Seizures and epilepsy

Last updated: September 11, 2023

Summarytoggle arrow icon

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). Provoked seizures occur as a result of various seizure triggers and underlying conditions (e.g., stroke, traumatic brain injury, alcohol withdrawal), while unprovoked seizures occur in the absence of an identifiable cause. Seizures can also be classified by onset and degree of CNS involvement (e.g., focal seizures, generalized seizures). Epilepsy 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. Rapidly reversible causes of seizures (e.g., hypoglycemia) should also be managed concurrently. The underlying cause is investigated based on a combination of clinical evaluation (e.g., seizure classification, identifying seizure triggers), 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 treatment of epilepsy 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.

For information on individual epilepsy syndromes, see “Generalized epilepsy in childhood.”

Definitiontoggle arrow icon

Seizures [1]

Epilepsy [1]

A single seizure or multiple provoked or triggered seizures (e.g., febrile seizures) without an underlying predisposition to seizures do not suffice for the diagnosis of epilepsy.

Epidemiologytoggle arrow icon

Epidemiological data refers to the US, unless otherwise specified.

Etiologytoggle arrow icon

Seizure triggers [9]

Seizure triggers are stimuli that can precipitate seizures both in people with and without epilepsy. [10]

Causes of acute symptomatic seizures [2]

Common causes of epilepsy [12]

Causes of epilepsy according to the age group [14]

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)

Classificationtoggle arrow icon

Classification of seizures according to the ILAE 2017 classification [15]

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
Focal Generalized Unknown
Location of abnormal neuronal activity
  • Originates within the networks of a single hemisphere
  • Originates from both hemispheres
  • Determination of focal or generalized onset is not possible
  • Aware
  • Impaired awareness
  • N/a
  • N/a
  • Motor onset
  • Nonmotor onset
  • Focal to bilateral tonic-clonic: focal progresses to a tonic-clonic pattern (characteristic of bilateral brain involvement)
  • N/a
  • Unclassified [16]

* Note: An expanded version of the ILAE 2017 classification also considers further subtypes of motor and nonmotor categories.

Classification of epilepsy [12]

Clinical featurestoggle arrow icon

Focal seizures (formerly partial seizures) [10][15][17]

  • Originate in one brain hemisphere [18]
  • 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 “Focal seizures and syndromes.”
Clinical features of focal seizures
Type Awareness Ictal Postictal
  • Residual transient neurologic deficits depending on the affected cerebral region
  • Todd paralysis: postictal weakness or paralysis of the involved limb or facial muscles (can last for minutes or up to 36 hours)
Focal to bilateral tonic-clonic
  • Prodromal aura may be present.
  • Starts as unilateral, localized focal symptoms that then progress into a bilateral generalized phase: Initial focal symptoms may go unnoticed if the condition progresses rapidly, leading to a potential misdiagnosis of generalized-onset seizures and inappropriate therapy.
  • Bilateral generalized phase
  • Confusion
  • Drowsiness
  • Agitation
  • Fatigue
  • May not recall the focal onset

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 [10][20][21]

Clinical features of generalized seizures
Type Ictal Postictal
Generalized motor seizure
Tonic-clonic seizure (grand mal)
Clonic seizure
Tonic seizure
  • Often occurs when the patient is drowsy, asleep, or after waking
  • Loss of consciousness
  • Muscle stiffening (extension or flexion of the head, trunk, and/or extremities)
    • Contraction can be bilateral or unilateral
  • Can be accompanied by autonomic symptoms (e.g., tachycardia, flushing)
  • Can be followed by atypical absence seizure
  • Amnesia of the event
  • Drowsiness or confusion may occur
Myoclonic seizure
  • Positive myoclonus: sudden jerk-like muscle twitching
  • Negative myoclonus: a brief loss of muscle activity during tonic contraction of a muscle
  • Myoclonus can affect the entire body or only a part.
  • Myoclonic seizures are nonrhythmic (i.e., jerks occur at different intervals) and irregular (i.e., jerks are asymmetric and may change laterality)
Myoclonic-atonic seizure
Myoclonic-tonic seizure
  • Myoclonus followed by a brief increase in tone
Atonic seizure (also known as “drop seizure” or “drop attack”)
  • Sudden loss of muscle tone: sudden head drop or collapse (lasts < 15 seconds)
  • Frequently mistaken for syncope
Generalized nonmotor seizure (absence seizure)
  • Interrupted motion or activity, blank stare, unresponsiveness
  • Can occur several hundred times a day and usually lasts < 10 seconds
  • Subtle automatisms (often go unnoticed): lip-smacking, eye fluttering, or head nodding are common.
  • Sudden onset and stop
  • Triggers: hyperventilation, flashing lights
  • None
  • Consciousness returns rapidly, without any impairment
  • Amnesia is common
  • Interrupted motion or activity, blank stare
  • Patients may be responsive
  • Automatisms: lip-smacking, eye fluttering, chewing
  • Small hand movements (e.g., rubbing of the fingers)
  • Longer than typical form (10–30 seconds)
  • Gradual onset and stop

It is important to distinguish between focal/bilateral tonic-clonic seizures and generalized tonic-clonic seizures, as they manifest similarly but are managed differently.

Diagnosticstoggle arrow icon

The following addresses evaluation following the resolution of an acute seizure. See “Management of acute seizures and status epilepticus” for actively seizing patients.


