Last Minute Review
Epilepsy — Last Minute Review
Rapid Review
A last-minute review of high-yield epilepsy facts for the RITE and board exams. Tables, key associations, and must-know one-liners — designed for a quick pass the night before.
Seizure Classification (ILAE 2025 Update)
| Old Term | 2017 Term | 2025 Term |
|---|---|---|
| Simple partial seizure | Focal aware seizure | Focal preserved consciousness seizure (FPC) |
| Complex partial seizure | Focal impaired awareness seizure | Focal impaired consciousness seizure (FIC) |
| Secondarily generalized tonic-clonic | Focal to bilateral tonic-clonic | Focal-to-bilateral tonic-clonic (FBTC) |
| Grand mal | Generalized-onset tonic-clonic | Generalized tonic-clonic (GTC) |
| Petit mal | Absence (non-motor) | Absence seizure (“non-motor” removed) |
| Aura | Focal aware seizure | Focal preserved consciousness seizure |
💎 Board Pearl
- 2025 key changes: “awareness” → consciousness (= awareness + responsiveness); “motor/non-motor” → observable/non-observable; “onset” dropped from class names; 63 → 21 seizure types
- New seizure type: generalized negative myoclonus (brief <500 ms interruption of tone)
- Epileptic spasms = seizure type only in generalized; in focal/unknown = descriptor
- Consciousness is a classifier for focal and unknown seizures only — generalized seizures always impair consciousness
Epilepsy Syndromes by Age of Onset
Neonatal (<2 months)
| Syndrome | Seizure Type | EEG Pattern | Key Gene/Etiology | Prognosis |
|---|---|---|---|---|
| Ohtahara (EIEE) | Tonic spasms | Burst suppression (wake + sleep) | STXBP1, KCNQ2, structural | Severe; may evolve to West → LGS |
| KCNQ2 neonatal epilepsy | Tonic, clonic | Burst suppression or multifocal | KCNQ2 | Good if self-limited; poor if DEE variant |
| Benign familial neonatal epilepsy | Clonic, apneic | May be normal interictally | KCNQ2, KCNQ3 | Excellent; remits by 6 months |
| Pyridoxine-dependent epilepsy | Multifocal clonic, myoclonic | Burst suppression or multifocal | ALDH7A1 | Seizure-free on B6; cognitive variable |
| Early myoclonic encephalopathy | Erratic myoclonus | Burst suppression (more in sleep) | Metabolic (NKH, organic acidurias) | Severe |
Infantile (2–12 months)
| Syndrome | Seizure Type | EEG Pattern | Key Gene/Etiology | Prognosis |
|---|---|---|---|---|
| Infantile epileptic spasms (West) | Epileptic spasms (clusters) | Hypsarrhythmia | TSC, structural, genetic (ARX, CDKL5) | Variable; 60–70% have cognitive impairment |
| Dravet syndrome | Prolonged febrile hemiclonic → myoclonic, absence, focal | Normal early; generalized spike-wave later | SCN1A (80%) | Poor; drug-resistant, cognitive decline |
| SCN2A encephalopathy | Tonic, clonic | Multifocal or burst suppression | SCN2A | Variable; early-onset → Na-blockers may help |
| CDKL5 encephalopathy | Epileptic spasms, tonic, hypermotor | Multifocal or hypsarrhythmia | CDKL5 | Severe; Rett-like features |
Childhood (1–12 years)
| Syndrome | Seizure Type | EEG Pattern | Key Feature | Prognosis |
|---|---|---|---|---|
| CAE | Typical absence (10–30 s, pluridaily) | 3 Hz generalized spike-wave | Peak 4–8 yr; hyperventilation provokes 100% | Good; 65–70% remit by adolescence |
| Doose (MAE) | Myoclonic-atonic | 2–3 Hz spike/polyspike-wave | Drop attacks; may have absence, GTCC | Variable; 50–60% seizure-free |
| SeLECTS (BECTS) | Focal hemifacial motor ± somatosensory; sleep predominant | Centrotemporal spikes (high-amplitude dipole) | Most common childhood epilepsy; age 3–13 yr | Excellent; all remit by age 16 |
