NeuroPCP · Primary Care Neurology & Epilepsy

The Epilepsy PathwayFrom "was that a seizure?" to a working diagnosis, a seizure type, and a first medication — organized the way the ILAE framework asks you to think.

Framework: ILAE 2017 classification Setting: Office / primary-care neurology Reading time: ~25 min
Educational reference only. This is a teaching document that summarizes published guidelines. It is not medical advice and does not replace clinical judgment, a full history and exam, specialist consultation, or current drug labeling. Doses, interactions, and contraindications must be verified against a primary source before any prescribing decision.
STEP 0

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.

Differentiating the three common paroxysmal events
FeatureEpileptic seizureConvulsive syncopePsychogenic (PNES)
Trigger / prodromeSometimes aura (rising epigastric, déjà vu, focal sensory)Upright posture, pain, heat, standing; greyout, tunnel vision, warmth, nauseaEmotional context; often prolonged, fluctuating build-up
OnsetAbruptGradual over secondsVariable, may be gradual
Motor patternRhythmic, synchronous, decrementing; tonic then clonicBrief (<15 s) arrhythmic multifocal jerks after collapseAsynchronous, side-to-side head, pelvic thrust, waxing/waning, stop-start
EyesOpen, may deviateOpen, rolled upOften forcibly closed, resist opening
Duration1–3 min typicalSecondsOften >2 min, can be very long
Tongue biteLateral tongue (specific)Rare; tip if anyTip of tongue, lips
RecoveryPost-ictal confusion, gradual over minutesRapid, oriented within secondsVariable; may have rapid reorientation or prolonged unresponsiveness
IncontinenceCan occurCan occurCan occur — not discriminating
Watch the classic traps

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.

STEP 1

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:

  1. At least two unprovoked (or reflex) seizures occurring more than 24 hours apart.
  2. 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.
  3. 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:

The "high-risk first seizure" call

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

Baseline evaluation after a first apparent unprovoked seizure
TestWhat it answersNote
History + witness / videoWas it a seizure? Focal features at onset?Highest yield of anything here
EEGEpileptiform activity → recurrence risk, classificationA normal routine EEG does not exclude epilepsy; sleep-deprived / repeat raises yield
MRI brain (epilepsy protocol)Structural lesion → focal epilepsy, surgical targetPreferred over CT except in the acute/emergent setting
LabsProvoked cause? (glucose, Na, Ca, Mg, renal, tox)Rules provocation in or out
ECGSyncope mimic, long-QT, arrhythmiaCheap, catches a dangerous mimic
STEP 2

Classify the seizure type

The ILAE 2017 framework classifies at three levels: seizure typeepilepsy typesyndrome. Everything starts with one question that colors the rest of the workup: where did the seizure begin?

The three onset categories

ONSET AXIS

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.

ONSET AXIS

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.

ONSET AXIS

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.

STEP 3

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.

The four ILAE epilepsy types
Epilepsy typeTypical evidencePrescribing implication
FocalFocal seizures; focal epileptiform EEG; structural MRI lesionBroad list works; the "narrow-spectrum" sodium-channel agents are safe here
GeneralizedGeneralized seizure types; generalized spike-wave EEG; usually normal MRIChoose a broad-spectrum drug. Narrow-spectrum agents can worsen absence/myoclonus
Combined focal & generalizedBoth seizure types (e.g., Dravet, Lennox-Gastaut)Broad-spectrum only
UnknownInsufficient information / normal EEG with unclear semiologyDefault to broad-spectrum to avoid aggravation
The single most useful safety heuristic

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.

ONSET 12–18 y

Juvenile myoclonic epilepsy

Early-morning myoclonic jerks (dropped coffee cup), generalized tonic-clonic seizures, sometimes absences. Photosensitive. Sleep deprivation & alcohol provoke.

First lineValproate (avoid in people who can become pregnant), levetiracetam, lamotrigine. Usually lifelong.
ONSET 4–10 y

Childhood absence epilepsy

Brief (5–10 s) staring spells, dozens/day, provoked by hyperventilation; 3 Hz generalized spike-wave. Normal development.

First lineEthosuximide (absence only) or valproate; lamotrigine second. Often remits by adolescence.
ONSET 3–13 y

Self-limited epilepsy with centrotemporal spikes

Nocturnal focal seizures — hemifacial twitching, drooling, speech arrest — from sleep. Centrotemporal spikes on EEG. Benign, self-limited.

