Epilepsy Mimics & DDx
Epilepsy Mimics & Differential Diagnosis
What Do You Need to Know?
- 20–30% of "drug-resistant epilepsy" referrals do not have epilepsy — misdiagnosis is one of the most common errors in neurology
- PNES is the most important mimic: mean diagnostic delay 7–10 years; ictal eye closure (approximately 50–88% sensitivity, 74–96% specificity across studies; Chung 2006 et al.) is one of the more reliable semiologic distinguishing signs
- ECG is MANDATORY for every first seizure presentation — cardiac channelopathies (Long QT, CPVT, Brugada) cause convulsive syncope and carry risk of sudden death
- Convulsive syncope — convulsive movements occur in up to 90% of syncope episodes (Lempert 1994); myoclonic jerks during syncope are common, not rare, and do NOT indicate epilepsy
- Dual diagnosis: 10–50% of PNES patients also have true epilepsy — never assume all events are the same type
- Gold standard: video-EEG monitoring with capture of a habitual event. A habitual event with no ictal scalp EEG correlate strongly supports PNES when semiology is compatible, but consider scalp-negative frontal/deep seizures before calling an event non-epileptic.
🚩 Don’t Miss — Test-Day Priorities
- PNES gold standard: video-EEG capturing the habitual spell with no ictal EEG correlate — treat with psychotherapy (CBT), NOT ASMs
- ECG on every first seizure: exclude Long QT, Brugada, CPVT, heart block — convulsive syncope from arrhythmia kills patients misdiagnosed as epilepsy
- Convulsive syncope is common: myoclonic jerks occur in up to 90% of syncopes — brief LOC <30 sec + prodrome + rapid recovery without postictal confusion = syncope, not seizure
- PKD (paroxysmal kinesigenic dyskinesia): brief <1 min movements triggered by sudden movement, preserved awareness, PRRT2 gene → dramatic response to carbamazepine (classic board point)
- PED + GLUT1 deficiency (SLC2A1): exercise-induced dyskinesia + low CSF glucose → ketogenic diet is both diagnostic and therapeutic
- RBD (REM sleep behavior disorder): dream enactment in older adults → prodromal α-synucleinopathy (PD, DLB, MSA); first-line treatment is melatonin
- TIA vs focal seizure: TIA = negative phenomena (weakness, numbness, loss of vision) in vascular distribution; seizure = positive phenomena (jerking, paresthesias, scintillations) with Jacksonian march
- Migraine aura march: slow 5–60 min spread of positive visual symptoms (fortification spectra, scintillating scotoma) — seizure aura is seconds, TIA is sudden-onset negative
- Cataplexy: sudden bilateral loss of muscle tone triggered by laughter/emotion with preserved consciousness — narcolepsy type 1 (low CSF hypocretin), NOT atonic seizure
- Pallid breath-holding spells in infants: vagally mediated after pain/startle → check hemoglobin/ferritin (iron deficiency association); treat with reassurance + iron if low
- Avoid the worst error: misdiagnosing PNES as refractory epilepsy → years of unnecessary ASMs, ICU admissions for "status," iatrogenic harm
🔍 Buzzwords & Pathognomonic FindingsDistinguishing features · Triggers / context · Workup / treatment
Distinguishing features
- Forced eye closure + pelvic thrusting + asynchronous flailing + side-to-side head shake + ictal crying + recall of event → PNES
- Brief LOC <30 sec + prodromal lightheadedness/nausea/visual greying + pallor + rapid recovery without postictal confusion → Syncope
- Convulsive jerks during cerebral hypoperfusion (myoclonic, brief, non-rhythmic) → Convulsive syncope (not epileptic)
- Dream enactment, punching/kicking bed partner in older adult → REM sleep behavior disorder (RBD)
- Screaming child sitting up in first third of night, inconsolable, no recall → NREM parasomnia (sleep terror)
- Brief <1 min abnormal movements + preserved awareness + dramatic carbamazepine response → PKD (PRRT2)
- Slow march of fortification spectra / scintillating scotoma over 5–60 min → Migraine aura
