Study guide
Continuous EEG & ACNS Standardized Critical Care Terminology
ABPN Neurocritical Care Study Guide Exam
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1 Chapter 1: Neurologic Examination & Coma Assessment in the ICU
Current Examination, Blueprint & Preparation Neurologic Examination in Critically Ill Patients Coma Evaluation & Consciousness Alterations Delirium & Toxic-Metabolic Encephalopathy in the ICU
2 Chapter 2: Cerebral Physiology & Intracranial Dynamics
Cerebral Blood Flow, Metabolism & Autoregulation Intracranial Pressure & Compliance Cerebral Edema & Herniation Syndromes
3 Chapter 3: Intracranial Hypertension & Cerebral Perfusion Management
Tiered ICP Management Protocols Hyperosmolar Therapy & Fluid Management Advanced & Refractory ICP Interventions
4 Chapter 4: Airway, Mechanical Ventilation & Pulmonary ICU Management
Emergency Airway Management & Neuro-Intubation Mechanical Ventilation Strategies in Acute Brain Injury Tracheostomy & Ventilator Weaning in Neurocritical Care Pulmonary Complications in the Neuro-ICU Obstructive Lung Disease, Pulmonary Hypertension & Bronchoscopy
5 Chapter 5: Hemodynamics, Shock & Cardiovascular Management
Hemodynamic Monitoring & Blood Pressure Targets Vasoactive Agents: Inotropes, Vasopressors & Antihypertensives Cardiac Complications of Brain Injury
6 Chapter 6: Neuropharmacology, Analgesia & Sedation
ICU Sedation & Analgesia Neuromuscular Blockade & Monitoring Propofol Infusion Syndrome & Drug Toxicities Antiseizure Drug Pharmacology in the ICU
7 Bleeding, Thrombosis & Hematologic Emergencies
Warfarin & Heparin Reversal Direct Oral Anticoagulant (DOAC) Reversal Antiplatelet Management & Platelet Dysfunction Venous Thromboembolism Prophylaxis & Management Transfusion, Coagulopathy, TMA & Cellular-Therapy Neurotoxicity
8 Chapter 8: Systemic ICU Care, Fluids, Electrolytes & Endocrine
Hyponatremia & Osmoregulation: SIADH vs Cerebral Salt Wasting Diabetes Insipidus, Hypernatremia & Endocrine Crises Critical Care Prophylaxis, Nutrition & Infection Prevention
9 Systemic Trauma & Environmental Injury
Polytrauma, Chest Injury & Abdominal Hemorrhage Burns, Electrical Injury & Hanging
10 Cardiac Emergencies & Mechanical Support
IABP, Ventricular Devices & ECMO Acute Coronary, Valvular, Rhythm & Aortic Emergencies
11 Kidney Injury, Acid–Base & Renal Replacement
Acute Kidney Injury & Renal Drug Clearance Acid–Base Disorders, Electrolytes & Renal Replacement
12 Systemic Infection & Endocrine Emergencies
Sepsis, Endocarditis & Antimicrobial Principles Thyroid, Adrenal & Dysglycemic Emergencies
13 Gastrointestinal & Hepatic Emergencies
Acute Abdomen, GI Bleeding & Abdominal Compartment Syndrome Acute Liver Failure, Cirrhosis & Hepatic Drug Effects
14 Chapter 9: Neuroimaging in the Neuro-ICU
Non-Contrast CT & CT Angiography CT Perfusion & Advanced Perfusion Imaging Magnetic Resonance Imaging in Critical Illness
15 Chapter 10: Electrophysiology & Neuromonitoring
Continuous EEG & ACNS Standardized Critical Care Terminology Invasive Neuromonitoring: ICP & External Ventricular Drains Multimodal Monitoring: PbtO2, Microdialysis & Transcranial Doppler
16 Angiography, Electrodiagnosis & CSF Analysis
Conventional Angiography & Cranial–Spinal Shunts EMG, Nerve Conduction & Acute Muscle Disease CSF Analysis: Infection, Inflammation & Hemorrhage
17 Chapter 11: Bedside Procedures, Ultrasound & Death by Neurologic Criteria
Critical Care Procedural Skills Critical Care Ultrasound & Echocardiography Determination of Death by Neurologic Criteria
