Nonconvulsive Status Epilepticus
Nonconvulsive status epilepticus (NCSE) is a prolonged seizure state in which continuous or near-continuous electrographic seizure activity occurs without prominent motor convulsions. It is frequently missed, particularly in elderly patients and those without a prior seizure history, and a delayed or missed diagnosis is independently associated with an odds ratio of 3.83 for failure to return to functional baseline. NCSE encompasses a broad spectrum of presentations — from ambulatory patients with subtle confusion to comatose ICU patients with only electrographic seizure activity — and the aggressiveness of treatment must be calibrated to the clinical context and underlying etiology.
Bottom Line
- Definition: Continuous absence, focal sensory, or focal impaired awareness seizures lasting ≥10 minutes (time point t1 for NCSE), or recurrent seizures without return to baseline awareness
- Prevalence: In the SENSE registry, NCSE (592 patients) outnumbered CSE (457 patients); cEEG monitoring detects NCSE in 8–37% of patients with unexplained coma
- Diagnosis: Requires EEG; the Salzburg EEG criteria provide a structured, validated diagnostic framework with high sensitivity and specificity
- Diagnostic delay: Median latency to first treatment is 150 minutes for NCSE vs. 30 minutes for CSE; clinical suspicion and urgent EEG are essential
- Treatment: No guideline-driven protocol; individualized approach based on etiology, seizure type, patient condition, and EEG patterns
- Mortality: Overall 18–19% in-hospital mortality in the SENSE registry; mortality correlates with acute medical etiology and severe mental status impairment, not the type of EEG discharge
Definition and Classification
NCSE is defined by the ILAE as status epilepticus without prominent motor symptoms. It is classified along the same four axes as convulsive SE (semiology, etiology, EEG, and age) but is distinguished by the absence of overt tonic-clonic activity. For NCSE, time point t1 (the duration after which the seizure should be considered continuous) is 10 minutes, though this is less firmly established than the 5-minute threshold for convulsive SE.
Types of Nonconvulsive Status Epilepticus
| Type | Clinical Presentation | EEG Pattern | Typical Setting | Prognosis |
|---|---|---|---|---|
| Absence SE | Prolonged confusional state with varying degrees of responsiveness; subtle eyelid fluttering or myoclonic jerks may be present; patients may walk, respond partially, and perform simple tasks | Generalized 2–4 Hz spike-and-wave discharges, often waxing and waning | Ambulatory patients with idiopathic generalized epilepsy (IGE); may be triggered by ASM withdrawal or sleep deprivation | Generally favorable; responds well to IV benzodiazepines; minimal long-term sequelae |
| Focal NCSE with impaired awareness | Confusion, behavioral changes, aphasia, automatisms, psychomotor slowing; may mimic psychiatric disorder, delirium, or stroke | Focal rhythmic or periodic discharges, often temporal or frontotemporal, evolving in frequency and morphology | Patients with known focal epilepsy; also acute presentations (stroke, encephalitis, tumor) | Variable; depends on etiology; more refractory than absence SE |
| Focal NCSE with preserved awareness | Persistent focal symptoms (sensory, visual, olfactory auras, dyscognitive phenomena) without alteration of consciousness | Focal discharges corresponding to symptomatology | Ambulatory patients; often overlooked or dismissed | Good; usually not immediately dangerous but indicates ongoing seizure activity |
| NCSE in coma (NCSE-coma) | Comatose or obtunded patient with no overt clinical seizure activity; may have subtle motor signs (nystagmoid eye movements, facial twitching, finger movements) | Continuous or near-continuous electrographic seizure activity or periodic discharges on cEEG | ICU: post-cardiac arrest, after convulsive SE, acute brain injury, septic encephalopathy, metabolic coma | Worst prognosis of all NCSE types; STESS score of 2 for this category alone; mortality >30% |
Clinical Presentation and Recognition
The clinical manifestations of NCSE are protean and frequently mimic other neurologic and psychiatric conditions. This diagnostic challenge is the fundamental reason NCSE is so commonly missed.
