cEEG · NON INVASIVE

Continuous EEG (cEEG)

Cortical electrical activity recorded continuously at the bedside, the only non-invasive tool that detects non-convulsive seizures and the canonical reference for SE drug-titration endpoints.

ElectricalBedsidePeds + adultNon-invasiveValidated
ALast reviewed 2026-05-1717-min read

1. Bedside vignettes: why this matters in the PICU

Vignette A. Post-arrest day 1, IIC or seizure?

A 6-year-old post out-of-hospital VF arrest, ROSC at 28 minutes, targeted temperature 33°C. Day 1: GCS 3 sedated; aEEG shows discontinuous pattern with intermittent bursts. cEEG (10–20 system) shows lateralised periodic discharges at 1.5 Hz with sharp morphology over the right hemisphere, lasting 30 seconds and recurring every 3 minutes. The bedside team asks: is this NCSE (treat) or the ictal-interictal continuum (less clear-cut)? Per ACNS 2021, frequency > 2.5 Hz with evolution is electrographic seizure; this is IIC. The team trials a midazolam bolus, the LPDs resolve, and the team interprets the resolution as functional evidence the LPDs were ictal: continue antiseizure therapy.

Vignette B. Refractory status epilepticus in a 5-year-old, the drug ladder

A 5-year-old with prolonged febrile seizure that has continued for 30 minutes despite two doses of midazolam IM and IV lorazepam. cEEG confirms ongoing generalised electrographic seizure. Per ESETT, second-line is levetiracetam 60 mg/kg IV, fosphenytoin 20 mg PE/kg IV, or valproate 40 mg/kg IV (all three equivalent in efficacy). The team chooses levetiracetam (least sedating). The clinical seizure stops; cEEG shows resolution of the electrographic seizure 10 minutes later. The team continues cEEG for 24 hours and detects two further brief electrographic seizures without clinical correlate, which they treat. Without cEEG, those NCSE episodes would be missed.

Vignette C. SAH day 6, qEEG alpha-delta ratio falls 6 hours before clinical signs of DCI

A 16-year-old with aneurysmal SAH post-coiling, day 6. cEEG running since day 2. Quantitative trends show the alpha-delta ratio (ADR) falling from 0.55 to 0.35 over 6 hours, which is statistically significant per the centre's algorithm. TCD MFV is rising in parallel but Lindegaard ratio is only 2.8 (borderline). The team escalates haemodynamics, repeats angiography (which confirms moderate vasospasm in the right MCA), and the patient is treated successfully. The clinical examination remained unchanged during the 6-hour ADR decline; qEEG was the earliest signal.


2. What EEG is, and what it is not

EEG records the summated post-synaptic potentials of cortical pyramidal neurons, measured at the scalp via differential amplification between electrode pairs. The signal amplitude at the scalp is ~10–100 μV, attenuated by the skull and scalp by a factor of ~100 from the underlying cortical surface.

Five things follow.

EEG samples cortex only. Deep structures (basal ganglia, thalamus, brainstem) are not directly seen on scalp EEG. Subcortical seizures (e.g., from a deep mesial focus) may show only as secondary cortical propagation.

EEG is highly state-dependent. Sedation, hypothermia, neuromuscular blockade, hypoglycaemia, and metabolic encephalopathy all change the baseline. Reading EEG requires knowing the clinical state.

EEG distinguishes NCSE from other altered-consciousness causes. This is its most uniquely valuable contribution: NCSE causes ~20% of comatose ICU patients' altered consciousness and is invisible without continuous monitoring.

EEG-based SE management has trial evidence. ESETT (second-line drugs) and ECLIPSE-SE (third-line) have established the modern drug ladder for SE. Endpoint definitions (electrographic seizure resolution, burst suppression) are EEG-based.

EEG is not seizure-detector only. Background continuity, reactivity, and pattern (e.g., GPD, LPD) carry independent prognostic and diagnostic information.

Clinical pearl

Reactivity matters as much as the pattern itself. A patient with sustained burst suppression who reactivates to a painful stimulus has a much better prognosis than one whose suppression is unchanged. Test reactivity before reading prognosis from the resting trace.

In children

Pediatric EEG differs by age in three important ways. (1) Background frequencies mature from delta (newborn) through theta (toddler) to alpha (school-age and adolescent); a "slow" trace in a 1-year-old is normal but pathological in a 14-year-old. (2) Seizure semiology in neonates is often subtle or invisible clinically; cEEG detects ~50% more seizures than clinical exam in neonates. (3) NCSE prevalence is higher in pediatric ICU than in adult ICU (some studies suggest 30–40% of comatose pediatric ICU patients).


