Study guide
24.1 Status Epilepticus and Seizures (03.N)
ABIM Neurocritical Care Subspecialty Certification Exam
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1 Introduction & Exam Overview
1.1 Current Exam Facts 1.2 Eligibility, Practice Pathway, and the IM Training Route 1.3 Format, Scoring, Pearson VUE, and Score Reports 1.4 How to Use This Independent Study Guide
2 ICU Neurologic Exam, Cerebral Physiology, and CSF
2.1 Neurological Examination in the ICU 2.2 Cerebral Physiology, ICP, CBF, and Autoregulation 2.3 CSF Physiology
3 Core Neuropharmacology
3.1 Osmotic Agents 3.2 Anti-Seizure Drugs 3.3 Anesthetics, Sedatives, Analgesia, and Paralytics 3.4 Antihypertensives, Vasopressors, and Inotropes
4 Reperfusion Drugs, Airway, and Ventilation
4.1 Thrombolytics, Anticoagulants, and Antiplatelets 4.2 Reversal of Anticoagulation After Acute Hemorrhage 4.3 Airway Management and Tracheostomy 4.4 Mechanical Ventilation
5 Hemodynamics and Shock
5.1 Hemodynamic Monitoring 5.2 IABP, Temporary VADs, LVAD, and ECMO 5.3 Diagnosis and Management of Shock
6 Nutrition, Temperature, and ICU Prophylaxis
6.1 Nutrition (01.J) 6.2 Temperature Control (01.K) 6.3 ICU Prophylaxis, Delirium, and Early Mobility (01.L)
7 General Trauma
7.1 Emergency Evaluation of Polytrauma, Chest, and Abdominal Trauma 7.2 Long-Bone Fractures and Fat Embolism 7.3 Burns, Electrical Injury, and Hanging/Strangulation
8 Pulmonary Critical Care
8.1 Pulmonary Physiology and ARDS (01.N.1–2) 8.2 PE, Pneumonia, and Pulmonary Edema (01.N.3, 7–8) 8.3 COPD, Asthma, PAH, and Bronchoscopy Basics (01.N.4–6, 9)
9 Cardiovascular Critical Care
9.1 Cardiovascular Physiology, Stress Cardiomyopathy, ACS, and Valves 9.2 Arrhythmias and Pacing 9.3 Acute Aortic Dissection and Cardiac Ultrasound
10 Renal and Infectious Disease
10.1 AKI, RRT, and Renal Drug Dosing 10.2 Acid-Base and Electrolyte Disorders 10.3 Severe Sepsis, Septic Shock, and Infective Endocarditis 10.4 Antimicrobial Use and Infection in the Immunosuppressed
11 Endocrine and Salt-Water Disorders
11.1 Pituitary Apoplexy, DI, and Panhypopituitarism (01.R.1–4) 11.2 SIADH and Cerebral Salt Wasting (01.R.5–6) 11.3 Thyrotoxicosis, Myxedema, Adrenal Crisis, and Dysglycemia (01.R.7–9)
12 Gastrointestinal Critical Care
12.1 GI Physiology, Acute Abdomen, Bleed, Ileus, and Perforation (01.S.1–5) 12.2 Mesenteric Ischemia and Abdominal Compartment Syndrome (01.S.6–7) 12.3 Fulminant Liver Failure, Cirrhosis Decompensation, and Hepatic Dosing (01.S.8–10)
13 Hematologic Disorders
13.1 Anemia, Transfusion, Thrombocytopenia, Coagulopathy, and DIC (01.T.1–4) 13.2 VTE in the Neuro ICU (01.T.5) 13.3 Chemo/Immune, SCT, CAR-T, Sickle Cell, and TMA (01.T.6–10)
14 Neuroimaging
14.1 CT of Brain and Spine 14.2 MRI and CT/MR Perfusion 14.3 Noninvasive Angiography and Catheter Angiography
15 EEG, EMG, and CSF Analysis
15.1 EEG, Standard and Processed (02.B) 15.2 Basic EMG Interpretation (02.G) 15.3 CSF Analysis (02.H)
16 ICP, TCD, and Multimodality Monitoring
16.1 ICP Monitoring (02.C) 16.2 Transcranial Doppler (02.D) 16.3 Brain-Tissue Oxygen and Multimodality Monitoring (02.E–F)
