A seizure is the 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 that may be temporary (e.g, due to electrolyte imbalances) or more permanent in nature (e.g., due to inherited or acquired neural abnormalities). Seizures can be triggered by a variety of circumstances depending on age, environmental factors, and underlying conditions. Acute symptomatic seizures (provoked seizures) have identifiable precipitating factors (e.g., stroke, traumatic brain injury, alcohol withdrawal), whereas unprovoked seizures occur in the absence of identifiable causes. Reflex seizures are seizures that occur consistently in response to a particular trigger. Seizures can also be classified by onset as focal (arising from discharges in one hemisphere), generalized (arising from discharges in both hemispheres), or of unknown onset. Epilepsy is a chronic neurological disorder defined as the occurrence of 2 or more unprovoked or reflex seizures at least 24 hours apart, the occurrence of a single unprovoked or reflex seizure in an individual with an underlying condition that increases the risk of subsequent seizures (e.g., a brain tumor), or the presence of an epilepsy syndrome (see also “Generalized epilepsy in childhood” for individual epilepsy syndromes).
Acute complications of seizures with potentially long-term consequences include physical trauma and CNS tissue damage due to hyperthermia, cardiorespiratory deficits, or excitatory toxicity. Status epilepticus is a potentially life-threatening acute complication characterized by ongoing seizure activity of more than 5 minutes that requires immediate medical treatment. An effort should be made to determine the cause of a seizure at initial presentation based on medical history (evaluation of provocative factors and seizure type), laboratory tests (to evaluate for metabolic abnormalities), and imaging (to evaluate for structural or metabolic causes). Electroencephalography (EEG) can provide additional evidence to support the diagnosis, although a normal EEG between the seizures does not rule out epilepsy. Important antiepileptic drugs include lamotrigine (first-line treatment in focal seizures), valproate (first-line treatment in generalized seizures), and ethosuximide (first-line treatment in absence seizures). With appropriate medical treatment, the majority of patients remain seizure‑free in the long term and prevent long-term complications such as psychiatric conditions (e.g., anxiety, depression, or psychosis), sleep disorders, and sudden unexpected death in epilepsy (SUDEP). Patients must be monitored for side effects of medications (e.g., bone disease).
- Seizure: an excessive and/or hypersynchronous activity of cortical neurons that results in transient neurological symptoms
- Acute symptomatic seizure (provoked seizure): a seizure that occurs at the time or soon after the onset of an acute systemic or CNS condition. Examples include: 
- Reflex seizure: a seizure constantly evoked by a particular stimulus (trigger) that lowers seizure threshold (e.g., flashing lights; see “Seizure triggers” in “Etiology” for more seizure triggers)
- Unprovoked seizure: a seizure that occurs in the absence of an identifiable cause or beyond the specified interval after an acute CNS condition 
- Descriptors: the following terms are used to describe events, clinical features, and EEG signs related to seizures 
Epilepsy: a chronic neurologic disorder characterized by a predisposition to seizures as defined by one of the following: 
- Two or more unprovoked or reflex seizures separated by more than 24 hours
- One unprovoked or reflex seizure in an individual with a high risk of subsequent seizures (e.g., after traumatic brain injury, stroke, CNS infections)
- Diagnosis of an epilepsy syndrome: a group of epileptic disorders characterized by a set of features typically occurring together.
Reflex epilepsy: Epilepsy in which seizures are consistently provoked by a certain trigger (e.g., lights, music, hormonal changes during menstrual cycle). Subtypes can be determined based on the trigger and include:
- Photosensitive epilepsy
- Musicogenic epilepsy
- Catamenial epilepsy
- Drug-resistant epilepsy: epilepsy in which at least two antiepileptic drugs (administered as sequential monotherapies or as combination therapy) have failed to prevent seizures 
- Resolved epilepsy
- Incidence of unprovoked seizures: 61 per 100,000 population 
- Incidence of epilepsy: 79.1 per 100,000 population 
- Prevalence of epilepsy: 8.5 per 1,000 population 
Epidemiological data refers to the US, unless otherwise specified.
