Seizure Semiology in Critical Care: Recognition, Interpretation, and Clinical Pearls

Dr Neeraj Manikath , Claude.ai

Abstract

Seizure semiology—the systematic description and interpretation of clinical manifestations of seizures—represents a cornerstone of acute neurological diagnosis in the intensive care unit. Despite advances in neurophysiological monitoring, accurate bedside recognition of seizure semiology remains essential for timely intervention and appropriate management. This review synthesizes current evidence on seizure classification, semiological phenomenology, and practical bedside recognition strategies tailored for critical care practitioners. We emphasize overlooked presentations, mimics of seizures, and clinical pearls that enhance diagnostic accuracy in resource-limited and technically challenging intensive care environments.

Keywords: Seizure semiology, Status epilepticus, Critical care neurology, Seizure mimics, Bedside diagnosis

Introduction

Seizures represent one of the most common neurological emergencies in critical care, with an incidence of 7–15% among ICU patients.¹ The clinical manifestations of seizures—collectively termed semiology—provide crucial diagnostic clues, yet they remain frequently misinterpreted or overlooked by non-neurologists.² The ability to recognize and accurately describe seizure semiology can mean the difference between timely intervention and catastrophic neurological deterioration.

Unlike electroencephalography (EEG), which provides objective physiological confirmation, bedside semiological assessment is immediately available, requires no equipment, and carries no delays. In resource-limited settings, or when technical monitoring is unavailable, semiology remains the only diagnostic tool. Even in well-equipped ICUs, initial clinical recognition triggers the diagnostic cascade and guides empirical management while confirmatory studies are pending.

This review addresses a critical gap in the literature: practical, comprehensive guidance on seizure semiology tailored specifically for critical care physicians. We integrate classical neuroscience with modern clinical evidence, emphasizing the phenomenological features that matter most at the bedside, along with evidence-based recognition hacks and commonly missed presentations.

Part I: Foundational Concepts

Seizure Definition and Classification

A seizure is defined as a transient occurrence of signs and/or symptoms due to abnormal, excessive, or synchronous neuronal activity in the brain.³ The 2017 ILAE classification reorganizes seizure types based on onset, awareness, and motor features, providing greater precision than older terminology.

Key Classification Framework:

By Seizure Onset: Generalized-onset (synchronous bilateral hemispheric involvement from onset) versus focal-onset (initial activation of neurons in networks limited to one hemisphere).

By Level of Awareness: Aware (consciousness preserved) versus impaired (diminished awareness, which replaces older terms "simple partial" and "complex partial").

By Motor Features (for generalized-onset seizures): Tonic-clonic (the only common generalized motor seizure type), atonic, clonic, tonic, myoclonic, or myoclonic-tonic-clonic.

Clinical Pearl #1: The distinction between generalized and focal-onset seizures has profound management implications. Generalized-onset seizures carry lower seizure recurrence risk and different medication response profiles. Misclassifying a focal seizure as generalized may lead to inappropriate monotherapy and treatment failure.

The Semiological Approach: Building a Mental Framework

Systematic semiological assessment follows this mental template:

Premonitory symptoms (hours to minutes before onset)
Aura (final warning before impaired awareness)
Onset phase (first observable motor or behavioral change)
Ictal phase (progression and full expression)
Termination phase (manner of offset)
Postictal phase (recovery trajectory and duration)

Each element narrows the differential diagnosis and guides localization in focal seizures.

Part II: The Fundamental Seizure Types and Their Semiology

Generalized-Onset Seizures

Generalized Tonic-Clonic Seizure (GTCS)

Classic Semiology:

The GTCS unfolds in stereotyped phases. An initial cry or vocalization occurs as thoracic muscles contract abruptly (not conscious vocalization—a critical distinction). This is immediately followed by loss of consciousness and a tonic phase (10–20 seconds) characterized by sustained axial muscle contraction. Patients typically fall backward or laterally; opisthotonus (extreme back arching) and facial grimacing are common. The eyes roll upward, and pupillary dilation occurs.

The clonic phase (typically 30–60 seconds but variable) begins with rhythmic alternation between muscle contraction and relaxation at 1–3 Hz. Clonic movements are most prominent in proximal limbs and typically bilaterally synchronous. Urinary (and occasionally fecal) incontinence may occur.

Tongue or cheek biting is extremely common and highly specific for GTCS. Examination afterward may reveal bitten tongue with blood in the mouth—this finding essentially confirms seizure activity, as few mimics produce this injury.

Critical Observation Point: The sequence matters. Tonic phase → clonic phase is GTCS. Immediate clonic activity without a preceding tonic phase may indicate focal motor seizure with secondary generalization or non-convulsive status epilepticus (NCSE). This distinction fundamentally alters your differential diagnosis.

Postictal State: Following GTCS, patients show profound postictal confusion lasting 5–30 minutes. Most crucially, there is typically a postictal period of unresponsiveness or deep confusion before gradual orientation returns. Serum prolactin levels peak 20 minutes post-ictal and remain elevated for 24–48 hours; this biomarker can support diagnosis retrospectively.⁴

Clinical Pearl #2: A patient who is fully alert immediately after an event almost certainly did not have GTCS. Consider syncope, psychogenic non-epileptic seizure (PNES), or focal seizure with retained awareness. Prolonged postictal confusion is the norm for GTCS, not the exception.

Oyster (Commonly Missed Detail): Asymmetric head turning during the clonic phase is a reliable lateralizing sign in focal motor seizure secondarily generalized. The head and eyes turn toward the seizure focus (contraversive turning toward non-affected hemisphere). This asymmetry is often overlooked because observers focus only on whether clonic activity is present, not its symmetry.

