NeuroLogic: Fundamentals
EEG Fundamentals
Welcome
This course is designed to take you all the way from a single neuron to the basics of reading a page and writing your own EEG report. You will not start by memorizing waveforms. You will start at the cell, then earn each later skill from the one before it.
Syllabus (each heading is a lesson in this course):
- What a scalp EEG channel measures
- International 10-20 electrode placement
- Bipolar montages and phase reversal
- Referential and common average reference
- Filters, sensitivity, and digital recording
- Frequency, amplitude, and how to describe a wave
- How to read the EEG background
- Sleep architecture and lookalike variants
- Interictal discharges, ICU patterns, and seizures
- The EEG report template
- From neuron to channel. How a synaptic current becomes a scalp field, and why the trace on the screen is a comparison, not a photograph of one electrode.
- Where the electrodes sit. Place the 10–20 array, then watch the same discharge on bipolar, transverse, circumferential, and average montages.
- What the machine keeps and loses. Filters, sensitivity, and the acquisition choices that cannot be undone later.
- How to read a page. Background and state first, then sleep, lookalikes, artifact and activation, spikes, ICU patterns, and seizures.
- How to write it down. The last page is the report template: each heading in order, from history to impression.
Use Next, or jump from Contents. Labs and real 10-second pages sit on the path. The first lesson starts at the source population.
From Cortex to Channel: What EEG Actually Measures
A scalp trace is the end of a five-step chain. Keep that chain in order and the later rules about polarity, montages, and localization become arithmetic rather than memorization.
- 1. Source population: Synaptic currents create graded postsynaptic potentials in cortical neurons. Single axonal action potentials are too brief and spatially scattered to dominate routine scalp EEG.
- 2. Open field: Thousands of similarly oriented pyramidal cells must be active with enough synchrony for their extracellular fields to add instead of cancel.
- 3. Volume conduction: The summed field spreads through brain, CSF, skull, and scalp. This passive journey attenuates and spatially blurs the signal; it does not create a new rhythm.
- 4. Electrode potential: Each scalp electrode samples the local extracellular potential produced by the mixture of fields that reaches it. An electrode has no meaningful absolute voltage by itself.
- 5. Channel difference: The amplifier displays Input 1 minus Input 2. The waveform therefore belongs to a channel (a comparison), not to either electrode alone.
A crowd is quiet at a distance when everyone speaks independently and loud when many people clap together. Cortical synchrony likewise emerges from interacting thalamocortical and intracortical networks; the thalamus is important for several rhythms, but it is not the sole conductor of EEG.
Scalp detection generally requires synchronous activation across several square centimeters of cortex; often-cited estimates begin around 6 cm², but detectability varies with depth, orientation, synchrony, amplitude, and competing background activity.
Quick check Follow the diagram from cortex to scalp. Which signal contributes most directly to routine scalp EEG?
Source population → open field → volume conduction → electrode potential → channel difference. That sequence is the conceptual spine of the course.
Why EEG Sees Synapses, Not Spikes
Step one of the chain said that routine scalp EEG reflects postsynaptic potentials rather than action potentials. That is usually stated and then left there. It is worth proving, because the reason is not biological preference; it is arithmetic about duration, and once you have seen it you can predict which signals will ever reach an electrode.
No cortical population fires in perfect lockstep. Each cell contributes the same little waveform at a slightly different moment, and the electrode adds them up. Adding jittered copies of something can never sharpen it; it can only spread and flatten it. How much it flattens depends on how long the event lasts compared with the spread in firing times.
A stadium is the everyday version. Thousands of people talking independently carry a long way as noise and nothing more; the same crowd clapping together produces something you can hear from outside the ground and even count the rhythm of. The crowd did not get bigger, and nobody got louder; the timing changed. That is the variable the slider below moves.
Try 5 ms of jitter on each in turn. The synaptic potential keeps almost all of its height; the spike keeps well under one percent. Five milliseconds is nothing to a 60 ms event and an eternity to a 1 ms one. By the time a neighboring cell fires, the first spike has been over for several milliseconds, so the two never overlap and there is nothing to add.
Why spikes never reach the scalp
This is why a cortex can be extremely busy and still look quiet at the scalp, and why EEG is a measure of synchrony at least as much as of activity. It is also the honest answer to a question that bothers most beginners: the spikes are absolutely there, firing constantly under the electrode. They are simply too brief to survive being added up.
Careful with the word "spike." The action potential here is the millisecond event of a single axon, and it is invisible to scalp EEG. The epileptiform spike you will learn to report is a 20–70 ms scalp waveform produced by a large population of synchronized postsynaptic currents. Same word, different phenomenon, three orders of magnitude apart in duration, and it is the slow one you can actually record.
Bioelectric Batteries: From Ion Flow to Waveform
Start with the extracellular space, because that is where the EEG electrode listens. A sink is a membrane region where conventional positive current enters the neuron. Removing positive charge makes the nearby extracellular space relatively negative. A source is the return-current region, where positive current leaves the cell and the extracellular space becomes relatively positive.
Pyramidal cells are aligned perpendicular to the cortical surface. When many of them activate together, the sink and source fields add as an open field. Move the synaptic current from the apical dendrites to the soma and the dipole flips, even though the cellular event can still be excitatory.
Move the synapse, then follow the charge
Why the IPSP uses chloride: GABAA commonly permits Cl− influx, making the extracellular region relatively positive. GABAB can instead produce K+ efflux. Both are inhibitory, which is why waveform polarity alone does not identify the neurotransmitter.
Keep the order straight: identify where current crosses the membrane, decide whether the nearby extracellular space is a sink or source, determine the dipole orientation, and only then predict the scalp polarity. Clinical EEG displays relative negativity upward.
Quick check Positive current enters a superficial apical dendrite during an EPSP. What does the nearby extracellular electrode sample?
Current in removes positive charge from the extracellular space. The sink is therefore relatively negative. Return current creates a source elsewhere, and the separation forms the dipole.
Continue the board-level review in Where the Signal Comes From.
Dipole Orientation: Why the Maximum Is Not Always Over the Source
Pyramidal cells stand perpendicular to the cortical surface, and the cortex is folded, so the fold decides which way the dipole points. A cell on a gyral crown points its dipole up at the scalp. A cell on a sulcal wall points sideways. That single geometric fact decides whether the electrode showing the biggest deflection is over the generator or not.
The number that matters: in this simplified model, at a fully tangential source the potential directly above the generator approaches zero, and the two largest deflections sit either side of it with opposite signs. So a sulcal spike is not faint; it is well formed and pointing at the wrong place. Real head geometry is less idealized, but the localization warning remains: both lobes may be real while neither maximum sits directly over the source.
Why deep sources hide
This is also why deep and sulcal sources need far more cortex firing together to be readable at all: a radial crown aims its whole field at the electrode, while a sulcal wall spends most of its field sideways and much of the rest cancelling against the opposite wall of the same sulcus.
Where this shows up: it is the reason MEG and EEG are complementary rather than redundant; MEG is most sensitive to exactly the tangential sources EEG localizes worst, while EEG reads radial crowns best. It is also why a spike that looks frontal on one montage may need re-reading on another before you believe where it is.
Once the field reaches the scalp, the next task is naming the electrode sites that sample it.
The International 10-20 Map
The International 10-20 system turns four reproducible bony landmarks into a proportional scalp map. Electrode sites fall at 10% and 20% intervals, so the same labels can be applied across different head sizes. A label is a scalp coordinate, not a promise that the same cortical gyrus lies directly beneath it in every patient.
