Is this event actually a seizure?
Most misdiagnosed "epilepsy" is something else entirely. Before you ever classify a seizure, decide whether the paroxysmal event was epileptic at all. The two big pretenders are syncope and psychogenic non-epileptic events.
The single most useful tool here is a careful witnessed history — a phone video of the event is worth more than any test you can order in clinic. Anchor the interview on what happened before, during, and after.
| Feature | Epileptic seizure | Convulsive syncope | Psychogenic (PNES) |
|---|---|---|---|
| Trigger / prodrome | Sometimes aura (rising epigastric, déjà vu, focal sensory) | Upright posture, pain, heat, standing; greyout, tunnel vision, warmth, nausea | Emotional context; often prolonged, fluctuating build-up |
| Onset | Abrupt | Gradual over seconds | Variable, may be gradual |
| Motor pattern | Rhythmic, synchronous, decrementing; tonic then clonic | Brief (<15 s) arrhythmic multifocal jerks after collapse | Asynchronous, side-to-side head, pelvic thrust, waxing/waning, stop-start |
| Eyes | Open, may deviate | Open, rolled up | Often forcibly closed, resist opening |
| Duration | 1–3 min typical | Seconds | Often >2 min, can be very long |
| Tongue bite | Lateral tongue (specific) | Rare; tip if any | Tip of tongue, lips |
| Recovery | Post-ictal confusion, gradual over minutes | Rapid, oriented within seconds | Variable; may have rapid reorientation or prolonged unresponsiveness |
| Incontinence | Can occur | Can occur | Can occur — not discriminating |
Convulsive syncope is the most common false-positive. Brief jerks and even incontinence happen with any cause of cerebral hypoperfusion — they do not make the event a seizure. Ask what came first: collapse then jerks (syncope) or jerks then fall (seizure). PNES and epilepsy co-exist in a meaningful minority of patients; the presence of one does not exclude the other, and definitive diagnosis usually needs video-EEG.
Does this patient have epilepsy?
A single seizure is not epilepsy. The ILAE gives a practical, operational definition — and, importantly, an updated one that lets you diagnose epilepsy after a first unprovoked seizure when recurrence risk is high.
The ILAE 2014 operational definition
Epilepsy is a disease of the brain defined by any one of the following three conditions:
- At least two unprovoked (or reflex) seizures occurring more than 24 hours apart.
- One unprovoked seizure and a probability of further seizures similar to the general recurrence risk after two unprovoked seizures (at least ~60%) over the next 10 years.
- Diagnosis of an epilepsy syndrome (e.g., juvenile myoclonic epilepsy on the strength of history + EEG, even after one clinical event).
Provoked vs. unprovoked — this changes everything
An acute symptomatic (provoked) seizure occurs in close temporal relationship to an acute insult and does not by itself indicate epilepsy. Treat the cause, not the "epilepsy." Common provokers:
- Metabolic: hyponatremia (<115), hypoglycemia, hypocalcemia, uremia, hepatic failure.
- Toxic / withdrawal: alcohol withdrawal (classically 6–48 h), benzodiazepine withdrawal, cocaine, bupropion, tramadol.
- Acute brain insult within ~7 days: stroke, trauma, CNS infection, hypoxic-ischemic injury.
- Fever in a young child meeting febrile seizure criteria.
Definition #2 is where primary-care neurology earns its keep. After a first unprovoked seizure, features that push recurrence risk toward or above 60% — and therefore justify a diagnosis and treatment — include an epileptiform EEG, a symptomatic lesion on MRI, a remote symptomatic cause (prior stroke, trauma, infection), and a nocturnal seizure. A first seizure with a normal EEG, normal imaging, and no clear cause carries roughly a 30–40% two-year recurrence risk — often watched rather than treated after shared decision-making.
The minimum first-seizure workup
| Test | What it answers | Note |
|---|---|---|
| History + witness / video | Was it a seizure? Focal features at onset? | Highest yield of anything here |
| EEG | Epileptiform activity → recurrence risk, classification | A normal routine EEG does not exclude epilepsy; sleep-deprived / repeat raises yield |
| MRI brain (epilepsy protocol) | Structural lesion → focal epilepsy, surgical target | Preferred over CT except in the acute/emergent setting |
| Labs | Provoked cause? (glucose, Na, Ca, Mg, renal, tox) | Rules provocation in or out |
| ECG | Syncope mimic, long-QT, arrhythmia | Cheap, catches a dangerous mimic |
Classify the seizure type
The ILAE 2017 framework classifies at three levels: seizure type → epilepsy type → syndrome. Everything starts with one question that colors the rest of the workup: where did the seizure begin?