| Panayiotopoulos | Autonomic (nausea, vomiting, pallor), eye deviation | Occipital ± multifocal spikes | Prolonged seizures; mimics gastroenteritis or encephalitis | Excellent; remits 1–2 yr after onset |
| LGS | Tonic (sleep), atonic, atypical absence, myoclonic, GTCC | Slow (<2.5 Hz) spike-wave + generalized paroxysmal fast activity (GPFA) in sleep | Onset 1–7 yr; multiple seizure types | Poor; drug-resistant, cognitive decline |
| CSWS / ESES | Variable; may be subtle | Continuous spike-wave in >85% of NREM sleep | Cognitive/behavioral regression | EEG normalizes by puberty; cognitive outcome variable |
| Landau-Kleffner | Focal, absence-like | ESES pattern over temporal/perisylvian | Acquired aphasia (auditory agnosia) | Language recovery variable; seizures remit |
Adolescent / Adult
| Syndrome | Seizure Type | EEG Pattern | Key Feature | Prognosis |
|---|---|---|---|---|
| JME | Myoclonic jerks (morning) + GTCC + absence (30%) | 4–6 Hz polyspike-wave | Onset 12–18 yr; photosensitive; lifelong Rx | Well-controlled but rarely remits (<10%); lifelong ASM |
| JAE | Absence (less frequent than CAE) + GTCC (80%) | 3–4 Hz spike-wave (faster fragments) | Onset 10–17 yr; GTCC common | Good control; lower remission rate than CAE |
| GTCA alone (epilepsy with GTCC only) | GTCC only | Generalized spike-wave / polyspike-wave | Onset 10–25 yr; often on awakening | Good control on ASM |
| TLE (mesial) | Focal impaired awareness — epigastric aura, déjà vu, oral/manual automatisms | Temporal intermittent rhythmic delta (TIRDA), anterior temporal sharp waves | Most common focal epilepsy in adults; hippocampal sclerosis | 30% drug-resistant; surgery 60–80% seizure-free |
| FLE | Brief, nocturnal, hypermotor, bilateral motor; rapid secondary generalization | May be normal interictally; vertex/frontal spikes | Clusters from sleep; bizarre semiology → misdiagnosed as PNES | Variable; surgery less successful than TLE |
💎 Board Pearl
- Ohtahara → West → LGS = classic electroclinical evolution of severe neonatal-onset epilepsy
- CAE: 3 Hz spike-wave provoked by hyperventilation; JME: 4–6 Hz polyspike-wave provoked by sleep deprivation/photic stimulation
- SeLECTS = most common childhood epilepsy; 100% remission by age 16
- GPFA in sleep = pathognomonic for LGS
EEG Patterns & Epilepsy Associations
| EEG Pattern | Association |
|---|---|
| 3 Hz generalized spike-wave | Childhood absence epilepsy |
| 3–4 Hz spike-wave (slightly faster fragments) | Juvenile absence epilepsy |
| 4–6 Hz generalized polyspike-wave | Juvenile myoclonic epilepsy |
| Hypsarrhythmia | Infantile spasms (West syndrome) |
| Burst suppression (neonatal) | Ohtahara / early myoclonic encephalopathy |
| Centrotemporal spikes (tangential dipole) | SeLECTS (BECTS) |
| Anterior temporal sharp waves / TIRDA | Mesial temporal lobe epilepsy |
| Slow (<2.5 Hz) spike-wave | Lennox-Gastaut syndrome |
| Generalized paroxysmal fast activity (GPFA) in NREM | LGS (pathognomonic) |
| Continuous spike-wave in NREM (>85%) | CSWS / ESES |
| Occipital spikes (shifting) | Panayiotopoulos syndrome |
| Photoparoxysmal response (PPR) | JME, progressive myoclonic epilepsies |
| 2–3 Hz polyspike-wave | Doose (myoclonic-atonic epilepsy) |
| Vertex positive sharp waves (neonatal) | Benign neonatal sleep myoclonus (not epilepsy) |