Vertex view of the scalp map
The four measurements that anchor the map
Reference, ground, and contact: A1/A2 are auricular sites; M1/M2 are mastoids. Check electrode-skin impedance before recording and when artifact appears. ACNS guidance ordinarily keeps it at or below 5 kΩ, balanced across the array, but a near-zero reading can indicate a salt bridge that shorts adjacent electrodes together.
Test the map now. Lead Placement is the next lesson, while these locations are still fresh.
Review the full technical framework in Instrumentation, Montage, and Localization.
Bipolar Montages: From Chains to Phase Reversal
A single electrode on the scalp cannot record an electrical potential. It has no value until it is compared to another point. This comparison (Input 1 minus Input 2) is executed by a differential amplifier.
An EEG montage is a logical display of differential channels. The longitudinal bipolar ("double banana") montage is an essential standard display, but no single montage is sufficient for every pattern. Clinical review uses complementary bipolar and referential displays and preserves the ability to reformat digitally.
- Left temporal
- Right temporal
- Left parasagittal
- Right parasagittal
- Midline
Common Mode Rejection (CMR): Differential amplifiers reject signals that affect both inputs equally (like line-frequency ambient hum) and amplify only the difference between Input 1 and Input 2. This is what lets a microvolt-scale cerebral rhythm survive alongside environmental interference that can be several orders of magnitude larger at the electrode.
Phase reversal is created by a shared electrode
In a Bipolar Montage, adjacent electrodes are linked sequentially in a chain (e.g., Channel 1: Fp1-F3, Channel 2: F3-C3). Each channel subtracts its second input from its first input.
Channel Output = Input 1 Voltage - Input 2 Voltage
If Input 1 is −50 μV and Input 2 is −20 μV:
(−50 μV) − (−20 μV) = −30 μV (Upward Deflection due to Negative-is-Up).
Follow the shared electrode
When a focal negative field is maximal at F3, it becomes the most negative point in the surrounding chain:
- Channel 1 (Fp1-F3): F3 is Input 2. Since Input 2 is negative, the subtraction formula outputs a positive value (Fp1 − F3 = 0 − (−100) = +100 μV). This projects Down (Divergence).
- Channel 2 (F3-C3): F3 is Input 1. Since Input 1 is negative, the formula outputs a negative value (F3 − C3 = (−100) − 0 = −100 μV). This projects Up (Convergence).
This creates a converging phase reversal at the negative chain maximum. A positive field creates a diverging reversal. A reversal localizes a voltage maximum in that chain; it does not, by itself, prove epilepsy or guarantee that the cortical generator lies directly beneath the electrode.
F3 is the field maximum at −100 µV, so the two channels that share F3 deflect toward each other. Channels farther along the chain barely move because their inputs sit at similar voltages.
Bipolar Math Simulator: Five Electrodes, Four Channels
Now isolate the arithmetic from the terminology. Change one electrode at a time and keep the five electrode voltages, all four subtractions, and all four traces visible together. Then apply the same reasoning to the clinical page immediately below.
1 / 9
Five electrodes, four channels. Each interior electrode is shared by the two channels either side of it; that is what makes a reversal possible.
Ch1 · Fp1 – F3
Ch2 · F3 – C3
Ch3 · C3 – P3
Ch4 · P3 – O1
Bipolar Math Spot Check: Find the Reversal
Spot check A real longitudinal bipolar page: the same double banana, on an actual recording. One sharp wave repeats through it. Click the chain where two channels turn to face each other.
The reversal is at T8. Walk the right temporal chain down: Fp2–F8, F8–T8, T8–P8, P8–O2. The two channels that share T8 deflect against each other, and that is the whole localization: T8 is the most negative electrode, so it drives F8–T8 one way and T8–P8 the other.
Notice what the reversal is not. It is not the largest deflection on the page, and it is not a property of the discharge; it is a property of subtraction. Put the same field in a referential montage and there is no reversal to find at all.
Spot check Ignore the blink and read the channel list on the left. What montage is this page?
Longitudinal bipolar, the double banana. Left temporal over right temporal, then left parasagittal over right parasagittal, then a short midline chain. Each channel is a neighboring pair subtracted front to back.
The blink at the front of the page is not the montage. Channel order is. Once you can name the banana from the labels, you can also name when a page has left it.
Referential Power & Common Average Reference (CAR)
While Bipolar montages are excellent for localizing sharp transients via phase reversals, they can falsely depress amplitude or completely miss broad, generalized discharges that span across multiple channels (since Input 1 and Input 2 would have identical voltage, subtracting to zero).
In a referential montage, each active scalp electrode is compared with a shared reference. A common average reference (CAR) is one useful computed option, not a universally superior standard:
- Mathematical Average: CAR sums the potentials of all active scalp electrodes (19 in the standard 10-20 array) and divides by the total number, creating a computed baseline reference.
- Amplitude and field distribution: The largest deflection helps identify the scalp maximum of a field, but source orientation, depth, reference composition, and volume conduction prevent a simple one-to-one equation between amplitude and generator proximity.
- Reference Contamination Warning: If a single electrode suffers a massive artifact (e.g., a loose electrode or localized muscle spike), that high voltage is mathematically distributed into the common average, causing a "paradoxical" ghost artifact to appear across every other channel.
Montage Spot Check: Same Event, New Reference
Spot check Compare the two views of the same field. What changes when the event is re-read against one reference?
Referential montages do not phase-reverse, and that is the point of running one. Every channel here is electrode − average. Adjacent channels no longer share an electrode, so the mechanism that produces a reversal is simply absent.
You pay for that with a different question. Bipolar asks where do two channels meet and disagree; referential asks which single channel is biggest. Read the amplitudes down the right temporal group and the maximum names the electrode directly; no walking the chain required.
This is why neither montage wins. Bipolar rejects the reference and localizes sharply but can hide a broad field; referential shows the true field shape but contaminates every channel if the reference is active.
After choosing which voltages to compare, display settings determine how those differences appear on the screen.
Transverse and Circumferential
Longitudinal chains run front to back, so they leave two gaps: a focus at a chain end has only one neighbor, and a midline focus is split across left and right chains. Transverse rows run left to right, so a midline field can sit inside a single chain. Circumferential closes the rim into a ring, giving occipital and frontopolar sites neighbors on both sides. Both layouts still use the same 10–20 array.
Switch the map, then click to enlarge
One Discharge, Four Montages
The 10–20 array is now fixed. Every electrode stays where you placed it. A montage is not a filter on the data: it is only a choice of subtractions. The same discharge can be obvious in one arrangement and invisible in another, which is why an unrevealing study gets re-read on a second montage rather than dismissed.
Below, the scalp field is computed once and every channel is re-derived from it. Switching Longitudinal (the double banana), Transverse, Circumferential, or Referential changes only which pairs get subtracted. The discharge never moves.
left temporal over right temporal, then left parasagittal over right parasagittal; no midline chain
The same right temporal sharp wave on four real pages. Switch montage; the generator does not move.
Try the occipital discharge on each montage in turn. On the longitudinal chains O1 sits at the end and can only give half a reversal. Put the same field on the circumferential ring, where O1 has neighbors on both sides, and the reversal completes; the data was never the problem.
Instrument Parameters: Filters & Sensitivity
Change one setting at a time (LFF, HFF, notch, or sensitivity) and watch the page. The recording underneath is the same 10-second longitudinal bipolar tracing; only the instrument changes.