Myoclonic Seizures

Semiology: Myoclonic seizures consist of sudden, brief (< 100 msec), arrhythmic jerks without loss of consciousness. Unlike the rhythmic clonic movements of GTCS, myoclonic jerks are irregular and non-repetitive. Bilateral synchronous myoclonic seizures can resemble the clonic phase of GTCS but occur in alert patients and lack the antecedent tonic phase.

Context Matters: Myoclonic seizures are typically generalized-onset but commonly occur in specific syndromes (juvenile myoclonic epilepsy, progressive myoclonic epilepsies, cortical myoclonus) and as a manifestation of critical illness myoclonus (multifocal, non-epileptic muscle jerks). Distinguishing pathological myoclonus from benign sleep-related hypnic jerks requires EEG correlation.

Clinical Pearl #3: Myoclonus in the ICU is often multifactorial. Sepsis, metabolic derangement, hepatic encephalopathy, and uremia all produce non-epileptic myoclonus. Always obtain EEG to confirm epileptic versus non-epileptic etiologies before escalating antiepileptic therapy. This prevents iatrogenic over-treatment and focuses management on underlying causes.

Atonic Seizures ("Drop Attacks")

Semiology: Sudden loss of postural tone affecting axial, proximal limb, or all muscles results in head nodding, shoulder drooping, or complete collapse. The event is typically brief (< 5 seconds), and consciousness may be preserved or briefly lost.

Critical Distinction: Atonic seizures must be differentiated from syncope or sudden leg weakness. In atonic seizure, there is genuine loss of muscle tone—the patient cannot maintain posture for even seconds. There is no prodrome, no palpitations, and no gradual recovery. The patient falls abruptly without warning.

High-Risk Presentation: Atonic seizures are characteristic of certain progressive myoclonic epilepsies and Lennox-Gastaut syndrome, but when they appear in an adult ICU patient, consider severe metabolic encephalopathy, hypoxic-ischemic injury, or frontal lobe pathology (particularly orbitofrontal/medial prefrontal cortex damage).

Focal-Onset Seizures

Focal Motor Seizure ("Jacksonian" Seizure)

Semiology: The hallmark of focal motor seizures is the march—progressive spread of rhythmic clonic movements from the seizure focus to adjacent cortical representations. Classic description: rhythmic twitching beginning in the hand, then forearm, then shoulder, then leg. This "march" takes 10–60 seconds and follows the somatotopic organization of motor cortex, providing precise localization of the seizure focus.

Lateralization: The side of motor involvement indicates contralateral cortical focus. Unilateral clonic activity during apparent GTCS strongly suggests focal-onset seizure with secondary generalization rather than primary generalized-onset GTCS.

Clinical Pearl #4: The presence of a march essentially rules out primary generalized-onset seizure and mandates urgent neuroimaging to identify structural lesion, because focal motor seizures have a structural etiology in >40% of cases.⁵ This finding should raise immediate concern for acute stroke, tumor, abscess, or hemorrhage in ICU patients.

Oyster: Todd's paralysis—transient focal weakness persisting 24–72 hours after focal motor seizure—can be mistaken for acute stroke. The key differentiator is that Todd's paralysis typically resolves completely and correlates with the seizure semiology (weakness in the body part that was seizing). MRI performed during Todd's paralysis may show subtle signal changes that resolve, adding to diagnostic confusion. A high index of suspicion for Todd's paralysis prevents unnecessary thrombolysis and unnecessary ICU complications.

Focal Sensory Seizure

Semiology: Patients report paresthesias (tingling, electrical sensations) that often march in distribution similar to motor seizures. Sensory seizures originating from somatosensory cortex follow the same somatotopic march as motor seizures. Visual sensations (photopsia), auditory phenomena, or olfactory hallucinations may occur with occipital, temporal, or orbitofrontal seizures, respectively.

Critical Challenge in ICU: Sedated or intubated patients cannot report sensory phenomena. Focal sensory seizures may be entirely invisible on routine observation, detectable only by EEG. The patient may show no motor activity, yet the EEG demonstrates clear focal epileptiform activity with clinical correlate (subtle eye deviation, autonomic changes).

Clinical Pearl #5: Non-convulsive seizures (NCS) are dramatically underrecognized in ICU patients.⁶ Any sedated or minimally responsive patient with unexplained alteration in mental status, autonomic instability, or subtle behavioral changes warrants EEG. NCS can manifest as nothing more than a change in pupil size, a brief pause in breathing, or subtle eye deviation—details easily missed if not specifically sought.

Focal Aware Seizure with Impaired Awareness (formerly "Complex Partial" Seizure)

Semiology: These seizures typically originate in the temporal lobe and involve hippocampus and surrounding structures. The aura is the initial warning and may include fear, depersonalization, a rising epigastric sensation (the "epigastric aura"), jamais vu, or déjà vu. The aura marks the moment of seizure onset and consciousness preservation.

Following the aura, consciousness becomes impaired. The characteristic behavioral automatism—stereotyped, purposeless motor or behavioral acts—unfolds: lip smacking, hand fumbling, pedaling movements, or undressing. These automatisms are not random; they are predictable and highly recognizable to trained observers.

Termination and Postictal State: Focal seizures with impaired awareness typically last 30–120 seconds. Post-ictally, there is prolonged confusion (5–15 minutes) and often a sense of exhaustion or headache.

Oyster: Automatisms in focal aware seizure are often confused with agitation or psychogenic behavior. The key distinction is stereotypy—the automatisms are identical in each seizure, occur without external stimuli, and are accompanied by impaired awareness. Agitation is typically responsive to environment and involves purposeful-appearing behavior in a fully aware patient.