In patients with an epilepsy diagnosis who present with an acute seizure, evaluate for medication-related issues, e.g., adherence, changes in drug doses or formulations, medication interactions.

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). [23]

Confirmation of seizure

Nonconvulsive status epilepticus is diagnosed based on the clinical presentation (e.g., changes in behavior and/or mental status from baseline) and the demonstration of seizure activity on EEG.

Evaluation for underlying conditions

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 diagnosestoggle arrow icon

Differential diagnosis of epilepsy
Condition Risk factors and triggers Clinical features Duration Diagnostics
Focal-onset seizure
  • Usually < 2 minutes

Generalized-onset motor seizure

  • Usually < 5 minutes
Febrile seizure
  • < 15 minutes
  • No more than 1 seizure per day
  • Simple (80% of cases)
    • < 15 minutes
    • < 1 seizure per 24 hours
  • Complex (20% of cases)
    • > 15 minutes
    • > 1 seizure per 24 hours
Psychogenic nonepileptic seizure (PNES)
  • Usually occur in presence of eyewitnesses [26][27]
  • Generalized asynchronous motor activity
  • Eyes are usually closed and resist being opened
  • Tongue-biting, other types of self-injury, and incontinence are rare.
  • Awareness is usually unimpaired
  • Aura and vocalizations are common
  • Individuals with PNES can recall the event
  • Postictal phase is uncommon
  • Typically > 5 minutes [28]
Panic attack
  • Seconds to hours
  • History
  • 1–2 minutes
  • History
  • ECG
  • Blood tests
  • Supine and orthostatic blood pressure measurements
  • Symptoms variable, depending on the location of the stroke or TIA
  • Usually negative symptoms (e.g., weakness, visual loss)
  • Consciousness preserved
  • TIA: Minutes to hours
  • Stroke: Days to years, often permanent damage
Migraine aura
  • Genetic predisposition
  • Female sex
  • Hormonal changes
  • Life stress
  • Typically positive symptoms (e.g., hallucinations) followed by negative ones (e.g., anesthesia)
  • Gradual onset
  • Consciousness preserved
  • Auras followed by headache
  • ≤ 1 hour
  • History
Breath-holding spell
  • Young age (6 months to 6 years)
  • Iron deficiency anemia
  • Distress due to strong emotions (e.g., anger, frustration, tantrums) or injury
  • Episodes of prolonged expiratory apnea
  • Transient paroxysms of cyanosis or pallor
  • Possibly generalized stiffness and jerky movements of the limbs
  • Post-event syncope
  • Vigorous cry: < 15 seconds
  • Cessation of breathing: ≤ 1 minute
  • Recovery: ≤ 1 minute
  • History
Self-stimulatory behavior
  • Repetitive movements performed to stimulate one's own senses
  • Examples of behaviors include tapping on a desk, twirling a lock of hair, and/or rocking back and forth.
  • Variable
  • History
Masturbation in children [30]
  • Normal behavior in children 5 months to 8 years
  • Dystonic posturing with rocking, grunting, and sweating
  • Median frequency: 7/week
  • Median duration: 2.5 minutes
  • History

The differential diagnoses listed here are not exhaustive.

Acute managementtoggle arrow icon

Acute management steps are determined by the time from seizure onset and include patient stabilization, identification and treatment of reversible acute causes of seizures, 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. [31]

Approach [31][32][33]

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.

Acute seizures are often self-limited and may not require immediate pharmacological intervention.

Initial stabilization for acute seizurestoggle arrow icon

A severe but self-limited metabolic acidosis due to marked and transient hyperlactatemia commonly occurs immediately after a seizure and usually does not require specific intervention. [35][36]

When indicated in an actively seizing patient, a nasopharyngeal airway is preferred over an oropharyngeal airway to avoid damaging intraoral structures in the setting of muscle spasms.

Phase-based acute seizure managementtoggle arrow icon

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. [31]


Overview of pharmacotherapy for acute seizures [31][34][37]
Seizure phase (time from seizure onset) Preferred agents Alternatives
Early seizure (0–5 minutes)
  • Often self-limited; pharmacotherapy is usually not indicated.

Early status epilepticus (5–20 minutes): first-line therapy

Administer push dose.
Repeat every 5–10 minutes if no response.

Persistent status epilepticus (20–40 minutes): second-line therapy

Administer loading dose.

Refractory status epilepticus (40–60 minutes)

Expert guidance is required.

Concurrently manage rapidly reversible causes of seizures (e.g., hypoglycemia, hyponatremia, hypocalcemia) without delay.

Early seizure (0–5 minutes)

Early status epilepticus (5–20 minutes)

Initiate first-line pharmacotherapy with a benzodiazepine (IV route is preferred).

Persistent status epilepticus (20–40 minutes)

If first-line pharmacotherapy is unsuccessful, initiate second-line pharmacotherapy.

Refractory status epilepticus (40–60 minutes)

If first and second-line pharmacotherapy are unsuccessful:

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. [34]

Management of rapidly reversible causes of seizurestoggle arrow icon

Management of rapidly reversible causes of seizures
Cause Recommended initial interventions
Electrolyte imbalance [41] Hyponatremia
Hypocalcemia [45]
Hypomagnesemia [46]
Eclampsia [47]
Hypertensive encephalopathy
Alcohol withdrawal [48]
Poisoning [49]

After seizure resolutiontoggle arrow icon

Dispositiontoggle arrow icon

  • Hospital admission and inpatient workup is recommended for patients with any of the following: [23][32][49]
    • Required > 1 dose of benzodiazepines to terminate the seizure
    • Failure to return to baseline clinical status after the seizure
    • Recurrent seizures
    • New-onset acute symptomatic seizures 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:

Driving requirements for individuals with epilepsy vary between jurisdictions but generally include a physician's evaluation and a seizure-free period of time (most commonly 6 months).

