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Seizure types

Epileptic seizures are transient occurrences of signs and/or symptoms due to abnormal excessive or synchronous neuronal activity in the brain.^[1] The classification of seizure types provides a standardized framework for identifying the onset, manifestations, and clinical features of these events, facilitating accurate diagnosis, targeted treatment, and improved patient management in epilepsy care.^[2] Developed by the International League Against Epilepsy (ILAE), this system emphasizes the distinction between focal and generalized onsets while incorporating levels of consciousness and observable motor behaviors to describe seizure semiology precisely.^[3] The most recent ILAE classification, updated in 2025, organizes epileptic seizures into four main classes: focal onset, generalized onset, unknown onset (whether focal or generalized), and unclassified.^[4] Focal onset seizures begin in networks limited to one hemisphere and may preserve or impair consciousness, potentially evolving into bilateral tonic-clonic seizures if they spread.^[3] Generalized onset seizures, in contrast, involve bilaterally distributed networks from the outset and include subtypes such as absence, tonic-clonic, myoclonic, clonic, tonic, atonic, and epileptic spasms, often affecting consciousness variably.^[3] Seizures of unknown onset are those where the initial site cannot be determined, subdivided similarly based on consciousness and motor features, while unclassified seizures lack sufficient information for categorization.^[4] This classification system, comprising 21 distinct seizure types, builds on prior frameworks by streamlining terminology and enhancing flexibility for clinical application, supported by tools like checklists and descriptors for semiology sequences.^[3] Accurate typing relies on clinical history, witness descriptions, and ancillary data such as electroencephalography (EEG) and neuroimaging, underscoring the role of multidisciplinary assessment in epilepsy.^[2] By prioritizing onset location and consciousness as primary classifiers, the ILAE approach aids in predicting seizure progression and guiding therapeutic decisions, such as selecting antiseizure medications tailored to specific types.^[4]

Classification Systems

Historical Development

The classification of seizures traces its origins to the late 19th century, when British neurologist John Hughlings Jackson (1835–1911) first distinguished focal seizures—characterized by localized symptoms arising from a specific brain region—from generalized seizures involving widespread cerebral involvement. Jackson's observations, drawn from clinical examinations and post-mortem analyses, emphasized that focal seizures could spread to produce more diffuse manifestations, laying the groundwork for understanding epilepsy as a disorder of brain excitability rather than a singular entity.^[5] A formalized international framework emerged in 1981 with the International League Against Epilepsy (ILAE) proposal, which categorized seizures into two primary groups: partial (later termed focal) and generalized. Partial seizures were subdivided into simple partial (without alteration of consciousness), complex partial (with impaired consciousness), and secondarily generalized (evolving from partial to bilateral involvement); generalized seizures encompassed absence, myoclonic, clonic, tonic, tonic-clonic, and atonic subtypes, based on clinical features and electroencephalographic (EEG) correlates. This system, developed through analysis of video-EEG recordings, aimed to standardize terminology for clinical and research purposes.^[6] Despite its influence, the 1981 classification faced criticism for several shortcomings, including reliance on archaic terms such as "grand mal" for tonic-clonic seizures and "petit mal" for absence seizures, which lacked descriptive precision. It also underemphasized key aspects like seizure onset location, level of awareness, and semiological details, leading to difficulties in classifying atypical or unclassifiable seizures that blurred category boundaries. These limitations hindered comprehensive application in diverse clinical scenarios.^[6]^[7] From the 1980s through the 2010s, technological advances profoundly shaped seizure understanding without prompting immediate classification overhauls. Video-EEG monitoring refined ictal pattern recognition and localization, while neuroimaging modalities like computed tomography (introduced in the 1970s), magnetic resonance imaging (MRI, widespread by the 1980s), and positron emission tomography (PET, advancing in the 1990s–2000s) revealed structural and functional abnormalities in focal epilepsies, enabling better differentiation from generalized forms. These tools supported syndrome identification and etiology assessment but highlighted the 1981 system's rigidity, setting the stage for the ILAE's 2017 revision as the first major update.^[6]^[8]

ILAE 2017 Classification

The International League Against Epilepsy (ILAE) introduced a revised operational classification of seizure types in 2017, building on and updating the 1981 framework that had become outdated due to advances in neuroimaging, genetics, and electroencephalography (EEG).^[9] This system emphasizes practical application in clinical settings, prioritizing the seizure's onset, level of awareness during the event, and prominent semiological features for accurate diagnosis and treatment selection.^[9] It defines seizures based on their initial manifestation, allowing for a hierarchical structure that facilitates communication among healthcare providers.^[9] Central to the 2017 classification is the concept of "onset," which categorizes seizures as focal onset (beginning in networks limited to one hemisphere), generalized onset (starting in bilateral networks), or unknown onset (when the beginning cannot be determined).^[9] For focal onset seizures, awareness is further specified as aware (consciousness fully preserved, allowing normal responsiveness), impaired awareness (altered responsiveness, often with confusion or automatisms), or without awareness information (if data is insufficient to assess).^[9] This distinction helps differentiate simple partial seizures (now termed focal aware) from those involving more widespread disruption.^[9] Generalized onset seizures, by contrast, do not require awareness assessment as they inherently involve bilateral involvement from the start, often leading to immediate loss of awareness.^[9] Focal onset seizures are subdivided based on the predominant early feature into motor and nonmotor types.^[9] Motor onset includes automatisms (e.g., repetitive lip-smacking or hand-rubbing), hyperkinetic (e.g., thrashing or pedaling movements), tonic (e.g., sudden stiffening of limbs), atonic (e.g., sudden loss of muscle tone), clonic (e.g., rhythmic jerking), myoclonic (e.g., brief jerks), and epileptic spasms (e.g., flexor or extensor contractions, often in clusters).^[9] Nonmotor onset encompasses sensory (e.g., tingling or visual auras), autonomic (e.g., piloerection or gastrointestinal sensations), cognitive (e.g., déjà vu or language arrest), emotional (e.g., fear or joy), and behavior arrest (e.g., sudden stillness without response).^[9] These categories allow focal seizures to evolve, such as progressing to bilateral tonic-clonic activity, which is noted separately.^[9] Generalized onset seizures are classified into motor and nonmotor (absence) subtypes, reflecting their diffuse bilateral activation.^[9] Motor types include tonic-clonic (e.g., stiffening followed by jerking), clonic (rhythmic shaking), tonic (sustained stiffening), myoclonic (brief jerks, often in legs), myoclonic-tonic-clonic (jerks leading to full convulsion), myoclonic-atonic (jerks followed by collapse), atonic (sudden falls), and epileptic spasms (brief, symmetric contractions).^[9] Absence seizures, as nonmotor generalized events, are divided into typical (brief staring spells with abrupt onset and offset, often with automatisms) and atypical (longer duration with gradual onset, more variable responsiveness).^[9] Additional absence variants include myoclonic absence (with jerks) and eyelid myoclonia (rapid blinking triggered by closure).^[9] The 2017 system delineates 63 distinct seizure types through combinations of onset, awareness, and manifestations, providing a comprehensive yet flexible taxonomy that underscores semiology—the detailed description of observable signs and symptoms—as essential for precise identification.^[9] EEG and video-EEG monitoring play a crucial role in confirming classifications by capturing electrical onset and behavioral correlates, particularly to distinguish focal from generalized events.^[9] If clinical history, witness accounts, or diagnostic tests provide insufficient data, seizures may be labeled as unknown onset or unclassified to avoid misdiagnosis.^[9] This approach supports individualized epilepsy management, including targeted therapies based on seizure type.^[9]