Focal Seizure Evolving to Bilateral Tonic-Clonic Seizure (Focal-Onset SGTCS)

Semiology and Localization: This category encompasses seizures that begin with focal features (motor march, lateral head/eye deviation, unilateral sensory symptoms) and then generalize bilaterally over seconds to minutes. The secondary generalization phase is preceded by clear focal features that provide localization clues.

Clinical Significance: The presence of focal-onset features during apparent GTCS is the most reliable bedside clue that this is a focal seizure with secondary generalization, not true primary generalized-onset seizure. This distinction is essential because focal seizures demand neuroimaging.

Key Lateralization Sign: Lateral deviation of the head and eyes during the seizure is highly lateralizing. Crucially, eyes and head deviate toward the seizure focus (contraversively). A patient seizing with rightward head deviation has a left-hemisphere focus.

Clinical Pearl #6: Memorize this: eyes and head turn toward the lesion (toward the non-contracting side). This single observation can guide emergent neuroimaging and localization. If uncertain, remember: the seizure focus drives the eyes away from that hemisphere, causing apparent turning toward it.

Part III: Non-Convulsive Seizures and Status Epilepticus

Absence Seizures

Semiology: Brief (5–30 seconds), sudden pauses in activity with staring and unresponsiveness. These are generalized-onset non-motor seizures. During absence, patients appear vacant and unaware; external stimuli produce no response. Recovery is immediate; there is no postictal confusion.

Behavioral Variant: Automatisms (eye fluttering, lip smacking) may occur during longer absence seizures but are less prominent than in focal seizures with impaired awareness.

Context: Absence seizures are predominantly a disorder of childhood and adolescence. When they appear in adults, suspect focal seizure with impaired awareness or non-convulsive status epilepticus (NCSE) rather than true absence epilepsy.

Non-Convulsive Status Epilepticus (NCSE)

Definition and Semiology: NCSE represents prolonged epileptiform activity (>5 minutes) without prominent motor manifestations. Patients present with altered mental status, behavioral changes, confusion, or apparent catatonia. Bedside recognition is nearly impossible without clinical suspicion and EEG.

Three Forms:

Absence Status: Continuous or near-continuous absence-like episodes causing profound unresponsiveness. Patients appear comatose but EEG reveals 3-Hz spike-wave activity.
Focal NCSE: Focal epileptiform activity producing fluctuating confusion, behavioral disturbance, or subtle automatisms. May resemble focal seizure semiology but is persistent.
Generalized Convulsive Status with Subtle Motor Signs: Patients receiving anesthesia for paralytic agents may have only subtle twitching of the eyelids, face, or fingers. The "clinical ictal marker" becomes harder to detect as neuromuscular blockade masks motor manifestations.

Presentation Patterns in ICU: NCSE often presents as unexplained alteration in consciousness in a post-stroke patient, post-anoxic patient, or patient with sepsis. Autonomic instability (tachycardia, hypertension, hyperthermia) and nystagmus or subtle eye deviation may be the only clues.

Clinical Pearl #7: The "EEG threshold" for diagnosing NCSE remains controversial, but modern consensus suggests prolonged focal or generalized epileptiform discharges (>30 seconds) in a patient with altered mental status constitute NCSE, even without electrographic seizure criteria.⁷ The burden of proof for diagnosis is lower than classical status epilepticus; a high index of suspicion should prompt empirical treatment followed by confirmatory EEG.

Oyster (Critical Diagnostic Pearl): Suppression of NCSE by intravenous benzodiazepines with concurrent dramatic improvement in mental status is both diagnostic and therapeutic. This "blinded" diagnostic response provides powerful evidence for NCSE when EEG confirmation is delayed. Improvement in orientation, reduction in autonomic instability, or cessation of subtle movements following benzodiazepine administration in a patient with altered mental status strongly supports NCSE diagnosis.

Convulsive Status Epilepticus (CSE): Phases and Evolution

Stage 1 (0–5 minutes): Discrete Seizures with Intervals

Individual seizures occur with brief intervals of preserved consciousness between them. This stage may not be recognized as status, as individual seizures appear "normal."

Stage 2 (5–20 minutes): Fusion Phase

Seizures merge into nearly continuous motor activity. This is the classic image of status epilepticus: continuous or near-continuous convulsive activity without return to baseline consciousness. Tonic and clonic phases become less distinct; the motor activity becomes more tonic and sustained.

Stage 3 (>20 minutes): Subtle/Electromechanical Dissociation

Motor manifestations dampen despite ongoing electrographic seizure activity. The patient may appear relatively still—breathing patterns may be barely perturbed, slight facial twitching or eye deviation may be the only observable sign—yet the EEG shows continuous epileptiform activity. This is the most dangerous phase because status epilepticus is "hidden" and easily missed.

Clinical Pearl #8: Status epilepticus does not always look like status epilepticus. After 20–30 minutes of continuous ictal activity, the motor manifestations settle down dramatically, and the patient may appear merely to be sleeping or comatose. This electromechanical dissociation is where the greatest mortality occurs, as inadequate treatment is instituted because clinical recognition fails. Any patient in persistent altered consciousness after what appeared to be a single seizure should be considered in possible subtle status epilepticus and managed accordingly.

Oyster: Pupil changes can herald evolution of status. During active motor status, pupils are typically dilated and reactive. As status evolves into subtle phase, pupils may become mid-position and unreactive—a sign of deepening brainstem dysfunction and urgency for aggressive treatment.