Long-term managementtoggle arrow icon

Long-term management following an isolated seizure [31][32][33]

Long-term medical therapy following a first unprovoked seizure is not required unless the patient meets the criteria for epilepsy or is at high risk of recurrence.

After the confirmation of PNES diagnosis with video-EEG, anticonvulsants should be withdrawn under medical supervision.

Patients with PNES may benefit from cognitive behavioral therapy. [53]

Long-term management of epilepsy [31][32][33]

Pharmacotherapy (antiepileptic drugs or AEDs) [54]

Treatment regimen

  • Monotherapy should be maintained if possible.
    • If initial monotherapy is ineffective, increase the dosage of the single agent or switch to an alternative agent before initiating combination therapy.
    • Approx. ⅔ of epilepsy patients become seizure-free with monotherapy. [55]
  • Combination therapy should only be given if monotherapy fails.
    • In this case, drugs from different classes and/or with different pharmacologic modes of action should be tried.
    • Combining two or three of the standard antiepileptic drugs is usually safe.
  • Failure of combination therapy : Consider nonpharmacological therapy. [56]

Termination of treatment

  • Evaluated on a case‑by‑case basis
  • May be considered if the patient meets all of the following:
    • < 2 seizures/year
    • An inconspicuous provocation EEG
    • Normal psychological findings
    • No hereditary predisposition
  • Generally possible after 2–5 seizure‑free years with normal EEG results
  • Medications should be tapered with caution.

Adverse effects of AEDs [57][58]

See “Overview of AEDs” for agent-specific adverse effects.

In patients with liver disease, hepatically metabolized anticonvulsants (e.g., valproic acid, phenytoin, felbamate, lamotrigine) should be avoided or dose adjusted. [57][59]

Nonpharmacological therapy

  • Indications: pharmacoresistant epilepsy
  • Surgery
    • Resection (surgical removal of pathological lesions)
    • Disconnection (surgical section of neuronal circuits)
      • Callosotomy: section of the corpus callosum [60]
        • Initially: partial disconnection only (usually the anterior ⅔)
        • If seizures persist: complete disconnection
      • 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 [61]
  • Stimulation techniques: vagus nerve stimulation, deep brain stimulation
  • Dietary measures: ketogenic diet [62]

Successful epilepsy therapy depends on determining whether the patient has focal or generalized seizures and prescribing medication accordingly.

Complicationstoggle arrow icon


Long term

Sudden unexpected death in epilepsy (SUDEP) [65]

  • 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.

Prognosistoggle arrow icon

  • Risk of seizure recurrence
    • After the first unprovoked seizure [66][67]
      • With no underlying brain insult (stroke, trauma, or CNS infection): ∼ 40–50% within 2 years
        • 80% of recurrences occur within 2 years of the initial seizure.
      • Occurring after at least 1 week after a brain insult: ∼ 65% over the next 10 years
    • After the second unprovoked seizure: 60% within 1 year
    • After an acute symptomatic seizure: ∼ 19% over the next 10 years
  • Treatment outcomes [68]
    • 60–70% of all treated patients become seizure-free at 10 years after first seizure
    • 60–90% of children and 35–57% of adults remain seizure-free after discontinuing medical therapy following a 2-year seizure-free period on antiepileptic drugs.
  • Legal regulations: State laws vary with regard to the requirements for individuals with epilepsy to operate vehicles and heavy machinery. [69]
  • Mortality [70]
    • Risk of all-cause mortality is 1.6–3 times higher in individuals with epilepsy than in the general population.
    • The worldwide incidence of SUDEP is 1.2–6.3 per 1,000 individuals with epilepsy.

Status epilepticustoggle arrow icon

Definition [31][71]

Etiology [72]

Classification [71]

  • With prominent motor features
  • Without prominent motor features: nonconvulsive status epilepticus (NCSE)
    • With coma
    • Without coma
      • Absence
      • Focal (e.g., aphasia, impaired consciousness, ongoing autonomic or sensory symptoms)


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.


  • Mortality is bimodal, with the highest risk in neonates (25–39%) and patients > 80 years of age (> 50%). [73][74]
  • Overall infant and child mortality: 3.6% [75]
  • Overall adult mortality: 15.9% [75]

Epilepsy and contraceptiontoggle arrow icon

General principles [76][77]

The CDC has developed a free app to help select a contraceptive method best suited to individual needs [78][79]

Contraceptive options in females with epilepsy [76][77]

Special considerations in patients on AEDs [76][77]

Hepatic enzyme-inducing AEDs can make combination hormonal contraceptives less effective and increase the risk of unplanned pregnancies. [76][77]

Combination OCPs may decrease serum concentrations of lamotrigine, thereby increasing the risk of seizures. [76][77]

Epilepsy in pregnancytoggle arrow icon

Folic acid supplementation is recommended in all individuals capable of pregnancy. [81]

Information on other seizure disorders that can occur in pregnancy (e.g., eclampsia, acute symptomatic seizure) is detailed separately.

