A seizure is a transient manifestation of abnormal excessive or synchronous electrical brain activity that causes convulsions, loss of consciousness, and/or lapses of consciousness. The underlying cause of seizures is a state of neuronal hyperexcitability, which may be temporary (e.g., due to electrolyte imbalances) or long-lasting (e.g., due to inherited or acquired neural abnormalities). occur as a result of various and underlying conditions (e.g., stroke, traumatic brain injury, alcohol withdrawal), while occur in the absence of an identifiable cause. Seizures can also be classified by onset and degree of CNS involvement (e.g., , ). is a chronic neurological disorder with diagnostic criteria that are based on seizure type, frequency, risk factors, and underlying conditions (e.g., epilepsy syndromes).
Acute complications of seizures include physical trauma and CNS tissue damage due to hyperthermia, cardiorespiratory deficits, or excitatory toxicity. Status epilepticus is a potentially life-threatening condition characterized by continuous seizure activity for more than 5 minutes that requires immediate management and stabilization. Acute seizures and status epilepticus in adults and children are most often initially treated with parenteral benzodiazepines, and then with the addition of other parenteral antiepileptic drugs (e.g., fosphenytoin) if there is no resolution. (e.g., hypoglycemia) should also be managed concurrently. The underlying cause is investigated based on a combination of clinical evaluation (e.g., , identifying ), laboratory studies, and neuroimaging. Electroencephalography (EEG) can provide additional evidence to support the diagnosis, although a normal EEG between seizures does not rule out epilepsy. Important antiepileptic drugs for the long-term include lamotrigine (first-line treatment in focal seizures), valproate (first-line treatment in generalized seizures), and ethosuximide (first-line treatment in absence seizures). Appropriate medical treatment allows the majority of patients to remain seizure‑free in the long term and prevents long-term complications such as psychiatric conditions (e.g., anxiety, depression, psychosis), sleep disorders, and sudden unexpected death in epilepsy (SUDEP); however, patients must be monitored for adverse effects of medications (e.g., bone disease). Epilepsy in certain groups (e.g., pregnant individuals, children) also may require specific considerations for management.
- Seizure: an excessive and/or hypersynchronous activity of cortical neurons that results in transient neurological symptoms
- Acute symptomatic seizure (provoked seizure): a seizure that occurs at the time or soon after the onset of an acute systemic or CNS condition. Examples include: 
- Reflex seizure: a seizure constantly evoked by a particular stimulus (trigger) that lowers seizure threshold (e.g., flashing lights; see “ ”)
- Unprovoked seizure: a seizure that occurs in the absence of an identifiable cause or beyond the specified interval after an acute CNS condition 
- Descriptors: the following terms are used to describe events, clinical features, and EEG signs related to seizures 
Epilepsy: a chronic neurologic disorder characterized by a predisposition to seizures as defined by one of the following: 
- Two or more unprovoked or reflex seizures separated by more than 24 hours
- One unprovoked or reflex seizure in an individual with a high risk of subsequent seizures (e.g., after traumatic brain injury, stroke, CNS infections)
- Diagnosis of an epilepsy syndrome: a group of epileptic disorders characterized by a set of features typically occurring together.
