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Seizure types
Seizure types
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In the field of neurology, seizure types refer to clinically and electrographically defined categories of seizures, based on observable features, underlying mechanisms, and diagnostic findings. A seizure is a paroxysmal episode of altered behavior, sensation, awareness, or autonomic function resulting from abnormal, excessive, or synchronous neuronal activity in the brain.[1]

Seizure classification plays a central role in the diagnosis and treatment of epilepsy and related disorders. It guides therapeutic decisions, informs prognosis, and supports communication among clinicians, researchers, and patients. The International League Against Epilepsy (ILAE) is the primary body responsible for defining seizure classifications. Its frameworks have evolved to reflect advances in neuroimaging, electrophysiology, and clinical semiology. The most recent system, published in 2025, introduces refined seizure categories aimed at improving diagnostic accuracy and clinical utility.[2]

Classification systems

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Historical background

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Descriptions of seizures date back to ancient Mesopotamia. Around 2500 B.C., Sumerian texts included early references to seizure-like events. By approximately 1050 B.C., Babylonian scholars had developed the first known classification of seizures, inscribed on the stone tablets of the Sakikku ("All Diseases"). This early system recognized seizure types that correspond to febrile seizures, absence seizures, generalized tonic-clonic seizures, focal seizures, impaired awareness seizures, and status epilepticus.[3][4] In the 18th century, Samuel-Auguste Tissot described grand état (now recognized as generalized tonic-clonic seizures) and petit état (absence seizures) in his work Traité de l’Épilepsie. Building on this, Jean-Étienne Dominique Esquirol introduced the terms grand mal and petit mal, which remained widely used until the late 20th century. In 1937, Gibbs and Lennox identified psychomotor seizures, characterized by mental, emotional, motor, and autonomic features. This clinical understanding laid the groundwork for formal classification systems.[3][5]

The first systematic international effort was led by Henri Gastaut, who directed the development of the ILAE 1969 classification, incorporating clinical features, electroencephalographic patterns, anatomical substrates, etiology, and age of onset.[6]  The ILAE published the International Classification of Epileptic Seizures (ICES) in 1981, which became a widely adopted standard in both clinical practice and research. The system divided seizures into partial and generalized types, based on clinical observation and electroencephalographic (EEG) findings, but excluded anatomical substrate, etiology, and age factors, as these factors were "historical or speculative" rather than directly observed.[7] Over time, the 1981 classification was seen as too limited to reflect advances in neuroscience and the diversity of seizure types. In response, the ILAE proposed a revised conceptual framework in 2010, though it was not adopted as a formal classification.[8]

In 2017, the ILAE introduced an operational classification of seizure types designed to better reflect clinical practice and improve communication across settings.[9] Seizures were categorized based on three key features: onset (focal, generalized, or unknown), awareness (for focal seizures: aware vs. impaired awareness), and predominant symptoms at onset (motor vs. non-motor). Seizure types were named using this structure — for example, a focal impaired awareness motor seizure with automatisms. Generalized seizures were divided into motor (e.g., tonic-clonic, myoclonic, atonic) and non-motor types (various absence seizures). While the 2017 system improved clarity over earlier frameworks, it retained some inconsistencies, such as the ambiguous role of "awareness" and overlap between seizure types and descriptive features.[9]

ILAE 2025 revision

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In 2025, the ILAE released a revised seizure classification that built on the 2017 operational framework.[2] The update introduced a taxonomic structure that distinguishes between classifiers, which define seizure types, and descriptors, which provide additional clinical detail. It also revised terminology, refined the use of consciousness as a classifier, and reduced the number of formally recognized seizure types to improve clarity and clinical utility.[2]

Classifiers are biologically meaningful categories that directly inform diagnosis and management. These include the main seizure classes — focal, generalized, unknown whether focal or generalized, and unclassified — as well as specific seizure types and the level of consciousness. Descriptors, in contrast, refer to observable or reported features of a seizure, including motor signs, automatisms, sensory symptoms, or affective changes. Although descriptors do not define a seizure type on their own, they provide important context when interpreted alongside clinical data, EEG, and imaging. In some cases, descriptors like epileptic spasms or myoclonus may carry therapeutic implications.[2]