Epidemiology [82][83][84]

  • 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.


Factors associated with an increased risk of epileptic seizures during pregnancy include:

Management [77][82][84][85]

General principles

Intrapartum exposure to teratogenic AEDs is associated with a 2–3 fold increase in the likelihood of major congenital malformations. [76]

AED management [77][82][84][85][87]

Adjust AED regimen as needed in consultation with a neurologist to maximize seizure control and minimize teratogenic risk. [84][87][89]

In patients planning pregnancy

  • Adjust AED therapy as needed early enough to: [82]
    • Measure AED levels before conception (if possible) and determine the lowest effective dose
    • Evaluate the efficacy of any new therapies
  • Consult the treating neurologist before discontinuing AEDs. [91]

During pregnancy

  • Measure AED levels regularly (e.g., monthly), especially for AEDs with increased clearance during pregnancy. [77][82]
  • Adjust target levels as needed, in consultation with neurology.

During the postpartum period

  • Encourage breastfeeding; counsel patients regarding the following: [82]
  • Adjust AED dosage in consultation with neurology; specialists may taper dosage to prepregnancy levels within 2–3 weeks after delivery. [90]

Valproate is the AED associated with the highest risk of major congenital malformations and should be avoided, if possible, in patients with epilepsy who may become pregnant. [57][77][82][87]

Complications [77][87]

Seizures in neonates (birth to 4 weeks of age)toggle arrow icon

Risk factors [92][93][94]

Clinical features [92][93]

Clinical features are often subtle or absent.

Diagnosis [92][93][94]

Management [92][93][94]

EEG screening and diagnostic confirmation are essential, as most seizures in neonates are subclinical and many other clinical entities can mimic true seizures.

Related One-Minute Telegramtoggle arrow icon

Interested in the newest medical research, distilled down to just one minute? Sign up for the One-Minute Telegram in “Tips and links” below.