Common Presentations
- Altered mental status or confusion: The most common presentation; may range from subtle inattention and psychomotor slowing to complete unresponsiveness
- Behavioral changes: Agitation, aggression, inappropriate laughter or crying, catatonia-like states, personality changes
- Speech and language disturbance: Aphasia (global, Broca, or Wernicke type), mutism, paraphasic errors, forced speech
- Subtle motor signs: Nystagmoid eye movements, facial twitching, perioral automatisms, eye blinking, subtle rhythmic limb movements, hippus
- Autonomic features: Salivation, urinary incontinence, blood pressure fluctuations
- Psychogenic features (mimic): Derealization, visual hallucinations, déjà vu, amnesia — may lead to misdiagnosis as psychiatric disorder
When to Suspect NCSE
- Unexplained prolonged confusion in any patient, especially after a witnessed convulsive seizure or in the setting of acute brain injury
- "Postictal" state lasting >30–60 minutes after a generalized tonic-clonic seizure — the patient may be in NCSE rather than truly postictal
- Fluctuating mental status in a critically ill patient not explained by metabolic derangements, medications, or structural lesions
- Acute aphasia or confusion with negative CT/MRI and no clear vascular etiology — NCSE can mimic stroke
- Comatose patient with subtle rhythmic movements (eye deviation, facial twitching, nystagmus) or unexplained failure to awaken
- Elderly patient with new confusion — NCSE is frequently missed in this population; age is independently associated with failure to receive benzodiazepines
- Any patient with known epilepsy presenting with prolonged atypical confusion or behavioral change
- Clinical rule: If in doubt, order an urgent EEG
Diagnosis: EEG and the Salzburg Criteria
The diagnosis of NCSE ultimately depends on electroencephalography. While the clinical picture may raise suspicion, EEG confirmation is essential because no clinical feature alone is sufficiently sensitive or specific. The Salzburg EEG Criteria for NCSE, developed in 2013 and validated in subsequent studies, represent the most widely used and rigorously evaluated diagnostic framework.
Salzburg EEG Criteria for Nonconvulsive Status Epilepticus
To qualify for a diagnosis of NCSE, the EEG abnormalities must be continuously present for at least 10 seconds. The criteria employ a stepwise decision algorithm:
| Step | Criterion | Outcome |
|---|---|---|
| 1 | Epileptiform discharges (EDs) at >2.5 Hz | NCSE |
| 2 | EDs at ≤2.5 Hz OR rhythmic delta/theta activity at >0.5 Hz | Proceed to Step 3 |
| 3 | Plus one of the following secondary criteria:
|
If any secondary criterion is met: NCSE If no secondary criterion is met: Possible NCSE |
| Special | Patients with known epileptic encephalopathy must fulfill additional criteria: increase in prominence or frequency compared with baseline AND observable clinical change OR improvement with IV ASM | Prevents over-diagnosis in patients with baseline abnormal EEGs |
Diagnostic Performance of Salzburg Criteria
- Validation studies demonstrate high sensitivity (97.7%) and specificity (95.9%) for the diagnosis of NCSE
- A 2024 study found moderate interrater agreement (Kappa = 0.55) in applying the Salzburg criteria, highlighting the need for expertise in interpretation
- The criteria are designed to be applied systematically, reducing subjectivity in EEG interpretation
- The "possible NCSE" category is clinically important — it should prompt a cautious IV ASM trial and continued monitoring rather than being dismissed
- The prognostic value has been formalized in the SACE (Salzburg Assessment for Classification and Evaluation) score (2024), which integrates Salzburg criteria with clinical variables for outcome prediction
The IV ASM Trial (Benzodiazepine Trial)
When the EEG shows patterns that are suspicious but not definitively ictal, a diagnostic IV benzodiazepine trial can help distinguish NCSE from non-ictal periodic or rhythmic patterns:
- Protocol: Administer sequential small doses of a short-acting benzodiazepine (e.g., lorazepam 0.5–1 mg IV or midazolam 1–2 mg IV) under continuous EEG monitoring with concurrent clinical assessment
- Positive response: Both EEG improvement (resolution or persistent reduction of the epileptiform pattern) AND clinical improvement (improved responsiveness, cessation of subtle motor signs)
- Important caveat: EEG improvement alone without clinical improvement does not confirm NCSE — benzodiazepines can suppress non-ictal periodic patterns and may simply sedate the patient
- False negatives: Chronically refractory NCSE may not respond to benzodiazepines due to GABAA receptor downregulation
Continuous EEG Monitoring in the ICU
Continuous EEG (cEEG) monitoring has become a cornerstone of neurologic critical care. The American Clinical Neurophysiology Society (ACNS) and the Neurocritical Care Society recommend cEEG monitoring for multiple indications.