17 Brain Death and Bedside Procedures
17.1 Brain Death Prerequisites and Clinical Exam (02.I) 17.2 Apnea Testing and Ancillary Studies (02.I) 17.3 Vascular Access, Thoracic Echo, and Lung Ultrasound (02.J–L)
18 Coma, Anoxia, and Intracranial Hypertension
18.1 Coma and Other States of Altered Consciousness (03.A) 18.2 Global Anoxia-Ischemia and Post-Resuscitation Encephalopathy (03.A.1) 18.3 Toxidromes, ICU Delirium, and Hypertensive Encephalopathy (03.A.2–4) 18.4 Intracranial Hypertension as a Disease State (03.B)
19 Acute Ischemic Stroke
19.1 IV Reperfusion Therapy (03.C.3) 19.2 Mechanical Thrombectomy Windows and Imaging Selection (03.C.3) 19.3 Malignant Hemispheric Infarction and Basilar Artery Occlusion (03.C.1–2)
20 Intraparenchymal Hemorrhage
20.1 Intracerebral Hematoma (03.D.1) 20.2 Cerebellar Hematoma (03.D.2) 20.3 Intraventricular Hemorrhage (03.D.3)
21 SAH, CVST, and Spinal Cord Infarction
21.1 Aneurysmal Subarachnoid Hemorrhage (03.E.1) 21.2 Non-Aneurysmal SAH (03.E.2) 21.3 Cerebral Venous Sinus Thrombosis (03.F) 21.4 Spinal Cord Infarction (03.G)
22 Vascular Anomalies and Traumatic Brain Injury
22.1 Unruptured Aneurysm, Cavernoma, AVM, and Dural AVF (03.H) 22.2 Diffuse Axonal Injury and Cerebral Contusions (03.I.1–2) 22.3 Epidural Hematoma, Subdural Hematoma, and Penetrating Injury (03.I.3–4, 7) 22.4 Arterial Dissection and Carotid-Cavernous Fistula (03.I.5–6)
23 Spine, Hydrocephalus, and CNS Infection
23.1 Spinal Cord Injury, Central Cord, and Neurogenic Shock (03.J) 23.2 Unstable Spine Fractures (03.K) 23.3 Hydrocephalus and CSF Diversion (03.L) 23.4 Acute CNS Infections (03.M)
24 Seizures and Neuromuscular Emergencies
24.1 Status Epilepticus and Seizures (03.N) 24.2 Guillain-Barré Syndrome (03.O.1) 24.3 Myasthenic Crisis (03.O.2) 24.4 Motor Neuron Disease, Acute Myopathies, Rhabdomyolysis, and CINM (03.O.3–6)
25 Inflammatory Disease, Neuro-Oncology, and Special Populations
25.1 Fulminant Demyelinating Diseases (03.P) 25.2 Autoimmune Encephalitis and Acute Autonomic Hyperactivity (03.Q–R) 25.3 Neuro-Oncology and Treatment Complications (03.S) 25.4 Pregnancy/Post-Partum, Post-Transplant, and Pediatric Patients (03.T–U)
26 Neurosurgical and Perioperative Complications
26.1 Postoperative Seizures, Hemorrhage, Ischemia, and Hyperperfusion (04.A, C, D, H) 26.2 Infection, CSF Leak, and Pneumocephalus (04.B, E, F) 26.3 Complications of EVD and Lumbar Drain (04.G, I)
27 Ethics, Prognostication, and Organ Donation
27.1 Communication, Decision-Makers, Advance Directives, and DNR (05.A, B, G) 27.2 Uncertainties of Prognostication and the Self-Fulfilling Prophecy (05.C) 27.3 Palliative Care, Withdrawal, Withholding, and Futility (05.D–F) 27.4 Donation After Cardiac Death and Care of the Organ Donor (05.H–I)
24.1 Status Epilepticus and Seizures (03.N)
Key Takeaways Explain This Topic AI
Convulsive status epilepticus is 5 or more minutes of continuous seizure, or 2 or more seizures without recovery of consciousness; start treatment at 5 minutes rather than waiting 30 minutes.