Reflex epilepsy: Epilepsy in which seizures are consistently provoked by a certain trigger (e.g., lights, music, hormonal changes during menstrual cycle). Subtypes can be determined based on the trigger and include:
- Photosensitive epilepsy
- Musicogenic epilepsy
- Catamenial epilepsy
- Drug-resistant epilepsy: epilepsy in which at least two antiepileptic drugs (administered as sequential monotherapies or as combination therapy) have failed to prevent seizures 
- Resolved epilepsy
Seizure triggers 
- Excessive physical exertion
- Alcohol consumption
- Fever (febrile seizures)
- Sleep deprivation
- Flashing lights (e.g., strobe lights, video games)
- Music 
- Hormonal changes (e.g., at different phases of the menstrual cycle, after menopause)
- Medication-related issues in patients with known epilepsy: e.g., poor adherence, recent changes in drug doses or formulation, new medication interactions
Causes of acute symptomatic seizures 
- Anoxic encephalopathy
- Intracranial surgery
- Acute CNS infections (e.g., meningitis, encephalitis)
- Electrolyte imbalance (e.g., hypoglycemia, hypocalcemia)
- Acute metabolic disturbances (e.g., uremia)
- Alcohol withdrawal
- Recreational drug use
- Prescription drug toxicity
- Exacerbations of autoimmune disorders (e.g., SLE)
Common causes of epilepsy 
- Genetic mutations affecting ion channels or transmitter receptors (e.g., mutations in KCNQ2 or SCN1A genes)
- Chromosomal abnormalities (e.g., Angelman syndrome, Prader-Willi syndrome, Rett syndrome)
- Genetic metabolic disorders (e.g., PKU, congenital disorders of glycosylation, lysosomal storage diseases, peroxisomal biogenesis disorders)
- Mitochondrial diseases (e.g., MELAS)
- Structural: chronic cerebral lesion or abnormality
- Immune: autoimmune encephalitides (e.g., anti-NMDA receptor encephalitis), Rasmussen encephalitis
- Infectious: : chronic CNS infection (e.g., toxoplasmosis, malaria, neurocysticercosis) or complication of acute CNS infection (e.g., viral or bacterial meningitis or encephalitis)
Causes of epilepsy according to the age group 
|Etiology of epilepsy in different age groups|
|Age group at manifestation||Causes|
|Neonates and infants (< 6 months)|
|Older infants (> 6 months) and children (< 10 years)|
|Adolescents (10–18 years)|
|Adults (18–60 years)|
|Older adults (> 60 years)|
Classification of seizures according to the ILAE 2017 classification 
Seizures are classified according to localization of abnormal neuronal activity and then further subcategorized based on symptoms and sometimes level of awareness.
|Basic classification of seizures|
|Location of abnormal neuronal activity|| || || |
|Awareness|| || || |
|Symptoms|| || || |
|Other|| || |
* Note: An expanded version of the ILAE 2017 classification also considers further subtypes of motor and nonmotor categories.
Classification of epilepsy 
- General considerations
Levels of classification
- For level 1, first determine the seizure type (see “Classification of seizures” above).
- For level 2, then determine the epilepsy type, which can be:
- Generalized: diagnosed in patients with generalized-onset seizures as evidenced by generalized ictal activity (e.g., 3 Hz spike-wave activity in absence seizures) and/or typical interictal discharges on EEG.
- Combined generalized and focal: diagnosed in patients who have both focal-onset and generalized-onset seizures (seen, e.g., in Dravet syndrome and Lennox-Gastaut syndrome)
- Unknown: diagnosed if there is not enough clinical information to classify seizures as focal, generalized, or combined
- For level 3, consider epilepsy syndromes (see “Focal seizures and syndromes” and “Generalized epilepsy in childhood” for discussion of specific syndromes)
Focal seizures (formerly partial seizures) 
- Originate in one brain hemisphere 
- Usually caused by focal structural abnormalities
- Symptoms depend on the anatomical location of the lesion or disturbance within the brain.
- For more information about the etiology and symptoms of seizures originating from the cortex of particular brain lobes, see “.”
|Clinical features of focal seizures|
|Focal|| || |
|Focal to bilateral tonic-clonic|| || || |
If focal to bilateral tonic-clonic type progresses rapidly to the bilateral generalized phase, initial focal symptoms may go unnoticed, leading to a potential misdiagnosis of generalized-onset seizures and inappropriate therapy.
Generalized-onset seizures 
|Clinical features of generalized seizures|
|Generalized motor seizure|
|Tonic-clonic seizure (grand mal)|| |
|Clonic seizure|| || |
|Tonic seizure|| || |
|Myoclonic seizure|| || |
|Myoclonic-atonic seizure|| |
|Myoclonic-tonic seizure|| |
|Atonic seizure (also known as “drop seizure” or “drop attack”)|| |
|Generalized nonmotor seizure (absence seizure)|
The following addresses evaluation following the resolution of an acute seizure. See “Management of acute seizures and status epilepticus” for actively seizing patients.
- Confirmation of seizure: Determine if the patient had a true seizure (see also “Differential diagnosis of a seizure”).
