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Neurology›Condition·Updated Apr 17, 2026·v1

Epilepsy

Epilepsy is a complex spectrum of disorders defined by recurrent unprovoked seizures. Diagnosis relies on clinical history, EEG, and high-resolution MRI. Management is primarily pharmacological, but early identification of drug resistance is vital for surgical referral. Special care must be taken in pregnancy and pediatric populations to minimize developmental and teratogenic risks.

High Evidence240 references·6,826 words·28 min read·v1
NeurologySeizure DisordersEpileptologyAntiseizure MedicationsStatus Epilepticus

Quick Reference

RxDrug of choiceLamotrigine or Levetiracetam (Focal); Valproate (Generalized, with caution in females)
AltAlternativesCenobamate (Refractory focal), Zonisamide, Lacosamide
⊘AvoidValproate in pregnancy (relative); Carbamazepine in Absence/Myoclonic seizures (may worsen)
DxTest of choiceEEG (Electrophysiology) and 3T MRI Epilepsy Protocol (Imaging)
ScKey scoreSeLECT score (predicts post-stroke epilepsy risk)
→When to referFailure of 2 appropriately chosen ASMs (Drug-Resistant Epilepsy); suspected surgical candidate
Epilepsy requires rapid diagnosis and tailored ASM therapy; failure of two drugs necessitates surgical evaluation to prevent long-term morbidity.
Epilepsy is a chronic neurological disorder characterized by an enduring predisposition to generate spontaneous, recurrent seizures due to abnormal, hypersynchronous neuronal activity. It is formally diagnosed by the occurrence of at least two unprovoked seizures more than 24 hours apart, or a single unprovoked seizure with a high probability (at least 60%) of recurrence over the next 10 years. The condition arises from a fundamental imbalance between excitatory (glutamatergic) and inhibitory (GABAergic) neurotransmission, often driven by genetic variants, structural brain lesions, or metabolic derangements. Management focuses on achieving seizure freedom through tailored antiseizure medications (ASMs), with early identification of drug-resistant epilepsy—defined as the failure of two appropriately chosen and tolerated ASM trials—to facilitate timely referral for surgical or neuromodulatory interventions. Special consideration is required for pediatric populations, where developmental and epileptic encephalopathies (DEEs) predominate, and for pregnant patients, where the risk of teratogenicity must be balanced against maternal seizure control.

Overview and Recommendations

Background

  • •Define epilepsy as a clinical syndrome of recurrent unprovoked seizures, distinguishing between ictogenesis (the acute transition to a seizure) and epileptogenesis (the chronic process of brain transformation into a seizure-prone state). The condition affects approximately 1% of the population and carries significant risks of morbidity, cognitive decline, and sudden unexpected death in epilepsy (SUDEP).
  • •Recognize the core pathophysiology involving the tripartite synapse, where disruptions in ion channels (e.g., SCN1A, KCNQ2) and glial regulation of glutamate (via TREK-1 channels) lead to neuronal hyperexcitability. In many cases, an initial insult such as traumatic brain injury or status epilepticus triggers neuroinflammation and maladaptive plasticity, cementing the epileptic network.
  • •Classify seizures by onset as focal (originating in one hemisphere), generalized (involving bilateral networks from the start), or unknown. Focal seizures are further categorized by the preservation or impairment of awareness, which is a primary classifier in the 2025 ILAE update.
  • •Identify key genetic variants that dictate clinical phenotypes, such as SCN1A loss-of-function in affecting inhibitory interneurons, or KCNQ2 variants leading to a spectrum from self-limited neonatal epilepsy to severe developmental and epileptic encephalopathy (DEE).
  • •Understand the role of metabolic and inflammatory triggers, including succinic semialdehyde dehydrogenase deficiency (SSADHD) and autoimmune encephalitis, which may present with drug-resistant seizures and require targeted metabolic or immunosuppressive therapy.

Evaluation

  • •Suspect epilepsy in any patient presenting with paroxysmal alterations in consciousness, motor activity, or sensory perception. Prioritize a meticulous reconstruction of the event from witnesses, as patient self-reporting is frequently inaccurate, especially in focal onset impaired awareness seizures (FIAS).
  • •Ask about the pre-ictal phase to identify triggers such as sleep deprivation, fever, or specific reflex stimuli like reading. In cases of Febrile Infection-Related Epilepsy Syndrome (FIRES), look for a febrile illness occurring 24 hours to 7 days prior to the onset of status epilepticus.
  • •Examine for systemic markers of genetic syndromes, such as macrocephaly in ODLURO syndrome (KMT2E variants) or distinct facial features and microcephaly in Mowat-Wilson syndrome. Assess for neurodevelopmental delays or regression, which suggest a DEE rather than a benign epilepsy syndrome.
  • •Obtain a routine or sleep-deprived EEG within 24 hours of the first seizure event to maximize the diagnostic yield for interictal epileptiform discharges (IEDs). If the initial EEG is normal, utilize functional tests or sleep induction (e.g., using melatonin 5 mg in children) to increase sensitivity.
  • •Order a high-resolution 3T MRI using a dedicated epilepsy protocol to rule out structural lesions such as focal cortical dysplasia (FCD), hippocampal sclerosis, or multinodular and vacuolating neuronal tumors (MVNT).
  • •Rule out non-epileptic mimics by assessing serum biomarkers within 60 minutes of the event; a serum lactate > 2.5 mmol/L or elevated prolactin and ammonia levels strongly suggest an epileptic seizure over syncope or functional/psychogenic non-epileptic seizures (PNES).
  • •Monitor for autonomic red flags, such as ictal heart rate increases > 50 bpm or significant peripheral oxygen desaturation (SpO2), which may serve as biomarkers for increased SUDEP risk.
  • •Screen for pediatric-specific red flags, including bruising in non-exploratory areas (ears, neck, torso) in infants < 1 year old, which may indicate abusive head trauma as the underlying cause of new-onset seizures.
  • •Consider genetic testing (e.g., epilepsy panels or whole-exome sequencing) in patients with early-onset seizures, developmental delay, or a family history of epilepsy, as over 1,000 genes are now associated with epileptic phenotypes.
  • •Utilize the STAMP scale (Scale for Objective Diagnostic Components of Paroxysmal Events) to objectively grade the likelihood of an epileptic seizure versus syncope based on clinical semiology.

