Seizure

Period of symptoms due to excessive or synchronous neuronal brain activity

This article is about epileptic seizures. For other types of seizures, see Non-epileptic seizure. For other uses, see Seizure (disambiguation).

Medical condition

Epileptic seizure

Other names| Epileptic fit,[1] seizure, fit, convulsions[2]
Generalized 3 Hz spike and wave discharges in an electroencephalogram (EEG) of a patient with epilepsy
Specialty| Neurology, emergency medicine
Symptoms| Variable[3]
Complications| Falling, drowning, car accidents, pregnancy complications, emotional health issues[4]
Duration| Typically less than 2 minutes[3]
Types| Focal, generalized; provoked, unprovoked[5]
Causes| Provoked: Low blood sugar, alcohol withdrawal, low blood sodium, fever, brain infection, traumatic brain injury[3][5]
Unprovoked: Flashing lights or colours, unknown causes, previous stroke, brain injury, brain tumor[5][6][3]
Diagnostic method| Based on symptoms, blood tests, medical imaging, electroencephalography[6]
Differential diagnosis| Syncope, psychogenic seizure, migraine aura, transient ischemic attack[3][7]
Treatment| Less than 5 min: Place person on their side, remove nearby dangerous objects
More than 5 min: Treat as status epilepticus[3][5][8]
Frequency| ≈10% of people (lifetime risk)[9][10]

A seizure is a sudden, brief disruption of brain activity caused by abnormal, excessive, or synchronous neuronal firing.[5][11] Depending on the regions of the brain involved, seizures can lead to changes in movement, sensation, behavior, awareness, or consciousness. Symptoms vary widely. Some seizures involve subtle changes, such as brief lapses in attention or awareness (as seen in absence seizures), while others cause generalized convulsions with loss of consciousness (tonic–clonic seizures).[12] Most seizures last less than two minutes and are followed by a postictal period of confusion, fatigue, or other symptoms.[13] A seizure lasting longer than five minutes is a medical emergency known as status epilepticus.[3][14]

Seizures are classified as provoked, when triggered by a known cause such as fever, head trauma, or metabolic imbalance, or unprovoked, when no immediate trigger is identified. Recurrent unprovoked seizures define the neurological condition epilepsy.[5][11]

## Clinical features

[edit]

Seizure manifestations vary depending on the brain regions involved and the type of seizure. They may affect movement, sensation, autonomic functions, or cognitive and emotional processing. Motor symptoms can include muscle stiffening (tonic activity), rhythmic jerking (clonic activity), sudden muscle jerks (myoclonus), or sudden loss of muscle tone (atonia). Sensory disturbances may involve tingling, visual phenomena, or hallucinated sounds. Autonomic features can include changes in heart rate, respiration, or gastrointestinal sensations. Cognitive or emotional symptoms may manifest as confusion, fear, or altered perception.

Some individuals experience an aura before the seizure progresses, characterized by subjective sensations such as unusual smells, a sudden emotional shift, or feelings of déjà vu.

Most seizures last less than two minutes and are followed by a recovery phase known as the postictal state, which may include confusion, fatigue, or other neurologic symptoms.[13] Seizures lasting more than five minutes, or occurring in rapid succession without recovery, are classified as status epilepticus, a medical emergency that can result in long-term brain injury or death.[12]

## Classification

[edit]

See also: Seizure types

Seizures are classified according to their site of onset in the brain, clinical features, and level of awareness during the episode. In 2025, the International League Against Epilepsy (ILAE) released an updated classification to improve clarity, clinical relevance, and global applicability. The system distinguishes four major types: focal, generalized, unknown onset, and unclassified seizures. Seizures are further characterized based on whether awareness is preserved or impaired, as determined by responsiveness during the event.[15]

### Focal seizures

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Focal seizures originate within a network limited to one hemisphere of the brain.[16] They may arise from the cerebral cortex or subcortical structures. For a given seizure type, the site of onset tends to be consistent across episodes. Once initiated, the seizure may remain localized or spread to adjacent areas, and in some cases, may propagate to the opposite hemisphere (contralateral spread). Despite this potential for spread, the initial focus remains consistent.

They are subdivided based on whether consciousness is preserved or impaired, a classifier defined by awareness and responsiveness during the event:[15]

* Focal preserved consciousness seizure: the person remains aware and responsive.
* Focal impaired consciousness seizure: awareness and/or responsiveness are affected.

They can manifest with motor, sensory, autonomic, cognitive, or emotional symptoms, depending on the regions involved. Some focal seizures can evolve into focal-to-bilateral tonic-clonic seizures, where abnormal brain activity spreads to both hemispheres.

### Generalized seizures

[edit]

Generalized seizures originate at a specific point within, and quickly spread across both hemispheres through interconnected brain networks. Generalized seizures can present in several forms, including:[15]

* Absence seizures (brief lapses in awareness)
* Generalized tonic–clonic seizures (stiffening followed by rhythmic jerking)
* Other generalized seizures (a grouping term encompassing various motor and non-motor types)

Generalized tonic–clonic seizures are associated with the highest morbidity and mortality, and are the primary risk factor for sudden unexpected death in epilepsy (SUDEP).[17]

### Unknown (whether focal or generalized) seizures

[edit]

When available information is insufficient to determine whether a seizure is focal or generalized, it is classified as unknown. These seizures may still be characterized based on consciousness and observable manifestations when possible.[15]

### Unclassified seizures

[edit]