ILAE 2025 Updates

The International League Against Epilepsy (ILAE) released an updated classification of epileptic seizures in 2025, building on the 2017 framework to enhance clinical utility and simplicity. This revision streamlines the system by reducing the number of distinct seizure types from 63 to 21, while retaining the four main classes: focal, generalized, unknown (whether focal or generalized), and unclassified. These changes aim to facilitate more precise communication among clinicians and alignment with epilepsy syndrome classifications, emphasizing practical shorthand notations for everyday use.^[10]^[4] Key revisions include the removal of "onset" from the names of the main seizure classes, shifting focus from initial localization to broader descriptors. The term "awareness" has been replaced by "consciousness," defined as a combination of awareness and responsiveness, to better capture the spectrum of cognitive involvement during seizures. Additionally, the previous distinction between motor and non-motor manifestations is now categorized as observable versus non-observable, providing a more neutral and comprehensive framework for describing seizure semiology.^[10]^[4] Further updates introduce the description of seizures through the chronological sequence of semiology, rather than relying solely on the initial manifestation, allowing for a more dynamic representation of seizure evolution. The classification now explicitly recognizes epileptic negative myoclonus as a distinct seizure type, addressing a previously underemphasized entity. To support treatment decisions, the system differentiates between classifiers—biological features that influence management—and descriptors for specific clinical signs, promoting the identification of subtypes with therapeutic implications.^[10]^[4] As of November 2025, the 2025 classification has received mixed reception, with some clinicians praising its practicality and stakeholder engagement, while others criticize lingering issues from the 2017 system, such as limited anatomofunctional detail for surgical planning, insufficient attention to external factors like sleep-activated or reflex seizures, and age-specific considerations. Ongoing debates include the "lumpers vs. splitters" approach to semiological overlaps and divergent needs across professions (e.g., neurosurgeons vs. pharmacists). Separate classifications for neonatal seizures and status epilepticus remain unresolved, and adoption varies among neurologists.^[11]

Focal Seizures

Definition and Onset

Focal seizures are defined as those originating within networks limited to one hemisphere of the brain, characterized by consistent ictal onset and preferential propagation patterns that may remain confined to the affected hemisphere or evolve further.^[12] According to the 2025 International League Against Epilepsy (ILAE) classification, these seizures are subdivided using key descriptors based on the level of consciousness and potential progression: focal preserved consciousness (FPC), where the individual remains aware and responsive; focal impaired consciousness (FIC), involving impaired awareness or responsiveness; and focal-to-bilateral tonic-clonic (FBTC), in which the seizure spreads to involve both hemispheres with complete loss of consciousness.^[12] This hemispheric limitation distinguishes focal seizures from generalized seizures, which involve bilateral networks from the outset.^[12] The initial semiology of focal seizures often begins with an aura, comprising subjective sensory experiences such as auditory hallucinations, psychic phenomena like déjà vu, or autonomic sensations including epigastric rising; these may be nonobservable to others, relying on patient recall.^[12] Observable manifestations can include focal clonic jerks or other motor signs, contrasting with nonobservable subjective cognitive changes that do not produce visible external signs.^[12] Onset can be discretely localized to specific cortical or subcortical structures or more widely distributed within one hemisphere, influencing the seizure's progression.^[12] Diagnosis of focal seizures typically involves electroencephalography (EEG) to identify unilateral ictal onset patterns, such as focal slow-wave activity, which supports the localized network involvement.^[12] Magnetic resonance imaging (MRI) is essential for detecting underlying structural causes, including cortical dysplasia or lesions that may trigger the seizure.^[12] Focal seizures account for approximately 60% of epilepsy cases, particularly predominant in adult-onset forms.^[13]

Seizures with Preserved Consciousness

Focal preserved consciousness seizures (FPC), classified as type 1.1 in the 2025 International League Against Epilepsy (ILAE) taxonomic hierarchy, originate within networks limited to one hemisphere while consciousness remains preserved, operationally defined by maintained awareness (recall of events) and responsiveness (normal response to verbal or motor tasks).^[3] These seizures, formerly known as simple partial seizures, allow the individual to remain fully aware of their surroundings and continue activities, though they may experience subjective symptoms without behavioral arrest.^[12] Semiology includes both observable and non-observable manifestations. Non-observable features often involve auras, such as epigastric sensations, olfactory hallucinations, or psychic phenomena like fear or déjà vu, originating from temporal or limbic structures. Observable signs may encompass focal motor phenomena (e.g., unilateral clonic jerks or versive head turning) or autonomic changes (e.g., piloerection or flushing), typically lasting seconds to a minute. For example, a patient might report an epigastric aura followed by brief arm twitching while remaining responsive and recalling the event fully.^[3] These seizures do not impair interaction and are often identified through patient history rather than witness observation alone. Diagnosis relies on detailed clinical history emphasizing preserved responsiveness and recall, supported by EEG showing unilateral ictal rhythms without bilateral spread during the event. Video-EEG monitoring can capture subtle focal discharges, such as rhythmic theta activity in the frontal lobe. Neuroimaging, including MRI, helps identify etiologies like tumors or malformations of cortical development. Challenges arise when symptoms are purely subjective, necessitating differentiation from non-epileptic events like migraines or panic attacks.^[12] Management focuses on treating the underlying epilepsy syndrome, with antiseizure medications such as carbamazepine or lamotrigine often effective for focal origins. Since consciousness is preserved, risks like injury are lower, allowing lifestyle accommodations like avoiding driving only if seizures evolve or cluster. Surgical options, such as resection, are considered for drug-resistant cases with identifiable foci.^[12]

Seizures with Impaired Consciousness

Focal impaired consciousness seizures (FIC), classified as type 1.2 in the 2025 International League Against Epilepsy (ILAE) taxonomic hierarchy, originate within networks limited to one hemisphere and involve impairment of consciousness, defined by lack of awareness (no recall) or responsiveness (failure to respond to verbal/motor prompts).^[3] Previously termed complex partial seizures, these events feature behavioral arrest or automatisms due to involvement of awareness-related networks, often in temporal or frontal lobes.^[12] Semiology typically begins with an aura (e.g., epigastric rising or auditory hallucination) transitioning to impaired responsiveness, with episodes lasting 30 seconds to 2 minutes. Observable manifestations include oroalimentary or manual automatisms (e.g., lip smacking, fumbling hands), dystonic posturing, or vocalizations, reflecting spread within the hemisphere. For instance, a temporal lobe seizure might present as staring with hand rubbing and no response to questions, followed by postictal confusion. Sensory or cognitive features like aphasia may occur without full generalization. Unlike preserved consciousness seizures, FIC inherently disrupts interaction, increasing risks of subtle progression unnoticed by witnesses.^[3] Diagnosis requires witness accounts of unresponsiveness combined with patient amnestic gaps, confirmed by EEG demonstrating unilateral ictal patterns (e.g., evolving spikes in the temporal region) evolving to impaired states. Video-EEG is essential to distinguish from absence seizures or psychogenic non-epileptic events, while MRI identifies structural lesions like hippocampal sclerosis. Caution is needed to exclude isolated aphasia or amnesia as the sole cause of apparent impairment.^[12] Management involves antiseizure medications tailored to focal epilepsy, such as levetiracetam or oxcarbazepine, with monitoring for evolution to bilateral tonic-clonic seizures. Due to impaired awareness, precautions against injury (e.g., driving restrictions) are critical. For refractory cases, interventions like vagus nerve stimulation or focal resection offer higher success rates when a seizure onset zone is localizable.^[12]

