2025 PACUPrep BCCCP Preparatory Course Neuromonitoring Techniques Neuromonitoring and Ventriculostomy Management in Neurocritical Care
Foundational Principles and Clinical Applications of Continuous EEG and BIS Monitoring in Critical Care

Foundational Principles and Clinical Applications of Continuous EEG and BIS Monitoring

Objective

Describe the foundational principles, indications, and clinical applications of continuous EEG (cEEG) and bispectral index (BIS) monitoring in critical care.

Learning Points Icon A checkmark inside a circle, symbolizing achieved learning goals.

Learning Points

  • Explain the physiological basis and technical aspects of cEEG.
  • Identify clinical indications for cEEG: seizure detection, ischemia monitoring, sedation depth assessment.
  • Describe BIS technology, algorithm, and scoring.
  • Discuss BIS use for sedation titration and anesthesia depth.
  • Interpret key EEG and BIS patterns in neurologic injury and sedation.

I. Introduction and Relevance

Continuous EEG (cEEG) and bispectral index (BIS) monitoring provide real-time, noninvasive assessment of cerebral electrical activity and sedation depth in critically ill patients.

  • Early detection of subclinical seizures reduces secondary brain injury.
  • EEG-based ischemia alerts facilitate timely interventions.
  • BIS-guided sedation protocols mitigate over- and under-sedation risks.
  • Pharmacists lead in protocol development, dose optimization, and drug interaction management.

Key Points

  • Up to 50% of ICU seizures are nonconvulsive and detectable only by cEEG.
  • Target BIS 40–60 for deep sedation in ventilated patients.

II. Physiological Basis and Technical Aspects of cEEG

cEEG captures summated cortical postsynaptic potentials across defined frequency bands using standardized electrodes and digital processing.

A. Neurophysiology (Frequency Bands)

Figure 1: EEG Frequency Bands. Visualization of the primary EEG frequency bands with their typical ranges and associated states of arousal or pathology.

B. Electrode Placement

  • International 10–20 system; silver/silver-chloride or gold cup electrodes
  • Montage options: bipolar, referential, Laplacian for spatial resolution

C. Signal Acquisition

  • Amplification of 10–100 µV signals; sampling ≥256 Hz
  • Analog/digital filtering to isolate clinical frequencies

D. Artifact Mitigation

  • Skin prep, secure leads, adjust montages
  • Recognize and exclude EMG, movement, and environmental noise
Pearl Icon A shield with an exclamation mark, indicating a clinical pearl. Clinical Pearl: Sampling Rate

Sampling rates ≥200 Hz are required to capture fast epileptiform activity accurately.

III. Clinical Indications for cEEG

cEEG is indicated for seizure detection, ischemia monitoring, sedation assessment, and prognostication in high-risk patients.

A. Seizure Detection

  • Convulsive vs nonconvulsive and subclinical events
  • Electrographic status epilepticus: continuous or recurrent seizures without return to baseline

B. Ischemia Monitoring

  • Loss of amplitude, slowing, periodic discharges signal perfusion deficits

C. Sedation Depth

  • Progressive background slowing, burst suppression, and suppression ratio guide titration

D. Prognostication

  • Continuity, reactivity, and burst suppression patterns inform outcome in coma and post-arrest care

Key Points

  • Recommend ≥24 h of monitoring for high-risk neonates and critically ill adults.
  • Early normalization of EEG background in HIE predicts improved neurodevelopmental outcome.

IV. BIS Monitoring Technology and Interpretation

BIS applies bispectral analysis to frontal EEG signals to generate a 0–100 index of cortical hypnosis.

A. Algorithm Components

  • Power spectral analysis
  • Bispectral (phase) relationships
  • Time-domain metrics

B. Sensor Placement

BIS Sensor Placement Diagram showing typical placement of a BIS sensor array on a patient’s forehead. BIS Sensor Placement on Forehead 1 2 3 (Ref) 4 (Gnd)
Figure 2: BIS Sensor Placement. A typical disposable BIS sensor array is placed across the forehead to acquire frontal EEG signals. Proper skin preparation and contact are crucial for accurate readings. Impedance should generally be <7.5 kΩ.

C. BIS Scale

BIS Scale and Corresponding Clinical States
BIS Range Clinical State
80–100 Awake/minimally sedated
60–80 Moderate sedation
40–60 Deep sedation/anesthesia
<40 Burst suppression

D. Limitations

  • EMG contamination elevates BIS
  • Hypothermia lowers BIS independent of sedation
  • Hemodynamic instability and neuromuscular blockade affect accuracy
Pearl Icon A shield with an exclamation mark, indicating a clinical pearl. Clinical Pearl: Context is Key

Always interpret BIS in the context of clinical exam and raw EEG when available.

