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2025 PACUPrep BCCCP Preparatory Course Neuromonitoring Techniques Neuromonitoring Data Interpretation and Clinical Application

Lesson 25, Topic 3

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Neuromonitoring Data Interpretation and Clinical Application

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Advanced Interpretation of cEEG and BIS

Advanced Interpretation of cEEG and BIS for Seizure Detection and Sedation Optimization

Objective

Interpret continuous EEG (cEEG) and Bispectral Index (BIS) data to detect neurologic complications and guide sedation management.

1. Introduction and Clinical Context

Continuous Electroencephalogram (cEEG) and Bispectral Index (BIS) monitoring enable real-time detection of subclinical seizures, hypoxic injury, and sedation depth, potentially improving neurologic outcomes and ICU efficiency.

cEEG is considered the gold standard for detecting nonconvulsive seizures, which are common in critically ill patients and can worsen outcomes if untreated.
BIS monitoring provides a processed EEG parameter that quantitates the level of sedation on a scale of 0 (no brain activity) to 100 (fully awake), particularly useful when clinical examination is limited by neuromuscular blockade or deep sedation.

Clinical Pearl: Integrated Assessment

Clinicians must integrate cEEG and BIS findings with the neurologic examination, other physiological monitors (e.g., intracranial pressure, cerebral oxygenation), and imaging data to tailor pharmacotherapy dynamically and make informed clinical decisions.

2. EEG Pattern Recognition for Neurologic Complications

Distinct EEG signatures guide the diagnosis of nonconvulsive seizures, status epilepticus, and ischemia, allowing for timely intervention.

A. Nonconvulsive Seizures (NCSz)

NCSz are characterized by electrographic seizure activity without overt clinical convulsions. Key patterns include:

Periodic Discharges (PDs): Formerly PLEDs (Periodic Lateralized Epileptiform Discharges), these are often associated with acute brain injury. PDs with a “plus” modifier (e.g., superimposed rhythmic activity) have a higher risk of evolving into seizures.
Rhythmic Delta Activity (RDA): Sustained rhythmic waves in the delta frequency range (0.5–4 Hz), particularly if evolving or associated with subtle clinical signs.
Evolving Electrographic Spikes/Sharp Waves: Clear evolution in frequency (typically increasing), amplitude, or spatial distribution of spike or sharp wave activity.

B. Nonconvulsive Status Epilepticus (NCSE)

NCSE is a state of continuous or rapidly recurring NCSz. EEG criteria often include:

Rhythmic discharges (e.g., spikes, sharp waves, spike-and-wave) at a frequency of ≥2.5 Hz lasting for at least 10 seconds.
Less frequent rhythmic discharges (<2.5 Hz) or periodic discharges if they show clear spatiotemporal evolution or are associated with subtle clinical ictal phenomena or EEG improvement with IV anti-seizure medication.
Progression to burst suppression pattern, which consists of periods of high-amplitude activity alternating with periods of isoelectric or very low amplitude background.

C. Ischemia and Hypoxic Injury

EEG changes can be early indicators of cerebral ischemia or hypoxic-ischemic brain injury:

Focal Slowing: Localized polymorphic delta waves, often the earliest sign of focal ischemia.
Generalized Attenuation: Diffusely low-voltage background activity (typically <20 μV), indicating widespread neuronal dysfunction.
Alpha Coma: Persistent, widespread, unreactive alpha frequency (8–13 Hz) activity, often associated with severe brainstem or diffuse cortical injury.
Triphasic Waves: Diffuse, bilaterally synchronous, high-amplitude waves with a characteristic positive-negative-positive morphology, often seen in metabolic encephalopathies but can also occur with anoxic injury.

Clinical Pearl: Prognostic Value of Burst Suppression

The presence of a burst suppression pattern on EEG, particularly if persistent or developing within 24-48 hours after a significant hypoxic-ischemic insult, is strongly associated with poor neurologic recovery.

3. BIS Monitoring Interpretation

BIS uses bispectral analysis of raw EEG signals, typically from a frontal sensor, to provide a numeric index of sedation depth. Values must be interpreted cautiously alongside clinical scales and raw EEG data.

