EEG Basics
EEG Basics
What Do You Need to Know?
- EEG physiology — measures cortical postsynaptic potentials (NOT action potentials); pyramidal neurons layer V; minimum 6 cm² cortex needed for scalp detection
- Normal rhythms — Beta (>13 Hz, frontal), Alpha (8–13 Hz, posterior, Berger effect), Mu (8–13 Hz, central, movement attenuation), Theta (4–7 Hz), Delta (<4 Hz)
- 10-20 system — odd = left, even = right, z = midline; bipolar montage (phase reversal localizes) vs referential montage (amplitude comparison)
- Sleep EEG — vertex waves (N1) → spindles + K-complexes (N2) → delta (N3) → low-voltage fast + sawtooth (REM)
- Normal variants — wicket spikes, BETS, 14&6 positive bursts, 6 Hz phantom spike-wave, RMTD, SREDA — these are NOT epileptiform
- Epileptiform patterns — 3 Hz spike-wave (absence), centrotemporal spikes (BECTS), temporal sharps (TLE), hypsarrhythmia (infantile spasms)
- Periodic patterns — GPDs (CJD), LPDs (HSV encephalitis), triphasic waves (hepatic encephalopathy); know the table
- Activation procedures — hyperventilation activates absence; photoparoxysmal response in JME; photic driving is normal
EEG Physiology
What Does EEG Actually Measure?
- Postsynaptic potentials (PSPs) of cortical pyramidal neurons — NOT action potentials
- Specifically, excitatory postsynaptic potentials (EPSPs) and inhibitory postsynaptic potentials (IPSPs) summed across large populations of neurons
- PSPs are slower and longer-lasting than action potentials → better temporal summation → detectable at the scalp
- Layer V pyramidal neurons are the primary generators — their apical dendrites are oriented perpendicular to the cortical surface
The Dipole Concept
- EPSPs on apical dendrites (superficial cortex) → current sink (negativity at surface) → upward deflection on EEG (by convention)
- EPSPs on deep layers/soma → positivity at surface → downward deflection
- IPSPs produce the opposite pattern
- The dipole orientation relative to the recording electrode determines the polarity of the scalp EEG signal
- Tangential dipoles (sulcal cortex) → maximum signal at a distance from the generator; radial dipoles (gyral crown) → maximum directly over the generator
Detection Requirements
- Minimum 6 cm² of synchronously active cortex is required to produce a detectable signal on scalp EEG
- Deeper sources (e.g., hippocampus, thalamus) are poorly represented on scalp EEG
- This is why many seizures (especially mesial temporal) may not be detected on scalp recordings
Board Pearl
EEG measures postsynaptic potentials, NOT action potentials. Action potentials are too brief and asynchronous to summate at the scalp. The generators are layer V cortical pyramidal neurons, and at least 6 cm² of cortex must be synchronously active for scalp detection.
Normal EEG Rhythms
| Rhythm | Frequency | Location | State | Clinical Significance |
|---|---|---|---|---|
| Beta | >13 Hz | Frontal (bifrontal) | Awake, alert | Enhanced by benzodiazepines, barbiturates; excess = medication effect |
| Alpha | 8–13 Hz | Posterior (occipital) | Awake, eyes closed, relaxed | Attenuates with eye opening (Berger effect); absent alpha → cortical dysfunction |
| Mu | 8–13 Hz | Central (C3, C4) | Awake, at rest | Attenuates with contralateral movement or thought of movement; arciform (comb-shaped) morphology |
| Theta | 4–7 Hz | Generalized / temporal | Drowsiness, light sleep | Normal in drowsiness/children; abnormal if persistent in awake adults → diffuse or focal dysfunction |
| Delta | <4 Hz | Generalized or focal | Deep sleep (N3) | Normal in deep sleep; abnormal if awake → structural lesion (focal) or encephalopathy (generalized) |
Key Points for Each Rhythm
- Alpha — the dominant posterior rhythm; should be symmetric (amplitude asymmetry >50% is abnormal); frequency <8 Hz in adults suggests encephalopathy
- Mu — often mistaken for alpha, but location (central) and reactivity (movement, not eye opening) distinguish it; can be asymmetric normally
- Beta — the most common medication-related change; asymmetrically reduced beta → consider structural lesion on the side with less beta (Bancaud phenomenon)
Board Pearl
Berger effect = alpha attenuation with eye opening. Mu rhythm attenuates with contralateral movement (not eye opening) — this distinction is a classic board question. Breach rhythm (increased amplitude, especially beta/mu, over a skull defect) is normal post-craniotomy and should not be mistaken for pathology.