- Sudden focal NEGATIVE deficit in vascular territory, no positive features → TIA
- Sudden bilateral loss of tone with preserved consciousness → Cataplexy (narcolepsy type 1)
- Diaphoresis + tremor + confusion + fingerstick glucose <70, reverses with dextrose → Hypoglycemia
Triggers / context
- Emotional stress, history of trauma/abuse, comorbid PTSD or conversion disorder → PNES
- Prolonged standing, hot environment, venipuncture, micturition, defecation, emotional → Neurocardiogenic (vasovagal) syncope
- Syncope on EXERTION or SUPINE, family history of sudden cardiac death, young athlete → Cardiogenic syncope (Long QT, HCM, CPVT, Brugada)
- Standing up from supine, autonomic neuropathy, Parkinsonism, dehydration, antihypertensives → Orthostatic syncope
- Sudden voluntary movement (rising from chair, startle) → PKD
- Alcohol, caffeine, stress, fatigue (no movement trigger) → PNKD (PNKD/MR1)
- Prolonged exercise + low CSF glucose → PED (GLUT1 / SLC2A1 deficiency)
- Laughter, joking, surprise → brief loss of tone → Cataplexy
- Pain or startle → pale infant becomes limp/loses consciousness → Pallid breath-holding spell (iron deficiency association)
- Frustration/crying → cyanotic infant during expiratory apnea → Cyanotic breath-holding spell
- Positional head movement → sudden drop attack → Third ventricle colloid cyst
Workup / treatment
- Video-EEG with capture of habitual event + normal ictal EEG → PNES confirmed; treat with CBT (CODES trial), gradual ASM taper
- ECG + Holter + tilt-table + echo (long QT in young, structural heart disease) → Syncope workup
- Polysomnography (PSG) with video → Parasomnia workup; RBD = REM without atonia → melatonin first-line
- PRRT2 genetic testing + therapeutic trial of carbamazepine → PKD confirmation
- CSF glucose + SLC2A1 sequencing + ketogenic diet trial → GLUT1 deficiency / PED
- Orthostatic vitals (drop ≥20 systolic / ≥10 diastolic within 3 min standing) → Orthostatic syncope
- CSF hypocretin-1 low + MSLT with ≥2 SOREMPs → Narcolepsy/cataplexy
- ABCD2 score + urgent MRI/MRA + carotid imaging + cardiac monitor → TIA workup
- Fingerstick glucose + IV D50 → Hypoglycemia (reverses event)
- Hemoglobin, ferritin + reassurance + iron supplementation if deficient → Pallid breath-holding spell
- Multidisciplinary care (neurology + psychiatry) + empathetic delivery of diagnosis → PNES management (itself therapeutic)
PNES (Psychogenic Nonepileptic Seizures) — The Most Important Mimic
Epidemiology & Impact
- 20–30% of patients referred to epilepsy monitoring units with "drug-resistant epilepsy" have PNES
- Mean diagnostic delay: 7–10 years of unnecessary ASM exposure
- Also termed functional seizures or dissociative seizures (FND spectrum)
- Consequences: iatrogenic ASM toxicity, ICU admissions for "status," psychosocial burden
Semiologic Features
| Feature | Sensitivity | Specificity | Notes |
|---|---|---|---|
| Ictal eye closure | ~50–88% | ~74–96% | One of the more reliable semiologic signs (Chung 2006 et al.); eyes are typically open during epileptic GTCS |
| Waxing/waning course | 94% | Very high (>90%) | Fluctuating intensity with pauses; seizures evolve but do not wax/wane; caveat: frontal lobe seizures can mimic |
| Asynchronous limb movements | 84% | Very high (>90%) | Out-of-phase alternating; caveat: frontal lobe seizures can mimic |
| Duration >2 minutes | 65% | 93% | GTCS typically 1–2 min; PNES often 5–30 min |
| Side-to-side head movement | 63% | Very high (>90%) | Lateral head shaking during event; caveat: frontal lobe seizures can mimic |
| Pelvic thrusting | 24% | 97% | Low sensitivity but highly specific; rarely in frontal lobe epilepsy |
| Ictal crying/weeping | Low | Very high | Virtually pathognomonic when present |
Dual Diagnosis
- 10–50% of PNES patients also have coexisting epilepsy
- Each event type must be independently identified on video-EEG
- Never assume all events in one patient are the same type
Diagnosis
- Gold standard: video-EEG capturing habitual event with normal ictal EEG