LFF (low-frequency filter) is a high-pass: it removes content below the cutoff. Sweat and electrode drift live there. HFF (high-frequency filter) is a low-pass: it removes content above the cutoff. Muscle lives there, and so does spike sharpness.
Analog LFF was specified as a time constant: LFF 0.5 Hz = 0.3 s TC. LFF 5.0 Hz or HFF 15 Hz will also blunt transients you need to keep.
Sensitivity (Calibration Scale): Governs visual wave height magnification. Standard baseline is 7 μV/mm.
At standard 7 μV/mm, a 70 μV spike will measure exactly 10 mm tall.
High display sensitivity (2 μV/mm) may be used when a protocol specifically evaluates electrocerebral inactivity. EEG alone does not establish brain death/death by neurologic criteria under the current U.S. consensus guideline; follow the applicable examination, apnea-testing, ancillary-testing, and local-policy requirements. Lower display sensitivity (15-20 μV/mm) can help display high-amplitude activity without channel overlap.
Left temporal over right temporal. Turn the knobs yourself and see what happens to the EEG.
Technical Troubleshooting: Fix the Source Before the Display
Use channel distribution to identify the shared bad electrode, correct the contact or environmental source, and only then adjust the display. These two checks apply that sequence.
Spot check Two channels on this page are buried under a 60 Hz buzz and the other fourteen are clean. The affected pair is Fp1–F7 and F7–T7. Which electrode is the problem?
Find the electrode the noisy channels share, and check it appears nowhere clean. Fp1–F7 and F7–T7 both contain F7; Fp1 also sits in a clean Fp1–F3 and T7 also sits in a clean T7–P7. Only F7 is implicated by every channel it touches. That is high impedance at one electrode: a loose or drying contact letting mains hum in.
So the notch filter is the wrong first move. A 60 Hz notch would make this page look clean while leaving a bad electrode in the montage, still degrading everything it records. Re-gel or reseat F7; use the notch only when the environment, not the electrode, is the source.
This is the general rule for localizing any single-electrode problem, including hum, an electrode pop, or a flat channel: list the channels that show it and take the electrode they have in common.
Spot check A different technical problem: the baselines on this page are swaying slowly, well below 1 Hz, and the sway is largest frontally. Which setting can attenuate it on the display while you correct the cause?
Sweat artifact occupies the lowest frequencies, so the low-frequency filter can attenuate it on the display. Salt bridges and slow changes in skin potential often produce sway below about 0.5 Hz. Raising the low-frequency filter modestly may improve readability, but it can also attenuate genuine cerebral delta.
Fix the cause too: cool the patient, dry the scalp. Filtering makes the page readable; it does not make the recording good, and a filter aggressive enough to bury sweat entirely will also flatten real delta, which matters when slowing is exactly what you are looking for.
The same logic runs the other way for muscle. EMG lives above the EEG band, so it is the high-frequency filter that touches it, and lowering that far enough to hide muscle will round off real spikes.
Digital Recording Essentials: What Cannot Be Recovered Later
A digital EEG is only as faithful as the analog signal that reached the converter. Display knobs can hide drift, muscle, or 60 Hz. They cannot restore a frequency the analog anti-alias filter removed, or un-alias a wave that was sampled too slowly.
Acquisition chain
The door only swings one way
Differential amplification, then analog anti-alias filtering, then analog-to-digital conversion, then digital filtering and display. The ADC is the cut. Everything after it is a view of the samples you already kept.
Still analog
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1
Differential amplifier Input 1 minus Input 2. Common-mode interference is rejected here, not later on the screen.
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2
Analog anti-alias filter A low-pass that must act before sampling. It throws away frequencies the ADC is not allowed to see.
Already a file
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3
Digital filtering and display LFF, HFF, notch, sensitivity, and montage reformatting. These change the view, not the samples.
Gone after conversion
- Content the analog anti-alias filter already removed
- The true frequency of an aliased oscillation
- Headroom, if the converter saturates
Still yours on the same file
- Display LFF, HFF, and notch
- Sensitivity, paper speed, and montage
- Any digital filter that was not in the analog path
Sampling does not guess the missing peaks
Nyquist requires a sampling rate at least twice the highest frequency of interest. In practice, sample about 3–5 times the high-frequency filter setting. Routine systems commonly use 256–512 Hz. The gray line is a true 60 Hz sine. The dots are what the ADC stored. Connect them and you see what the file actually contains.
True 60 Hz What the file kept
Impedance is a pattern, not one number
Routine electrode–skin impedances are ordinarily kept at or below about 5 kΩ and reasonably balanced. A near-zero value suggests a salt bridge. A high or mismatched contact weakens common-mode rejection. Trace a disturbance through every channel sharing the electrode before blaming the amplifier.
Electrical safety
Use approved isolated EEG equipment, hospital-grade grounded outlets, intact short leads, and one common patient ground according to local policy. Never create extra paths to ground through other appliances. Stop to investigate damaged cables, unexpected shocks, or equipment faults.
Acquisition rule. Troubleshoot the patient, electrode, environment, and analog chain before cleaning the display. A prettier trace is not necessarily a more accurate trace.
With the acquisition chain understood, the next step is learning the frequency and amplitude language used to describe the recorded waveforms.
Frequency: The Four Primary Bands
Interpretation foundation
EEG: A Language of Its Own
Every tracing begins with frequency, the number of cycles per second in hertz, and amplitude, the voltage difference in microvolts. Those measurements become meaningful only after you add location, morphology, state, symmetry, and reactivity.
Frequency classification is the baseline step of EEG analysis. Normal adult waking activity represents a balance across four physiological bands. Click through them. Every trace below is drawn at the same sensitivity, so the amplitudes are directly comparable.
The inverse frequency–amplitude relationship: Across the physiological bands, lower frequency tends to carry higher voltage and higher frequency lower voltage, a reflection of the roughly 1/f shape of the EEG power spectrum, and of the fact that slower rhythms recruit larger, more synchronous cortical populations. It is a useful expectation, not a law. The common departure from it is prominent high-voltage beta, which is far more often a sedative-hypnotic medication effect than a sign of cortical pathology.
Background reactivity: The posterior dominant rhythm normally attenuates with eye opening. Reactivity is interpreted alongside state, medications, technique, and the rest of the recording; absent or reduced reactivity can be concerning but is not diagnostic in isolation.
Amplitude & Voltage Scales
Amplitude is the voltage difference of the waveform, measured in microvolts (µV). Its physical height on the display is not intrinsic: it depends on both that voltage and the selected sensitivity in µV/mm. Lowering the µV/mm setting makes the same signal look taller; raising it makes the same signal look shorter. Routine scalp activity commonly falls in the tens of microvolts.
Calibrated display lab
Separate voltage from display height
Change the signal and sensitivity, then compare all three packets on the same calibrated baseline.
Amplitude changes when the underlying voltage changes.
Sensitivity changes only how tall every signal looks on screen.
Review display standards in Technical Standards and Recording Practice.
Intracranial vs. Scalp Voltages: Potentials recorded directly from the cortical surface are substantially larger than those at the scalp, often by roughly one to two orders of magnitude. Volume conduction through CSF, skull, and scalp both attenuates and spatially blurs the signal, which is why an intracranial electrode can resolve a discharge that the scalp never registers.