| Stimulus-induced rhythmic, periodic, or ictal discharges (SIRPIDs) | ICU artifact — significance debated |
| Lateralized periodic discharges (LPDs) | Acute structural lesion (stroke, HSV encephalitis); seizure risk 50–60% |
| Generalized periodic discharges (GPDs) | Metabolic/toxic encephalopathy, CJD, post-anoxic |
💎 Board Pearl
- Hypsarrhythmia = chaotic, high-amplitude, asynchronous slow waves + multifocal spikes — disappears during spasm (electrodecremental)
- TIRDA (temporal intermittent rhythmic delta activity) has the same localizing value as temporal sharp waves for TLE
- GPFA is seen in LGS only; slow spike-wave alone is insufficient for diagnosis
ASM Selection by Syndrome
| Syndrome / Seizure Type | First-Line ASM | Alternatives | Avoid |
|---|---|---|---|
| Focal seizures | LEV, LTG, OXC, CBZ | BRV, ZNS, LCM, cenobamate | — |
| Focal to bilateral tonic-clonic | LEV, LTG, OXC, CBZ | LCM, cenobamate, VPA | — |
| Generalized tonic-clonic (IGE) | VPA, LEV, LTG | TPM, PER, CLB | CBZ, OXC, PHT, GBP, TGB (worsen myoclonus/absence) |
| Typical absence | ETX, VPA, LTG | CLB | CBZ, OXC, PHT, GBP, TGB, VGB |
| JME | VPA (most effective), LEV, LTG (low dose) | TPM, CLB, PER | CBZ, OXC, PHT, GBP (worsen myoclonus) |
| Infantile spasms | ACTH (high dose), vigabatrin (especially if TSC) | Prednisolone (ICISS) | CBZ, OXC |
| Dravet syndrome | VPA + CLB; stiripentol + VPA + CLB | CBD (Epidiolex), fenfluramine | Na-channel blockers (CBZ, OXC, LTG, PHT, LCM) — worsen seizures |
| LGS | VPA, LTG, CLB, rufinamide | CBD, felbamate, TPM | CBZ, OXC (may worsen atonic/tonic) |
| CSWS/ESES | High-dose BZDs (clobazam, diazepam), VPA, ETX | Corticosteroids, IVIG, surgery if focal | — |
| TLE (drug-resistant) | Consider surgery early (ERSET: superior to 2 more ASM trials) | Cenobamate, LCM | Delay of surgical referral |
💎 Board Pearl
Drugs That Worsen Specific Syndromes
- Na-channel blockers (CBZ, OXC, LTG, PHT, LCM) → worsen Dravet (SCN1A loss-of-function)
- CBZ, OXC, PHT, GBP, TGB → worsen absence, myoclonus in JME and other IGEs
- LTG at high doses can worsen myoclonus in JME (use low dose, titrate slowly)
- Vigabatrin → irreversible visual field constriction (peripheral); requires visual field monitoring every 3 months
- VPA in women of childbearing age → highest teratogenicity (NTDs 6–10%, IQ ↓ 8–11 points); avoid if possible
Status Epilepticus Protocol
| Time | Stage | Treatment | Dose (Adult) | Key Notes |
|---|---|---|---|---|
| 0–5 min | Stabilization | ABCs, IV access, glucose, labs | D50W 25–50 mL; thiamine 100 mg IV | Note seizure onset time; call for cEEG |
| 5–10 min | First-line: BZDs | Midazolam IM or Lorazepam IV or Diazepam IV | Midazolam 10 mg IM; Lorazepam 4 mg IV (×2); Diazepam 10 mg IV (×2) | RAMPART: IM midazolam 73% vs. IV lorazepam 63%; repeat BZD ×1 if ongoing |
| 10–20 min | Second-line: IV ASMs | Fosphenytoin or Levetiracetam or Valproate | fPHT 20 mg PE/kg; LEV 60 mg/kg (max 4500 mg); VPA 40 mg/kg | ESETT: all 3 equivalent (~46–47%); choose based on patient factors |
| 20–40 min | Second second-line | Try another agent from above or lacosamide / phenobarbital | LCM 400 mg IV; PB 20 mg/kg | If still seizing after 2 agents → RSE |
| >40 min | Refractory SE → anesthetic infusions | Midazolam gtt or Propofol or Pentobarbital | MDZ: 0.2 mg/kg bolus → 0.05–2 mg/kg/h; Propofol: 1–2 mg/kg bolus → 20–65 mcg/kg/min; Pentobarbital: 5 mg/kg bolus → 1–5 mg/kg/h | Target: burst suppression on cEEG; intubation + vasopressors; avoid propofol >48 h (PRIS) |