Seizures are designated as unclassified when they are recognized as epileptic events, but insufficient information is available to assign them to any specific class. This is typically a temporary designation pending further clinical evaluation.[15]

## Causes

[edit]

Main article: Causes of seizures

Seizures can occur for many reasons and are broadly classified based on whether they are provoked (acute symptomatic) or unprovoked. Identifying the underlying cause is critical for guiding treatment and assessing the risk of recurrence.[12]

### Provoked seizures

[edit]

Provoked seizures, also known as acute symptomatic seizures, occur in direct response to an identifiable, transient cause affecting brain function. Common causes include:

* Metabolic disturbances: such as hypoglycemia (low blood sugar), hyponatremia (low sodium), or uremia.[3][14]
* Central nervous system infections: including meningitis, encephalitis, or neurocysticercosis.[12]
* Acute brain injuries: such as stroke, traumatic brain injury, or hemorrhage.[12]
* Substance-related factors: including alcohol withdrawal, drug intoxication, medication withdrawal, or certain toxins.[18][19]
* Fever: particularly in children, leading to febrile seizures.[12][20][21]

### Unprovoked seizures

[edit]

Unprovoked seizures occur without an immediate precipitating event. These include spontaneous seizures and reflex seizures, which are consistently triggered by specific stimuli (e.g., flashing lights) but arise due to an enduring predisposition, not a transient cause.[16]

They typically reflect an underlying neurological predisposition and are associated with a higher risk of recurrence,[12] meeting the diagnostic criteria for epilepsy when there are either two or more unprovoked (or reflex) seizures occurring more than 24 hours apart, or one unprovoked (or reflex) seizure with a recurrence risk of at least 60% over the next 10 years based on clinical and diagnostic findings.

Causes and contexts for unprovoked seizures include:

* Structural brain abnormalities, such as brain tumors, malformations of cortical development, and chronic lesions from prior brain trauma.[22]
* Genetic epilepsies: mutations affecting neuronal excitability or network function. Examples include Dravet syndrome, Lennox–Gastaut syndrome, and juvenile myoclonic epilepsy.[12]
* Infectious etiologies: sequelae of central nervous system infections, such as neurocysticercosis or viral encephalitis.[23]
* Metabolic disorders: inborn errors of metabolism or mitochondrial diseases affecting neuronal function.
* Immune-mediated epilepsies: such as autoimmune encephalitis.
* Unknown etiologies: in some cases, no clear cause is found despite thorough investigation (termed idiopathic seizures).

## Mechanism

[edit]

Seizures are the result of abnormal, excessive, and hypersynchronous neuronal activity in the brain. At a cellular level, they reflect a disruption of the normal balance between excitatory and inhibitory neurotransmission. Under healthy conditions, excitatory neurotransmission (mainly mediated by glutamate) and inhibitory neurotransmission (primarily via GABA) maintain cortical stability. An excess of excitation or a failure of inhibition can tip this balance, promoting hypersynchronous neuronal firing characteristic of seizures.[24][25][26] The generation of a seizure—the transition from an interictal to an ictal state—is known as ictogenesis. This process involves a cascade of physiological and network-level changes that lead to the sudden onset of pathological activity.

In provoked seizures (e.g., due to trauma, metabolic insults, or infections), acute disturbances in ionic gradients, neurotransmitter release, and neuronal membrane stability may transiently lower the threshold for seizure activity.

Brief seizures, such as absence seizures lasting 5–10 seconds, do not cause observable brain damage.[27] More prolonged seizures have a higher risk of neuronal death.[27] Prolonged and recurrent seizures, such as status epilepticus, typically cause brain damage.[27] Scarring of brain tissue (gliosis), neuronal death, and shrinking of areas of the brain (atrophy) are linked to recurrent seizures.[27][28] These changes may lead to the development of epilepsy, in a process called epileptogenesis.[28]

## Clinical evaluation

[edit]

The clinical evaluation after a seizure event involves confirming if the episode was epileptic in nature, determining its type and cause, and distinguishing it from other conditions that can mimic seizures. A careful clinical history and targeted investigations are essential.[12][3] The antecedent events preceding seizure onset, as well as the clinical signs observed during the episode, are critical for accurately classifying the seizure type. However, because most individuals do not recall the details of their own seizures, obtaining eyewitness accounts is often essential for an accurate diagnosis.[12][3][29] Video recordings, when available, provide valuable supplementary information, particularly in distinguishing epileptic seizures from mimics such as psychogenic nonepileptic seizures.[3]

The clinical history should include:

* Preictal symptoms (auras), such as unusual sensations, déjà vu, or fear
* Ictal features, including motor activity, awareness, automatisms, or autonomic signs
* Postictal symptoms, such as confusion, drowsiness, focal weakness (Todd’s paralysis), or headache

Medical history is also important, including:

* Previous neurological insults (e.g., traumatic brain injury, stroke, central nervous system infections)
* Developmental history in children
* Family history of epilepsy
* History of febrile seizures
* Use of medications, alcohol, or illicit substances

An individual who has bitten the tip of their tongue while having a seizure

### Physical examination

[edit]

A focused neurological examination can yield additional diagnostic clues, particularly soon after a seizure. Findings may include:[3]

* Tongue or oral injuries, such as lateral tongue bites, which strongly suggest a generalized tonic–clonic seizure, though they occur in only about one-third of cases
* Postictal focal neurological signs, such as weakness or asymmetric reflexes
* Urinary or fecal incontinence, which, while not specific, can support the diagnosis of a generalized seizure

Between seizures, the neurological examination is often normal.[3]

### Laboratory tests

[edit]

Laboratory testing is often performed in the evaluation of a new-onset seizure, particularly when a provoked cause is suspected.[12] Common investigations include:

* Serum glucose: to rule out hypoglycemia
* Electrolytes (sodium, calcium, magnesium): to identify metabolic disturbances[7]
* Renal and hepatic function panels: to assess for systemic dysfunction
* Toxicology screening: to detect alcohol, illicit substances, or prescription drug toxicity
* Infection markers (e.g., complete blood count, inflammatory markers): when infection is suspected

Laboratory findings can help identify treatable causes of seizures and guide management decisions.

