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Seizures and epilepsy

Last updated: June 7, 2021

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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).

For discussion of individual epilepsy syndromes, see “Generalized epilepsy in childhood.”

Seizures [1]

  • 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: [2]
  • 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 [1]
  • Descriptors: the following terms are used to describe events, clinical features, and EEG signs related to seizures [3]
    • Ictal: occurring during a seizure
    • Interictal: occurring between the seizures
    • Postictal: occurring signs after a seizure

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.

Epidemiological data refers to the US, unless otherwise specified.

Seizure triggers [9]

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

  • Excessive physical exertion
  • Alcohol consumption
  • Fever (febrile seizures)
  • Sleep deprivation
  • Flashing lights (e.g., strobe lights, video games)
  • Music [11]
  • Hormonal changes (e.g., at different phases of the menstrual cycle, after menopause)

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)

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]

Focal seizures (formally 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 hours)
Focal to bilateral tonic-clonic
  • Progresses to loss of consciousness
  • Prodromal aura may be present.
  • Focal symptoms may be clinically inapparent due to the rapid spread and bilateral activation
  • 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]

  • Symptoms are produced by bilateral cerebral cortex disturbances.
  • Start with loss of consciousness.
  • Patients do not recall the seizure.
Clinical features of generalized seizures
Type Ictal Postictal
Generalized motor seizure
Tonic-clonic seizure (grand mal)
  • Prodromal symptoms may occur up to hours before seizure onset (e.g., sleep disturbances, lightheadedness, mood changes, anxiety/irritability, impaired concentration)
  • Loss of consciousness (sudden and without warning)
  • Motor symptoms
    1. Tonic phase
    2. Clonic phase: rhythmic muscle twitching
  • Bladder or bowel incontinence
  • Tongue-bite lacerations
  • Usually lasts 1–3 minutes
Clonic seizure
  • Loss of consciousness
  • Bilateral rhythmic jerking (of the entire body or only a part)
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
  • 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.

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

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.

Presurgical evaluation for epilepsy surgery [23]

  • 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
    • To identify structural abnormalities/lesions and their location (e.g., focal cortical dysplasia)
    • Done with MRI with a minimum power of 1.5 T and epilepsy-specific protocols [22]
  • Functional imaging
    • If structural imaging identifies no lesion or more than one lesion
    • Done with PET, ictal SPECT, or fMRI
  • 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
  • Prior seizure
  • Excessive physical exertion
  • Sleep deprivation
  • Flashing lights
  • Usually < 2 minutes

Generalized-onset motor seizure

  • Aura is uncommon
  • Loss of consciousness
  • Tongue biting
  • Bladder and bowel incontinence
  • Postictal phase: confusion, amnesia, fatigue
  • Eyes often open or do not resist opening
  • Usually < 5 minutes
Febrile seizure
  • Young age (6 months to 5 years)
  • Genetic predisposition
  • High fever (> 40°C/104°F)
  • Viral infection (e.g., HHV-6, influenza)
  • Postimmunization fever
  • < 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 seizures (PNES)
  • Usually occur in presence of eyewitnesses [24][25]
  • Generalized asynchronous motor activity
  • Forced eye closure
  • Eyes are usually closed and resist being opened
  • Tongue-biting and other types of self-injury are rare.
  • Awareness is usually unimpaired
  • Individuals with PNES can recall the event
  • Typically > 5 minutes [26]
  • Video-EEG monitoring
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

The differential diagnoses listed here are not exhaustive.


Acute management of a seizure

Management of the first unprovoked seizure [29][30]

  • 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 [31]

Treatment options
Seizure type First line Second line
Generalized Tonic-clonic
Typical absence
Atypical absence
  • Treatment regimen
    • Monotherapy should be maintained, if possible.
      • Increase the dosage of a single agent or switch drug if treatment proves ineffective before initiating combination therapy.
      • ∼ ⅔ of epilepsy patients become seizure-free with monotherapy [32]
    • 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. [33]
  • 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.

Nonpharmacological therapy

  • Indications: pharmacoresistant epilepsy
  • Surgery
    • Procedures
      • Resection (surgical removal of pathological lesions)
      • Disconnection (surgical section of neuronal circuits)
        • Callosotomy: section of the corpus callosum [34]
          • Initially, partial disconnection only (usually the anterior ⅔)
          • Complete disconnection if seizures persist
        • 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 [35]
  • Stimulation techniques: vagus nerve stimulation, deep brain stimulation
  • Dietary measures: ketogenic diet [36]

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

We list the most important complications. The selection is not exhaustive.

General considerations

Stages and treatment [41]

Treatment of SE is staged according to the time elapsed from the seizure onset. For initial assessment and supportive treatment, see “Acute management of a seizure” in “Treatment.”

Status epilepticus is a life‑threatening event! If not interrupted, it can lead to cerebral edema, a dangerous rise in body temperature, rhabdomyolysis, and cardiovascular failure!

  • Risk of seizure recurrence
    • After the first unprovoked seizure [29][43]
      • 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 [44]
    • 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. [45]
  • Mortality [46]
    • 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.
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