Evolution to Bilateral Tonic-Clonic

Focal to bilateral tonic-clonic (FBTC) seizures represent a subtype of focal seizures in which ictal activity originates in one hemisphere and propagates to involve both hemispheres, leading to impaired consciousness and bilateral motor manifestations. Under the International League Against Epilepsy (ILAE) classifications of 2017 and 2025, these seizures are categorized within the focal seizure domain (type 1.3), emphasizing their evolution from a localized onset to widespread bilateral involvement, distinct from seizures that remain confined to one hemisphere. This propagation mechanism underscores the dynamic nature of epileptiform activity in focal epilepsies, where network connectivity facilitates secondary generalization.^[4] The clinical sequence typically begins with a focal onset phase, which may include an aura (such as epigastric rising or déjà vu in temporal lobe cases), focal motor symptoms (e.g., unilateral clonic jerking or versive head movement), sensory disturbances, or impaired awareness lasting seconds. This is rapidly followed by bilateral tonic stiffening, characterized by rigid extension of the limbs and trunk, often accompanied by a cry or fall if the individual is upright, due to sudden loss of postural control. The tonic phase transitions into the clonic phase, marked by rhythmic, bilateral jerking movements that progressively decrease in frequency and amplitude, culminating in flaccid recovery. Postictally, patients experience prolonged confusion, fatigue, and sometimes focal deficits such as Todd's paralysis, with the entire event lasting 1-3 minutes on average.^[14]^[15]^[16] Electroencephalographic (EEG) findings during FBTC seizures illustrate this progression: initial unilateral rhythmic discharges, often delta or theta frequencies with evolving spikes, arise from the focal onset zone (e.g., temporal or frontal regions). As propagation occurs, these patterns synchronize bilaterally, showing low-voltage fast activity (20-50 Hz) during the tonic phase, followed by bilateral spike-and-wave complexes at 2-4 Hz during clonic jerking, which attenuate toward the end. Video-EEG monitoring is crucial for capturing this evolution, as surface EEG may miss subtle early focal changes in up to 20-30% of cases without intracranial recordings.^[17]^[18]^[19] Risk factors for the evolution to bilateral tonic-clonic involvement include underlying structural lesions, such as hippocampal sclerosis in mesial temporal lobe epilepsy, cortical dysplasias, or low-grade tumors, which disrupt normal inhibitory networks and promote spread. These seizures occur more frequently in adults with chronic focal epilepsies compared to children, with incidence rates up to 50% in temporal lobe epilepsy cohorts. Genetic predispositions and prior brain insults (e.g., trauma or infection) further elevate risk by altering cortical excitability.^[20]^[21]^[13] Distinction from primary generalized tonic-clonic seizures relies on identifying focal features, such as asymmetric onset in history (e.g., aura or unilateral symptoms), EEG evidence of unilateral ictal rhythms preceding bilateral synchronization, or neuroimaging revealing a focal etiology. In the absence of such indicators, seizures of unknown onset are classified separately under ILAE guidelines.^[15]^[4]

Generalized Seizures

Definition and Characteristics

Generalized seizures are epileptic events that originate within and rapidly engage bilaterally distributed networks, encompassing both cortical and subcortical structures, without detectable focal onset or involvement of the entire cortex from the beginning; onset may appear localized or asymmetric but engages bilateral networks swiftly.^[3] This contrasts with focal seizures, which start in networks confined to one cerebral hemisphere and may propagate secondarily.^[3] The International League Against Epilepsy (ILAE) 2025 classification organizes generalized seizures into three main categories: absence seizures, generalized tonic-clonic seizures, and other generalized seizures (including myoclonic, clonic, negative myoclonic, epileptic spasms, tonic, atonic, and myoclonic-atonic types).^[3] These seizures frequently arise from genetic or idiopathic etiologies, as exemplified in idiopathic generalized epilepsies such as juvenile myoclonic epilepsy, where hereditary factors predominate without identifiable structural lesions.^[22] Electroencephalography (EEG) characteristically reveals bilateral synchronous discharges, such as 3 Hz spike-and-wave complexes or polyspike-wave patterns, reflecting the widespread network involvement from seizure inception. Symmetric clinical manifestations across both hemispheres underscore their distinguishing feature, differentiating them from asymmetrical or unilateral focal presentations. Generalized seizures commonly manifest in childhood or adolescence, with syndromes like juvenile myoclonic epilepsy typically emerging around ages 12-18.^[3] They comprise approximately 15-20% of all epilepsy syndromes, highlighting their significant epidemiological impact.^[23]

Absence Seizures

Absence seizures are generalized nonmotor seizures characterized by a sudden, brief cessation of ongoing activity accompanied by impaired consciousness, without any preceding aura or subsequent postictal confusion.^[3] These episodes typically manifest as a blank stare or unresponsiveness, with the individual appearing momentarily "frozen" in place, and they resolve abruptly without residual effects.^[24] Under the ILAE 2025 classification, absence seizures are subdivided into four main subtypes based on clinical and electroencephalographic (EEG) features: typical absence seizures, atypical absence seizures, myoclonic absence seizures, and eyelid myoclonia with or without absence.^[3] Typical absence seizures involve a sudden onset of impaired awareness with minimal motor signs, such as subtle eyelid fluttering or lip smacking, and are associated with a characteristic 3 Hz generalized spike-and-wave discharge on EEG.^[25] Atypical absence seizures feature a more gradual onset and offset, with longer durations and less complete impairment of consciousness, often showing slower (<2.5 Hz) spike-and-wave patterns on EEG and occurring in individuals with developmental or neurological impairments.^[25] Myoclonic absence seizures combine impaired awareness with rhythmic bilateral myoclonic jerks, typically at 3 Hz, affecting the shoulders and arms, leading to progressive arm elevation during the event.^[25] Eyelid myoclonia with or without absence presents as rapid (4-6 Hz) myoclonic jerks of the eyelids, often triggered by eye closure, and may include brief lapses in awareness.^[25] Typical absence seizures generally last 5-10 seconds and are most prevalent in children diagnosed with childhood absence epilepsy, a common idiopathic generalized epilepsy syndrome with onset between ages 4 and 10 years.^[26] These seizures lack convulsive motor activity, distinguishing them from other generalized seizure types that involve prominent tonic or clonic movements.^[3] Hyperventilation is a well-established trigger, reliably provoking episodes in over 90% of susceptible individuals during EEG testing.^[27] Differentiation from focal seizures with impaired awareness relies on EEG findings, where absence seizures show bilateral synchronous generalized discharges, whereas focal onset seizures exhibit unilateral or regional abnormalities.^[28]

