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Epilepsy

SNOMED: 847570091063 wordsUpdated 03/03/2026
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Exam Tips

  • In paediatric OSCEs, start with event classification: focal, generalized, or unknown onset; then state whether awareness is impaired and whether focal events evolved to bilateral tonic-clonic.
  • A seizure lasting 5 minutes or more is treated as convulsive status epilepticus: this is a time-critical emergency.
  • Normal EEG does not rule out epilepsy; diagnosis is primarily clinical and witness history is pivotal.
  • Name one high-yield safety point: SUDEP risk rises with uncontrolled tonic-clonic and nocturnal seizures, and falls with better seizure control.
  • State key prescribing caution unprompted: avoid or tightly restrict sodium valproate in females of childbearing potential because of major teratogenic risk.

Definition

Epilepsy is a chronic brain disorder with an enduring tendency to generate unprovoked seizures due to abnormal, excessive, and synchronous neuronal activity. Clinically, it is diagnosed by either at least two unprovoked seizures more than 24 hours apart, one unprovoked seizure with a high (about 60% or more) 10-year recurrence risk, or a recognized epilepsy syndrome with characteristic clinical and EEG features.

Pathophysiology

Epileptic seizures arise when cortical networks become hyperexcitable and hypersynchronous because inhibitory-excitatory balance is disrupted (typically reduced GABAergic inhibition, increased glutamatergic drive, or both). At a systems level, seizures may begin in a focal cortical network (focal-onset) or in bilaterally distributed thalamo-cortical circuits (generalized-onset), with possible secondary spread from focal to bilateral tonic-clonic activity. In children, mechanisms commonly include genetic channelopathies, developmental cortical malformations, immune-mediated inflammation, and metabolic defects; repeated uncontrolled seizures can promote network reorganization and drug resistance. See Figure: ILAE-style focal versus generalized seizure network schematic (helpful for viva explanations of semiology-anatomy correlation).

Risk Factors

  • Preterm birth and perinatal brain injury
  • Congenital cortical malformations and neurocutaneous syndromes (for example tuberous sclerosis, Sturge-Weber syndrome, neurofibromatosis)
  • Family history of epilepsy or known genetic epilepsy syndrome (for example Dravet syndrome, Lennox-Gastaut syndrome)
  • Previous CNS infection, head injury, intracranial tumour, or prior neurosurgery
  • Complicated febrile seizures (prolonged, focal, or with post-ictal weakness)
  • Neurodevelopmental disorders (autism spectrum disorder, ADHD, learning disability)
  • Stroke and cerebrovascular disease (major risk in older age groups but relevant for lifetime counselling)
  • Poor antiseizure medication adherence, alcohol/drug misuse, frequent nocturnal tonic-clonic seizures, and sleeping alone (important SUDEP risk modifiers)

Clinical Features

Symptoms

  • Recurrent transient episodes of altered awareness, behaviour, sensation, motor activity, or emotion
  • Focal sensory phenomena (for example paraesthesia, visual or auditory aura, epigastric rising sensation)
  • Motor jerking, tonic stiffening, atonic drops, or myoclonic jerks
  • Absence episodes with brief behavioural arrest and unresponsiveness
  • Post-ictal confusion, headache, myalgia, or sleepiness
  • Possible tongue biting, urinary incontinence, and amnesia for the event

Signs

  • Observed focal onset signs (head/eye deviation, unilateral clonic movements) with or without progression to bilateral tonic-clonic seizure
  • Generalized tonic-clonic seizure pattern: tonic phase then rhythmic clonic movements
  • Impaired awareness during focal impaired-awareness seizures
  • Prolonged convulsive seizure lasting 5 minutes or more (convulsive status epilepticus emergency threshold)
  • Lateral tongue bite and prolonged post-ictal phase supporting epileptic rather than syncopal event
  • Interictal neurological abnormalities may suggest an underlying structural cause

Investigations

Detailed history from child and eyewitness (including smartphone video):Most diagnostically useful test; helps classify seizure type and distinguish mimics (syncope, non-epileptic events, movement disorders)
Capillary blood glucose and basic metabolic screen (U&E, calcium, magnesium):Excludes acute provoked causes such as hypoglycaemia or electrolyte disturbance
12-lead ECG:Screens for arrhythmic syncope (for example long QT) that can mimic seizures
EEG (including sleep-deprived EEG where indicated):May show epileptiform discharges; supports syndrome diagnosis but a normal EEG does not exclude epilepsy
Brain MRI (epilepsy protocol):Detects structural aetiology such as cortical dysplasia, tumour, vascular malformation, prior infarct or haemorrhage
Genetic testing in suspected epilepsy syndrome:May identify monogenic causes (important for prognosis, counselling, and treatment selection)
Lumbar puncture or autoimmune/infectious work-up when clinically indicated:Used if encephalitis, CNS infection, or immune-mediated epilepsy is suspected