Describing What You See: Phases, Morphology & Rhythmicity
Frequency and amplitude describe a wave in numbers. Everything below describes its shape, and the shape is what separates a spike from a wicket, or an encephalopathic rhythm from a seizure. Every term used in the sections that follow is defined here.
Phases: count the crossings
A phase is one excursion to one side of the baseline. You count phases by counting baseline crossings, not peaks; a wave with three phases crosses twice. Spikes and sharp waves are usually mono- or biphasic; a discharge with many phases is polyphasic.
Each phase is shaded and numbered. Red phases point up (surface-negative), blue point down (surface-positive).
“Triphasic” means two different things. As a shape it just means three phases. As an ACNS pattern, GPDs with triphasic morphology is a specific critical-care finding: generalized, usually frontally predominant, often with an anterior-to-posterior lag. A three-phased spike is not a triphasic wave.
One wave, or a run of them?
Once you are describing more than a single wave, the question becomes whether the shape repeats. Polymorphic activity varies from wave to wave; monomorphic activity keeps the same shape and frequency. Focal polymorphic delta over a tumor and a monomorphic run of temporal theta are different findings precisely because of this.
If a monomorphic run continues for at least six cycles, it earns one of two names, and the distinction is a gap:
- Periodic: discrete discharges with a measurable interval between the end of one and the start of the next.
- Rhythmic: each wave runs straight into the next, with no interval at all.
Current ACNS terminology does not use the older quasi-periodic or quasi-rhythmic modifiers. A pattern remains periodic or rhythmic when cycle length varies by less than 50% across most consecutive cycle pairs; greater variation falls outside those labels.
The lower two traces run at the same rate for the same number of cycles. Only the interval tells them apart.
Why this vocabulary is worth the trouble: it is the entire basis of the ACNS critical-care terminology: LPDs, GPDs, LRDA and GRDA are just lateralized or generalized crossed with periodic or rhythmic. Learn the four words here and that nomenclature reads itself.
Reading the Background: What You Do First
Everything above this point describes individual waves. But no one reads an EEG wave by wave; you read the background first, and only then hunt for discrete events. A record can contain no epileptiform discharge at all and still be unmistakably abnormal. Four questions, in this order:
- Organization. Continuous, symmetric, and does it have an anterior–posterior gradient?
- Posterior dominant rhythm. Present, in range, and symmetric; does it react?
- Variability and reactivity. Does the tracing change on its own, and change when you stimulate?
- State. Awake, drowsy, or asleep? Everything else is judged against the answer.
The next three pages take organization apart. Continuity, symmetry, and the anterior–posterior gradient each get their own comparison.
Organization: Continuity
Continuity: a healthy child or adult record is never interrupted by attenuated stretches. (Discontinuity is normal in the premature neonate; that is tracé discontinu, not pathology.)
Each pair uses the same montage. Only the background differs. Look for flat stretches. If they are there, the record is discontinuous.
Organization: Symmetry
Symmetry: the two hemispheres should broadly match in amplitude and frequency. Compare homologous chains, not a single channel against memory.
A persistent left-right mismatch in frequency or amplitude is an organization failure, even if no spike is present.
Organization: Anterior–Posterior Gradient
The anterior–posterior gradient is faster and lower-amplitude at the front, slower and higher-amplitude at the back. Losing that gradient is itself an abnormality.
When the front looks like the back, organization has failed on this question even if the page is continuous and symmetric.
The Posterior Dominant Rhythm
The PDR is a reactive occipital rhythm in an awake person with the eyes closed. Alpha names a frequency band. PDR names a finding with a location, behavioral state, and response to eye opening. Follow the complete longitudinal bipolar page before measuring it.
10-second longitudinal bipolar page
Watch the PDR appear, settle, and attenuate
The posterior temporal and parasagittal derivations are highlighted only when the finding is established.
Count before you call it
How many complete cycles are inside the one-second bracket?
Open the stable PDR stage above, then count complete peaks between the two green lines. That window is one second.
One cycle per second is one hertz.
Continue with PDR maturation and normal lookalikes in Normal Variants and Artifacts.
Measurement traps and adult asymmetry thresholds
Alpha squeak: the first second after eye closure may briefly run faster. Measure the stable awake segment that follows.
Drowsiness: the rhythm may look clearer but slow as arousal falls. Use the best awake sample.
Reactivity: attenuation with eye opening helps establish that the posterior rhythm is a PDR.
| Measure | Expected adult finding | Concerning difference |
|---|---|---|
| Frequency | 8–13 Hz in an awake adult | Below 8 Hz while fully awake |
| R vs L frequency | Within 1 Hz | Persistent difference greater than 1 Hz |
| R vs L amplitude | Right may be up to about 50% higher | Persistent left excess or right excess beyond about 50% |
Variability and Reactivity
Both are reduced or lost under sedation, and their absence carries real prognostic weight after cardiac arrest: background continuity and reactivity sit alongside SSEPs and imaging in post-arrest prognostication, never alone, and never before sedation and hypothermia have cleared.
State: Awake, Drowsy, or Asleep
Decide whether the patient is awake, drowsy, or asleep, because every other judgment depends on the answer. Delta in an awake adult is abnormal; the same delta in slow-wave sleep is expected.
Age-related findings not to over-read
| Finding | What it is |
|---|---|
| Posterior slow waves of youth | 2.5–4.5 Hz mixed into the posterior rhythm in children and adolescents, attenuating with eye opening |
| Slow / fast alpha variant | Half or double the alpha frequency; both react like alpha, and that reactivity is what identifies them |
| Benign temporal slowing | Scattered temporal theta or delta in the elderly |
Adult Background Check: Apply the Four Questions
Spot check This is a fully awake adult during sustained eyes-closed recording; drowsiness has been excluded. You have run the four background questions on the page. How would you describe it? (There is muscle on the frontal channels; read past it.)
Diffuse, symmetric, continuous slowing. The background is theta-dominant across the page rather than alpha-dominant posteriorly, both hemispheres look alike, and there are no periodic or rhythmic runs. That combination is mild diffuse slowing, the commonest abnormal EEG finding there is.
It is non-specific on its own. Diffuse slowing says cerebral function is abnormal in this known-awake adult; it does not say why. Toxic, metabolic, post-ictal, infectious, and degenerative processes may look like this. If behavioral state were unknown, drowsiness could mimic the appearance and would have to be excluded before calling it abnormal.
Note the trap this page sets. The frontal channels carry muscle, and muscle is fast; if you judge the background where the EMG is, you will call a slow record normal. Judge it posteriorly, where the rhythm lives.
Spot check Awake adult, eyes closed after a mixed-frequency stretch. Where is the posterior dominant rhythm maximal?
The PDR is an occipital rhythm. After the first seconds of mixed activity, a regular alpha-range oscillation appears and stays maximal at O1 and O2. Measure it there, on the stable eyes-closed stretch, not through the frontal muscle.
Frequency, symmetry, and reactivity are the three questions that follow. Count cycles in a one-second bracket on the posterior channels; compare left with right; then confirm that eye opening attenuates it.
Developmental Orientation: The Normal Target Moves With Age
The adult rules in this course are not universal across development. Interpret pediatric and neonatal EEG against conceptional age, behavioral state, and sleep–wake organization before calling slowing or discontinuity abnormal.