Indications for cEEG Monitoring
- Unexplained alteration of consciousness in a critically ill patient
- Post-convulsive SE — to detect ongoing electrographic seizures or NCSE after clinical convulsions have stopped
- After acute brain injury (stroke, TBI, subarachnoid hemorrhage, hypoxic-ischemic encephalopathy)
- Monitoring during and after anesthetic infusions for refractory SE (titration to burst suppression, detection of seizure recurrence during weaning)
- Paroxysmal events of uncertain etiology in an ICU patient
- Assessment of level of sedation and detection of subclinical seizures in patients receiving neuromuscular blockade
Duration and Yield of cEEG Monitoring
| Patient Population | Seizure Detection Rate | Recommended Duration | Notes |
|---|---|---|---|
| Unexplained coma (medical ICU) | 8–37% | ≥24 hours; 48 hours if high suspicion | Over 90% of patients with seizures will have their first seizure detected within 24 hours of monitoring |
| Post-convulsive SE | 14–48% have ongoing NCSE | ≥24 hours after clinical seizure cessation | Critical to confirm that clinical seizure cessation corresponds to electrographic seizure cessation |
| Acute brain injury (stroke, TBI, SAH) | 10–30% | 24–48 hours | Seizures correlate with secondary brain injury and worse outcomes |
| Post-cardiac arrest | 10–35% | ≥24 hours; may extend to 72 hours | EEG also used for prognostication; postanoxic SE carries very poor prognosis |
| Refractory SE on anesthetic infusion | Continuous monitoring required | Throughout infusion + 24–48 hours after weaning | Target: burst suppression (interburst intervals 5–15 seconds); detect breakthrough seizures |
The Diagnostic Dilemma: EEG Patterns of Uncertain Significance
Not all periodic or rhythmic EEG patterns in critically ill patients represent NCSE. The ACNS 2021 Critical Care EEG Terminology provides a standardized nomenclature for these patterns, which fall on a continuum between interictal activity and definite seizures. This "ictal-interictal continuum" represents one of the greatest diagnostic and therapeutic challenges in neurocritical care.
Key Patterns on the Ictal-Interictal Continuum
| Pattern | Description | Clinical Significance | Treatment Approach |
|---|---|---|---|
| LPDs (Lateralized Periodic Discharges) | Periodic sharp waves or complexes arising from one hemisphere at 0.5–3 Hz; formerly PLEDs | Associated with acute structural lesions (stroke, herpes encephalitis), seizures in 40–60% of cases; may represent NCSE if plus-features present | Low threshold for treatment if associated with clinical change; consider cautious IV ASM trial |
| GPDs (Generalized Periodic Discharges) | Bilaterally synchronous periodic discharges at 0.5–3 Hz; includes triphasic waves | Most commonly metabolic (hepatic encephalopathy, uremia) or post-anoxic; may also represent NCSE | Treat underlying cause first; IV ASM trial if clinical doubt; triphasic waves from hepatic encephalopathy typically resolve with metabolic correction |
| LRDA (Lateralized Rhythmic Delta Activity) | Rhythmic delta activity >0.5 Hz from one hemisphere | High risk of acute seizures (>60%); often considered "pre-ictal" or on the ictal side of the continuum | Strong consideration for ASM treatment; close monitoring |
| GRDA (Generalized Rhythmic Delta Activity) | Bilateral synchronous rhythmic delta activity; includes FIRDA | Usually non-ictal; associated with diffuse encephalopathy | Typically does not require ASM treatment; address underlying encephalopathy |
| "Plus" features | Superimposed fast activity ("+F") or superimposed rhythmic/sharp activity ("+R", "+S") on any of the above patterns | Moves the pattern toward the ictal end of the continuum; increases the probability that the pattern represents NCSE | Lower threshold for treatment |
Practical Approach to the Ictal-Interictal Continuum
- Context is everything: The same EEG pattern may warrant aggressive treatment in one clinical scenario and observation in another
- Apply Salzburg criteria: If the pattern meets criteria for NCSE (either definite or possible), treatment is warranted
- Consider the IV ASM trial: For "possible NCSE," a structured benzodiazepine trial with concurrent EEG monitoring and clinical assessment can clarify the diagnosis
- Weigh risks vs. benefits: In a young patient with a treatable etiology (autoimmune encephalitis, infection), err on the side of treatment. In an elderly patient with severe anoxic injury, aggressive treatment of periodic patterns is unlikely to improve outcome and may cause harm
- Treat the patient, not the EEG: EEG-guided therapy should always be interpreted in the full clinical context. Suppressing an EEG pattern with sedating medications without clinical improvement is not a therapeutic success
- Multidisciplinary input: These decisions benefit from collaboration between epileptologists, neurointensivists, and the primary team
Treatment of NCSE
Unlike convulsive SE, which follows a relatively standardized treatment algorithm, the management of NCSE is not driven by consensus guidelines. Instead, it is individualized based on the clinical scenario, NCSE subtype, underlying etiology, and the patient's overall condition and goals of care.
