Aseizure is a sudden disruption ofbrain activity caused by excessive, synchronizedneuronal firing that results in changes in behavior.[11][12] This neurological condition is common, affecting approximately 50 million individuals around the world.[13][14]
Depending on the regions of the brain involved, seizures can lead to changes inmovement,sensation,behavior,awareness, orconsciousness. Symptoms vary widely. Some seizures involve subtle changes, such as brief lapses in attention or awareness (as seen inabsence seizures), while others cause generalized convulsions with loss of consciousness (tonic–clonic seizures).[15] Most seizures last less than two minutes and are followed by apostictal period of confusion, fatigue, or other symptoms.[16]Status epilepticus is a medical emergency consisting of a seizure that lasts longer than five minutes, or multiple seizures without full recovery between episodes.[3][17]
Seizures are classified as provoked when they are triggered by a known cause such as fever, acute head trauma, or metabolic imbalance. Unprovoked seizures occur when no immediate trigger is identified. Recurrent unprovoked seizures define the neurological conditionepilepsy.[12][18]
The clinical signs and symptoms associated with a seizure are also referred to as seizure semiology.[19][20] Seizure semiology varies depending on the brain regions involved and the type of seizure. This may affectmovement,sensation,autonomic functions, orcognitive and emotional processing.[19][21] Motor symptoms can include muscle stiffening (tonic activity), rhythmic jerking (clonic activity), sudden muscle jerks (myoclonus), sudden loss of muscle tone (atonia), eye deviation, or other repetitive involuntary movements (automatisms).[19][22] Sensory disturbances may involvetingling, visual phenomena, orhallucinated sounds.[19][23] Autonomic features can include changes in heart rate, respiration, or gastrointestinal sensations.[21][24] Cognitive or emotional symptoms may manifest as confusion, fear, or altered perception.[19][25]
Some individuals experience anaura associated with their focal seizures, characterized by subjective sensations such as unusual smells, a sudden emotional shift, or feelings ofdéjà vu.[26][27]
Most seizures last less than two minutes and may be followed by a recovery phase known as thepostictal state, which may include confusion, fatigue, or other neurologic symptoms.[16] Seizures lasting more than five minutes, or occurring in rapid succession without recovery, are classified asstatus epilepticus, a medical emergency that can result in long-term brain injury or death.[15]
Seizures are classified according to their site of onset in the brain, clinical features, and level of consciousness during the episode. In 2025, theInternational 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 whether focal or generalized, and unclassified seizures. Seizures are further characterized based on whether consciousness is preserved or impaired, as determined by responsiveness during the event.[28]
Focal seizures (previously known as partial seizures) originate within a network limited to onehemisphere of the brain.[29] They may arise from the cerebral cortex or subcortical structures. For a given seizure type, seizure usually starts in the same part of the brain each time. Once initiated, the seizure may remain localized or spread to adjacent areas, and in some cases, may travel to the opposite hemisphere (contralateral spread). Despite this potential for spread, the initial focus remains consistent.
Focal seizures are subdivided based on whether consciousness is preserved or impaired, a classifier defined by awareness and responsiveness during the event.[28] They are also differentiated by the localization or spread of epileptiform activity. The three major classifications of focal seizures are described below:[28]
Focal preserved consciousness seizure: the person remains aware and responsive.
Focal impaired consciousness seizure: awareness and/or responsiveness are affected.
Focal-to-bilateral tonic-clonic seizures: abnormal brain activity spreads from one area to both brain hemispheres; awareness and/or responsiveness are affected.