Referencestoggle arrow icon

  1. ACOG. Gynecologic Management of Adolescents and Young Women With Seizure Disorders. ACOG Committee Opinion, Number 806.. Obstetrics & Gynecology. 2020; 135 (5): p.e213-e220.doi: 10.1097/aog.0000000000003827 . | Open in Read by QxMD
  2. Li Y, Meador KJ. Epilepsy and Pregnancy. Continuum (Minneap Minn). 2022; 28 (1): p.34-54.doi: 10.1212/con.0000000000001056 . | Open in Read by QxMD
  3. CDC USMEC USSPR Contraception App. Updated: May 19, 2022. Accessed: January 7, 2023.
  4. Clark EA, Curtis KM. Contraception Recommendations: Updates for the Busy Clinician.. Am Fam Physician. 2022; 106 (3): p.227-228.
  5. ACOG. ACOG Practice Bulletin No. 206: Use of Hormonal Contraception in Women With Coexisting Medical Conditions. Obstet Gynecol. 2019; 133 (2): p.e128-e150.doi: 10.1097/aog.0000000000003072 . | Open in Read by QxMD
  6. Soul JS. Acute symptomatic seizures in term neonates: Etiologies and treatments. Semin Fetal Neonatal Med.. 2018; 23 (3): p.183-190.doi: 10.1016/j.siny.2018.02.002 . | Open in Read by QxMD
  7. Glass HC. Neonatal Seizures. Clin Perinatol. 2014; 41 (1): p.177-190.doi: 10.1016/j.clp.2013.10.004 . | Open in Read by QxMD
  8. Co JPT, Elia M, Engel J, et al. Proposal of an Algorithm for Diagnosis and Treatment of Neonatal Seizures in Developing Countries. Epilepsia. 2007; 48 (6): p.1158-1164.doi: 10.1111/j.1528-1167.2007.01008.x . | Open in Read by QxMD
  9. Renée A. Shellhaas, Taeun Chang, Tammy Tsuchida, Mark S. Scher, James J. Riviello, Nicholas S. Abend, Sylvie Nguyen, Courtney J. Wusthoff, Robert R. Clancy. The American Clinical Neurophysiology Society's Guideline on Continuous Electroencephalography Monitoring in Neonates. Journal of Clinical Neurophysiology. 2011; 28 (6): p.611-617.doi: 10.1097/wnp.0b013e31823e96d7 . | Open in Read by QxMD
  10. Kaminiów K, Kozak S, Paprocka J. Neonatal Seizures Revisited. Children. 2021; 8 (2): p.155.doi: 10.3390/children8020155 . | Open in Read by QxMD
  11. Fisher RS, Acevedo C, Arzimanoglou A, et al. ILAE official report: a practical clinical definition of epilepsy. Epilepsia. 2014; 55 (4): p.475-482.doi: 10.1111/epi.12550 . | Open in Read by QxMD
  12. Beghi E, Carpio A, Forsgren L, et al. Recommendation for a definition of acute symptomatic seizure. Epilepsia. 2010; 51 (4): p.671-675.doi: 10.1111/j.1528-1167.2009.02285.x . | Open in Read by QxMD
  13. Fisher RS, Scharfman HE, deCurtis M. How Can We Identify Ictal and Interictal Abnormal Activity?. Springer Netherlands ; 2014: p. 3-23
  14. Fisher RS, Boas W van E, Blume W, et al. Epileptic Seizures and Epilepsy: Definitions Proposed by the International League Against Epilepsy (ILAE) and the International Bureau for Epilepsy (IBE). Epilepsia. 2005; 46 (4): p.470-472.doi: 10.1111/j.0013-9580.2005.66104.x . | Open in Read by QxMD
  15. Kalilani L, Sun X, Pelgrims B, Noack-Rink M, Villanueva V. The epidemiology of drug-resistant epilepsy: A systematic review and meta-analysis. Epilepsia. 2018; 59 (12): p.2179-2193.doi: 10.1111/epi.14596 . | Open in Read by QxMD
  16. Kwan P, Arzimanoglou A, Berg AT, et al. Definition of drug resistant epilepsy: Consensus proposal by the ad hoc Task Force of the ILAE Commission on Therapeutic Strategies. Epilepsia. 2009; 51 (6): p.1069-1077.doi: 10.1111/j.1528-1167.2009.02397.x . | Open in Read by QxMD
  17. Hauser WA, Beghi E. First seizure definitions and worldwide incidence and mortality. Epilepsia. 2008; 49: p.8-12.doi: 10.1111/j.1528-1167.2008.01443.x . | Open in Read by QxMD
  18. Helmers SL, Thurman DJ, Durgin TL, Pai AK, Faught E. Descriptive epidemiology of epilepsy in the U.S. population: A different approach. Epilepsia. 2015; 56 (6): p.942-948.doi: 10.1111/epi.13001 . | Open in Read by QxMD
  19. Anna Szűcs, Beáta Rosdy, Anna Kelemen, András Horváth, Péter Halász. Reflex seizure triggering: Learning about seizure producing systems. Seizure. 2019; 69: p.25-30.doi: 10.1016/j.seizure.2019.03.019 . | Open in Read by QxMD
  20. Blume WT, Lüders HO, Mizrahi E, Tassinari C, van Emde Boas W, Engel J Jr.. Glossary of descriptive terminology for ictal semiology: report of the ILAE task force on classification and terminology. Epilepsia. 2001; 42 (9): p.1212-1218.doi: 10.1046/j.1528-1157.2001.22001.x . | Open in Read by QxMD
  21. Ellis L. The potential mechanism of musicogenic epilepsy and future research avenues. Bioscience Horizons: The International Journal of Student Research. 2017; 10.doi: 10.1093/biohorizons/hzx004 . | Open in Read by QxMD
  22. $The Organization of the Epilepsies: Report of the ILAE Commission on Classification and Terminology.
  23. Maschio M. Brain Tumor-Related Epilepsy. Current Neuropharmacology. 2012; 10 (2): p.124-133.doi: 10.2174/157015912800604470 . | Open in Read by QxMD
  24. Ropper A, Klein J, Samuels M. Adams and Victor's Principles of Neurology 10th Edition. McGraw-Hill Education / Medical ; 2014