In the basic version of the classification, seizures are described as either with or without observable manifestations. In the expanded version, semiological features may be listed in chronological order, with optional somatotopic modifiers (such as face, arm, or leg) to specify the distribution of clinical signs. This structure supports more precise interpretation and seizure localization.[2]

The use of consciousness as a classifier replaced the earlier term awareness for focal and unknown seizures. Consciousness is defined as the combination of awareness — assessed after the seizure through recall — and responsiveness, which can be tested during the event using verbal or motor cues. Focal seizures are now classified as involving either preserved or impaired consciousness, and this framework also applies to seizures of unknown origin. Generalized seizures are considered to impair consciousness by definition.[2]

The revision also simplified terminology by removing the word onset from the names of the major seizure classes. As a result, focal-onset seizures became focal seizures, generalized-onset seizures became generalized seizures, and unknown-onset seizures became unknown whether focal or generalized. Other notable changes include the formal recognition of epileptic negative myoclonus as a seizure manifestation, and the removal of the label nonmotor from absence seizures, which are now described without this qualifier. Epileptic spasms remain a seizure type within the generalized seizure class but are also recognized as semiological descriptors that can occur in focal or unknown seizures. Overall, the number of seizure types was reduced from 63 in the 2017 classification to 21 in 2025, reflecting a shift toward greater clarity, biological relevance, and clinical applicability.[2]

Comparison of 2017 and 2025 ILAE seizure classifications
Feature 2017 ILAE classification 2025 ILAE classification
Terminology for seizure classes Focal-onset, generalized-onset, unknown-onset Focal, generalized, unknown whether focal or generalized
Subclassification of focal seizures Based on awareness (aware vs. impaired awareness) Based on consciousness (preserved vs. impaired)
Consciousness definition Awareness assessed via recall Consciousness defined as both awareness (recall) and responsiveness (tested)
Motor/nonmotor subtypes Motor vs. nonmotor onset in focal and generalized seizures Replaced by "seizures with" vs. "without observable manifestations"
Use of semiology Listed features; not always chronologically ordered Seizure features described in chronological sequence (expanded version)
Number of recognized seizure types 63 types 21 types
Status of epileptic spasms Seizure type under generalized seizures Still a generalized seizure type; now also a descriptor for focal and unknown seizures
Recognition of epileptic negative myoclonus Not formally included Included as a recognized seizure manifestation
Terminology for absence seizures Labeled as "nonmotor" seizures "Nonmotor" label removed; simply classified as absence seizures


Focal seizures

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Focal seizures originate within a network limited to one hemisphere of the brain and may remain confined to that region or propagate to adjacent areas or to the contralateral hemisphere. Despite possible spread, the initial site of onset remains consistent across episodes and defines the seizure as focal.[2]

Under the 2025 classification, focal seizures are subdivided into three biologically defined types:[2]

  • Focal preserved consciousness seizure (FPC): The person remains aware of and responsive to their environment throughout the event.
  • Focal impaired consciousness seizure (FIC): There is diminished awareness and/or responsiveness.
  • Focal to bilateral tonic-clonic seizure (FBTC): The seizure begins focally and evolves to involve bilateral tonic-clonic activity.

Focal seizures are inherently diverse in their clinical manifestations, depending on the region involved. These manifestations are described using descriptors, which do not define the seizure type but add critical clinical detail. The ILAE defines two levels of descriptors for focal (and unknown) seizures:

  • Basic descriptors: Indicate whether the seizure has observable manifestations or not. Seizures with impaired consciousness are presumed to have observable features.
  • Expanded descriptors: Present a chronological sequence of semiological signs, such as automatisms, motor symptoms, sensory phenomena, or speech arrest. These may be further modified using somatotopic terms (e.g., facial clonic movements, right arm tonic posturing) to aid in localization.

