On this page
Quick Reference
Overview and Recommendations
Background
- •Define status epilepticus (SE) using the two-timepoint framework: Timepoint 1 (t1) is 5 minutes of continuous activity, indicating the seizure is unlikely to self-terminate; Timepoint 2 (t2) is 30 minutes, indicating a high risk of long-term neuronal injury.
- •Recognize the receptor trafficking hypothesis, which explains why SE becomes pharmacoresistant: prolonged seizures cause the internalization (endocytosis) of synaptic GABA-A receptors and the increased surface expression of excitatory NMDA and AMPA receptors.
- •Distinguish between the two physiological stages of SE: Stage 1 (Compensated) involves massive autonomic discharge with , tachycardia, and hyperglycemia; Stage 2 (Uncompensated) involves hemodynamic collapse, hypotension, hyperkalemia, and metabolic (lactic) acidosis.
- •Identify common etiologies including medication non-compliance, acute structural brain injury (stroke, hemorrhage, trauma), metabolic derangements, and .
- •Understand the concept of (NORSE), a clinical construct describing a previously healthy patient presenting with refractory SE without an obvious acute cause, often requiring an aggressive workup for autoimmune or paraneoplastic triggers.
Evaluation
- •Suspect SE in any patient presenting with rhythmic motor activity, fluctuating mental status, or persistent coma following a witnessed seizure.
- •Obtain a fingerstick glucose immediately upon arrival to rule out hypoglycemia, which is a rapidly reversible cause of status-like activity.
- •Time the seizure activity from the moment of onset or arrival; clinical protocols for first-line therapy must be activated at the 5-minute mark.
- •Examine the patient for signs of "subtle" status epilepticus, such as nystagmus, rhythmic eye blinking, or small-amplitude twitching of the face or extremities, which may persist after overt convulsions cease.
- •Order emergent laboratory studies including a comprehensive metabolic panel (to check for hyponatremia or hypocalcemia), toxicology screen, and serum levels of known antiseizure medications (ASMs).
- •Perform a pregnancy test in all women of reproductive age to guide ASM selection and screen for , which requires different management (magnesium sulfate).
- •Obtain a non-contrast CT as soon as the patient is stabilized to rule out intracranial hemorrhage, large masses, or acute hydrocephalus.
- •Order an emergent (EEG) within 30–60 minutes if the patient does not regain consciousness after motor seizures stop to rule out nonconvulsive status epilepticus (NCSE).
- •Utilize point-of-care EEG (pocEEG) in the emergency department for rapid screening if full continuous EEG (cEEG) is not immediately available.
- •Consider a lumbar puncture for cerebrospinal fluid (CSF) analysis if there is clinical suspicion of meningitis, encephalitis, or if the patient has a fever of unknown origin.
- •Calculate the STESS (Status Epilepticus Severity Score) or EMSE (Etiology, Age, Comorbidities, EEG) score to assist in prognostic stratification and mortality risk assessment.
- •Look for specific MRI findings such as Crossed Cerebellar Diaschisis (CCD)—reversible hyperintensity in the contralateral cerebellum—which indicates high metabolic demand from a supratentorial seizure focus.
Management
- •Administer first-line benzodiazepines immediately at the 5-minute mark: IV Lorazepam 4 mg (may repeat once) or IM Midazolam 10 mg for patients weighing >40 kg.
- •Initiate second-line non-sedating intravenous ASMs if seizures persist after the first benzodiazepine dose: IV Levetiracetam 60 mg/kg (maximum 4500 mg) is often preferred for its safety profile.
- •Consider alternative second-line agents: IV Fosphenytoin 20 mg PE/kg (maximum 1500 mg PE) or IV Valproate 40 mg/kg (maximum 3000 mg).
- •Avoid IV Valproate in pregnant patients due to high teratogenic risk unless all other options have failed.
- •Escalate to Refractory Status Epilepticus (RSE) management if seizures continue despite one benzodiazepine and one appropriately dosed second-line ASM.
- •Induce anesthesia for RSE using IV Midazolam: 0.2 mg/kg bolus followed by a continuous infusion of 0.05–2.0 mg/kg/hr.
- •Utilize IV Propofol as an alternative anesthetic: 1–2 mg/kg bolus followed by 20–100 μg/kg/min; monitor closely for Propofol-Related Infusion Syndrome (PRIS) characterized by metabolic acidosis and bradycardia.
- •Incorporate NMDA antagonism for super-refractory cases: IV Ketamine 1–2 mg/kg bolus followed by 1–5 mg/kg/hr infusion.
- •Maintain continuous EEG (cEEG) monitoring to guide anesthetic titration; the goal is typically the cessation of electrographic seizures or a burst-suppression pattern.
- •Administer Magnesium Sulfate 4–6 g IV loading dose followed by 1–2 g/hr infusion if the patient is pregnant and eclampsia is suspected.
- •Monitor for systemic complications including , acute kidney injury, and neurogenic pulmonary edema.
- •Avoid underdosing in elderly patients; while they are more sensitive to side effects, subtherapeutic dosing is a primary cause of treatment failure.
- •Consult neurocritical care early for patients requiring anesthetic infusions or those with suspected NORSE.
- •Initiate gradual weaning of anesthetics only after at least 24 hours of electrographic seizure control to prevent rebound status epilepticus.
- •Consider adjunctive Tocilizumab 8 mg/kg IV (max 800 mg) in cases of refractory SE with a suspected autoimmune or neuroinflammatory component.
- •Refer for surgical evaluation or (VNS) in cases of super-refractory SE that fail all pharmacological interventions.
Board Review — High Yield
- •GABA-A Internalization — The primary molecular mechanism for benzodiazepine resistance in prolonged SE.
- •T1 vs T2 — T1 (5 min) is when to start treatment; T2 (30 min) is when permanent damage begins.
- •Crossed Cerebellar Diaschisis — A reversible MRI finding in SE showing contralateral cerebellar hyperintensity.
- •Propofol-Related Infusion Syndrome (PRIS) — Metabolic acidosis, rhabdomyolysis, and cardiac failure during high-dose propofol use.
- •Eclampsia Treatment — Magnesium sulfate is the drug of choice, not standard antiseizure medications.
- •Subtle Status — The transition from convulsive SE to electrographic SE with minimal motor movements.
- •Ketamine Mechanism — Non-competitive NMDA receptor antagonist used for refractory SE when GABAergic drugs fail.
- •NORSE — New-onset refractory status epilepticus in a healthy person, often autoimmune.
