Epilepsy

Overview

Focal - originate within one hemisphere; may secondarily generalise
Generalised - engage bilaterally distributed networks from onset
Juvenile myoclonic epilepsy (JME) - triad of early-morning myoclonic jerks, absence seizures, and generalised tonic-clonic seizures; precipitated by sleep deprivation and alcohol; lifelong in most cases

Presentation

Aura - focal onset symptom (e.g. rising epigastric sensation in temporal lobe epilepsy); represents the start of the seizure
Automatisms - lip-smacking, fumbling, chewing; focal impaired-awareness seizures, classically temporal lobe
Tonic-clonic - sudden stiffening (cry), apnoea, then rhythmic bilateral jerking that decelerates before stopping
Absence - abrupt-onset blank stare <30 seconds, immediate full recovery, no post-ictal phase
Myoclonic jerks - brief shock-like bilateral contractions; most prominent in the morning in JME
Post-ictal phase - confusion, drowsiness, headache lasting minutes to hours; key differentiator from syncope
Todd's paresis - transient focal weakness after a focal motor seizure, localising to the hemisphere of onset
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Prolonged post-ictal confusion strongly favours epilepsy over syncope. Vasovagal episodes resolve within seconds to minutes with rapid lucidity.

Investigations

🥇 First-line

12-lead ECG (exclude cardiac cause), bloods (FBC, U&E, glucose, calcium, magnesium, LFTs), EEG, MRI brain (epilepsy protocol preferred)

🥈 Second-line

autoimmune encephalitis antibody screen (serum and CSF) if autoimmune aetiology suspected

🏆 Gold standard

prolonged video-telemetry EEG - for definitive diagnosis when doubt remains and pre-surgical assessment; essential to distinguish epilepsy from NEAD
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A normal EEG does not exclude epilepsy. Epilepsy remains a clinical diagnosis supported by investigations. Refer urgently to neurology within two weeks after a first suspected seizure.

Differential diagnosis

Epilepsy vs key mimics
FeatureEpilepsySyncopeNEAD
ProdromeAura (positive symptoms)Nausea, greyout, tunnel visionVariable
Post-ictal confusionMinutes to hoursSeconds to minutes, rapid lucidityOften absent
Eye closure during eventEyes usually openEyes usually closedEyes often closed
DiagnosisClinical + EEG + MRIECG, tilt-table testVideo-EEG (gold standard)
NEAD features - prolonged duration, pelvic thrusting, eye closure, ictal crying, no post-ictal confusion

Management

Start ASM after confirmed diagnosis - not usually after a single seizure unless recurrence risk is high
First-line ASM by seizure/syndrome type
Seizure typeFirst-lineAvoid
Focal epilepsyLamotrigine or levetiracetamCarbamazepine (enzyme-inducing)
Generalised tonic-clonic (male/post-menopausal)Sodium valproate-
Generalised tonic-clonic (female of childbearing potential)Lamotrigine or levetiracetamSodium valproate (teratogenic)
Absence seizuresEthosuximide-
JMESodium valproate (male/post-menopausal) or levetiracetam/lamotrigine (females of childbearing potential)Carbamazepine (worsens myoclonic seizures)
Second-line (drug-resistant epilepsy): failure of 2 ASMs - refer to tertiary centre; consider clobazam, topiramate, zonisamide, perampanel

🥉 Third-line

epilepsy surgery (resective for focal structural lesion); vagus nerve stimulation, responsive neurostimulation, deep brain stimulation
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Sodium valproate must NOT be prescribed to women of childbearing potential unless enrolled in the MHRA Valproate Pregnancy Prevention Programme, using effective contraception, and no suitable alternative exists. Review at every consultation.

Follow-up

At least annual structured review: seizure control, ASM adherence and side effects, mental health, driving and employment
Women of childbearing potential: discuss enzyme-inducing ASMs reducing hormonal contraception efficacy, pre-conception counselling, folic acid 5 mg daily from ≥3 months before conception through first trimester

Complications

Status epilepticus - convulsive seizure ≥5 minutes or ≥2 seizures without recovery; medical emergency
First-line: lorazepam IV (in hospital); midazolam buccal or diazepam rectal if no IV access
SUDEP - ~1 in 1000 person-years; highest risk with poorly controlled generalised tonic-clonic seizures, nocturnal seizures, young adults; discuss openly with all patients
Teratogenicity - sodium valproate carries highest risk (neural tube defects, neurodevelopmental delay); all ASMs carry some pregnancy risk
Psychiatric comorbidity - depression and anxiety in ~30-50%; must be actively screened
Seizure-related injury - posterior shoulder dislocation after tonic-clonic seizure is a classic association

Prognosis

~70% achieve long-term seizure freedom with ASMs; ~47% on first ASM
Only 11-16% respond to a second drug; failure of 2 adequate ASM trials = drug-resistant epilepsy - refer for surgical evaluation
After 2 years seizure-free, discuss ASM withdrawal in selected patients (consider EEG findings, driving status, patient preference)

Driving regulations

Group 1 (cars/motorcycles): 12 months seizure-free before driving may resume
Group 2 (lorries/buses): 10 years seizure-free, off all ASMs, no structural cause or EEG tendency
Clinician must advise patient of obligation to notify the DVLA; patient must self-report