| ≥24 h on anesthetics | Super-refractory SE | Multimodal: ketamine, immunotherapy, ketogenic diet | Ketamine 1–5 mg/kg/h; anakinra; IVIG/PLEX if autoimmune | Consider NORSE/FIRES → immunotherapy ≤72 h; ketogenic diet ≤7 days |
💎 Board Pearl
- RAMPART → IM midazolam is non-inferior AND superior to IV lorazepam for prehospital SE
- ESETT → fosphenytoin = levetiracetam = valproate as second-line (all ~47%); choose by comorbidities
- VA Cooperative → stepwise efficacy decline: 1st agent 55% → 2nd agent 7% → 3rd agent 2%
- >75% of SE patients receive subtherapeutic BZD doses — apparent “refractoriness” may be underdosing
Presurgical Evaluation Checklist
| Modality | Purpose | Key Details |
|---|---|---|
| MRI epilepsy protocol | Identify structural lesion | 3T; thin-cut coronal FLAIR/T2 perpendicular to hippocampus; 3D T1 volumetric; look for hippocampal sclerosis, FCD, tumors, vascular malformations |
| Video-EEG monitoring | Capture habitual seizures; localize onset | Phase I: scalp; Phase II: intracranial (SEEG or subdural grids); need ≥3 concordant seizures |
| Neuropsychological testing | Lateralize/localize cognitive function; predict postop deficits | Memory asymmetry suggests lateralization; low baseline → less to lose |
| Wada test (IAP) | Lateralize language and memory | Amobarbital into ICA; being replaced by fMRI in many centers |
| Functional MRI (fMRI) | Map eloquent cortex (language, motor) | Replacing Wada for language lateralization; concordance >90% |
| FDG-PET | Interictal hypometabolism at seizure focus | Sensitivity 80–90% for TLE; hypometabolism = seizure focus |
| Ictal SPECT | Ictal hyperperfusion at seizure focus | Must inject within 30 s of seizure onset; SISCOM (subtraction ictal-interictal SPECT co-registered to MRI) |
| MEG | Localize interictal dipole sources | Complement to EEG; better for deep/tangential sources; useful for MRI-negative cases |
| Stereo-EEG (SEEG) | Intracranial recording via depth electrodes | Phase II; preferred for bilateral, deep, or non-lesional cases; lower morbidity than grids |
| Subdural grids/strips | Cortical mapping + seizure localization | Phase II; better for neocortical mapping/stimulation; higher morbidity than SEEG |
💎 Board Pearl
- Concordance model: surgery most successful when MRI, EEG, PET, semiology all point to same focus
- PET = interictal hypometabolism; SPECT = ictal hyperperfusion
- SEEG is now preferred over grids in most centers — lower infection/hemorrhage rate, better for bilateral hypotheses
Epilepsy Surgery Types & Outcomes
| Procedure | Indication | Seizure-Free Rate (Engel I) | Key Notes |
|---|---|---|---|
| Anterior temporal lobectomy (ATL) | Drug-resistant mTLE with hippocampal sclerosis | 60–80% | Gold standard for mTLE; ERSET: ATL superior to continued ASM trials |
| Selective amygdalohippocampectomy (SAH) | mTLE with hippocampal sclerosis | 50–70% | May preserve more lateral temporal function; less naming decline in dominant hemisphere |
| MRI-guided laser ablation (LITT/SLAH) | mTLE, hypothalamic hamartoma, small lesions | 50–60% (mTLE) | Minimally invasive; shorter recovery; slightly lower seizure-free rate than open ATL |
| Lesionectomy | Focal lesion (tumor, cavernoma, FCD) | 60–90% | Best outcomes when complete resection + concordant EEG |
| Corpus callosotomy | Drop attacks (atonic/tonic) in LGS; palliative | 50–75% reduction in drop attacks | Palliative — not curative; anterior 2/3 first; complete if drops persist |