The American Epilepsy Society 2016 clock is stabilize 0–5 minutes, benzodiazepine 5–20 minutes, a full second antiseizure load 20–40 minutes, then another antiseizure drug or anesthetic coma with continuous EEG after 40 minutes.
ESETT 2019 found fosphenytoin 20 mg PE/kg (max 1500 mg PE), levetiracetam 60 mg/kg (max 4500 mg), and valproate 40 mg/kg (max 3000 mg) equivalent after benzodiazepines, each succeeding in about half of patients.
Refractory status epilepticus is failure of an adequate benzodiazepine plus a second antiseizure drug; super-refractory status epilepticus continues or recurs 24 hours after anesthetic therapy, including seizures that return during weaning.
Avoid valproate in pregnancy, POLG-related mitochondrial disease, and liver failure. Early post-anoxic myoclonus is not, by itself, a reason to withdraw life-sustaining treatment.
Last updated: September 2026
Why the clock starts at five minutes
Status epilepticus (SE) is one of the few neurologic crises in which minutes of under-treatment convert a reversible electrographic storm into hypotension, aspiration, neuronal injury, and death. The neurocritical care examination tests whether you apply an operational definition, move through time-based stages without waiting for imaging, give first- and second-line drugs at trial doses, and know when continuous electroencephalography (cEEG) and anesthetic coma are required.
Operational definition
The International League Against Epilepsy (ILAE) 2015 framework treats SE as failure of the mechanisms that should stop a seizure, or as mechanisms that abnormally prolong one. Two times matter. t1 is when a seizure is already abnormally prolonged and treatment should start. t2 is when long-term consequences—neuronal injury and network reorganization—become likely.
For convulsive (tonic–clonic) SE , t1 is 5 minutes and t2 is 30 minutes . The bedside rule is therefore: 5 or more minutes of continuous convulsive activity, or 2 or more convulsive seizures without recovery of consciousness between them. Do not wait 30 minutes to treat. Thirty minutes is the injury horizon, not the treatment start time.
Focal SE with impaired awareness has a longer t1 (about 10 minutes) and t2 (about 60 minutes). Absence SE is longer still. Those distinctions matter for nonconvulsive syndromes. They do not justify delaying a benzodiazepine while a patient is convulsing in front of you.
Time-based stages
The American Epilepsy Society (AES) 2016 algorithm is the framework most examination items assume. The clock starts at seizure onset , not at hospital arrival. Benzodiazepines should be given as soon as SE is recognized. The 0–5 minute window is stabilization , not an excuse to withhold a benzodiazepine if the patient is already seizing on arrival. Many neurointensive care protocols therefore give the benzodiazepine during those first minutes and have a second antiseizure drug (ASD) infusing by 5–20 minutes if convulsions continue—compressing the AES labels because delayed benzodiazepine therapy is the dominant failure mode.
Clock Stage Priority Typical adult agents
0–5 min Stabilization Airway, oxygen, vital signs, finger-stick glucose, ECG, IV access, time the seizure, send electrolytes, complete blood count, ASD levels, and toxicology. If glucose is under 60 mg/dL, give thiamine 100 mg IV then 50 mL of D50W in adults. Treat hypoglycemia. Do not wait for a CT scan before a benzodiazepine.
5–20 min Initial therapy A benzodiazepine is first-line (AES Level A). Choose one adequate dose . Underdosing is the most common treatment failure. Lorazepam 0.1 mg/kg IV, maximum 4 mg per dose, may repeat once. Midazolam 10 mg IM if weight is over 40 kg (5 mg if 13–40 kg). IV diazepam 0.15–0.2 mg/kg, maximum 10 mg, may repeat once.