- If possible, identify the underlying cause at the initial presentation.
- Obtain an EEG. 
Previously diagnosed epilepsy
- Assess for common causes of seizure frequency, e.g.:  and increased
- Check antiepileptic drug levels.
- Consider further investigations based on clinical suspicion, e.g., neuroimaging.  , selective
- Consider EEG for patients with treatment-refractory seizures, those who have had a change in seizure type, or if there is insufficient information for .
Obtain neuroimaging in patients with an epilepsy diagnosis if there is a change in seizure pattern or other concerning features are present (e.g., recent head injury, new neurological deficit, persistent headache). 
Confirmation of seizure
- History of present illness: description of the event by the patient (aware seizure) and/or witnesses (seizure with impaired awareness)
- Past medical history
- Physical examination: attention should be paid to visual inspection (e.g., for bruises from falls, tongue bites, phakomatosis-specific skin manifestations) and evaluation for cardiovascular disorders
- Performed in individuals who present with first seizure, with insufficient information for seizure classification, and/or treatment-refractory seizures
Characteristic EEG findings help to establish the diagnosis of epilepsy; the absence of such findings cannot, however, rule out epilepsy.
- During the seizure (ictal)
- Epileptiform discharges (e.g., spikes, sharp waves, spike waves) are usually detected.
- Certain types of conditions characterized by seizures have characteristic discharge patterns (e.g., hypsarrhythmia in West syndrome, 3 Hz spike-and-wave in typical absence seizures, burst suppression in anoxic encephalopathy or barbiturate administration)
- If no epileptiform discharges are detected during a seizure, alternative diagnoses (e.g., psychogenic nonepileptic seizures) should be considered.
- After a seizure or between seizures (postictal or interictal)
- Video-EEG telemetry in hospitalized patients
- Continuous EEG in ambulatory patients
- During the seizure (ictal)
Evaluation for underlying conditions
- ECG: Rule out cardiogenic causes (e.g., cardiac arrhythmias resulting in cerebral hypoxia) in all patients with loss of consciousness during a seizure.
- MRI: Modality of choice for investigating potential underlying structural abnormalities. 
- CT: : May be used if MRI is not available, but is less sensitive for identifying soft-tissue lesions 
- Angiography: if vascular cause (e.g., cerebral arteriovenous malformation) is suspected
Laboratory screening: to identify metabolic disorders and infectious diseases, if suspected
- Bacterial cultures
- Cerebrospinal fluid analysis
- Endocrine studies
In adults, an isolated unprovoked focal or focal to bilateral tonic-clonic seizure typically indicates a structural or metabolic origin and should receive further evaluation.
|Differential diagnosis of epilepsy|
|Condition||Risk factors and triggers||Clinical features||Duration||Diagnostics|
|Focal-onset seizure|| |
Generalized-onset motor seizure
|Febrile seizure|| |
|Psychogenic nonepileptic seizure (PNES)|| || |
|Panic attack|| || || |
|Migraine aura|| || || |
|Breath-holding spell|| || || |
|Self-stimulatory behavior|| || || |
|Masturbation in children || || || || |
The differential diagnoses listed here are not exhaustive.
Acute management steps are determined by the time from seizure onset and include patient stabilization, identification and treatment of , and pharmacotherapy to terminate the seizure. Treatment recommendations are consistent with the 2016 American Epilepsy Society (AES) guidelines on the treatment of convulsive status epilepticus in adults and children. 
- Start as needed.
- Identify and treat .
- Implement .
Status epilepticus is a life‑threatening condition. If not interrupted, it can lead to cerebral edema, hyperthermia, rhabdomyolysis, and cardiovascular failure. If the time from seizure onset is unknown, begin management for status epilepticus.
- Call for help and remove or control hazards (e.g., remove sharp objects in the patient's vicinity).
- Perform an cardiopulmonary resuscitation.; if needed, perform
- Initiate , start , and place the patient in the .
- Check POC glucose and vital signs.
- Initiate continuous ECG monitoring if available and start pulse oximetry.
- Obtain IV access and blood samples for investigations.