3. Montage and electrode placement

Fig. 1
EEG MONTAGE · 10-20 SYSTEMTop-down view · highlighted = PICU reduced 8-channel arrayNASIONLRINIONFp1Fp2F7F3FzF4F8T3C3CzC4T4T5P3PzP4T6O1O2ARRAYSFull 10-2019 standard channelsPICU reducedFp1/Fp2 · C3/C4 · T3/T4 · O1/O2FREQUENCY BANDSβ beta13–30 Hzα alpha8–13 Hzθ theta4–8 Hzδ delta0.5–4 HzSETUP TARGETSimpedance < 5 kΩcollodion (long stay) / pasteNAMING CONVENTIONLetters: Fp frontopolar · F frontal · C central · T temporal · P parietal · O occipitalNumbers: odd = left, even = right, z = midlineMNM-Edu original schematic · 10-20 international electrode placement · ACNS standardised terminology
The 10-20 international system. Electrode positions are labelled by region (F, T, C, P, O for frontal, temporal, central, parietal, occipital) and side (odd numbers left, even numbers right, Z midline). Standard adult montage uses 19 electrodes plus a reference; pediatric and neonatal montages reduce to 9–11 electrodes for practicality. Bipolar (longitudinal 'Banana') montage shows differences between adjacent electrode pairs along anterior-posterior chains, useful for localising focal patterns. Referential (average reference) montage shows each electrode against an average of all others, useful for global pattern recognition.
MNM-Edu, original schematic.

Electrode placement. The 10-20 international system places electrodes at proportional distances (10% or 20%) along the head circumference. Standard adult ICU montage uses 19 electrodes plus a reference. Pediatric NICU/PICU montages often reduce to 9 or 11 electrodes (less coverage but faster placement, less coverage but better fit on small heads).

Montages. Two principal display modes:

  • Bipolar (longitudinal "Banana"): each channel shows the difference between two adjacent electrodes. Useful for localising focal patterns; "phase reversal" in bipolar identifies the seizure focus.
  • Referential (average reference): each channel shows one electrode against an average of all others. Useful for global pattern recognition (burst suppression, generalised discharges).

Bedside teams often run both simultaneously and switch view depending on the question.

Pediatric considerations. Neonatal EEG uses a reduced montage (typically Fp1, Fp2, C3, C4, T3, T4, O1, O2, Cz; 9 electrodes) per ACNS 2013 neonatal guidelines. Head size, scalp thinness, and the need to balance coverage against placement time guide the choice.


4. The signal: bands, rhythms, reactivity, continuity

A bedside EEG reading covers four dimensions:

Frequency bands (the basic vocabulary):

BandFrequencyWhere it appears normally
Delta0.5–3 HzDeep sleep, newborns awake
Theta4–7 HzToddlers awake; drowsiness in older children
Alpha8–12 HzAwake adult posterior dominant rhythm (PDR)
Beta13–30 HzFrontal in awake adult; often pharmacological
Gamma> 30 HzHigh cognition; mostly outside ICU concern

Rhythms: posterior dominant rhythm (PDR) is the canonical awake-resting alpha over occipital cortex; loss of PDR is a non-specific marker of encephalopathy.

Reactivity: does the background change when the patient is stimulated (loud noise, painful stimulus)? Reactive background is favourable; unreactive is concerning regardless of the resting frequency.

Continuity: is the background continuous (always present) or discontinuous (bursts separated by silence)? Severely discontinuous patterns (suppression, burst-suppression) reflect deep encephalopathy or anaesthesia.

Clinical pearl

Continuity + reactivity + dominant frequency is the three-axis snapshot every bedside team should chart. A discontinuous, unreactive, low-amplitude trace in an unsedated patient is severe; a continuous, reactive, alpha-dominant trace is essentially normal.