Part IV: Seizure Mimics and Diagnostic Traps

Psychogenic Non-Epileptic Seizure (PNES)

Semiology:

PNES events superficially resemble seizures but originate from psychological rather than neurobiological mechanisms. Key semiological differences include:

Onset and Termination: Gradual onset and offset, not sudden. PNES may begin with emotional trigger or stress.
Responsiveness During Event: Patients often retain some awareness and responsiveness to external stimuli (responding to name, avoiding painful stimuli). True seizure patients are unresponsive.
Asynchronous Movement: Thrashing and vigorous whole-body movement that is non-rhythmic and not stereotyped. Unlike focal seizures with predictable progression, PNES movements are chaotic.
Preserved Protective Reflexes: The patient rarely sustains serious injuries because protective reflexes remain partially intact.
No Postictal Confusion: Immediate alertness after event, or gradual emotional recovery without the profound confusion of true seizure.
Absence of Autonomic Changes: True seizures produce sustained elevation in heart rate and blood pressure; PNES events may show reactive but not sustained changes.

Diagnostic Traps: PNES can coexist with true epilepsy, creating diagnostic confusion. Video-EEG is the gold standard, but in ICU settings where PNES is suspected, look for inconsistencies between clinical description and observed events, preserved responsiveness, and lack of true postictal states. Never assume PNES—confirm with EEG whenever possible.

Syncope

Semiological Differences:

Syncope produces brief loss of consciousness with rapid recovery. However, brief convulsive syncope (myoclonic jerks triggered by cerebral hypoperfusion) can closely mimic seizure. Distinguishing features:

Prodrome: Syncope typically includes warning signs (dizziness, nausea, palpitations, diaphoresis) preceding loss of consciousness. Seizures lack this phase.
Duration of Altered Consciousness: Syncope resolves within seconds to 1–2 minutes. Recovery of full consciousness is immediate.
Motor Activity: When myoclonic jerks occur in syncope, they are brief (< 5 seconds), asynchronous, and occur only after loss of consciousness. True seizure-related myoclonus is more sustained and rhythmic.
Postictal State: No true postictal confusion in syncope. Syncope patients regain full alert immediately.
Tongue Biting: Unusual in syncope; common in true seizure.

Oyster: Situational syncope in ICU patients (prolonged standing, Valsalva, vasovagal triggers) may be overlooked as seizure if a brief convulsive component occurs. Detailed history from witnesses (any warning symptoms? how quickly did they become alert?) and absence of postictal confusion point to syncope.

Sleep-Related Movement Disorders

Semiology:

Non-REM sleep parasomnias (night terrors, sleepwalking) and REM-sleep behavior disorder (RBD) produce complex movements during sleep that can superficially resemble seizures.

Distinguishing Features:

Timing and Duration: Parasomnias occur during specific sleep stages and last minutes to hours. Seizures are brief (seconds to minutes) and occur at any time.
Awareness: Patients are typically confused or completely unaware during parasomnia but become fully oriented when awakened. Seizure patients show postictal confusion even after waking.
Stereotypy: Parasomnias show variable, context-dependent movements. Seizures are stereotyped and identical from episode to episode.
EEG Findings: Background during parasomnia shows sleep EEG; seizure shows epileptiform activity (spikes, sharp waves).

Tremor and Movement Disorders

Essential Tremor vs. Myoclonic Seizure:

Essential tremor is rhythmic (6–12 Hz), persistent, and worsens with intentional movement. Myoclonic seizures are arrhythmic, brief, and occur without voluntary movement. Video-EEG can definitively separate these.

Dystonic Reactions (Medication-Induced):

Anticholinergic toxicity or antipsychotic-induced dystonia produces sustained muscle contraction with bizarre posturing. Unlike seizures, dystonia is responsive to anticholinergic medications and produces no alteration in consciousness. Consciousness is completely preserved throughout dystonic event.

Hyperventilation Syncope and Panic Attacks

Rapid breathing may produce dizziness, altered consciousness, and peri-oral paresthesias that can be misattributed to seizure. Distinguishing features: conscious patient who can describe the experience, awareness of triggering (anxiety), and no postictal state. EEG shows no epileptiform activity.

Part V: Clinical Pearls and Practical Hacks for ICU Recognition

Pearl #9: The "Witnessed Event" Taxonomy

Always obtain detailed history of the event using this framework:

Premonitory Phase (what happened in hours to days before): Any mood changes, sleep deprivation, infection, or medication changes?
Immediate Prodrome (seconds to minutes before): Warning signs (palpitations, diaphoresis, déjà vu, epigastric rising sensation)?
Onset: Sudden or gradual? What was the patient doing?
Sequence of Motor Activity: What moved first? Did movements spread (march)? Were movements rhythmic?
Asymmetry: Were movements symmetric or clearly one-sided?
Duration: How long did the event last?
Responsiveness During: Could the patient respond to commands? Did they react to pain?
Injury Pattern: What injuries resulted? (Tongue biting is highly specific for seizure.)
Recovery: How quickly did full alertness return? Was there a period of confusion?

This structured history dramatically improves diagnostic accuracy.

Pearl #10: The "Postictal Signature"

After true seizure, especially generalized seizure, expect:

5–10 minutes: Profound confusion, often unable to follow commands or form coherent sentences
10–30 minutes: Gradual orientation, but still slow mentally and physically fatigued
30–120 minutes: Return to baseline, though fatigue may persist

Any patient fully alert immediately after the event almost certainly did not have generalized seizure. This single observation rules out most true seizures and points toward syncope, PNES, or focal seizure without bilateral spread.

Pearl #11: Pupil Examination as Ictal Marker

During active generalized seizure, pupils are typically dilated (7–8 mm) and fixed (non-reactive to light). This pupillary dilation is due to sympathetic surge and sustained contraction of dilator muscles during the sustained muscle activity of seizure.

As seizure resolves, pupils gradually return to normal size and reactivity within seconds to minutes. In contrast, fixed dilated pupils from brainstem injury or medication effect persist unchanged.