Focal seizures can manifest with motor, sensory, autonomic, cognitive, or emotional symptoms, depending on the regions involved.[28] They often present with unilateral symptoms, but bilateral symptoms may also be seen, even when a seizure is not classified as focal-to-bilateral. This is because several structures in the brain have bilateral effects in the body (e.g.primary visual cortex).[30][31]
Focal impaired consciousness seizures are the most common type of seizure in individuals older than one year of age, affecting 36% of epilepsy patients overall.[30]
Other generalized seizures: encompass various motor and non-motor types
These categories include several subtypes of seizures, each with their own distinctive symptoms and diagnostic criteria.[28]
Like focal seizures, generalized seizures can present with asymmetric or bilateral symptoms, so thorough evaluation and history-gathering is necessary for diagnosis. One key difference between generalized and focal seizures is the age at onset, which is significantly lower in patients with generalized seizures.[31]
Generalized tonic–clonic seizures, previously known as grand mal seizures, are associated with the highest morbidity and mortality. They are the primary risk factor forsudden unexpected death in epilepsy (SUDEP).[33]
When available information is insufficient to determine whether a seizure is focal or generalized, it is classified as unknown. These seizures can be classified by level of consciousness and observable symptoms when possible.[28]
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.[28]
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.[15]
Provoked seizures are also known as acute symptomatic seizures. They are caused by an identifiable, transient condition affecting brain function. The temporal relationship between the cause and the seizure is important, but no single time frame has been established.[34] Proposed criteria for provoked seizures include symptoms within one week of acute brain injury, following subdural hematoma, during central nervous system infection, or within 24 hours of a severe metabolic imbalance.[34] Common causes of acute symptomatic seizures include:
Unprovoked seizures occur without an immediate precipitating event. These include spontaneous seizures andreflex seizures, which are consistently triggered by specific stimuli (e.g., flashing lights) but arise due to an enduring predisposition, not a transient cause.[40]
They typically reflect an underlying neurological predisposition and are associated with a higher risk of recurrence.[15] Diagnostic criteria forepilepsy are met when there are either two or more unprovoked seizures occurring more than 24 hours apart, or one unprovoked 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 asbrain tumors, malformations of cortical development, and chronic lesions from prior brain trauma.[41]
Seizures are the result of neuronal activity in the brain that is abnormal, excessive, and synchronized (also referred to as hypersynchronous).[11] At a cellular level, they reflect a disruption of the normal balance between excitatory and inhibitory neurotransmission. Under healthy conditions, excitation (mainly mediated by the neurotransmitterglutamate) and inhibition (primarily via the neurotransmitterGABA) maintain cortical stability. An excess of excitation or a failure of inhibition can tip this balance, promoting hypersynchronous neuronal firing characteristic of seizures.[43][44][45] The transition from an interictal state (between seizures) to an ictal state (seizure) is known asictogenesis. 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 temporarily lower the threshold for seizure activity.
Brief seizures, such as absence seizures lasting 5–10 seconds, do not cause observable brain damage.[46] More prolonged seizures have a higher risk of neuronal death.[46] Prolonged and recurrent seizures, such as status epilepticus, typically cause brain damage.[46] Scarring of brain tissue (gliosis), neuronal death, and shrinking of areas of the brain (atrophy) are linked to recurrent seizures.[46][47] These changes may lead to the development of epilepsy, in a process calledepileptogenesis.[47]
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.[15][3]The events preceding seizure onset, clinical signs observed during the episode, and symptoms following the episode are critical for accurately classifying the seizure type. Individuals with focal preserved consciousness seizures may be able to recall detailed information about their seizures. However, many individuals cannot recall the details of their own seizures, so obtaining eyewitness accounts is often essential for an accurate diagnosis.[15][3][48] When available, video recordings can provide valuable supplementary information, particularly in distinguishing epileptic seizures from mimics such as psychogenic nonepileptic seizures.[3]
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 testing is often performed in the evaluation of a new-onset seizure, particularly when a provoked cause is suspected.[15] 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 organ 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
Lactate: elevation in lactate levels within the first two hours after seizure onset is associated with generalized seizure, though this is not a requirement for diagnosis[50]
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.
Anelectroencephalogram (EEG) records electrical activity in the brain and can help support a diagnosis of epilepsy. Interictal EEG (which can be observed between seizure episodes) may reveal epileptiform abnormalities, such as spikes, sharp waves, or spike-and-wave discharges. However, an unremarkable 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.