An EEG can aid in locating the focus of the epileptic seizure.

### Electroencephalography (EEG)

[edit]

An electroencephalogram (EEG) records electrical activity in the brain and can help support a diagnosis of epilepsy.Interictal EEG may reveal epileptiform abnormalities, such as spikes, sharp waves, or spike-and-wave discharges. However, a normal EEG does not exclude epilepsy.

In certain cases, prolonged video EEG monitoring is used to capture seizures in real time and clarify seizure type, localization, or the diagnosis when psychogenic nonepileptic seizures are suspected.

### Neuroimaging

[edit]

Brain imaging is recommended in most cases of new-onset unprovoked seizures to identify structural abnormalities that may predispose to epilepsy. Imaging techniques include:[3]

* Magnetic resonance imaging (MRI): the preferred modality for detecting cortical dysplasia, tumors, mesial temporal sclerosis, and other lesions
* Computed tomography (CT): often used in emergency settings to exclude acute hemorrhage or trauma

### Differential diagnosis

[edit]

Several conditions can mimic epileptic seizures and must be considered:

* Syncope (transient loss of consciousness due to cerebral hypoperfusion)
* Psychogenic nonepileptic seizures (PNES)
* Transient ischemic attacks (TIAs)
* Paroxysmal movement disorders
* Migraine aura

Differentiating these conditions from epileptic seizures relies on careful history-taking, examination, EEG findings, and, when necessary, additional cardiac, metabolic, or psychiatric evaluations.

## Management

[edit]

Management of seizures depends on the clinical context, including whether the seizure is isolated or part of an ongoing epileptic disorder, and whether it is provoked or unprovoked.

### First aid during a seizure

[edit]

Basic first aid during a tonic-clonic seizure focuses on ensuring the person's safety and preventing injury:[30]

* Protect the person: Gently guide them to the ground if they are standing, and remove sharp or dangerous objects nearby.
* Do not restrain movements: Allow the seizure to occur without attempting to hold the person down.
* Do not place objects in the mouth: This can cause choking or injury.
* Turn onto the side: Once convulsions stop, or if vomiting occurs, gently roll the person onto their side into the recovery position to maintain an open airway and prevent aspiration.
* Stay calm and reassure: Stay with the person until they have regained full awareness.

For nonconvulsive seizures (such as absence seizures or focal impaired consciousness seizures), active physical first aid is often unnecessary. In these cases, observers should ensure the person is safe from harm, gently guide them away from danger if needed, and offer support and reassurance as they regain awareness.

### Emergency medical treatment

[edit]

If a convulsive seizure lasts longer than five minutes or if repeated seizures occur without full recovery between events, the situation is classified as status epilepticus, a medical emergency requiring rapid intervention.[31] In emergency care, the first-line therapy for status epilepticus is the administration of a benzodiazepine to terminate the seizure, with most guidelines recommending lorazepam, midazolam or diazepam. Early benzodiazepine treatment is associated with better seizure control and improved outcomes.[3]

If seizures persist despite benzodiazepine administration (second-line therapy), an intravenous antiseizure medication is given. Recommended options include fosphenytoin, valproate, or levetiracetam, depending on patient-specific factors and institutional protocols.[32] In cases of refractory status epilepticus (seizures continuing despite first- and second-line treatments), patients typically require intensive care unit management. This involves continuous EEG monitoring and administration of anesthetic agents such as propofol or continuous infusion of midazolam.[3]

Prompt recognition and treatment of status epilepticus are critical to prevent permanent neuronal injury, systemic complications, and death.

### Management of provoked seizures

[edit]

If a seizure is provoked by an acute reversible cause, treatment focuses on addressing the underlying condition. Long-term antiseizure medications are typically not needed once the acute cause has been resolved, unless seizures recur.

### Management after unprovoked seizures

[edit]

After a first unprovoked seizure, management depends on assessing the risk of recurrence. Antiseizure medication may be considered after a single event if risk factors for epilepsy are identified, such as epileptiform abnormalities on EEG or structural lesions on MRI. In other cases, careful observation may be appropriate.

### Long-term management of epilepsy

[edit]

See also: Epilepsy § Management

Long-term management applies to individuals diagnosed with epilepsy. The goals are seizure control, minimizing adverse effects, and optimizing quality of life.[3]

It is recommended to start with one anti-seizure medication.[3][33] Another may be added if one is not enough to control the seizure occurrence.[33] Approximately 70% of people can obtain full control with continuous use of medication.[34] The type of medication used is based on the type of seizure.[3][33]

Anti-seizure medications may be slowly stopped after some time if a person has just experienced one seizure and has not had any more.[3] The decision to stop anti-seizure medications should be discussed between the doctor and patient, weighing the benefits and risks.