Tonic-Clonic Seizures

Generalized tonic-clonic seizures (GTCS), also known as grand mal seizures, are a type of generalized seizure characterized by bilateral symmetric involvement of the cerebral cortex and subcortical structures, leading to loss of consciousness and convulsive motor activity. According to the International League Against Epilepsy (ILAE) 2025 classification, GTCS originate within and rapidly engage bilaterally distributed networks without evidence of a focal onset. The seizure progresses through distinct phases: an initial tonic phase involving widespread muscle stiffening and increased electromyographic tone, often accompanied by a cry or vocalization due to diaphragmatic contraction, followed by a clonic phase of rhythmic jerking movements that gradually slow and transition to a flaccid postictal state.^[3]^[12]^[29] In the ILAE 2025 update, GTCS include specific variants such as myoclonic GTCS, which are preceded by brief myoclonic jerks, and absence-to-tonic-clonic seizures that follow an absence episode. Electroencephalography (EEG) during GTCS typically shows generalized polyspike-and-wave discharges at 3-6 Hz, particularly in associated syndromes like juvenile myoclonic epilepsy (JME). These seizures are strongly linked to idiopathic generalized epilepsies, including JME, where GTCS occur in nearly all affected individuals, often in the morning shortly after awakening. Common triggers include sleep deprivation, which is the most potent precipitant, as well as stress, alcohol consumption, and photic stimulation from flashing lights.^[3]^[12]^[30]^[29] GTCS typically last 1 to 3 minutes before spontaneous resolution, though durations up to 5 minutes are common without indicating status epilepticus. The postictal phase involves confusion, somnolence, headache, and muscle soreness, lasting from minutes to hours. These seizures carry significant risks, including physical injuries such as tongue biting (occurring in about 22% of cases due to trismus during the tonic phase), falls leading to fractures or bruises, and urinary incontinence; they are also associated with higher morbidity, including sudden unexpected death in epilepsy (SUDEP). Unlike focal-to-bilateral tonic-clonic seizures, GTCS lack any initial focal clinical or EEG features.^[31]^[32]^[29]^[3]

Other Motor Seizures

Other motor seizures in the generalized category encompass a range of bilateral, symmetric motor manifestations distinct from tonic-clonic seizures, including myoclonic, clonic, tonic, atonic, myoclonic-atonic, and epileptic negative myoclonus types. These seizures typically arise from widespread cortical networks and are classified under the 2025 ILAE framework as "other generalized seizures" to highlight their non-progressive nature and varied electroclinical features.^[3] Myoclonic seizures involve sudden, brief (<200 ms), shock-like muscle jerks that are bilaterally distributed, often affecting proximal limbs such as the shoulders or arms. These jerks may occur singly or in clusters upon awakening and are a hallmark of syndromes like juvenile myoclonic epilepsy (JME), where they represent the primary seizure type in up to 90% of cases. Electroencephalographic (EEG) correlates typically show generalized spike-and-wave or polyspike-and-wave discharges time-locked to the jerks, reflecting synchronous thalamocortical activation.^[3]^[33] Clonic seizures are characterized by sustained, rhythmic, repetitive muscle jerking (1-3 Hz) across bilateral body regions without an initial tonic phase, distinguishing them from the more common tonic-clonic progression. These events are less frequent in isolation but can manifest in certain generalized epilepsies, with EEG patterns featuring generalized rhythmic spike-and-wave discharges that evolve in frequency during the seizure.^[3] Tonic seizures entail abrupt, sustained muscle contraction leading to stiffening of the limbs, trunk, or axial muscles, often resulting in sudden drops or falls if postural control is affected. They are prominent in Lennox-Gastaut syndrome (LGS), where nocturnal tonic events occur in over 70% of patients and contribute to the syndrome's refractory nature. EEG during these seizures commonly displays generalized low-voltage fast activity (around 10-20 Hz) or an electrodecremental pattern, indicating diffuse cortical suppression amid hypertonia.^[3]^[34] Atonic seizures feature a sudden loss of postural muscle tone, causing head nods, slumps, or complete falls (drop attacks) that are brief (1-2 seconds) and bilateral. These are particularly hazardous due to injury risk and often cluster in syndromes like LGS. EEG findings include generalized spike-and-wave or polyspike-and-wave complexes correlating with the atonic phase.^[3] Myoclonic-atonic seizures combine a rapid myoclonic jerk with immediate loss of tone, leading to abrupt falls; this sequence is emblematic of epilepsy with myoclonic-atonic seizures (EMAS, or Doose syndrome), affecting children aged 2-5 years with multiple daily events. The EEG typically mirrors that of myoclonic seizures, with generalized spike-and-wave discharges preceding the atonic component.^[3]^[35] A novel addition in the 2025 ILAE classification is epileptic negative myoclonus, defined as brief (<500 ms) interruptions in ongoing muscle activity without a positive jerk, manifesting as involuntary pauses or lapses in limb movement during voluntary actions. This type, previously underrecognized, is now formalized as a distinct entity, often linked to generalized epilepsies with subtle semiology; EEG shows generalized spike-and-wave or sharp-wave discharges precisely time-locked to electromyographic (EMG) silence, enabling diagnosis via video-EEG.^[3]

Unknown Onset Seizures

Definition and Classification

Unknown onset seizures are classified as such when there is insufficient information to determine whether the seizure is focal or generalized in origin, serving as a provisional category for epileptic events confirmed by clinical history or other data but lacking definitive onset details.^[4] This classification applies in situations where electroencephalography (EEG) or detailed witness accounts are unavailable or inconclusive, distinguishing it from unclassified seizures that lack even basic epileptic confirmation.^[4] In the 2025 International League Against Epilepsy (ILAE) update, unknown onset seizures are subcategorized based on level of consciousness and semiology, using terms such as preserved consciousness (PC), impaired consciousness (IC), and bilateral tonic-clonic (BTC).^[4] These descriptors allow for structured description without specifying onset: PC seizures involve maintained awareness, IC seizures feature altered responsiveness, and BTC seizures exhibit symmetric motor involvement evolving to tonic-clonic activity.^[4] Unlike definitive focal (unilateral onset) or generalized (bilateral onset) classes, this framework emphasizes observable features to guide initial management.^[4] Common scenarios leading to unknown onset classification include unwitnessed events, such as nocturnal seizures occurring during sleep without video-EEG monitoring, or observed episodes without access to real-time neurophysiological data.^[4] For instance, bilateral tonic-clonic seizures presenting with normal postictal EEG or imaging often fall into this category initially due to obscured onset.^[4] Reclassification is possible and encouraged with additional diagnostic tools, such as prolonged EEG, video monitoring, or refined patient history, potentially shifting the seizure to focal or generalized based on emerging evidence of onset patterns.^[4] In clinical settings, particularly emergencies, a notable proportion of new-onset seizures may initially receive an unknown onset designation due to limited immediate data, underscoring its relevance for prompt symptomatic treatment while awaiting further evaluation.^[36] This provisional approach facilitates standardized care in resource-constrained environments like emergency departments.^[36]