Pediatric PDR maturation
| Approximate age | Expected milestone |
|---|---|
| ~4 months | Posterior rhythm around 4 Hz |
| ~1 year | Posterior rhythm around 6 Hz |
| ~3 years | Posterior rhythm around 8 Hz |
| ~8 years onward | Adult-range 8–13 Hz PDR |
Sleep spindles appear at roughly 6–8 weeks and may remain asynchronous until about 2 years. Posterior slow waves of youth can be normal when they remain tied to the reactive posterior rhythm.
Neonatal preview
In neonates, state and continuity are maturational variables. Tracé discontinu is expected at very premature ages; delta brushes peak before term; tracé alternant belongs to term quiet sleep; and wakefulness/active sleep should become continuous by term. A pattern normal at 29 weeks postmenstrual age may signal severe dysfunction in an adult.
This is orientation, not neonatal interpretation training. Continue to Neonatal EEG and Neonatal Seizures for conceptional-age windows, neonatal seizures, and full recording standards.
Normal neonatal patterns must be anchored to conceptional age and state; adult continuity rules cannot be carried backward unchanged.
Sleep Architecture: Diagnostic Graphoelements
Sleep is a dynamic neurophysiological process. Differentiating sleep stages is critical, as many sleep waveforms mimic epilepsy spikes, and certain epilepsy syndromes manifest exclusively during NREM sleep transitions. Every figure is the same longitudinal bipolar page (left temporal over left parasagittal, then right temporal over right parasagittal) across the same ten seconds at the same sensitivity, so they can be compared with each other. The channels carrying the finding are in red.
Stage N1 (Light Sleep)
Drowsiness. N1 is scored when the posterior dominant rhythm attenuates to less than 50% of the epoch, replaced by low-amplitude, mixed-frequency activity. Differentiated by:
• Vertex Sharp Waves (V-waves): Brief, sharp, negative transients maximal at the midline central region (Cz).
• Slow Rolling Eye Movements (SREMs): Gentle, slow horizontal oscillations.
How you know: Vertex waves are surface-negative, so they reverse phase at C3 and C4 rather than appearing in one channel alone.
Same waves, transverse montage: use the Transverse button on the tracing. The reversal then falls on Cz, where the wave actually is. Strip the midline chain out, as the bare double banana in One Discharge, Four Montages does, and the same wave reverses at C3 and C4 instead: a real reversal at the wrong electrode.
Stage N2 (Stable Sleep)
Differentiated by two distinct, diagnostic waveforms:
• Sleep Spindles: Rhythmic sinusoidal runs of 11–16 Hz (classically 12–14 Hz) activity lasting >0.5 seconds, maximal in central/frontal channels.
• K-Complexes: A well-delineated negative sharp wave immediately followed by a positive component, total duration >0.5 seconds, maximal over the frontal derivations, often elicited by sound stimuli.
How you know: A K-complex is a sharp negative followed by a slow positive, and a spindle is a brief 11–16 Hz waxing-and-waning run. Their state-appropriate morphology, distribution, and relationship to the surrounding sleep architecture identify them; lack of evolution alone does not exclude every electrographic seizure.
Stage N3 (Slow Wave Sleep)
Deep NREM sleep. In adults, N3 is scored when slow-wave activity at 0.5–2 Hz and at least 75 μV measured over the frontal derivations occupies at least 20% of a 30-second epoch. Other activity may still be present; spindles can occur and are not scored separately from the N3 epoch.
How you know: The delta is generalized but frontally maximal; a completely uniform field would cancel out in a bipolar chain and show nothing at all.
Stage REM (Dreaming State)
Low-voltage, mixed-frequency background resembling an active, awake state, with reduced chin and axial tonic EMG; brief phasic muscle activity may still occur:
• Sawtooth Waves: 2–6 Hz triangular, jagged waveforms maximal in central channels, preceding rapid eye movements.
• Rapid Eye Movements (REMs): Sharp, irregular horizontal deflections.
How you know: The eye movements are SHARP here, not the slow rolling drift of N1, and the left and right frontal chains move in opposite directions.
Sleep Spot Checks: Stage, Field, and Symmetry
Spot check A real sleep page, longitudinal bipolar. Which stage is this?
N2 is defined by what interrupts the background, not by the background itself. Between the transients this page is low-voltage mixed-frequency, which on its own is N1 or REM. What makes it N2 is the presence of K-complexes and spindles.
That is why N2 is worth recognizing deliberately: it is the stage that most reliably brings out epileptiform discharges, and it is also the stage whose normal graphoelements get over-read as pathology. A K-complex is a large, sharply contoured, midline-maximal transient, on a bad day, exactly what a sharp wave looks like.
The discriminator is context and morphology. Vertex waves and K-complexes have expected sleep-stage timing, topography, and associated architecture. Interictal epileptiform discharges may be strongly activated by NREM sleep or even appear only in sleep, so absence during wakefulness does not make a sharp transient benign. Look instead for a reproducible physiologic field, appropriate duration and morphology, an after-going slow wave, and disruption of the background.
Spot check Same idea, a different sleep page: one bilateral central transient stands out. Click either parasagittal chain carrying its symmetric maximum.
A vertex wave is a central, midline generator, so it appears on both sides at once. The two parasagittal chains carry it simultaneously and symmetrically, and the temporal chains hardly see it. That bilateral symmetry is the finding, not the sharpness.
This is a useful habit in reading sharp transients: before asking how sharp is it, define its field and relationship to state. A true interictal epileptiform discharge may be focal or generalized, so symmetry alone does not make a waveform benign. Here the expected midline maximum, bilateral parasagittal expression, sleep state, and morphology together support a vertex wave.
The trap runs the other way too. A vertex wave that happens to be a little larger on one side (which is common and normal) gets reported as a central sharp wave. Judge asymmetry across several transients, never one.
Spot check Another real sleep page, same longitudinal bipolar layout. Which stage is this?
N3 is scored from the background, not from a single graphoelement. In adults, slow-wave activity at 0.5–2 Hz and at least 75 μV over the frontal derivations must occupy at least 20% of a 30-second epoch. This page is already there: high-voltage delta in every chain, largest in front.
Spindles may still appear in N3 and are not scored separately. What you should not do is call this N2 because you can still find a spindle, or call it abnormal awake delta. State first, then the voltage makes sense.
Physiological Variants: Differentiating the Lookalikes
One of the most common errors in clinical neurology is the misdiagnosis of normal, benign physiological variants as epilepsy spikes (false positives). Master these key benign variants to prevent clinical errors: Every figure is the same longitudinal bipolar page (left temporal over left parasagittal, then right temporal over right parasagittal) across the same ten seconds at the same sensitivity, so they can be compared with each other. The channels carrying the finding are in red.
Mu Rhythm
Arch-shaped or comb-like 7–11 Hz central rhythm (C3/C4). Unlike Alpha, it has no reaction to eye opening. Differentiated because it blocks instantly upon motor movement (or even thinking about movement) of the contralateral hand.
How you know: It lives over the central electrodes, not the occiput, and eye opening does not abolish it. Movement of the opposite hand is the test that separates mu from the PDR.
Wicket Spikes
Arciform, comb-like 6–11 Hz runs in the temporal chains during drowsiness and light sleep. Distinguished from epileptiform discharges because they are rhythmic and repetitive rather than isolated, symmetric in waveform, have no aftercoming slow wave, and do not disturb the surrounding background. Because they appear in runs across neighboring temporal electrodes, they do not behave like a focal discharge; treating a wicket run as a localizing finding is one of the commonest over-reads in clinical EEG.
How you know: They come in runs with no after-going slow wave, and the background runs on underneath.