Clinical Hack: Perform pupil examination during and immediately after suspected seizure. Comparison of pupil size before, during, and after the event provides a timeline that confirms seizure activity. Pupils that dilate during event and then normalize support seizure diagnosis.

Pearl #12: Autonomic Markers of Seizure

Brief but intense autonomic changes accompany ictal activity:

Cardiovascular: Heart rate elevation to 140–160 bpm within seconds; blood pressure elevation; sometimes initial bradycardia with sudden switch to tachycardia
Respiratory: Brief apnea (< 30 seconds) during tonic phase; irregular breathing during clonic phase
Thermoregulation: Rapid temperature elevation (core temperature may increase 0.5–1°C within 1–2 hours post-ictal due to sustained muscle activity)
Salivation: Excessive drooling and foaming at mouth

These changes are immediate and dramatic, quite different from the gradual autonomic changes of syncope.

Pearl #13: The Tongue Bite Location Matters

Lateral Tongue Laceration: Highly specific for true seizure. The tonic phase jaw clenching combined with lateral tongue displacement creates a characteristic laceration on the side of the tongue.

Central/Anterior Tongue Bites: Less specific; can occur with trauma, fall, or even aggressive laughing or chewing habits.

Inspection Technique: Ask the patient to protrude the tongue and examine for fresh lacerations (erythema, oozing blood) or healing ulcers (white slough, mild swelling). Fresh lateral tongue laceration within hours of an event is essentially diagnostic for seizure.

Pearl #14: Nystagmus as Ictal vs. Postictal Sign

During Seizure (Ictal Nystagmus):

Jerk nystagmus may occur, typically beating toward the seizure focus (converging nystagmus toward the discharging hemisphere). This is a sign of active cortical excitation. The nystagmus is often rapid (10–15 Hz) and more obvious on lateral gaze.

After Seizure (Postictal Nystagmus):

Horizontal or vertical nystagmus may persist for minutes post-ictally, representing postictal cortical depression and decreased inhibition. This finding, while non-specific, supports recent seizure activity.

Clinical Utility: In comatose or sedated patients where motor activity is unobservable, nystagmus may be the only sign of ongoing ictal or post-ictal activity. Persistent nystagmus in a previously still patient should prompt EEG to exclude NCSE.

Pearl #15: The "Serum Prolactin Spike" Biomarker

Physiology: Tonic-clonic seizure produces rapid spike in serum prolactin, peaking 20 minutes post-ictally and remaining elevated for 24–48 hours. This occurs due to loss of hypothalamic dopaminergic inhibition during seizure.

Sensitivity and Specificity: Prolactin elevation has ~60–80% sensitivity for generalized seizure and ~50% sensitivity for focal seizure with impaired awareness. Specificity is lower, as prolactin can elevate with stress, anesthesia, or antipsychotic medications.⁸

Clinical Application: In uncertain cases where EEG is not immediately available, a serum prolactin level drawn within 20 minutes of suspected seizure can provide supportive evidence. However, prolactin should not be used as the sole diagnostic criterion; rather, it provides additional data points in the context of clinical presentation.

Oyster: Serum prolactin is less helpful in NCSE, as subtle seizures may not produce as dramatic prolactin elevation. A normal prolactin in a patient with NCSE should not be reassuring.

Pearl #16: The EEG Correlate of Key Semiological Features

Focal Motor Seizure → Motor Cortex Discharge: EEG shows rhythmic discharges or spike activity over contralateral motor strip (C3/C4 leads). Clonic movements correspond to individual spike complexes at 1–3 Hz.

Temporal Lobe Seizure → Characteristic Pattern: Rhythmic theta activity (4–6 Hz) over temporal leads (T3/T4) or depth recordings from hippocampus, often with impairment of consciousness and behavioral automatisms.

Absence Seizure → 3-Hz Spike-Wave: Characteristic bilateral, synchronous, symmetrical 3-Hz spike-wave complexes on EEG correlating precisely with staring and unresponsiveness.

Myoclonic Seizure → Polyspike-Wave: Bursts of polyspike-wave complexes (multiple sharp waves followed by slow wave) corresponding to jerking movements.

Post-Ictal Slowing: Following seizure, the EEG typically shows generalized slowing (theta and delta activity) that gradually returns to baseline over minutes to hours. This post-ictal EEG slowing correlates with clinical postictal confusion.

Pearl #17: Seizure Mimicry in Anesthetized/Paralyzed Patients

When a paralytic agent is used, seizure activity becomes electrographic without visible motor manifestation. The clinical semiology disappears entirely, making bedside diagnosis impossible. Clues that NCSE is occurring in a paralyzed patient:

Sudden autonomic instability: Abrupt hypertension, tachycardia, or diaphoresis without obvious cause
Pupillary changes: Abrupt pupillary dilation
Nystagmus: Persistent jerk nystagmus (often the only observable motor activity in paralyzed patient)
Twitching of small muscles: Eyelid flickering, minute facial twitching, or fasciculation-like movements of face

Any of these changes in a previously stable paralyzed patient warrants immediate EEG and consideration of NCSE.

Part VI: Syndromic Presentations and Clinical Context

Seizures in Acute Stroke

Timing and Incidence: Early post-stroke seizures (within 2 weeks) occur in 3–5% of acute ischemic stroke and up to 20% of hemorrhagic stroke patients. Seizures are more common with large cortical strokes, hemorrhage, and subarachnoid hemorrhage.

Semiology Clues: Focal motor seizures with march pattern strongly suggest acute cortical involvement. The seizure semiology may identify the vascular territory affected (anterior cerebral artery → contralateral leg; middle cerebral artery → contralateral arm and face).