- Perform a neurological assessment and collect relevant history.
The following addresses acute seizure management in adults and children. For other patient groups see “Neonatal seizures”, “Eclampsia”, or “Febrile seizures.” If initial contact is ≥ 5 minutes from seizure onset or the time from seizure onset is unknown, implement interventions for early seizure and early status epilepticus simultaneously. 
|Overview of pharmacotherapy for acute seizures |
|Seizure phase (time from seizure onset)||Preferred agents||Alternatives|
|Early seizure (0–5 minutes)|| |
Early status epilepticus (5–20 minutes): first-line therapy
Administer push dose.
Persistent status epilepticus (20–40 minutes): second-line therapy
Administer loading dose.
Refractory status epilepticus (40–60 minutes)
Expert guidance is required.
Early seizure (0–5 minutes)
- Perform initial stabilization for acute seizures.
- Monitor vital signs, oxygen saturation, and ECG.
- Identify and treat rapidly reversible causes of seizures.
- Preemptively prepare for benzodiazepine administration
Early status epilepticus (5–20 minutes)
Initiate first-line pharmacotherapy with a benzodiazepine (IV route is preferred).
- If IV access is available, administer:
- If IV access is unavailable, administer one of the following:
- If there is no response to the initial dose, repeat IV benzodiazepine after 5 minutes (after 10 minutes for other routes).
- Monitor for benzodiazepine-induced hypotension and respiratory suppression.
- Consider ICU consult if there is no response to the first dose of benzodiazepine.
Persistent status epilepticus (20–40 minutes)
If first-line pharmacotherapy is unsuccessful, initiate second-line pharmacotherapy.
- Preferred: loading dose of any ONE of the following
- Alternative: IV phenobarbital 
- If second-line pharmacotherapy successfully stops the seizure, consult neurology regarding the need for maintenance therapy.
- Monitor for medication adverse effects, including:
- Prepare for possible intubation and ICU transfer if there is no response to second-line pharmacotherapy.
Refractory status epilepticus (40–60 minutes)
If first and second-line pharmacotherapy are unsuccessful:
- Consult a specialist: e.g., neurology, anesthesia, and/or critical care.
- Consider intubation and ICU admission.
- Start continuous EEG monitoring.
A recurrent seizure following full neurological recovery from a preceding seizure should be managed as a discrete episode: repeat first-line pharmacotherapy with benzodiazepines while carefully monitoring for respiratory depression.
Focal motor status epilepticus is often drug-resistant but rarely life-threatening. Phase-based management is similar to that of generalized motor seizures but general anesthesia is NOT typically required. 
|Management of rapidly reversible causes of seizures|
|Cause||Recommended initial interventions|
|Electrolyte imbalance ||Hyponatremia|| |
|Hypocalcemia || |
|Hypomagnesemia || |
|Eclampsia || |
|Hypertensive encephalopathy|| |
|Alcohol withdrawal |
|Poisoning || |
After seizure resolution
- Continue close monitoring until the GCS returns to baseline.
- If a normal level of consciousness is not regained within 20–30 minutes: Consider EEG to rule out ongoing .
- Complete the history, physical examination, and neurological assessment and consider further investigations.
- See “ .”
- For children, see also “ .”
- Hospital admission and inpatient workup is recommended for patients with any of the following: 
- Required > 1 dose of benzodiazepines to terminate the seizure
- Failure to return to baseline clinical status after the seizure
- Recurrent seizures
- New-onset for which the immediate cause has not been definitively corrected
- Acute illness (including isolated fever) or trauma
- New neurological abnormalities preceding or following the seizure
- Persistent headache
- Concerns regarding adherence or inability to ensure follow-up
- In patients who have returned to their baseline clinical status and do not require hospitalization:
Long-term management following an isolated seizure 
- Consult neurology.
- Remove cause or provoking factors (e.g., cessation of recreational drug use, treatment of underlying disorders).
- Assess for risk of recurrence; patients with a CNS insult or lesion , abnormality on brain imaging or EEG, or nocturnal seizure are at higher risk of recurrence.
Long-term management of epilepsy 
- Start, continue, or optimize long-term antiepileptic drugs.
