pressure features or a changing examination requires structural imaging and urgent review.
Mood change, suicidality, severe rash, bruising, jaundice, pancreatitis symptoms or marked sedation may represent serious antiseizure-medicine toxicity.
Sodium valproate initiation and continuation require current MHRA safeguards, specialist documentation and pregnancy-prevention measures where applicable.
Baseline medicine safety assessment
Why
Record weight, organ function, blood count, mood, reproductive context and interacting medicines before treatment.
Interpretation and limitations
Choose tests from the selected drug; not every antiseizure medicine needs routine serum-level monitoring.
Measure seizures, injuries, cognition, mood and school function rather than drug concentration alone.
03Review failureRecheck before escalatingEscalationSeizures continue despite a prescribed first medicine.+
1Confirm events are epileptic and review adherence, sleep, dose, interactions and syndrome fit.
2AlternativeIntroduce an alternative carefully and taper the ineffective medicine only after control and safety planning.
3Refer to tertiary epilepsy services after failure of two appropriate tolerated regimens.
04Whole-life careReduce avoidable harmA child or young person lives with ongoing epilepsy risk.+
1Maintain rescue, school, water, sleep, travel and transition plans appropriate to seizure type.
2Discuss SUDEP and reproductive safety proportionately and revisit them as circumstances change.
3Coordinate learning, mental-health and family support with named clinical follow-up.
Key medicines and prescribing safety4 treatments · regimens, roles and cautions+
NICE first-line monotherapy for absence seizures when no other seizure type is present.
Ethosuximide
For typical absence alone, children aged 6 years and older commonly start 500 mg daily in divided doses and younger children 250 mg daily, increasing by 250 mg every 4–7 days; specialist dosing is usually about 20 mg/kg/day, maximum 2 g/day.
Monitor gastrointestinal effects, fatigue, rash, mood and rare blood dyscrasia; it does not treat tonic-clonic or myoclonic seizures, so recheck syndrome if these occur.
Broad-spectrum first-line option for focal and several generalised seizure types with few pharmacokinetic interactions.
Levetiracetam
For adjunctive treatment from 6 months, a common specialist start is 10 mg/kg twice daily, increasing by 10 mg/kg twice daily every 2 weeks to 30 mg/kg twice daily; use product-specific age limits and renal adjustment.
Ask specifically about irritability, aggression, depression and suicidality, adjust for renal impairment and avoid assuming behavioural deterioration is merely adolescence.
NICE first-line option for focal seizures and selected generalised tonic-clonic epilepsy, chosen after syndrome review.
Lamotrigine
In children aged 2–12 years not taking valproate or enzyme inducers, specialist initiation commonly uses 0.3 mg/kg/day for 2 weeks then 0.6 mg/kg/day for 2 weeks, followed by increases of up to 0.6 mg/kg every 1–2 weeks; interactions require different schedules.
Slow titration is essential because rapid escalation, high starting dose and valproate increase serious rash risk; stop and seek urgent review for rash, mucosal lesions or systemic illness.
Effective broad-spectrum treatment for selected generalised epilepsies when safer effective alternatives are unsuitable.
Sodium valproate
Specialist paediatric dosing often begins at 10–15 mg/kg/day in divided doses and increases by 5–10 mg/kg at weekly intervals to the lowest effective dose, commonly 20–30 mg/kg/day, only within current MHRA safeguards.
Two-specialist initiation restrictions apply below age 55 unless formal exceptions are met; address pregnancy prevention, paternal risk advice, liver and pancreatic toxicity, weight, thrombocytopenia and suspected mitochondrial disease.