Seizure triggers 
- Excessive physical exertion
- Alcohol consumption
- Fever (febrile seizures)
- Sleep deprivation
- Flashing lights (e.g., strobe lights, video games)
- Music 
- Hormonal changes (e.g., at different phases of the menstrual cycle, after menopause)
Causes of acute symptomatic seizures 
- Anoxic encephalopathy
- Intracranial surgery
- Acute CNS infections (e.g., meningitis, encephalitis)
- Electrolyte imbalance (e.g., hypoglycemia, hypocalcemia)
- Acute metabolic disturbances (e.g., uremia)
- Alcohol withdrawal
- Recreational drug use
- Prescription drug toxicity
- Exacerbations of autoimmune disorders (e.g., SLE)
Common causes of epilepsy 
- Genetic mutations affecting ion channels or transmitter receptors (e.g., mutations in KCNQ2 or SCN1A genes)
- Chromosomal abnormalities (e.g., Angelman syndrome, Prader-Willi syndrome, Rett syndrome)
- Genetic metabolic disorders (e.g., PKU, congenital disorders of glycosylation, lysosomal storage diseases, peroxisomal biogenesis disorders)
- Mitochondrial diseases (e.g., MELAS)
- Structural: chronic cerebral lesion or abnormality
- Immune: autoimmune encephalitides (e.g., anti-NMDA receptor encephalitis), Rasmussen encephalitis
- Infectious: : chronic CNS infection (e.g., toxoplasmosis, malaria, neurocysticercosis) or complication of acute CNS infection (e.g., viral or bacterial meningitis or encephalitis)
Causes of epilepsy according to the age group 
|Etiology of epilepsy in different age groups|
|Age group at manifestation||Causes|
|Neonates and infants (< 6 months)|
|Older infants (> 6 months) and children (< 10 years)|
|Adolescents (10–18 years)|
|Adults (18–60 years)|
|Older adults (> 60 years)|
Classification of seizures according to the ILAE 2017 classification 
Seizures are classified according to localization of abnormal neuronal activity and then further subcategorized based on symptoms and sometimes level of awareness.
|Basic classification of seizures|
|Location of abnormal neuronal activity|| || || |
|Awareness|| || || |
|Symptoms|| || || |
|Other|| || |
* Note: An expanded version of the ILAE 2017 classification also considers further subtypes of motor and nonmotor categories.
Classification of epilepsy 
- General considerations
Levels of classification
- For level 1, first determine the seizure type (see “Classification of seizures” above).
- For level 2, then determine the epilepsy type, which can be:
- Generalized: diagnosed in patients with generalized-onset seizures as evidenced by generalized ictal activity (e.g., 3 Hz spike-wave activity in absence seizures) and/or typical interictal discharges on EEG.
- Combined generalized and focal: diagnosed in patients who have both focal-onset and generalized-onset seizures (seen, e.g., in Dravet syndrome and Lennox-Gastaut syndrome)
- Unknown: diagnosed if there is not enough clinical information to classify seizures as focal, generalized, or combined
- For level 3, consider epilepsy syndromes (see “Focal seizures and syndromes” and “Generalized epilepsy in childhood” for discussion of specific syndromes)
Focal seizures (formally partial seizures) 
- Originate in one brain hemisphere 
- Usually caused by focal structural abnormalities
- Symptoms depend on the anatomical location of the lesion or disturbance within the brain.
- For more information about the etiology and symptoms of seizures originating from the cortex of particular brain lobes, see “.”
|Clinical features of focal seizures|
|Focal|| || |
|Focal to bilateral tonic-clonic|| || || |
If focal to bilateral tonic-clonic type progresses rapidly to the bilateral generalized phase, initial focal symptoms may go unnoticed, leading to a potential misdiagnosis of generalized-onset seizures and inappropriate therapy.
Generalized-onset seizures 
- Symptoms are produced by bilateral cerebral cortex disturbances.
- Start with loss of consciousness.
- Patients do not recall the seizure.
|Clinical features of generalized seizures|
|Generalized motor seizure|
|Tonic-clonic seizure (grand mal)|| |
|Clonic seizure|| || |
|Tonic seizure|| || |
|Myoclonic seizure|| || |
|Myoclonic-atonic seizure|| |
|Myoclonic-tonic seizure|| |
|Atonic seizure (also known as “drop seizure” or “drop attack”)|| |
|Generalized nonmotor seizure (absence seizure)|
Determining if a patient is having or had a seizure is primarily a clinical diagnosis. An effort should be made to determine the cause at initial presentation based on medical history (evaluation of provocative factors and seizure type), laboratory tests (to evaluate for metabolic abnormalities), and possibly imaging (to evaluate for structural or metabolic causes). For first seizures with unclear cause, insufficient classification, or treatment-refractory seizures, electroencephalography (EEG) should be performed to help in diagnosing potential underlying epilepsy.