Deep Dive — Evidence Details
Pathophysiology and Mechanisms of Neuronal Injury
- ▸SE becomes self-sustaining through progressive loss of GABA_A-mediated inhibition and increased synaptic/extrasynaptic NMDA and AMPA receptor activity. [3][5][17]
- ▸Excessive glutamatergic signaling causes calcium overload, mitochondrial depolarization, oxidative stress, and excitotoxic neuronal injury. [3][113]
- ▸GluN2B-containing NMDA receptors, BDNF-TrkB signaling, and P2X7 purinergic signaling are experimentally implicated in SE-associated hyperexcitability and injury. [12][18]
- ▸p53/Puma-dependent apoptosis and region-specific ubiquitin–proteasome responses contribute to neuronal injury, but reducing acute neuronal death does not necessarily prevent prolonged seizures or epileptogenesis. [19][110][14][6]
- ▸Neuronal injury is regionally heterogeneous and is influenced by excitotoxic burden, neurovascular coupling, spreading depolarization, inflammation, blood–brain barrier disruption, and systemic complications. [7][1][111][113][2]
Overview
Status epilepticus (SE) is defined clinically as a seizure lasting more than 5 minutes or recurrent seizures without complete recovery of consciousness between events. [3]D The transition from a self-limited seizure to self-sustaining SE reflects failure of seizure-termination mechanisms and progressive molecular, cellular, metabolic, and systemic injury. [3]D[5]D[2]D Although seizure termination is itself the simplest neuroprotective intervention, preservation of neuronal function and network integrity is a broader objective than preventing neuronal death alone; preventing cell loss does not necessarily prevent epileptogenesis. [6]D
Failure of inhibition and maladaptive receptor trafficking
A central mechanism is progressive impairment of γ-aminobutyric acid type A (GABA_A)-mediated inhibition. During experimental SE, GABA_A receptors are internalized, reducing the effectiveness of endogenous inhibition and of benzodiazepines. [5]D[3]D At the same time, glutamatergic receptors, particularly NMDA and AMPA receptors, are transported toward or accumulated at the synaptic membrane, increasing excitatory transmission and helping sustain seizure activity. [3]D Experimental models demonstrate increased surface expression of NMDA receptor NR1 subunits and increased synaptic and extrasynaptic NMDA currents in dentate granule cells during SE. [17]D
These changes help explain why benzodiazepine responsiveness declines as seizure duration increases, whereas NMDA-receptor antagonism may retain efficacy in experimental SE. [5]D In prolonged convulsive SE, GABA signaling may become functionally excitatory, and benzodiazepine resistance increases with time; this has prompted the proposed concept of “Stage 1 plus,” in which combined therapy rather than benzodiazepine monotherapy may be required from the outset. [4]D Evidence from immature rats also indicates that SE can modify the subsequent anticonvulsant effects of ifenprodil, an antagonist preferential for NMDA receptors containing the NR2B/GluN2B subunit, demonstrating age- and time-dependent changes in NMDA-receptor pharmacology. [13]D
Excitotoxicity, calcium overload, and mitochondrial injury
Increased glutamatergic drive produces excessive NMDA- and AMPA-receptor activation, with substantial calcium influx and elevation of intracellular calcium. [3]D[5]D Calcium loading can exceed mitochondrial buffering capacity, causing mitochondrial membrane depolarization and mitochondrial injury. [3]D The resulting energetic failure and oxidative stress amplify neuronal dysfunction and injury. [3]D Experimental observations support a role for reactive oxygen species, glutamate, inflammatory cytokines, and related tissue-injuring molecules in the post-SE microenvironment. [113]D
BDNF-TrkB signaling also contributes to seizure-related hyperexcitability and synaptic plasticity. Recent experimental work specifically implicates synaptic accumulation of GluN2B-containing NMDA receptors as a mediator of BDNF-dependent changes in hippocampal glutamatergic synapses during SE. [12]D ATP-dependent purinergic signaling may further promote injury: SE selectively increases hippocampal P2X7-receptor expression, with dentate granule neurons identified as a major transcriptional source in mice; targeting P2X7 reduced seizures and provided neuroprotection in that model. [18]D
Cell-death pathways and intracellular stress responses
SE activates programmed neuronal-death pathways. In mice, intra-amygdala kainate-induced SE produces rapid p53 accumulation, followed by increased expression of the p53-regulated proapoptotic protein Puma and hippocampal injury; pharmacological inhibition of p53 or genetic loss of Puma reduces hippocampal damage. [110]D However, p53 deficiency also causes more prolonged electrographic seizures and an aggravated chronic epileptic phenotype despite reduced acute neuronal death, illustrating that neuronal death, seizure duration, and epileptogenesis are related but nonidentical processes. [19]D
The ubiquitin–proteasome system, which regulates degradation of proteins involved in survival, synaptic plasticity, and neurotransmitter signaling, is altered after SE in a region- and cell-specific manner. [14]D The spatiotemporal pattern of proteasome inhibition after SE may represent a protective adaptation against hippocampal injury rather than uniformly harmful dysfunction. [14]D Endogenous signaling pathways can likewise have opposing effects: ERK1/2 activation may be neuroprotective or may promote neuronal death depending on the timing and pattern of activation. [6]D
Neuroinflammation, network remodeling, and regional vulnerability
Experimental SE produces neuronal death in the hippocampus, amygdala, piriform cortex, and entorhinal cortex, while microglial activation extends across broader limbic regions. [111]D SE-associated inflammation, blood–brain barrier leakage, altered cell genesis, and subsequent spontaneous recurrent seizures have been documented in experimental models. [113]D Aberrant neurogenesis, gliogenesis, and inflammation are implicated in epileptogenesis, and post-SE changes extend beyond the hippocampus to extrahippocampal regions. [111]D Altered corticostriatal synaptic physiology and plasticity has also been investigated in pilocarpine models of temporal-lobe epilepsy, indicating that network remodeling is not restricted to limbic structures. [20]D
Prolonged or super-refractory SE can produce progressive cortical and subcortical atrophy on serial MRI, consistent with continuing neuronal loss and structural reorganization. [16]D The distribution and severity of injury are heterogeneous. In a patient with nonconvulsive SE, cortical diffusion-weighted and FLAIR abnormalities were associated with increased frontal cerebral blood flow, whereas a contralateral cerebellar lesion-like signal abnormality occurred without increased cerebellar blood flow and later resolved; the authors attributed the cerebellar sparing to substantially lower excitotoxicity than in the involved cerebrum. [7]C
Metabolic, vascular, and systemic contributors
Ictal activity markedly increases neuronal energy demand and can contribute to lesion progression when neurovascular coupling is impaired. [1]C Spreading depolarization causes sustained neuronal and astroglial depolarization, translocation of ions, cytotoxic edema, and electrical silencing; it may facilitate neuronal death through toxic effects, increased metabolic demand, and inverse neurovascular coupling with severe hypoperfusion. [1]C Ictal events may similarly contribute to injury through increased metabolic demand, particularly in an acutely injured brain. [1]C
SE also rapidly induces systemic complications, including programmed neuronal death, cardiopulmonary insults, hemodynamic collapse, and multisystem organ failure; these complications can worsen secondary cerebral injury and contribute to mortality. [2]D Potential protective strategies studied experimentally include early NMDA-receptor antagonism, inhibition of later apoptotic pathways, modulation of oxidative and inflammatory injury, and rapid seizure cessation, although these approaches do not necessarily preserve network function or prevent later epilepsy. [6]D[113]D
| Mechanism | Consequence | Evidence |
|---|---|---|
| GABA_A receptor internalization | Reduced inhibition and declining benzodiazepine responsiveness | [3]D[5]D |
| NMDA/AMPA receptor recruitment | Sustained excitation and glutamate-mediated excitotoxicity | [3]D[17]D |
| Calcium influx and mitochondrial overload | Membrane depolarization, energetic failure, and oxidative injury | [3]D |
| Apoptotic signaling | p53/Puma-associated hippocampal neuronal death | [110]D[19]D |
| Inflammation and barrier dysfunction | Microglial activation, tissue injury, and epileptogenesis | [111]D[113]D |
| Metabolic and vascular stress | Hypermetabolism, hypoperfusion, cytotoxic edema, and lesion progression | [1]C[2]D |
Etiology and Triggering Factors
- ▸Identifying the underlying etiology is the most critical predictor of mortality (approx. 27.8% in NORSE) and functional recovery [32].