Clinical Pearl
A focal reduction in beta activity over one hemisphere in a patient on benzodiazepines suggests an underlying structural lesion on that side (Bancaud phenomenon). Beta should be symmetrically enhanced by medications — asymmetry is always suspicious.
The 10-20 System
Electrode Placement
- Standardized system based on 10% and 20% intervals between skull landmarks (nasion, inion, preauricular points)
- Odd numbers = left hemisphere (F3, C3, P3, T3/T7, O1)
- Even numbers = right hemisphere (F4, C4, P4, T4/T8, O2)
- "z" = midline (Fz, Cz, Pz)
Electrode Labels
| Letter | Region | Electrodes |
|---|---|---|
| Fp | Frontopolar | Fp1, Fp2 |
| F | Frontal | F3, F4, F7, F8, Fz |
| C | Central | C3, C4, Cz |
| P | Parietal | P3, P4, Pz |
| O | Occipital | O1, O2 |
| T | Temporal | T3/T7, T4/T8, T5/P7, T6/P8 |
Montages
| Montage Type | Method | Advantages | Localization Technique |
|---|---|---|---|
| Bipolar (longitudinal) | Each channel = difference between two adjacent electrodes in anterior–posterior chains | Excellent localization; good artifact rejection | Phase reversal — the electrode common to two channels showing opposite deflections is the maximum |
| Bipolar (transverse) | Adjacent electrodes in left–right chains | Lateralization of parasagittal/midline activity | Phase reversal in the transverse plane |
| Referential | Each electrode compared to a common reference (ear, Cz, average) | True amplitude comparison across channels; no phase reversal | Amplitude comparison — highest amplitude channel = closest to maximum |
| Average reference | Each electrode compared to the average of all electrodes | Minimizes reference contamination | Amplitude comparison; can show artificial phase reversals |
Board Pearl
Phase reversal on bipolar montage localizes the source. In a bipolar (longitudinal) montage, the electrode shared between two channels showing opposite deflections is the site of the maximum. On a referential montage, there is no phase reversal — instead, you compare amplitudes to localize.
Normal Sleep EEG
Sleep Stage Progression
| Stage | EEG Features | Key Findings |
|---|---|---|
| Wakefulness | Alpha rhythm (posterior), beta (frontal) | Alpha attenuates with eye opening (Berger effect) |
| Drowsiness | Alpha dropout, slow lateral eye movements | Transition — intermittent theta, alpha fragmenting |
| N1 | Low-voltage mixed frequency; theta predominant | Vertex sharp waves (V-waves) — central (Cz), surface-negative; POSTs begin |
| N2 | Theta background | Sleep spindles (12–14 Hz, central, generated by thalamic reticular nucleus) + K-complexes (high-amplitude biphasic waves, frontal) |
| N3 | >20% of epoch is high-amplitude delta (≥75 µV, <2 Hz) | Slow-wave sleep; deep sleep; spindles may persist |
| REM | Low-voltage, fast (desynchronized) | Sawtooth waves (frontally maximal, 2–6 Hz, notched); rapid eye movements; muscle atonia on EMG |
Normal Sleep Variants (Benign Transients of Sleep)
- POSTs (positive occipital sharp transients of sleep) — positive polarity, occipital, N1/N2; bilateral, may be asymmetric; completely benign
- BETS (benign epileptiform transients of sleep) — also called small sharp spikes (SSS); low amplitude, temporal, broad field; occur in drowsiness/light sleep; NOT epileptiform
- Wicket spikes — arciform, temporal, adults >30 years; monophasic; no aftergoing slow wave; resemble mu rhythm; NOT epileptiform
Board Pearl
Sleep spindles are generated by the thalamic reticular nucleus and are a hallmark of N2 sleep along with K-complexes. Absent or asymmetric sleep spindles suggest thalamic or hemispheric dysfunction on the affected side. K-complexes are the largest normal EEG waveforms and are maximal frontally.