18 Chapter 12: Acute Ischemic Stroke & Reperfusion Therapies
Acute Ischemic Stroke Management & Thrombolysis Endovascular Thrombectomy & Large Vessel Occlusion Malignant Hemispheric & Cerebellar Infarction
19 Chapter 13: Spontaneous Intracerebral Hemorrhage & Intraventricular Hemorrhage
Acute Intraparenchymal Hemorrhage Management Intraventricular Hemorrhage & Hydrocephalus Surgical Evacuation & Minimally Invasive Surgery in ICH
20 Chapter 14: Aneurysmal Subarachnoid Hemorrhage & Delayed Cerebral Ischemia
Aneurysmal Subarachnoid Hemorrhage: Acute Resuscitation & Securing Delayed Cerebral Ischemia & Cerebral Vasospasm Non-Aneurysmal Subarachnoid Hemorrhage & Vascular Malformations
21 Venous, Spinal & Traumatic Vascular Disease
Cerebral Venous Thrombosis & Spinal Cord Infarction Traumatic Dissection, Carotid–Cavernous Fistula & Penetrating Injury
22 Chapter 15: Traumatic Brain & Spinal Cord Injury
Severe Traumatic Brain Injury & Contusions Acute Traumatic Spinal Cord Injury & Neurogenic Shock Spine Trauma, Fractures & Cord Syndromes
23 Chapter 16: Status Epilepticus, Seizures & Neuromuscular Emergencies
Status Epilepticus: Convulsive & Non-Convulsive Refractory & Super-Refractory Status Epilepticus Acute Neuromuscular Respiratory Failure
24 Chapter 17: Post-Cardiac Arrest Care, CNS Infections & Encephalitis
Targeted Temperature Management & Post-Cardiac Arrest Care Post-Cardiac Arrest Neuroprognostication Acute CNS Infections, Encephalitis & Inflammatory Emergencies
25 Neuroinflammation & Neurooncology
Fulminant Demyelination & Autoimmune Encephalitis Brain, Spinal & Leptomeningeal Cancer Emergencies
26 Pregnancy, Transplantation & Pediatric Care
Pregnancy, Postpartum & Post-Transplant Neurologic Care Pediatric Neurocritical Care
27 Chapter 18: Neurosurgical & Perioperative Emergencies
Postoperative Neurosurgical Complications Device Complications: EVDs, Shunts & ICP Monitors Cerebral Hyperperfusion Syndrome & Post-Interventional Emergencies
28 Chapter 19: Ethics, Palliative Care & Organ Donation in the Neuro-ICU
Communication, Surrogate Decision-Making & Conflict Resolution Neuroprognostication Ethics, Withdrawal of Life Support & Palliative Care Organ Donation & Management of the Deceased Donor
Continuous EEG & ACNS Standardized Critical Care Terminology
Key Takeaways Explain This Topic AI
Use cEEG when nonconvulsive seizures are suspected, for EEG-guided status treatment, and in selected secondary-injury surveillance.
ACNS 2021 standardizes background continuity, rhythmic and periodic patterns, distribution, modifiers, seizure duration, and burden.
An electrographic seizure is distinct from electrographic status; an IIC pattern is not automatically a mandate for anesthetic coma.
Post-arrest EEG prognosis requires appropriate timing, confounder assessment, and other modalities; no early pattern establishes invariant outcome.
Quantitative trends support screening but require raw EEG review and clinical correlation.
Last updated: October 2026
Continuous EEG & ACNS Standardized Critical Care Terminology
Continuous electroencephalography (cEEG) has transitioned from an elective diagnostic modality into an indispensable real-time monitor of cerebral cortical function in the neurocritical care unit. Because clinical examination in comatose or deeply sedated patients cannot reliably distinguish secondary ischemic deterioration, metabolic encephalopathy, or occult epileptic activity, cEEG provides continuous bedside functional neuro-monitoring.