Common features of focal seizures include clonic or tonic movements, automatisms (such as lip-smacking or hand fumbling), sensory or visual phenomena, emotional experiences such as fear or déjà vu, and autonomic symptoms like nausea or flushing. These features, when carefully described, contribute to localizing the seizure onset zone and guiding treatment decisions, particularly in presurgical evaluation.[2]

Descriptors

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In the ILAE 2025 classification, descriptors provide additional clinical detail for seizures classified as focal or unknown whether focal or generalized. They are not used for generalized seizures, which are considered biologically complete seizure types. These semiological features are often modified by somatotopic terms (e.g., left hand clonic movement, bilateral asymmetric tonic posturing), and their evolution over time can support localization of the seizure onset zone and identification of specific syndromes. Although additional clinical characteristics — such as seizure triggers, sleep-related onset, or epileptogenic zone — are not formally part of the classification, they remain highly relevant in clinical and research settings.[2]

Some focal seizures may present with rare or striking phenomena that, while not formally classified as distinct seizure types, are recognized as semiological descriptors in the ILAE 2025 framework. These include ecstatic or blissful sensations, sexual automatisms, ictal fear or laughter (gelastic seizures), and mystic experiences. Such features often reflect activation of specific brain regions; for instance, ecstatic seizures are typically associated with the anterior insula or mesial temporal structures.[10]

Categories of semiological descriptors (ILAE 2025)
Category Example features
Elementary motor Clonic, tonic, myoclonic, versive, eye deviation, head turning
Complex motor Automatisms, hyperkinetic behavior, ictal grasping
Sensory Visual flashes, auditory hallucinations, paresthesia, epigastric rising
Autonomic Flushing, piloerection, nausea, tachycardia, urinary urge
Affective/emotional Fear, laughter (gelastic), sadness, ecstasy, anxiety
Indescribable aura A vague or unnamable warning sensation
Postictal phenomena Confusion, paresis (Todd’s), headache, nose-wiping

Generalized seizures

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Generalized seizures originate in bilateral, distributed brain networks and typically affect both hemispheres from the outset. Although generalized seizures often appear symmetric, some types may have subtle asymmetries in their clinical features or EEG patterns. In the 2025 classification, generalized seizures are defined as a biologically meaningful class and are not subclassified by level of consciousness, as consciousness is presumed to be impaired from onset.

In the basic classification, generalized seizures are grouped into three categories: absence seizures, generalized tonic-clonic seizures, and a third group labeled other generalized seizures. The latter is not a biologically distinct category but serves as a grouping term for a variety of seizure types (myoclonic, clonic, tonic, and atonic seizures).

Expanded classification of generalized seizures (ILAE 2025)
Category Seizure type
Absence seizures (AS) Typical absence seizure
Atypical absence seizure
Myoclonic absence seizure
Eyelid myoclonia with or without absence
Generalized tonic-clonic seizures (GTC) Myoclonic-tonic-clonic seizure
Absence-to-tonic-clonic seizure
Other generalized seizures Generalized myoclonic seizure
Generalized clonic seizure
Generalized negative myoclonic seizure
Generalized epileptic spasms
Generalized tonic seizure
Generalized atonic seizure
Generalized myoclonic-atonic seizure

Special considerations

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Unknown and unclassified seizures

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The 2025 classification includes two categories for seizures that cannot be confidently assigned to a known class. Seizures of unknown type are those in which the onset cannot be determined — for example, when an event is unwitnessed, occurs during sleep, or lacks sufficient EEG or clinical detail to distinguish between focal and generalized onset. In contrast, unclassified seizures refer to cases where there is insufficient information of any kind to support classification, even temporarily. This designation may be used early in the diagnostic process or in resource-limited settings. Both categories recognize that seizure classification is a dynamic process, and events initially labeled as unknown or unclassified may be reclassified as more information becomes available.