- Staged approach (ILAE): documented → clinically established → confirmed (EEG-video confirmed)
- Prolactin: elevated after GTCS (not after PNES or absence)
- AAN guideline: serum prolactin >2× baseline, drawn 10–20 minutes post-event, supports GTCS or complex partial seizure (but does NOT exclude epilepsy if normal)
- Must draw within 10–20 minutes of the event
- Limited sensitivity; NOT reliable as sole diagnostic tool
- Often not elevated after frontal lobe seizures (variable across focal epilepsies)
Treatment
- Psychotherapy is the treatment — NOT ASMs
- CBT has the best evidence (CODES trial: CBT-informed therapy reduced seizure frequency)
- Empathetic communication of the diagnosis is itself therapeutic
- Gradual ASM taper if no concurrent epilepsy is safe and avoids iatrogenic harm; symptomatic improvement requires psychotherapy (CODES trial)
- Avoid iatrogenic harm: no IV benzodiazepines for prolonged PNES events
💎 Board Pearl
- Ictal eye closure throughout a convulsive event strongly suggests PNES. Eyes are typically open during epileptic GTCS; ictal eye closure throughout a convulsive event strongly suggests PNES. Reported sensitivity ~50–88% and specificity ~74–96% across studies (Chung 2006 et al.) — one of the more reliable semiologic signs, but not pathognomonic
Syncope vs. Seizure
Comparison Table
| Feature | Syncope | Epileptic Seizure (GTCS) |
|---|---|---|
| Trigger | Positional/situational (standing, pain, heat) | Usually spontaneous; sleep deprivation, alcohol |
| Prodrome | Lightheadedness, tunnel vision, warmth, nausea | Focal aura (déjà vu, epigastric rising) or none |
| Position | Usually upright | Any position (including supine or from sleep) |
| Skin color | Pale, diaphoretic | Cyanotic (respiratory compromise) |
| Motor features | Brief myoclonus (<15 sec), irregular, multifocal — occurs in up to 90% of syncope (Lempert 1994) | Sustained tonic → rhythmic clonic (1–2 min) |
| Duration of LOC | Seconds (<30 sec) | Minutes (1–3 min + postictal) |
| Recovery | Rapid (<1 min), oriented quickly | Prolonged postictal confusion (5–30+ min) |
| Tongue bite | Tip of tongue (if any) | Lateral tongue laceration (specific) |
| Incontinence | Uncommon | Common in GTCS |
Convulsive Syncope
- Convulsive movements occur in up to 90% of syncope episodes (Lempert 1994 videometric analysis); myoclonic jerks during syncope are common, not rare
- Mechanism: transient cerebral hypoperfusion → cortical disinhibition → subcortical motor release
- Brief (<15 sec) tonic stiffening or irregular, multifocal myoclonic jerks
- Does NOT indicate epilepsy; does NOT require ASMs
- No prolonged postictal confusion
💎 Board Pearl
- Lateral tongue laceration = seizure. Tip tongue bite = syncope (if any). Lateral tongue bite specificity ~99% but sensitivity only ~24% — absence does not exclude seizure. This is the highest-yield tongue-bite distinction for boards
Cardiac Mimics — Critical for Boards
ECG Is Mandatory
- ECG must be obtained for EVERY first seizure presentation
- Cardiac channelopathies cause convulsive syncope indistinguishable from GTCS by observation alone
- Family history of unexplained sudden death (<40 years) = critical red flag
Key Cardiac Channelopathies
| Condition | Gene | Presentation Clue | Diagnosis |
|---|---|---|---|
| Long QT (LQT1) | KCNQ1 | "Seizure" during swimming = LQT1 until proven otherwise | Prolonged QTc on resting ECG |
| Long QT (LQT2) | KCNH2 | Syncope with auditory startle | Prolonged QTc on resting ECG |
| Long QT (LQT3) | SCN5A | Events during sleep/rest | Prolonged QTc on resting ECG |
| CPVT | RYR2 (AD), CASQ2 (AR) | 30% misdiagnosed as epilepsy; resting ECG is NORMAL | Exercise stress test: bidirectional VT (pathognomonic) |
| Brugada | SCN5A | Nocturnal syncope/SCD (may be convulsive); SE Asian males in 3rd–4th decade; SUNDS phenotype | Coved ST elevation V1–V3; Na channel blocker provocation |
SUDEP & Cardiac Overlap