Management

Lifestyle Modifications

  • Provide an individualized seizure action plan for home and school, including when to give rescue medication and when to call emergency services
  • Safety counselling: supervised bathing/swimming, heights/fire/cooking precautions, cycling helmet use
  • Address adherence, sleep deprivation, alcohol/recreational drugs (adolescents), and mental health comorbidity
  • Discuss SUDEP risk honestly and proportionately, emphasizing seizure control and nocturnal supervision strategies
  • Offer education support and neuropsychology input where cognition/learning are affected

Pharmacological Treatment

Focal-onset seizure maintenance therapy

  • Lamotrigine (child specialist titration; typical start 0.3 mg/kg/day, slowly up-titrate to maintenance based on response and co-medication)
  • Levetiracetam (usually start 10 mg/kg twice daily; increase every about 2 weeks to up to 30 mg/kg twice daily, max commonly 1.5 g twice daily)
  • Carbamazepine (often start about 5 mg/kg/day in divided doses; usual maintenance around 10-20 mg/kg/day)

Choice is syndrome- and comorbidity-dependent. Titrate slowly to limit adverse effects. Check interactions (enzyme induction with carbamazepine).

Generalized tonic-clonic / generalized epilepsies

  • Levetiracetam (as above, weight-based titration)
  • Lamotrigine (slow titration required; rash risk if escalated too quickly)
  • Sodium valproate (typically start 10-15 mg/kg/day, increase by 5-10 mg/kg/week; common maintenance 20-30 mg/kg/day)

Valproate is highly teratogenic; in girls/adolescents who could become pregnant, avoid unless no suitable alternative and strict MHRA pregnancy prevention requirements are met.

Absence seizure therapy

  • Ethosuximide (commonly 10-15 mg/kg/day initially, titrated to about 20 mg/kg/day; max often 1.5 g/day)
  • Sodium valproate (useful if mixed generalized seizure types coexist)
  • Lamotrigine (alternative where ethosuximide/valproate unsuitable)

Match drug to syndrome; ethosuximide is effective for typical absence without prominent tonic-clonic seizures.

Rescue treatment for prolonged convulsive seizures in community

  • Buccal midazolam (age-banded: 2.5 mg at 3-11 months, 5 mg at 1-4 years, 7.5 mg at 5-9 years, 10 mg at 10 years and over)
  • Rectal diazepam (alternative when buccal route unavailable or ineffective)

Give according to individualized protocol; call emergency services for ongoing seizure, respiratory compromise, or recurrent seizures without recovery.

Hospital treatment of convulsive status epilepticus

  • Lorazepam IV 0.1 mg/kg (max 4 mg), repeat once if needed
  • Levetiracetam IV 40 mg/kg (max 2.5 g) or phenytoin/fosphenytoin per local protocol if benzodiazepine-refractory

Airway-breathing-circulation first. Continuous monitoring required; watch for respiratory depression and hypotension with sedatives.

Surgical / Interventional

  • Epilepsy surgery assessment for drug-resistant focal epilepsy (for example lesionectomy or temporal lobe surgery after specialist multidisciplinary work-up)
  • Vagus nerve stimulation when resective surgery is unsuitable or as adjunct in refractory epilepsy
  • Ketogenic diet (specialist-led) in selected refractory childhood epilepsies

Complications

  • Status epilepticus with significant morbidity and mortality
  • Injuries during seizures (falls, fractures, burns, drowning, head injury, road traffic incidents)
  • Psychiatric comorbidity (depression, anxiety, psychosis) and increased suicide risk
  • Cognitive and developmental impact, especially in complex childhood epileptic encephalopathies
  • Social and educational consequences (stigma, school absence, reduced attainment)
  • Sudden unexpected death in epilepsy (SUDEP), especially with poorly controlled generalized tonic-clonic or nocturnal seizures

Prognosis

Many individual seizures stop spontaneously, but recurrence risk after a first unprovoked seizure is highest in the first year. Overall recurrence risk is roughly 30-40%, falling to less than 10% after two years in many cohorts; risk is higher with epileptiform EEG changes, structural brain abnormalities, and certain comorbid mental health conditions. Long-term outcome is strongly predicted by early seizure burden and response to the first appropriately chosen antiseizure medicine.

Sources & References

💊BNF Drug References(50)

NICE Guidelines(1)

📖Textbook References(1)

  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 967)[context]

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