- ▸Autoimmune triggers, including AQP4 and Anti-Hu antibodies, often present as highly refractory focal SE or EPC [27, 28].
Status epilepticus (SE) arises from a fundamental failure of endogenous seizure-termination mechanisms or the activation of pathways that promote abnormally prolonged, self-sustaining electrical activity [2]D. The transition from a self-terminating seizure to SE is characterized by a critical physiological shift, often involving the internalization of GABA-A receptors and the synaptic recruitment of NMDA receptors, which creates a cycle of refractory hyperexcitability [34]D. Identifying the specific etiology is the most significant predictor of both short-term mortality and long-term functional recovery [24][32]D.
Recognition and Triage
- ▸The operational threshold for status epilepticus is 5 minutes of continuous seizure activity, necessitating immediate pharmacological intervention.
- ▸Nonconvulsive status epilepticus (NCSE) requires EEG for diagnosis and should be suspected in any patient with unexplained altered mental status or failure to wake after a convulsive seizure.
Status epilepticus (SE) is a critical neurologic emergency requiring rapid identification to mitigate the high risk of mortality and permanent neurological damage [40][43]C. The modern approach to SE recognition utilizes a patient-specific framework organized into four axes: semiology, etiology, electroencephalogram (EEG) correlate, and age [43]C. Clinical recognition is often straightforward in convulsive status epilepticus (CSE), but nonconvulsive status epilepticus (NCSE) presents a significant diagnostic challenge, frequently requiring specialized monitoring to distinguish it from other forms of encephalopathy [45]D[52]D.
Refractory and Super-Refractory Status Epilepticus Management
- ▸Refractory status epilepticus (RSE) requires immediate ICU admission and escalation to continuous anesthetic infusions like midazolam or propofol.
- ▸Ketamine is a critical adjunctive therapy that targets NMDA receptor upregulation, which occurs as GABAergic medications lose efficacy during prolonged seizures.
Refractory status epilepticus (RSE) is defined as seizure activity that persists despite the administration of a first-line and at least one appropriately dosed second-line non-sedating intravenous (IV) antiseizure medication (ASM) [60][66]D. Approximately 10% to 40% of pediatric status epilepticus cases progress to RSE [54]. Super-refractory status epilepticus (SRSE) occurs when seizures continue or recur 24 hours or more after the initiation of anesthetic therapy, including instances where seizures return during the weaning of anesthetic infusions [55][63]D[71]C.
Secondary Assessment and Diagnostic Workup
- ▸Status epilepticus is defined by the t1 (failure to terminate) and t2 (risk of neuronal injury) timepoints, with 5 minutes being the threshold for generalized convulsive SE.
- ▸EEG is mandatory for the diagnosis of nonconvulsive status epilepticus (NCSE), as clinical signs are often subtle or absent in critically ill patients.
The diagnosis of status epilepticus (SE) is a time-sensitive neuro-emergency that requires a parallel approach: stabilizing the patient while simultaneously identifying the seizure type and underlying etiology [83]D[84]D. Because prolonged seizure activity leads to progressive changes in neurotransmission—specifically the internalization of GABA receptors and the mobilization of NMDA receptors—prompt recognition is vital to prevent the transition to refractory states [84]D. The diagnostic process is guided by the International League Against Epilepsy (ILAE) framework, which classifies SE across four axes: semiology, EEG correlates, etiology, and age [89]D.
Special Populations: Pediatrics, Pregnancy, and Elderly
- ▸The elderly have the highest incidence of SE (89.6/100,000) and a fourfold higher mortality rate compared to younger adults [97].
- ▸In pregnancy, differentiating SE from eclampsia is critical, as eclampsia requires Magnesium sulfate rather than standard ASMs [88].
of (SE) requires significant modification when encountered in specific patient cohorts. Physiological variations, altered pharmacokinetics, and distinct etiologic profiles necessitate a departure from standard adult protocols to optimize outcomes and minimize iatrogenic harm [88]D[97]D. ### Pediatrics In the pediatric population, SE is a common neurological emergency where rapid intervention is critical to prevent long-term developmental and cognitive sequelae [99]D.
Guidelines and Resources
- ▸The Neurocritical Care Society (NCS) 2012 guidelines establish a three-tiered pharmacological framework: Emergent (Benzodiazepines), Urgent (AEDs), and Refractory (Anesthetic infusions).
- ▸Continuous EEG (cEEG) is recommended by the NCS within 60 minutes of seizure onset to rule out non-convulsive status epilepticus in patients who do not regain consciousness.
Clinical practice guidelines for (SE) emphasize a time-sensitive, tiered approach to . Because SE is a neurological emergency with high morbidity, standardized protocols are essential to reduce institutional variability and improve patient outcomes [107]. The primary objectives of all major guidelines are the rapid termination of clinical and electrographic seizure activity and the prevention of seizure recurrence.