Seizures with Preserved Consciousness

Seizures with preserved consciousness of unknown onset, as defined in the International League Against Epilepsy (ILAE) 2025 classification, occur when the initial brain involvement cannot be determined as focal or generalized due to unobserved or obscured onset, yet the individual maintains full awareness of self and surroundings throughout the event.^[3] These are termed "unknown whether focal or generalized - preserved consciousness seizure (PC)" and are characterized by the absence of any impairment in responsiveness or recall, distinguishing them from seizures involving altered states.^[12] This category applies to brief events where consciousness is explicitly preserved, allowing the person to continue activities or respond appropriately despite the seizure activity.^[3] Manifestations of these seizures are typically subtle and short-lived, often involving sudden motor phenomena such as myoclonic jerks—brief, shock-like muscle contractions—or nonmotor sensory experiences like tingling or visual flashes, without any disruption to ongoing behavior.^[6] For instance, observable signs may include piloerection (goosebumps) or facial flushing in a fully aware individual, as seen in case examples from clinical reports.^[3] These features may closely resemble those of focal preserved consciousness seizures but lack sufficient evidence to confirm localized onset.^[12] In some cases, such as idiopathic generalized myoclonus with unclear onset, the events present as isolated jerks upon awakening, maintaining complete awareness.^[6] Diagnosing these seizures poses significant challenges, primarily relying on patient history and witness descriptions since the onset is not captured, often leading to initial classification as unknown.^[3] Electroencephalography (EEG), particularly video-EEG monitoring, may later reveal patterns to reclassify the event as focal or generalized, but in the absence of such data, assessment focuses on preserved responsiveness during the episode.^[6] This diagnostic uncertainty underscores the need for detailed semiology to differentiate from nonepileptic events or other seizure types. Management of unknown onset seizures with preserved consciousness emphasizes a conservative approach, treating them as the lowest risk category until further evaluation allows reclassification, often involving observation, lifestyle adjustments, or low-dose antiseizure medications if recurrent.^[12] Supportive tests like EEG or imaging guide potential adjustments to therapy, prioritizing minimal intervention given the preserved awareness and typically benign course.^[3]

Seizures with Impaired Consciousness

Seizures with impaired consciousness of unknown onset, as defined in the 2025 International League Against Epilepsy (ILAE) classification, involve a loss of awareness and/or responsiveness without identifiable focal or generalized origin, often manifesting as staring or behavioral arrest.^[4] These events may represent equivalents to absence seizures when onset details are unavailable, such as in unwitnessed episodes.^[37] Consciousness impairment is operationally assessed by the inability to recall the event or respond to verbal or motor prompts during its occurrence.^[4] The semiology typically includes automatisms, such as repetitive lip-smacking or hand fumbling, alongside periods of unresponsiveness, with episodes lasting 10-30 seconds on average.^[38] In cases without video-EEG confirmation, classification relies on witness descriptions, highlighting the need for prompt diagnostic evaluation. Misclassification of these seizures can elevate injury risks, as unaddressed episodes may lead to falls or accidents without appropriate interventions.^[39] Urgent electroencephalography (EEG) is recommended to clarify onset and guide treatment, potentially reclassifying the event as focal or generalized.^[37] Differentiation from syncope is aided by the absence of prodromal pallor or sweating, which are characteristic of vasovagal events but rare in epileptic impairments.^[40] In contrast to seizures with preserved consciousness, which allow maintained responsiveness as a milder variant, impaired consciousness events disrupt interaction entirely.^[4]

Bilateral Tonic-Clonic Seizures

Bilateral tonic-clonic seizures of unknown onset, abbreviated as BTC, occur when a full convulsive seizure is observed without sufficient information to determine whether it begins focally or diffusely across both hemispheres of the brain. These seizures are classified under the "unknown onset" category in the International League Against Epilepsy (ILAE) 2025 updated classification system, serving as the default designation for unwitnessed or incompletely observed convulsions that exhibit bilateral motor involvement.^[4] This classification applies particularly to scenarios where the onset phase is missed, such as during sleep or in unattended settings, ensuring a practical approach to diagnosis when detailed history or electroencephalographic (EEG) data is unavailable at the time of the event.^[3] The clinical sequence of bilateral tonic-clonic seizures of unknown onset mirrors that of generalized tonic-clonic seizures (GTCS) or focal to bilateral tonic-clonic (FBTC) seizures, beginning with a tonic phase characterized by sudden bilateral stiffening of the extremities, trunk, and often the face, accompanied by a cry and loss of consciousness. This is followed by a clonic phase of rhythmic, bilateral jerking movements that gradually decrease in frequency, culminating in a postictal period of flaccidity, confusion, and exhaustion lasting minutes to hours.^[4] These seizures typically last 1-3 minutes but can recur or evolve into status epilepticus if untreated.^[29] Bilateral tonic-clonic seizures represent the most common subtype among unknown onset seizures, frequently encountered in emergency settings where onset details are obscured. In population-based studies of first-time seizures in adults, unknown onset tonic-clonic events comprise a substantial portion, with generalized or unknown onset seizures accounting for over 50% of cases and focal to bilateral tonic-clonic adding nearly 30%.^[41] Moreover, convulsive status epilepticus—predominantly bilateral tonic-clonic—constitutes about 42.5% of all status epilepticus episodes in adults, highlighting its prevalence in prolonged seizure scenarios.^[42] To clarify the underlying onset, video-EEG monitoring is the gold standard investigation, capturing ictal EEG patterns to distinguish focal origins (e.g., unilateral rhythmic activity spreading bilaterally) from truly generalized discharges, often combined with neuroimaging like MRI to identify structural etiologies.^[4] Prognosis aligns closely with that of equivalently classified known-onset seizures, influenced by underlying etiology, age, and prompt intervention, though these events carry high treatment priority due to risks of respiratory compromise, injury, and progression to refractory status epilepticus with mortality rates of 16-20% for initial episodes.^[43]