  25. Scheffer IE, Berkovic S, Capovilla G, et al. ILAE classification of the epilepsies: Position paper of the ILAE Commission for Classification and Terminology. Epilepsia. 2017; 58 (4): p.512-521.doi: 10.1111/epi.13709 . | Open in Read by QxMD
  26. Fisher RS, Cross JH, D’Souza C, et al. Instruction manual for the ILAE 2017 operational classification of seizure types. Epilepsia. 2017; 58 (4): p.531-542.doi: 10.1111/epi.13671 . | Open in Read by QxMD
  27. Daroff RB, et al.. Bradley's Neurology in Clinical Practice. Elsevier
  28. Epilepsy Diagnosis - Focal Onset Seizure. . Accessed: September 2, 2020.
  29. Berg AT, Berkovic SF, Brodie MJ et al. Revised terminology and concepts for organization of seizures and epilepsies: Report of the ILAE Commission on Classification and Terminology, 2005–2009. Epilepsia. 2010; 51 (4): p.676-685.doi: 10.1111/j.1528-1167.2010.02522.x . | Open in Read by QxMD
  30. Kasper DL, Fauci AS, Hauser SL, Longo DL, Lameson JL, Loscalzo J. Harrison's Principles of Internal Medicine. McGraw-Hill Education ; 2015
  31. Seizure Disorders. Updated: June 1, 2016. Accessed: March 29, 2017.
  32. Jagoda A, Gupta K. The Emergency Department Evaluation of the Adult Patient Who Presents with a First-Time Seizure. Emerg Med Clin North Am. 2011; 29 (1): p.41-49.doi: 10.1016/j.emc.2010.08.004 . | Open in Read by QxMD
  33. Galizia EC, Faulkner HJ. Seizures and epilepsy in the acute medical setting: presentation and management. Clin Med (Northfield Il). 2018; 18 (5): p.409-413.doi: 10.7861/clinmedicine.18-5-409 . | Open in Read by QxMD
  34. Bernasconi A, Cendes F, Theodore WH, et al. Recommendations for the use of structural magnetic resonance imaging in the care of patients with epilepsy: A consensus report from the International League Against Epilepsy Neuroimaging Task Force. Epilepsia. 2019.doi: 10.1111/epi.15612 . | Open in Read by QxMD
  35. Walters RJL, Hutchings AD, Smith DF, Smith PEM. Inappropriate requests for serum anti-epileptic drug levels in hospital practice. QJM.. 2004; 97 (6): p.337-341.doi: 10.1093/qjmed/hch057 . | Open in Read by QxMD
  36. Woollacott IOC, Scott C, Fish DR, Smith SM, Walker MC. When do psychogenic nonepileptic seizures occur on a video/EEG telemetry unit?. Epilepsy & Behavior. 2010; 17 (2): p.228-235.doi: 10.1016/j.yebeh.2009.12.002 . | Open in Read by QxMD
  37. Szabó L, Siegler Z, Zubek L, et al. A detailed semiologic analysis of childhood psychogenic nonepileptic seizures. Epilepsia. 2012; 53 (3): p.565-570.doi: 10.1111/j.1528-1167.2012.03404.x . | Open in Read by QxMD
  38. Seneviratne U, Minato E, Paul E. How reliable is ictal duration to differentiate psychogenic nonepileptic seizures from epileptic seizures?. Epilepsy Behav. 2017; 66: p.127-131.doi: 10.1016/j.yebeh.2016.10.024 . | Open in Read by QxMD
  39. Gedzelman E, LaRoche S. Long-term video EEG monitoring for diagnosis of&nbsp;psychogenic nonepileptic seizures. Neuropsychiatric Disease and Treatment. 2014: p.1979.doi: 10.2147/ndt.s49531 . | Open in Read by QxMD
  40. Nechay A, Ross LM, Stephenson JB, O'Regan M. Gratification disorder ("infantile masturbation"): a review.. Arch Dis Child. 2004; 89 (3): p.225-6.doi: 10.1136/adc.2003.032102 . | Open in Read by QxMD
  41. Tellez-Zenteno JF, Patten SB, Jetté N, Williams J, Wiebe S. Psychiatric Comorbidity in Epilepsy: A Population-Based Analysis. Epilepsia. 2007: p.070728063136006-???.doi: 10.1111/j.1528-1167.2007.01222.x . | Open in Read by QxMD
  42. Schmitt B. Sleep and Epilepsy Syndromes. Neuropediatrics. 2015; 46 (03): p.171-180.doi: 10.1055/s-0035-1551574 . | Open in Read by QxMD
  43. Nashef L, So EL, Ryvlin P, Tomson T. Unifying the definitions of sudden unexpected death in epilepsy. Epilepsia. 2011; 53 (2): p.227-233.doi: 10.1111/j.1528-1167.2011.03358.x . | Open in Read by QxMD
  44. Berg AT. Risk of recurrence after a first unprovoked seizure. Epilepsia. 2008; 49 (Suppl 1): p.13-18.doi: 10.1111/j.1528-1167.2008.01444.x . | Open in Read by QxMD
  45. Hesdorffer DC, Benn EK, Cascino GD, Hauser WA. Is a first acute symptomatic seizure epilepsy? Mortality and risk for recurrent seizure.. Epilepsia. 2009; 50 (5): p.1102-8.doi: 10.1111/j.1528-1167.2008.01945.x . | Open in Read by QxMD
  46. Beghi E, Giussani G, Sander JW. The natural history and prognosis of epilepsy.. Epileptic Disord. 2015; 17 (3): p.243-53.doi: 10.1684/epd.2015.0751 . | Open in Read by QxMD
  47. State Driving Laws Database. . Accessed: April 14, 2021.
  48. Thurman DJ, Logroscino G, Beghi E, et al. The burden of premature mortality of epilepsy in high-income countries: A systematic review from the Mortality Task Force of the International League Against Epilepsy.. Epilepsia. 2017; 58 (1): p.17-26.doi: 10.1111/epi.13604 . | Open in Read by QxMD
  49. Bibbins-Domingo et al. Folic Acid Supplementation for the Prevention of Neural Tube Defects. JAMA. 2017; 317 (2): p.183-189.doi: 10.1001/jama.2016.19438 . | Open in Read by QxMD