BETS (SSS)
Benign Epileptiform Transients of Sleep (also known as Small Sharp Spikes / SSS). These are very brief (<50ms), low-amplitude (<50μV), monophasic or biphasic spikes occurring in N1/N2 NREM sleep. Differentiated because they have a broad, shallow dipole field across hemispheres, but absolutely no aftercoming slow wave disruption.
How you know: Very brief, di-phasic, and independent on the two sides; no after-going slow wave and no disruption of the background.
RMTD (Psychomotor Variant)
Rhythmic Mid-Temporal Drowsiness. Runs of monomorphic, flat-topped temporal theta waves (5–7 Hz) lasting several seconds during drowsiness. Typical RMTD remains monomorphic, does not spread, sits in its characteristic drowsy temporal field, and has no clinical correlate.
How you know: The characteristic notched temporal morphology, drowsy state, fixed rate and field, and preserved background support RMTD. Evolution would argue against it, but not every electrographic seizure must evolve.
POSTS and lambda: same shape, different state
Positive Occipital Sharp Transients of Sleep are sail-shaped, surface-positive transients maximal over the occipital regions during N1/N2 sleep, often in runs. Lambda waves are the awake counterpart: the same occipital positive sharp transients while the patient is scanning a patterned field with the eyes open. Identical morphology; the diagnosis is the state.
How you know: Surface positive. POSTS arrive in sleep, usually in trains. Lambda is isolated and tied to visual scanning. Use the Lambda button on the tracing to switch the page. When a patient is awake and looking around, call it lambda; when asleep, call it POSTS.
Variant Spot Check: State Is Part of the Diagnosis
Spot check The technologist documents stable N1–N2 sleep with the eyes closed and no visual scanning. Sharply contoured transients appear over the posterior head. What are they?
POSTS are the posterior equivalent of vertex waves: normal sleep transients that look epileptiform. Checkmark-shaped, surface-positive, occipital, usually bilateral, and characteristically in runs of several rather than one at a time.
The discriminators against a real occipital spike are state, company and rhythm. POSTS occur in sleep, arrive in trains, and have no after-going slow wave; an occipital spike focus does not need sleep, does not travel in packs, and usually drags a slow wave behind it.
Their awake counterpart is lambda: the same morphology in the same place, produced by scanning eye movements with the eyes open. Same waveform, different state: when a patient is awake and looking around, call it lambda; when asleep, call it POSTS.
Interictal Epileptiform Discharges: More Than “Sharp”
An interictal epileptiform discharge (IED) is a transient with a plausible cerebral field, not simply a pointy waveform. Measure duration first: an EEG spike is 20–70 ms, while a sharp wave is 70–200 ms. Then ask whether the event has a reproducible field, an appropriate phase relationship across channels, a common after-going slow wave, and disruption of the surrounding background. No single feature is mandatory or diagnostic by itself.
Work through the same discharge in three full-width views. You already found the bipolar reversal at T8; now name the transient, re-read its field in average reference, then confirm that same T8 maximum on a second bipolar montage. Circumferential does not invent neighbors F8 already had on the banana.
Select a view to begin.
- Duration: Measure at the baseline crossings instead of judging sharpness by eye.
- Field: Confirm a plausible voltage gradient across neighboring electrodes on more than one montage.
- Context: Decide whether the transient belongs to sleep architecture, artifact, a benign variant, or an abnormal background.
- Repeatability: Find the same morphology and field again before diagnosing from an ambiguous transient.
Continue with Interictal Epileptiform Discharges and Focal Epilepsy: Semiology to Localization in Board Review.
Activation Procedures
Activation procedures (hyperventilation, photic stimulation, and sleep) stress the brain to bring out epileptiform activity that a resting record may miss.
We perform specific activation procedures to stress the brain and induce diagnostic abnormalities:
Hyperventilation (HV)
Typically 3 minutes of deep, rapid breathing (some laboratories extend to 5 minutes when absence seizures are suspected). Hypocapnia produces cerebral vasoconstriction and a fall in cerebral blood flow.
- Normal Response: "HV Buildup" consisting of high-voltage, rhythmic, generalized delta slowing (promoted by hypoglycemia).
- Abnormal Response: Induction of asymmetric focal slowing or generalized 3 Hz Spike-and-Wave discharges (classic absence seizure trigger).
Photic Stimulation
Flashing strobe light at progressive frequencies (1–30 Hz).
- Photic Driving (Normal): Occipital channels synchronize and match the flashing frequency.
- Photoparoxysmal Response (Abnormal): Generalized spike-and-wave or polyspike-and-wave discharges provoked by the strobe. A PPR may be confined to the flash train or persist after it; persistence increases concern but is not required for the definition. A PPR indicates photosensitivity, a largely heritable trait; it is strongly associated with the generalized epilepsies but also occurs in people who never have seizures, so it is interpreted with the clinical history rather than as a diagnosis on its own.
Spot check A real photic stimulation page; the flash train is marked along the bottom of the page. What makes a response to the flashes normal rather than epileptogenic?
Photic driving is the normal answer. It is a symmetric posterior rhythm locked to the stimulus frequency or a harmonic and lacks a generalized epileptiform discharge.
A photoparoxysmal response is generalized spike-wave or polyspike-wave provoked by flashes. It may remain limited to the stimulus train or continue afterward; persistence strengthens the abnormality but is not required to call a PPR.
Read the stimulus markers first. Timing, distribution, and morphology must be interpreted together: ending with the train does not by itself make an epileptiform response normal.
Activation can reveal epileptiform potential. Name those transients next by duration, field, and disruption of the background, not by how pointy they look.
Continuity, Attenuation, and Suppression: Describe Voltage Over Time
Continuity asks whether activity persists across time. Attenuation and suppression ask how far voltage falls. Keep these four terms in view while you work the cases: they are the vocabulary the later ACNS names depend on.
| Term | What it means |
|---|---|
| Focal attenuation | Regional voltage drop; activity continues on that side |
| Discontinuity | Repeated interruptions; activity returns between them |
| Suppression | Background below 10 µV |
| Burst suppression | High-voltage bursts alternating with suppression |
Select a view to begin.
Continue with Encephalopathy, Coma, and the ICU and Neonatal EEG and Neonatal Seizures in Board Review.
Once voltage over time has a name, ACNS terminology can name the sustained pattern without deciding whether it is a seizure.
ACNS and the Ictal–Interictal Continuum: Name Before You Interpret
ACNS critical-care terminology separates description from clinical interpretation. Build the main term from distribution plus pattern, then add modifiers. The name communicates what is on the tracing without presuming cause, seizure status, prognosis, or treatment.
Start with where the pattern is, then whether it is periodic or rhythmic, then add frequency, prevalence, plus-modifiers, fluctuation/evolution, and stimulus relationship.
| Family | Core names | First distinction |
|---|---|---|
| Periodic discharges (PDs) | LPDs, BIPDs, GPDs | Discrete discharges separated by a measurable interval |
| Rhythmic delta activity (RDA) | LRDA, GRDA | Continuous repeating delta without an interval between waves |
- Plus modifiers: +F adds fast activity, +R adds superimposed rhythmic activity to PDs, and +S adds sharp waves/spikes to RDA. An LRDA+R atlas example belongs in advanced modifier practice rather than being mislabeled as plain LRDA.