Special Seizure Types

Epileptic Spasms

Epileptic spasms are characterized by clusters of brief, symmetric flexor or extensor contractions involving the trunk, neck, and limbs, typically occurring in infants. These spasms often present as sudden flexion of the trunk with elevation and extension of the arms, resembling a "jackknife" motion, and last 1-2 seconds each, with clusters of 3-15 spasms happening multiple times daily, particularly upon waking. They peak in incidence between 4 and 8 months of age and are a hallmark of infantile epileptic spasms syndrome (IESS), formerly known as West syndrome.^[3]^[44] In the 2025 International League Against Epilepsy (ILAE) classification, epileptic spasms are categorized under generalized other motor seizures, specifically as generalized epileptic spasms (GES). This placement reflects their bilateral, symmetric nature without a clear focal onset in most cases, distinguishing them from focal motor seizures. Electroencephalography (EEG) during spasms typically shows hypsarrhythmia—a chaotic, high-amplitude, multifocal spike-and-wave pattern—or electrodecremental suppression, which is pathognomonic for IESS and aids in diagnosis.^[12]^[3]^[44] The etiology of epileptic spasms is predominantly structural or genetic, with up to 60% of cases linked to identifiable causes such as brain malformations, perinatal insults, or genetic mutations. Common genetic associations include mutations in TSC1 or TSC2 genes causing tuberous sclerosis complex (TSC), as well as variants in ARX, CDKL5, and STXBP1, which disrupt neuronal development and are unique to the infantile period due to age-specific brain vulnerability. Their presentation is distinct from other infantile seizures owing to this developmental window, where immature cortical networks facilitate the spasm clusters. Untreated spasms may evolve into more refractory epilepsy syndromes, such as Lennox-Gastaut syndrome, in approximately one-third of cases.^[44]^[45]^[46] Treatment focuses on rapid cessation of spasms to optimize neurodevelopmental outcomes, with adrenocorticotropic hormone (ACTH) or vigabatrin as first-line therapies. ACTH, administered as high-dose intramuscular injections, achieves spasm cessation in 50-80% of cases within two weeks, while vigabatrin—a GABA analog—is particularly effective in TSC-associated spasms, with response rates exceeding 90% in those subgroups. These interventions are prioritized over other antiseizure medications due to their targeted efficacy in IESS, and early treatment within weeks of onset significantly reduces the risk of cognitive impairment.^[44]^[47]^[48]

Neonatal Seizures

Neonatal seizures are defined as sudden, paroxysmal electrographic events occurring in newborns within the first 28 days of life, with an incidence of 1 to 4 per 1,000 live births in full-term infants and up to 130 per 1,000 in preterm infants.^[49] These seizures often present with subtle clinical manifestations due to the immature neonatal brain, such as rowing or bicycling limb movements, ocular deviation, or minor myoclonic jerks, which can be difficult to distinguish from normal neonatal behaviors.^[50] Focal clonic seizures are the most common type, while generalized seizures are less frequent; notably, 60% to 80% of confirmed electrographic seizures are subclinical, lacking visible signs and detectable only through EEG monitoring.^[51] This high rate of electrical-only activity underscores the limitations of clinical observation alone in neonates.^[49] The primary causes of neonatal seizures include hypoxic-ischemic encephalopathy (HIE), accounting for 35% to 45% of cases, metabolic disturbances such as hypoglycemia, and genetic etiologies like mutations in the KCNQ2 gene.^[49] HIE often results from perinatal asphyxia, leading to brain injury that manifests as seizures shortly after birth.^[50] Metabolic causes, including electrolyte imbalances or inborn errors of metabolism, are provoked by transient factors and may resolve with correction, whereas genetic forms, such as self-limited neonatal epilepsy due to KCNQ2 variants, represent unprovoked events comprising about 15% of neonatal seizure cases.^[50] Diagnosis relies heavily on electroencephalography (EEG), as clinical signs are unreliable; video-EEG monitoring is the gold standard, with recommendations for at least 24 hours of continuous recording to capture subclinical events.^[50] Common EEG patterns include burst suppression, characterized by alternating periods of high-voltage bursts and suppression, particularly in severe cases like those associated with HIE or early-onset epileptic encephalopathies.^[49] Recent guidelines emphasize quantitative EEG and amplitude-integrated EEG for improved detection in neonatal intensive care settings.^[49] Prognosis for neonatal seizures is guarded, with high rates of mortality and long-term morbidity, including neurodevelopmental delays, influenced by seizure burden and underlying etiology; for instance, HIE-related seizures carry poorer outcomes compared to benign genetic forms.^[51] These seizures are distinct from epileptic spasms seen in older infants, differing in timing, typical EEG features, and clustering patterns.^[50] Subclinical seizures, which may persist continuously, further contribute to brain injury risk if undetected.^[49]

Continuous and Subclinical Seizures

Continuous seizures refer to prolonged or ongoing epileptic activity that does not resolve spontaneously, distinguishing them from discrete, self-limited events. A primary example is nonconvulsive status epilepticus (NCSE), characterized by continuous or nearly continuous electrographic seizure activity lasting more than 10 minutes, accompanied by subtle cognitive, behavioral, or autonomic changes without prominent motor manifestations.^[52] This condition contrasts with convulsive status epilepticus by lacking overt convulsions, yet it requires urgent recognition due to its potential for neuronal injury.^[53] Subclinical seizures, also known as electrographic-only seizures, involve epileptiform activity detected exclusively on electroencephalography (EEG) without corresponding clinical signs. These are prevalent in critically ill populations, occurring in 8–27% of comatose intensive care unit (ICU) patients and frequently post-stroke, where they may contribute to unexplained encephalopathy.^[53]^[54] In the 2025 International League Against Epilepsy (ILAE) classification, both continuous and subclinical seizures can be categorized as focal (originating in one hemisphere), generalized (engaging bilateral networks), or of unknown onset when the distinction is unclear.^[3] Negative myoclonus, recognized as a distinct generalized seizure type, exemplifies a brief continuous form involving abrupt interruptions of muscle tone lasting less than 500 milliseconds, often linked to ongoing epileptiform discharges.^[3]^[55] Diagnosis of continuous and subclinical seizures relies on continuous EEG (cEEG) monitoring, which is essential in high-risk settings like ICUs or post-stroke care to identify rhythmic delta activity, repetitive spikes, or evolving patterns indicative of ictal activity.^[56] The modified Salzburg Consensus Criteria, for instance, require EEG changes persisting for at least 10 seconds in abnormal recordings, integrated with clinical context, achieving over 90% diagnostic accuracy.^[56] Treatment typically begins with intravenous benzodiazepines such as lorazepam for acute termination, followed by second-line agents like levetiracetam or phenytoin, and refractory cases may necessitate anesthetic coma induction with propofol or pentobarbital.^[53] These seizure forms carry significant risks, including cognitive decline, with survivors of NCSE facing elevated probabilities of memory, learning, and executive function deficits compared to those with multiple discrete seizures.^[57] In post-stroke contexts, undetected subclinical activity heightens the likelihood of neurological deterioration and epilepsy recurrence.^[54] For example, subclinical seizures in neonates, identified via amplitude-integrated EEG, underscore the need for vigilant monitoring across age groups to mitigate long-term neurodevelopmental impacts.^[58]