General Principles
- Treat the underlying cause: Identify and correct metabolic derangements, infections, medication toxicity, and structural lesions. In many cases, NCSE will resolve once the precipitant is treated.
- Benzodiazepines remain first-line: IV lorazepam or midazolam at standard SE doses should be administered for established NCSE, though response rates are lower than in CSE.
- Non-sedating IV ASMs: Fosphenytoin, valproate, levetiracetam, and lacosamide are used as second-line agents, following the same general principles as CSE treatment.
- Calibrate aggressiveness to clinical context: The aggressiveness of treatment should be proportional to the potential for harm from ongoing seizure activity versus the potential for harm from aggressive pharmacotherapy.
Treatment Stratification by NCSE Subtype
| NCSE Type | Treatment Aggressiveness | Rationale | Approach |
|---|---|---|---|
| Absence SE | Moderate | Generally responds well to benzodiazepines; minimal long-term neuronal injury from absence seizures | IV benzodiazepine (often curative); if recurrent, load valproate or optimize IGE therapy |
| Focal NCSE with preserved awareness | Low to moderate | Patient is conscious and communicative; risk of neuronal injury is lower than in convulsive SE | Non-sedating ASMs; avoid anesthetic infusions; optimize chronic ASM regimen; address triggers |
| Focal NCSE with impaired awareness | Moderate to high | Impaired awareness indicates significant cortical dysfunction; potential for hippocampal injury with prolonged temporal lobe SE | Benzodiazepines → non-sedating IV ASMs → consider anesthetic infusion if refractory and etiology is treatable |
| NCSE in coma (treatable etiology) | High | Ongoing electrographic seizures compound primary brain injury; treatment of seizures may unmask recoverable function | Aggressive protocol mirroring CSE: benzodiazepines → non-sedating IV ASMs → anesthetic infusion; concurrent treatment of underlying cause |
| NCSE in coma (post-anoxic) | Low (palliative) | Post-anoxic NCSE is highly refractory and carries a dismal prognosis regardless of treatment; excluded from most SE treatment trials | Non-sedating ASMs for symptom management; anesthetic infusions rarely change outcome; goals-of-care discussion essential |
Aggressive vs. Conservative Treatment: Navigating the Controversy
- The argument for aggressive treatment: Ongoing electrographic seizures cause excitotoxic neuronal injury; animal models demonstrate hippocampal damage from prolonged NCSE; human studies show worse outcomes with missed or delayed NCSE diagnosis
- The argument for conservative treatment: In critically ill patients with severe underlying conditions (anoxia, widely metastatic cancer, advanced dementia), aggressive SE treatment with anesthetic infusions may prolong dying without improving functional outcome; anesthetics themselves carry significant morbidity (hypotension, infections, prolonged ICU stays)
- Resolution: The decision must be individualized. The key question is: "If I successfully stop the electrographic seizures, does this patient have a realistic chance of meaningful neurologic recovery?"