Tonic-clonic seizures

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In the 2025 classification, tonic-clonic seizures are positioned as a final category within each major seizure onset type — focal to bilateral tonic-clonic, generalized tonic-clonic, and bilateral tonic-clonic of unknown onset — in recognition of their high clinical relevance. These seizures are associated with increased morbidity, risk of injury, and are a major contributor to sudden unexpected death in epilepsy (SUDEP).[2]

Epileptic spasms

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Epileptic spasms are a distinct seizure type that can occur with generalized, focal, or unknown onset. In the ILAE 2025 classification, generalized epileptic spasms (GES) are formally recognized as a seizure type, most commonly associated with infantile epileptic spasms syndrome (IESS). In focal or unknown-onset seizures, spasms are considered semiological features; for instance, a seizure may be described as a focal epileptic spasm. Early identification of epileptic spasms, particularly in infancy, is critical, as delays in treatment are associated with worse developmental outcomes. Although classically associated with infancy, epileptic spasms can also occur outside this age range.[2]

Neonatal seizures

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The 2025 ILAE classification does not encompass neonatal seizures, which are addressed in a separate position paper.[2] The ILAE has recognized the unique characteristics of seizures in neonates and proposed a classification tailored to this age group. Unlike older children and adults, neonatal seizures often lack overt clinical manifestations and are frequently identified through electroencephalography (EEG) monitoring. Consequently, the neonatal classification emphasizes EEG findings over clinical observation.[11]

Continuous and subclinical seizures

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Certain seizure types deviate from the typical episodic pattern by occurring in a near-continuous or subclinical manner. Status epilepticus is a medical emergency defined as a seizure lasting more than 30 minutes, or a series of seizures without return to baseline consciousness between episodes.[12]

A rare subtype is epilepsia partialis continua (EPC), characterized by focal motor seizures — often clonic movements of the face or distal limbs — that recur at intervals of seconds or minutes and may persist for days, weeks, or longer. EPC is most often caused by structural lesions such as strokes in adults, or inflammatory conditions like Rasmussen’s encephalitis or autoimmune encephalitis in children.[13]

Subclinical seizures are electrographic events without overt clinical manifestations. These may occur in individuals with epilepsy or in critically ill patients undergoing EEG monitoring. While subclinical seizures cause little or no observable behavior, they can still contribute to cumulative neuronal injury and cognitive impairment if left unrecognized.[14]

References

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Revisions and contributorsEdit on WikipediaRead on Wikipedia
from Grokipedia
Epileptic seizures are transient occurrences of signs and/or symptoms due to abnormal excessive or synchronous neuronal activity in the . The classification of seizure types provides a standardized framework for identifying the onset, manifestations, and clinical features of these events, facilitating accurate , targeted treatment, and improved patient management in care. Developed by the (ILAE), this system emphasizes the distinction between focal and generalized onsets while incorporating levels of and observable motor behaviors to describe seizure semiology precisely. 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. Focal onset seizures begin in networks limited to one hemisphere and may preserve or impair , potentially evolving into bilateral tonic-clonic seizures if they spread. 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 variably. Seizures of unknown onset are those where the initial site cannot be determined, subdivided similarly based on and motor features, while unclassified seizures lack sufficient information for categorization. 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. 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. 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.

Classification Systems

Historical Development

The classification of seizures traces its origins to the late , when British neurologist John Hughlings Jackson (1835–1911) first distinguished focal seizures—characterized by localized symptoms arising from a specific 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 as a disorder of brain excitability rather than a singular entity. 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. 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 , and semiological details, leading to difficulties in classifying or unclassifiable seizures that blurred category boundaries. These limitations hindered comprehensive application in diverse clinical scenarios. From the 1980s through the 2010s, technological advances profoundly shaped seizure understanding without prompting immediate classification overhauls. Video-EEG monitoring refined ictal and localization, while modalities like computed tomography (introduced in the 1970s), (MRI, widespread by the 1980s), and (PET, advancing in the 1990s–2000s) revealed structural and functional abnormalities in focal epilepsies, enabling better differentiation from generalized forms. These tools supported identification and assessment but highlighted the 1981 system's rigidity, setting the stage for the ILAE's 2017 revision as the first major update.