In severe cases where seizures are uncontrolled by at least two anti-seizure medications, brain surgery can be a treatment option.[3][33] Epilepsy surgery is especially useful for those with focal seizures, where the seizures are coming from a specific part of the brain.[33] The amount of brain removed during the surgery depends on the extent of the brain involved in the seizures. It can range from just removing one lobe of the brain (temporal lobectomy) to disconnecting an entire side of the brain (hemispherectomy).[3] The procedure can be curative, where seizures are eliminated.[3] However, if it is not curative, it can be palliative, reducing the frequency of seizures but not eliminating them.[35]

#### Other

[edit]

Helmets may be used to protect the head during a seizure. Some claim that seizure response dogs, a form of service dog, can predict seizures.[36] Evidence for this, however, is poor.[36] Cannabis has also been used for the management of seizures that do not respond to anti-seizure medications. Research on its effectiveness is ongoing, but current research shows that it does reduce seizure frequency.[37][38] A ketogenic diet or modified Atkins diet may help in those who have epilepsy who do not improve following typical treatments, with evidence for its effectiveness growing.[39][40]

## Prognosis

[edit]

The prognosis after a first seizure depends on the underlying cause, seizure type, and patient-specific factors. In general, individuals who experience a single provoked seizure due to an acute and reversible cause (such as hypoglycemia or head trauma) have a low risk of recurrence once the underlying issue is treated. Following a first unprovoked seizure, the risk of more seizures in the next two years is around 40%.[41] Starting anti-seizure medications reduces the recurrence of seizures by 35% within the first two years. The greatest predictors of more seizures are problems either on the EEG or on imaging of the brain. Those with normal EEG and normal physical exam following a first unprovoked seizure had less risk of recurrence in the next two years, with a risk of 25%. In adults, after 6 months of being seizure-free after a first seizure, the risk of a subsequent seizure in the next year is less than 20% regardless of treatment.[42]

## Epidemiology

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Seizures are relatively common neurological events, with an estimated lifetime risk of experiencing at least one seizure approaching 8-10% within the general population. However, not all seizures are indicative of epilepsy; numerous episodes are provoked by transient factors such as infections, metabolic abnormalities, or trauma. In adults, the risk of seizure recurrence within the five years following a new-onset seizure is 35%; the risk rises to 75% in persons who have had a second seizure.[43] In children, the risk of seizure recurrence within the five years following a single unprovoked seizure is about 50%; the risk rises to about 80% after two unprovoked seizures.[44] In the United States in 2011, seizures resulted in an estimated 1.6 million emergency department visits; approximately 400,000 of these visits were for new-onset seizures.[43]

Global variations exist, with higher rates of seizures and epilepsy reported in regions with elevated prevalence of risk factors such as central nervous system infections, traumatic brain injury, and limited access to perinatal care. Seizures contribute significantly to the global burden of neurological disease, affecting individuals' quality of life, social participation, and access to education and employment.

## History

[edit]

Seizures have been recognized throughout recorded history. Early descriptions date back to ancient Mesopotamia around 2000 BCE, where seizures were often attributed to supernatural causes or demonic possession.[45][46] Similar beliefs persisted across ancient cultures, including in Egypt, India, and Greece.[45] In the 5th century BCE, the physician Hippocrates challenged supernatural explanations in his treatise On the Sacred Disease, proposing that epilepsy was a disorder of the brain.[45] However, stigma surrounding seizures remained widespread for centuries.

## Society and culture

[edit]

### Economics

[edit]

Seizures result in direct economic costs of about one billion dollars in the United States.[6] Epilepsy results in economic costs in Europe of around €15.5 billion in 2004.[47] In India, epilepsy is estimated to result in costs of US$1.7 billion or 0.5% of the GDP.[34] They make up about 1% of emergency department visits (2% for emergency departments for children) in the United States.[48]

## Research

[edit]

Scientific work on the prediction of epileptic seizures began in the 1970s. Several techniques and methods have been proposed, but evidence regarding their usefulness is still lacking.[49]

Two promising areas include: (1) gene therapy,[50] and (2) seizure detection and seizure prediction.[51]

Gene therapy for epilepsy consists of employing vectors to deliver pieces of genetic material to areas of the brain involved in seizure onset.[50]

Seizure prediction is a special case of seizure detection in which the developed systems can issue a warning before the clinical onset of the epileptic seizure.[49][51]

Computational neuroscience has brought a new perspective on seizures by considering the dynamical aspects.[52]