5. ACNS 2021 terminology: GPD, LPD, RDA, BIRDS, IIC

The ACNS 2021 standardised terminology is the modern reference for ICU EEG reading. The key categories:

CategoryAcronymWhat it is
Generalised periodic dischargesGPDSharp waves recurring at regular intervals across both hemispheres
Lateralised periodic dischargesLPDSame but over one hemisphere
Rhythmic delta activityRDAContinuous 0.5–4 Hz waves, lateralised or generalised
Brief intermittent rhythmic dischargesBIRDSShort (< 10 s) rhythmic bursts
Ictal-interictal continuumIICPattern that does not meet seizure criteria but is concerning

Seizure criteria (ACNS 2021): rhythmic activity > 2.5 Hz with evolution in frequency, location, or morphology lasting ≥ 10 seconds; OR rhythmic activity ≤ 2.5 Hz with clinical correlate; OR repeated rhythmic activity meeting threshold.

The IIC dilemma: many patterns (LPDs at 1–2 Hz, GPDs at 1.5 Hz, rhythmic delta) are below the seizure cutoff but may still drive metabolic distress. The bedside approach: trial of antiseizure medication; resolution of the pattern and clinical/electrographic improvement supports an ictal interpretation. Non-resolution suggests interictal or post-ictal pattern.


6. Pattern library: what to recognise on cEEG

Fig. 2
ICU EEG PATTERN LIBRARYeight canonical patterns · ACNS / Hirsch 2021 terminology · each tracing ~3 seconds(a) NORMAL AWAKEposterior alpha 9-10 Hz(b) DROWSYalpha attenuates, theta appears(c) ASLEEP, STAGE 2KspindleK-complexes + sleep spindles(d) GENERALISED SE3 Hz generalised spike-wave(e) FOCAL SE~4 Hz sharp, left temporal(f) LPDlateralised periodic ~1.5 Hz(g) GPDgeneralised periodic ~1 Hz(h) BURST SUPPRESSIONbursts + flat suppressionMNM-Edu schematic · ACNS standardised critical-care EEG terminology (Hirsch 2021; Herman 2015) · morphologies illustrative
Eight canonical ICU EEG patterns. (a) Normal awake adult: posterior alpha rhythm 9–10 Hz, normal frontal beta. (b) Drowsy: alpha attenuates, theta appears. (c) Asleep stage 2: K-complexes and sleep spindles. (d) Generalised electrographic SE: continuous spike-wave at 3 Hz, generalised. (e) Focal electrographic SE: 4 Hz sharp waves over left temporal, evolving. (f) LPD: lateralised periodic discharges at 1.5 Hz over right hemisphere. (g) GPD: generalised periodic discharges at 1 Hz, low amplitude. (h) Burst suppression: alternating bursts and isoelectric periods, characteristic of barbiturate coma or severe HIE.
MNM-Edu, original schematic. ACNS 2021 standardised terminology (Hirsch 2021; Herman 2015).
PatternMeaningAction
Continuous alpha-dominantNormal awake adultNone
Continuous theta-dominantMild encephalopathy or drowsyInvestigate; usually metabolic / mild
Continuous delta-dominantModerate encephalopathyInvestigate; metabolic, structural, or post-ictal
DiscontinuousSevere encephalopathy or deep anaesthesiaInvestigate cause; consider sedation withdrawal trial
Burst suppressionDeep anaesthesia, severe HIE, barbiturate comaContext-dependent; SE endpoint if therapeutic
Isoelectric (flat)Cerebral electrical silenceSevere HIE, brain death (with ancillary testing), drug overdose
GPD (generalised periodic discharges)IIC, post-anoxic, sepsis-associated encephalopathyConsider antiseizure trial; pair with clinical
LPD (lateralised periodic discharges)Focal cortical injury, focal SEConsider antiseizure trial; investigate structural cause
Electrographic seizureRhythmic > 2.5 Hz with evolutionTreat per SE protocol
RDA (rhythmic delta)IIC; less ictal than LPD/GPDTrial antiseizure if encephalopathic
BIRDSBrief (< 10 s) rhythmic dischargesOften pre-ictal; monitor closely

7. Try it: interactive widgets

EEGPatternLibrary
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aEEGGenerator
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qEEGSpectrogram
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BISDemo
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8. Status epilepticus management section

The modern SE ladder is based on trial evidence (ESETT, ECLIPSE-SE, RAMPART). EEG is used at three points: (1) confirming initial diagnosis (especially NCSE), (2) titrating second- and third-line therapy, (3) defining endpoints (electrographic seizure resolution; burst suppression for super-refractory).

8.1 First-line: benzodiazepines

  • Midazolam 0.2 mg/kg IM (max 10 mg) per RAMPART, or lorazepam 0.1 mg/kg IV (max 4 mg).
  • Repeat once if seizure continues at 5 minutes.