ILAE 2017 Classification

The (ILAE) introduced a revised operational of seizure types in , building on and updating the 1981 framework that had become outdated due to advances in , , and (EEG). 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 and treatment selection. It defines seizures based on their initial manifestation, allowing for a hierarchical structure that facilitates communication among healthcare providers. 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). 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). This distinction helps differentiate simple partial seizures (now termed focal aware) from those involving more widespread disruption. 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. Focal onset seizures are subdivided based on the predominant early feature into motor and nonmotor types. 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 ), clonic (e.g., rhythmic jerking), myoclonic (e.g., brief jerks), and epileptic spasms (e.g., flexor or extensor contractions, often in clusters). Nonmotor onset encompasses sensory (e.g., tingling or visual auras), autonomic (e.g., piloerection or gastrointestinal sensations), cognitive (e.g., or language ), emotional (e.g., or joy), and behavior (e.g., sudden stillness without response). These categories allow focal seizures to evolve, such as progressing to bilateral tonic-clonic activity, which is noted separately. Generalized onset seizures are classified into motor and nonmotor (absence) subtypes, reflecting their diffuse bilateral activation. 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 ), myoclonic-atonic (jerks followed by collapse), atonic (sudden falls), and epileptic spasms (brief, symmetric contractions). 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). Additional absence variants include myoclonic absence (with jerks) and myoclonia (rapid blinking triggered by closure). The 2017 system delineates 63 distinct seizure types through combinations of onset, awareness, and manifestations, providing a comprehensive yet flexible that underscores semiology—the detailed description of observable —as essential for precise identification. 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. If clinical history, witness accounts, or diagnostic tests provide insufficient data, seizures may be labeled as unknown onset or unclassified to avoid misdiagnosis. This approach supports individualized management, including targeted therapies based on seizure type.

ILAE 2025 Updates

The (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 syndrome classifications, emphasizing practical shorthand notations for everyday use. 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 and , to better capture the spectrum of cognitive involvement during s. Additionally, the previous distinction between motor and non-motor manifestations is now categorized as versus non-, providing a more neutral and comprehensive framework for describing semiology. Further updates introduce the description of 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 as a distinct seizure type, addressing a previously underemphasized entity. To support treatment decisions, the system differentiates between classifiers—biological features that influence —and descriptors for specific clinical signs, promoting the identification of subtypes with therapeutic implications. As of November 2025, the 2025 classification has received mixed reception, with some clinicians praising its practicality and , 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 remain unresolved, and adoption varies among neurologists.

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. 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. This hemispheric limitation distinguishes focal seizures from generalized seizures, which involve bilateral networks from the outset. The initial semiology of focal seizures often begins with an aura, comprising subjective sensory experiences such as auditory hallucinations, psychic phenomena like , or autonomic sensations including epigastric rising; these may be nonobservable to others, relying on patient recall. Observable manifestations can include focal clonic jerks or other motor signs, contrasting with nonobservable subjective cognitive changes that do not produce visible external signs. Onset can be discretely localized to specific cortical or subcortical structures or more widely distributed within one hemisphere, influencing the seizure's progression. Diagnosis of focal seizures typically involves (EEG) to identify unilateral ictal onset patterns, such as focal slow-wave activity, which supports the localized network involvement. (MRI) is essential for detecting underlying structural causes, including cortical or lesions that may trigger the seizure. Focal seizures account for approximately 60% of epilepsy cases, particularly predominant in adult-onset forms.

Seizures with Preserved Consciousness

Focal preserved consciousness seizures (FPC), classified as type 1.1 in the 2025 (ILAE) taxonomic hierarchy, originate within networks limited to one hemisphere while remains preserved, operationally defined by maintained awareness (recall of events) and responsiveness (normal response to verbal or motor tasks). 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. 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 , 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 . For example, might report an epigastric followed by brief arm twitching while remaining responsive and recalling fully. These seizures do not impair interaction and are often identified through history rather than alone. Diagnosis relies on detailed clinical emphasizing preserved 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 . , 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. Management focuses on treating the underlying epilepsy syndrome, with antiseizure medications such as or often effective for focal origins. Since 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.