Normal Variants (Benign Patterns)
| Pattern | Location | Age/State | Key Features | Why It Matters |
|---|---|---|---|---|
| Wicket spikes | Temporal | Adults >30 yr; drowsiness/sleep | Arciform, monophasic, no aftergoing slow wave; trains or single | Mimics temporal sharp waves; no treatment needed |
| BETS / SSS | Temporal (widespread field) | Drowsiness/light sleep | Low amplitude (<50 µV), brief, broad field, diphasic | Mimics epileptiform spikes; benign |
| 14&6 positive bursts | Posterior temporal | Adolescents; drowsiness | Positive polarity, arciform; 14 Hz or 6 Hz; comb-like | Previously overcalled; completely benign |
| 6 Hz phantom spike-wave | Generalized (frontal or occipital max) | Young adults; drowsiness | Very low-amplitude spike, prominent slow wave; "FOLD" = Female, Occipital, Low amplitude, Drowsiness | Benign FOLD variant vs WHAM (Wake, High amplitude, Anterior, Male) which may have epilepsy association |
| RMTD | Midtemporal | Adults; drowsiness | Rhythmic theta (5–7 Hz); sharply contoured but no evolution | Previously called "psychomotor variant"; NOT a seizure pattern |
| SREDA | Parietal / posterior | Elderly; awake or drowsy | Rhythmic theta/delta; bilateral, widespread; abrupt onset/offset; NO clinical correlate | Mimics a seizure pattern on EEG but patient is asymptomatic; no treatment |
Mnemonic: FOLD vs WHAM for 6 Hz Spike-Wave
- FOLD (benign) — Female, Occipital predominance, Low amplitude spike, Drowsiness
- WHAM (possibly epileptiform) — Wake, High amplitude, Anterior predominance, Male
Clinical Pearl
SREDA is one of the most commonly misread EEG patterns. It appears as a sudden onset of rhythmic theta activity that looks electrographically like a seizure, but the patient is completely asymptomatic. It is most common in elderly patients and requires no treatment. Always correlate with clinical behavior.
Epileptiform Discharges
Spikes vs Sharp Waves
- Spike — duration <70 ms; sharply contoured; stands out from background; followed by aftergoing slow wave
- Sharp wave — duration 70–200 ms; otherwise similar morphology to spikes
- Both are interictal epileptiform discharges (IEDs) — indicate epileptogenic cortex but do NOT by themselves constitute a seizure
Classic Epileptiform Patterns
| Pattern | Frequency/Morphology | Location | Associated Syndrome |
|---|---|---|---|
| 3 Hz spike-wave | Regular, 3 Hz, spike followed by wave; lasts seconds to minutes | Generalized, bifrontal maximum | Childhood absence epilepsy; activated by hyperventilation |
| 4–6 Hz polyspike-wave | Irregular, 4–6 Hz, multiple spikes before each wave | Generalized | Juvenile myoclonic epilepsy (JME); activated by photic stimulation, sleep deprivation |
| Centrotemporal spikes | High-amplitude spike with horizontal dipole; activated by sleep | Centrotemporal (C3/C4, T3/T4) | BECTS / Rolandic epilepsy; benign, outgrown by adolescence |
| Temporal sharp waves | Sharp waves ± focal slowing | Anterior temporal (F7/F8, T3/T4) | Temporal lobe epilepsy |
| Hypsarrhythmia | Chaotic, high-amplitude, multifocal spikes + slow waves; disorganized | Generalized | Infantile spasms (West syndrome) |
| Slow spike-wave (<2.5 Hz) | Slow, irregular spike-wave complexes | Generalized | Lennox-Gastaut syndrome |
| GPFA | Generalized paroxysmal fast activity (10–25 Hz bursts) | Generalized, frontal maximum | Lennox-Gastaut syndrome (during sleep; tonic seizures) |
| Electrodecremental pattern | Sudden diffuse voltage attenuation | Generalized | Infantile spasms (ictal correlate); also tonic seizures in LGS |
Board Pearl
3 Hz generalized spike-wave = absence epilepsy; activated by hyperventilation. HV is the single best activation procedure for absence seizures. The discharge begins and ends abruptly, the child stares and is unresponsive during the discharge, and returns to normal immediately. Frequency <2.5 Hz suggests Lennox-Gastaut instead.