## References

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1. ^ Shorvon S (2009). Epilepsy. OUP Oxford. p. 1\. ISBN 9780199560042.
2. ^ "Epileptic Seizures - National Library of Medicine". PubMed Health. Retrieved 16 October 2018.
3. ^ a b c d e f g h i j k l m n o p q r s t u v w Abou-Khalil, Bassel W.; Gallagher, Martin J.; Macdonald, Robert L. (2022). "Epilepsies". Bradley and Daroff's Neurology in Clinical Practice (8th ed.). Elsevier. pp. 1614–1663\. ISBN 978-0323642613.
4. ^ Mayo Clinic Staff. "Seizures – Symptoms and causes". Mayo Clinic. Retrieved 4 June 2023.
5. ^ a b c d e f Fisher, Robert S.; Acevedo, Carlos; Arzimanoglou, Alexis; Bogacz, Alicia; Cross, J. Helen; Elger, Christian E.; Engel, Jerome; Forsgren, Lars; French, Jacqueline A.; Glynn, Mike; Hesdorffer, Dale C.; Lee, B.I.; Mathern, Gary W.; Moshé, Solomon L.; Perucca, Emilio (2014). "ILAE Official Report: A practical clinical definition of epilepsy". Epilepsia. 55 (4): 475–482\. doi:10.1111/epi.12550. ISSN 0013-9580.
6. ^ a b c Wilden JA, Cohen-Gadol AA (August 2012). "Evaluation of first nonfebrile seizures". American Family Physician. 86 (4): 334–340\. PMID 22963022.
7. ^ a b Winkel, Daniel; Cassimatis, Dimitri (2022). "Episodic Impairment of Consciousness". Bradley and Daroff's Neurology in Clinical Practice (8th ed.). Elsevier. pp. 8–16\. ISBN 978-0323642613.
8. ^ Cruickshank, Moira; Imamura, Mari; Booth, Corinne; Aucott, Lorna; Counsell, Carl; Manson, Paul; Scotland, Graham; Brazzelli, Miriam (2022). "Pre-hospital and emergency department treatment of convulsive status epilepticus in adults: an evidence synthesis". Health Technology Assessment. 26 (20): 1–76\. doi:10.3310/RSVK2062. ISSN 2046-4924. PMC 8977974. PMID 35333156.
9. ^ Ferri FF (2018). Ferri's Clinical Advisor 2019 E-Book: 5 Books in 1. Elsevier Health Sciences. p. 959\. ISBN 9780323550765.
10. ^ "Epilepsy". World Health Organization. 9 February 2023. Retrieved 4 June 2023.
11. ^ a b Fisher, Robert S.; Boas, Walter van Emde; Blume, Warren; Elger, Christian; Genton, Pierre; Lee, Phillip; Engel Jr., Jerome (2005). "Epileptic Seizures and Epilepsy: Definitions Proposed by the International League Against Epilepsy (ILAE) and the International Bureau for Epilepsy (IBE)". Epilepsia. 46 (4): 470–472\. doi:10.1111/j.0013-9580.2005.66104.x. ISSN 1528-1167.
12. ^ a b c d e f g h i j k Berkowitz, Aaron L. (2022), "Seizures & Epilepsy", Clinical Neurology & Neuroanatomy: A Localization-Based Approach (2 ed.), New York, NY: McGraw Hill, retrieved 28 April 2025
13. ^ a b Pottkämper, Julia C. M.; Hofmeijer, Jeannette; van Waarde, Jeroen A.; van Putten, Michel J. A. M. (2020). "The postictal state-What do we know?". Epilepsia. 61 (6): 1045–1061\. doi:10.1111/epi.16519. ISSN 1528-1167. PMC 7317965. PMID 32396219.
14. ^ a b Nardone, Raffaele; Brigo, Francesco; Trinka, Eugen (2016). "Acute Symptomatic Seizures Caused by Electrolyte Disturbances". Journal of Clinical Neurology. 12 (1): 21–33\. doi:10.3988/jcn.2016.12.1.21. ISSN 1738-6586. PMC 4712283. PMID 26754778.
15. ^ a b c d e Beniczky, Sándor; Trinka, Eugen; Wirrell, Elaine; Abdulla, Fatema; Al Baradie, Raidah; Alonso Vanegas, Mario; Auvin, Stéphane; Singh, Mamta Bhushan; Blumenfeld, Hal; Bogacz Fressola, Alicia; Caraballo, Roberto; Carreno, Mar; Cendes, Fernando; Charway, Augustina; Cook, Mark (23 April 2025). "Updated classification of epileptic seizures: Position paper of the International League Against Epilepsy". Epilepsia. doi:10.1111/epi.18338. ISSN 0013-9580. PMC 12169392.
16. ^ a b Berg, Anne T.; Berkovic, Samuel F.; Brodie, Martin J.; Buchhalter, Jeffrey; Cross, J. Helen; Van Emde Boas, Walter; Engel, Jerome; French, Jacqueline; Glauser, Tracy A.; Mathern, Gary W.; Moshé, Solomon L.; Nordli, Douglas; Plouin, Perrine; Scheffer, Ingrid E. (2010). "Revised terminology and concepts for organization of seizures and epilepsies: Report of the ILAE Commission on Classification and Terminology, 2005–2009". Epilepsia. 51 (4): 676–685\. doi:10.1111/j.1528-1167.2010.02522.x. ISSN 1528-1167.
17. ^ Salas-Puig, Xavier; Iniesta, Marc; Abraira, Laura; Puig, Josep; QUIN-GTC study group (2019). "Accidental injuries in patients with generalized tonic-clonic seizures. A multicenter, observational, cross-sectional study (QUIN-GTC study)". Epilepsy & Behavior. 92: 135–139\. doi:10.1016/j.yebeh.2018.10.043. ISSN 1525-5069. PMID 30658321.