8.2 Second-line: ESETT-equivalent

ESETT (Kapur 2019) compared levetiracetam 60 mg/kg, fosphenytoin 20 mg PE/kg, valproate 40 mg/kg. All three were equivalent at 60 minutes. Choose by patient context:

  • Levetiracetam: least sedating, no hepatic interactions; often first choice.
  • Fosphenytoin: established, but cardiac monitoring required.
  • Valproate: avoid in hepatic disease, suspected metabolic disease, age < 2 years.

8.3 Third-line (refractory SE)

Continuous IV anaesthetic infusion:

  • Midazolam 0.2 mg/kg bolus, then 0.05–2 mg/kg/h infusion.
  • Propofol 1–2 mg/kg bolus, then 1–4 mg/kg/h (caution in children, risk of PRIS).
  • Pentobarbital 5–15 mg/kg load, then 1–5 mg/kg/h (super-refractory; reserved when above fails).

EEG endpoint: resolution of electrographic seizures for refractory; burst suppression (typically 60% suppression ratio for 24 hours) for super-refractory.

8.4 ECLIPSE-SE (third-line trial)

ECLIPSE-SE (Kapur 2019) is the ongoing trial comparing midazolam vs propofol vs pentobarbital for RSE in adults; pediatric extension data are accumulating. Until results are definitive, choice is centre- and clinician-dependent.

Caveat

Decision support, not a clinical protocol. Every drug, dose, and endpoint above is age-, centre-, and patient-dependent. Defer to your unit's protocols and senior clinical team.

Educational algorithm, not a clinical protocol. This walkthrough is a teaching aid. Defer to your unit's pediatric protocols, current PBTF / Kochanek / local guidelines, and your senior clinical team. Doses, thresholds, and decision points are starting points, not prescriptions.

9. Clinical contexts: cEEG across acute brain injuries

9.1 Convulsive and non-convulsive status epilepticus

The canonical indication. NCSE causes ~20% of comatose ICU patients' altered consciousness. cEEG is the only way to detect it. ESETT and ECLIPSE-SE define the modern drug ladder.

9.2 HIE and post-cardiac arrest neuroprognosis

Post-arrest cEEG patterns carry strong prognostic information:

  • Continuous, reactive background within 24–48 h: favourable.
  • Discontinuous, unreactive, low-amplitude: unfavourable.
  • Burst suppression with identical bursts: highly unfavourable.
  • Status epilepticus, especially myoclonic SE: unfavourable but not invariably fatal.
  • Isoelectric at > 72 h: very poor.

The AHA 2020 pediatric post-arrest guidelines and Topjian 2021 pediatric statement endorse cEEG as part of routine post-arrest neuroprognostication.

9.3 SAH and DCI (qEEG)

Quantitative EEG trends, particularly the alpha-delta ratio (ADR), detect DCI hours before clinical signs in adult SAH cohorts. Pediatric SAH data are sparse but the principle applies. The Sandsmark 2024 review and Foreman 2022 cohort summarise modern qEEG-for-DCI evidence.

9.4 Bacterial meningitis with seizures

cEEG is recommended when seizures are suspected (subtle motor signs, fluctuating consciousness) or in severely encephalopathic patients per European meningitis and IDSA encephalitis guidelines.

9.5 Sepsis-associated encephalopathy

Sepsis-associated encephalopathy presents with delirium, altered consciousness, and a spectrum of EEG findings from diffuse slowing to GPD and NCSE. cEEG detects NCSE in 10–20% of comatose septic patients.

9.6 Severe TBI: subclinical seizures

cEEG detects subclinical / non-convulsive seizures in 15–25% of severe TBI patients in the first 7 days, particularly in those with intra-axial haemorrhage or cortical contusion. PBTF 4 pediatric guidelines recommend cEEG for severe TBI with GCS ≤ 8 or for refractory ICP suggestive of seizure-driven elevation.

9.7 Neonatal seizures

Neonatal seizures are often subtle or invisible clinically. The 2017 ILAE neonatal seizure classification (Pressler 2017) uses cEEG as the diagnostic standard. Sansevere 2023 Pediatric Neurology cEEG review summarises modern neonatal cEEG practice. aEEG remains the bedside trend tool, but cEEG (10–20 system, ideally video) is the diagnostic standard.

9.8 ECMO

cEEG on ECMO detects seizures (~20% of pediatric ECMO patients) and provides background continuity / reactivity for ongoing prognostication. Movement artefact from circuit and ventilator is a recurrent challenge. Cho 2024 pediatric ECMO outcomes endorses cEEG as standard monitoring on neuro-ECMO indications.