Periodic Patterns
| Pattern | Morphology/Interval | Location | Associated Conditions |
|---|---|---|---|
| GPDs (generalized periodic discharges) | Periodic sharp/triphasic complexes at ~1–2 Hz intervals | Generalized, bifrontal max | CJD (1 Hz periodic sharp complexes); anoxic brain injury; late status epilepticus |
| Long-interval GPDs | Periodic complexes every 4–14 seconds | Generalized | SSPE (subacute sclerosing panencephalitis); very long intervals, high amplitude |
| LPDs (lateralized periodic discharges) | Periodic sharp waves/complexes, lateralized; 1–3 Hz | Focal/lateralized (often temporal) | HSV encephalitis (temporal LPDs); acute stroke; tumor; abscess |
| BiPDs (bilateral independent PDs) | Independent periodic discharges from each hemisphere | Bilateral but asynchronous | Poor prognosis; anoxia, severe encephalopathy, bilateral structural lesions |
| Triphasic waves | Three phases: initial small negative, large positive, trailing negative; anterior-to-posterior lag | Generalized, frontal max | Hepatic encephalopathy; uremia; other metabolic encephalopathies |
| SIRPIDs | Stimulus-induced rhythmic, periodic, or ictal discharges | Variable | Critically ill patients; triggered by stimulation; uncertain significance — may or may not require treatment |
Triphasic Waves vs GPDs of CJD
- Triphasic waves (metabolic) — anterior-to-posterior time lag; reactive to stimulation; slower frequency; improve with treatment of metabolic cause
- GPDs of CJD — shorter duration complexes; ~1 Hz; may NOT show anterior-posterior lag; progressive; associated with myoclonus
- The distinction can be challenging — clinical context is essential
Board Pearl
Temporal LPDs in a febrile patient with altered mental status = think HSV encephalitis until proven otherwise. LPDs (formerly PLEDs) are seen in acute destructive focal lesions. GPDs at 1 Hz with rapidly progressive dementia and myoclonus = CJD. BiPDs carry a poor prognosis regardless of etiology.
EEG in Specific Conditions
| Condition | Classic EEG Pattern | Key Features |
|---|---|---|
| Absence epilepsy | 3 Hz generalized spike-wave | Activated by hyperventilation; abrupt onset/offset; bilateral synchronous |
| JME | 4–6 Hz generalized polyspike-wave | Activated by photic stimulation + sleep deprivation; normal background |
| Temporal lobe epilepsy | Temporal spikes/sharp waves | Anterior temporal max; ictal: rhythmic theta evolving to delta |
| BECTS (Rolandic) | Centrotemporal spikes | Activated by sleep; horizontal dipole; outgrown by adolescence |
| Infantile spasms | Hypsarrhythmia | Chaotic, high-amplitude, disorganized; ictal: electrodecrement |
| Lennox-Gastaut | Slow spike-wave (<2.5 Hz) + GPFA | GPFA seen in sleep (tonic seizures); diffusely slow background |
| CJD | Periodic sharp wave complexes (~1 Hz GPDs) | Progressive; associated with myoclonus; may be absent early |
| HSV encephalitis | Temporal LPDs | Usually unilateral initially; periodic at 1–3 second intervals |
| Hepatic encephalopathy | Triphasic waves | Frontal maximum; anterior-to-posterior lag; resolve with treatment |
| Brain death | Electrocerebral inactivity (ECI) | No cerebral activity >2 µV; 30-min recording; interelectrode distance ≥10 cm; sensitivity 2 µV/mm |
Clinical Pearl
For brain death determination by EEG, specific technical standards must be met: recording duration at least 30 minutes, interelectrode distances of at least 10 cm, sensitivity of 2 µV/mm, and the EEG must show no reactivity to stimulation. Drug intoxication and hypothermia must be excluded as they can cause reversible electrocerebral inactivity.