Unclassified Seizures

Unclassified seizures represent a category in the 2025 International League Against Epilepsy (ILAE) classification for epileptic events that cannot be assigned to focal, generalized, or unknown onset classes due to inadequate or absent information about their characteristics. This designation applies when clinicians are confident the event is epileptic but lack sufficient data, such as detailed semiology, electroencephalographic (EEG) findings, or video-EEG documentation, to enable more precise categorization. Unlike other classes, unclassified seizures serve as a provisional label, emphasizing the need for additional evaluation rather than a definitive subtype.^[4] The criteria for classifying a seizure as unclassified are stringent and typically arise in scenarios with limited historical or observational details, such as brief, unwitnessed events or incomplete medical records. These seizures are rare in clinical practice, comprising less than 5% of documented epileptic events, as most can be reclassified with targeted investigations. In experimental models of epilepsy, unclassified seizures may occur when induced phenomena do not align with standard focal or generalized patterns, providing opportunities to study atypical mechanisms. The 2025 ILAE update simplifies this category by eliminating subtypes, focusing instead on encouraging comprehensive follow-up to facilitate reclassification into more informative groups.^[4]^[59] Clinically, management of unclassified seizures involves a multidisciplinary approach, including neurologists, epileptologists, and sometimes neuropsychologists, to review available semiology and pursue diagnostic tools like prolonged EEG monitoring or neuroimaging. Provisional treatment is guided by observable features, such as motor manifestations or duration, often starting with broad-spectrum antiseizure medications while prioritizing further investigation. This category plays a key role in research, acting as a placeholder in databases that supports the identification of novel seizure types through accumulated data and advanced analytics.^[4]^[60]