- Monotherapy is preferred unless the seizures are not adequately controlled.
- Drug-resistant epilepsy may be managed with nonpharmacological methods (e.g., surgery, neurostimulation, ketogenic diet).
Pharmacotherapy (antiepileptic drugs or AEDs) 
- AEDs reduce the risk of future seizures by raising the seizure threshold, which is pathologically lowered in individuals with epilepsy.
- Criteria for the choice of antiepileptic drugs:
- Seizure type
- Patient age
|Pharmacotherapy for epilepsy|
|Seizure type||First line||Second line|
|Atypical absence|| |
- Monotherapy should be maintained if possible.
- Combination therapy should only be given if monotherapy fails.
- Failure of combination therapy : Consider nonpharmacological therapy. 
Termination of treatment
- Evaluated on a case‑by‑case basis
- May be considered if the patient meets all of the following:
- Generally possible after 2–5 seizure‑free years with normal EEG results
- Medications should be tapered with caution.
Adverse effects of AEDs 
See “Overview of AEDs” for agent-specific adverse effects.
- Neurocognitive changes (e.g., sedation, headache, dizziness, tremor, memory impairment)
- Skin disorders (e.g., rash, SJS, DRESS)
- Psychiatric symptoms (e.g., depression, psychosis)
- Laboratory abnormalities (e.g., hyponatremia, neutropenia, thrombocytopenia)
- Gastrointestinal symptoms (e.g., nausea, vomiting, constipation)
- Weight gain or loss
- Indications: pharmacoresistant epilepsy
Resection (surgical removal of pathological lesions)
- Patients with temporal lobe epilepsy (e.g., due to hippocampal sclerosis): resection of the anteromedial temporal lobe or of the amygdala and the hippocampus
- Patients with severe intractable seizures due to structural cerebral abnormalities confined to one hemisphere: resection of an entire hemisphere (hemispherectomy)
Disconnection (surgical section of neuronal circuits)
- Callosotomy: section of the corpus callosum 
- Hemispherotomy: disconnection of the cortex of one hemisphere from the ipsilateral subcortical structures and cortex of the other hemisphere without removal of the affected hemisphere 
- Resection (surgical removal of pathological lesions)
- Stimulation techniques: vagus nerve stimulation, deep brain stimulation
- Dietary measures: ketogenic diet 
- Hyperthermia, cardiorespiratory deficits, and excitatory toxicity, which can cause irreversible tissue damage, especially to the CNS (e.g., cortical laminar necrosis) and, in turn, increase the risk of further seizures
- Postictal lactic acidosis: postictal transient anion gap metabolic acidosis with increased lactic acid and reduced serum bicarbonate (usually resolves spontaneously within 60–90 minutes after seizure activity stops)
- Physical trauma, such as:
- Status epilepticus
- Psychiatric 
- Sleep disturbances and insomnia 
- Bone disease (osteomalacia, osteoporosis) associated with antiepileptic drugs
Sudden unexpected death in epilepsy (SUDEP) 
- The sudden death of a person with diagnosed epilepsy that cannot be attributed to trauma or drowning and occurs with or without evidence of preceding seizure in the absence of any underlying medical conditions that could explain the event
- Usually occurs while the patient is asleep
- Is more common in patients with intractable epilepsy, frequent seizures (especially tonic-clonic seizures), and early age of onset
We list the most important complications. The selection is not exhaustive.
Risk of seizure recurrence
- After the first unprovoked seizure 
- After the second unprovoked seizure: 60% within 1 year
- After an acute symptomatic seizure: ∼ 19% over the next 10 years
- Treatment outcomes 
- Legal regulations: State laws vary with regard to the requirements for individuals with epilepsy to operate vehicles and heavy machinery. 
- Mortality 
- Status epilepticus is a seizure that lasts ≥ 5 minutes or a series of seizures in rapid succession without full neurological recovery in the interictal period, which increases the risk of long-term consequences such as neuronal injury and functional deficits.