- BIRDs: Brief potentially ictal rhythmic discharges are focal or generalized rhythmic activity above 4 Hz, lasting at least 0.5 but under 10 seconds, without a definite clinical correlate. They must not be a known normal/benign pattern or part of burst suppression/attenuation, and must show evolution, resemble this patient’s IEDs or seizures, or have a sharp contour. They are short by definition but carry a strong seizure association.
- SIRPIDs: Stimulus-induced rhythmic, periodic, or ictal-appearing discharges are an umbrella description tied to stimulation, not one morphology or an automatic seizure diagnosis.
- IIC: The ictal–interictal continuum is a risk-bearing gray zone, not a diagnosis by appearance alone. Frequency, plus features, evolution, clinical state, medications, imaging, response testing, and temporal context all matter.
Do not add “epileptiform” back into the legacy names. PLEDs, BIPLEDs, and GPEDs are now LPDs, BIPDs, and GPDs precisely because the descriptive label should not decide ictal significance in advance.
Pathology Showcase: Diagnostic Signatures
Compare one full-size tracing at a time. Every figure uses the same longitudinal bipolar montage, ten-second time base, and sensitivity. Red traces show the involved chains, so distribution can be compared without a scale or montage change.
Focal Slowing (PDA)
Continuous, polymorphic delta activity localized to a single hemisphere or lobe. Strong indicator of focal structural injury (e.g., tumor, stroke, abscess).
How you know: Polymorphic means several rates at once, and it is CONTINUOUS; that plus a strictly regional field is what points to structural injury.
Generalized Periodic Discharges (GPDs)
The synchronized complexes are intentionally higher in amplitude here so their three successive phases are easy to inspect. Triphasic describes morphology, not cause. It can occur in toxic-metabolic encephalopathy and other settings; it is not specific to hepatic encephalopathy.
How you know: A measurable interval separates near-identical complexes, and every chain participates at the same time. GPDs are not automatically seizures; frequency, evolution, plus features, duration, and clinical context determine ictal significance.
Lateralized Periodic Discharges (LPDs)
Discrete complexes recur over the right posterior temporal and parasagittal chains, with a clear interval between them and no mirror field on the left. LPDs commonly accompany acute focal brain injury and carry a meaningful seizure association.
How you know: Distribution first gives lateralized, and the measurable gap gives periodic discharges. LPDs alone do not prove an electrographic seizure; assess frequency, plus modifiers, evolution, clinical findings, and response over time.
Continue with Periodic Patterns by Etiology and BIRDs and the Ictal-Interictal Continuum in Board Review.
ACNS Pattern Spot Checks: Periodic, Rhythmic, and Lateralized
Spot check Repetitive complexes in every chain on a real page. ACNS asks one question before any other. Periodic or rhythmic?
Periodic and rhythmic are the two branches of the whole ACNS nomenclature, and the test is the gap. If discharges are separated by an interval you can measure, the pattern is periodic. If the waveform is continuous with no return to baseline, it is rhythmic. This page is periodic: roughly one complex per second in every chain, on a background that is markedly attenuated between them.
Generalized distribution plus periodicity gives GPDs, which point to a diffuse insult: hypoxic-ischemic injury, drug toxicity, or CJD. The same complexes over one hemisphere would be LPDs, and a structural lesion moves to the top of the list instead.
Sharpness is not what makes them worrying. Frequency, prevalence, plus-modifiers, fluctuation or evolution, and clinical context determine where a pattern sits on the ictal–interictal continuum. GPDs are not automatically seizures. An electrographic seizure is present if epileptiform discharges average more than 2.5 Hz for at least 10 seconds, or if a pattern shows definite evolution for at least 10 seconds.
Spot check Rhythmic delta on a real page, and it is not everywhere. Click the chain where it is largest.
Right lateralized rhythmic delta activity (LRDA). Two things make the call: the waveform is rhythmic (successive waves repeat without a measurable interval between them), and it is lateralized (largest over the right parasagittal region compared with the mirror chain on the left).
Lateralization is always a comparison, never a single-chain judgment. Read each temporal and parasagittal chain against its opposite number, then identify the maximum within the involved hemisphere.
LRDA matters because it carries meaningful seizure association, but plain LRDA is not automatically on the ictal–interictal continuum. Under ACNS criteria, lateralized RDA qualifies for IIC when it is above 1 Hz for at least 10 seconds and has a plus modifier or fluctuation. Distinguish it from polymorphic focal slowing, which is irregular rather than rhythmic and usually points toward focal cerebral dysfunction.
Spot check Discrete complexes recur about once a second, and they are not everywhere. How should this page be named?
Right posterior LPDs. ACNS naming is distribution, then pattern: the complexes are lateralized (right posterior temporal and parasagittal, no left mirror) and periodic (a clear, near-constant interval). That is LPDs, not GPDs and not a seizure by itself.
LPDs commonly accompany acute focal injury and raise seizure risk. Frequency, plus modifiers, evolution, and the clinical examination decide where they sit on the ictal–interictal continuum. Do not put “epileptiform” back into the name.
Seizure Dynamics: Two Electrographic Pathways
ACNS recognizes two routes to an electrographic seizure: (1) epileptiform discharges averaging more than 2.5 Hz for at least 10 seconds, or (2) any EEG pattern with definite evolution lasting at least 10 seconds. Definite evolution is sequential change in frequency, morphology, or location under the ACNS criteria; the pattern does not have to change in all three dimensions. Drag through this left temporal example to see several dimensions change as neighboring cortex is recruited.
Seizure Spot Checks: Focal Chain and Generalized Onset
Spot check This page begins with background, then a right-sided seizure evolves. Click the full horizontal chain that carries the sustained ictal maximum once it begins.
The right lateral chain becomes the sustained ictal maximum. Read its four derivations from top to bottom, then follow them horizontally. The early background is not ictal. After onset, frequency, amplitude, and morphology change as the seizure evolves across the right lateral derivations.
The spatial answer is a chain, not a vertical slice of time. A vertical “onset” target would include every channel at one moment and would not test localization. The full horizontal highlight shows the field the learner must follow.
The right parasagittal and midline channels are recruited later. Spread does not erase the earlier and sustained right lateral maximum.
Spot check This page starts normal and then does not. Click where the generalized burst begins.
Abrupt onset, generalized from the first complex, normal background before and after. That triad is the signature of a generalized spike-and-wave burst, and each part of it is doing work.
Abrupt and generalized separates it from a focal seizure, which starts in one region and spreads over seconds; there is no march here, every chain starts together. Normal background points toward a genetic generalized epilepsy rather than a symptomatic one; a slow or attenuated background between bursts suggests an encephalopathic syndrome instead.
Duration matters, but duration alone does not label the event. A brief generalized spike-wave burst may be electroclinical or subclinical depending on careful testing and video correlation. Absence status epilepticus requires a prolonged generalized epileptiform pattern together with a compatible sustained change in responsiveness or mental state; do not infer it from “a longer-looking burst” without the electroclinical context.
Continue with Ictal EEG and Generalized Epilepsies in Board Review.
Before accepting an apparent seizure pattern as cerebral, exclude physiologic and technical artifacts that can mimic rhythmicity or evolution.
Artifacts: The Biophysics of Noise
A large share of what appears on a routine EEG is not cerebral at all; it originates from the eyes, muscle, heart, movement, the electrodes themselves, or the environment. Each one below has a DISTRIBUTION that gives it away, which is why they are all drawn on the same page: Every figure is the same longitudinal bipolar page (left temporal over left parasagittal, then right temporal over right parasagittal) across the same ten seconds at the same sensitivity, so they can be compared with each other. The channels carrying the finding are in red.