References

[1]
Epileptic seizures and epilepsy: definitions proposed by ... - PubMed
An epileptic seizure is a transient occurrence of signs and/or symptoms due to abnormal excessive or synchronous neuronal activity in the brain.<|control11|><|separator|>
[2]
A practical guide to the updated seizure classification 2025
Oct 13, 2025 · The ILAE seizure classification offers a logical, structured framework and standardized terminology, a common language for managing people with ...
[3]
[PDF] Updated classification of epileptic seizures: Position paper of the ...
Feb 14, 2025 · The four main classes are: Focal, Generalized, Unknown (whether focal or generalized), and Unclassified.
[4]
Updated classification of epileptic seizures: Position paper of the ...
Apr 23, 2025 · The main seizure classes include Focal, Generalized, Unknown (whether focal or generalized), and Unclassified. Figures 1 and 2 illustrate the ...
[5]
The evolution of the concepts of seizures and epilepsy: What's in a ...
It was during the time of John Hughlings Jackson (1835‐1911) that the field of neurology and epileptology was beginning to establish itself. Jackson used the ...
[6]
[PDF] Operational classification of seizure types by the International ...
Mar 8, 2017 · The new classification does not represent a fundamental change, but allows greater flexibility and transparency in naming seizure types. KEY ...
[7]
Evaluation of the International League Against Epilepsy 1981, 1989 ...
In ILAE‐1981, the seizures were classified into partial, generalized, and unclassifiable seizure onset. The partial seizures involved initial clinical and EEG ...
[8]
Neuroimaging in the Definition and Organization of the Epilepsies
Neuroimaging significantly impacts the diagnosis and treatment of epilepsy patients. Despite its importance, MRI has been marginally incorporated into concepts ...
[9]
Operational classification of seizure types by the International ...
Mar 8, 2017 · The expanded ILAE 2017 operational classification of seizure types. The following clarifications should guide the choice of seizure type.
[10]
Updated classification of epileptic seizures (2025)
Apr 23, 2025 · The updated classification maintains four main seizure classes: Focal, Generalized, Unknown (whether focal or generalized), and Unclassified — ...Operational Classification 2017Separate position paper
[11]
https://pmc.ncbi.nlm.nih.gov/articles/PMC12618206/
[12]
Focal (Partial) Epilepsy: Background, Pathophysiology, Etiology
Feb 25, 2025 · Approximately 60% of adult-onset epilepsies are focal epilepsies. Males are slightly more affected; however, this is thought to be related ...Background · Pathophysiology · Etiology · Epidemiology
[13]
[PDF] Instruction manual for the ILAE 2017 operational classification of ...
Mar 8, 2017 · The International League Against Epilepsy (ILAE) has released a 2017 version of seizure-type classification (ac- companying manuscript).
[14]
Seizures and epilepsy - Knowledge @ AMBOSS
Jul 22, 2025 · If the time from seizure onset is unknown, begin management for status epilepticus. Acute seizures are often self-limited and may not ...
[15]
Clinical and paraclinical features of first unprovoked seizures in the ...
Previous research on elderly patients with new-onset epilepsy indicated that 12.5 %–22.3 % of seizures were of unknown origin [8], [9]. Few studies focused on ...
[16]
The causes of new-onset epilepsy and seizures in the elderly - PMC
New-onset epilepsy in elderly people often has underlying etiology, including cerebrovascular diseases, primary neuron degenerative disorders, intracerebral ...Missing: semiology syncope
[17]
How to Differentiate Syncope from Seizure - PubMed
The most important step to an accurate diagnosis is a fastidious history. Inducing syncope with tilt table testing and documenting heart rate changes during ...
[18]
Focal Bilateral Tonic Clonic Seizures - Epilepsy Foundation
These seizures are called focal to bilateral tonic-clonic, because they start in a limited area on one side of the brain and spread to involve both sides.
[19]
FOCAL TO BILATERAL TONIC-CLONIC SEIZURE
A focal seizure may spread to involve wider brain networks, resulting in a focal to bilateral tonic-clonic seizure. This was previously known as a 'secondary ...
[20]
Bilateral tonic-clonic seizure: MedlinePlus Medical Encyclopedia
Mar 31, 2024 · The seizures often result in rigid muscles (tonic phase). This is followed by violent muscle contractions (clonic phase). Other symptoms that ...
[21]
Seizures - Learning EEG
Focal seizures have a single area from which they originate. They can be categorized into focal aware, focal impaired aware, or focal to bilateral tonic clonic ...
[22]
Predictors of focal to bilateral tonic-clonic seizures during long-term ...
Objective: To determine predictors of focal to bilateral tonic-clonic seizures (FBTCS) during video-electroencephalography (EEG) monitoring (VEM).
[23]
Detection of focal to bilateral tonic–clonic seizures using a ...
May 23, 2024 · This study was undertaken to develop and evaluate a machine learning-based algorithm for the detection of focal to bilateral tonic–clonic seizures (FBTCS)
[24]
Secondarily generalized seizures in temporal lobe epilepsy - PubMed
Secondarily generalized tonic-clonic seizure (SGTCS) may occur rarely in temporal lobe epilepsy (TLE), but SGTCS is the major risk factor for sudden death.
[25]
Temporal Lobe Epilepsy (TLE)
One of the most common findings is scarring in the temporal lobe. This is called hippocampal sclerosis (sclerosis means hardening or scarring).Main Navigation Sidebar · What Type Of Seizures Are... · How Is Tle Diagnosed?
[26]
Idiopathic (Genetic) Generalized Epilepsy - StatPearls - NCBI - NIH
It is estimated that over 50 million people are affected by epilepsy worldwide. The pathophysiology of epilepsy will depend on its etiology, with ...Introduction · Epidemiology · History and Physical · Treatment / Management
[27]
Genetic generalized and focal epilepsy prevalence in the North ...
Sixty-eight percent (28/41) of GGE, 100% (24/24) of DEE, and 66% (63/95) of FE cases were medically refractory, defined as failing at least 2 ASMs. The last ...
[28]
Absence Seizure - StatPearls - NCBI Bookshelf - NIH
Apr 20, 2024 · Absence seizures are characterized by behavioral arrest and EEG showing 3-Hz spike and wave discharges. Episodes usually occur multiple times ...
[29]
[PDF] Definitions of generalized epileptic seizure types
Duration is typically 7–12 s, but occasionally longer (up to 60 s) and may occur multiple times per day. Ictal EEG shows regular 3Hz, bilateral-synchronous (“ ...
[30]
Absence seizures - Symptoms, diagnosis and treatment
May 7, 2025 · Absence seizures with special features include myoclonic absence and eyelid myoclonia, characteristic of Jeavons syndrome. History and exam ...
[31]
Out of thin air: Hyperventilation-triggered seizures - ScienceDirect.com
Jan 15, 2019 · Hyperventilation triggers absence seizures. SWDs are triggered by voluntary hyperventilation in over 90% of patients with absence epilepsy ...
[32]
Focal Impaired Awareness Seizure - StatPearls - NCBI Bookshelf - NIH
Mar 19, 2024 · Focal impaired awareness seizures refer to focal seizures that start in one hemisphere of the brain and are associated with impairment in consciousness.
[33]
Generalized Tonic-Clonic Seizure - StatPearls - NCBI Bookshelf - NIH
Patients with generalized tonic-clonic seizures are at increased risk of psychiatric disorders, cognitive impairment, sleep disorders, cardiovascular disease, ...
[34]
Juvenile Myoclonic Epilepsy (JME)
Mar 12, 2019 · Generalized tonic-clonic seizures are seen in nearly all people with JME. They usually begin a few months after the myoclonic jerks start.
[35]
Duration of epileptic seizure types: A data‐driven approach - NIH
Most typical absence seizures had durations less than 27 s (with outliers up to 32 s), whereas atypical absence seizures had durations up to 100 s. Most focal ...
[36]
https://www.sciencedirect.com/science/article/pii/S152550502400307X
[37]
Juvenile Myoclonic Epilepsy - StatPearls - NCBI Bookshelf - NIH
Myoclonic seizures are the hallmark of this condition and are necessary for the diagnosis of JME. Only occasionally they will manifest as the only seizure type.Continuing Education Activity · Pathophysiology · History and Physical · Evaluation
[38]
Lennox-Gastaut Syndrome
Jul 19, 2024 · Common seizure types include: Tonic seizures (stiffening of the body, upward eye gaze, dilated pupils, and altered breathing patterns)
[39]
Myoclonic Atonic Epilepsy Doose Syndrome
Nov 23, 2019 · Drop seizures, characterized by an abrupt fall with loss of body tone (atonic) or by a brief body jerk followed by an abrupt fall (myoclonic ...
[40]
Causes and prognosis of adults experiencing a first seizure in ...
Feb 17, 2024 · Most seizures had a generalized onset/unknown onset (53.9%) or were focal to bilateral tonic–clonic (28.3%), with fewer being focal with ...
[41]
Epidemiology of status epilepticus in adults: A population‐based ...
Nov 26, 2018 · We assume that the high incidence is due to a high proportion (34.4%) of NCSE in our study. This is more than 2.5 times higher than the 13% of “ ...<|control11|><|separator|>
[42]
Status Epilepticus - StatPearls - NCBI Bookshelf - NIH
May 8, 2023 · The findings of convulsive status epilepticus include generalized tonic-clonic movements of the extremities and impaired mental status.
[43]
Infantile Epileptic Spasms Syndrome (West Syndrome) - NCBI - NIH
Infantile spasms is a seizure disorder that was first described by William West in 1841 and has been referred to as West syndrome.
[44]
West Syndrome - Symptoms, Causes, Treatment | NORD
These spasms usually begin in the early months after birth and can sometimes be helped with medication. They can also occur in older patients; if this happens, ...
[45]
West syndrome: a comprehensive review - PMC - PubMed Central
Aug 22, 2020 · Mutations in either the TSC1 ... Mutations of CDKL5 cause a severe neurodevelopmental disorder with infantile spasms and mental retardation.
[46]
Management of infantile spasms - Nelson - Translational Pediatrics
Treatment of infantile spasms has little class I data, but adrenocorticotropic hormone (ACTH), prednisolone and vigabatrin have the best evidence as first-line ...<|control11|><|separator|>
[47]
Infantile Spasms | West Syndrome - Epilepsy Foundation
Jan 6, 2020 · Infantile spasms (West Syndrome) begins at 3-12 months, usually ending by age 4. Learn more at the Epilepsy Foundation.
[48]
Neonatal Seizures: New Evidence, Classification, and Guidelines
This review will provide updated knowledge about the pathophysiology of neonatal seizures, classification of the provoked seizures and neonatal epilepsies.Neonatal Seizures: New... · Eeg Monitoring In Complex... · Quantitative Eeg And...
[49]
Neonatal Seizures and Neonatal Epilepsy - StatPearls - NCBI - NIH
Nov 14, 2024 · Seizures are common in neonates, particularly in the first month of life. Neonatal seizures can be either provoked or unprovoked.
[50]
Neonatal Seizures | Pediatrics In Review - AAP Publications
Jul 1, 2024 · Neonatal seizures are difficult to recognize clinically and require electroencephalographic monitoring for accurate diagnosis; ...
[51]
Epidemiology, diagnosis, and management of nonconvulsive status ...
Nonconvulsive status epilepticus (NCSE) is a state of continuous seizure activity for at least 30 minutes, with cognitive or behavioral changes.
[52]
Poststroke Seizure and Epilepsy: A Review of Incidence, Risk ...
If the early EEG shows epileptiform discharge, there is a 3.8 times greater risk of seizures than patients with a normal early poststroke EEG [29]. It is ...
[53]
Myoclonic seizures | MedLink Neurology
Epileptic negative myoclonus. Focal or generalized, epileptic negative myoclonus is a motor symptom characterized by abrupt and brief (< 500 ms) interruption ...
[54]
EEG criteria for diagnosing nonconvulsive status epilepticus in ... - NIH
Nov 17, 2023 · The mainstay of diagnosing NCSE is an electrographic seizure (ESz) and electrical status epilepticus (ESE) detected on EEG in the presence of clinical ...
[55]
Status epilepticus in older adults: A critical review
May 14, 2025 · Survivors of SE are also at increased risk of cognitive impairment, including deficits in memory, learning, and executive function, suggesting ...
[56]
Nonconvulsive Status Epilepticus: The Encephalopathic Pediatric ...
Mar 1, 2012 · The presence of clinical seizures and acute neuroimaging abnormality was associated with an 82% probability of NCSE. All but 1 patient with NCSE ...
[57]
(PDF) Experimental Epilepsy Models and Morphologic Alterations of ...
Jun 3, 2015 · ... Unclassified. seizures. In experimental epilepsy studies, animal models have been developed according to this. classification (Table-1) ...<|separator|>
[58]
Updated Classification of Epileptic Seizures: Position paper of the ...
It would define if other people perceive the seizures, or the only one who perceives them is the patient. This new categorization could help to define social ...