| Hemispherectomy / hemispherotomy | Hemispheric syndromes (Rasmussen, Sturge-Weber, large hemispheric malformations) | 60–80% | Functional hemispherotomy preferred; best outcomes in children (neuroplasticity) |
| VNS | Drug-resistant epilepsy; not a surgical candidate | ~5% seizure-free; 50% responder rate ~50% at 2–3 yr | Palliative; left vagus; side effects: hoarseness, cough; improves over years |
| RNS (NeuroPace) | 1–2 foci in eloquent cortex; bilateral temporal | ~18% seizure-free at 9 yr; median 75% reduction | Closed-loop responsive stimulation; efficacy improves over years; FDA-approved 2013 |
| DBS (anterior nucleus of thalamus) | Drug-resistant focal epilepsy (≥2 foci ok) | ~20% seizure-free at 7 yr; median 75% reduction | SANTE trial; open-loop; can target CMN for generalized epilepsy |
💎 Board Pearl
- ERSET trial: early surgery (ATL) superior to continued ASM trials for drug-resistant TLE — do not delay surgical referral after failure of 2 appropriate ASMs
- ATL = highest seizure-free rate; LITT/SLAH = lower morbidity but slightly lower efficacy
- RNS and DBS both improve over years (unlike ASMs which have stable efficacy)
- Corpus callosotomy: palliative for drops — risk of disconnection syndrome if complete
Key Genetics in Epilepsy
| Gene | Channel / Protein | Syndrome | Key Features |
|---|---|---|---|
| SCN1A | Nav1.1 (sodium channel) | Dravet syndrome (LOF); GEFS+ (GOF) | 80% of Dravet; Na-blockers worsen LOF variants |
| SCN2A | Nav1.2 (sodium channel) | Neonatal/infantile DEE; self-limited familial neonatal-infantile epilepsy | Early onset GOF → Na-blockers may help; late onset LOF → avoid |
| KCNQ2 | Kv7.2 (potassium channel) | Self-limited neonatal epilepsy (mild); KCNQ2-DEE (severe) | Na-channel blockers (CBZ) effective; burst suppression in severe form |
| KCNQ3 | Kv7.3 (potassium channel) | Benign familial neonatal epilepsy | Usually self-limited |
| CDKL5 | Kinase (signaling) | CDKL5 deficiency disorder | Rett-like; epileptic spasms; X-linked; ganaxolone FDA-approved |
| STXBP1 | Syntaxin-binding protein (synaptic) | Ohtahara, West, non-syndromic DEE | Burst suppression; one of most common DEE genes |
| TSC1 / TSC2 | Hamartin / Tuberin (mTOR pathway) | Tuberous sclerosis complex | Cortical tubers, infantile spasms; vigabatrin first-line; everolimus (mTOR inhibitor) for refractory |
| ARX | Transcription factor | X-linked infantile spasms, lissencephaly | Males; brain malformations; severe |
| SLC2A1 | GLUT1 (glucose transporter) | GLUT1 deficiency syndrome | Low CSF glucose (CSF:serum glucose ratio <0.4); ketogenic diet = treatment of choice |
| DEPDC5 | mTOR pathway regulator | Familial focal epilepsy with variable foci (FFEVF) | AD; different family members have different focal seizure types; FCD IIa on MRI |
| PCDH19 | Protocadherin (cell adhesion) | PCDH19-related epilepsy | X-linked; affects females (cellular interference); clusters with fever; males are carriers |
| ALDH7A1 | Antiquitin (lysine metabolism) | Pyridoxine-dependent epilepsy | Neonatal seizures; give pyridoxine (B6) trial; elevated pipecolic acid / α-AASA |
| KCNT1 | KNa1.1 (potassium channel) | Epilepsy of infancy with migrating focal seizures; SHE | GOF; quinidine trial (variable success) |
💎 Board Pearl
- SCN1A LOF = Dravet → avoid Na-channel blockers; SCN1A GOF = GEFS+
- GLUT1 deficiency: low CSF glucose, normal serum glucose → ketogenic diet is the treatment