References
- [1]
Winkler MK, Chassidim Y, Lublinsky S et al.. “Impaired neurovascular coupling to ictal epileptic activity and spreading depolarization in a patient with subarachnoid hemorrhage: possible link to blood-brain barrier dysfunction.” Epilepsia (2012). PMID: 23134492 ↗
L4CASE_REPORTCited in: Pathophysiology and Mechanisms of Neuronal Injury - [2]
Iglesias AH, Balabanov A, Raedy A. “Systemic Complications of Status Epilepticus.” Current neurology and neuroscience reports (2025). PMID: 41068542 ↗
L5REVIEW_NARRATIVECited in: Pathophysiology and Mechanisms of Neuronal Injury, Etiology and Triggering Factors - [3]
Alshehri RS, Alrawaili MS, Zawawi BMH et al.. “Pathophysiology of Status Epilepticus Revisited.” International journal of molecular sciences (2025). PMID: 40806628 ↗
L5REVIEW_NARRATIVECited in: Pathophysiology and Mechanisms of Neuronal Injury - [4]
Magro G, Laterza V. “Status epilepticus: Is there a Stage 1 plus?” Epilepsia (2024). PMID: 38507275 ↗
L5REVIEW_NARRATIVECited in: Pathophysiology and Mechanisms of Neuronal Injury - [5]
Wasterlain CG, Chen JW. “Mechanistic and pharmacologic aspects of status epilepticus and its treatment with new antiepileptic drugs.” Epilepsia (2008). PMID: 19087119 ↗
L5REVIEW_NARRATIVECited in: Pathophysiology and Mechanisms of Neuronal Injury - [6]
Walker M. “Neuroprotection in epilepsy.” Epilepsia (2007). PMID: 18330004 ↗
L5REVIEW_NARRATIVECited in: Pathophysiology and Mechanisms of Neuronal Injury - [7]
Ohe Y, Hayashi T, Deguchi I et al.. “A case of nonconvulsive status epilepticus with a reversible contralateral cerebellar lesion: temporal changes in magnetic resonance imaging and single-photon emission computed tomography finding.” Journal of stroke and cerebrovascular diseases : the official journal of National Stroke Association (2013). PMID: 23910513 ↗
L4CASE_REPORTCited in: Pathophysiology and Mechanisms of Neuronal Injury - [8]
Specchio N, Auvin S. “To what extent does status epilepticus contribute to brain damage in the developmental and epileptic Encephalopathies.” Epilepsy & behavior : E&B (2025). PMID: 39883989 ↗
L5REVIEW_NARRATIVECited in: Pathophysiology and Mechanisms of Neuronal Injury - [9]
Niquet J, Lumley L, Baldwin R et al.. “Early polytherapy for benzodiazepine-refractory status epilepticus.” Epilepsy & behavior : E&B (2019). PMID: 31636007 ↗
L5REVIEW_NARRATIVECited in: Pathophysiology and Mechanisms of Neuronal Injury - [10]
Scott RC. “What are the effects of prolonged seizures in the brain?” Epileptic disorders : international epilepsy journal with videotape (2014). PMID: 25323416 ↗
L5REVIEW_NARRATIVECited in: Pathophysiology and Mechanisms of Neuronal Injury - [11]
Engrand N, Crespel A. “[Pathophysiologic basis of status epilepticus].” Revue neurologique (2009). PMID: 19243800 ↗
L5REVIEW_NARRATIVECited in: Pathophysiology and Mechanisms of Neuronal Injury - [12]
De Luca P, Mele M, Tanqueiro S et al.. “Synaptic accumulation of GluN2B-containing NMDA receptors mediates the effects of BDNF-TrkB signalling on synaptic plasticity and in hyperexcitability during status epilepticus.” Journal of biomedical science (2025). PMID: 40890771 ↗
L5OTHERCited in: Pathophysiology and Mechanisms of Neuronal Injury - [13]
Abbasova K, Kubová H, Mareš P. “Does status epilepticus modify the effect of ifenprodil on cortical epileptic afterdischarges in immature rats?” Pharmacological reports : PR (2018). PMID: 29355816 ↗
L5OTHERCited in: Pathophysiology and Mechanisms of Neuronal Injury - [14]
Engel T, Martinez-Villarreal J, Henke C et al.. “Spatiotemporal progression of ubiquitin-proteasome system inhibition after status epilepticus suggests protective adaptation against hippocampal injury.” Molecular neurodegeneration (2017). PMID: 28235423 ↗
L5OTHERCited in: Pathophysiology and Mechanisms of Neuronal Injury - [15]
Shao H, Yang Y, Qi AP et al.. “Gastrodin Reduces the Severity of Status Epilepticus in the Rat Pilocarpine Model of Temporal Lobe Epilepsy by Inhibiting Nav1.6 Sodium Currents.” Neurochemical research (2017). PMID: 27743286 ↗
L5OTHERCited in: Pathophysiology and Mechanisms of Neuronal Injury - [16]
Hocker S, Nagarajan E, Rabinstein AA et al.. “Progressive Brain Atrophy in Super-refractory Status Epilepticus.” JAMA neurology (2016). PMID: 27533350 ↗
L5OTHERCited in: Pathophysiology and Mechanisms of Neuronal Injury - [17]
Wasterlain CG, Naylor DE, Liu H et al.. “Trafficking of NMDA receptors during status epilepticus: therapeutic implications.” Epilepsia (2013). PMID: 24001081 ↗
L5OTHERCited in: Pathophysiology and Mechanisms of Neuronal Injury - [18]
Engel T, Gomez-Villafuertes R, Tanaka K et al.. “Seizure suppression and neuroprotection by targeting the purinergic P2X7 receptor during status epilepticus in mice.” FASEB journal : official publication of the Federation of American Societies for Experimental Biology (2012). PMID: 22198387 ↗
L5OTHERCited in: Pathophysiology and Mechanisms of Neuronal Injury - [19]
Engel T, Tanaka K, Jimenez-Mateos EM et al.. “Loss of p53 results in protracted electrographic seizures and development of an aggravated epileptic phenotype following status epilepticus.” Cell death & disease (2010). PMID: 21368852 ↗
L5OTHERCited in: Pathophysiology and Mechanisms of Neuronal Injury - [20]
Avchalumov Y, Kirschstein T, Köhling R. “Altered physiology and pharmacology in the corticostriatal system in a model of temporal lobe epilepsy.” Epilepsia (2011). PMID: 21070218 ↗
L5OTHERCited in: Pathophysiology and Mechanisms of Neuronal Injury - [21]
Peng W, Lu L, Yin J et al.. “Factors associated with long-term outcomes in people with new onset refractory epilepticus: A single-center cohort study.” Epilepsia (2026). PMID: 41277767 ↗
L2bCOHORTCited in: Etiology and Triggering Factors, Special Populations: Pediatrics, Pregnancy, and Elderly - [22]
Lopez-Espejo M, Skorin I, Mesa T et al.. “Three-year incidence and acute setting predictors of epilepsy after neonatal and childhood arterial ischaemic stroke: a disease-based cohort study.” European journal of pediatrics (2024). PMID: 38170290 ↗
L2bCOHORTCited in: Etiology and Triggering Factors - [23]
Wang X, Wang YY, Gao Q et al.. “Development and validation of a nomogram to provide individualized predictions of functional outcomes in patients with convulsive status epilepticus at 3 months: The modified END-IT tool.” CNS neuroscience & therapeutics (2023). PMID: 37334755 ↗