10. Multimodal integration: EEG in the MMM/MNM stack

Fig. 3
ALPHA-DELTA RATIO: THE EARLIEST DCI SIGNALqEEG ADR in SAH · the decline precedes TCD and clinical changeDCI-risk window0.200.350.550.70ADR (alpha / delta)6080120160TCD MFV (cm/s)day 2day 3day 4day 5day 6day 7ADR decline0.55 → 0.35 (~36%), 6 hearliest DCI signalTCD MFV rising →Lindegaard borderline, lags ADRclinical exam unchanged during the declineADRTCD MFVMNM-Edu schematic · adapted from Claassen 2004 and Foreman 2022 · illustrative, not patient data
qEEG alpha-delta ratio (ADR) trend in a SAH patient on cEEG. Stable at 0.55 for days 2–6 post-bleed; on day 6 morning the ADR begins declining (0.55 → 0.35 over 6 hours). TCD MFV is rising in parallel but Lindegaard ratio is only borderline. Clinical examination remained unchanged during the decline. The ADR trend was the earliest objective signal of evolving DCI. Treatment escalation (induced hypertension, angiography) confirmed moderate right MCA vasospasm. Recovery of the ADR mirrored vasospasm resolution.
MNM-Edu, original schematic adapted from Claassen 2004 and Foreman 2022.

The qEEG alpha-delta ratio as an early marker of delayed cerebral ischaemia in SAH is established by Claassen 2004 and extended by Foreman 2022.

Pair with…What you gainWorked scenario
TCDNCSE drives flow changes (high MFV during seizure); seizure-vs-spasm discriminationTCD page
NIRSrSO2 reactivity loss + isoelectric EEG = worst-case post-arrest signatureNIRS page
ICPSeizure-driven ICP spikes; NCSE causes metabolic stress and ICP riseICP page
aEEGCompressed bedside trend (NICU mainstay)aEEG page
qEEGSpectrogram, ADR, suppression ratio for shift-level trendsqEEG page
BISOperating-room sedation depth surrogate (not for SE titration)BIS page
Evoked potentialsSubcortical and brainstem function alongside corticalEP page
Clinical examAlways; EEG without clinical context can misleadAlways

11. Setup and technique: a step-by-step

11.1 Electrode placement (10-20 system)

Measure scalp landmarks (nasion, inion, preauricular points). Place electrodes at proportional 10% / 20% distances. Standard adult ICU montage uses 19 electrodes (Fp1, Fp2, F3, F4, C3, C4, P3, P4, O1, O2, F7, F8, T3, T4, T5, T6, Fz, Cz, Pz) plus reference and ground.

Pediatric reduction (9 electrodes): Fp1, Fp2, C3, C4, T3, T4, O1, O2, Cz. Trades coverage for placement time and fit on small heads.

11.2 Skin preparation

  • Mark the position, abrade lightly with prep gel.
  • Apply conductive paste or gel.
  • Place the electrode, secure with collodion or adhesive disk.
  • Verify impedance < 5 kΩ ideally (< 10 kΩ acceptable).

11.3 Filters and sampling

  • Sample rate: 200–512 Hz typical for ICU cEEG; > 256 Hz for high-frequency oscillation work.
  • Low-frequency filter (HFF): 0.5–1 Hz (preserve delta).
  • High-frequency filter (LFF): 70 Hz (reject muscle/EMG).
  • Notch filter: 50 or 60 Hz mains.

11.4 Artefact reduction

  • Common artefacts: EMG (muscle), ECG (cardiac), eye movement, electrode pop, ventilator, sweat.
  • EMG: paralyse only when essential; otherwise filter and accept some contamination.
  • Eye movement: dominant in frontal channels; usually obvious morphology.
  • Electrode pop: sudden high-amplitude spike on a single channel; re-secure the electrode.
  • Ventilator: rhythmic at ~12–20/min; isolated by frequency.

11.5 Video EEG

Continuous video alongside EEG is the standard for SE management and seizure semiology characterisation. The video stream captures eye deviation, automatisms, head turn, and post-ictal state, all of which add diagnostic information.