Confirmation of seizure
- History of present illness: description of the event by the patient (aware seizure) and/or witnesses (seizure with impaired awareness)
- Past medical history
- Physical examination: attention should be paid to visual inspection (e.g., for bruises from falls, tongue bites, phakomatosis-specific skin manifestations) and evaluation for cardiovascular disorders
- Performed in individuals who present with first seizure, with insufficient information for seizure classification, and/or treatment-refractory seizures
Characteristic EEG findings help to establish the diagnosis of epilepsy; the absence of such findings cannot, however, rule out epilepsy.
- During the seizure (ictal)
- Epileptiform discharges (e.g., spikes, sharp waves, spike waves) are usually detected.
- Certain types of conditions characterized by seizures have characteristic discharge patterns (e.g., hypsarrhythmia in West syndrome, 3 Hz spike-and-wave in typical absence seizures, burst suppression in anoxic encephalopathy or barbiturate administration)
- If no epileptiform discharges are detected during a seizure, alternative diagnoses (e.g., psychogenic nonepileptic seizures) should be considered.
- After a seizure or between seizures (postictal or interictal)
- Video-EEG telemetry in hospitalized patients
- Continuous EEG in ambulatory patients
- During the seizure (ictal)
Evaluation for underlying conditions
- ECG: Rule out cardiogenic causes (e.g., cardiac arrhythmias resulting in cerebral hypoxia) in all patients with loss of consciousness during a seizure.
- MRI: Modality of choice for investigating potential underlying structural abnormalities. 
- CT: : May be used if MRI is not available, but is less sensitive for identifying soft-tissue lesions 
- Angiography: if vascular cause (e.g., cerebral arteriovenous malformation) is suspected
Laboratory screening: to identify metabolic disorders and infectious diseases, if suspected
- Bacterial cultures
- Cerebrospinal fluid analysis
- Endocrine studies
In adults, an isolated unprovoked focal or focal to bilateral tonic-clonic seizure typically indicates a structural or metabolic origin and should receive further evaluation.
Presurgical evaluation for epilepsy surgery 
- Neuropsychological testing: to detect possible cognitive dysfunction associated with epilepsy and assess risks for postsurgical dysfunction
- Video-EEG monitoring: : to review seizure semiology and ensure it corresponds with EEG and structural and functional imaging
- Structural imaging
- Functional imaging
- Intracranial EEG recording (electrocorticography): performed if structural and functional imaging fail to definitively localize the epileptogenic focus
|Differential diagnosis of epilepsy|
|Condition||Risk factors and triggers||Clinical features of the event||Duration||Diagnostics|
|Focal-onset seizure|| || |
Generalized-onset motor seizure
|Febrile seizure|| |
|Psychogenic nonepileptic seizures (PNES)|| || |
|Panic attack|| || || |
|Migraine aura|| || || |
|Breath-holding spell|| || || |
The differential diagnoses listed here are not exhaustive.
- Seizures are usually self-limiting and may not require administration of antiseizure drugs.
- Long-term therapy with antiepileptic drugs is required for individuals who meet the criteria for epilepsy; the goal is to achieve seizure freedom.
- Monotherapy should be maintained unless it fails to control seizures.
- Drug-resistant epilepsy is managed with nonpharmacological methods (e.g., with surgery, neurostimulation, ketogenic diet).
Acute management of a seizure
- Remove or control hazards (e.g., remove sharp objects in the patient's vicinity)
- Check ABCs; if needed, perform cardiopulmonary resuscitation
- Place the patient in the recovery position to prevent injury.
- If in a health care setting:
- Monitor vital signs (especially oxygenation via pulse oximetry)
- Establish secure IV access
- Perform laboratory studies
- Administer supportive therapy as necessary (e.g., oxygen, glucose, thiamine , naloxone )
- If acute brain injury (e.g., intracerebral hemorrhage) is suspected: obtain a cranial CT
- If CNS infection is suspected: perform a lumbar puncture
- Acute seizures are usually self-limiting and do not require pharmacological treatment.
If a seizure has not ceased after 5 minutes (indicating status epilepticus), the patient should receive ; antiseizure medications, starting with benzodiazepines (see “Treatment of SE”). 