- 10–15% of SUDEP autopsy cases have cardiac channel gene variants
- Overlap between epilepsy and cardiac channelopathy genes (e.g., SCN5A, SCN1A)
- Some "SUDEP" cases may be primary cardiac arrhythmia deaths
💎 Board Pearl
- CPVT has the highest misdiagnosis rate of all cardiac channelopathies because the resting ECG is completely normal. Exercise stress test is required. Exercise-triggered "seizures" + normal resting ECG = think CPVT before epilepsy
Paroxysmal Dyskinesias
| Type | Gene | Trigger | Duration | Treatment |
|---|---|---|---|---|
| PKD | PRRT2 | Sudden movement (standing, starting to walk) | <1 min (seconds) | Dramatic response to low-dose CBZ |
| PNKD | MR-1/PNKD | Alcohol, caffeine, stress (NOT movement) | 10 min–hours | Clonazepam; CBZ NOT effective |
| PED | SLC2A1 (GLUT1) | Sustained exercise (10–15 min continuous) | 5–30 min | Ketogenic diet |
PRRT2: One Gene, Three Phenotypes
- BFIS: seizure clusters in infancy, resolve by age 2
- PKD: movement-triggered dyskinesias in childhood/adolescence
- ICCA syndrome: BFIS in infancy followed by PKD in adolescence (same individual)
- All three respond to low-dose carbamazepine; all have excellent prognosis
Key Principle
- Paroxysmal dyskinesias are NOT epileptic — consciousness preserved; EEG normal during events
- PKD is one of the most gratifying diagnoses: dramatic response to minimal treatment
💎 Board Pearl
- PRRT2 = one gene, three phenotypes (BFIS + PKD + ICCA). All respond to low-dose CBZ. Exercise-induced dystonia + low CSF glucose = think GLUT1 (SLC2A1); treat with ketogenic diet
Benign Paroxysmal Events of Infancy
| Condition | Key Features | Distinguishing Clue |
|---|---|---|
| Shuddering attacks | Brief tremor-like shivering; head tremor, shoulder elevation | Normal development; resolves by age 2; family history of essential tremor |
| Jitteriness (neonatal) | Rhythmic tremulous movements; stimulus-sensitive; symmetric | Stops with passive flexion (seizures do NOT); higher frequency/lower amplitude |
| Sandifer syndrome | Dystonic posturing with GERD; arching, head rotation during feeds | Related to feeding; resolves with antireflux treatment (PPI) |
| Benign tonic upgaze | Sustained upward gaze; compensatory head retroflexion | Consciousness preserved; horizontal movements normal; resolves by age 2–4 |
| Spasmus nutans | Triad: head bobbing + nystagmus + torticollis | MRI MANDATORY to exclude chiasmal/hypothalamic glioma |
| Benign neonatal sleep myoclonus | Myoclonic jerks ONLY in sleep; may be dramatic | STOPS on awakening; WORSENED by benzos; resolves by 3–6 months |
| Non-epileptic head drops | Brief head drops mimicking epileptic spasms | Normal EEG (no hypsarrhythmia); self-gratification behavior |
💎 Board Pearl
- Benign neonatal sleep myoclonus: sleep-only, stops on waking, WORSENED by benzos — the paradoxical benzodiazepine worsening is a classic board question
- Jitteriness vs. seizure: jitteriness is stimulus-sensitive and suppressible by passive flexion; seizures are NOT suppressible — key bedside maneuver
Sleep Events vs. Nocturnal Seizures
| Condition | Key Features | Distinguishing Clue |
|---|---|---|
| SHE (Sleep-related Hypermotor Epilepsy) | Brief (<2 min); hypermotor; stereotyped; multiple per night; NREM | Any time of night; frequent (5–10+/night); genes: nAChR subunits CHRNA4, CHRNB2, CHRNA2; KCNT1 (severe SHE, often drug-resistant; some response to quinidine reported); mTOR pathway DEPDC5, NPRL2, NPRL3 (often with focal cortical dysplasia on MRI) |
| NREM parasomnias | Sleep terrors, sleepwalking, confusional arousals; longer; N3 | First third of night; variable/non-stereotyped; difficult to arouse |
| REM behavior disorder | Dream enactment; violent movements; vivid dream recall | Latter third of night; older adults; PSG shows REM sleep without atonia (diagnostic); >80% phenoconvert to synucleinopathy (PD/DLB/MSA) within 10–15 years |
| Hypnagogic jerks | Single brief myoclonic jerk at sleep onset; falling sensation | Sleep-wake transition ONLY; single jerk; universal (60–70%) |