11.6 qEEG trend display

Modern ICU EEG systems compress 24-hour traces into:

  • Spectrogram: colour map of frequency power over time (per electrode).
  • Alpha-delta ratio: ratio of 8–12 Hz to 1–4 Hz power; falls in DCI.
  • Suppression ratio: percentage of time with EEG below an amplitude threshold; rises in deep anaesthesia.
  • Asymmetry index: left-vs-right power; flags unilateral pathology.

12. Pitfalls and artefacts

  • Under-reading: missing GPD or NCSE under deep sedation; the encephalopathy can mask the pattern.
  • Over-reading: calling RDA or GPD an electrographic seizure without meeting ACNS criteria.
  • Inter-rater variability: even among trained epileptologists, agreement on IIC patterns is moderate.
  • Sedation-induced patterns: propofol-induced burst suppression looks like post-anoxic burst suppression; clinical context is essential.
  • Movement artefact: ventilator, ECMO circuit, CRRT.
  • Montage choice obscuring focal patterns: bipolar may miss a true generalised pattern; always verify with referential.
  • Electrode dislodgement: long ICU recordings; verify impedance every shift.
  • Salt-bridges: conductive paste connecting adjacent electrodes; falsely suggests synchrony.
  • Pseudo-seizure artefact: chewing, shivering, eye flutter; verify with video.
  • Pediatric montage limits: 9-electrode neonatal montage will miss some focal patterns; accept the trade-off for placement feasibility.

13. Combine with…

  • qEEG: for the alpha-delta ratio, spectrogram, suppression ratio.
  • aEEG: for the compressed bedside trend (NICU).
  • BIS: for operating-room sedation depth.
  • Evoked potentials: for subcortical and brainstem function.
  • TCD: for the NCSE-vs-spasm discrimination in SAH.
  • NIRS: for the rSO2 reactivity pair in HIE.
  • ICP: for the seizure-driven ICP spike pair.

14. Evidence summary and recent literature

14.1 Evidence summary

TopicSourceGrade
Original EEG descriptionfoundational
ACNS 2021 standardised terminology expert
ACNS cEEG indications expert
Neonatal EEG (ACNS 2013)expert
Pediatric cEEG (Tasker 2018) review
NCSE prevalence (Claassen 2004, 2013) B
Subclinical seizures in TBI (Vespa 2010)B
ESETT (second-line SE)A
ECLIPSE-SE (third-line SE) A
Status epilepticus definition (Trinka 2015)expert
Neonatal seizure classification (Pressler 2017)expert
Sansevere 2023 neonatal cEEGreview
Topjian 2021 AHA pediatric post-arrest expert
Foreman 2022 qEEG and DCI B
Sandsmark 2024 qEEG DCI reviewreview
Naim 2023 brain injury in pediatric CHDexpert
Abend 2011 pediatric cEEGB
Pediatric MNM consensus 2025expert
NCS MMM consensusexpert
Williams 2024 qEEGreview

14.2 Recent literature (2022–2025)

  • ACNS 2021 standardised terminology (Hirsch): the modern reference for ICU EEG reading; GPD, LPD, RDA, BIRDS, IIC defined.
  • Topjian 2021 AHA pediatric post-arrest: cEEG endorsed as routine post-arrest neuroprognostication tool.
  • Naim 2023 PCCM brain injury in pediatric CHD: integrates cEEG into multimodal CHD neurosurveillance.
  • Sansevere 2023 neonatal cEEG: practical review of modern neonatal cEEG; reduced montages, aEEG-cEEG combination, video integration.
  • Sandsmark 2024 qEEG DCI review: contemporary synthesis of qEEG-for-DCI evidence base; ADR as the workhorse trend.
  • Williams 2024 qEEG: review of contemporary qEEG metrics in ICU.
  • Figaji 2025 Pediatric MNM consensus: cEEG endorsed as essential pediatric neurocritical-care monitoring.

15. Self-check

Retrieval check
A 6-year-old post-arrest day 1 on targeted temperature. cEEG shows LPDs at 1.5 Hz with sharp morphology over the right hemisphere, lasting 30 seconds, recurring every 3 minutes. Per ACNS 2021, what is this pattern, and what should be done?
A 5-year-old with convulsive status epilepticus continues to seize after benzodiazepines. Per ESETT, which second-line drug should be administered?
A 16-year-old with aneurysmal SAH post-coiling, day 6. cEEG running since day 2. The alpha-delta ratio (ADR) has fallen from 0.55 to 0.35 over 6 hours. TCD MFV is rising, Lindegaard ratio 2.8 (borderline). Clinical examination is unchanged. Best interpretation?

References

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