- PCDH19: X-linked but affects females (not males) — unique mechanism of cellular interference
- TSC + infantile spasms → vigabatrin first-line (not ACTH)
SUDEP
Risk Factors
| Risk Factor | Details |
|---|---|
| Frequent GTCC | #1 risk factor; ≥3 GTCC/year → OR 15; prone position post-ictally |
| Drug-resistant epilepsy | Uncontrolled seizures = highest modifiable risk |
| Young adult (20–40 yr) | Peak SUDEP risk age range |
| Nocturnal seizures | Unwitnessed; no repositioning; MORTEMUS: 73% occur in prone position |
| Polytherapy with subtherapeutic levels | Proxy for poor seizure control |
| Male sex | Slightly higher risk |
| Duration of epilepsy >15 yr | Cumulative risk |
| Absence of nocturnal supervision | Living alone ↑ risk |
Prevention Strategies
| Strategy | Details |
|---|---|
| Seizure control | Most important — optimize ASMs; consider surgery for drug-resistant cases |
| Nocturnal supervision / monitoring | Seizure detection devices, bed alarms; someone in the room ↓ SUDEP risk |
| Avoid prone sleeping post-ictally | MORTEMUS: prone position in 73% of SUDEP cases |
| SUDEP counseling | AAN practice parameter recommends discussing SUDEP with all epilepsy patients |
| Adherence to ASMs | Missed doses → breakthrough GTCC → ↑ SUDEP risk |
💎 Board Pearl
- SUDEP incidence: ~1/1000 patient-years (general epilepsy); up to 9/1000 in drug-resistant epilepsy
- MORTEMUS mechanism: post-ictal generalized EEG suppression (PGES) → central apnea → cardiac arrest
- #1 modifiable risk factor = GTCC frequency
Special Populations
Pregnancy & ASMs
| ASM | Teratogenicity | Key Malformation | Breastfeeding |
|---|---|---|---|
| Valproate | Highest risk (6–10% MCM rate; dose-dependent) | Neural tube defects, cardiac, craniofacial; IQ ↓ 8–11 points | Low transfer; generally safe |
| Topiramate | Elevated (3–5%) | Cleft lip/palate; SGA infants | Moderate transfer; monitor infant |
| Phenobarbital | Elevated (5–7%) | Cardiac; cognitive effects | Sedation risk; monitor |
| Phenytoin | Moderate (3–5%) | Fetal hydantoin syndrome (craniofacial, digital hypoplasia) | Low transfer; safe |
| Carbamazepine | Moderate (2–3%) | NTDs (lower than VPA); craniofacial | Safe |
| Lamotrigine | Lowest risk (~2%) | No specific pattern | Safe; significant transfer but well-tolerated |
| Levetiracetam | Low (~2%) | No specific pattern | Safe |
| Oxcarbazepine | Low (~2–3%) | Limited data | Generally safe |
Pregnancy Management Pearls
| Item | Details |
|---|---|
| Folic acid | All WWE: 0.4–4 mg/day preconception through 1st trimester (higher dose if on VPA or prior NTD) |
| LTG in pregnancy | Clearance ↑ 50–100% by 3rd trimester → monthly levels; dose ↑ often needed; taper postpartum |
| VPA in pregnancy | Avoid if at all possible; if used, lowest effective dose; dose-dependent IQ effects (NEAD study) |
| Seizure risk | ~15–30% have ↑ seizure frequency; GTCC = greatest fetal risk (placental abruption, fetal hypoxia) |
| Registry | NAAED Pregnancy Registry; EURAP; all WWE should be enrolled |
Driving Regulations
| Item | Details |
|---|---|
| Seizure-free interval | 3–12 months depending on state (most common: 6 months) |
| Reporting | 6 states = mandatory physician reporting (CA, DE, NV, NJ, OR, PA); rest = voluntary/patient responsibility |
| Commercial driving (CDL) | FMCSA: 8 years seizure-free AND off all ASMs (essentially excludes epilepsy) |