Indications for Continuous EEG in the Neuro-ICU
Use cEEG when nonconvulsive seizures are suspected, consciousness does not recover as expected after convulsive status, or high-risk injury and an unreliable examination warrant surveillance. Monitoring should begin promptly when the indication is present; one universal admission deadline or prevalence estimate does not apply to every ICU coma. At least 24 hours is often needed, with longer recordings for coma, ongoing treatment, or high-risk patterns. Duration is individualized from the evolving findings.
During continuous anesthetic treatment of status epilepticus, cEEG verifies electrographic seizure control because paralysis and sedation can hide clinical activity. The target may be seizure cessation or selected burst suppression under a defined protocol. A fixed number of bursts per screen is not a universal validated target. Review raw EEG with trends and bedside events rather than treating a quantitative display as the diagnosis.
The 2021 ACNS Standardized Critical Care EEG Terminology
To eliminate ambiguous subjective descriptors (e.g., "triphasic waves," "PLEDs," "subclinical seizures"), the American Clinical Neurophysiology Society (ACNS) established an objective, highly reproducible nomenclature updated in 2021. Rhythmic and periodic patterns (RPPs) are classified by pairing a Main Term 1 (spatial localization) with a Main Term 2 (pattern morphology), supplemented by Plus Modifiers .
Spatial Localization (Main Term 1)
Generalized (G): Bilaterally synchronous, symmetric, and uniform discharge across both hemispheres.
Lateralized (L): Unilateral, asymmetric, or focal discharge predominantly involving one hemisphere or a specific lobar distribution.
Bilateral Independent (BI): Synchronous or asynchronous discharges occurring independently and simultaneously in both hemispheres.
Multifocal (Mf): At least three distinct, independent foci of discharges across both hemispheres.
Core Morphology (Main Term 2)
Periodic Discharges (PDs): Waveforms of relatively uniform morphology repeating at regular intervals with intervening flat or lower-amplitude inter-discharge baseline segments.
Rhythmic Delta Activity (RDA): Continuous, rhythmic waves repeating without an intervening flat baseline, exhibiting a regular, sinusoidal or rhythmic delta ( < 4 Hz <4\text{ Hz} < 4 Hz ) frequency.
Spike-and-Wave / Sharp-and-Wave (SW): Polyspike, spike, or sharp-wave components persistently followed by a slow-wave deflection in a repetitive rhythmic cycle.
Plus (+) Modifiers
Plus modifiers designate specific features that increase the intrinsic epileptogenicity of an underlying rhythmic or periodic pattern:
+F (Fast activity): Superimposed fast frequencies (beta or gamma bands) occurring over the main rhythmic or periodic waveform.
+R (Rhythmic activity): Rhythmic background activity interlaced with periodic complexes.
+S (Sharp or Spiky): Spiky or sharp morphology embedded within otherwise sinusoidal rhythmic slow activity.
ACNS Nomenclature Historical Term Waveform Features Typical Etiology Seizure Association
LPDs PLEDs Unilateral periodic sharp waves or spikes separated by static baseline intervals Acute focal cortical lesion (stroke, abscess, focal encephalitis, neoplasm) Increased; frequency and modifiers matter
LPDs+F PLEDs-Plus Unilateral periodic complexes with superimposed rhythmic fast beta/gamma frequencies Acute destructive cortical injury with active epileptogenic transition Higher-risk pattern; interpret frequency and burden
LRDA Rhythmic delta localized to one hemisphere or region; TIRDA is a specific temporal pattern Unilateral rhythmic sinusoidal delta waves without intervening flat baseline Deep subcortical white matter ischemia, focal cortical contusion, focal epilepsy Increased in relevant acute injury settings
GPDs Triphasic waves / GPEDs Generalized synchronous periodic complexes with frontocentral or anteroposterior lag Toxic-metabolic encephalopathy (hepatic, uremic, anoxic, baclofen, cefepime toxicity) Variable; etiology, frequency, and modifiers matter
GRDA FIRDA / OIRDA Generalized rhythmic delta activity with anterior (FIRDA) or posterior predominance Diffuse metabolic encephalopathy, increased ICP, midline subcortical lesions Generally not an IIC pattern by itself
BIPDs BiPLEDs Independent periodic discharges occurring across both hemispheres asynchronously Severe bilateral destructive lesions (herpes simplex encephalitis, bilateral watershed infarcts) Increased in severe bilateral injury
The Ictal-Interictal Continuum & Salzburg Criteria for NCSE
The Ictal-Interictal Continuum (IIC) represents a neurophysiological twilight zone. Patterns on the IIC do not meet strict electrographic seizure criteria but reflect marked neuronal hypersynchrony driven by intense metabolic demand. On advanced multimodal monitoring, IIC patterns frequently trigger profound neurovascular uncoupling, marked elevations in the cerebral microdialysis lactate-to-pyruvate ratio ( L P R > 40 LPR > 40 L PR > 40 ), and critical reductions in brain tissue oxygenation ( P b t O 2 < 15 mmHg PbtO_2 < 15\text{ mmHg} P b t O 2 < 15 mmHg ), culminating in secondary metabolic exhaustion.