- The time threshold after which a seizure is considered status epilepticus differs according to the type of seizure:
- Withdrawal from antiepileptic drugs
- Electrolyte imbalance (e.g., hyponatremia, hypocalcemia)
- Metabolic disturbances (e.g., hypoglycemia, uremia, porphyria)
- Structural brain lesions and/or injury (e.g., tumors, trauma, stroke)
- Anoxic brain injury
- Alcohol withdrawal
- Recreational drug use
- Drug toxicity (e.g., from tricyclic antidepressants, isoniazid)
- CNS infections (e.g., cerebral malaria, neurocysticercosis, viral encephalitis, prion diseases)
- Late-stage neurodegenerative diseases (e.g., Alzheimer disease)
- With prominent motor features
- Without prominent motor features: nonconvulsive status epilepticus (NCSE)
- See “Management of acute seizures and status epilepticus.”
- Maintain a high level of suspicion for NCSE: Consider continuous EEG and urgent neurology consult. 
Consider NCSE in patients with persistently altered mental status following a seizure or with otherwise unexplained altered mental status, bizarre behavior, autonomic dysfunction, or sensory symptoms.
General principles 
- Ongoing education on relevant techniques is essential
- Contraception selection should be a shared decision (ideally with neurologist) 
Contraceptive options in females with epilepsy 
Special considerations in patients on AEDs 
- Any AED: Progestin implant not recommended
- Hepatic enzyme-inducing AEDs: can decrease efficacy of combination hormonal contraceptives and progestin-only pills → avoid use or consider additional barrier method .
- Nonhepatic enzyme-inducing AEDs
- Approximately 1.5 million female individuals of reproductive age in the US have epilepsy.
- Approximately 24,000 female individuals with epilepsy become pregnant per year.
- In the majority of cases, pregnancy does not affect seizure frequency.
- Reduced plasma concentration of AEDs due to physiologic changes in pregnancy (e.g., steroid-hormone induced hepatic enzyme induction, increased renal clearance)
- Psychosocial stress
- Sleep deprivation
- Hormonal changes (e.g., increased estrogen:progesterone ratio)
- For all female individuals with epilepsy who are currently pregnant or expecting to be pregnant:
- If possible, obtain AED drug levels prior to pregnancy to determine a baseline level for continued monitoring. 
- Strict management of therapeutic AED levels during pregnancy is the gold standard of care for pregnant individuals with epilepsy. 
- Vitamin K supplementation to prevent vitamin K deficiency bleeding of the newborn (VKDB) 
- Epilepsy alone is not an indication for cesarean delivery. 
AED management 
- Reduce AED-associated risk of major congenital malformations (MCMs).
- Monotherapy is associated with a lower risk of MCMs compared to polytherapy. 
In patients planning pregnancy
- Adjust AED therapy as needed early enough to: 
- Consult the treating neurologist before discontinuing AEDs. 
- Measure AED levels regularly (e.g., monthly), especially for AEDs with increased clearance during pregnancy. 
- Adjust target levels as needed, in consultation with neurology.
During the postpartum period
- Encourage breastfeeding; counsel patients regarding the following: 
- Adjust AED dosage in consultation with neurology; specialists may taper dosage to prepregnancy levels within 2–3 weeks after delivery. 
- Fetal complications
- Maternal complications: increased risk of the following
Risk factors 
Clinical features 
Clinical features are often subtle or absent.
- Focal seizures (tonic or clonic)
- Myoclonic seizures
- Behavioral arrest
- See also “Apparent life-threatening event.”
- Clinical evaluation: E.g., determine the patient's age at seizure onset (i.e., in days or weeks) and perform a full history and physical examination.
- POC glucose, electrolytes
- Neonatal sepsis workup (See “Neonatal infection.”)
- Continuous video-EEG for at least 24 hours 
- Neuroimaging: cranial ultrasound and/or brain MRI
- Consider further investigations on a case-by-case basis: e.g., testing for nonaccidental trauma , evaluating for
- Stabilize the patient while focusing on supporting (see also “ ” and “ ”).
- Treat the underlying cause: e.g., correction of hypoglycemia and electrolyte abnormalities, empiric antibiotics for .
- Administer an antiepileptic agent to terminate clinical and subclinical neonatal seizures. 
- Consult neonatology and pediatric neurology.