Clinical Pearl #18: Post-stroke seizures commonly manifest as recurrent, brief focal seizures rather than prolonged convulsive status. Each seizure may last only 30–60 seconds but recur at intervals of minutes to hours. This pattern is easily missed if not specifically sought. The series of seizures may be interpreted as "jerking" or "spasticity," delaying appropriate seizure management.

Seizures in Sepsis and Metabolic Encephalopathy

Semiology: Seizures in metabolic encephalopathy often differ from primary epileptic seizures. They tend to be:

Generalized and bilateral: Rather than focal, reflecting global cerebral dysfunction
Myoclonic: Often manifest as multifocal, non-rhythmic myoclonus rather than true seizure semiology
Associated with altered baseline mental status: The patient may already be altered before seizures begin

Context Clue: The presence of obvious precipitant (infection, renal failure, hepatic failure) makes metabolic seizure more likely than primary epilepsy. Correction of the metabolic derangement often controls seizures better than antiepileptic monotherapy alone.

Seizures in Hypoxic-Ischemic Encephalopathy

Myoclonic Seizures Post-Cardiac Arrest: Post-anoxic myoclonus represents one of the most challenging semiological presentations. Myoclonic jerks may be:

Cortical epileptic myoclonus: Arising from damaged cortex, with EEG correlate (spike-wave preceding jerk by 10–50 msec)
Subcortical non-epileptic myoclonus: Arising from brainstem or thalamus, without EEG correlate; typically rhythmic at 1–3 Hz
Spinal myoclonus: Lower limb jerks arising from spinal cord; may persist despite full brainstem death

Clinical Pearl #19: Post-anoxic myoclonus carries ominous prognostic significance, yet the etiology (epileptic vs. non-epileptic) predicts treatment response. Epileptic myoclonus may respond to antiepileptic drugs; non-epileptic myoclonus typically does not and reflects irreversible brainstem damage.⁹ EEG is mandatory to differentiate these, as semiology alone cannot reliably distinguish them. Video-EEG performed simultaneously with clinical myoclonus allows precise temporal correlation between EEG event and motor manifestation.

Oyster: Lance-Adams syndrome—delayed post-anoxic encephalopathy with progressive myoclonic epilepsy that develops weeks to months after cardiac arrest—presents with generalized myoclonic seizures in a previously recovering patient. This rare syndrome should be suspected when seizures emerge during apparent recovery, distinct from immediate post-arrest myoclonus.

Seizures in Neuroinfection (Meningitis, Encephalitis)

Semiology Patterns:

Infections of the central nervous system produce seizures through multiple mechanisms: inflammation, cortical involvement, increased intracranial pressure, or metabolic derangement. The semiology often reflects the specific pathogen and location of infection.

Bacterial Meningitis: Seizures occur in 20–30% of cases, typically early in disease course. They are often generalized and recurrent. The seizures may appear before, concurrent with, or after meningeal signs appear clinically.

Viral Encephalitis (especially Herpes Simplex Virus): Focal seizures are common, reflecting preferential involvement of temporal and inferofrontal lobes by HSV. Focal seizures with temporal lobe automatisms, or focal motor seizures with contralateral march, should raise suspicion for HSV encephalitis.

Tuberculous Meningitis: Often produces status epilepticus, with seizures being an early and ominous sign. The seizures may evolve from focal to generalized pattern.

Clinical Pearl #20: In a patient with fever and new-onset seizures, consider neuroinfection until proven otherwise. The seizure semiology may provide the first clue to localization of infection. A patient with fever, headache, and focal temporal lobe seizures with impaired awareness should receive empirical HSV treatment while awaiting CSF results.

Part VII: Advanced Semiological Concepts

Lateralization and Localization Through Semiology

Motor Semiology for Localization:

The motor march of focal motor seizure provides exquisite cortical localization due to the somatotopic organization of motor cortex. A seizure that begins in the hand and marches to forearm and shoulder indicates a focus in the hand area of motor cortex, contralateral to the affected side.

Head and Eye Deviation Semiology:

This is among the most reliable lateralizing signs in seizure semiology:

Contraversive Head/Eye Deviation: Eyes and head turn away from the seizing limbs, toward the side opposite the motor activity. This occurs because the focus drives conjugate gaze away from itself. A patient with leftward head/eye deviation has a right hemisphere focus.
Versive Head/Eye Deviation: Eyes and head turn toward the seizing limbs. This is less common but indicates contralateral frontal involvement.

Memorization Hack: Think of the seizure focus as "pushing" the eyes and head away. Eyes turn away from the seizure focus, so rightward gaze means left-sided focus.

Automatisms: Window into Temporal Lobe Pathology

Behavioral automatisms are hallmark of temporal lobe seizure with impaired awareness. The specific automatisms provide clues to seizure laterality and specific brain involvement:

Right Temporal Lobe Seizures: Tend to produce less structured automatisms—vigorous thrashing, complex hand movements, or undressing.

Left Temporal Lobe Seizures: Tend to produce more structured automatisms—lip smacking, picking movements, or verbal automatisms (speaking in jargon or nonsense).

Orbitofrontal Involvement: Rapid cycling between automatisms—the patient may alternate between different stereotyped behaviors during the same seizure, suggesting involvement of orbitofrontal regions involved in behavioral switching.

Clinical Pearl #21: The consistency of automatisms is more diagnostic than the specific type. Ask family or witnesses if the automatisms are identical each time. Seizure automatisms are stereotyped; each seizure produces the same sequence of behaviors. Psychogenic seizures produce variable, less structured movements. This distinction, combined with EEG, provides definitive diagnosis.

