Non-Convulsive Status Epilepticus (NCSE)



Non-Convulsive Status Epilepticus (NCSE) is a persistent change in the level of consciousness, behaviour, autonomic function, and sensorium from baseline associated with continuous epileptiform EEG changes, but without major motor signs

  • NCSE comprises a group of syndromes with a wide range of response to anticonvulsants from virtually self-limiting forms to refractory forms
  • No universally accepted definition yet exists
  • Time limits for the definition of NCSE have not been determined (often considered >10 minutes or shorter  recurrences without full recovery)
  • NCSE lacks prominent motor features, but may have subtle motor signs (e.g. twitching, blinking, eye movements)
  • NCS and NCSE are likely underdiagnosed, including in the ICU setting


  • NCS occur in about 50% of patients with coma or convulsive status epilepticus
  • NCS occur in 8-37% of the general ICU population
  • NCSE affects:
    • 12-33% of post-cardiac arrest patients in ICU
    • 8-35% of TBI patients in ICU


Two main types, though recent literature has further subdivisions:

  • absence SE, or primary generalized NCSE
  • complex partial SE, or secondary generalized NCSE



  • Requires high index of suspicion in patients with risk factors and suggestive clinical features
  • Little agreement on diagnostic criteria, clinical forms, consequences and treatment
  • Difficulty telling when coma is due to ictal symptomatology and differentiating it from non-ictal symptoms associated with underlying pathology such as post-hypoxic, metabolic or septic encephalopathies and effects of sedative drugs
  • No clinical findings are 100% specific
  • No EEG findings are100% specific – on EEG there are crossover features between epilepsy and encephalopathies which are being still standardized and the diagnosis of NCSE should not be based on EEG changes alone
  • Availability of continuous EEG monitoring (cEEG) is lacking in many centres
  • Diagnosis is often delayed (e.g. >24 hours)

Suspect NCSE in these patients:

  • Patients who have a generalized tonic-clonic seizure and a prolonged postictal period (NCSE complicates 10-40% of convulsive status epilepticus)
  • Patients with altered sensorium who demonstrate subtle signs, such as twitching or blinking or other eye movement signs and/or fluctuating mental status
  • Patients in whom no other cause is available to explain the altered sensorium, especially in those who have a history of a previous seizure, even if remote
  • Unexplained stupor or confusion in the elderly, especially those taking neuroleptic medications
  • Stroke patients who look clinically worse than expected
  • Patients with altered mental status in whom no other cause is available to explain the altered sensorium
  • Paradoxical response (improved alertness) in a patient with altered sensorium who receives anti-epileptic therapy (e.g. benzodiazepine, propofol)


  • Systemic infection in a patient with pre-existing epilepsy
  • Ischaemic stroke
  • Intracerebral and subarachnoid haemorrhages
  • post cardiac arrest
  • severe traumatic brain injury
  • Encephalitis
  • Dementia
  • Neoplasia
  • Previous neurosurgery
  • Also: benzodiazepine or other medication withdrawal, excessive use of psychotropic drugs, infections, trauma, metabolic derangements and alcohol use


None are specific for NCS or NCSE

  • Coma, altered consciousness, or altered sensorium
  • Catatonia
  • Behaviour changes and psychotic symptoms (e.g. delusions, paranoia, hallucinations)
  • Subtle motor signs (e.g. automatism, cyclonic jerks, myoclonus, eye twitching, eye deviation)
  • Speech disorders (e.g. verbal perseveration, aphasia, speech arrest, disorganized speech)
  • Autonomic dysfunction


May be difficult to differentiate from, or may coexist with:

  • Metabolic encephalopathy
  • Epileptic encephalopathy
  • Infective or autoimmune encephalitis
  • Complex migraine
  • Post-traumatic amnesia
  • Hypoglycaemia
  • Prolonged postictal state
  • Psychogenic pseudocoma
  • Psychogenic non-epileptic status
  • Substance intoxication (lithium, baclofen, tricyclics, tiagabine)
  • Detoxification from medications/drugs (alcohol, benzodiazepines)
  • Transient ischaemic attack or stroke
  • Transient global amnesia


  • Blood tests (exclude hypoglycaemia, electrolyte abnormalities (low Ca, low Mg), liver and renal dysfunction, haematological causes (e.g TTP))
  • Lumbar puncture (CNS infection or inflammation)
  • EEG and response on EEG and clinically to treatments such as benzodiazepines — without continuous EEG >50% of NCSE is missed in ICUs
  • MRI brain (to exclude structural cause not evident on CT)
  • Other advanced brain imaging modalities may be useful

Criteria for EEG diagnosis

  • Unequivocal electrographic seizure activity in which there is a typical evolution of changes in the EEG recording with a build-up of rhythmic activity
  • Periodical epileptiform discharges or rhythmic discharge with clinical seizure activity
  • Rhythmic discharge with either clinical or electrographic response to treatment

More difficult situations are when there are epileptiform discharges (EDs) on EEG but they do not reach the diagnostic criteria for seizure activity; look for:

  • subtle motor signs time-locked with EDs
  • spatiotemporal evolution
  • EEG and clinical improvement with IV anti-epileptic drugs (e.g. midazolam) (but may be delayed or confounded by drug-induced sedation)