L1bRCTCited in: Etiology and Triggering Factors, Recognition and Triage - [24]
Lee S, Kim SH, Kim HD et al.. “Identification of etiologies according to baseline clinical features of pediatric new-onset refractory status epilepticus in single center retrospective study.” Seizure (2024). PMID: 38908141 ↗
L2bCOHORTCited in: Etiology and Triggering Factors - [25]
Mikdashi J, Krumholz A. “Long-term outcome of status epilepticus-related to systemic lupus erythematosus: An observational study and a systematic review.” Seminars in arthritis and rheumatism (2023). PMID: 37595509 ↗
L2aSR_OBSCited in: Etiology and Triggering Factors - [26]
Tabaee Damavandi P, Bosque-Varela P, Santos HBH et al.. “Crossed cerebellar diaschisis in status epilepticus: A systematic review of the literature.” Epileptic disorders : international epilepsy journal with videotape (2026). PMID: 41483388 ↗
L2aSR_OBSCited in: Etiology and Triggering Factors, Secondary Assessment and Diagnostic Workup - [27]
Romozzi M, Vollono C, Calabresi P et al.. “Epilepsia Partialis Continua as a manifestation of aquaporin-4 autoimmunity.” Multiple sclerosis (Houndmills, Basingstoke, England) (2024). PMID: 39077880 ↗
L4CASE_REPORTCited in: Etiology and Triggering Factors - [28]
Cabreira V, Ferreira D, Melo C et al.. “Child Neurology: Anti-Hu Encephalitis in an Adolescent With a Mediastinal Seminoma.” Neurology (2023). PMID: 37527936 ↗
L4CASE_REPORTCited in: Etiology and Triggering Factors - [29]
Gaillard JR, Whitt Z, Selwa LM et al.. “Pearls & Oy-sters: Whole-Genome Sequencing in Critically Ill Neurologic Patient Leads to Diagnosis With Treatment Implications.” Neurology (2023). PMID: 37460236 ↗
L4CASE_REPORTCited in: Etiology and Triggering Factors - [30]
Marini C, Rosati A, Fusco L et al.. “Genetic Etiologies of Epilepsies With Status Epilepticus: Insights From the Italian Pediatric Status Epilepticus Group Cohort.” Neurology (2026). PMID: 41915870 ↗
L5OTHERCited in: Etiology and Triggering Factors - [31]
Damiano M, Lambrecq V, Nguyen-Michel VH et al.. “EEG, clinical, and MRI features of status epilepticus associated with mitochondrial diseases.” Journal of neurology (2026). PMID: 41729327 ↗
L5OTHERCited in: Etiology and Triggering Factors, Special Populations: Pediatrics, Pregnancy, and Elderly - [32]
Jayalakshmi S, Pachipala S, Patil A et al.. “Clinical characteristics, etiology and outcome of new onset refractory status epilepticus in adults.” Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology (2026). PMID: 41498863 ↗
L5OTHERCited in: Etiology and Triggering Factors, Special Populations: Pediatrics, Pregnancy, and Elderly - [33]
Lattanzi S, Matricardi S, Vogrig A et al.. “Predicting epilepsy after new onset refractory status epilepticus due to autoimmune encephalitis: The DAME score.” Epilepsia (2026). PMID: 41467927 ↗
L5OTHERCited in: Etiology and Triggering Factors - [34]
Pelletier J, Merriman W, Koyfman A et al.. “Benzodiazepine-refractory status epilepticus: A narrative review.” The American journal of emergency medicine (2026). PMID: 40974752 ↗
L5REVIEW_NARRATIVECited in: Etiology and Triggering Factors, Recognition and Triage, Refractory and Super-Refractory Status Epilepticus Management - [35]
Kilmer J, Ransley G, Murphy E et al.. “The Role of Metabolic Testing in the Diagnostic Evaluation of Adult NORSE: A Retrospective, Single-Centre Study.” European journal of neurology (2025). PMID: 40470573 ↗
L5OTHERCited in: Etiology and Triggering Factors - [36]
Steriade C, Thomas SC, Xu F et al.. “Patients with status epilepticus and new-onset refractory status epilepticus display drastically altered fecal microbiomes compared to chronic epilepsy patients.” Epilepsia (2025). PMID: 40387216 ↗
L5OTHERCited in: Etiology and Triggering Factors - [37]
Ferreira JHF, Gomes AM, Zetehaku AC et al.. “Performance of cryptogenic new onset refractory status epilepticus score in a Brazilian cohort after testing for antineuronal antibodies with tissue-based and cell-based assays.” Epilepsia (2025). PMID: 40318023 ↗
L5OTHERCited in: Etiology and Triggering Factors - [38]
Halawani LM, Myers KA. “Comparative analysis of new-onset refractory status epilepticus in adult and pediatric patients: immunotherapy timing and functional outcomes.” Journal of neurology (2025). PMID: 40251332 ↗
L5OTHERCited in: Etiology and Triggering Factors - [39]
Ferhat L, Soussi R, Masse M et al.. “A peptide-neurotensin conjugate that crosses the blood-brain barrier induces pharmacological hypothermia associated with anticonvulsant, neuroprotective, and anti-inflammatory properties following status epilepticus in mice.” eLife (2025). PMID: 40152901 ↗
L5OTHERCited in: Etiology and Triggering Factors - [40]
Vignatelli L, Tontini V, Meletti S et al.. “Clinical practice guidelines on the management of status epilepticus in adults: A systematic review.” Epilepsia (2024). PMID: 38606469 ↗
L1cGUIDELINECited in: Recognition and Triage - [41]
Simma L, Kammerl A, Ramantani G. “Point-of-care EEG in the pediatric emergency department: a systematic review.” European journal of pediatrics (2025). PMID: 40053132 ↗
L2aSR_OBSCited in: Recognition and Triage, Secondary Assessment and Diagnostic Workup - [42]
Limotai C, Jirasakuldej S, Wongwiangiunt S et al.. “Efficacy of delivery of care with Tele-continuous EEG in critically ill patients: a multicenter randomized controlled trial (Tele-cRCT study) study.” Critical care (London, England) (2025). PMID: 39773282 ↗
L1bRCTCited in: Recognition and Triage, Secondary Assessment and Diagnostic Workup - [43]
Rubinos C. “Emergent Management of Status Epilepticus.” Continuum (Minneapolis, Minn.) (2024). PMID: 38830068 ↗
L4CASE_REPORTCited in: Recognition and Triage, Refractory and Super-Refractory Status Epilepticus Management - [44]
Shen JY, Saffari SE, Yong L et al.. “Evaluation of prognostic scores for status epilepticus in the neurology ICU: A retrospective study.” Journal of the neurological sciences (2024). PMID: 38490090 ↗
L2bCOHORTCited in: Recognition and Triage - [45]
Gélisse P, Crespel A. “Nonconvulsive status epilepticus in patients under intensive care: Should we view epilepsy as a sleep disorder?” Epilepsia (2025). PMID: 39821147 ↗
L5REVIEW_NARRATIVECited in: Recognition and Triage, Secondary Assessment and Diagnostic Workup - [46]
Gélisse P, Crespel A. “When patients with Creutzfeldt-Jakob disease are misdiagnosed as having nonconvulsive status epilepticus.” Epilepsia (2025). PMID: 39754446 ↗