Seizures with Impaired Consciousness

Focal impaired consciousness seizures (FIC), classified as type 1.2 in the 2025 (ILAE) taxonomic , originate within networks limited to one hemisphere and involve impairment of , defined by lack of (no recall) or responsiveness (failure to respond to verbal/motor prompts). 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. Semiology typically begins with an aura (e.g., epigastric rising or ) 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 seizure might present as with and no response to questions, followed by postictal . Sensory or cognitive features like may occur without full generalization. Unlike preserved consciousness seizures, FIC inherently disrupts interaction, increasing risks of subtle progression unnoticed by witnesses. 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 . Caution is needed to exclude isolated or as the sole cause of apparent impairment. Management involves antiseizure medications tailored to focal epilepsy, such as or , with monitoring for evolution to bilateral tonic-clonic seizures. Due to impaired , precautions against (e.g., restrictions) are critical. For cases, interventions like or focal resection offer higher success rates when a seizure onset zone is localizable.

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 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. The clinical sequence typically begins with a focal onset phase, which may include an (such as epigastric rising or in 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. 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 occurs, these patterns synchronize bilaterally, showing low-voltage fast activity (20-50 Hz) during the tonic phase, followed by bilateral 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. Risk factors for the evolution to bilateral tonic-clonic involvement include underlying structural lesions, such as 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 cohorts. Genetic predispositions and prior brain insults (e.g., trauma or ) further elevate risk by altering cortical excitability. Distinction from primary generalized tonic-clonic seizures relies on identifying focal features, such as asymmetric onset in history (e.g., or unilateral symptoms), EEG evidence of unilateral ictal rhythms preceding bilateral synchronization, or revealing a focal . In the absence of such indicators, seizures of unknown onset are classified separately under ILAE guidelines.

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. This contrasts with focal seizures, which start in networks confined to one and may propagate secondarily. The (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). These seizures frequently arise from genetic or idiopathic etiologies, as exemplified in idiopathic generalized epilepsies such as , where hereditary factors predominate without identifiable structural lesions. (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 typically emerging around ages 12-18. They comprise approximately 15-20% of all syndromes, highlighting their significant epidemiological impact.

Absence Seizures

Absence seizures are generalized nonmotor seizures characterized by a sudden, brief cessation of ongoing activity accompanied by impaired , without any preceding aura or subsequent postictal confusion. 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. 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. Typical absence seizures involve a sudden onset of impaired with minimal motor signs, such as subtle eyelid fluttering or lip smacking, and are associated with a characteristic 3 Hz generalized discharge on EEG. 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) patterns on EEG and occurring in individuals with developmental or neurological impairments. Myoclonic absence seizures combine impaired with rhythmic bilateral myoclonic jerks, typically at 3 Hz, affecting the shoulders and arms, leading to progressive arm elevation during the event. 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 . Typical absence seizures generally last 5-10 seconds and are most prevalent in children diagnosed with childhood absence , a common syndrome with onset between ages 4 and 10 years. These seizures lack convulsive motor activity, distinguishing them from other generalized seizure types that involve prominent tonic or clonic movements. is a well-established trigger, reliably provoking episodes in over 90% of susceptible individuals during EEG testing. 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.

Tonic-Clonic Seizures

Generalized tonic-clonic seizures (GTCS), also known as grand mal seizures, are a type of generalized characterized by bilateral symmetric involvement of the and subcortical structures, leading to loss of and convulsive motor activity. According to the (ILAE) 2025 classification, GTCS originate within and rapidly engage bilaterally distributed networks without evidence of a focal onset. The 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 . 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. (EEG) during GTCS typically shows generalized polyspike-and-wave discharges at 3-6 Hz, particularly in associated syndromes like (). These seizures are strongly linked to idiopathic generalized epilepsies, including , where GTCS occur in nearly all affected individuals, often in the morning shortly after awakening. Common triggers include , which is the most potent precipitant, as well as stress, alcohol consumption, and photic stimulation from flashing lights. GTCS typically last 1 to 3 minutes before spontaneous resolution, though durations up to 5 minutes are common without indicating . The postictal phase involves , , , 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 ; they are also associated with higher morbidity, including (SUDEP). Unlike focal-to-bilateral tonic-clonic seizures, GTCS lack any initial focal clinical or EEG features.