Often no drugTreat only if frequent/daytime; low-dose narrow-spectrum agents fine. Remits by mid-teens.
ADULT, ANY AGE

Mesial temporal lobe epilepsy

Focal impaired-awareness seizures with rising epigastric aura, déjà vu, automatisms. Hippocampal sclerosis on MRI. Frequently drug-resistant.

First lineAny focal-appropriate agent; refer early for surgical evaluation if drug-resistant — high cure rate.
PROFILE

Who these patients are — traits & comorbidities by type

Epilepsy is a network disorder, and the same network that generates the seizures also shapes cognition, mood and behaviour. That is why the "traits" cluster by type. But group-level tendencies are not verdicts about a person — read this as clinical texture, not a personality horoscope.

Read this first — the myth to retire

There is no valid "epileptic personality." The 19th- and 20th-century idea of a global temperament shared by everyone with epilepsy is discredited, stigmatising, and wrong. What is real and evidence-based is two things: (1) psychiatric and cognitive comorbidity is far more common in epilepsy than in the general population, and (2) specific epilepsy types carry characteristic cognitive-behavioural profiles tied to their brain network. Both are reasons to screen and support — never to label.

Comorbidity is the rule, not the exception

Across all epilepsy types, the biggest driver of quality of life is often not the seizures but the company they keep. The relationship is bidirectional — depression, for instance, is both more common after epilepsy begins and an independent risk factor for developing it — which points to shared underlying biology rather than a simple reaction to diagnosis.

Cross-cutting comorbidities to screen for in every patient
ComorbidityPattern in epilepsyPractical move
DepressionThe most common; affects roughly a third; frequently under-recognised and under-treated; bidirectional riskScreen routinely (a tool like the NDDI-E takes a minute); SSRIs are generally safe and do not meaningfully lower the seizure threshold at therapeutic dose
AnxietyVery common; distinguish an ictal fear aura (seconds, stereotyped) from sustained interictal anxiety and anticipatory fear of seizuresAsk specifically; treat; ictal fear points toward a focal (often temporal) onset
ADHD / attentionStrongly over-represented, especially in childhood epilepsies; the inattentive presentation predominatesScreen children; stimulants are generally safe in controlled epilepsy
PsychosisInterictal and postictal psychosis, most linked to temporal lobe epilepsy; "forced normalisation" — psychiatric symptoms emerging as the EEG normalises — is a recognised paradoxAsk about the postictal window; refer
SuicidalityElevated relative to the general population — a sensitive but important part of the pictureAsk directly when screening for mood; have resources ready
CognitionAttention, memory and processing speed, driven by the underlying cause, seizure burden, interictal discharges and medicationSeparate what is fixed (etiology) from what is reversible (drug, seizure control) before attributing decline

Type-specific profiles

These are the characteristic textures each classification tends to carry. Every card describes a tendency at the group level — many individuals show none of it.

FOCAL · TEMPORAL

Temporal lobe epilepsy

The richest subjective world of any epilepsy. Auras of déjà vu / jamais vu, a rising epigastric sensation, sudden fear, dreamy states, or odd smells and tastes. Memory is affected in a material-specific way — dominant (usually left) temporal networks hit verbal memory, non-dominant hit visuospatial. Carries the highest psychiatric burden of the epilepsies: interictal dysphoric disorder, depression, anxiety, and the strongest tie to interictal and postictal psychosis.

Contested historical noteThe old "Geschwind / interictal behaviour syndrome" (hyperreligiosity, hypergraphia, intensified emotionality, interpersonal "viscosity", usually reduced sexuality) is controversial, non-specific, and not diagnostic. Most patients show none of it; use network and mood language, not this label.
FOCAL · FRONTAL

Frontal lobe epilepsy

Seizures are brief, often nocturnal, hyperkinetic and bizarre with fast recovery — and are frequently mistaken for psychogenic events. The interictal profile follows the lobe: executive dysfunction — planning, working memory, inhibition and sustained attention — plus a tendency toward impulsivity and blunted social cognition when the seizures are frequent or the cause is diffuse.

Watch forExecutive-load difficulties that look "behavioural" but track with seizure burden and frontal involvement.
GENERALIZED · 12–18 y

Juvenile myoclonic epilepsy

Intelligence is typically normal, but a frontal-executive behavioural signature has been described — impulsivity, mood lability, difficulty with planning and time management, sometimes framed (unkindly and debatably) as "immaturity". Whatever the label, the clinically decisive fact is that seizures here are driven by sleep deprivation, alcohol and non-adherence.

