Seizure

A seizure is a brief, sudden disturbance in normal brain activity caused by abnormal, excessive or synchronous neuronal firing. Depending on the regions affected, seizures can alter movement, sensation, behaviour, awareness or consciousness. Symptoms range widely from subtle lapses in attention, characteristic of absence seizures, to the dramatic loss of consciousness and convulsive movements seen in tonic–clonic seizures. Most episodes last under two minutes and are followed by a postictal period marked by confusion, fatigue or other neurological changes. When a seizure persists beyond five minutes, it is classified as status epilepticus, a medical emergency associated with a substantial risk of long-term brain injury. Seizures may be provoked by identifiable triggers or occur spontaneously; recurrent unprovoked seizures define the condition known as epilepsy.

Clinical Features

Seizure manifestations vary according to the brain regions involved and the specific type of seizure. Motor signs may include muscle stiffening (tonic activity), rhythmic jerking (clonic activity), sudden muscle jerks (myoclonus) or loss of muscle tone (atonia). Sensory disturbances can arise in the form of tingling, visual phenomena or auditory hallucinations. Autonomic changes may involve fluctuations in heart rate, breathing or gastrointestinal sensations. Some seizures affect cognitive and emotional processes, producing confusion, fear or altered perception.
Many individuals experience an aura, often representing the earliest phase of a focal seizure. Auras are subjective sensations such as unusual smells, déjà vu, or sudden emotional shifts. Most seizures resolve rapidly and are followed by a postictal recovery phase characterised by tiredness, impaired memory and slowed responsiveness. Status epilepticus occurs when seizures last longer than five minutes or recur without a return to baseline, creating a risk of permanent neuronal injury.

Classification

Seizures are broadly categorised by their site of onset, clinical characteristics and the person’s level of awareness during the event. The updated International League Against Epilepsy classification, released in 2025, distinguishes focal, generalised, unknown-onset and unclassified seizures. These types are further refined by noting whether awareness is preserved or impaired, assessed through responsiveness during the episode.
Focal seizures arise within a localised network confined to one cerebral hemisphere. They may originate in cortical or subcortical regions and typically have a consistent site of onset across episodes. Focal seizures can remain localised, spread to neighbouring areas or propagate to the opposite hemisphere. They are traditionally divided into:• Focal preserved consciousness seizures, in which awareness and responsiveness remain intact.• Focal impaired consciousness seizures, in which awareness or responsiveness is reduced.These seizures may produce motor, sensory, autonomic, cognitive or emotional symptoms. Some evolve into focal-to-bilateral tonic–clonic seizures, where abnormal activity spreads across both hemispheres.
Generalised seizures involve rapidly spreading activity that engages networks in both hemispheres from onset. They include several clinical forms, notably absence seizures involving brief lapses in awareness, and tonic–clonic seizures characterised by stiffening followed by rhythmic jerking. Other generalised types comprise motor and non-motor variants. Generalised tonic–clonic seizures carry notable morbidity and are linked to an increased risk of sudden unexpected death in epilepsy.
Unknown-onset seizures are diagnosed when the available information cannot determine whether the seizure began focally or generally. These may still be classified according to awareness and clinical signs when such features are observable.
Unclassified seizures represent events recognised as epileptic but lacking sufficient information for definitive categorisation. This designation is usually provisional pending further assessment.

Causes

The underlying causes of seizures are grouped into provoked (acute symptomatic) and unprovoked categories. Identifying the mechanism is crucial for treatment planning and predicting recurrence.
Provoked seizures occur as direct responses to transient disturbances in brain function. Common causes include:• Metabolic abnormalities, such as low glucose, low sodium or renal failure.• Central nervous system infections, including meningitis or encephalitis.• Acute neurological injuries, such as stroke, head trauma or intracranial haemorrhage.• Substance-related triggers, including alcohol withdrawal, intoxication or abrupt cessation of certain medications.• Fever, which is a leading cause of febrile seizures in children.
Unprovoked seizures occur without immediate triggers and usually reflect a lasting predisposition to abnormal neuronal excitability. Recurrent unprovoked events meet the diagnostic criteria for epilepsy when either two unprovoked seizures occur more than twenty-four hours apart or a single unprovoked seizure is accompanied by a high risk of recurrence. Causes may include:• Structural abnormalities, such as tumours, cortical malformations or chronic lesions from past injuries.• Genetic epilepsies, involving mutations affecting ion channels or neuronal networks, as seen in Dravet syndrome, Lennox–Gastaut syndrome and juvenile myoclonic epilepsy.• Infectious sequelae, including residual effects of neurocysticercosis or viral encephalitis.• Metabolic disorders, including inherited metabolic defects or mitochondrial diseases.• Immune-mediated causes, such as autoimmune encephalitis.In some patients, no clear cause is identified, leading to a diagnosis of idiopathic seizures.

Mechanism

Seizures arise when the normal balance between excitatory and inhibitory neuronal activity is disrupted. Under physiological conditions, equilibrium is maintained primarily by the interplay of glutamate-mediated excitation and GABA-mediated inhibition. When excitation becomes excessive or inhibitory processes fail, hypersynchrony develops, producing the hallmark patterns of seizure activity.
The transition from a non-seizure (interictal) to seizure (ictal) state, known as ictogenesis, involves rapid changes in ionic gradients, neurotransmitter release and neuronal membrane stability. In provoked seizures, acute disturbances such as metabolic derangements or inflammation can transiently lower the threshold for neuronal firing. Brief seizures, including absence seizures lasting only a few seconds, do not cause detectable structural damage. However, prolonged or recurrent seizures—especially status epilepticus—are associated with neuronal injury. Recurrent episodes may lead to gliosis, neuronal loss and regional atrophy, which can contribute to the development of chronic epilepsy through a process termed epileptogenesis.

Provoked and Unprovoked Seizures in Context

The distinction between provoked and unprovoked seizures has major clinical significance. Provoked seizures are usually linked to reversible causes, and the risk of recurrence is low once the underlying problem is corrected. Conversely, unprovoked seizures suggest an enduring susceptibility to epileptic activity, with a substantially higher likelihood of future episodes. Modern diagnostic approaches employ neuroimaging, electrophysiological studies and metabolic or genetic testing to identify contributing factors and inform long-term management.