Implications of NCSE are poorly defined

  • associated with poorer prognosis, however the underlying cause is typically the major determinant of mortality
    • Patients with pre-existing epilepsy have a lower mortality (3%) than where NCSE is due to acute medical disorders (27%)
  • associated with surrogate markers of harm such as increased neuron-specific enolase and hippocampal atrophy
  • increased mortality with:
    • increased duration of NCSE (with exceptions, e.g. absence NCOSE)
    • increased delay to diagnosis
  • worse prognosis with use of IV anaesthetic agents (possible marker of severity/ refractoriness)

The significance of ictal-interictal continuum disorders, that do not meet criteria for NCS, is uncertain



  • Early recognition and treatment are essential to optimize response to treatment and to prevent neurological (for which there is little evidence base) and systemic sequelae
  • Overdiagnosis and aggressive use of anticonvulsants can contribute to morbidity and mortality
  • Treatment is poorly understood and follows standard status epilepticus regimens


  • Seek and treat life threats
    • compromised airway and breathing
    • hypoglycemia
    • hyperthermia
  • Treatment of underlying cause
    • Reversal of factors that lower seizure threshold e.g. drugs such as cefepime, fever, hypoxia, hypoglycaemia, hyponatraemia
    • optimise existing AEDs in patients with known epilepsy (e.g. ensure therapeutic levels)
  • Treatment of seizures
    • Benzodiazepines: diazepam or lorazepam
    • Valproate or phenytoin: if failure to respond to benzodiazepines
    • Keppra increasingly used
  • Often unresponsive to initial treatments
    • progress rapidly to anaesthetic agents and endotracheal intubation if not responding
      • midazolam
      • propofol
      • barbiturates
    • Ketamine can be used for refractory status epilepticus (observational studies suggest ketamine is an effective option for refractory status epilepticus due to antagonism of excitotoxic NMDA receptors) (Hofler and Trinka, 2018)
    • Common practice is to continue anaesthetic agents until 12-24 hours of burst suppression or absence of epileptic activity before stopping
  • Use cEEG monitoring if available to detect and diagnose NCSE and to assess response to treatment
  • Seek and treat complications
    • e.g. compartment syndrome, pressure injury, aspiration, hypoxia, hypoglycaemia
  • Admit to ICU if not responsive to initial management
    • absence SE rarely requires ICU care and is typically responsive to IV benzodiazepines
  • Consults
    • Neurology


  • robust evidence for different NCSE therapies is lacking

CCC Neurocritical Care Series

Journal articles

  • Höfler J, Trinka E. Intravenous ketamine in status epilepticus. Epilepsia. 2018;59 Suppl 2:198-206. [PMID 30146731]
  • Kinney MO, Craig JJ, Kaplan PW. Non-convulsive status epilepticus: mimics and chameleons. Pract Neurol. 2018;18(4):291-305.[PMID 29650639]
  • Kinney MO, Kaplan PW. An update on the recognition and treatment of non-convulsive status epilepticus in the intensive care unit. Expert Rev Neurother. 2017;17(10):987-1002. [PMID 28829210]
  • Meierkord H, Holtkamp M. Non-convulsive status epilepticus in adults: clinical forms and treatment. Lancet Neurol. 2007 Apr;6(4):329-39. [pubmed] [PMID ]
  • Shah AM, Vashi A, Jagoda A. Review article: Convulsive and non-convulsive status epilepticus: an emergency medicine perspective. Emerg Med Australas. 2009  Oct;21(5):352-66. [PMID 19840084]
  • Sutter R. Are We Prepared to Detect Subtle and Nonconvulsive Status Epilepticus in Critically Ill Patients?. J Clin Neurophysiol. 2016;33(1):25-31. [pubmed] [PMID ]
  • 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):1515-23. [PMID 26336950]
  • Trinka E, Leitinger M. Which EEG patterns in coma are nonconvulsive status epilepticus?. Epilepsy Behav. 2015;49:203-22. [PMID 26148985]

Critical Care


Chris is an Intensivist and ECMO specialist at the Alfred ICU in Melbourne. He is also a Clinical Adjunct Associate Professor at Monash University. He is a co-founder of the Australia and New Zealand Clinician Educator Network (ANZCEN) and is the Lead for the ANZCEN Clinician Educator Incubator programme. He is on the Board of Directors for the Intensive Care Foundation and is a First Part Examiner for the College of Intensive Care Medicine. He is an internationally recognised Clinician Educator with a passion for helping clinicians learn and for improving the clinical performance of individuals and collectives.

After finishing his medical degree at the University of Auckland, he continued post-graduate training in New Zealand as well as Australia’s Northern Territory, Perth and Melbourne. He has completed fellowship training in both intensive care medicine and emergency medicine, as well as post-graduate training in biochemistry, clinical toxicology, clinical epidemiology, and health professional education.

He is actively involved in in using translational simulation to improve patient care and the design of processes and systems at Alfred Health. He coordinates the Alfred ICU’s education and simulation programmes and runs the unit’s education website, INTENSIVE.  He created the ‘Critically Ill Airway’ course and teaches on numerous courses around the world. He is one of the founders of the FOAM movement (Free Open-Access Medical education) and is co-creator of litfl.com, the RAGE podcast, the Resuscitology course, and the SMACC conference.

His one great achievement is being the father of three amazing children.

On Twitter, he is @precordialthump.

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