Actionable traitCounselling on sleep, alcohol and taking the drug matters as much as the drug itself — the "traits" and the triggers are the same lifestyle axis.
GENERALIZED · 4–10 y

Childhood absence epilepsy

Development is called "normal", yet subtle attention deficits and higher rates of ADHD (inattentive type), plus academic and psychosocial difficulty, are common — the absences themselves fragment attention dozens of times a day, and discharges can be subclinical.

Watch forFalling grades and "daydreaming" that is actually seizure activity; screen attention even after seizures stop.
DEVELOPMENTAL & EPILEPTIC ENCEPHALOPATHIES

West · Lennox-Gastaut · Dravet

Here the traits are central, not incidental. The epilepsy and the developmental impairment usually share a cause, and the relentless seizures and discharges themselves worsen development — the "encephalopathy". Expect intellectual disability, behavioural dysregulation, and autism-spectrum features (prominent in Dravet). Controlling the electrical activity can protect development, which is why these are treat-today diagnoses.

Watch forRegression or plateau in a child with frequent seizures — the EEG burden is part of the cognitive problem.
FOCAL · SELF-LIMITED (BECTS)

Self-limited centrotemporal epilepsy

Usually cognitively normal and outgrown by mid-teens, but during the active period transient difficulties with language, reading and attention are recognised. A reminder that "benign" describes the seizures, not always the school year.

Watch forTemporary literacy/attention dips while the epilepsy is active; they typically recover.

Before you call it a "trait" — check the drug

A large share of what looks like personality is iatrogenic and reversible. Anti-seizure medications have their own behavioural fingerprints; changing the agent can change the "trait".

Behaviourally relevant medication effects
AgentCharacteristic behavioural / cognitive effect
LevetiracetamIrritability, aggression, anxiety and low mood are common — the well-known "behavioural" downside; pyridoxine sometimes helps, or switch to brivaracetam
PerampanelIrritability and aggression, dose-related (carries a behavioural warning)
TopiramateCognitive slowing, word-finding difficulty, paraesthesia, occasionally low mood — the classic "cognitive" ADR profile
ZonisamideSimilar cognitive slowing and mood effects to topiramate
Phenobarbital / barbituratesSedation and depression in adults; paradoxical hyperactivity in children
LamotrigineGenerally favourable — often mood-brightening and cognitively "clean"; watch for rash on fast titration
ValproateBroadly mood-neutral to stabilising; watch tremor, weight, and hyperammonaemic encephalopathy
The mental model — where a "trait" comes from

When a patient seems changed, sort the contribution before you attribute it: the underlying etiology / lesion (fixed), the network location (temporal vs frontal shapes which functions), the seizure and discharge burden (improves with control), the medication (often reversible), and psychosocial and stigma factors (driving loss, employment, autonomy). Name the specific, modifiable contributor — never the diagnosis as a whole.

Clinic takeaways
  • Screen every visit for depression and anxiety; they hurt quality of life more than seizure frequency does and they respond to treatment.
  • Ask what the medication did to mood and thinking before concluding anything about the person.
  • Match the profile to the network: temporal → memory + mood + psychosis risk; frontal → executive + impulsivity; generalized → attention + adherence.
  • Refuse the stereotype. "Epilepsy" is not a personality; describe specifics — a network, a burden, a drug — that you can actually act on.
STEP 4

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.

◉ REC · Simulated single-channel EEG
Report language → what it points to
  • 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%.
STEP 5

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.

Two non-negotiable safety gates before any prescription
  • 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.
Epilepsy / seizure classification
Key patient factor

Broad- vs. narrow-spectrum: the mental model

Broad-spectrum — safe across the board

Cover both focal and generalized seizures. When onset is uncertain, these are the safe default: lamotrigine, levetiracetam, valproate, topiramate, zonisamide, lacosamide (adjunct), perampanel, brivaracetam.

Narrow-spectrum — focal only

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.

Universal titration principles
  • 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.
STEP 6

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.

0–5 min · Stabilization

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.
5–20 min · First-line: benzodiazepine

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.
20–40 min · Second-line: IV AED

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.
40+ min · Refractory status

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.
STEP 7

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.

Referral triggers
TriggerWhy
Drug-resistant epilepsyFailure of two tolerated, appropriately chosen and dosed regimens. Surgery, neurostimulation, and dietary therapy become options with high value in the right patient.
Diagnostic uncertaintyEvents that could be PNES, or seizures that won't classify — video-EEG resolves both.
Structural lesionMRI shows a resectable focus (e.g., hippocampal sclerosis, focal cortical dysplasia).
Pregnancy / planningRegimen optimization and folate before conception; specialist co-management.
Infantile spasms / hypsarrhythmiaEmergency — time-sensitive treatment protects development.
SUDEP risk counselingPoorly-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)