- Post-anoxic periodic discharges: The TELSTAR trial (2023) randomized post-cardiac arrest patients with periodic or rhythmic patterns to aggressive step-up ASM treatment vs. no treatment; there was no difference in neurologic outcome, supporting a conservative approach in this specific population
NCSE Epidemiology and Outcomes
Data from the SENSE Registry
The SENSE (Sustained Effort Network for Treatment of Status Epilepticus) clinical registry provides the most comprehensive real-world data on NCSE treatment and outcomes:
- Of 1,049 patients, 592 (56.4%) had NCSE (including NCSE in coma, focal aware SE, focal unaware SE, and absence SE)
- Median age of NCSE patients was 72 years (older than CSE patients)
- Baseline modified Rankin Score of 0–2 was present in only 45% of NCSE patients
- STESS score ≤2 in 55% of NCSE patients
- In-hospital mortality was 19%
- Treatment delays were profound: Median latency from SE onset to first-line treatment was 150 minutes for NCSE vs. 30 minutes for CSE
- Benzodiazepine dosing was suboptimal in 78% of NCSE patients
- Underdosing was even more pronounced in patients who went on to develop refractory NCSE, suggesting that refractoriness was partly iatrogenic
- Factors associated with shorter time to SE cessation: lower STESS score, fewer comorbidities, benzodiazepine use as first-line, and higher cumulative standard ASM doses within the first hour
Mortality Predictors in NCSE
A US study of 100 consecutive patients with NCSE found an 18% mortality rate. Mortality was associated with:
- NCSE due to an acute medical cause (strongest predictor)
- Severe mental status impairment at presentation
- Development of acute systemic complications during hospitalization
- Notably, the type of EEG ictal discharge pattern was not associated with mortality
Key Differences Between CSE and NCSE Management
- Urgency of treatment: While CSE demands immediate, protocolized intervention to prevent neuronal death, NCSE allows a more measured approach in many subtypes, particularly absence SE and focal SE with preserved awareness
- Diagnostic confirmation required: CSE is a clinical diagnosis; NCSE requires EEG confirmation
- Treatment targets differ: In CSE, the goal is complete seizure cessation. In NCSE, the goal may be clinical improvement rather than complete electrographic seizure resolution, particularly in comatose patients with uncertain prognosis
- Anesthetic infusions carry higher risk-to-benefit ratio in NCSE: Given the lack of evidence that aggressive pharmacologic suppression of NCSE improves outcomes in many subtypes, the morbidity of anesthetic coma must be weighed more carefully
- Treatment of the underlying cause is paramount: In NCSE, correcting the precipitant (metabolic, infectious, medication-related) may resolve seizures without the need for aggressive ASM escalation
Special Scenarios
NCSE After Convulsive SE ("Subtle SE")
After prolonged convulsive SE, the overt motor manifestations may fade while electrographic seizure activity persists. This "subtle SE" or electrographic SE occurs in 14–48% of patients after clinical cessation of convulsions. Continuous EEG monitoring after CSE is essential to detect this phenomenon, which carries the same neuronal injury risk as ongoing convulsive seizures.
NCSE Mimicking Stroke
Focal NCSE can present with acute focal neurologic deficits (hemiparesis, aphasia, hemianopia, neglect) that are clinically indistinguishable from stroke. This "epileptic pseudostroke" accounts for approximately 1–3% of cases initially diagnosed as stroke. EEG should be considered in patients with acute focal deficits and negative or discordant vascular imaging.
NCSE in the Elderly
NCSE has a predilection for elderly patients, often presenting as new-onset confusion without a prior seizure history. In the SENSE registry, the median age of NCSE patients was 72 years. Swiss investigators found that increasing age was an independent predictor for not receiving benzodiazepines and that a missed NCSE diagnosis was associated with poor functional outcomes (OR 3.83). Clinicians should have a low threshold for ordering EEG in elderly patients with unexplained confusion.
De Novo Absence SE of Late Onset
A well-recognized entity in elderly patients is de novo absence SE occurring without a prior history of IGE. It is often precipitated by benzodiazepine or barbiturate withdrawal, psychotropic medications, or metabolic disturbances. It presents as a prolonged confusional state and is usually rapidly responsive to IV benzodiazepines. The key diagnostic clue is generalized spike-and-wave discharges on EEG in a patient without prior seizure history.
EEG Monitoring: Practical Considerations
ACNS Critical Care EEG Terminology (2021)
The ACNS standardized nomenclature provides a structured framework for describing and communicating EEG findings in critically ill patients. Key terms relevant to NCSE diagnosis include:
- Main Term 1 — Location: Generalized (G), lateralized (L), bilateral independent (BI), multifocal (Mf)
- Main Term 2 — Pattern type: Periodic discharges (PDs), rhythmic delta activity (RDA), spike-and-wave or sharp-and-wave
- Modifiers: Prevalence, frequency, number of phases, sharpness, amplitude, polarity
- "Plus" features: +F (fast activity), +R (rhythmic), +S (sharp or spike), +FR, +FS
- Electrographic seizure: Evolving pattern lasting ≥10 seconds with definite evolution in frequency, morphology, or spatial distribution
Quantitative EEG (qEEG) Trends
Quantitative EEG provides color-coded compressed spectral arrays and other trend displays that allow rapid screening of hours of cEEG data. While not a substitute for expert raw EEG review, qEEG trends assist in:
- Early detection of seizure onset during overnight monitoring
- Assessment of seizure burden over time
- Monitoring the response to treatment changes
- Facilitating communication between neurology and ICU teams
Outcomes and Prognostication
Outcomes in NCSE are highly dependent on the underlying etiology rather than NCSE per se. In the SENSE registry, 54.7% of all SE patients (both CSE and NCSE) progressed to refractory SE; among those with refractory SE, 52.7% ultimately had good outcomes (mRS 0–2 or unchanged from baseline), which correlated with lower STESS score, lack of intubation, adequate first-phase benzodiazepine dose, absence of acute etiology, and shorter SE duration.
