Neonatal and pediatric EEG is its own subspecialty within clinical neurophysiology. Patterns vary dramatically with age — particularly conceptional age in neonates — and patterns considered abnormal in adults can be entirely normal at specific developmental stages. Misapplying adult criteria to children is the most common source of pediatric EEG over-reading. This page covers the developmental EEG patterns from neonates to adolescents, neonatal seizure recognition, the use of amplitude-integrated EEG (aEEG) in NICU monitoring, and the specific pediatric epilepsy syndromes with diagnostic EEG patterns.

Neonatal EEG Fundamentals

Behavioral State Coding

  • Active sleep (REM-like): low-voltage mixed-frequency, eye movements, irregular breathing, muscle activity.
  • Quiet sleep (deep): tracé alternant or continuous high-voltage delta; regular breathing; minimal motor activity.
  • Awake: low-voltage mixed-frequency; variable motor activity; eyes open.
  • Recording neonatal EEG requires correlation with behavioral state.

Conceptional Age (CA) Patterns

CA (weeks) Key features
24–28 Tracé discontinue (discontinuous activity with interburst intervals); little reactivity
29–32 Tracé discontinu reducing; delta brushes appear (occipital/central rolandic spindles superimposed on delta)
33–36 Tracé alternant in quiet sleep (alternating high-voltage and lower-voltage epochs); delta brushes; concordance increasing
37–40 (term) Tracé alternant in quiet sleep; continuous activity awake and active sleep; mature sleep spindles NOT yet present at term
1–3 months post-term Mature sleep spindles begin to emerge (typically ~6–8 weeks post-term, often asynchronous between hemispheres); hypnagogic hypersynchrony develops
4–6 months PDR begins (3–4 Hz); K complexes appear
9–12 months PDR 5–6 Hz

Delta Brushes

  • Bursts of fast activity (beta) superimposed on slow waves (delta).
  • Normal in premature infants (29–35 weeks CA).
  • Maximum at central or occipital regions.
  • Often misread as epileptiform.

Tracé Discontinue and Tracé Alternant

  • Tracé discontinue: in very preterm; bursts of activity separated by quiet periods.
  • Tracé alternant: in term neonates in quiet sleep; alternating high-voltage delta and lower-voltage mixed-frequency epochs.
  • Normal at appropriate developmental stages.
  • Maturation: discontinue → alternant → continuous (term).

Neonatal Encephalopathy Patterns

Abnormal Backgrounds

  • Burst-suppression: most severe; very poor prognosis; HIE, severe metabolic disorders.
  • Low-amplitude: severe encephalopathy.
  • Discontinuous beyond expected CA: pathologic discontinuity.
  • Lack of concordance: state regulation impaired.
  • Asymmetric background: unilateral injury (stroke, hemorrhage).

Hypoxic-Ischemic Encephalopathy (HIE)

  • Mild: continuous background with mild slowing; good prognosis.
  • Moderate: discontinuous background; intermediate prognosis.
  • Severe: burst-suppression or flat; poor prognosis without intervention.
  • Therapeutic hypothermia improves outcomes if started within 6 hours.

Neonatal Seizures

Recognition Challenge

  • Neonatal seizures are subtle:
    • Eye deviation, eyelid flutter.
    • Lip smacking, oral automatisms.
    • Bicycling or pedaling movements.
    • Apnea (especially with eye deviation).
    • Brief tonic posturing.
  • Many neonatal seizures are electroclinical-dissociated: electrographic seizures without clinical correlate, or clinical events without EEG correlate.
  • EEG is essential for diagnosis.

EEG Patterns of Neonatal Seizures

  • Focal rhythmic activity in delta-alpha range.
  • Often unilateral; spread possible.
  • Evolution in frequency, location, amplitude.
  • Duration typically 30 seconds to several minutes.
  • Sharply contoured rhythmic waves.

Causes

  • Hypoxic-ischemic encephalopathy (most common in term).
  • Intracranial hemorrhage (germinal matrix in premature; intraventricular in others).
  • Metabolic: hypoglycemia, hypocalcemia, hyponatremia, hyperammonemia.
  • Infections (sepsis, meningitis, encephalitis).
  • Stroke (neonatal arterial ischemic stroke).
  • Inborn errors of metabolism.
  • Pyridoxine-dependent epilepsy (treatable with B6 trial).
  • Genetic epileptic encephalopathies.