ACNS Seizure, Status, and IIC Definitions
An electrographic seizure is epileptiform discharges averaging more than 2.5 Hz for at least ten seconds, or a pattern with definite evolution lasting at least ten seconds. Electrographic status epilepticus is a seizure lasting at least ten continuous minutes or seizure activity occupying at least 20% of any 60-minute period. A ten-second electrographic seizure is not automatically status epilepticus.
The ictal–interictal continuum (IIC) is an electrographic description, not a diagnosis by itself. Under ACNS 2021, applicable patterns include PDs or spike-and-wave above 1 and up to 2.5 Hz; PDs or spike-and-wave at 0.5–1 Hz with a plus modifier or fluctuation; and lateralized RDA above 1 Hz with a plus modifier or fluctuation. Generalized RDA is not included simply because it is rhythmic. Patterns already meeting seizure criteria are classified accordingly rather than remaining on the IIC.
Clinical correlation, the underlying lesion, metabolic and drug effects, pattern burden, and response to treatment guide management. A time-locked clinical correlate can establish an electroclinical seizure even with a brief pattern. In a diagnostic medication trial, EEG improvement alone after a sedative does not prove that an encephalopathy was ictal; clinical improvement and the complete criteria matter. Salzburg criteria provide another structured clinical framework and should not be conflated with a rule that any ten-second fast pattern is status.
A 2-Hz LPD pattern with superimposed fast activity may lie on the IIC and carry substantial seizure risk. In contrast, a clearly evolving 20-second pattern can meet seizure criteria. The distinction affects monitoring and treatment but does not imply that all IIC patterns require anesthetic coma. Correct a toxic or metabolic trigger, assess clinical effects, and balance treatment benefit against hypotension, ventilation, and loss of examination.
Background Architecture, Reactivity, and Suppression
ACNS describes continuity by the proportion of suppression or attenuation: continuous below 1%, nearly continuous 1–9%, discontinuous 10–49%, and burst attenuation/suppression 50–99%. Suppression involves activity below 10 microvolts; attenuation and suppression are distinct descriptors. Background voltage, symmetry, state changes, and medication exposure must be evaluated together.
Reactivity is a reproducible background change with stimulation. Test using an appropriate protocol and avoid mistaking muscle or movement artifact for cerebral response. A reactive background can be reassuring in context, but absent reactivity alone is not a reliable standalone poor-outcome predictor. Sedatives, temperature, technical factors, and injury affect interpretation.
Spontaneous suppression or burst suppression after arrest can be concerning, particularly at delayed, confounder-free assessment. It does not supply a universal zero-error prediction or a histologic diagnosis of cortical necrosis. Drug-induced burst suppression during seizure or ICP treatment has a different context. Use the dedicated neuroprognostication framework rather than transferring an early pattern directly into a withdrawal decision.
Quantitative EEG (qEEG) Bedside Trends
Alpha–delta ratio: A sustained decline can raise concern for ischemia in aSAH, but changes also reflect sedation, sleep, seizures, artifact, or other illness. Review raw EEG and correlate with examination, TCD, imaging, and other monitoring. No single percentage decline reliably diagnoses every DCI event.