- Some experts also recommend considering medical therapy already before 5 minutes. 
Management of the first unprovoked seizure 
- Remove cause or provoking factors (e.g., cessation of recreational drug use, treatment of underlying disorders).
- Long-term medical therapy is not required unless the patient meets the criteria for epilepsy.
Management of epilepsy
Medical therapy 
- Antiepileptic drugs raise the seizure threshold that is pathologically lowered in individuals with epilepsy, thereby reducing the risk of future seizures.
- Criteria for the choice of antiepileptic drugs
- Seizure type
- Patient age
- Comorbidities and contraindications
|Seizure type||First line||Second line|
|Atypical absence|| |
- Monotherapy should be maintained, if possible.
- 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. 
Termination of treatment
- To be evaluated on a case‑by‑case basis
- May be considered if the patient has < 2 seizures/year, an inconspicuous provocation EEG, normal psychological findings, and no hereditary predisposition
- Generally possible after 2–5 seizure‑free years with normal EEG results
- Medications should be tapered with caution.
- Indications: pharmacoresistant epilepsy
Resection (surgical removal of pathological lesions)
- Resection of the anteromedial temporal lobe or of the amygdala and the hippocampus in patients with temporal lobe epilepsy, e.g., due to hippocampal sclerosis
- Resection of an entire hemisphere (hemispherectomy) in patients with severe intractable seizures due to structural cerebral abnormalities confined to one hemisphere
Disconnection (surgical section of neuronal circuits)
- Callosotomy: section of the corpus callosum 
- Hemispherotomy: disconnection of the cortex of one hemisphere from the ipsilateral subcortical structures and the cortex of the other hemisphere without removal of the affected hemisphere 
- Resection (surgical removal of pathological lesions)
- Stimulation techniques: vagus nerve stimulation, deep brain stimulation
- Dietary measures: ketogenic diet 
- Hyperthermia, cardiorespiratory deficits, and excitatory toxicity potentially causing irreversible tissue damage (especially to the CNS; e.g., cortical laminar necrosis) and, in turn, increase the risk of further seizures.
- Postictal transient anion gap metabolic acidosis with increased lactic acid and reduced serum bicarbonate (usually resolves spontaneously within 60–90 minutes after seizure activity stops)
- Physical trauma, such as:
- Status epilepticus
- Psychiatric 
- Sleep disturbances and insomnia
- Bone disease (osteomalacia, osteoporosis) associated with antiepileptic drugs
Sudden unexpected death in epilepsy (SUDEP): 
- The sudden death of a person with a 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 (esp. tonic-clonic), and early age of onset
We list the most important complications. The selection is not exhaustive.
- Definition: Status epilepticus (SE) is a seizure that lasts ≥ 5 minutes or a series of seizures in rapid succession without recovery in the interictal period, which increases the risk of long-term consequences such as neuronal injury and functional deficits. 
- Withdrawal from antiepileptic drugs
- Metabolic disturbances (e.g., hyponatremia, porphyria)
- Drug toxicity (e.g., tricyclic antidepressants)
- Structural brain lesions/injury (e.g., tumors, trauma, stroke)
- CNS infections (e.g., cerebral malaria, neurocysticercosis viral encephalitis, prion diseases)
- Late-stage neurodegenerative diseases (e.g., Alzheimer disease)
- Anoxic brain injury
- Classification 
- Prognosis: mortality is 16–17% in adults with convulsive SE 
Stages and treatment 
- Stage 1 (5–20 minutes after the onset of a seizure): benzodiazepines (lorazepam, midazolam, or clonazepam)
- Stage 2 (20–40 minutes after the onset of a seizure or after stage 1 treatment failed): a single dose of IV phenytoin or fosphenytoin, valproic acid, or levetiracetam
- Stage 3 (40–60 minutes after the onset of seizures or after stage 1 and 2 treatment failed): induction of coma with IV propofol, midazolam, thiopental, or phenobarbital
Risk of seizure recurrence
- After the first unprovoked seizure 
- After the second unprovoked seizure: 60% within 1 year
- After an acute symptomatic seizure: ∼ 19% over the next 10 years
- Treatment outcomes 
- Legal regulations: State laws vary with regard to the requirements for individuals with epilepsy to operate vehicles and heavy machinery. 
- Mortality