L5REVIEW_NARRATIVECited in: Recognition and Triage, Secondary Assessment and Diagnostic Workup - [47]
O'Kula SS, Hill CE. “Improving Quality of Care for Status Epilepticus: Putting Protocols into Practice.” Current neurology and neuroscience reports (2024). PMID: 38995482 ↗
L5REVIEW_NARRATIVECited in: Recognition and Triage - [48]
Gélisse P, Tatum WO, Crespel A et al.. “Stimulus-induced arousal with transient electroencephalographic improvement distinguishes nonictal from ictal generalized periodic discharges.” Epilepsia (2024). PMID: 38624097 ↗
L5REVIEW_NARRATIVECited in: Recognition and Triage - [49]
Green A, Wegman ME, Ney JP. “Economic review of point-of-care EEG.” Journal of medical economics (2024). PMID: 38014443 ↗
L5REVIEW_NARRATIVECited in: Recognition and Triage - [50]
Davey Z, Gupta PB, Li DR et al.. “Rapid Response EEG: Current State and Future Directions.” Current neurology and neuroscience reports (2022). PMID: 36434488 ↗
L5REVIEW_NARRATIVECited in: Recognition and Triage - [51]
De Stefano P, Kaplan PW, Quintard H et al.. “Nonconvulsive status epilepticus following cardiac arrest: overlooked, untreated and misjudged.” Journal of neurology (2023). PMID: 36076090 ↗
L5REVIEW_NARRATIVECited in: Recognition and Triage - [52]
Alkhachroum A, Appavu B, Egawa S et al.. “Electroencephalogram in the intensive care unit: a focused look at acute brain injury.” Intensive care medicine (2022). PMID: 35997792 ↗
L5REVIEW_NARRATIVECited in: Recognition and Triage - [53]
Rosati A, Bartolotta P, Marini C et al.. “Optimizing pediatric status epilepticus management: The role of early midazolam infusion and adherence to clinical practice guidelines.” Epilepsia (2025). PMID: 40377450 ↗
L1cGUIDELINECited in: Refractory and Super-Refractory Status Epilepticus Management - [54]
Chiriboga N, Spentzas T, Abu-Sawwa R. “A systematic review and meta-analysis of ketamine in pediatric status epilepticus.” Epilepsia (2024). PMID: 38881333 ↗
L2aSR_OBSCited in: Refractory and Super-Refractory Status Epilepticus Management - [55]
Yan M, Sun T, Liu J et al.. “The efficacy and safety of ketamine in the treatment of super-refractory status epilepticus: a systematic review.” Journal of neurology (2024). PMID: 38782798 ↗
L2aSR_OBSCited in: Refractory and Super-Refractory Status Epilepticus Management - [56]
Au YK, Kananeh MF, Rahangdale R et al.. “Treatment of Refractory Status Epilepticus With Continuous Intravenous Anesthetic Drugs: A Systematic Review.” JAMA neurology (2024). PMID: 38466294 ↗
L2aSR_OBSCited in: Refractory and Super-Refractory Status Epilepticus Management - [57]
Cornwall CD, Piilgaard H, Engedal TS et al.. “Fast Acute Sedation at Intensive Care vs. High-Dose IV Anti-seizure Medication for Treatment of Non-convulsive Status Epilepticus: A Randomized, Multicenter Trial.” Critical care explorations (2025). PMID: 40953286 ↗
L2bTRIAL_NONRANDOMCited in: Refractory and Super-Refractory Status Epilepticus Management - [58]
Vossler DG. “First Seizures, Acute Repetitive Seizures, and Status Epilepticus.” Continuum (Minneapolis, Minn.) (2025). PMID: 39899098 ↗
L4CASE_REPORTCited in: Refractory and Super-Refractory Status Epilepticus Management - [59]
El-Haggar SM, Hegazy SK, Mustafa W et al.. “Possible immuno-modulatory effects of tocilizumab in patients with refractory status epilepticus.” European review for medical and pharmacological sciences (2023). PMID: 36876691 ↗
L1bRCTCited in: Refractory and Super-Refractory Status Epilepticus Management - [60]
Chiu WT, Campozano V, Schiefecker A et al.. “Management of Refractory Status Epilepticus: An International Cohort Study (MORSE CODe) Analysis of Patients Managed in the ICU.” Neurology (2022). PMID: 35918156 ↗
L2bCOHORTCited in: Refractory and Super-Refractory Status Epilepticus Management - [61]
Daniels ZS, Srdanovic N, Rychlik K et al.. “High-Dose Midazolam for Pediatric Refractory Status Epilepticus: A Single-Center Retrospective Study.” Pediatric critical care medicine : a journal of the Society of Critical Care Medicine and the World Federation of Pediatric Intensive and Critical Care Societies (2022). PMID: 35894600 ↗
L2bCOHORTCited in: Refractory and Super-Refractory Status Epilepticus Management - [62]
Aboul-Fotouh S, Habib MZ, Magdy SM et al.. “Tranexamic acid-associated fatal status epilepticus in a paediatric non-cardiac surgery: A case report and literature review.” British journal of clinical pharmacology (2022). PMID: 35244235 ↗
L4CASE_REPORTCited in: Refractory and Super-Refractory Status Epilepticus Management - [63]
Hu Y, Peng X, Wang X. “Therapeutic approaches for super-refractory status epilepticus: an update of the literature.” Expert review of neurotherapeutics (2025). PMID: 40583044 ↗
L5REVIEW_NARRATIVECited in: Refractory and Super-Refractory Status Epilepticus Management - [64]
Kapur J. “Strategies to innovate emergency care of status epilepticus.” Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics (2025). PMID: 39701892 ↗
L5REVIEW_NARRATIVECited in: Refractory and Super-Refractory Status Epilepticus Management - [65]
Finney JD, Schuler PD, Rudloff JR et al.. “Evaluation of the Use of Ketamine in Prehospital Seizure Management: A Retrospective Review of the ESO Database.” Prehospital emergency care (2025). PMID: 39058382 ↗
L5REVIEW_NARRATIVECited in: Refractory and Super-Refractory Status Epilepticus Management - [66]
Rossetti AO, Claassen J, Gaspard N. “Status epilepticus in the ICU.” Intensive care medicine (2024). PMID: 38117319 ↗
L5REVIEW_NARRATIVECited in: Refractory and Super-Refractory Status Epilepticus Management - [67]
Buratti S, Giacheri E, Palmieri A et al.. “Ketamine as advanced second-line treatment in benzodiazepine-refractory convulsive status epilepticus in children.” Epilepsia (2023). PMID: 36792542 ↗
L5REVIEW_NARRATIVECited in: Refractory and Super-Refractory Status Epilepticus Management - [68]
Roberti R, Rocca M, Iannone LF et al.. “Status epilepticus in pregnancy: a literature review and a protocol proposal.” Expert review of neurotherapeutics (2022). PMID: 35317697 ↗
L5REVIEW_NARRATIVECited in: Refractory and Super-Refractory Status Epilepticus Management - [69]
Mastroianni G, Iannone LF, Roberti R et al.. “Management of status epilepticus in patients with liver or kidney disease: a narrative review.” Expert review of neurotherapeutics (2021). PMID: 33297776 ↗