V. Clinical Applications of BIS in ICU Sedation

BIS-guided sedation targets reduce variability and may shorten ventilation duration compared to clinical scales alone.

A. Target Ranges

  • 60–80: light to moderate sedation (RASS –1 to –3)
  • 40–60: deep sedation (RASS –4 to –5)

B. Correlation with RASS (Richmond Agitation-Sedation Scale)

  • BIS 60–70 ≈ RASS –2 to –3
  • BIS 50–60 ≈ RASS –4 to –5

C. Advantages

  • Quantitative, easy bedside implementation

D. Drawbacks

  • Cannot detect focal EEG changes or seizures
  • Cost and intermittent validation in neurocritical care

E. BIS Sedation Target Table

BIS Sedation Targets and Clinical Goals
BIS Range Clinical State Goal
80–100 Awake/minimally sedated Baseline assessment
60–80 Moderate sedation Light sedation (RASS –2)
40–60 Deep sedation ICU sedation target
<40 Burst suppression Avoid unless clinically indicated (e.g., status epilepticus, intracranial hypertension)

F. Case Example

An ARDS patient on propofol is titrated to BIS 50 to minimize overshoot and facilitate earlier weaning. This quantitative target helps maintain adequate sedation for ventilator synchrony while avoiding excessive drug administration, potentially reducing time on mechanical ventilation and ICU length of stay.

VI. Neuromonitoring-Guided Pharmacotherapy

Sedative and anticonvulsant regimens should be aligned with neuromonitoring endpoints to optimize efficacy and safety.

A. Sedative Agents Comparison

Comparison of Common ICU Sedative Agents
Agent Mechanism Dose Notes
Propofol GABAA potentiation 5–50 µg/kg/min infusion Rapid offset; risk of hypotension and PRIS (Propofol Infusion Syndrome)
Midazolam GABAA agonist 0.02–0.1 mg/kg/hr infusion Accumulates, especially with renal/hepatic dysfunction; risk of delirium
Dexmedetomidine α2-agonist 0.2–1.5 µg/kg/hr infusion Minimal respiratory depression; cooperative sedation; risk of bradycardia/hypotension
Ketamine NMDA antagonism 0.1–0.5 mg/kg/hr infusion (analgesic/sedative doses) Preserves airway reflexes; bronchodilator; may increase ICP in some patients; psychomimetic effects

B. Anticonvulsant Regimens

  • Levetiracetam: Load 20–60 mg/kg; maintenance 500–3000 mg/day (divided doses). Favorable side effect profile.
  • Phenytoin/Fosphenytoin: Load 15–20 mg/kg phenytoin equivalents (PE); monitor ECG for arrhythmias and hypotension during loading. Multiple drug interactions.
  • Valproate: Load 20–30 mg/kg; monitor liver function and platelets. Teratogenic.

C. Pharmacokinetic/Pharmacodynamic (PK/PD) Considerations

  • Context-sensitive half-times increase with infusion duration for many sedatives (e.g., fentanyl, midazolam).
  • Dose adjustments required in renal/hepatic impairment for many sedatives and anticonvulsants.

Key Points

  • Use EEG/BIS to titrate doses and avoid excessive suppression or inadequate treatment.
  • Monitor for accumulation, hemodynamic effects, and drug interactions, especially with prolonged infusions or organ dysfunction.

VII. Interpretation of Key EEG and BIS Patterns

Recognize pathologic patterns and differentiate artifacts to guide therapy adjustments.

A. Common EEG/BIS Patterns

  • Burst suppression: Alternating periods of high-amplitude activity (bursts) and very low amplitude or flat EEG (suppression). Indicates deep anesthesia, severe encephalopathy, or therapeutic coma. BIS typically <40.
  • Periodic discharges (PDs): Repetitive, stereotyped waveforms occurring at regular intervals (e.g., GPDs – Generalized Periodic Discharges). Can be ictal, interictal, or non-specific. Consider anticonvulsant escalation if frequent or associated with clinical changes.
  • EMG artifact: High-frequency muscle activity, often from frontalis or temporalis muscles, contaminates the EEG signal. This artifactually elevates BIS values, potentially leading to under-sedation if not recognized. Confirm with clinical exam (e.g., facial grimacing, movement).