A. Technology and Signal Processing

BIS is derived from several EEG features, including spectral power (frequency content), phase coupling (synchrony between frequencies), and time-domain characteristics.
Proprietary algorithms filter out common artifacts like electromyographic (EMG) activity and electrical noise to enhance signal quality.

B. Numeric Ranges and Sedation Levels

BIS values generally correlate with sedation depth as follows:

>80: Awake or light sedation.
60–80: Moderate sedation (conscious sedation).
40–60: Deep sedation and general anesthesia (often the target range in ICU for sedated, mechanically ventilated patients).
<40: Very deep sedation, potentially indicating burst suppression or profound coma. Values near 0 suggest isoelectric EEG.

C. Clinical Correlation and Pitfalls

Accuracy and reliability of BIS are improved when correlated with validated clinical sedation scales like the Richmond Agitation-Sedation Scale (RASS) or Sedation-Agitation Scale (SAS).
Hypothermia and the use of neuromuscular blocking agents (NMBAs) can artifactually lower BIS values, even if the patient is inadequately sedated. NMBAs reduce EMG artifact, which can unmask underlying low BIS values or cause the algorithm to interpret the quiet signal as deeper sedation.
High EMG activity (e.g., from agitation, shivering) can artifactually elevate BIS. Electrocautery and other sources of electrical interference can distort readings or cause signal dropout.

Clinical Pearl: Verify Unexpected BIS Changes

Always verify unexpected or sudden changes in BIS values by reviewing the raw EEG strip (if available through the BIS monitor or cEEG), checking for artifacts, assessing for changes in EMG activity, and performing a focused clinical assessment of the patient’s sedation level and neurologic status.

4. Pharmacotherapy Integration and Dose Adjustment

Neuromonitoring data, including cEEG and BIS, direct targeted anticonvulsant and sedative titration to balance seizure control with optimal sedation depth, minimizing adverse effects.

A. Anticonvulsant Pharmacotherapy

Selection and dosing of anticonvulsants are guided by EEG findings, patient characteristics, and drug properties.

Anticonvulsant Agents for Seizure Management in Critical Care
Agent	Mechanism	Loading Dose	Maintenance	Monitoring & Pearls
Phenytoin	Na⁺ channel blocker	15–20 mg/kg IV (≤50 mg/min)	4–6 mg/kg/day divided	Trough 10–20 μg/mL; monitor ECG (arrhythmias, hypotension with rapid infusion), BP. Multiple drug interactions.
Levetiracetam	SV2A modulator	1000–4000 mg IV (typically 20-60 mg/kg)	500–1500 mg IV q12h	Renal dose adjustment required. Minimal drug interactions. Generally well-tolerated.
Valproate	↑GABA, Na⁺/Ca²⁺ blocker	20–40 mg/kg IV (≤6 mg/kg/min)	15–60 mg/kg/day divided	Monitor LFTs, platelets, ammonia. Avoid in hepatic failure and urea cycle disorders.
Lacosamide	Slow Na⁺ channel inactivation	200–400 mg IV over 15-30 min	100–200 mg IV q12h	Monitor ECG for PR prolongation, especially with other AV nodal blocking agents. Renal dose adjustment.
Phenobarbital	GABA-A agonist	15–20 mg/kg IV (≤100 mg/min)	1–3 mg/kg/day IV	Respiratory depression, hypotension. Monitor drug levels. Used for refractory status epilepticus.

Clinical Pearl: EEG-Guided Anticonvulsant Loading

Use EEG suppression targets (e.g., cessation of electrographic seizures, significant reduction in epileptiform discharges) to guide loading doses and subsequent titration of anticonvulsants, especially in status epilepticus, to prevent under-treatment of electrographic seizures.

B. Sedative Pharmacotherapy

Sedative choice and dose are influenced by BIS targets, cEEG background activity, and patient-specific factors.