SHE vs. Parasomnias — Quick Comparison
- SHE: brief, stereotyped, frequent, any time of night, rapid return to sleep
- Parasomnias: longer, variable, infrequent, first third of night, hard to arouse
- Frontal seizures may have no scalp EEG correlate — video-EEG with extended sleep montage often required
Other Mimics
Hyperekplexia (Startle Disease)
- Gene: GLRA1 (glycine receptor α1-subunit); NOT epileptic
- Exaggerated startle to unexpected stimuli (especially nose tap); neonatal hypertonia
- Vigevano maneuver (forced head/limb flexion) aborts attacks; treatment: clonazepam
Tics & Stereotypies
- Suppressible (with effort); premonitory urge unique to tics
- Stereotypies: interruptible by distraction; no postictal state; normal EEG
Migraine with Aura vs. Seizure
- Migraine aura: gradual march over 20–30 minutes (cortical spreading depolarization)
- Seizure aura: rapid spread over seconds
- Key: minutes to develop = migraine; seconds = seizure
Migraine Variants That Mimic Seizures
- Hemiplegic migraine — genes CACNA1A, ATP1A2, SCN1A (gene overlap with epilepsy); unilateral motor weakness with aura that can persist hours; can mimic focal motor seizure or postictal Todd paralysis. Familial (FHM) and sporadic forms; SCN1A overlap links to Dravet spectrum.
- Migraine with brainstem aura (formerly basilar migraine) — bilateral visual disturbance, vertigo, dysarthria, ataxia, tinnitus, diplopia; can include LOC and confusional state; mimics posterior (occipital/temporal) seizure or syncope. Diagnosed when ≥2 fully reversible brainstem symptoms accompany typical migraine.
TIA vs. Seizure
- TIA: negative symptoms (weakness, numbness, vision loss)
- Seizure: positive symptoms (jerking, tingling, flashing lights)
- Exception: limb-shaking TIA (hemodynamic insufficiency) mimics focal motor seizures
Daydreaming vs. Absence Seizure
- Daydreaming: interruptible; longer duration; no automatisms
- Absence: NOT interruptible; abrupt onset/offset; eyelid flutter; 3 Hz spike-wave
- Hyperventilation provokes absences but NOT daydreaming — useful bedside test
Transient Global Amnesia (TGA)
- Duration 4–8 hours; pure anterograde amnesia with retrograde gradient
- Repetitive questioning (“Where am I? What happened?”) is classic
- Preserved personal identity and procedural skills; no other focal neurologic deficit
- Single lifetime event typical; mid-to-late adulthood; often triggered by emotional/physical stress, Valsalva, cold water immersion
- MRI may show transient punctate DWI hyperintensity in CA1 hippocampus 24–72h after onset
TGA vs. TEA (Transient Epileptic Amnesia)
- TGA: single-lifetime event, hours-long (4–8h), no recurrence, no ASM response
- TEA: recurrent, brief (<1 hour), often on awakening; interictal/long-term autobiographical memory loss and topographical amnesia; responds to ASMs (usually carbamazepine or lamotrigine)
- TEA is a form of temporal lobe epilepsy — consider in older adults with recurrent brief amnestic spells
Cataplexy / Narcolepsy
- Cataplexy: sudden bilateral loss of muscle tone triggered by emotion (especially laughter); consciousness is preserved throughout
- Classic atonic seizure / drop attack mimic; preserved awareness is the key distinguishing feature
- Narcolepsy type 1 (with cataplexy): hypocretin/orexin deficiency (CSF orexin-A <110 pg/mL); strong HLA-DQB1*06:02 association
- REM intrusion phenomena — hypnagogic/hypnopompic hallucinations and sleep paralysis — can also mimic seizures or PNES
- Diagnosis: MSLT showing mean sleep latency ≤8 min and ≥2 sleep-onset REM periods (SOREMPs); treat with modafinil/pitolisant/sodium oxybate
Episodic Ataxias
- EA1 (KCNA1, Kv1.1) — brief attacks (seconds to minutes) of ataxia/dysarthria triggered by startle or exertion; interictal myokymia (continuous fine muscle rippling, often periorbital/hand); can mimic focal motor seizures. Some patients have comorbid epilepsy.