18. ^ Chen, Hsien-Yi; Albertson, Timothy E.; Olson, Kent R. (2015). "Treatment of drug-induced seizures". British Journal of Clinical Pharmacology. 81 (3): 412–419\. doi:10.1111/bcp.12720. ISSN 0306-5251. PMC 4767205. PMID 26174744.
19. ^ Phillips, Haley N.; Tormoehlen, Laura (November 2020). "Toxin-Induced Seizures". Neurologic Clinics. 38 (4): 867–879\. doi:10.1016/j.ncl.2020.07.004. ISSN 1557-9875. PMID 33040866.
20. ^ Xixis, Kathryn L.; Samanta, Debopam; Smith, Travis; Keenaghan, Michael (2024), "Febrile Seizure", StatPearls, Treasure Island (FL): StatPearls Publishing, PMID 28846243, retrieved 1 November 2024
21. ^ Graves RC, Oehler K, Tingle LE (January 2012). "Febrile seizures: risks, evaluation, and prognosis". American Family Physician. 85 (2): 149–153\. PMID 22335215.
22. ^ Chen, Jiayu; Ye, Haijiao; Zhang, Jie; Li, Aihong; Ni, Yaohui (2022). "Pathogenesis of seizures and epilepsy after stroke". Acta Epileptologica. 4 (1): 2. doi:10.1186/s42494-021-00068-8. ISSN 2524-4434.
23. ^ Vezzani, Annamaria; Fujinami, Robert S.; White, H. Steve; Preux, Pierre-Marie; Blümcke, Ingmar; Sander, Josemir W.; Löscher, Wolfgang (2015). "Infections, inflammation and epilepsy". Acta Neuropathologica. 131 (2): 211–234\. doi:10.1007/s00401-015-1481-5. ISSN 0001-6322. PMC 4867498. PMID 26423537.
24. ^ Tatti, Roberta; Haley, Melissa S.; Swanson, Olivia K.; Tselha, Tenzin; Maffei, Arianna (15 May 2017). "Neurophysiology and Regulation of the Balance Between Excitation and Inhibition in Neocortical Circuits". Biological Psychiatry. 81 (10): 821–831\. doi:10.1016/j.biopsych.2016.09.017. ISSN 1873-2402. PMC 5374043. PMID 27865453.
25. ^ Sarlo, Gabrielle L.; Holton, Kathleen F. (2021). "Brain concentrations of glutamate and GABA in human epilepsy: A review". Seizure - European Journal of Epilepsy. 91: 213–227\. doi:10.1016/j.seizure.2021.06.028. PMID 34233236 – via Elsevier Science Direct.
26. ^ Treiman, David M. (2001). "GABAergic Mechanisms in Epilepsy". Epilepsia. 42 (s3): 8–12\. doi:10.1046/j.1528-1157.2001.042suppl.3008.x. ISSN 0013-9580. PMID 11520315 – via Wiley Online Library.
27. ^ a b c d Dingledine, Ray; Varvel, Nicholas H.; Dudek, F. Edward (2014), Scharfman, Helen E.; Buckmaster, Paul S. (eds.), "When and How Do Seizures Kill Neurons, and Is Cell Death Relevant to Epileptogenesis?", Issues in Clinical Epileptology: A View from the Bench, vol. 813, Dordrecht: Springer Netherlands, pp. 109–122, doi:10.1007/978-94-017-8914-1_9, ISBN 978-94-017-8913-4, PMC 4624106, PMID 25012371
28. ^ a b Jerome Engel Jr.; Timothy A. Pedley, eds. (2008). Epilepsy: a comprehensive textbook (2nd ed.). Philadelphia: Wolters Kluwer Health/Lippincott Williams & Wilkins. p. 483\. ISBN 978-0-7817-5777-5.
29. ^ Rowland, Kate; Lambert, Carl Earl (1 May 2022). "Evaluation After a First Seizure in Adults". American Family Physician. 105 (5): 507–513\. ISSN 1532-0650. PMID 35559631.
30. ^ Asadi-Pooya, Ali A.; Hosseini, Seyed Ali; Hashemizadeh Fard Haghighi, Leila; Asadi-Pooya, Hanieh (2022). "Seizure first aid for people with epilepsy: opinions and knowledge of caregivers and healthcare professionals". Seizure. 102: 1–5\. doi:10.1016/j.seizure.2022.09.007. ISSN 1532-2688. PMID 36130455 – via PubMed.
31. ^ Al-Mufti, Fawaz; Claassen, Jan (1 October 2014). "Neurocritical Care: Status Epilepticus Review". Critical Care Clinics. 30 (4): 751–764\. doi:10.1016/j.ccc.2014.06.006. ISSN 0749-0704. PMID 25257739.
32. ^ De Waele L, Boon P, Ceulemans B, Dan B, Jansen A, Legros B, et al. (December 2013). "First line management of prolonged convulsive seizures in children and adults: good practice points". Acta Neurologica Belgica. 113 (4): 375–380\. doi:10.1007/s13760-013-0247-x. hdl:1854/LU-4182539. PMID 24019121. S2CID 17641491.
33. ^ a b c d e Liu, Gerald; Slater, Nicole; Perkins, Allen (15 July 2017). "Epilepsy: Treatment Options". American Family Physician. 96 (2): 87–96\. ISSN 1532-0650. PMID 28762701.
34. ^ a b "Epilepsy". Fact Sheets. World Health Organization. October 2012. Archived from the original on 11 March 2016. Retrieved 24 January 2013.
35. ^ Matern, Tyson S.; DeCarlo, Rebecca; Ciliberto, Michael A.; Singh, Rani K. (2021). "Palliative Epilepsy Surgery Procedures in Children". Seminars in Pediatric Neurology. 39: 100912. doi:10.1016/j.spen.2021.100912. ISSN 1558-0776. PMID 34620461 – via PubMed.