B. Troubleshooting Checklist for Neuromonitoring

  1. Verify electrode/sensor placement and impedance. Ensure good skin-electrode contact.
  2. Optimize skin preparation and secure leads to minimize movement artifact.
  3. Identify and minimize sources of EMG (e.g., patient discomfort, shivering) and electrical interference (e.g., nearby equipment).
  4. Correlate neuromonitoring data (EEG waveforms, BIS value) with the patient’s clinical assessment (RASS, neurological exam).
  5. Consult neurophysiology or an experienced clinician for interpretation of complex or uncertain patterns.
Pearl Icon A shield with an exclamation mark, indicating a clinical pearl. Clinical Pearl: Integrated Assessment

Integrate cEEG, BIS, and bedside clinical examination to avoid misinterpretation and guide safe, effective therapy. No single monitor replaces comprehensive clinical judgment.

References

  1. Castillo-Pinto C, Sen K, Gropman A. Neuromonitoring in Rare Disorders of Metabolism. Yale J Biol Med. 2021;94:645–655.
  2. Chock VY, Rao A, Van Meurs KP. Optimal neuromonitoring techniques in neonates with hypoxic ischemic encephalopathy. Front Pediatr. 2023;11:1138062.
  3. Herman ST, Abend NS, Bleck TP, et al. Consensus statement on continuous EEG in critically ill adults and children, part I: indications. J Clin Neurophysiol. 2015;32(2):87–95.
  4. Glass HC, Shellhaas RA, Wusthoff CJ, et al. Contemporary profile of seizures in neonates: a prospective cohort study. J Pediatr. 2016;174:98–103.e1.
  5. Nash KB, Bonifacio SL, Glass HC, et al. Video-EEG monitoring in newborns with hypoxic-ischemic encephalopathy treated with hypothermia. Neurology. 2011;76(6):556–62.
  6. Wiwattanadittakul N, Prust M, Gaillard WD, et al. The utility of EEG monitoring in neonates with hyperammonemia due to inborn errors of metabolism. Mol Genet Metab. 2018;125(3):235–40.
  7. Shellhaas RA, Chang T, Tsuchida T, et al. The American Clinical Neurophysiology Society’s Guideline on continuous electroencephalography monitoring in neonates. J Clin Neurophysiol. 2011;28(6):611–617.
  8. Smith M. Multimodality neuromonitoring in adult traumatic brain injury: a narrative review. Anesthesiology. 2018;128(2):401–415.
  9. Appavu B, Burrows BT, Foldes S, Adelson PD. Approaches to multimodality monitoring in pediatric traumatic brain injury. Front Neurol. 2019;10:1261.
  10. Pacreu S, Vilà E, Moltó L, et al. Effect of dexmedetomidine on evoked-potential monitoring in patients undergoing brain stem and supratentorial cranial surgery. Acta Anaesthesiol Scand. 2021;65:1043–1053.
  11. Adkins GB, Mirallave Pescador A, Koht AH, Gosavi SP. Intraoperative neuromonitoring in intracranial surgery. BJA Educ. 2024;24(5):173–182.
  12. Aldana E, Alvarez Lopez-Herrero N, Benito H, et al. Consensus document for multimodal intraoperative neurophysiological monitoring in neurosurgical procedures. Rev Esp Anestesiol Reanim. 2021;68:82–98.
  13. Hoh BL, Ko NU, Amin-Hanjani S, et al. 2023 Guideline for the management of patients with aneurysmal subarachnoid hemorrhage. Stroke. 2023;54:e314–e370.
  14. Sloan TB, Jameson LC, Janik DJ, Koht A. Evoked potentials. In: Cottrell and Patel’s Neuroanesthesia. 6th ed. Elsevier; 2017:114–126.
  15. Spitzmiller RE, Phillips T, Meinzen-Derr J, Hoath SB. Amplitude-integrated EEG is useful in predicting neurodevelopmental outcome in full-term infants with hypoxic-ischemic encephalopathy: a meta-analysis. J Child Neurol. 2007;22(9):1069–1078.
  16. Koskela T, Kendall GS, Memon S, et al. Prognostic value of neonatal EEG following therapeutic hypothermia in survivors of hypoxic-ischemic encephalopathy. Clin Neurophysiol. 2021;132(9):2091–2100.
  17. Srinivasakumar P, Zempel J, Trivedi S, et al. Treating EEG seizures in hypoxic ischemic encephalopathy: a randomized controlled trial. Pediatrics. 2015;136(5):e1302–1309.
Previous Lesson
Back to Lesson
Next Topic