- EA2 (CACNA1A) — hours-long attacks of ataxia with nystagmus (often downbeat) and vertigo; responds dramatically to acetazolamide; allelic with familial hemiplegic migraine type 1 and SCA6 (gene overlap with epilepsy and migraine).
- Consciousness preserved; ictal EEG normal — not epileptic
Diagnostic Approach to Paroxysmal Events
Systematic Algorithm
- Step 1 — Detailed history: patient AND witnesses; triggers, timing, position, motor features, awareness, recovery
- Step 2 — Home video: smartphone recording; reviewed by specialist achieves ~89% PPV
- Step 3 — ECG for ALL: mandatory 12-lead; measure QTc; exclude cardiac channelopathies
- Step 4 — Routine EEG: sensitivity 50–60% on first study; normal EEG does NOT exclude epilepsy
- Step 5 — Sleep-deprived EEG: increases yield; serial studies reach 80–90%
- Step 6 — Prolonged video-EEG: gold standard; habitual event with no ictal scalp EEG correlate strongly supports PNES when semiology is compatible, but consider scalp-negative frontal/deep seizures before excluding epilepsy
- Step 7 — MRI brain: epilepsy protocol if epilepsy suspected
- Consider: ambulatory EEG, exercise stress test, tilt-table test, PSG
Red Flags for Non-Epileptic Events
- Failure to respond to 2+ appropriately chosen ASMs
- Prolonged duration (>5 min) without postictal state
- Eye closure during convulsive event; waxing/waning motor activity
- Preserved responsiveness during bilateral motor event
Red Flags for Cardiac Cause
- Event during exercise, swimming, or emotional stress
- Abrupt LOC WITHOUT prodrome; rapid full recovery
- Family history of sudden cardiac death at young age (<40)
Board Pearls
💎 Board Pearl
- Ictal eye closure throughout a convulsive event strongly suggests PNES (approximately 50–88% sensitivity, 74–96% specificity across studies; Chung 2006 et al.); eyes are typically open during epileptic GTCS — one of the more reliable semiologic signs
- "Seizure" during swimming = Long QT type 1 (KCNQ1) until proven otherwise — ECG with QTc measurement is the critical first test
- CPVT: 30% epilepsy misdiagnosis rate; resting ECG is NORMAL — exercise stress test showing bidirectional VT is diagnostic; the normal resting ECG is why it gets missed
- Benign neonatal sleep myoclonus: sleep-only, stops on waking, WORSENED by benzos — the paradoxical benzodiazepine worsening is a classic board question
- Lateral tongue bite = seizure; tip tongue bite = syncope — specificity ~99% but sensitivity only ~24%; absence does NOT exclude seizure. Only objectively confirmed lateral laceration is specific; self-reported biting occurs equally in PNES and epilepsy
- Drug-resistant epilepsy failing 2 ASMs = mandatory diagnostic reassessment — 20–30% of these patients do not have epilepsy at all
- 10–15% of SUDEP autopsy cases have cardiac channel gene variants — overlap between epilepsy and cardiac channelopathy genetics
Clinical Pearls
Clinical Pearl
Prolactin for seizure diagnosis is a trap. While prolactin elevation after GTCS (not after PNES or absence) seems useful, it must be drawn within 10–20 minutes, is often not elevated after frontal lobe seizures (variable across focal epilepsies), and has limited sensitivity. A normal prolactin does NOT exclude epileptic seizures. Video-EEG remains the gold standard.