L5REVIEW_NARRATIVECited in: Refractory and Super-Refractory Status Epilepticus Management - [70]
Machado RA, Patel J, Elsayed MS. “The role of ketamine-induced beta activity in the treatment of refractory status epilepticus. Is the EEG useful to determine responder's rate? A retrospective study.” Epilepsy & behavior : E&B (2022). PMID: 34974373 ↗
L2bCOHORTCited in: Refractory and Super-Refractory Status Epilepticus Management - [71]
Chakravartty A, Gilmore EJ, Hirsch LJ et al.. “Clinical Reasoning: A 40-Year-Old Man With Refractory Status Epilepticus After Small Bowel Resection for Volvulus.” Neurology (2025). PMID: 40986431 ↗
L4CASE_REPORTCited in: Refractory and Super-Refractory Status Epilepticus Management - [72]
Finney JD, Kowalski M, Wang J et al.. “Prehospital Ketamine Administration in Benzodiazepine Refractory Status Epilepticus: A Case Series Review.” Prehospital emergency care (2026). PMID: 40193549 ↗
L4CASE_REPORTCited in: Refractory and Super-Refractory Status Epilepticus Management - [73]
Syed MJ, Zutshi D, Muzammil SM et al.. “Ketamine to Prevent Endotracheal Intubation in Adults with Refractory Non-convulsive Status Epilepticus: A Case Series.” Neurocritical care (2024). PMID: 37783825 ↗
L4CASE_REPORTCited in: Refractory and Super-Refractory Status Epilepticus Management - [74]
Kimmons LA, Alzayadneh M, Metter EJ et al.. “Safety and Efficacy of Ketamine Without Intubation in the Management of Refractory Seizures: A Case Series.” Neurocritical care (2024). PMID: 37610640 ↗
L4CASE_REPORTCited in: Refractory and Super-Refractory Status Epilepticus Management - [75]
Perlmutter M, Price M, Kothari K et al.. “Prehospital Treatment of Benzodiazepine-Resistant Pediatric Status Epilepticus with Parenteral Ketamine: A Case Series.” Prehospital emergency care (2023). PMID: 37276174 ↗
L4CASE_REPORTCited in: Refractory and Super-Refractory Status Epilepticus Management - [76]
Pirgit ML, Beniczky S. “EEG and semiology in the elderly: A systematic review.” Seizure (2025). PMID: 39294074 ↗
L2aSR_OBSCited in: Secondary Assessment and Diagnostic Workup - [77]
Peña-Ceballos J, Moloney PB, Kinney MO et al.. “How are we doing? The electroclinical diagnosis of status epilepticus in idiopathic generalized epilepsy in a tertiary referral center: A case series and scoping review of 40 years of literature.” Journal of the neurological sciences (2026). PMID: 41807915 ↗
L4CASE_REPORTCited in: Secondary Assessment and Diagnostic Workup - [78]
Hirsch LJ, Gopaul MT. “EEG in the critical care setting.” Clinical neurophysiology : official journal of the International Federation of Clinical Neurophysiology (2026). PMID: 41297117 ↗
L5REVIEW_NARRATIVECited in: Secondary Assessment and Diagnostic Workup - [79]
Spagnoli C, Ramantani G, Sharpe C et al.. “Rethinking the definition of neonatal status epilepticus.” European journal of pediatrics (2025). PMID: 40906263 ↗
L5REVIEW_NARRATIVECited in: Secondary Assessment and Diagnostic Workup - [80]
De Stefano P. “Reconsidering the management and prognostic implications of myoclonus and status epilepticus post-cardiac arrest.” Clinical neurophysiology : official journal of the International Federation of Clinical Neurophysiology (2026). PMID: 40436658 ↗
L5REVIEW_NARRATIVECited in: Secondary Assessment and Diagnostic Workup - [81]
Nagarajan L, Ghosh S. “Status epilepticus in the neonate.” BMJ paediatrics open (2025). PMID: 40121015 ↗
L5REVIEW_NARRATIVECited in: Secondary Assessment and Diagnostic Workup - [82]
Lévi-Strauss J, Marois C, Worbe Y et al.. “Utility and Value of Movement Recording with Combined EEG-EMG Monitoring in the Intensive Care Unit.” Neurocritical care (2025). PMID: 40032771 ↗
L5REVIEW_NARRATIVECited in: Secondary Assessment and Diagnostic Workup - [83]
Haider HA. “Initial Management of Acute Seizures and Status Epilepticus.” The Medical clinics of North America (2025). PMID: 39893025 ↗
L5REVIEW_NARRATIVECited in: Secondary Assessment and Diagnostic Workup - [84]
Gettings JV, Mohammad Alizadeh Chafjiri F, Patel AA et al.. “Diagnosis and management of status epilepticus: improving the status quo.” The Lancet. Neurology (2025). PMID: 39637874 ↗
L5REVIEW_NARRATIVECited in: Secondary Assessment and Diagnostic Workup - [85]
Chiarello D, Perrone A, Ricci E et al.. “The Role of Electroencephalography in Children with Acute Altered Mental Status of Unknown Etiology: A Prospective Study.” Neuropediatrics (2024). PMID: 39106957 ↗
L2bCOHORTCited in: Secondary Assessment and Diagnostic Workup - [86]
Gomutbutra P, Krongsut S, Lott J. “A Systematic Review and Meta-Analysis Evaluating the Clinical Impact and Accuracy of Artificial Intelligence in EEG for the Early Detection of Nonconvulsive Seizures.” The Neurodiagnostic journal (2025). PMID: 40679314 ↗
L2aSR_OBSCited in: Secondary Assessment and Diagnostic Workup - [87]
Neves Briard J, Duquette A, Cayrol R et al.. “Refractory Status Epilepticus in a Patient With Aducanumab-Induced Amyloid-Related Imaging Abnormalities.” Neurology (2024). PMID: 39121445 ↗
L4CASE_REPORTCited in: Secondary Assessment and Diagnostic Workup - [88]
Siegel CR, Khoujah D. “Status Epilepticus.” Emergency medicine clinics of North America (2026). PMID: 41260851 ↗
L5REVIEW_NARRATIVECited in: Secondary Assessment and Diagnostic Workup, Special Populations: Pediatrics, Pregnancy, and Elderly - [89]
Leitinger M, Bosque-Varela P, Kuchukhidze G et al.. “Seminars in epileptology: How to diagnose status epilepticus in adults and children.” Epileptic disorders : international epilepsy journal with videotape (2025). PMID: 40528536 ↗
L5REVIEW_NARRATIVECited in: Secondary Assessment and Diagnostic Workup - [90]
Ford H, Seneviratne U. “The electroencephalogram in the diagnosis and classification of status epilepticus: a practical guide.” Practical neurology (2025). PMID: 39890455 ↗
L5REVIEW_NARRATIVECited in: Secondary Assessment and Diagnostic Workup - [91]
Zehtabchi S, Beall J, Silbergleit R et al.. “Chronological Sequence of Convulsive Status Epilepticus Treatment Steps in a Real-Life Scenario for Patients Enrolled in a Large Multicenter Trial.” Academic emergency medicine : official journal of the Society for Academic Emergency Medicine (2026). PMID: 41854499 ↗
L1bRCTCited in: Special Populations: Pediatrics, Pregnancy, and Elderly - [92]