36. ^ a b Doherty MJ, Haltiner AM (January 2007). "Wag the dog: skepticism on seizure alert canines". Neurology. 68 (4): 309. CiteSeerX 10.1.1.1003.1543. doi:10.1212/01.wnl.0000252369.82956.a3. PMID 17242343. S2CID 33328776.
37. ^ Lattanzi, Simona; Trinka, Eugen; Striano, Pasquale; Rocchi, Chiara; Salvemini, Sergio; Silvestrini, Mauro; Brigo, Francesco (2021). "Highly Purified Cannabidiol for Epilepsy Treatment: A Systematic Review of Epileptic Conditions Beyond Dravet Syndrome and Lennox–Gastaut Syndrome". CNS Drugs. 35 (3): 265–281\. doi:10.1007/s40263-021-00807-y. PMC 8005394. PMID 33754312.
38. ^ Elliott, Jesse; DeJean, Deirdre; Clifford, Tammy; Coyle, Doug; Potter, Beth K.; Skidmore, Becky; Alexander, Christine; Repetski, Alexander E.; Shukla, Vijay; McCoy, Bláthnaid; Wells, George A. (2020). "Cannabis-based products for pediatric epilepsy: An updated systematic review". Seizure. 75: 18–22\. doi:10.1016/j.seizure.2019.12.006. ISSN 1532-2688. PMID 31865133 – via PubMed.
39. ^ Martin-McGill, Kirsty J.; Bresnahan, Rebecca; Levy, Robert G.; Cooper, Paul N. (24 June 2020). "Ketogenic diets for drug-resistant epilepsy". The Cochrane Database of Systematic Reviews. 2020 (6): CD001903. doi:10.1002/14651858.CD001903.pub5. ISSN 1469-493X. PMC 7387249. PMID 32588435.
40. ^ Devi, Nagita; Madaan, Priyanka; Kandoth, Nidhun; Bansal, Dipika; Sahu, Jitendra Kumar (2023). "Efficacy and Safety of Dietary Therapies for Childhood Drug-Resistant Epilepsy: A Systematic Review and Network Meta-analysis". JAMA Pediatrics. 177 (3): 258–266\. doi:10.1001/jamapediatrics.2022.5648. PMC 9887534. PMID 36716045.
41. ^ Neligan, Aidan; Adan, Guleed; Nevitt, Sarah J; Pullen, Angie; Sander, Josemir W; Bonnett, Laura; Marson, Anthony G (23 January 2023). Cochrane Epilepsy Group (ed.). "Prognosis of adults and children following a first unprovoked seizure". Cochrane Database of Systematic Reviews. 2023 (1): CD013847. doi:10.1002/14651858.CD013847.pub2. PMC 9869434. PMID 36688481.
42. ^ Bonnett LJ, Tudur-Smith C, Williamson PR, Marson AG (December 2010). "Risk of recurrence after a first seizure and implications for driving: further analysis of the Multicentre study of early Epilepsy and Single Seizures". BMJ. 341: c6477. doi:10.1136/bmj.c6477. PMC 2998675. PMID 21147743.
43. ^ a b Gavvala JR, Schuele SU (December 2016). "New-Onset Seizure in Adults and Adolescents: A Review". JAMA. 316 (24): 2657–2668\. doi:10.1001/jama.2016.18625. PMID 28027373.
44. ^ Camfield P, Camfield C (June 2015). "Incidence, prevalence and aetiology of seizures and epilepsy in children". Epileptic Disorders. 17 (2): 117–123\. doi:10.1684/epd.2015.0736. PMID 25895502. S2CID 20719640.
45. ^ a b c Ali R, Connolly ID, Feroze AH, Awad AJ, Choudhri OA, Grant GA (June 2016). "Epilepsy: A Disruptive Force in History". World Neurosurgery. 90: 685–690\. doi:10.1016/j.wneu.2015.11.060. PMID 26709155.
46. ^ Magiorkinis E, Sidiropoulou K, Diamantis A (January 2010). "Hallmarks in the history of epilepsy: epilepsy in antiquity". Epilepsy & Behavior. 17 (1): 103–108\. doi:10.1016/j.yebeh.2009.10.023. PMID 19963440. S2CID 26340115.
47. ^ National Institute for Health and Clinical Excellence (January 2012). "Chapter 1: Introduction" (PDF). The Epilepsies: The diagnosis and management of the epilepsies in adults and children in primary and secondary care. National Clinical Guideline Centre. pp. 21–28\. Archived (PDF) from the original on 16 December 2013.
48. ^ Martindale JL, Goldstein JN, Pallin DJ (February 2011). "Emergency department seizure epidemiology". Emergency Medicine Clinics of North America. 29 (1): 15–27\. doi:10.1016/j.emc.2010.08.002. PMID 21109099.
49. ^ a b Litt B, Echauz J (May 2002). "Prediction of epileptic seizures". The Lancet. Neurology. 1 (1): 22–30\. doi:10.1016/S1474-4422(02)00003-0. PMID 12849542. S2CID 10109539.
50. ^ a b Walker MC, Schorge S, Kullmann DM, Wykes RC, Heeroma JH, Mantoan L (September 2013). "Gene therapy in status epilepticus". Epilepsia. 54 (Suppl 6): 43–45\. doi:10.1111/epi.12275. PMID 24001071. S2CID 13942394.
51. ^ a b Mormann F, Andrzejak RG, Elger CE, Lehnertz K (February 2007). "Seizure prediction: the long and winding road". Brain. 130 (Pt 2): 314–333\. doi:10.1093/brain/awl241. PMID 17008335.
52. ^ Depannemaecker D, Destexhe A, Jirsa V, Bernard C (August 2021). "Modeling seizures: From single neurons to networks". Seizure. 90: 4–8\. doi:10.1016/j.seizure.2021.06.015. PMID 34219016. S2CID 235468072.