Clinical Pearl
SHE vs. parasomnias — the key is stereotypy. If the family describes the same bizarre nocturnal behavior happening identically multiple times per night, think SHE. If events are variable, prolonged, and happen only in the first hours of sleep, think parasomnia. Frontal seizures may have NO scalp EEG correlate.
Clinical Pearl
Convulsive syncope is not epilepsy. Convulsive movements occur in up to 90% of syncope episodes (Lempert 1994) — brief (<15 sec) tonic stiffening or irregular myoclonic jerks from cerebral hypoperfusion. Myoclonic jerks during syncope are common, not rare. These do NOT indicate epilepsy, do NOT require ASMs, and should not lead to an epilepsy diagnosis. Key: positional trigger, pallor, rapid recovery without postictal confusion.
References
- LaFrance WC Jr, Baker GA, Duncan R, et al. Minimum requirements for the diagnosis of psychogenic nonepileptic seizures: a staged approach. Epilepsia 2013;54(11):2005–2018.
- Goldstein LH, Robinson EJ, Mellers JDC, et al. Cognitive behavioural therapy for adults with dissociative seizures (CODES): a pragmatic, multicentre, randomised controlled trial. Lancet Psychiatry 2020;7(6):491–505.
- Chung SS, Gerber P, Kirlin KA. Ictal eye closure is a reliable indicator for psychogenic nonepileptic seizures. Neurology 2006;66(11):1730–1731.
- Lempert T, Bauer M, Schmidt D. Syncope: a videometric analysis of 56 episodes of transient cerebral hypoxia. Ann Neurol 1994;36(2):233–237.
- Schwartz PJ, Ackerman MJ, Antzelevitch C, et al. Inherited cardiac arrhythmias. Nat Rev Dis Primers 2020;6(1):58.
- Leenhardt A, Lucet V, Denjoy I, et al. Catecholaminergic polymorphic ventricular tachycardia in children. Circulation 1995;91(5):1512–1519.
- Tinuper P, Bisulli F, Cross JH, et al. Definition and diagnostic criteria of sleep-related hypermotor epilepsy. Neurology 2016;86(19):1834–1842.
- Bruno MK, Hallett M, Gwinn-Hardy K, et al. Clinical evaluation of idiopathic paroxysmal kinesigenic dyskinesia: new diagnostic criteria. Neurology 2004;63(12):2280–2287.
- Chen WJ, Lin Y, Xiong ZQ, et al. Exome sequencing identifies truncating mutations in PRRT2 that cause paroxysmal kinesigenic dyskinesia. Nat Genet 2011;43(12):1252–1255.
- Derry CP, Duncan JS, Berkovic SF. Paroxysmal motor disorders of sleep: the clinical spectrum and differentiation from epilepsy. Epilepsia 2006;47(11):1775–1791.
- Hallett M, Aybek S, Dworetzky BA, et al. Functional neurological disorder: new subtypes and shared mechanisms. Lancet Neurol 2022;21(6):537–550.
- Ertan D, Aybek S, LaFrance WC Jr, et al. Functional (psychogenic non-epileptic/dissociative) seizures: updated review. J Neurol Neurosurg Psychiatry 2022;93(10):1029–1037.
- Uldall P, Alving J, Hansen LK, et al. The misdiagnosis of epilepsy in children admitted to a tertiary epilepsy centre with paroxysmal events. Arch Dis Child 2006;91(3):219–221.
- Kotagal P, Costa M, Wyllie E, et al. Paroxysmal nonepileptic events in children and adolescents. Pediatrics 2002;110(4):e46.
- Continuum (Minneap Minn). Epilepsy. Volume 31, Number 1, February 2025.
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