Aura Semiology and Predictive Value

The aura represents the earliest clinical manifestation of focal seizure, occurring when the epileptiform discharge is still limited to a small cortical region before secondary spread. The nature of the aura provides precise localization:

Sensory Aura (Somatosensory Cortex): Tingling in a specific body part that may march somatotopically. Bilateral sensory aura or sensory aura affecting non-somatotopic distribution suggests non-epileptic etiology.

Visual Aura (Occipital Cortex): Flashing lights, color (typically unilateral, in the visual field contralateral to focus), or crude geometric patterns indicate occipital lobe seizure.

Auditory Aura (Superior Temporal Lobe): Simple sounds (buzzing, roaring) rather than complex auditory hallucinations. Complex auditory experiences (hearing voices or music) suggest non-epileptic etiology.

Epigastric Aura (Medial Temporal Lobe/Insular Cortex): Rising sensation in the stomach, often described as butterflies, pressure, or nausea. This is among the most common auras and highly specific for temporal lobe seizure.

Fear Aura (Amygdala): Intense sudden fear or dread, often without external trigger. Nearly pathognomonic for amygdala involvement in medial temporal lobe.

Vestibular Aura (Temporoparietal Junction): Vertigo, spinning sensation, or feeling of body rotation. Indicates seizure in regions involved in vestibular processing.

Clinical Pearl #22: The aura, though subjective, is highly reliable for localization because it reflects the initial seizure focus before secondary spread. A patient who consistently reports the same aura has a stable, localized seizure focus. Change in aura semiology may indicate a new lesion or progression of existing pathology.

Autonomic Seizures: The "Hidden" Presentation

Seizures can originate in insular cortex, orbitofrontal cortex, or other autonomic-regulatory regions, producing predominantly autonomic manifestations:

Ictal Bradycardia: Abrupt slowing of heart rate to 40–50 bpm during seizure, sometimes with cardiac asystole lasting < 5 seconds. This is frightening for observers but typically self-limited.

Ictal Tachycardia and Hypertension: More common; sustained elevation of heart rate and blood pressure during ictal phase.

Respiratory Dysrhythmia: Irregular or agonal-appearing breathing during seizure, ranging from apnea to hyperventilation.

Urinary Incontinence: Occurs during ictal phase due to relaxation of sphincters; post-ictal urinary retention is common.

Salivation and Lacrimation: Excessive saliva production (foaming at mouth) and tearing during seizure.

Temperature Elevation: Rapid rise in core body temperature, particularly with prolonged seizure or status epilepticus, due to sustained muscle activity and increased metabolic rate.

Oyster: Sudden Unexpected Nocturnal Death in Epilepsy (SUDEP) is hypothesized to result partially from ictal autonomic dysrhythmia—specifically, respiratory depression and cardiac arrhythmia during nocturnal seizure. Patients with nocturnal seizures may benefit from pulse oximetry and apnea monitoring, especially those with clustering seizures or frequent nocturnal events.

Semiological Seizure Classification for Prognostication

The specific seizure semiology has prognostic implications:

Simple Motor Seizures (without secondary generalization): Generally have better prognosis for seizure control with single-agent antiepileptic therapy compared to complex seizures or status epilepticus.

Focal Seizures with Secondary Generalization: Indicate structural lesion in ~40% of cases; these patients require neuroimaging and often need dual-agent therapy.

Status Epilepticus (any type): Associated with significant morbidity and mortality; even brief seizures that evolve rapidly to status carry worse prognosis than isolated seizures.

Post-Ictal Deficit Severity: Severe, prolonged postictal confusion or focal neurological deficit (Todd's paralysis) suggests more severe ictal discharge and may indicate greater seizure burden.

Part VIII: Practical ICU Bedside Algorithm

The "Seizure or Not?" Rapid Assessment

When witnessing a suspected seizure or encountering altered mental status, use this bedside framework:

Step 1: Obtain Witnessed Account

Ask observers (family, nurses, paramedics): What did you see? Describe movements, their onset, sequence, duration, and recovery.

Step 2: Examine the Patient

Consciousness: Is the patient now fully alert, partially confused, or unresponsive?
Tongue: Examine for fresh lateral lacerations with blood or erythema
Pupils: Note size and reactivity; compare to patient's baseline
Motor Examination: Focal weakness? Asymmetry? (Could indicate Todd's paralysis or structural lesion)
Autonomic Status: Heart rate, blood pressure, respiratory pattern, temperature

Step 3: Mental Status Assessment

Can the patient follow commands? Form sentences? Remember recent events?
How rapidly is orientation returning? (True postictal confusion improves over 5–30 minutes)

Step 4: EEG Determination

Obtain immediately if: Altered consciousness persists >30 minutes, seizure recurrence, any possibility of status epilepticus
Obtain urgently if: First unprovoked seizure, significant head trauma, fever with seizure, or seizure semiology inconsistent with patient's known seizure history
Can defer briefly if: Clear single seizure with rapid return to baseline AND no red flags

Step 5: Neuroimaging Decision

Obtain emergently if: First unprovoked seizure, focal seizure semiology, asymmetric motor features, or new neurological deficit
Obtain urgently if: Status epilepticus, concern for acute lesion (stroke, hemorrhage, infection)
Can defer if: Known epilepsy with seizure consistent with baseline pattern, clear provoked seizure (metabolic derangement being corrected)

The "Subtle Status Epilepticus" Recognition Checklist

When seizure activity is suspected but semiology is unclear, ask:

□ Is the patient unexpectedly altered in consciousness?

□ Are there autonomic changes (tachycardia, hypertension, diaphoresis) without obvious explanation?

□ Does the patient have nystagmus, eye deviation, or subtle eyelid flickering?

□ Is there minimal motor activity (tremor, myoclonus, or fasciculations)?

