EEG Basics
EEG Basics
What You'll Learn
- EEG physiology — measures cortical postsynaptic potentials (NOT action potentials); layers III and V pyramidal neurons; 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–<8 Hz (≥4 to <8 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
HighYield Pearls
- 3 Hz generalized spike-wave activated by hyperventilation: childhood absence epilepsy (CAE) — HV is the highest-yield activation procedure for absence
- Hypsarrhythmia (chaotic high-amplitude >200 µV delta + multifocal spikes, disorganized background): infantile spasms / West syndrome / IESS — treat with ACTH, vigabatrin (vigabatrin first if tuberous sclerosis)
- Periodic sharp waves at ~1 Hz on suppressed background: sporadic CJD — pair with 14-3-3, RT-QuIC, cortical ribboning on DWI
- Extreme delta brush (rhythmic delta with superimposed beta): anti-NMDA receptor encephalitis (young woman, ovarian teratoma, psych + dyskinesias)
- Lateralized periodic discharges (LPDs/PLEDs) in temporal region with febrile encephalopathy: HSV-1 encephalitis — start acyclovir empirically; do NOT wait for PCR
- Burst-suppression in a neonate with intractable seizures: Ohtahara syndrome (tonic spasms, structural cause) or early myoclonic encephalopathy (EME, myoclonus, metabolic)
- Triphasic waves with frontal predominance + anterior–posterior lag: hepatic / uremic / cefepime / lithium toxicity — check ammonia, BUN, drug list before calling it NCSE
- Non-reactive generalized alpha frontally (alpha coma): post-anoxic injury or high pontine lesion — poor prognosis post-cardiac-arrest
- Photoparoxysmal response (generalized polyspike-wave to intermittent photic stim): juvenile myoclonic epilepsy (JME) and other IGE — avoid sodium channel blockers (carbamazepine, phenytoin) that can worsen
- Electrical status epilepticus in sleep (ESES/CSWS): classic threshold SWI ≥85% in NREM, but lower SWI can still be clinically significant when there is cognitive/language regression — interpret with the clinical syndrome (Landau-Kleffner / CSWS); treat with steroids, high-dose benzos, valproate
- EEG & brain death (BD/DNC): historical electrocerebral inactivity criteria are NOT accepted as a current ancillary test for BD/DNC. Per 2023 AAN/AAP/CNS/SCCM, acceptable ancillary tests are 4-vessel catheter angiography, radionuclide cerebral blood-flow scan, and TCD in adults only.
- Centrotemporal sharps activated by drowsiness/sleep in a school-age child with nocturnal hemifacial seizures: BECTS (self-limited epilepsy with centrotemporal spikes) — benign, often no treatment needed
- A normal routine EEG does NOT rule out epilepsy: routine ~30–50% sensitivity, sleep-deprived ~80%; repeat or capture sleep if suspicion is high
🔍 Quick ReferenceFrequency / stage · Pattern · Disease association
Frequency / stage / variant
- δ <4 Hz / θ 4–<8 Hz / α 8–13 Hz / β >13 Hz / γ >30 Hz → EEG frequency bands (memorize the cutoffs exactly)
- Posterior dominant rhythm 8–13 Hz, attenuates with eyes opening (Berger effect) → normal awake alpha rhythm in adults
- Mu rhythm, 8–13 Hz arciform/wicket-shaped over central head, blocked by contralateral movement → normal sensorimotor rhythm
- Vertex sharp waves + slow rolling eye movements + theta → stage N1 sleep
- Sleep spindles (12–14 Hz) + K complexes → stage N2 sleep
- High-amplitude delta >75 µV occupying ≥20% of epoch → stage N3 (slow-wave) sleep
- Sawtooth waves + REMs + muscle atonia (low-voltage mixed-frequency) → REM sleep
- Tracé alternant / tracé discontinu → normal neonatal EEG (term / preterm respectively)
- Lambda waves (positive occipital sharp during visual scanning, eyes open) → normal awake variant
- POSTS (positive occipital sharp transients of sleep) → normal drowsy/sleep variant, NOT epileptiform
Pattern / waveform
- Spike <70 ms / sharp wave 70–200 ms → epileptiform discharges (by duration definition)
- Generalized 3 Hz spike-and-wave activated by hyperventilation → childhood absence epilepsy
- Slow (<2.5 Hz) generalized spike-and-wave + paroxysmal fast activity in sleep → Lennox-Gastaut syndrome
- Generalized 4–6 Hz polyspike-and-wave with photoparoxysmal response → juvenile myoclonic epilepsy (JME)
- Centrotemporal sharps activated by sleep, horizontal dipole → BECTS (self-limited childhood epilepsy with centrotemporal spikes)
- Hypsarrhythmia (chaotic, high-amplitude, multifocal spikes, disorganized) → infantile spasms / West syndrome
- Burst-suppression → Ohtahara, EME, post-anoxic injury, deep anesthesia, hypothermia
- Triphasic waves with anterior–posterior lag → metabolic/toxic encephalopathy
- FIRDA (frontal intermittent rhythmic delta activity) → nonspecific encephalopathy / deep midline dysfunction (adults)
- OIRDA (occipital IRDA) → children, often with absence epilepsy
- LPDs / GPDs / LRDA / GRDA → ictal-interictal continuum (high seizure risk, cEEG indicated)
- Extreme delta brush (rhythmic delta with superimposed beta "brushes") → anti-NMDA receptor encephalitis
- Spike-wave index ≥85% during NREM sleep → ESES / CSWS (classic threshold; lower SWI may be clinically meaningful with cognitive/language regression — interpret with clinical syndrome)
- Isoelectric (electrocerebral inactivity) recording, ≥30 min, technical criteria met → historical brain-death finding only; NOT an accepted ancillary test under the 2023 AAN/AAP/CNS/SCCM BD/DNC guideline (acceptable: 4-vessel angiography, nuclear CBF, TCD adults only)
Disease association
- Periodic sharp waves at ~1 Hz on suppressed background → sporadic Creutzfeldt-Jakob disease (CJD)
- Periodic complexes every 4–15 sec (long-interval periodicity) → subacute sclerosing panencephalitis (SSPE)
- Temporal LPDs/PLEDs in febrile encephalopathy → HSV-1 encephalitis
- Non-reactive alpha frontally (alpha coma) → post-anoxic injury / high pontine stroke (poor prognosis)
- Beta coma (non-reactive frontal beta) → benzodiazepine / barbiturate intoxication
- Spindle coma (sleep-like spindles in unresponsive patient) → upper brainstem lesion (better prognosis than alpha coma)
- Triphasic waves → hepatic, uremic, cefepime, lithium, anoxic encephalopathy
- Acquired aphasia in a child + ESES pattern → Landau-Kleffner syndrome
- Photoparoxysmal response to intermittent photic stimulation → idiopathic generalized epilepsies (JME, JAE, CAE)
- 14-and-6 Hz positive spikes / 6 Hz phantom spike-wave / wicket spikes / BETS (SSS) / SREDA → benign normal variants, NOT epilepsy
- Generalized periodic discharges (GPDs) post-cardiac-arrest → anoxic brain injury / myoclonic status (poor prognosis if non-reactive)
- BIRDs (brief potentially ictal rhythmic discharges, <10 s) → high seizure risk in critically ill patients
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
- Layers III and 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 layers III and V pyramidal neurons, and at least 6 cm² of cortex must be synchronously active for scalp detection.
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