| Aura-only seizures | Some states allow driving if auras never impair awareness; document with video-EEG |
| ASM changes | Many states restart seizure-free interval after ASM change (varies) |
Clinical Pearl
VPA in Women of Childbearing Age
- VPA is FDA category X in pregnancy for migraine — contraindicated
- NEAD study: VPA exposure → mean IQ 8–11 points lower at age 6 vs. other ASMs
- FDA boxed warning: VPA contraindicated for migraine/bipolar in pregnant women or women of childbearing potential not using effective contraception
- If VPA must be used for epilepsy: lowest effective dose, divided dosing, high-dose folic acid
Classic Board Traps
💎 Board Pearl
Na-Channel Blockers & Specific Syndromes
- Dravet + CBZ/OXC/LTG/PHT/LCM → seizure exacerbation (SCN1A loss-of-function; blocking already impaired Nav1.1 on inhibitory interneurons)
- JME + CBZ/OXC/PHT/GBP → worsens myoclonus and absence
- CAE + CBZ/OXC/PHT/GBP/TGB → worsens absence seizures; may precipitate absence SE
- LGS + CBZ → may worsen tonic and atonic seizures
Clinical Pearl
Mesial Temporal Sclerosis — MRI Features
- Hippocampal atrophy (volume loss) on T1
- Hippocampal hyperintensity on T2/FLAIR
- Loss of internal hippocampal architecture (loss of digitations)
- Best seen on coronal thin-cut FLAIR perpendicular to long axis of hippocampus
- May have associated temporal pole blurring/atrophy
- Board favorite: given MRI → identify hippocampal sclerosis → recommend surgical evaluation
Clinical Pearl
PNES (Psychogenic Non-Epileptic Seizures) Clues
- Eyes closed during event (epileptic seizures: eyes typically open)
- Asynchronous, side-to-side head/body movements; waxing/waning intensity
- Prolonged duration (>2 min for convulsive events)
- Preserved awareness during bilateral motor activity
- Pelvic thrusting (not specific — can occur in frontal lobe seizures)
- Immediate postical return to baseline; crying/emotional distress post-event
- Normal EEG during event is diagnostic (video-EEG = gold standard)
- Elevated prolactin 10–20 min post-event supports epileptic GTCC (not reliable for focal seizures or PNES)
💎 Board Pearl
Other High-Yield Board Traps
- Hyperventilation provokes absence seizures 100% — if no absence with 3 min HV, reconsider diagnosis
- JME: lifelong treatment — >90% relapse with ASM withdrawal (unlike CAE)
- Panayiotopoulos: prolonged autonomic seizures in children — do NOT misdiagnose as gastroenteritis or encephalitis
- FLE vs. PNES: frontal lobe seizures are brief, stereotyped, nocturnal, with rapid postictal recovery — bizarre semiology ≠ PNES
- KCNQ2 neonatal epilepsy: responds to sodium channel blockers (CBZ/PHT) — opposite of Dravet
- GLUT1 deficiency: low CSF glucose with normal serum glucose → ketogenic diet (not ASMs) is the treatment
- Drug-resistant epilepsy definition: failure of 2 tolerated, appropriately chosen, and adequately dosed ASMs (ILAE 2010)
- Vigabatrin visual field loss is irreversible (retinal toxicity) — requires VF monitoring q3 months
- LTG rash: risk ↑ with rapid titration, VPA co-therapy (VPA doubles LTG levels); SJS/TEN risk
- Felbamate: aplastic anemia (1:5000) + hepatic failure (1:10,000) — requires CBC/LFT monitoring; reserved for LGS
💎 Board Pearl
- Eyes open = epileptic seizure; eyes closed = think PNES
- If a question says “seizures worsened after starting carbamazepine” → think Dravet, JME, or absence epilepsy
- Prolactin: ↑ post-GTCC/focal with impaired awareness (NOT post-PNES); measure at 10–20 min