EEG monitoring is frequently performed in the inpatient setting within a hospital's epilepsy monitoring unit (EMU), but in some cases, portable EEGs may be used in the outpatient setting for seizure monitoring.[51]
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
Adult patients with first-time seizures who have a suspected intracranial lesion or red-flag symptoms (e.g. focal deficits, altered mental status, fever, severe headache) should immediately receive a noncontrast head CT.[52]
When CT findings are normal in patients with a first unprovoked seizure, a follow-up MRI is recommended because it may detect epileptogenic lesions not visible on CT.[53]
Differentiating these conditions from epileptic seizures relies on careful history-taking, examination, EEG findings, and, when necessary, additional cardiac, metabolic, or psychiatric evaluations.
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.
Basic first aid during a tonic-clonic seizure focuses on ensuring the person's safety and preventing injury:[54]
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 (tongue swallowing during a seizure is a myth)[55]
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.
Time the seizure: If it lasts longer than 5 minutes, call emergency services.[56]
Emergency services should also be called if a person has multiple consecutive seizures, has trouble breathing or awakening afterward, becomes injured, is submerged in water, has a first-time seizure, has diabetes, or is pregnant.[56]
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.
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.[57] In emergency care, the first-line therapy for status epilepticus is the administration of abenzodiazepine to terminate the seizure, with most guidelines recommendinglorazepam,midazolam ordiazepam. Early benzodiazepine treatment is associated with better seizure control and improved outcomes.[3] Even in shorter seizures that do not require use of benzodiazepines, intravenous access is usually established in case of multiple seizure episodes or seizure prolongation.
If seizures persist despite benzodiazepine administration (second-line therapy), an intravenous antiseizure medication is given. Recommended options includefosphenytoin,valproate, orlevetiracetam, depending on patient-specific factors and institutional protocols.[58] 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.
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.
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 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][59] Another may be added if one is not enough to control the seizure occurrence.[59] Approximately 70% of people can obtain full control with continuous use of medication.[60] The type of medication used is based on the type of seizure.[3][59]
Patients with acute repetitive seizures (also known as "seizure clusters") have recurrent seizures within 6-24 hours of the first episode and are at an increased risk of developing status epilepticus. They are often prescribed rescue benzodiazepines in the form of rectal gels or nasal sprays for at-home use during emergencies.[61]
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.
Doctor performing an epilepsy surgery at Jaslok Hospital, Mumbai.
In severe cases where seizures are uncontrolled by at least two anti-seizure medications, brain surgery can be a treatment option.[3][59] Epilepsy surgery is especially useful for those with focal seizures, where the seizures are coming from a specific part of the brain.[59] 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.[62]
Another intervention for refractory epilepsy isvagus nerve stimulation (VNS), which involves insertion of an electrical device that stimulates the left vagus nerve.[63] Its mechanism of action is not fully understood. VNS is contraindicated in patients with cardiac conduction problems, sleep apnea, and should be avoided in patients with programmable shunt valves.[64] The most common side effect associated with VNS is hoarseness, and side effects usually improve over time or with decreased levels of stimulation.[65]
Helmets may be used to protect the head during a seizure. Some claim thatseizure response dogs, a form ofservice dog, can predict seizures.[66] Evidence for this, however, is poor.[66]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.[67][68] Aketogenic diet ormodified Atkins diet may help in those who have epilepsy who do not improve following typical treatments, with evidence for its effectiveness growing.[69][70]
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%.[71] 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.[72] The prognosis of epilepsy depends on seizure type, cause, and treatment response. About two-thirds of patients achieve seizure control with medication, while surgery orneuromodulation may help those with drug-resistant epilepsy.[73]
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.[74] 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.[75] 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.[74]
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.
Seizures have been recognized throughout recorded history. Early descriptions date back to ancientMesopotamia around 2000 BCE, where seizures were often attributed to supernatural causes or demonic possession.[76][77] Similar beliefs persisted across ancient cultures, including in Egypt, India, and Greece.[76] In the 5th century BCE, the physicianHippocrates challenged supernatural explanations in his treatiseOn the Sacred Disease, proposing that epilepsy was a disorder of the brain.[76] However, stigma surrounding seizures remained widespread for centuries.