The three onset categories
Focal onset
Begins in networks limited to one hemisphere. Sub-classify by awareness (aware vs. impaired) and by first prominent feature (motor vs. non-motor). May evolve to a focal-to-bilateral tonic-clonic seizure.
Generalized onset
Engages bilateral networks from the start. Awareness is not used to sub-classify (it's usually impaired). Split into motor (tonic-clonic, myoclonic, tonic, atonic) and non-motor / absence.
Unknown onset
Used when onset isn't witnessed or is unclear. Still describe observable features (e.g., "unknown-onset tonic-clonic"). Reclassify later as data arrive.
Interactive classifier
Work through the same questions you'd ask a witness. This walks the ILAE branch points and lands on a seizure-type label. It is a teaching aid, not a diagnosis.
Classify the epilepsy type & look for a syndrome
Once you know the seizure type(s), the epilepsy type usually follows. The 2017 framework adds a category most primary-care neurologists under-use: combined generalized and focal epilepsy.
| Epilepsy type | Typical evidence | Prescribing implication |
|---|---|---|
| Focal | Focal seizures; focal epileptiform EEG; structural MRI lesion | Broad list works; the "narrow-spectrum" sodium-channel agents are safe here |
| Generalized | Generalized seizure types; generalized spike-wave EEG; usually normal MRI | Choose a broad-spectrum drug. Narrow-spectrum agents can worsen absence/myoclonus |
| Combined focal & generalized | Both seizure types (e.g., Dravet, Lennox-Gastaut) | Broad-spectrum only |
| Unknown | Insufficient information / normal EEG with unclear semiology | Default to broad-spectrum to avoid aggravation |
When you are unsure whether an epilepsy is focal or generalized, prescribe as if it were generalized and pick a broad-spectrum agent. Narrow-spectrum sodium-channel blockers (carbamazepine, oxcarbazepine, phenytoin, and to a degree gabapentin/pregabalin) can aggravate absence and myoclonic seizures. The cost of guessing "generalized" wrong is small; the cost of guessing "focal" wrong can be worsened seizures.
Common syndromes worth recognizing on sight
A syndrome bundles seizure type(s), age of onset, EEG signature, and prognosis into a package that often dictates drug choice directly.
Juvenile myoclonic epilepsy
Early-morning myoclonic jerks (dropped coffee cup), generalized tonic-clonic seizures, sometimes absences. Photosensitive. Sleep deprivation & alcohol provoke.
Childhood absence epilepsy
Brief (5–10 s) staring spells, dozens/day, provoked by hyperventilation; 3 Hz generalized spike-wave. Normal development.
Self-limited epilepsy with centrotemporal spikes
Nocturnal focal seizures — hemifacial twitching, drooling, speech arrest — from sleep. Centrotemporal spikes on EEG. Benign, self-limited.
Mesial temporal lobe epilepsy
Focal impaired-awareness seizures with rising epigastric aura, déjà vu, automatisms. Hippocampal sclerosis on MRI. Frequently drug-resistant.
Reading the EEG signatures
The EEG doesn't diagnose epilepsy on its own, but a handful of interictal patterns are strongly tied to specific classifications. This viewer animates the waveform morphology behind the words in your report.
- Generalized 3 Hz spike-and-wave: typical absence; classic in childhood absence epilepsy.
- Generalized polyspike-wave, often photosensitive: juvenile myoclonic epilepsy and other generalized epilepsies.
- Focal sharp waves / spikes: focal epilepsy; localization hints at the seizure network (e.g., temporal, centrotemporal).
- Hypsarrhythmia: chaotic high-voltage disorganization — the signature of infantile epileptic spasms; a can't-miss, refer-today pattern.
- Normal posterior-dominant α rhythm: reassuring but never rules epilepsy out — sensitivity of a single routine EEG is only ~30–50%.
Choosing a first medication
Drug choice follows classification, then gets tuned to the person — age, sex and pregnancy potential, comorbidities, other medications. Pick a rational agent, start low, titrate slowly, aim for monotherapy at the lowest effective dose.
- Pregnancy potential: valproate is teratogenic and impairs neurodevelopment — avoid in anyone who could become pregnant unless no alternative exists and under specialist oversight. Lamotrigine and levetiracetam are the usual preferred broad-spectrum choices in this group.
- HLA-B*15:02: in patients of Southeast/East Asian ancestry, screen before carbamazepine (and consider before oxcarbazepine/phenytoin) for risk of Stevens-Johnson syndrome / toxic epidermal necrolysis.