Wang P, Lu L, Gao H et al.. “Will Memantine Exacerbate Seizures in People With Epilepsy? A Prospective Cohort Study.” Annals of clinical and translational neurology (2026). PMID: 41288262 ↗
L2bCOHORTCited in: Special Populations: Pediatrics, Pregnancy, and Elderly - [93]
Pichardo-Rojas D, Camarena-Rubio KJ, Gómez-Oropeza I et al.. “Optimizing vagus nerve stimulation for Super Refractory Status Epilepticus: A case series and systematic review.” Epileptic disorders : international epilepsy journal with videotape (2025). PMID: 40539748 ↗
L2aSR_OBSCited in: Special Populations: Pediatrics, Pregnancy, and Elderly - [94]
Yoo JY, Bloomfield J, Eka O et al.. “Vagus nerve stimulation as an adjunctive therapy for super-refractory status epilepticus including NORSE: a retrospective cohort study.” Epilepsy & behavior : E&B (2026). PMID: 41875755 ↗
L2bCOHORTCited in: Special Populations: Pediatrics, Pregnancy, and Elderly - [95]
Manai H, Kharraz T, Zouari H et al.. “Prognostic performance of STESS and qSOFA scores in pre-hospital status epilepticus: A prospective cohort study.” Seizure (2026). PMID: 41679101 ↗
L2bCOHORTCited in: Special Populations: Pediatrics, Pregnancy, and Elderly - [96]
Nakamura Y, Aso S, Yasunaga H et al.. “In-hospital outcomes of lacosamide versus levetiracetam for early adjunctive treatment of status epilepticus: A Nationwide Japanese retrospective cohort study.” Epilepsia open (2026). PMID: 41222404 ↗
L2bCOHORTCited in: Special Populations: Pediatrics, Pregnancy, and Elderly - [97]
Woodward MR, Armahizer MJ, Wang TI et al.. “Status epilepticus in older adults: A critical review.” Epilepsia (2025). PMID: 40365943 ↗
L5REVIEW_NARRATIVECited in: Special Populations: Pediatrics, Pregnancy, and Elderly - [98]
Alghadeer SM, Alsuwayegh A, AlMuqati H et al.. “Underdosing and response to pharmacotherapy in patients with status epilepticus: a retrospective study from Saudi Arabia.” Annals of medicine (2025). PMID: 40317249 ↗
L2bCOHORTCited in: Special Populations: Pediatrics, Pregnancy, and Elderly - [99]
Al Wahaibi A, Kazazian K, Gopaul M et al.. “The spectrum of cognitive outcomes following admission to hospital for refractory status epilepticus (RSE): A scoping review.” Seizure (2025). PMID: 40972237 ↗
L5REVIEW_NARRATIVECited in: Special Populations: Pediatrics, Pregnancy, and Elderly - [100]
Spuler K, Kaukas L, Tawfik S et al.. “Fatal Status Epilepticus After Elective Revision Cranioplasty: Case Report and Literature Review.” The American journal of case reports (2026). PMID: 41719224 ↗
L4CASE_REPORTCited in: Special Populations: Pediatrics, Pregnancy, and Elderly - [101]
Lanzone J, Bellini A, Cursi M et al.. “Structured EEG report complements the prognostic stratification of status epilepticus.” Journal of neurology (2026). PMID: 41986752 ↗
L5OTHERCited in: Special Populations: Pediatrics, Pregnancy, and Elderly - [102]
Schlabitz S, Doerrfuss JI, Hebel JM et al.. “Neurofilament light-chain (Nf-L) as a biomarker in seizures and status epilepticus of varying duration.” Journal of neurology (2026). PMID: 41927849 ↗
L5OTHERCited in: Special Populations: Pediatrics, Pregnancy, and Elderly - [103]
Orav K, Bosque-Varela P, Lauth W et al.. “Peri-Ictal MRI Abnormalities and Risk of Unprovoked Seizures After De Novo Status Epilepticus.” Neurology (2026). PMID: 41838966 ↗
L5OTHERCited in: Special Populations: Pediatrics, Pregnancy, and Elderly - [104]
Sala Padró J, Fonseca E, Quintana M et al.. “Impact of Treatment Delays in Epileptic Seizures: Time to Hospital Care and to EEG Increases Risk of Status Epilepticus and ICU Admission in Epileptic Seizures.” European journal of neurology (2026). PMID: 41778530 ↗
L5OTHERCited in: Special Populations: Pediatrics, Pregnancy, and Elderly - [105]
De Stefano P, Baumann SM, Fisch U et al.. “Impact of Etiology on Mortality and Recovery in Patients With Status Epilepticus.” Neurology (2026). PMID: 41637681 ↗
L5OTHERCited in: Special Populations: Pediatrics, Pregnancy, and Elderly - [106]
Krishnamurthy PV, Philibert-Rosas S, Rivkin M et al.. “Duration of EEG monitoring needed to ensure a low risk of seizure recurrence in hospitalized patients.” Journal of neurology (2026). PMID: 41507611 ↗
L5OTHERCited in: Special Populations: Pediatrics, Pregnancy, and Elderly - [107]
Brophy GM, Bell R, Claassen J et al.. “Guidelines for the evaluation and management of status epilepticus.” Neurocritical care (2012). PMID: 22528274 ↗
L1cGUIDELINECited in: Guidelines and Resources - [108]
Harden CL, Hopp J, Ting TY et al.. “Practice parameter update: management issues for women with epilepsy--focus on pregnancy (an evidence-based review): obstetrical complications and change in seizure frequency: report of the Quality Standards Subcommittee and Therapeutics and Technology Assessment Subcommittee of the American Academy of Neurology and American Epilepsy Society.” Neurology (2009). PMID: 19398682 ↗
L1cGUIDELINECited in: Guidelines and Resources - [109]
Harden CL, Hopp J, Ting TY et al.. “Management issues for women with epilepsy-Focus on pregnancy (an evidence-based review): I. Obstetrical complications and change in seizure frequency: Report of the Quality Standards Subcommittee and Therapeutics and Technology Assessment Subcommittee of the American Academy of Neurology and the American Epilepsy Society.” Epilepsia (2009). PMID: 19496807 ↗
L1cGUIDELINECited in: Guidelines and Resources - [110]
Engel T, Murphy BM, Hatazaki S et al.. “Reduced hippocampal damage and epileptic seizures after status epilepticus in mice lacking proapoptotic Puma.” FASEB journal : official publication of the Federation of American Societies for Experimental Biology (2009). PMID: 19890018 ↗
L5Cited in: Pathophysiology and Mechanisms of Neuronal Injury - [111]
Jung KH, Chu K, Lee ST et al.. “Region-specific plasticity in the epileptic rat brain: a hippocampal and extrahippocampal analysis.” Epilepsia (2008). PMID: 19054393 ↗
L5Cited in: Pathophysiology and Mechanisms of Neuronal Injury - [112]
Coleman BR, Ratcliffe RH, Oguntayo SA et al.. “[+]-Huperzine A treatment protects against N-methyl-D-aspartate-induced seizure/status epilepticus in rats.” Chemico-biological interactions (2008). PMID: 18588864 ↗
L5Cited in: Pathophysiology and Mechanisms of Neuronal Injury - [113]
Chu K, Jung KH, Lee ST et al.. “Erythropoietin reduces epileptogenic processes following status epilepticus.” Epilepsia (2008). PMID: 18479396 ↗
L5Cited in: Pathophysiology and Mechanisms of Neuronal Injury