Move the eye and watch the frontal channels
Centered gaze: the corneoretinal field is balanced. Move the eyes or run a blink to see why the artifact is frontal and how channel subtraction sets its direction.
The Artifact Gallery: Four Noise Sources on One Page
Eye Blinks (Bell's Phenomenon)
The eyeball behaves as a dipole: the cornea is relatively positive and the retina relatively negative. During a blink, the positive field is commonly maximal at Fp1/Fp2. In an Fp1–F3 derivation, Fp1 is Input 1; a relatively positive Input 1 produces a downward deflection when negative is displayed upward.
How you know: Both sides move together and DOWNWARD, and the field is almost gone one electrode back; real frontal slowing does not drop off that fast.
Lateral Eye Movements
Looking to the Left brings the positive left cornea close to F7 and the negative right retina close to F8.
Resulting Trace: An immediate positive/downward deflection at F7 and a simultaneous negative/upward deflection at F8. This is accompanied by rapid "lateral rectus spikes" (myogenic contractions) in the temporal leads.
How you know: The mirror-image frontal field matches the corneoretinal dipole and is time-locked to eye movement on video or eye leads. Watch for lateral rectus spikes at each onset.
Myogenic (EMG) Artifacts
Extremely high-frequency, narrow, jagged buzz caused by jaw clenching, chewing, or tension. Classically maximal in temporal channels (T7/T8). Oversmoothing with filters to remove this can artificially round the muscle spikes, causing them to look like cerebral Beta waves.
How you know: Individual motor-unit spikes are visible in the expanded inset. Filtering them rounds them off until they look like cerebral beta, which is the trap.
60Hz Line Hum
A regular fast artifact from mains interference, poor or unbalanced electrode contact, nearby equipment, or grounding problems. First inspect electrodes and the environment. A notch filter may reduce residual interference but can distort activity near the filtered frequency and should not replace troubleshooting.
How you know: It appears in exactly the chains sharing the bad electrode, and in OPPOSITE phase between them. Fix the electrode first; a notch filter only hides it.
Artifact Spot Checks: Distribution Before Shape
Spot check Brief, repeated, frontally maximal deflections on a real page, and the posterior background is untouched. What are they?
The eye is a dipole with the cornea positive relative to the retina, so any eye movement is a voltage generator sitting two centimeters from Fp1 and Fp2. A blink rolls the globes up, driving the frontal electrodes positive: brief, bilateral, and steeply falling off behind the frontal chains.
Three features identify it and all three matter: the distribution is frontal and drops away immediately, the events align with blinking on video or eye leads, and the background elsewhere is unaffected. The repeated shape is compatible with blinks, but epileptiform discharges can also be stereotyped, so stereotypy is not the discriminator.
The related trap is eye flutter: rhythmic, roughly 3 Hz, frontally maximal, and a convincing imitation of FIRDA. The tell is the same: it is maximal right at Fp and vanishes posteriorly, whereas a cerebral rhythmic pattern has a broader field. Eye leads settle it in a second, which is what they are for.
Spot check A rhythmic pattern is running through this record. Before calling it a seizure, what should you check?
Mechanical devices can drive a highly regular rhythm through the patient and electrode array. A percussor, ventilator, or vibrating bed may produce a fixed rate with no physiologic field, no independent cerebral evolution, and exact temporal coupling to the device.
Lack of evolution alone does not exclude an electrographic seizure, because qualifying epileptiform discharges above 2.5 Hz for at least 10 seconds provide the other pathway. Here, however, the waveform is not an epileptiform discharge and the bedside/video correlation identifies its mechanical source.
Two habits catch these in seconds. Read the non-cerebral channels (the EKG and any respiratory or movement channel), because a mechanical rhythm usually shows up there too. And read the technologist’s notes and the video: chest PT written on the page is the fastest EEG interpretation you will ever make.
Spot check High-amplitude bursts march through this page about once a second. The EKG underneath is regular. What is contaminating the record?
Chewing is muscle, at the frequency of the jaw. Each burst is packed with high-frequency motor-unit spikes, maximal in the temporal chains, and the EKG is unaffected. Ask the technologist to pause chewing, or watch the video: the page quiets when the jaw does.
The trap is to call the cadence periodic and write LPDs or a seizure. Periodicity of the bursts is the chewing rate. Distribution (temporalis/masseter), morphology (EMG needles, not a sharp-and-slow dipole), and video separate it in seconds.
Artifact Hunter: Clean the Trace at Its Source
Artifact Hunter: Clean the Trace
Six artifacts are contaminating this record, on the same longitudinal bipolar page as every figure above. Each has a distribution, a shape and a rhythm that give it away: blinks are frontal and bilateral, muscle sits on the temporal electrodes, line hum and an electrode pop each follow one single electrode, sweat sways the baseline below 0.5 Hz, and the ECG keeps perfect time, which is what the EKG channel at the bottom is for. Click any channel to see what reaches it and why, then fix each artifact at its source and watch the posterior rhythm reappear.
From Tracing to Report: Fill Each Heading in Order
A technically accurate waveform name is only one part of an EEG interpretation. State, medications, stimulation, video, and behavior can change the meaning of the same pattern. Write the report in this order so those qualifiers are not lost. Each heading is one line of the clinical template.
Clinical report template
- STUDY DATE AND TIME:
- Start time, recording type, duration, electrodes, montages, and any technical limitations.
- CLINICAL HISTORY:
- @AGE@ with possible seizures. Age and the clinical question. Note recent seizures, temperature, and other major confounders when known.
- CNS ACTIVE MEDICATIONS:
- Sedation, antiseizure medications, and other CNS-active drugs that change the tracing.
- DAY 1
- Day header for serial or long-term recordings. Repeat the fields below for each day.
- BACKGROUND:
- The background activity is organization, symmetry, predominant frequencies, anterior–posterior gradient, PDR frequency and reactivity, variability, and stimulus reactivity.
- SLEEP:
- Architecture and state changes, separate from the waking background. State whether sleep was captured.
- CONTINUITY/VOLTAGE:
- Whether activity persists across time, and how far voltage falls (attenuation or suppression).
- SLOWING:
- Distribution and prevalence. Do not bury this inside the background sentence.
- ACTIVATION PROCEDURES:
- Hyperventilation and photic stimulation: performed or not, and the response.
- EPILEPTIFORM DISCHARGES, RHYTHMIC OR PERIODIC PATTERNS:
- IED morphology, field, location, and abundance. Name rhythmic or periodic patterns with ACNS terms and modifiers.
- SEIZURES OR CLINICAL EVENTS:
- Onset, duration, evolution, and spread. Review video and technologist notes. State whether an electrographic correlate was present and whether awareness was tested.
- QEEG FINDINGS:
- Record quantitative EEG findings if they were reviewed. If QEEG was not part of this study, say so.
- EKG:
- Heart rate and rhythm from the EKG channel. Confirm ECG artifact on the scalp against this channel.
Impression: after the template, summarize the most important findings in priority order, connect them cautiously to the clinical question, compare with prior recordings when available, and state meaningful limitations.
Continue with Technical Standards and Recording Practice for the full reporting framework.
Measure first. Place second.
Build a standard adult 10–20 array from reproducible cranial landmarks. This schematic training tool is not a substitute for supervised technologist training or local laboratory protocol.
With a reproducible electrode array in place, connect those sites into bipolar and referential channels and learn how each subtraction changes what the field looks like.