Other Motor Seizures

Other motor seizures in the generalized category encompass a range of bilateral, symmetric motor manifestations distinct from tonic-clonic seizures, including , 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. 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 (JME), where they represent the primary seizure type in up to 90% of cases. Electroencephalographic (EEG) correlates typically show generalized or polyspike-and-wave discharges time-locked to the jerks, reflecting synchronous thalamocortical activation. 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 discharges that evolve in frequency during the . 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 . 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 or polyspike-and-wave complexes correlating with the atonic phase. Myoclonic-atonic seizures combine a rapid myoclonic jerk with immediate loss of tone, leading to abrupt falls; this sequence is emblematic of with myoclonic-atonic seizures (EMAS, or Doose ), affecting children aged 2-5 years with multiple daily events. The EEG typically mirrors that of myoclonic seizures, with generalized discharges preceding the atonic component. A novel addition in the 2025 ILAE classification is epileptic negative , 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 or sharp-wave discharges precisely time-locked to electromyographic (EMG) silence, enabling diagnosis via video-EEG.

Unknown Onset Seizures

Definition and Classification

Unknown onset s are classified as such when there is insufficient information to determine whether the 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. This classification applies in situations where (EEG) or detailed witness accounts are unavailable or inconclusive, distinguishing it from unclassified s that lack even basic epileptic confirmation. In the 2025 International League Against Epilepsy (ILAE) update, unknown onset seizures are subcategorized based on level of and semiology, using terms such as preserved consciousness (PC), impaired consciousness (IC), and bilateral tonic-clonic (BTC). These descriptors allow for structured description without specifying onset: PC seizures involve maintained , IC seizures feature altered , and BTC seizures exhibit symmetric motor involvement evolving to tonic-clonic activity. Unlike definitive focal (unilateral onset) or generalized (bilateral onset) classes, this framework emphasizes features to guide initial management. Common scenarios leading to unknown onset classification include unwitnessed events, such as nocturnal seizures occurring during without video-EEG monitoring, or observed episodes without access to real-time neurophysiological . For instance, bilateral tonic-clonic seizures presenting with postictal EEG or often fall into this category initially due to obscured onset. 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. 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. This provisional approach facilitates standardized care in resource-constrained environments like emergency departments.

Seizures with Preserved Consciousness

Seizures with preserved of unknown onset, as defined in the (ILAE) 2025 classification, occur when the initial involvement cannot be determined as focal or generalized due to unobserved or obscured onset, yet the maintains full of self and surroundings throughout the event. These are termed "unknown whether focal or generalized - preserved seizure (PC)" and are characterized by the absence of any impairment in responsiveness or recall, distinguishing them from seizures involving . This category applies to brief events where is explicitly preserved, allowing the person to continue activities or respond appropriately despite the activity. 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. For instance, observable signs may include piloerection (goosebumps) or facial flushing in a fully aware individual, as seen in case examples from clinical reports. These features may closely resemble those of focal preserved consciousness seizures but lack sufficient evidence to confirm localized onset. In some cases, such as idiopathic generalized myoclonus with unclear onset, the events present as isolated jerks upon awakening, maintaining complete awareness. 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. (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. 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 category until further evaluation allows reclassification, often involving , adjustments, or low-dose antiseizure medications if recurrent. Supportive tests like EEG or guide potential adjustments to , prioritizing minimal intervention given the preserved and typically benign course.

Seizures with Impaired Consciousness

Seizures with impaired 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. These events may represent equivalents to absence seizures when onset details are unavailable, such as in unwitnessed episodes. Consciousness impairment is operationally assessed by the inability to recall the event or respond to verbal or motor prompts during its occurrence. 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. In cases without video-EEG confirmation, classification relies on 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. Urgent (EEG) is recommended to clarify onset and guide treatment, potentially reclassifying the event as focal or generalized. Differentiation from syncope is aided by the absence of prodromal or sweating, which are characteristic of vasovagal events but rare in epileptic impairments. In contrast to seizures with preserved consciousness, which allow maintained responsiveness as a milder variant, impaired consciousness events disrupt interaction entirely.