Broad- vs. narrow-spectrum: the mental model
Cover both focal and generalized seizures. When onset is uncertain, these are the safe default: lamotrigine, levetiracetam, valproate, topiramate, zonisamide, lacosamide (adjunct), perampanel, brivaracetam.
Effective for focal seizures but can worsen absence and myoclonic seizures: carbamazepine, oxcarbazepine, phenytoin, gabapentin, pregabalin, eslicarbazepine, vigabatrin. Don't reach for these when the epilepsy might be generalized.
- Monotherapy first. ~50% are controlled on the first well-chosen drug; another ~15% on the second.
- Start low, go slow — especially lamotrigine, where fast titration drives serious rash. Slow titration is a safety measure, not a delay.
- Titrate to effect or to tolerability, not to a target level. Levels guide adherence and toxicity, not the goal.
- If the first two appropriate drugs fail at adequate doses → drug-resistant epilepsy. That's a referral trigger, not a third-drug trigger.
Status epilepticus — the time-critical branch
A convulsive seizure lasting ≥5 minutes, or repeated seizures without recovery of awareness between them, is status epilepticus. This is a neurological emergency where the algorithm is a clock, not a decision tree.
ABCs, clock, glucose
- Airway, oxygen, IV access, continuous monitoring. Note the time.
- Check fingerstick glucose; treat hypoglycemia (with thiamine first if malnourished/alcohol).
- Send labs: electrolytes, Ca/Mg, renal, LFTs, AED levels, toxicology, consider ABG.
Give an adequately-dosed benzodiazepine — under-dosing is the classic error
- IM midazolam (no IV), IV lorazepam, or IV diazepam at weight-appropriate doses.
- May repeat once. Do not stall on this step — a second full dose beats waiting.
Load a second-line agent if seizures continue
- Choices with comparable efficacy: IV levetiracetam, IV fosphenytoin, or IV valproate.
- Choose by comorbidities and interactions; any one of the three is a reasonable first pick.
ICU, continuous EEG, anesthetic infusion
- Refractory status → continuous infusion (midazolam, propofol, or pentobarbital) with intubation.
- Continuous EEG monitoring, because ongoing seizures can become non-convulsive.
When to escalate or refer
Primary-care neurology handles the common, well-classified epilepsies. These situations should route to epileptology, video-EEG monitoring, or a comprehensive epilepsy center.
| Trigger | Why |
|---|---|
| Drug-resistant epilepsy | Failure of two tolerated, appropriately chosen and dosed regimens. Surgery, neurostimulation, and dietary therapy become options with high value in the right patient. |
| Diagnostic uncertainty | Events that could be PNES, or seizures that won't classify — video-EEG resolves both. |
| Structural lesion | MRI shows a resectable focus (e.g., hippocampal sclerosis, focal cortical dysplasia). |
| Pregnancy / planning | Regimen optimization and folate before conception; specialist co-management. |
| Infantile spasms / hypsarrhythmia | Emergency — time-sensitive treatment protects development. |
| SUDEP risk counseling | Poorly-controlled convulsive seizures carry real mortality; the conversation belongs in the plan. |
A reproducible classifier, in code
The onset-first logic above expressed as a small GNU Octave function — a compact way to encode the branch points so the reasoning is explicit and testable rather than implicit.
% classify_seizure.m — teaching model of the ILAE 2017 onset-first branch % Inputs are strings; returns a seizure-type label. Educational only. function label = classify_seizure(onset, awareness, feature) onset = lower(onset); % 'focal' | 'generalized' | 'unknown' awareness = lower(awareness); % 'aware' | 'impaired' | 'na' feature = lower(feature); % 'motor' | 'nonmotor' | 'tonicclonic' | 'absence' | 'myoclonic' switch onset case 'focal' aw = 'aware'; if strcmp(awareness,'impaired'), aw = 'impaired awareness'; end label = sprintf('Focal %s, %s onset', aw, feature); if strcmp(feature,'tonicclonic') label = 'Focal to bilateral tonic-clonic'; end case 'generalized' switch feature case 'absence', label = 'Generalized non-motor (absence)'; case 'myoclonic', label = 'Generalized motor: myoclonic'; case 'tonicclonic', label = 'Generalized motor: tonic-clonic'; otherwise, label = 'Generalized motor (specify)'; end otherwise label = sprintf('Unknown-onset %s', feature); end endfunction % >> classify_seizure('focal','impaired','motor') % ans = Focal impaired awareness, motor onset % >> classify_seizure('generalized','na','absence') % ans = Generalized non-motor (absence)