Activation Procedures
| Procedure | Technique | Normal Response | Abnormal Response |
|---|---|---|---|
| Hyperventilation (HV) | 3–5 minutes of deep breathing | Bilateral, symmetric high-amplitude slowing (especially in young patients); resolves within 1–2 min of stopping | 3 Hz spike-wave (absence seizures); focal slowing (may unmask focal lesion); asymmetric slowing |
| Photic stimulation | Strobe light at various frequencies (1–30 Hz) | Photic driving — occipital response time-locked to flash frequency (normal, physiologic) | Photoparoxysmal response (PPR) — generalized spike-wave discharges outlasting the stimulus; associated with JME, generalized epilepsies |
| Sleep deprivation | Partial or total sleep deprivation prior to recording | Patient falls asleep during recording | Increases yield of interictal epileptiform discharges; activates centrotemporal spikes (BECTS), generalized epilepsies |
| Sleep recording | Natural or induced sleep during EEG | Normal sleep architecture | Many epileptiform discharges are activated by NREM sleep (especially N2); BECTS, ESES (electrical status epilepticus of sleep) |
Key Points
- HV is the most important activation for absence epilepsy — provokes 3 Hz spike-wave in nearly all untreated patients
- HV-induced slowing in normal individuals is more prominent in children and resolves quickly; persistent or asymmetric slowing is abnormal
- Photic driving is NORMAL; photoparoxysmal response is ABNORMAL — do not confuse the two
- Photic stimulation should be stopped immediately if a photoparoxysmal response occurs to prevent seizure provocation
Board Pearl
Photic driving = normal. Photoparoxysmal response = abnormal. Photic driving is a time-locked occipital response that follows the flash frequency. A photoparoxysmal response is generalized spike-wave activity that outlasts the stimulus and indicates a predisposition to photosensitive epilepsy, classically JME.
EEG Artifacts
| Artifact | Appearance | Location | How to Distinguish from Cerebral Activity |
|---|---|---|---|
| Muscle (EMG) | High-frequency, spiky, irregular | Frontalis, temporalis (frontotemporal electrodes) | Too fast for cerebral rhythms; decreases with relaxation; corresponds to tense muscles |
| Eye movement (EOG) | Slow, rolling deflections (lateral); blink = frontal positive-negative | Fp1, Fp2 (frontopolar) | Eye blink: in-phase deflection at Fp1/Fp2; conjugate eye movements affect frontal channels; cornea is positive relative to retina |
| Electrode pop | Abrupt, high-amplitude, single-channel | Isolated to one electrode | Confined to one channel; sharp, vertical; no physiologic field |
| 60 Hz (electrical interference) | Regular, sinusoidal, 60 Hz | Any electrode (often one with high impedance) | Perfectly regular frequency; improves with impedance reduction; notch filter eliminates it |
| ECG artifact | Periodic, QRS-like complexes; coincides with heart rate | Any channel (especially ear references) | Correlate with ECG channel; regular at heart rate; time-locked to QRS |
| Glossokinetic | Slow, rhythmic delta; related to tongue movement | Frontal, temporal | Associated with talking, chewing; tongue acts as a dipole (tip negative) |
| Sweat artifact | Very slow, undulating baseline drift | Any electrode | Ultra-slow (<0.5 Hz); improves with cooling/drying skin; not in typical EEG frequency range |
Eye Movement Physiology
- The eye is a dipole: cornea = positive, retina = negative
- Eye blink → Bell phenomenon (eyes roll up) → positive potential at Fp1/Fp2
- Lateral eye movements produce opposite deflections at F7 vs F8 (one electrode closer to cornea, the other to retina)
Board Pearl
The cornea is electrically positive relative to the retina. This is why eye blinks produce a positive deflection at frontopolar electrodes (Fp1/Fp2). An eye flutter artifact can mimic frontal rhythmic delta activity. Always check for simultaneous deflections at Fp1 and Fp2 with opposite polarity on a bipolar montage to identify lateral eye movements.