Amplitude-Integrated EEG (aEEG)

Concept

  • Single-channel (or 2-channel) EEG.
  • Signal rectified and time-compressed.
  • Displays band of activity over time (hours).
  • Smoothed and amplitude-integrated.

Normal aEEG Patterns

  • Continuous normal voltage (CNV): band between 5–10 μV (lower margin) and 25–50 μV (upper margin).
  • Discontinuous normal voltage (DNV): periods of lower voltage (<5 μV).
  • Sleep-wake cycling: cyclic alternation between higher and lower amplitudes; emerges in term neonates after first day.

Abnormal aEEG Patterns

  • Burst-suppression: clearly alternating high-voltage bursts and low-voltage suppressions.
  • Continuous low-voltage: band always below 5–10 μV.
  • Flat: band below 5 μV.
  • Seizures: brief upward shifts of the band (“saw-tooth” appearance).

aEEG in NICU

  • Bedside continuous monitoring by nurses and intensivists.
  • Detects seizures, burst-suppression, sleep-wake cycling.
  • Sensitivity for neonatal seizures: ~50–80% (depends on duration; brief seizures may be missed).
  • Should be supplemented with full cEEG for definitive diagnosis.

Specific Pediatric Epilepsy Syndromes

West Syndrome (Infantile Spasms)

  • 4–10 months of age.
  • Infantile spasms (clusters of brief flexion or extension), psychomotor regression.
  • EEG: hypsarrhythmia (chaotic high-amplitude with multifocal spikes); modified hypsarrhythmia.
  • Ictal spasm: brief electrodecremental response (diffuse high-amplitude slow wave + brief attenuation).
  • Treatment: ACTH, vigabatrin (especially in tuberous sclerosis), prednisolone.
  • Prognosis: variable; many evolve to Lennox-Gastaut.

Lennox-Gastaut Syndrome

  • 1–8 years.
  • Multiple seizure types (tonic, atonic, atypical absence, myoclonic, focal).
  • Cognitive impairment.
  • EEG: 1.5–2.5 Hz slow spike-wave; GPFA in sleep.
  • Pharmacoresistant; ketogenic diet, VNS, corpus callosotomy in refractory.

Childhood Absence Epilepsy

  • 4–10 years.
  • Multiple daily absences.
  • EEG: 3-Hz spike-wave with HV.
  • Treatment: ethosuximide, valproate, lamotrigine.
  • Good prognosis.

BECTS (Benign Epilepsy with Centrotemporal Spikes / Benign Rolandic)

  • School-age children.
  • Nocturnal facial seizures.
  • EEG: centrotemporal sharp waves, activated by sleep.
  • Treatment often unnecessary; remits in adolescence.

Panayiotopoulos Syndrome

  • 3–10 years.
  • Autonomic seizures (vomiting, pallor, cyanosis).
  • EEG: occipital spikes activated by eye closure.
  • Good prognosis.

Gastaut Type Childhood Occipital Epilepsy

  • Older children.
  • Visual hallucinations, ictal blindness.
  • EEG: occipital spikes.

Doose Syndrome (Myoclonic-Atonic Epilepsy)

  • 2–5 years.
  • Myoclonic-atonic seizures (drop attacks).
  • EEG: generalized 2–4 Hz spike-wave.
  • Often responds to ketogenic diet.

Dravet Syndrome

  • SCN1A mutation in 80%.
  • First-year onset with febrile status epilepticus.
  • Multiple seizure types: febrile, myoclonic, absence, focal, atypical absence.
  • EEG: variable; SW, polyspike-wave, photoparoxysmal response.
  • AVOID Na⁺-channel blockers (carbamazepine, oxcarbazepine, lamotrigine, phenytoin).
  • Use valproate, clobazam, stiripentol, cannabidiol, fenfluramine.

Continuous Spike-Wave of Sleep (CSWS / ESES)

  • School-age children.
  • Cognitive regression, especially language.
  • EEG: bilateral continuous spike-wave occupying >85% of slow-wave sleep.
  • Landau-Kleffner syndrome: specific form with language regression.
  • Treatment: valproate, ethosuximide, steroids, IVIG.

Children’s EEG Differences from Adults

  • Higher amplitudes generally.
  • Slower PDR (see development table).
  • Hypnagogic hypersynchrony in drowsy/sleep (rhythmic theta, normal until ~10 years).
  • Anterior slow waves during drowsiness (normal in young children).
  • Posterior slow waves of youth (fused with PDR, normal up to 20s).
  • Photic driving usually present.
  • Greater variability and lability.