Sedative Agents for ICU Sedation and Neuromonitoring
Agent	Mechanism	Dose Range (IV Infusion)	Monitoring & Pearls
Propofol	GABA-A agonist	5–80 μg/kg/min	Rapid onset/offset. Hypotension, respiratory depression, hypertriglyceridemia. Risk of propofol-related infusion syndrome (PRIS) with high doses/prolonged use. Can induce burst suppression on EEG.
Midazolam	Benzodiazepine (GABA-A agonist)	0.02–0.2 mg/kg/h (can be higher)	Accumulates in renal/hepatic dysfunction, prolonged emergence. Anterograde amnesia. Risk of delirium. Can suppress seizures.
Dexmedetomidine	α₂ agonist	0.2–1.5 μg/kg/h	Bradycardia, hypotension. Minimal respiratory depression (“cooperative sedation”). Preserves EEG background activity better than propofol or benzodiazepines, facilitating neurologic checks and cEEG interpretation. Not a primary anticonvulsant.
Ketamine	NMDA antagonist	0.1-2 mg/kg/h (analgesic/sedative doses)	Bronchodilation, sympathomimetic effects (↑HR, ↑BP). Can cause hypersalivation, emergence reactions. Has anticonvulsant properties. EEG shows increased fast activity or rhythmic delta.

Clinical Pearl: Dexmedetomidine and EEG

Dexmedetomidine is often favored when ongoing neurologic assessment or clear cEEG interpretation is critical, as it typically preserves EEG background activity and sleep spindles, unlike propofol or benzodiazepines which can cause diffuse slowing or burst suppression at higher doses.

5. Limitations, Artifacts, and Quality Improvement

Recognizing technical and physiologic artifacts is crucial to prevent misinterpretation of cEEG and BIS data and avoid inappropriate clinical interventions.

EEG Artifacts: Common artifacts include electromyographic (EMG) interference from scalp/facial muscles, electrode displacement or high impedance, 50/60 Hz electrical noise, movement artifact, and EKG artifact.
BIS Artifacts: EMG activity can falsely elevate BIS values. Conversely, profound muscle relaxation (e.g., with NMBAs) or very low signal quality can falsely lower BIS. Electrocautery, patient movement, and poor sensor contact can cause erratic readings or signal dropout.
Mitigation Strategies: Regular checks of electrode integrity and impedance, meticulous skin preparation, use of artifact-suppression software features, and education of staff are important. Multidisciplinary communication between neurology, critical care, and nursing staff is key to interpreting ambiguous findings.

Clinical Pearl: Standardized Workflows

Implement standardized artifact-recognition workflows and ensure prompt communication of significant neuromonitoring signal changes or concerns to the entire care team. Regular training sessions for ICU staff on basic EEG/BIS interpretation and artifact identification can improve monitoring quality.

6. Clinical Decision Algorithm and Case Studies

A structured approach to interpreting neuromonitoring data ensures rapid detection of critical changes and timely intervention, integrating these tools into overall patient management.

Detect Neuromonitoring Change (e.g., New PLEDs, ↓BIS, ↑ICP)

Perform Focused Clinical Assessment (Neurologic exam, hemodynamics, artifact check, review trends)

Adjust Pharmacotherapy (Anticonvulsant, sedative, osmotic agent per protocol/clinical judgment)

Reassess (Repeat EEG/BIS, exam, labs, imaging)

Figure 1: Clinical Decision Algorithm. A simplified algorithm for responding to changes in neuromonitoring parameters in the ICU.

Case Vignette

A 58-year-old male admitted with subarachnoid hemorrhage develops new rhythmic delta activity with superimposed fast activity in the left temporal region on cEEG, without clear clinical correlate. His BIS is stable at 55 on propofol 30 μg/kg/min. The neurologist interprets this as evolving nonconvulsive seizures. Levetiracetam 2000 mg IV is administered as a loading dose, followed by 1000 mg IV q12h. Within 2 hours, the cEEG shows resolution of the rhythmic activity. The propofol infusion is continued, and BIS remains 50-60. Daily neurologic examinations are performed during brief sedation holds, showing no new focal deficits.

References

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