Continuous EEG Monitoring (cEEG)
Indications
- Refractory status epilepticus — monitor burst-suppression or seizure-free target during treatment
- Unexplained altered mental status — rule out nonconvulsive status epilepticus (NCSE)
- Post-cardiac arrest — prognostication; detect subclinical seizures
- Subarachnoid hemorrhage — monitor for delayed cerebral ischemia (alpha-delta ratio changes)
- After acute brain injury — detect nonconvulsive seizures (occur in 10–30% of critically ill neurologic patients)
Nonconvulsive Status Epilepticus (NCSE)
- Definition — electrographic seizure activity without prominent motor symptoms; patient typically has impaired consciousness
- Salzburg criteria — periodic discharges >2.5 Hz OR periodic discharges ≤2.5 Hz with: (1) spatiotemporal evolution, OR (2) subtle clinical correlate, OR (3) improvement with IV antiseizure medication
- Must monitor for at least 24–48 hours in high-risk patients — brief routine EEGs miss many nonconvulsive seizures
Post-Cardiac Arrest Prognostication
- Highly malignant patterns — suppression (<10 µV), suppression-burst with identical bursts, status epilepticus → poor prognosis
- Malignant patterns — periodic/rhythmic discharges without background reactivity
- Benign patterns — continuous, reactive background with normal sleep architecture → favorable prognosis
- EEG reactivity and background continuity are the most important prognostic features
Quick Reference
Summary — EEG at a Glance
| Question | Answer |
|---|---|
| What does EEG measure? | Postsynaptic potentials of cortical pyramidal neurons (layer V); NOT action potentials. |
| Minimum cortex for scalp detection? | 6 cm² of synchronously active cortex. |
| Alpha rhythm attenuation? | Berger effect — alpha blocks with eye opening. |
| Mu rhythm attenuation? | Contralateral limb movement (or thought of movement); NOT eye opening. |
| Odd vs even electrodes? | Odd = left hemisphere; even = right hemisphere; z = midline. |
| How does bipolar montage localize? | Phase reversal — shared electrode between two channels with opposite deflections. |
| N2 sleep hallmarks? | Sleep spindles (12–14 Hz, thalamic reticular nucleus) + K-complexes. |
| 3 Hz spike-wave? | Absence epilepsy; activated by hyperventilation. |
| Centrotemporal spikes in a child? | BECTS / Rolandic epilepsy; benign, activated by sleep, outgrown by adolescence. |
| Hypsarrhythmia? | Infantile spasms (West syndrome); chaotic, high-amplitude, disorganized. |
| Temporal LPDs in febrile patient? | HSV encephalitis until proven otherwise. |
| 1 Hz GPDs + rapid dementia? | CJD (Creutzfeldt-Jakob disease). |
| Triphasic waves + liver disease? | Hepatic encephalopathy. |
| FOLD mnemonic? | 6 Hz phantom spike-wave (benign): Female, Occipital, Low amplitude, Drowsiness. |
| Photic driving vs PPR? | Driving = normal (occipital, time-locked). PPR = abnormal (generalized spike-wave, outlasts stimulus). |
| Brain death EEG criteria? | Electrocerebral inactivity: no activity >2 µV; 30-min recording; sensitivity 2 µV/mm; distance ≥10 cm. |
References
- Ebersole JS, Husain AM, Nordli DR. Current Practice of Clinical Electroencephalography. 4th ed. Wolters Kluwer; 2014.
- Tatum WO. Handbook of EEG Interpretation. 3rd ed. Demos Medical; 2021.
- Hirsch LJ, LaRoche SM, Gaspard N, et al. American Clinical Neurophysiology Society's Standardized Critical Care EEG Terminology: 2021 version. J Clin Neurophysiol. 2021;38(1):1–29.
- Niedermeyer E, Schomer DL, Lopes da Silva FH. Niedermeyer's Electroencephalography. 7th ed. Oxford University Press; 2018.
- American Clinical Neurophysiology Society (ACNS). Guidelines for standard electrode position nomenclature and EEG recording in clinical practice.
- Continuum (AAN). EEG and Epilepsy Monitoring review articles.