Management

  • •Administer first-line monotherapy for focal epilepsy using Lamotrigine (titrated slowly to 100-200 mg BID) or Levetiracetam (500-1500 mg BID). Lamotrigine is preferred in patients of childbearing potential due to its lower teratogenic risk compared to other agents.
  • •Avoid Valproate in women of childbearing potential whenever possible due to high risks of major congenital malformations and adverse neurodevelopmental outcomes; if required, use the lowest effective dose with concurrent folic acid supplementation.
  • •Manage Infantile Epileptic Spasms Syndrome (IESS) urgently by initiating ACTH monotherapy, followed by a clinical and EEG assessment on Day 7; if spasms persist, add Vigabatrin (50 mg/kg/day, titrated up to 150 mg/kg/day) to the regimen.
  • •Treat status epilepticus (seizure > 5 minutes) as a neurological emergency: start with IV Lorazepam 4 mg (repeated once if needed), followed immediately by a second-line ASM such as IV Levetiracetam 60 mg/kg (max 4500 mg) or Fosphenytoin 20 mg PE/kg.
  • •Escalate to Cenobamate (starting at 12.5 mg/day and titrating slowly to 200-400 mg/day) for adults with drug-resistant focal seizures, as it has shown high potency in reducing seizure frequency across all focal subtypes.
  • •Refer patients for a comprehensive presurgical evaluation if they fail two appropriately chosen and tolerated ASM trials (drug-resistant epilepsy). Surgical options include anterior temporal lobectomy (ATL) for mesial temporal lobe epilepsy or Laser Interstitial Thermal Therapy (LITT) for deep-seated lesions.
  • •Consider palliative procedures such as Vagus Nerve Stimulation (VNS) or Responsive Neurostimulation (RNS) for patients who are not candidates for resective surgery or who have multifocal seizure onsets.
  • •Monitor for medication-induced autonomic changes, such as hypohidrosis (reduced sweating) and hyperthermia in patients taking Zonisamide or Topiramate, particularly in warm environments.
  • •Perform therapeutic drug monitoring (TDM) during pregnancy, as physiological changes (increased glomerular filtration) can significantly lower ASM plasma levels, necessitating dose adjustments to maintain seizure control.
  • •Implement an Acute Seizure Action Plan for all patients, including rescue medications (e.g., intranasal Midazolam 5-10 mg) for clusters or prolonged events to prevent progression to status epilepticus.
  • •Avoid routine ASM prophylaxis in seizure-naive patients with newly diagnosed brain tumors, as evidence from the SPRING trial suggests it does not meaningfully reduce the risk of a first seizure.
  • •Evaluate for ASM withdrawal only after a minimum of 2 years of seizure freedom, counseling the patient that the risk of recurrence is approximately 15% compared to 7% if treatment is continued.
  • •Refer for specialized metabolic management in cases of vitamin B6-dependent epilepsy (PLPBP-related), where high-dose pyridoxine is the definitive treatment.
  • •Monitor cognitive and neuropsychiatric comorbidities, particularly ADHD (present in ~30% of pediatric cases) and depression, which can significantly impact quality of life and ASM adherence.

Board Review — High Yield

  • •SCN1A mutation — The hallmark of Dravet Syndrome; avoid sodium channel blockers as they worsen seizures.
  • •3 Hz spike-and-wave — Classic EEG finding for Childhood Absence Epilepsy.
  • •Hypsarrhythmia — The chaotic EEG pattern associated with West Syndrome (Infantile Spasms).
  • •Drug-Resistant Epilepsy — Defined as failure of 2 tolerated and appropriately chosen ASM schedules.
  • •SUDEP — Sudden Unexpected Death in Epilepsy; risk is highest with uncontrolled generalized tonic-clonic seizures and nocturnal events.
  • •Gelastic seizures — Associated with hypothalamic hamartomas; present as inappropriate bursts of laughter.
  • •Todd's Paralysis — Focal neurological deficit (usually hemiparesis) following a focal seizure, typically resolving within 24 hours.
  • •BECTS (SeLECTS) — Most common childhood epilepsy; characterized by centrotemporal spikes and nocturnal orofacial seizures.

Deep Dive — Evidence Details

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