## External links

[edit]

Look up seizure in Wiktionary, the free dictionary.

Wikimedia Commons has media related to Seizures.

Classification|

* ICD-11: 8A63–8A68
* ICD-10: R56, G40.9
* ICD-9-CM: 780.3, 345.9
* MeSH: D012640
* DiseasesDB: 19011

|

External resources|

* MedlinePlus: 003200
* eMedicine: neuro/415 neuro/694

* v
* t
* e

Seizures and epilepsy

Basics|

* Seizure types
* Aura (warning sign)
* Postictal state
* Epileptogenesis
* Neonatal seizure
* Epilepsy in children

Management|

* Anticonvulsants
* Investigations
* Electroencephalography
* Epileptologist

Personal issues|

* Epilepsy and driving
* Epilepsy and employment

Seizure types|

| Focal|

Seizures
Preserved consciousness
Impaired consciousness
Gelastic seizure

Epilepsy
Temporal lobe epilepsy
Frontal lobe epilepsy
Rolandic epilepsy
Sleep-related hypermotor epilepsy
Panayiotopoulos syndrome
Vertiginous epilepsy

|

Generalised|

* Tonic–clonic
* Absence seizure
* Atonic seizure
* Automatism
* Benign familial neonatal seizures
* Lennox–Gastaut syndrome
* Myoclonic astatic epilepsy
* Epileptic spasms
* Febrile seizure

Status epilepticus|

* Epilepsia partialis continua
* Complex partial status epilepticus

Myoclonic epilepsy|

* Progressive myoclonus epilepsy
* Dentatorubral–pallidoluysian atrophy
* Unverricht–Lundborg disease
* MERRF syndrome
* Lafora disease
* Early myoclonic encephalopathy
* Juvenile myoclonic epilepsy

Related disorders|

* Sudden unexpected death in epilepsy
* Todd's paresis
* Landau–Kleffner syndrome
* Psychogenic non-epileptic seizure
* Epilepsy in animals

Organizations|

* International League Against Epilepsy
* Citizens United for Research in Epilepsy (US)
* Epilepsy Action (UK)
* Epilepsy Action Australia
* Epilepsy Foundation (US)
* Epilepsy Outlook (UK)
* Epilepsy Research UK
* Epilepsy Society (UK)

* v
* t
* e

Diseases of the nervous system, primarily CNS

Inflammation|

| Brain|

* Encephalitis
* Viral encephalitis
* Herpesviral encephalitis
* Limbic encephalitis
* Encephalitis lethargica
* Cavernous sinus thrombosis
* Brain abscess
* Amoebic

|

Brain and spinal cord|

* Encephalomyelitis
* Acute disseminated
* Meningitis
* Meningoencephalitis

Brain/
encephalopathy|

| Degenerative|

| Extrapyramidal and
movement disorders|

* Basal ganglia disease
* Parkinsonism
* PD
* Postencephalitic
* NMS
* PSP
* CBD
* NBIA
* PKAN
* Striatonigral degeneration
* Hemiballismus
* Huntington's disease
* Olivopontocerebellar atrophy

* Dyskinesia
* Dystonia
* Status dystonicus
* Spasmodic torticollis
* Meige's
* Blepharospasm
* Athetosis
* Chorea
* Choreoathetosis
* Myoclonus
* Myoclonic epilepsy
* Akathisia

* Tremor
* Essential tremor
* Intention tremor
* Restless legs
* Stiff-person

|

Dementia|

* Alzheimer's
* Early-onset
* Primary progressive aphasia
* Frontotemporal dementia/Frontotemporal lobar degeneration
* Lewy body dementia
* Posterior cortical atrophy

* Creutzfeldt–Jakob disease

* Vascular dementia

Mitochondrial disease|

* Leigh syndrome

Demyelinating|

* Autoimmune
* Inflammatory
* Multiple sclerosis
* For more detailed coverage, see Template:Demyelinating diseases of CNS

Episodic/
paroxysmal|

| Seizures and epilepsy|

* Focal
* Generalised
* Status epilepticus
* For more detailed coverage, see Template:Epilepsy

|

Headache|

* Migraine
* Cluster
* Tension
* For more detailed coverage, see Template:Headache

Cerebrovascular|

* TIA
* Stroke
* For more detailed coverage, see Template:Cerebrovascular diseases

Other|

* Sleep disorders
* For more detailed coverage, see Template:Sleep

CSF|

* Intracranial hypertension
* Hydrocephalus
* Normal pressure hydrocephalus
* Choroid plexus papilloma
* Idiopathic intracranial hypertension
* Cerebral edema
* Intracranial hypotension

Other|

* Brain herniation
* Reye syndrome
* Hepatic encephalopathy
* Toxic encephalopathy
* Hashimoto's encephalopathy
* Static encephalopathy

Both/either|

| Degenerative|

| SA|

* Friedreich's ataxia
* Ataxia–telangiectasia

|

MND|

* UMN only:
* Primary lateral sclerosis
* Pseudobulbar palsy
* Hereditary spastic paraplegia

* LMN only:
* Distal hereditary motor neuronopathies
* Spinal muscular atrophies
* SMA
* SMAX1
* SMAX2
* DSMA1
* Congenital DSMA
* Spinal muscular atrophy with lower extremity predominance (SMALED)
* SMALED1
* SMALED2A
* SMALED2B
* SMA-PCH
* SMA-PME
* Progressive muscular atrophy
* Progressive bulbar palsy
* Fazio–Londe
* Infantile progressive bulbar palsy

* both:
* Amyotrophic lateral sclerosis

Portal:

* Medicine

Authority control databases: National |

* Germany
* Czech Republic

|

*[v]: View this template
*[t]: Discuss this template
*[e]: Edit this template