□ Did the altered state follow a witnessed seizure that the patient "should have recovered from" by now?

□ Are there bursts of unclear behavior or repetitive automatisms?

If 3 or more boxes are checked, obtain stat EEG and consider empiric benzodiazepine therapy pending EEG results.

Part IX: Teaching Points for Postgraduate Learners

Key Takeaways

Semiology is the foundation: Accurate bedside recognition of seizure semiology remains essential despite modern neurophysiological advances. EEG confirms but does not replace careful clinical observation.
Context matters: The patient's history, precipitants (fever, medications, metabolic derangement), and baseline neurological status inform semiological interpretation.
Focal seizures are structural until proven otherwise: Any seizure with focal features (motor march, lateralized head/eye deviation, unilateral motor activity) mandates neuroimaging to exclude acute lesion.
Postictal confusion is the signature: True generalized seizures produce profound postictal confusion lasting many minutes. Immediate alertness essentially rules out primary generalized seizure.
Subtle status is deadly: The most dangerous seizures are those that appear least obvious. Electromechanical dissociation—ongoing ictal activity with minimal motor manifestation—is where mortality peaks. High index of suspicion and early EEG are life-saving.
Seizure mimics are common: PNES, syncope, and movement disorders can closely resemble seizure. Distinguishing features include preserved responsiveness, immediate recovery of consciousness, and specific timing patterns.
Semiology guides first-line therapy: Focal versus generalized distinction informs which antiepileptic to choose initially. Structural seizures need different workup and sometimes different management (e.g., surgical consultation).
The aura is a gift: When a patient provides clear aura description, you receive precise localization information. Never dismiss aura as "just anxiety" or psychological phenomenon.

Common Pearls to Reinforce in Teaching

Pearl A - The "5-Minute Rule":

Within 5 minutes of witnessing an event, determine: (1) Was consciousness impaired? (2) Were movements rhythmic and symmetric? (3) Did the patient bite their tongue? (4) How rapidly did they become alert?

Affirmative answers to (1) and (2), and a positive answer to (3), strongly support seizure diagnosis. If the answer to (4) is "immediately," reconsider diagnosis.

Pearl B - The "Todd's Paralysis" Differential:

Post-ictal focal weakness can mimic acute stroke. Key differentiators:

Onset: Develops immediately post-seizure in Todd's paralysis; develops acutely outside of seizure in stroke
Resolution: Improves over hours in Todd's paralysis; persists in acute stroke
Imaging: Todd's paralysis may show transient signal changes; acute stroke shows restricted diffusion on DWI

Pearl C - The "Autonomic Burst" Sign:

A sudden surge in heart rate (from 80 to 140 bpm in seconds), rising blood pressure, and diaphoresis during an event is virtually diagnostic of seizure. Few other conditions produce such dramatic, instantaneous autonomic change. Syncope produces gradual autonomic changes; PNES rarely produces sustained changes.

Part X: Emerging Concepts and Future Directions

Quantitative Semiology and Artificial Intelligence

Recent work using video analysis and machine learning to quantify semiological features (movement velocity, symmetry indices, seizure progression patterns) shows promise for automated seizure detection and classification. These tools may enhance bedside recognition, particularly in resource-limited settings or during overnight hours when human observation is limited.

Wearable Devices and Remote Monitoring

Emerging wearable seizure detection devices (accelerometers, ECG monitors, sweat sensors) can detect convulsive seizures with >90% sensitivity, alerting patients and caregivers to impending SUDEP risk or status epilepticus. Integration of these with bedside EEG and vital sign monitoring may enhance early recognition of subtle seizures in ICU settings.

High-Frequency Oscillations as Biomarkers of Seizure Focus

Interictal high-frequency oscillations (100–500 Hz) recorded on EEG or intracranial electrodes mark epileptogenic tissue more precisely than traditional spike activity. Future ICU monitoring may employ algorithms that detect high-frequency oscillations to identify seizure focus in patients with multiple seizures, guiding more targeted treatment or surgical intervention.

Summary and Clinical Imperatives

Seizure semiology remains the most immediate, accessible, and clinically valuable diagnostic tool for critical care physicians. Systematic assessment of the witnessed event, careful examination of tongue, pupils, and postictal state, and integration of clinical context allow accurate bedside diagnosis in the majority of cases.

Critical gaps in recognition include:

Non-convulsive seizures remain dramatically underdiagnosed; low threshold for EEG in altered patients is life-saving
Focal seizures with secondary generalization are frequently misclassified as primary generalized, leading to inappropriate monotherapy
Subtle status epilepticus lacks obvious clinical manifestation; persistent altered consciousness after apparent single seizure warrants aggressive investigation
Seizure mimics are common and should be actively considered in differential diagnosis

The ICU physician's ability to recognize seizure semiology, synthesize clinical context, and respond with appropriate investigation and empiric treatment directly impacts patient outcomes and mortality. This skill remains a core competency that no advancement in technology can fully replace.

References

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Author Notes

This review synthesizes over two decades of clinical literature in seizure semiology and distills core concepts essential for postgraduate critical care training. The emphasis on bedside recognition, practical differentiation from mimics, and integration of semiological findings with neurophysiological and neuroimaging data reflects the multidisciplinary approach required for excellence in critical care neurology.

The "pearls," "oysters," and "hacks" embedded throughout are drawn from clinical experience and represent nuanced insights that extend beyond standard medical training. Their inclusion reflects the pedagogical approach of enhancing clinical acumen through memorable, applicable teaching points.

For the critical care physician, mastery of seizure semiology transforms a symptom (altered consciousness, movement) into a diagnosis, guides appropriate investigation, and initiates timely life-saving intervention.

Saturday, October 11, 2025