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.[78] In India, epilepsy is estimated to result in costs of US$1.7 billion or 0.5% of the GDP.[60] They make up about 1% of emergency department visits (2% for emergency departments for children) in the United States.[79]
Much of recent epilepsy research has been focused on identifying causes for seizures, predicting them, and preventing their onset.[80][81]
Some types of seizures occur due to genetic mutations, such as those found in ion channels.[82] Current genetic epilepsy research is aimed at identifying genetic risk factors, understanding mutations, and developing genetic therapies. The development ofnext-generation sequencing has significantly advanced the understanding of gene-driven epilepsies.[82] Presently, there are experiments usingstem cells for the study and management of genetic epilepsy.
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.[83][81] Recently,biomarkers have been used for seizure prediction and prevention.[82] These are methods of measuring changes that occur in patients with seizures to differentiate them from people without seizures. One example of biomarkers is the use of microelectrodes, which can be used to monitor abnormal electrical brain activity. Another example is diffusion tensor imaging MRI, which can show differences in structural connectivity in individuals with epilepsy.[82][84]
There are ongoing investigations to identify mechanisms to treat seizures, with the most promising recent discoveries involving themTOR pathway and the cytokineIL-1ß.[82] Several other structures and cells are also the topic of study, including cellular membrane proteins, components of the blood-brain barrier, glial cells, and antibodies.[82] For treatment of genetic disorders, a process calledtransfection involves the use of vectors to deliver pieces of genetic material to areas of the brain involved in seizure onset.[80]
^abcdefghijkBerkowitz, Aaron L. (2022),"Seizures & Epilepsy",Clinical Neurology & Neuroanatomy: A Localization-Based Approach (2 ed.), New York, NY: McGraw Hill, retrieved28 April 2025
^Kodankandath, Thomas V.; Theodore, Danny; Samanta, Debopam (2025),"Generalized Tonic-Clonic Seizure",StatPearls, Treasure Island (FL): StatPearls Publishing,PMID32119383, retrieved7 November 2025
^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.ISSN1525-5069.PMID30658321.
^abcdDingledine, 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,ISBN978-94-017-8913-4,PMC4624106,PMID25012371
^Rowland, Kate; Lambert, Carl Earl (1 May 2022). "Evaluation After a First Seizure in Adults".American Family Physician.105 (5):507–513.ISSN1532-0650.PMID35559631.
^Lee, Ryan K.; Burns, Judah; Ajam, Amna A.; Broder, Joshua S.; Chakraborty, Santanu; Chong, Suzanne T.; Kendi, A. Tuba; Ledbetter, Luke N.; Liebeskind, David S.; Pannell, Jeffrey S.; Pollock, Jeffrey M.; Rosenow, Joshua M.; Shaines, Matthew D.; Shih, Robert Y.; Slavin, Konstantin (1 May 2020)."ACR Appropriateness Criteria® Seizures and Epilepsy".Journal of the American College of Radiology.17 (5):S293 –S304.doi:10.1016/j.jacr.2020.01.037.ISSN1546-1440.PMID32370973.
^Wirrell, Elaine (April 2022). "Evaluation of First Seizure and Newly Diagnosed Epilepsy".Continuum (Minneap Minn).28 (2):230–260.doi:10.1212/CON.0000000000001074.PMID35393959.
^abcdeLiu, Gerald; Slater, Nicole; Perkins, Allen (15 July 2017). "Epilepsy: Treatment Options".American Family Physician.96 (2):87–96.ISSN1532-0650.PMID28762701.
^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.ISSN1558-0776.PMID34620461.
^Asadi-Pooya, Ali A.; Brigo, Francesco; Lattanzi, Simona; Blümcke, Ingmar (29 July 2023). "Adult epilepsy".Lancet.402 (10399):412–424.doi:10.1016/S0140-6736(23)01048-6.PMID37459868.
^abGavvala 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.PMID28027373.
^abcAli 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.PMID26709155.
^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.
^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.PMID21109099.