  50. Tomson T, Battino D, Bromley R, et al. Executive Summary: Management of epilepsy in pregnancy: A report from the International League Against Epilepsy Task Force on Women and Pregnancy. Epilepsia. 2019; 60 (12): p.2343-2345.doi: 10.1111/epi.16395 . | Open in Read by QxMD
  51. Sazgar M. Treatment of Women With Epilepsy. CONTINUUM: Lifelong Learning in Neurology. 2019; 25 (2): p.408-430.doi: 10.1212/con.0000000000000713 . | Open in Read by QxMD
  52. Voinescu PE, Meador KJ. Epilepsy Complicating Pregnancy. Curr Obstet Gynecol Rep. 2022.doi: 10.1007/s13669-022-00344-5 . | Open in Read by QxMD
  53. Patel SI, Pennell PB. Management of epilepsy during pregnancy: an update. Therapeutic Advances in Neurological Disorders. 2015; 9 (2): p.118-129.doi: 10.1177/1756285615623934 . | Open in Read by QxMD
  54. Harden CL, Pennell PB, Koppel BS, et al. Practice Parameter update: Management issues for women with epilepsy--Focus on pregnancy (an evidence-based review): Vitamin K, folic acid, blood levels, and breastfeeding: Report of the Quality Standards Subcommittee and Therapeutics and Technology Assessment Subcommittee of the American Academy of Neurology and American Epilepsy Society. Neurology. 2009; 73 (2): p.142-149.doi: 10.1212/wnl.0b013e3181a6b325 . | Open in Read by QxMD
  55. Spiegel R, Merius H. Principles of Epilepsy Management for Women in Their Reproductive Years. Front Neurol. 2020; 11.doi: 10.3389/fneur.2020.00322 . | Open in Read by QxMD
  56. Hand I, Noble L, Abrams SA. Vitamin K and the Newborn Infant. Pediatrics. 2022; 149 (3).doi: 10.1542/peds.2021-056036 . | Open in Read by QxMD
  57. Harden CL, Hopp J, Ting TY, et al. Practice Parameter update: Management issues for women with epilepsy--Focus on pregnancy (an evidence-based review): Obstetrical complications and change in seizure frequency: Report of the Quality Standards Subcommittee and Therapeutics and Technology Assessment Subcommittee of the American Academy of Neurology and American Epilepsy Society. Neurology. 2009; 73 (2): p.126-132.doi: 10.1212/wnl.0b013e3181a6b2f8 . | Open in Read by QxMD
  58. Bui E. Women’s Issues in Epilepsy. Continuum (Minneap Minn). 2022; 28 (2): p.399-427.doi: 10.1212/con.0000000000001126 . | Open in Read by QxMD
  59. Hessler A, Dolbec K. Seizures. Obstet Gynecol. 2021; 137 (1): p.207-207.doi: 10.1097/aog.0000000000004211 . | Open in Read by QxMD
  60. Kanner AM, Bicchi MM. Antiseizure Medications for Adults With Epilepsy. JAMA. 2022; 327 (13): p.1269.doi: 10.1001/jama.2022.3880 . | Open in Read by QxMD
  61. Glauser T, Shinnar S, Gloss D, et al. Evidence-Based Guideline: Treatment of Convulsive Status Epilepticus in Children and Adults: Report of the Guideline Committee of the American Epilepsy Society. Epilepsy Currents. 2016; 16 (1): p.48-61.doi: 10.5698/1535-7597-16.1.48 . | Open in Read by QxMD
  62. Huff JS, Melnick ER, Tomaszewski CA, et al. Clinical Policy: Critical Issues in the Evaluation and Management of Adult Patients Presenting to the Emergency Department With Seizures. Ann Emerg Med. 2014; 63 (4): p.437-447.e15.doi: 10.1016/j.annemergmed.2014.01.018 . | Open in Read by QxMD
  63. Krumholz A, Wiebe S, Gronseth GS, et al. Evidence-based guideline: Management of an unprovoked first seizure in adults: Report of the Guideline Development Subcommittee of the American Academy of Neurology and the American Epilepsy Society. Neurology. 2015; 84 (16): p.1705-1713.doi: 10.1212/wnl.0000000000001487 . | Open in Read by QxMD
  64. Goldstein LH, Chalder T, Chigwedere C, et al. Cognitive-behavioral therapy for psychogenic nonepileptic seizures: A pilot RCT. Neurology. 2010; 74 (24): p.1986-1994.doi: 10.1212/wnl.0b013e3181e39658 . | Open in Read by QxMD
  65. Kanner AM, Ashman E, Gloss D, et al. Practice guideline update summary: Efficacy and tolerability of the new antiepileptic drugs I: Treatment of new-onset epilepsy. Neurology. 2018; 91 (2): p.74-81.doi: 10.1212/wnl.0000000000005755 . | Open in Read by QxMD
  66. Glauser T, Ben-Menachem E, Bourgeois B, et al. Updated ILAE evidence review of antiepileptic drug efficacy and effectiveness as initial monotherapy for epileptic seizures and syndromes. Epilepsia. 2013; 54 (3): p.551-563.doi: 10.1111/epi.12074 . | Open in Read by QxMD
  67. St. Louis E. Truly “Rational” Polytherapy: Maximizing Efficacy and Minimizing Drug Interactions, Drug Load, and Adverse Effects. Current Neuropharmacology. 2009; 7 (2): p.96-105.doi: 10.2174/157015909788848929 . | Open in Read by QxMD
  68. Vossler DG, Weingarten M, Gidal BE. Summary of Antiepileptic Drugs Available in the United States of America. Epilepsy Curr. 2018; 18 (4_suppl): p.1-26.doi: 10.5698/1535-7597.18.4s1.1 . | Open in Read by QxMD
  69. Vidaurre J, Gedela S, Yarosz S. Antiepileptic Drugs and Liver Disease. Pediatr Neurol. 2017; 77: p.23-36.doi: 10.1016/j.pediatrneurol.2017.09.013 . | Open in Read by QxMD