Prognostic Factors
| Factor | Favorable | Unfavorable |
|---|---|---|
| Etiology | ASM non-adherence, absence SE, reversible metabolic cause | Anoxic brain injury, acute stroke, CNS infection, malignancy |
| NCSE type | Absence SE, focal aware SE | NCSE in coma (STESS score 2 for this category alone) |
| Age | <65 years | ≥65 years (STESS score 2) |
| STESS | 0–2 | ≥3 |
| Treatment | Adequate first-line benzodiazepine dosing, short time to treatment, seizure cessation within 12 hours | Delayed diagnosis, subtherapeutic ASM dosing, progression to refractory SE |
| MRI | No peri-ictal MRI abnormalities | Peri-ictal DWI/FLAIR abnormalities (cortical, thalamic, hippocampal) |
| Duration | Short (<24 hours) | Prolonged; longer duration associated with worse outcomes regardless of treatment |
References
- Trinka E, Cock H, Hesdorffer D, et al. A definition and classification of status epilepticus — report of the ILAE Task Force on Classification of Status Epilepticus. Epilepsia. 2015;56(10):1515-1523.
- Leitinger M, Beniczky S, Rohracher A, et al. Salzburg Consensus Criteria for Non-Convulsive Status Epilepticus — approach to clinical application. Epilepsy Behav. 2015;49:158-163.
- Leitinger M, Trinka E, Gardella E, et al. Diagnostic accuracy of the Salzburg EEG criteria for non-convulsive status epilepticus: a retrospective study. Lancet Neurol. 2016;15(10):1054-1062.
- Hirsch LJ, Fong MWK, Leitinger M, et al. American Clinical Neurophysiology Society's Standardized Critical Care EEG Terminology: 2021 Version. J Clin Neurophysiol. 2021;38(1):1-29.
- Glauser T, Shinnar S, Gloss D, et al. Evidence-based guideline: treatment of convulsive status epilepticus in children and adults. Epilepsy Curr. 2016;16(1):48-61.
- Vossler DG. First seizures, acute repetitive seizures, and status epilepticus. Continuum (Minneap Minn). 2025;31(1, Epilepsy):93-128.
- Ruijter BJ, Keijzer HM, Tjepkema-Cloostermans MC, et al. Treating rhythmic and periodic EEG patterns in comatose survivors of cardiac arrest (TELSTAR). N Engl J Med. 2023;388(10):906-916.
- Sutter R, Semmlack S, Kaplan PW. Nonconvulsive status epilepticus in adults — insights into the invisible. Nat Rev Neurol. 2016;12(5):281-293.
- Misirocchi F, Vandelli L, Bedin R, et al. Prognostic value of Salzburg nonconvulsive status epilepticus criteria: the SACE score. Epilepsia. 2024;65(4):922-933.
- Rossetti AO, Lowenstein DH. Management of refractory status epilepticus in adults: still more questions than answers. Lancet Neurol. 2011;10(10):922-930.
- Foreman B, Claassen J, Abou Khaled K, et al. Generalized periodic discharges in the critically ill: a case-control study of 200 patients. Neurology. 2012;79(19):1951-1960.
- DeLorenzo RJ, Waterhouse EJ, Towne AR, et al. Persistent nonconvulsive status epilepticus after the control of convulsive status epilepticus. Epilepsia. 1998;39(8):833-840.
- Vignatelli L, Rinaldi R, Gallo C, et al. Clinical practice guidelines on the management of status epilepticus in adults: a systematic review. Epilepsia. 2024;65(4):894-912.
- Gómez Domínguez A, Mateo Montero RC, Díaz Cid A, et al. Salzburg Criteria, a useful tool in non-convulsive status epilepticus diagnosis: a retrospective study. Clin EEG Neurosci. 2021;52(4):280-287.
- Kaplan PW. Nonconvulsive status epilepticus in the emergency room. Epilepsia. 1996;37(7):643-650.