20–40 min Second therapy If convulsions continue, give a full loading dose of a second ASD. AES lists fosphenytoin, valproate, and levetiracetam as reasonable; phenobarbital if those are unavailable. See ESETT doses below. Infuse over about 10 minutes as in the trial. Do not trickle a maintenance dose and call it a load.
40–60+ min Third therapy Second-line failure predicts further ASD failure. Repeat a different second-line load or proceed to anesthetic doses with cEEG. Midazolam, propofol, or pentobarbital/thiopental infusions. Ketamine is used for super-refractory SE.
The RAMPART trial (2012) showed that intramuscular midazolam 10 mg was at least as effective as intravenous lorazepam 4 mg in prehospital convulsive SE, because IM injection avoids the delay of obtaining a line. If there is no IV, do not delay for access: give IM midazolam.
Underdosing lorazepam (for example 1–2 mg in a 70 kg adult) is a classic error. 0.1 mg/kg in a 70 kg adult is 7 mg, capped at 4 mg per dose, with a second 4 mg dose permitted—so many adults should receive 4 mg, then another 4 mg if still seizing, not a timid 2 mg. Respiratory depression after a correctly dosed benzodiazepine is more often a consequence of ongoing SE than of the drug; placebo-controlled data in the AES evidence review showed more respiratory problems with untreated convulsions than with benzodiazepines.
ESETT 2019: benzodiazepine-refractory convulsive SE
Once an adequate benzodiazepine has failed, the patient has established SE . The Established Status Epilepticus Treatment Trial (ESETT; Kapur and colleagues, New England Journal of Medicine 2019) randomized children and adults 2 years and older in the emergency department to one of three 10-minute infusions:
- Levetiracetam 60 mg/kg IV, maximum 4500 mg
- Fosphenytoin 20 mg phenytoin equivalents (PE)/kg IV, maximum 1500 mg PE
- Valproate 40 mg/kg IV, maximum 3000 mg
The primary outcome—clinically evident seizure cessation and improving consciousness at 60 minutes without additional ASD—occurred in 47% with levetiracetam, 45% with fosphenytoin, and 46% with valproate. The trial stopped for futility of showing superiority or inferiority. About half of patients still need further therapy. Numerically more hypotension and intubation occurred with fosphenytoin and more deaths with levetiracetam; those differences were not statistically significant. About 10% of enrollments were psychogenic nonepileptic events, a reminder to verify that the event is epileptic.
Choose among the three by contraindication and logistics , not by a belief that one agent is stronger:
Prefer levetiracetam when liver disease, mitochondrial disease, pregnancy, or thrombocytopenia make valproate or fosphenytoin unattractive. Expect psychiatric or behavioral effects later, not hemodynamic collapse during the load.
Prefer fosphenytoin when a sodium-channel agent is desired and the patient is not hypotensive or in high-grade atrioventricular block. Monitor blood pressure and ECG. Infuse no faster than 150 mg PE/min.
Prefer valproate when idiopathic generalized epilepsy is the background (myoclonus, absence) or when a sodium-channel agent recently failed, unless the patient is pregnant, might be pregnant, has mitochondrial disease (especially POLG ), or has liver failure.
Avoid valproate in pregnancy (neural-tube defects and valproate embryopathy), in suspected POLG-related mitochondrial disease (fulminant hepatic failure), and in significant hepatic synthetic failure or active pancreatitis. Carbapenems collapse serum valproate levels—do not add meropenem and expect valproate to hold.
Refractory and super-refractory SE
Refractory status epilepticus (RSE) is SE that continues despite an adequate benzodiazepine plus a correctly dosed second ASD. Roughly one-quarter to one-third of convulsive SE becomes refractory.