  70. Asadi-Pooya AA, Sharan A, Nei M, Sperling MR. Corpus callosotomy.. Epilepsy Behav. 2008; 13 (2): p.271-8.doi: 10.1016/j.yebeh.2008.04.020 . | Open in Read by QxMD
  71. De Ribaupierre S, Delalande O. Hemispherotomy and other disconnective techniques.. Neurosurg Focus. 2008; 25 (3): p.E14.doi: 10.3171/FOC/2008/25/9/E14 . | Open in Read by QxMD
  72. Bough KJ, Rho JM. Anticonvulsant mechanisms of the ketogenic diet.. Epilepsia. 2007; 48 (1): p.43-58.doi: 10.1111/j.1528-1167.2007.00915.x . | Open in Read by QxMD
  73. Crawshaw AA, Cock HR. Medical management of status epilepticus: Emergency room to intensive care unit. Seizure. 2020; 75: p.145-152.doi: 10.1016/j.seizure.2019.10.006 . | Open in Read by QxMD
  74. Lipka K, Bülow H-H. Lactic acidosis following convulsions. Acta Anaesthesiol Scand. 2003; 47 (5): p.616-618.doi: 10.1034/j.1399-6576.2003.00115.x . | Open in Read by QxMD
  75. Orringer CE, Eustace JC, Wunsch CD, Gardner LB. Natural History of Lactic Acidosis after Grand-Mal Seizures. N Engl J Med. 1977; 297 (15): p.796-799.doi: 10.1056/nejm197710132971502 . | Open in Read by QxMD
  76. Brophy GM, Bell R, et al. Guidelines for the Evaluation and Management of Status Epilepticus. Neurocrit Care. 2012; 17 (1): p.3-23.doi: 10.1007/s12028-012-9695-z . | Open in Read by QxMD
  77. Manno EM. Status Epilepticus. Neurohospitalist. 2011; 1 (1): p.23-31.doi: 10.1177/1941875210383176 . | Open in Read by QxMD
  78. Dhir S, Tarasenko M, Napoli E, Giulivi C. Neurological, Psychiatric, and Biochemical Aspects of Thiamine Deficiency in Children and Adults.. Front psychiatry. 2019; 10: p.207.doi: 10.3389/fpsyt.2019.00207 . | Open in Read by QxMD
  79. Smith TJ, Johnson CR, Koshy R, et al. Thiamine deficiency disorders: a clinical perspective. Ann N Y Acad Sci. 2020; 1498 (1): p.9-28.doi: 10.1111/nyas.14536 . | Open in Read by QxMD
  80. Castilla-Guerra L, Fernández-Moreno M del C, López-Chozas JM, Fernández-Bolaños R. Electrolytes Disturbances and Seizures. Epilepsia. 2006; 47 (12): p.1990-1998.doi: 10.1111/j.1528-1167.2006.00861.x . | Open in Read by QxMD
  81. Fleisher GR, Ludwig S. Textbook of Pediatric Emergency Medicine . Lippincott Williams & Wilkins ; 2010
  82. Verbalis JG, Goldsmith SR, Greenberg A, et al. Diagnosis, evaluation, and treatment of hyponatremia: expert panel recommendations. Am J Med. 2013; 126 (10): p.S1-S42.doi: 10.1016/j.amjmed.2013.07.006 . | Open in Read by QxMD
  83. Watson S, Thompson A. Pediatric Intensive Care. Oxford University Press ; 2017
  84. Hypocalcemia: Diagnosis and Treatment. Updated: January 3, 2016. Accessed: July 4, 2019.
  85. Chen BB, Prasad C, Kobrzynski M, Campbell C, Filler G. Seizures Related to Hypomagnesemia. Child Neurology Open. 2016; 3: p.2329048X1667483.doi: 10.1177/2329048x16674834 . | Open in Read by QxMD
  86. Leeman L, Dresang LT, Fontaine P. Hypertensive Disorders of Pregnancy. Am Fam Physician. 2016; 93 (2): p.121-7.
  87. Alvanzo et al.. The ASAM Clinical Practice Guideline on Alcohol Withdrawal Management. Journal of Addiction Medicine. 2020; 14 (3S): p.1-72.doi: 10.1097/adm.0000000000000668 . | Open in Read by QxMD
  88. Walls R, Hockberger R, Gausche-Hill M. Rosen's Emergency Medicine. Elsevier Health Sciences ; 2018
  89. Ten Things Physicians and Patients Should Question. Updated: March 6, 2015. Accessed: March 19, 2021.
  90. Daly FFS. A risk assessment based approach to the management of acute poisoning. Emerg Med J. 2006; 23 (5): p.396-399.doi: 10.1136/emj.2005.030312 . | Open in Read by QxMD
  91. Nelson LS, Howland M, Lewin NA, Smith SW, Goldfrank LR, Hoffman RS. Goldfrank's Toxicologic Emergencies, 11th edition. McGraw-Hill Education ; 2019
  92. Trinka E, Cock H, Hesdorffer D, et al. A definition and classification of status epilepticus - Report of the ILAE Task Force on Classification of Status Epilepticus. Epilepsia. 2015; 56 (10): p.1515-1523.doi: 10.1111/epi.13121 . | Open in Read by QxMD
  93. Trinka E, Höfler J, Zerbs A. Causes of status epilepticus. Epilepsia. 2012; 53: p.127-138.doi: 10.1111/j.1528-1167.2012.03622.x . | Open in Read by QxMD
  94. Pisani F, Cerminara C, Fusco C, Sisti L. Neonatal status epilepticus vs recurrent neonatal seizures: Clinical findings and outcome. Neurology. 2007; 69 (23): p.2177-2185.doi: 10.1212/01.wnl.0000295674.34193.9e . | Open in Read by QxMD
  95. Boggs JG. Mortality Associated with Status Epilepticus. Epilepsy Currents. 2004; 4 (1): p.25-27.doi: 10.1111/j.1535-7597.2004.04110.x . | Open in Read by QxMD
  96. Neligan A, Noyce AJ, Gosavi TD, Shorvon SD, Köhler S, Walker MC. Change in Mortality of Generalized Convulsive Status Epilepticus in High-Income Countries Over Time: A Systematic Review and Meta-analysis.. JAMA neurology. 2019.doi: 10.1001/jamaneurol.2019.1268 . | Open in Read by QxMD

Icon of a lockAccess full content

Sign up and get unlimited access.
 Evidence-based content, created and peer-reviewed by physicians. Read the disclaimer