Bilateral Tonic-Clonic Seizures

Bilateral tonic-clonic seizures of unknown onset, abbreviated as BTC, occur when a full convulsive is observed without sufficient information to determine whether it begins focally or diffusely across both hemispheres of the . These seizures are classified under the "unknown onset" category in the International League Against Epilepsy (ILAE) 2025 updated system, serving as the default designation for unwitnessed or incompletely observed convulsions that exhibit bilateral motor involvement. This applies particularly to scenarios where the onset phase is missed, such as during or in unattended settings, ensuring a practical approach to when detailed history or electroencephalographic (EEG) data is unavailable at the time of the event. 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. These seizures typically last 1-3 minutes but can recur or evolve into if untreated. 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%. Moreover, convulsive —predominantly bilateral tonic-clonic—constitutes about 42.5% of all status epilepticus episodes in adults, highlighting its prevalence in prolonged seizure scenarios. 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 like MRI to identify structural etiologies. 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 with mortality rates of 16-20% for initial episodes.

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. 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. (EEG) during spasms typically shows —a chaotic, high-amplitude, multifocal spike-and-wave pattern—or electrodecremental suppression, which is for IESS and aids in . The etiology of epileptic spasms is predominantly structural or genetic, with up to 60% of cases linked to identifiable causes such as 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, , and , which disrupt neuronal development and are unique to the infantile period due to age-specific 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 syndromes, such as Lennox-Gastaut syndrome, in approximately one-third of cases. Treatment focuses on rapid cessation of spasms to optimize neurodevelopmental outcomes, with (ACTH) or as first-line therapies. ACTH, administered as high-dose intramuscular injections, achieves spasm cessation in 50-80% of cases within two weeks, while —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 .

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. These seizures often present with subtle clinical manifestations due to the neonatal , such as or bicycling limb movements, ocular deviation, or minor myoclonic jerks, which can be difficult to distinguish from normal neonatal behaviors. 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. This high rate of electrical-only activity underscores the limitations of clinical observation alone in neonates. The primary causes of neonatal seizures include hypoxic-ischemic encephalopathy (HIE), accounting for 35% to 45% of cases, metabolic disturbances such as , and genetic etiologies like mutations in the KCNQ2 gene. HIE often results from , leading to brain injury that manifests as seizures shortly after birth. Metabolic causes, including electrolyte imbalances or , 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. Diagnosis relies heavily on (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. Common EEG patterns include , characterized by alternating periods of high-voltage bursts and suppression, particularly in severe cases like those associated with HIE or early-onset epileptic encephalopathies. Recent guidelines emphasize quantitative EEG and amplitude-integrated EEG for improved detection in neonatal intensive care settings. Prognosis for neonatal seizures is guarded, with high rates of mortality and long-term morbidity, including neurodevelopmental , influenced by seizure burden and underlying ; for instance, HIE-related s carry poorer outcomes compared to benign genetic forms. These s are distinct from epileptic spasms seen in older infants, differing in timing, typical EEG features, and clustering patterns. Subclinical s, which may persist continuously, further contribute to brain injury risk if undetected.

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 (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. This condition contrasts with convulsive by lacking overt convulsions, yet it requires urgent recognition due to its potential for neuronal injury. Subclinical seizures, also known as electrographic-only seizures, involve epileptiform activity detected exclusively on (EEG) without corresponding clinical signs. These are prevalent in critically ill populations, occurring in 8–27% of comatose (ICU) patients and frequently post-stroke, where they may contribute to unexplained . 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. Negative , recognized as a distinct generalized seizure type, exemplifies a brief continuous form involving abrupt interruptions of lasting less than 500 milliseconds, often linked to ongoing epileptiform discharges. 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. The modified 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. Treatment typically begins with intravenous benzodiazepines such as for acute termination, followed by second-line agents like or , and refractory cases may necessitate anesthetic coma induction with or . These seizure forms carry significant risks, including cognitive decline, with survivors of NCSE facing elevated probabilities of , learning, and executive function deficits compared to those with multiple discrete seizures. In post-stroke contexts, undetected subclinical activity heightens the likelihood of neurological deterioration and recurrence. 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.

Unclassified Seizures

Unclassified seizures represent a category in the 2025 (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. 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 , 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. Clinically, 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 . 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 that supports the identification of novel seizure types through accumulated data and advanced analytics.

References

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