Super-refractory status epilepticus (super-RSE) is SE that continues or recurs 24 hours or more after the start of anesthetic therapy , including seizures that return while anesthesia is being weaned. Super-RSE should trigger a hunt for new-onset RSE (NORSE) etiologies: autoimmune encephalitis, occult infection, inborn errors of metabolism, and inflammatory syndromes such as FIRES in younger patients. Immunotherapy is considered when those diagnoses are plausible, not as a default third-line ASD.
Anesthetic coma, cEEG, and weaning
When third-line therapy is anesthesia, intubate, support blood pressure, and place cEEG . Clinical cessation of convulsions does not mean electrographic cessation. After convulsive SE, a substantial minority have nonconvulsive status epilepticus (NCSE) or frequent electrographic seizures. Treat electrographic SE, not only visible shaking.
Common ICU infusions:
Midazolam : high-dose infusion; tachyphylaxis after many hours; an active metabolite accumulates in renal failure.
Propofol : rapid on and off. Watch for propofol infusion syndrome after high dose for a prolonged time, especially in catecholamine-supported patients: unexplained metabolic acidosis, rhabdomyolysis, hyperkalemia, and cardiac failure. Cap prolonged high-dose use.
Pentobarbital or thiopental : effective but long half-life, hypotension, ileus, immunosuppression, and delayed awakening that confounds prognosis.
Ketamine : NMDA antagonism used increasingly in super-RSE; often raises blood pressure (helpful in anesthetic vasodilatation) and increases secretions.
The usual electrographic goal is seizure suppression . Burst-suppression is often targeted with barbiturates but is not proven to improve outcome compared with seizure control without deep suppression. After 24–48 hours of control, wean the anesthetic slowly on cEEG. If seizures recur, resume anesthesia, add or change a maintenance ASD, and re-investigate etiology. Do not extubate a patient who is still in NCSE simply because the motor activity stopped.
Nonconvulsive SE
Suspect NCSE in unexplained coma, fluctuating consciousness after a convulsion, subtle nystagmus or facial twitching, or failure to wake after sedation is lightened. Diagnosis is EEG-based; Salzburg criteria are the research standard. Treatment follows the same ladder. A carefully observed benzodiazepine trial on EEG can be diagnostic as well as therapeutic in selected patients. Do not declare anoxic injury or sedation hangover until NCSE is excluded with EEG.
Post-anoxic myoclonus
Early myoclonus after cardiac arrest is not a single entity and is not , by itself, a reason to withdraw life-sustaining treatment.
Malignant myoclonus or myoclonic status in a still-comatose patient, especially with a highly malignant EEG (suppression, burst-suppression, or identical bursts time-locked to jerks), is associated with poor outcome. Even then, Neurocritical Care Society 2023 neuroprognostication guidance, affirmed by the American Academy of Neurology, requires a multimodal approach. Myoclonus is one data point, not a death sentence, and assessment waits until after rewarming and clearance of sedatives (typically 72 hours or more).
Lance–Adams syndrome is chronic action and intention myoclonus that typically declares itself as consciousness returns, often after a primarily hypoxic (respiratory) arrest. Vertex-predominant spikes on a continuous background, described by Elmer and colleagues, mark a phenotype with a meaningful chance of recovery. These patients may need levetiracetam, valproate, or clonazepam for the myoclonus—not an automatic pentobarbital coma and not early withdrawal.
The examination trap is a vignette of a temperature-managed post-arrest patient with multifocal jerks at hour 12. The correct move is cEEG, continued temperature control in the 32–37.5 °C range, and delayed multimodal prognosis—not myoclonus equals no chance.
Examination traps
Giving 2 mg of lorazepam and calling benzodiazepines a failure.
Starting fosphenytoin before any benzodiazepine.
Combining tiny doses of three ASDs instead of one full load.
Using valproate in a woman who might be pregnant, or in unexplained liver failure.
Stopping the workup after a CT: missed meningitis, autoimmune encephalitis, and ASD nonadherence still need a search.
Treating all post-arrest myoclonus as super-RSE or as certain poor outcome.