Practical Pediatric EEG

  • Shorter recording sessions tolerated by children.
  • Parent presence often helpful.
  • Recording during natural sleep is best.
  • Video synchronization essential.
  • Pediatric-trained interpreters strongly preferred.
  • Documentation of state (awake, drowsy, sleep, crying) throughout recording.

🔍 Did You Know?

The electroclinical dissociation in neonatal seizures — where electrographic seizure activity occurs without clinical correlate, or clinical events occur without EEG correlate — has profoundly shifted how neonatologists and pediatric neurologists approach the seizing newborn. Studies have shown that ~80% of neonatal seizures are subclinical (EEG-only), particularly in patients receiving anti-seizure medication who may continue to seize electrographically while clinical signs are masked by the medication. Conversely, many “seizure-like” clinical events (jitteriness, abnormal movements, autonomic changes) in neonates have no EEG correlate. The implication: EEG (or aEEG) is essential for diagnosis and management of neonatal seizures, and treatment decisions cannot rely on clinical observation alone. Modern NICU practice combines continuous aEEG monitoring at the bedside (for trend recognition and seizure detection by NICU staff) with intermittent full cEEG review (for diagnostic confirmation and pattern characterization). When seizures are confirmed, treatment (phenobarbital, phenytoin, levetiracetam, or — in refractory cases — pyridoxine trial for pyridoxine-dependent epilepsy) is guided by ongoing EEG response. The lesson generalizes: brain injury in the developing nervous system can produce profound effects with subtle clinical signs, and objective monitoring (EEG) reveals what clinical observation misses. For practicing neurologists and neonatologists, the take-home is that EEG is no longer a luxury in the modern NICU — it’s standard of care for any seizing or encephalopathic neonate.

Pitfalls and Pearls

  • Neonatal EEG patterns vary by conceptional age: don’t apply adult criteria.
  • Tracé discontinue (very preterm): normal at <30 weeks.
  • Tracé alternant (term): normal in quiet sleep.
  • Mature sleep spindles are post-term: typically begin ~6–8 weeks after term (often asynchronous initially); they are NOT a normal feature of the term neonatal EEG.
  • Delta brushes (29–35 weeks): bursts of beta on delta; normal.
  • Behavioral state coding: active vs quiet sleep vs awake.
  • HIE: burst-suppression = severe; therapeutic hypothermia within 6 hr.
  • Neonatal seizures: subtle; often electrographic-dissociated; EEG essential.
  • Pyridoxine-dependent epilepsy: trial B6 in refractory neonatal seizures.
  • aEEG: bedside NICU monitoring; ~50–80% seizure sensitivity; supplement with full cEEG.
  • West syndrome (infantile spasms): hypsarrhythmia; ACTH, vigabatrin.
  • Hypsarrhythmia: chaotic high-amplitude with multifocal spikes; modified variants.
  • Lennox-Gastaut: 1.5–2.5 Hz SW; GPFA in sleep.
  • CSWS / Landau-Kleffner: continuous spike-wave of sleep with language regression.
  • BECTS: centrotemporal spikes; benign; nocturnal facial seizures.
  • Dravet: SCN1A; AVOID Na⁺ blockers.
  • Hypnagogic hypersynchrony: normal pediatric drowsy theta.
  • Anterior slow waves of drowsiness: normal in young children.
  • Pediatric-trained interpreter: essential for accurate reading.

References

  1. Mizrahi EM, Hrachovy RA. Atlas of Neonatal Electroencephalography. 4th ed. Demos Medical; 2016.
  2. Hrachovy RA, Frost JD Jr. The EEG in selected generalized seizures. J Clin Neurophysiol. 2006;23(4):312-332.
  3. Wusthoff CJ. How to interpret an EEG in pediatric epilepsy. Continuum (Minneap Minn). 2013;19(3 Epilepsy):632-665.
  4. Tsuchida TN, Wusthoff CJ, Shellhaas RA, et al. American Clinical Neurophysiology Society standardized EEG terminology and categorization for the description of continuous EEG monitoring in neonates. J Clin Neurophysiol. 2013;30(2):161-173.
  5. Hellström-Westas L. Amplitude-integrated electroencephalography for seizure detection in newborn infants. Semin Fetal Neonatal Med. 2018;23(3):175-182.
  6. Scheffer IE, Berkovic S, Capovilla G, et al. ILAE classification of the epilepsies: position paper of the ILAE Commission for Classification and Terminology. Epilepsia. 2017;58(4):512-521.